Iactacon 2016

19th Annual
National
Conference
Souvenir & Lecture Notes
Presidents Message:
Today, the Chennai city has been bestowed with a rare honor of holding the IACTA annual national conference for
the 3rd time. The only city in the country to get this distinction and it fills me with pride as a Chennaite, and as the
President of IACTA to welcome you all to the IACTACON 2016.
Our association has grown immensely from a mere 30 40 founding members in the year 1997 to its present strength
of 1500 members. I am convinced that this growth will be sustained to shape our organization into a much stronger
and larger one. But, that in itself should not be sufficient or satisfying, because we also have to ensure that this growth
goes in the right direction. To ensure we are doing just that, we need to set some goals and objectives for the next
decade for IACTA. Hence, I propose the following,
Academics: We should strive to be the best academic group among all the medical fraternities in the country. We
have a large volume of data in our country and we should encourage the translation of our clinical work into
academic work. We need to encourage and promote publications. Our associations journal is indexed and it is
currently one of the only two English journals of the official societies in the world for cardiothoracic anesthesia.
Our continued focus in this area would lead to more research and thereby establish our associations standing as a
pioneer in this field.
Becoming leaders in the global field of cardiothoracic anesthesia: We must make it our mission to be the leaders in
the practice of cardiac anesthesia in the world. This can only be possible by having a uniform standard of patient
care across the country that is based on safety and quality. Only that can help us achieve our goal and reach the
zenith of excellence in cardiothoracic anesthesia in the world.
We must ensure that we nurture, encourage and protect young talent and mentor them, so as to establish a strong
and learned, future generation of cardiac anesthesiologists, who will focus on patient care, education and research.
To develop robust and country specific good practice guidelines
To collaborate with other co-specialties
Let us Learn, Advance and Excel..

We also need to increase our membership further. We need to embark on and promote the formation of regional
associations and encourage them to enroll more members and conduct periodic scientific meetings.
History has been created in IACTA, The IACTA education and research cell has transformed into the more formal
Indian College of Cardiac Anesthesia, this will help us not only to sustain but also to advance further in all our
academic endeavors.
Tremendous amount of effort has been put in by the IACTA TEE committee under the guidance of IERC into the
development of curriculum and guidelines along with the conduct of perioperative TEE fellowship examination and
certification. Many, national and international collaborations have strengthened these efforts. A new set of guidelines
for centre recognition for TEE training have been developed. IACTA wishes to take the perioperative TEE training
to greater heights to benefit many more patients, provide easy training opportunities to many young aspiring cardiac
anesthesiologists and practicing anesthesiologists.
So, friends, let us all join hands to advance the IACTA to achieve these goals and reach greater heights!!
With these words, I once again welcome you to this conference, Have a wonderful time at this lovely venue!
Regards
Dr.Mahesh Vakamudi
President, IACTA
Message
Dear distinguished guest of this conference,

As the secretary, it is my honor and privilege to extend a warm invitation to all
the participants of the 19th Annual National Conference ofIndian Association of
Cardiovascular Thoracic Anaesthesiologists. The overwhelming response to this
conference is a signal that our commitment to IACTAs objectives remains steadfast.
The organizing committee has managed to bring together a host of eminent faculty
of national and international repute to share their expertise with us. The scientific
committee have arranged an array of basic and advanced workshops in addition to
thematic academic sessions. The scientific deliberations will widen the understanding
of postgraduate students and practicing cardiac anesthesiologists in the safe patient
management and also will create a research aptitude. I am sure that the galaxy of
international faculty will impart the latest knowledge to teachers, students and
practitioners so that our day to day practice rises to international standards.
Furthermore, the scientific deliberations (75 plus lectures, pro-con sessions,panel
discussions, problem based learning discussions and workshops} of this meeting will
help leveraging the intersection of leadership, practices and technologies to generate
transformational performance in cardiothoracic anesthesia & critical care where
failure is not an option.
Apart from the scientific program, I invite you to enjoy your stay and sightseeing.
The conference venue, RadissonBlu Temple Bay Mamallapuramis a prime location off
the East Coast Road (ECR) near fantastic attractions like Shore Temple and Krishna
Mandapam. It is a much sought after tourist destination in Tamil Nadu. I am sure you
will return from IACTACON 2016 more than satisfied.
Jai IACTA.
With warm regards
Dr. Thomas Koshy
National Secretary, IACTA
Professor in Cardiac Anesthesiology& Associate Dean
SreeChitraTirunal Institute for Medical Sciences & Technology
Trivandrum, Kerala, India
Message
Dear colleagues,
Greetings from IACTA Chennai.
On behalf of IACTACON 2016 organising committee it is my great pleasure and
privilege to extend a warm welcome to you all to the 19th Annual Conference of
Indian Association of Cardiovascular and Thoracic Anaesthesiologists to be held
at Chennai from 12th to 14th February 2016. I take this opportunity to thank the
IACTA National Committee for entrusting upon us the responsibility of organising
this prestigious annual meet.
IACTA Chennai is fortunate to host this conference for the third time. The first
national conference of IACTA was conducted in the year 1997 and the second one in
2009. Apart from the three national conferences IACTA Chennai branch has hosted
Annual Cardiac Anaesthesia update 11 times so far.
The IACTACON 2016 scientific program has been carefully planned to include entire
gamut of topics from basics to recent advances in the field of Cardiac anaesthesia and
Cardiac Critical Care. Renowned National and international faculty will be deliberating
and discussing these topics.
Besides the scientific programme the social events will give you the opportunity to
experience the essence of local culture and cuisine. The venue of the conference
Radisson Blue Temple Bay resort provides a perfect ambience with its sylvan
atmosphere, an ideal locale for academic activity and relaxation. The organising
committee under the stewardship of Dr Mahesh Vakamudi, has left no stone unturned
to make your stay comfortable and memorable.
With Warm Regards,
Dr P.S.N.Raju
Message
Dear Colleagues,
It gives me great pleasure to welcome you all for the scientific sessions of IACTA 2016.
The scientific committee did the hard yards to put up a well-crafted programme for
the conference. The senior Chennai faculty extended their helping hand in preparing
the scientific schedule.
We have introduced PBLD (Problem Based Learning Discussion) and audience
response system for the first time in this conference. We have also incorporated
workshops on Trans-Esophageal Echo, ECMO, Thoracic anesthesia, ultra sound in
critical care, Pro & Con sessions, Panel discussions, and didactic lectures on relevant
topics. We have also encouraged the free scientific paper presentations by providing a
dedicated hall for the same.
We were very fortunate to have renowned faculty from both India and abroad for this
conference. We have provided enough opportunity for the younger upcoming speakers
keeping the futuristic view. The scientific committee has taken greater efforts to choose
the faculty best in the field for each topic. I am sure you will have an excellent scientific
extravaganza at the conference.
On behalf of the scientific committee, I express my sincere gratitude to all the faculty
members who readily accepted our invitations in spite of their busy schedule and
co-operated with us within a short notice. I thank you all anticipating your active
participation.
Dr. Suresh Rao K.G

Chairperson
Scientific Committee-IACTA 2016
IACTA NATIONAL EXECUTIVE COMMITTEE

President
Secretary
Treasurer
Senior Vice President
Assoc: Vice President
Chief Editor
Special Invitees

Dr. Mahesh Vakamudi

Dr.Thomas Koshy
Dr. Abraham Cherian
Dr. Mukul Kapoor
Dr. Rajeev Lochan Tiwari
Dr. Poonam Malhotra/Dr. Praveen Kumar Neema
Dr. Gopinath R
Dr. Kanchi Muralidhar
Dr. Rajiv Juneja
Dr. Yatin Mehta
Executive Council
Dr. Dheeraj Arora

Dr. Jacob Abraham

Dr. Jayaprakash K

Dr. Kumar S

Dr. Navneet Mehta
Ex-officio Members

Dr. Neeti Makhija

Dr. Pradeep Goyal
Dr. Pradeep Poswal
Dr. Rajesh Arya
Dr. Saibal Roy Chowdhury
Dr. Murali Chakravarthy

Dr. Suresh G.Nair
IACTA CHENNAI CITY BRANCH

PRESIDENT
Dr. SHASHIDHAR.B
SECRETARY
Dr. KANAGARAJAN.N
JOINT SECRETARY
Dr. NEDUMARAN .K
ADDITIONAL JOINT SECRETARY Dr. SITARAM .A.K

TREASURER
Dr. RANJITHA B.KARTHEKEYAN
EXECUTIVE COMMITEE
Dr. CHARANJIT KAUR
Dr. SATHISH .R
Dr. SHAPNAVARMA
Dr. ASHOK .K
Dr. MUTHUVIJAYA SANKAR
Dr. GOKULAKRISHNAN .M
Dr. MURALIKRISHNA .T
Dr. SUJATHA D.I
ADVISORS
Dr. NAIDU .I.S
Dr. BHASKARAN .K
Dr. RAJU .P.S.N
Dr. MAHESH VAKAMUDI
Dr. BENJAMIN NINAN
Dr. SURESH RAO .K.G
International Fuculty - IACTA CHENNAI 2016

Dr. Chandra Ramamoorthy
Dr. Roy Sheinbaum
Dr.Madhav Swaminathan
Dr.Francois Roodt
Dr. Suresh Chengode
Dr. Ruben
Dr.Chirojeet
Dr. Kumar Belani
Dr.Joerg Ender
Dr. Madan Mohan Maddali
Dr. Peter Norman
Dr.Jagtar Singh Heir
Dr. Achal Dhir
Dr. Mahesh Prabhu
Dr. Douglas B Coursin
Dr.Sheela Cole
Dr.William Zev Rymer
Dr. Suresh Santhanam
Dr.Swaroop Margale
Dr. Rajagopal Kailasam
Dr.Justiaan Swanevelder
Dr.Harikrishnan Kothandan
Dr. Shital Shah
Dr. Sudhakar Subramani
Dr. Dilip Thaker
Dr. Rajesh Bhavsar
National Faculty - IACTA CHENNAI 2016

Dr. K.Muralidhar
Dr. Deepak Tempe
Dr. Ganapathy
Dr. Gopinath R
Dr. Praveen Kumar Neema
Dr. Manjula Sarkar
Dr. Murali Chakravarthy
Dr.Srinivas Gondhi
Dr. Rahul Guhabiswas
Dr. Sreedhar Joshi
Dr. Selvakumar
Dr. Rajesh Chand
Dr.Nedumaran
Dr.Sandeep Mutha
Dr. Shapna verma
Dr Kumar S
Dr.T A Patil
Dr.Kumar C
Dr.Pankaj Kundra
Dr.Rajesh Kumar Kodali
Dr.Prabhakar
Dr.Navneet Mehta
Dr.Srinivas C
Dr.Sanjeeta Umbarkar
Dr.Satyen Parida
Dr.Jayaprakash
Dr.Sathish Dharmalingam
Dr.Vinod Parashar
Dr.Sanjivini Inamdar
Dr.N M Kumar
Dr.Nithya
Dr.Vijay Shety
Dr.Hanumantha Rao
Dr.Prasanna salvi
Dr.Srikanth
Dr.Ravi Shankar
Dr.Puneet Goyal
Dr.Alok Kumar
Dr.Shashi Kiran
Dr.Usha Kiran
Dr.Sachin Patil
Dr.Y.Ramesh
Dr.Vijaya Shankar
Dr. Suresh G Nair

Dr. Mukul Kapoor
Dr. Abraham Cherian
Dr. Thomas Koshy
Dr. Benjamin Ninan
Dr. Poonam Malhotra Kapoor
Dr. Prabhat Tiwari
Dr. Bhaskaran
Dr. Deepak borde
Dr. Kanakaraj
Dr. Satish R
Dr. Dharmesh Agarwal
Dr.Sujatha DI
Dr. Neethi Makhija
Dr. Rajeev Tiwari
Dr.Nilesh Juvekar
Dr.Venugopal Kulkarni
Dr.Murali Krishna T
Dr.Sharan Patil
DR. Jagadeesh, A M
Dr.Nagarajan
Dr.Ashok
Dr.Deepa Kane
Dr.Minal Vora
Dr.Masthanamma
Dr.Rakesh
Dr.Balamurugan
Dr.Jayaraman
Dr.Manjunath
Dr.Pradeep Goyal
Dr.Ravikant
Dr.Sibal Roy Chowdhary
Dr.Garach
Dr.Ajmer Singh
Dr.Shrinivas
Dr.Shastri
Dr.Vellingiri
Dr.Mohan Swami
Dr.Subramanian C
Dr.Vijeesh Venugopal
Dr.Anil Sant
Dr.Arun Maheswari
Dr.Ayya Syama Sundar
Dr. Naman Shastri

Dr.Dheeraj Arora
Dr. Udhay Gandhe
Dr. Vipul Sharma
Dr. Sitaram A K
Dr. Rajiv Juneja
Dr. Yatin Mehta
Dr. Manju Bhutani
Dr. Rajesh Arya
Dr. Rakhi B
Dr. Vishwas Malik
Dr. Suresh Rao K G
Dr. Shrinivas Gadhinjkar
Dr. Shashidhar
Dr. Jacob Abraham
Dr.Vinayak Desurkar
Dr.Harish R
Dr.PSN Raju
Dr.Ranjith Karthekeyan
Dr. Gokula Krishnan
Dr.Kamalesh Tailor
Dr.Palaniappan
Dr.Prabhu Mayakesavan
Dr.Alok Samantaray
Dr.Anand Vagrali
Dr.Manikandan
Dr.Pradeep Poswal
Dr.Malleswar
Dr.Rupa Sreedhar
Dr.Vishwas Nivargi
Dr.Tomar
Dr.Leena Pawar
Dr.Sunil Dhole
Dr.Anuradha Mahendar
Dr.Minnati
Dr.Pravin Saxena
Dr.Ramesh Kashav
Dr.Ponnambalan
Dr.Mahesh Vakamudi
Dr.Unni Krishnan
Dr.Shilpa Bojraj
Dr. Ramesh Srigiri
Dr.Raj Sahajanandam
TIME
8:30 - 9:30
9:30 - 9:40
REGISTRATION
LAMP LIGHTING
HALL A
Lectures
Chairperson-Dr.Prabhakar, Bangalore &
Dr.Nagaraj, Hyderabad
9:45 - 10.10 Perioperative MI after CABG: Classification and

management- New insights
Dr. K.Muralidhar, Bangalore
10:15-10:40 Single ventricle physiology: A comprehensive

review
Dr. Chandra Ramamoorthy, USA
10:45-11:10 Myocardial protection during cardiac surgery
Dr. Suresh Nair, Kochi
Integrating 3D TEE in the OR workflow
Dr. Naman Shastri, Ahmedabad
Mediastinal mass: Anesthesiologists' Nightmare?
Pro and Con Session

Moderator- Dr.Narendra Garach, Mumbai
Cell salvage is beneficial in all patients

undergoing vascular surgery
Anesthesiologists should routinely be present in

cardiac cath lab
Pro : Dr.Dheeraj Arora, Delhi

Con : Dr. Ganapathy, Chennai
Chairperson-Dr.Prabhu
Mayakesavan,Chennai & Dr.K.Ashok,
Chennai
How I do it
Pro : Dr. Abraham Cherian, Kochi

Con : Dr. Uday Gandhe, Mumbai
Chairperson-Dr.Hari Krishnan, Singapore &
Dr.Leena Pawar, Mumbai
12:25-12:50 Heart Brain Cross talk: What do we need to

know?
Dr. Gopinath, Hyderabad
12:55 - 1:20 Management of failing Fontan
2:25 - 2:50
Perioperative management of the congenital

cyanotic Parturient
Pro and Con Session

Moderator- Dr.Jayaraman, Chennai
Dr. Mukul Kapoor, Delhi

Lectures
Dr.Chandra Ramamoorthy, USA

LUNCH
Chairperson-Dr.Srinivas C ,Chennai &
Dr.Deepa Kane,Mumbai
How I do it
HALL C
Lectures
Chairperson-Dr.Shital Shah, Singapore &
Dr.Prasanna Salvi, Mumbai
Dr. Thomas Koshy, Thiruvananthapuram
12:00-12:20 Fluid management in cardiac surgery - Which

fluid and how much?
2:00 - 2:20
HALL B
Dr. Deepak Tempe, Delhi
11:10-11:25 TEA
11:25-11:55
1:20 - 2:00
DAY 1
How I do it
Renal protection in cardiac surgery - An overview
Dr.Madhav Swaminathan, USA

Lectures
Regional anesthesia in adult cardiac surgery
Dr. Roy Sheinbaum, USA
Understanding diastolic dysfunction and diastolic

Heart failure
Dr.Francois Roodt, South Africa

Chairperson-Dr.Ravikant,Hyderabad &
Dr.Sanjeeta Umbarkar,Mumbai
How I do it
Perioperative management of an adult with

congenital heart disease
Anesthesia for pneumonectomy
Dr. Suresh Chengode, Muscat

Lectures
Dr. Ruben, Singapore

Lectures
Heart as a pump
Echo Navigation in interventional cardiac surgery
Dr. Pankaj Kundra, Puducherry

Chairperson-Dr.Minal Vora,Chennai &
Dr.Vijish Venugopal,Calicut
Dr.Chirojeeth Mukerjee, Germany

Chairperson-Dr.Satyen Parida, Puducherry &
Dr.Masthanamma, Chennai
Executive Council
Meeting
2:55 - 3:20
Perioperative temperature management in

cardiac surgery - The ill effects!
Anesthetic challenges in patients with

multivalvular heart disease coming for a double
valve replacement
3:25 - 3:50
Analgesia and sedation post cardiac surgery - Do What is new in ventricular support: Review of
we need to bother?
VAD technologies
Dr. Vipul Sharma, Delhi
Dr. Praveen Neema, Raipur
Dr. Kumar Belani,USA

TEA
Chairperson-Dr.Anand Vagrali, Belgaum &
Dr.Jayaprakash K, Bangalore
Dr.Jeorge Ender,Germany
3:50 - 4:05
Chairperson-Dr.Rakesh, Mangalore &

Dr.Ramesh Kashav, New Delhi
4:05 - 4:30
Anticoagulation in cardiac surgery: Problems

with heparin sensitivity, resistance, dosing and
alternatives
4:35 - 5:00
Antiplatelet agents and cardiac anesthesia: Quo

vadis?
5:05 - 5:30
Preop preparation and optimization for cardiac

surgery
Post cardiac surgery hemodynamic monitoring:

how to interpret the data?
Dr. Rajiv Juneja,Delhi
Dr. Madan Mohan Maddali,Muscat
Dr. Benjamin Ninan,Chennai

Dr. Manjula Sarkar,Mumbai
Risk factors for periop sepsis in cardiac surgery
Dr. Seetaram, Chennai
Advanced Hemodynamic monitoring (GEDV):

What, when and why?
Dr.PoonamKapoor,Delhi
PBLD
5:30 - 6:15
Prosthetic valve assessment on echo
Dr.Madhav Swaminathan,USA
ST elevation post grafting in a CABG
6:30 onwards
Dr.Jagdeesh A M,Bangalore
Difficult weaning of a paediatric patient post

cardiac surgery from ventilator
Dr. Chandra Ramamoorthy,USA

INAUGURATION/LIFE TIME ACHIEVEMENT AWARD
DAY 2
TIME
7:30 - 8:25
HALL A
BREAKFAST SESSION
HALL B
Arrest in post cardiac surgery ICU - current

guidelines
Lung Isolation - Newer techniques
Dr. Peter Norman,USA

Chairperson-Dr.Sathish Dharmalingam,
Vellore/Dr.Balamurugan,Madurai
Dr.Jagathar Singh,USA
Chairperson-Dr.Pradeep Poswal,New Delhi /
Dr.Unni Krishnan,Thiruvananthapuram
Lectures
Free Papers
Lectures
8:30 - 8:55
Hemodynamic rescue in the OR: TEE as a

compass
9:00 - 9:25
Management of RV Dysfunction in Cardiac

Surgery
Predicting new onset AF in cardiac surgery

patients
Dr. Ranjith Karthekeyan,Chennai
Dr. Mahesh Prabhu,UK
Dr. Achal Dhir,Canada
HALL C
Practice changing publications in the field of

cardiac anesthesia and intensive care in the last
five years
Dr. Murali Chakravarthy,Benguluru
9:30 - 10:00 Plenary Session - (Chairpersons-Dr.Vinod Parashar,Jaipur & Dr.P.S.N.Raju,Chennai)
Transfusion Therapy in Perioperative or Critically Ill Patients - Dr. Douglas Coursin,USA
10:00 - 10:45 Brig P N Bhatt Oration - (Chairperson - Dr.Mahesh Vakamudi,Chennai) Electronic data management in OR and
10:45 - 11:00
11:00 - 12:30
ICU: Accurate information begets enhanced patient care -Dr. Prabhat Tiwari,Lucknow
TEA
Janak Mehta Best Paper Award
Chairperson-Dr.Malleshwar,Hyderabad &
Dr.Sanjivini Inamdar,Pune
Lectures
12:35 - 12:55 Anesthetic management of robotic cardiac

surgery
Dr. Yatin Mehta,Delhi
Chairperson-Dr.C.Subramanian,Hyderabad &
Dr.Sachin Patil,Mumbai
Lectures
Anesthetic management of interrupted aortic

arch / Hypoplastic LV
Dr.Kamlesh Tailor,Mumbai
1:00 - 1:20
Anesthesia for VAD placement: Clinical pearls
TAPVC - Anesthetic Management
1:20 - 2:00
2:00 - 3:00
Dr.Sheela Cole, USA

LUNCH
Panel Discussion
Dr.Shastri,Hyderabad
3:00 - 3:30
Panel Discussion
Low cardiac output syndrome
Organ protection on CPB
Moderator: Dr. P.S.N.Raju,Chennai

Panel List -Dr.Alok
Samantharay,Tirupathi/Dr.Anil
Sant,Pune/Dr.Shilpa Bojraj,Mumbai/
Dr.Y.Ramesh,Vijayawada/Dr.N M
Kumar,Chennai
Pro and Con Session
Moderator:Dr.Rupa
Sreedhar,Thiruvananthapuram
Moderator: Dr. Manju Bhutani,Mumbai

Panel List -Dr.Arun Maheswari,Delhi/Dr.
Ramesh Srigiri,Delhi/Dr.Usha
Kiran,Delhi/Dr.Manjunath,Benguluru/Dr.Nar
endra Garach,Mumbai
Pro: Dr. Rahul Guha,Kolkata

Con: Dr. Deepak borde,Mumbai
Chairperson-Dr.Pradeep Goyal,Rajastan &
Dr.Shrinivas,Chennai
Symposium - CPB Disasters
Pro: Dr. Rajesh Arya,Ludhiana

Con: Dr. Sreedhar Joshi,Bangalore
Chairperson-Dr.Nithya,Delhi & Dr.
Pro and Con Session

Moderator: Dr.Ponnambalan,Chennai
TIVA vs inhalational anesthesia in cardiac surgery Liberal vs restrictive transfusion in cardiac

surgery
3:30 - 3:45
Sudden unexpected aortic dissection
Symposium - Pulmonary Circulation
Anesthesia for pulmonary endarterectomy
ICCA Board
Meeting
Dr.Vijaya Shankar,Chennai
3:45 - 4:00
Massive air embolism
4:00 - 4:15
Vasoplegia and its management
4:15 - 4:25
Discussion on all topics
Dr. Sharan Patil,Belgaum

Dr. Selvakumar,Madurai
Dr. Kanakarajan N,Chennai
Perioperative Implications of Severe Pulmonary

HTN
Dr. Rakhi B,Kochi
Inhaled Pulmonary Vasodilator Therapy
Dr. Satish R,Chennai
Chairperson-Dr.Vishwas Nivargi,Pune &

Dr.Manikandan,Madurai
Chairperson-Dr.Ashok Shankar
Badhe,Puduchery & Dr.Navneet Mehta,
Jaipur
Symposium - Monitoring in cardiac surgery
Symposium - Minimally invasive CABG
4:30 - 4:45
Cardiac biomarkers
4:45 - 5:00
Should we be monitoring depth of anesthesia

during CPB?
5:00 - 5:15
Monitoring Cerebral Blood Flow during CPB
Dr.Viswas Malik,Delhi
Dr. Rajesh Chand,Delhi
Dr.Srinivas Gondhi,Vijayawada
5:15 - 5:25
5:30 - 7:00
GBM
7:00 onwards BANQUET
OPCAB Vs ONCAB - Do we have the final

judgement?
Dr.Bhaskar, Chennai
Percutanous Aortic Valve Replacement
Dr. Rajagopal,UK
Minimally invasive CABG
Dr. Dharmesh Agarwal,Bangalore
DAY 3
TIME
8:30 - 8:55
9:00 - 9:25
HALL A
HALL B
Chairperson-Dr.Vellaingiri,Chennai & Dr.Sibal Chairperson-Dr.Minnati,Delhi &

Roy Chowdhary,Kolkata
Dr.Palaniappan,Coimbatore
Anesthesia for heart transplantation
Predictors of failures in fast track cardiac surgery
HALL C
Editorial Board
Meeting
Dr.Suresh Rao,Chennai
Dr.Nedumaran,Chennai
Plenary Session-Acute Intermittent Hypoxia (AIH) As Therapy For Incomplete Spinal Cord Injury: Exploratory
Findings-Dr.William Zev Rymer,USA - (Chairperson- Dr.M.Hanumantha Rao, Tirupathi& Dr Mohan
swami,Pune)
Plenary Session-Regional anesthesia in pediatric cardiac surgery - is it time to make it a standard of practice?
Dr. Suresh Santhanam,USA - (Chairperson-Dr.Vipul Sharma,Delhi)
10:00 - 10:45 Dr V A Punnose Oration-The Value of Cardiovascular Anaesthesia to Perioperative Medicine-Dr.Justiaan
Swanevelder, South Africa - (Chairperson - Dr.Mukul Kapoor,Delhi)
10:45 - 11:00
TEA
Chairperson-Dr.Sunil Dhole,Delhi & Dr.Alok Chairperson-Dr.Pravin Saxena ,New Delhi&
Kumar,Chandigarh
Dr.Puneet Goyal,New Delhi
Symposium - Blood
Symposium - Vascular
11:00 - 11:15 Albumin in cardiac surgery -current status
Managing anestheisa for Arch Aneurysm repair. Executive Council
Meeting
Dr.Sujatha,Chennai
Dr.Vijay Shety,Mumbai
9:30 - 9:55
11:15 - 11:30 Factor concentrates: An update
Dr.Shashi Kiran,Rohtak
Endovascular repair: Anesthetic management
Dr. Shrinivas
Gadhinjkar,Thiruvananthapuram
11:30 - 11:45 Point of care coagulation monitoring: Which tests Aortic dissections - Anesthetic Challenges
and when?
Dr.Sandeep Mutha,Pune
11:45 - 11:55 Discussion on all topics
Chairperson-Dr.Ajmer Singh,New Delhi &

Dr.Ravi Shankar,Hyderabad
Symposium - Drugs
12:00 - 12:15 Dexmedetomidine in cardiac surgery
Dr. Shashidhar,Chennai
12:15 - 12:30 Antifibrinolytics in cardiac surgery- No more

contriversies?
Dr. Rajeev Tiwari,Jaipur
12:30 - 12:45 Myocardial protection by inhalational agents
Dr.Ayya Syama Sundar,Hyderabad
12:45 - 12:55 Discussion on all topics

1:00 - 2:00 LUNCH
2:00 - 5:00 WORKSHOP
Advanced TEE
Dr. Neethi Makhija,Delhi
Chairperson-Dr.Srikanth, Hyderabad &

Dr.Anuradha Mahendar,Chennai
Symposium - Critical Care
Is there a place for corticosteroid treatment

anymore?
Dr. Shapna,Chennai
Is low tidal volume ventilation low enough?
Dr. Jacob Abraham,Kochi
What are the best glucose and HbA1C values for

patients undergoing cardiac surgery
Dr Kumar S,Madurai
Thoracic Anesthesia
Dr.Thomas Koshy/Dr.T A Patil /

Dr.Venugopal Kulkarni / Dr.Harish.R /
Dr.Sudhakar Subramani/Dr.Kumar
Dr.Dilip Thaker/Dr.Gokula Krishnan/Dr.Roy

Sheinbaum/Dr.Peter Norman /
Dr.J.Singh/Dr.Raj Sahajanandam
ECMO Simulation
USG in Cardiac Critical Care
Dr.Swaroop Margale/Dr.Rajesh
Bhavar/Dr.Nilesh/Dr.Vinayak
Desurkar/Dr.Murali Krishna
Dr.Suresh Santhanam/Dr.Francois
Roodt/Dr.Douglas Cousin/Dr.Rajesh Kodali
Contents
Topic
Page No.
LECTURES
ALBUMIN IN CARDIAC SURGERY CURRENT STATUS
31
Dr. D. I. Sujatha,
Anaesthetic challenges in patients with multi-valvular heart disease coming for a

double valve replacement
38
Dr Praveen Kumar Neema, MD, PDCC
Aortic Arch Surgery-
44
Dr Vijay Shetty,
Acute Intermittent Hypoxia (AIH) As Therapy For Incomplete Spinal Cord Injury:
Exploratory Findings
48
William Z Rymer MD PhD
Predictors of Failures in
Fast Track cardiac Surgery
51
Dr.K.Nedumaran
Post cardiac surgery hemodynamic monitoring: how to interpret the data?
54
Dr. Madan Mohan Maddali, MD
Cell salvage is beneficial in all patients undergoing vascular surgery (CON)
60
Dr. Ganapathy Arumugam. C,
Cell salvage is beneficial in all patients undergoing vascular surgery (PRO)
66
Dheeraj Arora
Diastolic Function
69
Justiaan LC Swanevelder, Francois Roodt
73
Dr.R.Satish
TIVA Vs. Inhalational Anesthesia in Cardiac Surgery: Con
80
Liberal v/s restrictive use of transfusion in cardiac surgery: Pro
83
CARDIAC BIOMARKERS
88
HEART BRAIN CROSS TALK: WHAT DO WE NEED TO KNOW
91
PERIOPERATIVE MANAGEMENT OF INTERRUPTED AORTIC ARCH (IAA)
97
Dr. Deepak Borde, MD, DNB, FCA, FTEE.

Dr. Rajesh Arya,
Dr. Vishwas Malik, Dr. ArunSubramanium

DR.R.GOPINATH
Dr.Kamlesh Tailor
Renal Protection in Cardiac Surgery: An overview
104
Antiplatelet agents and cardiac anaesthesia: quo vadis
110
Madhav Swaminathan, MD, FASE, FAHA

Dr Manjula Sarkar
Contents
POINT OF CARE COAGULATION WHICH TEST AND WHEN? DR SANDEEP MUTHA
(PACPL PUNE)
120
PRO/CON - Liberal versus restrictive strategy of blood transfusion (CON)
133
Monitoring Cerebral Blood Flow during cardiopulmonary bypass
136
Anterior mediastinal masses, Anaesthesiologists nightmare
143
Anaesthesia for robotic cardiac surgery
149
TIVA Vs Inhalational Anesthesia in Cardiac Surgery
155
PRO/CON - Liberal versus restrictive strategy of blood transfusion (CON)
157
Low Tidal Volume Ventillation in ARD
159
Myocardial protection by inhalational agents
170
CPB DISASTERS - SUDDEN UNEXPECTED AORTIC DISSECTION
179
Dr SHREEDHAR S JOSHI MD., DM

Prof. Srinivas Rao G
Dr. Thomas Koshy,
Dr Yatin Mehta
Dr. Rahul Guhabiswas,
Dr Jacob Abraham
Dr A. Syama Sundar,
Dr.M.Vijayasankar., M.D.
JANAK MEHTA AWARD PAPERS

COMPARISON BETWEEN NON INVASIVE MEASUREMENT OF CENTRAL VENOUS
PRESSURE USING NEAR INFRARED SPECTROSCOPY WITH AN INVASIVE CENTRAL
VENOUS PRESSURE MONITORING IN CARDIAC SURGICAL ICU.
205
Dr N. Sathish, Dr Nagaraja P S, Dr Naveen G Singh, Dr. Sarala B M , Dr Manjunath N
FEASIBILITY OF MEASURING SUPERIOR MESENTERIC ARTERY BLOOD FLOW DURING

CARDIAC SURGERY UNDER HYPOTHERMIC CARDIOPULMONARY BYPASS USING TRANS
ESOPHAGEAL ECHOCARDIOGRAPHY AN OBSERVATIONAL STUDY.
211
Dr Nagaraja P S, Dr Naveen G Singh, Dr Divya Gopal, Dr Manjunath N
EFFECT OF DEXMEDETOMIDINE ON CORONARY VESSEL DIAMETER AND MYOCARDIAL

PROTECTION IN PERCUTANEOUS CORONARY INTERVENTIONAL PATIENTS
218
Dr Tanveer Singh Kundra, Dr Nagaraja P.S, Dr Naveen G Singh, Dr Manjunatha.N
THE ROLE OF NEUTROPHIL GELATINASE ASSOCIATED LIPOCALIN (NGAL) IN

PREDICTING ACUTE KIDNEY DISEASE IN PATIENTS UNDERGOING OPCABG: A PILOT
STUDY 224
Monitoring diastolic function using a simplified algorithm in patients undergoing off
pump coronary artery bypass grafting (OPCABG) surgery
230
Deepak Borde
Contents
ABSTRACTS
EuroSCORE II, STS and ACEF Scoring systems fail to predict outcome after Minimally
Invasive Direct Coronary Artery Bypass graft surgeries in Asian patients.
259
Dr.Antony George, Dr. Murali Chakravarthy,
2 mg/kg heparin is non-inferior to 3mg/kg in off-pump coronary artery bypass

surgeries: randomized, single center, blinded, noninferiority study
260
TRANSCATHETER AORTIC VALVE IMPLANTATION OUR EXPERIENCE.
261
HEMODYNAMIC EFFECTS OF PERIOPERATIVE DEXMEDETOMIDINE THERAPY IN

VALVULAR HEART SURGERIES A RANDOMIZED CONTROL TRIAL
262
APPLICATION OF BLOOD CONSERVATION STRATEGY IN A RARE BLOOD GROUP

PATIENT - CHALLENGES FACED IN PERIPHERAL CENTRES
263
MITRAL VALVE REPLACEMENT USING CHITRA HEART VALVE PROSTHESIS:

INTRAOPERATIVE TRANSESOPHAGEAL ECHOCARDIOGRAPHY EVALUATION
264
LA Aneurysm A case report
265
Minimizing blood and blood product usage in open heart surgery by simple
approach of blood conservation.
266
Experience of an anaesthetist in a HYBRID operating room.
267

DR ASHUTOSH V. SHARMA,
Sambhunath Das, Neeti Makhija, Balram Airan, Gautam Sharma
Dr Satwik Telkar,Dr Madhuprakash,S C.Dr Manjunatha B N,Dr Srinivas Kulkarni
Dr Shrinivas Gadhinglajkar, Dr Jagadeesh N Vaggar, Dr Neelam Aggarwal,

Dr Rupa Sreedhar.
Dr Yogesh Z , Dr Amol T , Dr V.R. Shrotey
Dr. Sachin K. Nachane et al
Dr.KARUPPIAH.R, Dr. Mrugesh Prajapati
COMPARATIVE STUDY BETWEEN EFFECTS OF TRANEXAMIC ACID AND EPSILON AMINO

CAPROIC ACID IN ADULT VALVULAR HEART SURGERIES- RAMDOMIZED CONTROL
TRIAL
268
DR ISHA SAMADHIYA
MINIMALLY INVASIVE MITRAL VALVE REPAIR IN POST RENAL TRANSPLANT PATIENTPERIOPERATIVE MANAGEMENT
269
Dr. Jigisha Pujara, Dr. Nirav Parikh, Dr. Alpesh Sarvaiya
INTRA-OPERATIVE AUTOLOGOUS DONATION REGULATES INCREASE IN THORACIC

FLUID CONTENT IN PATIENTS UNDERGOING HEART VALVE REPLACEMENT ON
CARDIOPULMONARY BYPASS
270
Jitin Narula, Usha Kiran, Poonam Malhotra Kapoor, Minati Choudhury,
Ujjwal Kumar Chowdhary,
An innovative way to reinsert dislodged Arndt blocker using urological glide wire 271
Melvin Alex Abraham, Rahul Pillai, Sneha Ann Ancheri, Sathish Kumar,
Raj Sahajanandan*
CARDIAC TUBERCULOSIS AN UNUSUAL PRESENTATION

Dr.Naresh Kumar T, GKNM hospital, Coimbatore
272
Contents
LEARNING EXPERIENCES OF TRANS-CATHETER AORTIC VALVE IMPLANTATION AT
MEDANTA: A CASE SERIES OF SIXTEEN PATIENTS
Dr Neeraj Kumar Sharma, Dr Rajeev Juneja, Dr Yatin Mehta, Dr Anand Kumar,
Dr Ravindra Sawhney, Dr Nagendra Chouhan, Dr Praveen Chandra,
Dr Naresh Trehan, Medanta,
273
IMPACT OF RETROGRADE AUTOLOGOUS PRIMING OF THE CARDIOPULMONARY

BYPASS CIRCUIT ON POST OPERATIVE HEMODILUTION AND BLOOD TRANSFUSION
REQUIREMENTS 274
Prashant A Biradar, C Ganesan, Krishnanand Pai, P R Murugesan, M S Murugan,
CATASTROPHIC CORONARY STENT THROMBOSIS SECONDARY TO REVERSAL OF DUAL

ANTI-PLATELET THERAPY WITH PLATELETS.
275
Dr.RAJASEKAR.A
Early extubation in cases of septuagenarian and octagenarians undergoing on

pump CABG. A 2 yr single centre prospective study .
276
Dr Rakhi.K.R, Dr Nikhil,Dr Sunil Agarwal, Dr Gee Varghese, Dr Sajiv
QUANTIFYING THE PROPOSED BENEFITS FOLLOWING GOAL-DIRECTED THERAPY

(GDT) IN HIGH RISK CARDIAC PATIENTS UNDERGOING CORONARY ARTERY BYPASS
GRAFTING: A CLINICAL OUTCOME & BIOMARKER BASED STUDY
277
Dr.Rohan Magoon
MINIMALLY INVASIVE APPROACH FOR REDO VALVE SURGERY-A CASE SERIES
278
PHLEGMASIA CERULEA DOLENS FOLLOWING HEPARIN INDUCED

THROMBOCYTOPENIA {HIT} A CASE REPORT
279
LUTEMBACHER SYNDROME: DILEMMA OF DOING A TRICUSPID ANNULOPLASTY
280
TITLE: ANESTHETIC MANAGEMNT OF PULMONARY EMBOLISM-A CASE SERIES OF

TEN PATIENTS
281
Asias first heart and liver en bloc transplant case report
282
DIFFICULTY IN WEANING OFF CPB IN A CASE OF WILLIAMS SYNDROME WITH

SUPRAVALVULAR AORTIC STENOSIS
283
TRACHEAL INJURY FOLLOWING DOUBLE LUMEN ENDOTRACHEAL INTUBATION

A CASE REPORT
284
Posterior aortic root widening during aortic valve replacement : Role of

intraoperative transesophageal echocardiography
285
ULTRASOUND GUIDED SYMPATHETIC BLOCK AS A TREATMENT MODALITY

FOR ACUTE AS WELL AS CHRONIC ISCHEMIA OF THE UPPER LIMB
286
Mechanical circulatory support as a bridge to transplant: Our experience
287
Dr.Satya Swaroop Patnaik,
Dr.Shilpa bhojraj, Simin Mehta, Aliasgar Behranwalla,

Varsha A V, Gladdy George, Raj Sahajanandan
Dr Dhawal Wadaskar, Dr Bharati Tendolkar,Dr Shakuntala Basantwani

Dr Minal Vora, Dr Disha Khanpara, Dr Bhaskaran K,
Dr. Subha C.P, ,Dr.Minal Vora, Dr.Bhaskaran .K,
Dr Neelam Aggarwal ,Dr Srinivas Gadhinglajkar ,Dr Rupa Sreedhar
Dr. Rupa Sreedhar,Dr.Shrinivas Vitthal Gadhiglajkar
Dr. Ajay Aravind, Dr. Murali Krishna, Dr. Suresh Rao K G, Dr. K R Balakrishnan
Contents
Role of Transesophageal echocardiography during repair of Double Chambered
Right Ventricle (DCRV)
288
Amit Mathew, Melvin Alex Abraham, Raj Sahajanandan
BRIDGING BRONCHUS IN ASSOCIATION WITH CONGENITAL HEART DEFECT IN A 2

MONTH OLD INTERESTING CASE REPORT.
289
Dr.Anupama Mallappa, Dr .Shivanand Nandimiti,
Dr.Gangadhar Tagada Basavaiah, Dr Devananda Nijagal Shivanna
EFFICACY OF CONTINUOUS LOCAL ANAESTHETIC INFILTRATION AT STERNAL

WOUND SITE FOR POSTOPERATIVE ANALGESIA IN PATIENTS UNDERGOING
CARDIAC SURGERY BY MEDIAN STERNOTOMY
290
ASD closure in postpneumonectomy patient- Anaesthesia management
291
Banerjee Anusua, Sen Dasgupta Chaitali, Goswami Anupam
Dr Dhawal Wadaskar,Dr Bharati Tendolkar,Dr Shakuntala Basantwani
IMMEDIATE AND LONG-TERM OUTCOMES AFTER REPAIR OF ANOMALOUS

ORIGIN OF LEFT CORONARY ARTERY FROM PULMONARY ARTERY: RESULTS FROM
A LARGE SINGLE CENTER EXPERIENCE FROM A LIMITED RESOURCE ENVIRONMENT 292
Dr Jessin P Jayashankar, Dr Sunil GS, Dr Rakhi Balachandran,
Dr Amitabh C Sen, Dr Abraham Cherian , Dr Raman Krishnakumar
ANESTHETIC MANAGEMENT OF A 3.2 Kg JEHOVAHS WITNESS PATIENT FOR

SURGICAL REPAIR OF TRUNCUS ARTERIOSUS - A CASE REPORT
293
Effect of induction with etomidate and thiopentone on hemodynamic

responses in patients with left ventricular dysfunction due to coronary artery
disease undergoing coronary artery bypass graft surgery a pilot study
294
Transesophageal Pacing in a Neonate with Sick Sinus Syndrome Posted for

Emergency Laparotomy
295
MINIMAL ACCESS ATRIAL SEPTAL DEFECT CLOSURE- A SINGLE INSTITUTIONAL

RETROSPECTIVE REVIEW OF 56 CASES
296
PERIOPERATIVE VARIATIONS IN SERUM ALBUMIN PREDICT ADVERSE OUTCOME

AFTER CARDIAC SURGERY FOR TETRALOGY OF FALLOT REPAIR.
298
ELECTRICAL CARDIOMETRY: A RELIABLE SOLUTION TO CARDIAC OUTPUT

ESTIMATION IN CHILDREN WITH STRUCTURAL HEART DISEASE.
299
Outcomes of Midcab Vs Conventional CABG
300
EMPIRICAL TRANSFUSION OF BLOOD PRODUCTS IN CARDIAC SURGERY.

CAN YOU TRUST YOUR CLINICAL JUDGEMENT? AN AUDIT
308
Dr. Kaushik Jothinath, Dr. Vindhya Kumar, Dr. Shivananda Nadiminti,

Dr. Anupama Mallappa, Dr.Thirumuruga Pandian, Dr. Greeshma Prabhakar Gowdar,
Mr. Elayaraja, Ms. Vedasree Satyanarayana, Dr.Gangadhar, Dr. Devananda
Arindam Choudhury, Agarwal SMilind Hote,Chauhan U,Kiran U
Gladdy George, Varsha A.V, Raj Sahajanandan
DR ISHA SAMADHIYA
Jitin Narula, Poonam Malhotra Kapoor,Ujjwal Kumar Chowdhury, Sameer Taneja
Jitin Narula, Sandeep Chauhan, Saurabh Gupta, M Ramakrishnan

DR. JITUMONI BAISHYA , DR. MURALI CHAKRAVARTHY
Joseph Punnoose Paarel , Sathish Kumar D, Raj Sahajanandan
Contents
TITLE - A RARE CASE OF ADULT TOTAL ANOMALOUS PULMONARY VENOUS RETURN
(SUPRA CARDIAC TYPE) INTERESTING TRANSESOPHAGEAL ECHOCARDIOGRAPHIC
VIDEOS AND IMAGE
309
Dr. KARTHIK N, Dr. PARIMALA P SIMHA, Dr. MANJUNATHA N, Dr. LAKSHMI
SURGERY FOR TRUNCUS AND HEMITRUNCUS ARTERIOSUS: ANESTHESIA AND

ECHOCARDIOGRAP
310
Use of Methylprednisolone In Neonatal Cardiac SurgeryA Randomized Control Single Centre Trial
311
Comparison of USG guided Internal Jugular Vein Cannulation with traditional

landmark technique in paediatric patients for Cardiac Surgery.
312
Pediatric heart transplant our experience
313
Dr.Keerthi Chigurupati, Dr.Shrinivas Gadhinglajkar, Dr.Rupa Sreedhar,
Leena V. Chaudhari, Kamlesh B. Tailor, Shankar V. Kadam,

Smrutiranjan R. Mohanty, Suresh G. RaO
Dr Munir Ahmad Khan, Dr Devashish Chakravarty, Dr Milan Pendse.
Murali Krishna.T, Ajay Aravind, Suresh Rao.K.G. , K.R. Bala Krishnan
Pretreatment with Methylprednisolone versus lidocaine for attenuating propofol

injection pain: a randomized controlled trial.
314
Dr.Shivaprakash, Dr.Shiopriye , Dr.Satya Narayana Jagannath
Conscious sedation using dexmedetomidine for percutaneous transcatheter

closure of atrial septal defects: A single centre experience
315
Efficacy of Clonidine, as adjuvant,to 0.75% Ropivacaine for potentiation of

postoperative analgesia, when added in Supraclavicular Brachial plexus
blocks for upper limb vascular surgery
316
RED BULL IN PEDIATRIC CARDIAC INTENSIVE CARE UNIT
317
Pushkar M Desai, Dr Manjula Sarkar, Dr Sanjeeta Umbarkar
Rahul maria*, Ritesh Shah , M.H Parmar, Vaishali Sarvariya
Dr.Rahul Norawat, Dr.Deepa Sarkar, Dr.Reetesh Gupta, Dr.Jothi Muthu.
ABRUPT CARDIOVASCULAR COLLAPSE ON PARALYSIS IN A CHILD WITH TRAUMATIC

LEFT DIAPHRAGMATIC HERNIATION OF ABDOMINAL VISCERA.
318
Dr.Rajasekar A.
Diarrhea in a post heart transplant patient: Challenging as always
319
SUCCESSFUL REVASCULARIZATION OF THE CONGENTIAL LEFT MAIN CORONARY

ARTERY ATRESIA IN AN INFANT.
320
Dr. Rohit, Dr. Vidya Devarajan, Dr. Murali Krishna, Dr. Suresh Rao,
Dr. K.R. Bala Krishnan
Samrat. S. Madanaik, Anand Vagarali,Sharan Patil,Abhijeet Shitole.
ATRIAL SEPTAL DEFECT WITH HYPOPLASTIC RIGHT VENTRICLE: THERAPEUTIC DILEMMA 321
Varsha A.V, Gladdy George, Raj Sahajanandan
TITLE INTRAOPERATIVETRANSESOPHAGEAL ECHOCARDIOGRAPHY IN AV SEPTAL

DEFECTS; WHAT AND WHEN TO LOOK?
322
Dr Deepak Mathew ,Dr Srinivas Gadhinglajkar,Dr Rupa Sreedhar
LOBECTOMY FOR PULMONARY ARTERIOVENOUS MALFORMATIONS: ANAESTHESIA

AND PERIOPERATIVE CARE.
323
Dr Manjusha N. Pillai, Dr.Shrinivas Gadhinglajkar, Dr.Rupa Sreedhar,
Dr.UnniKrishnan.M,
Contents
ANAESTHETIC MANAGEMENT FOR PULMONARY THROMBO-ENDARTERECTOMY
324
SURGERY FOR LEFT ATRIAL MYXOMA: OUR TWELVE YEAR EXPERIENCE OF

ANAESTHESIA AND PERIOPERATIVE CARE
325
CARDIAC SURGERY POSTOPERATIVE ARREST AND RESUSCITATION- A SINGLE

INSTITUTION 3 YEAR RETROSPECTIVE STUDY OF PROTOCOL AND OUTCOME
326
CASE REPORT; LEFT VENTRICULAR MYXOMA, A RARE CASE
328
Dr Thushara Madathil, Dr Balasubrahmaniam, Dr.Poornima Kasthuri,

Dr Abraham Cherian,
Dr. Saravana Babu M.S, Dr. Shrinivas Gadhinglajkar, Dr. Rupa Sreedhar,
Dr. Vivek Pillai, Dr. Vargheese T. Panicker,
Ultrasound guided measurement of minimal transverse diameter of subglottic

airway (MTDSA) in determining the endotracheal tube size in paediatric patients. 330
Sureshkumaran, Rahul Pillai, Raj Sahajanandan
Stenting of carinal tumor in a patient with significant CAD (coronary artery disease) 331
Bilateral Stellate ganglion block and Cardiac denervation in case of long QT

syndrome with refractory ventricular tachycardia (Electrical storm)
Dr Dinesh Kumar DM, PDCC 1, Dr Prashant Kulkarni DM 2, Dr Shivanand Mch 3, Dr Murugesh
332
PATIENT OF SV ASD WITH PAPVC AND LSVC FOR MINIMAL ACCESS CARDIAC
SURGERY 333
ASD closure in postpneumonectomy patient- Anaesthesia management
334
A rare case of Idiopathic Tri-saccular Left Ventricular Outflow Tract (LVOT)

pseudo aneurysm masquerading as ruptured sinus of valsalva (RSOV)
compressing all major coronary arteries role of TransEsophageal
Echocardiography (TEE) in surgical correction
337
SIBBLINGS WITH JERVELL AND LANGE-NIELSEN SYNDROME FOR

VIDEOSCOPIC LEFT CARDIAC SYMPATHETIC DENERVATION
338
Dr Dhawal Wadaskar
Dr.M.Karthik Babu Murugessan,
Dr.T.Vikram Kumar Naidu, Dr.Hemang Gandhi, Dr.Rajesh Thosani,

Dr.Arvind Kumar Bishnoi, Dr.Varsha Sarvaiya
Anaesthetic management of a case of Gilberts syndrome for mitral and aortic valve
replacement with tricuspid valve plasty Role of
Transesophageal echocardiography.
339
Dr.Sundar Subash Singh
IMMEDIATE HYPOXIA AFTER ASD REPAIR CASE REPORT
340
RARE CAUSE OF EPICARDIAL PACING DYSFUNCTION - A NOVEL METHOD

TO DEAL WITH IT.
342
Dr.Amol Thakre
Dr Satwik Telkar,Dr Madhuprakash S C,Dr Srinivas Kulkarni.
A rare case of ruptured sinus of valsalva in the left coronary sinus into the left atrium 343
Dr Sathyanarayan J, Dr Syed Mudassar A, Dr Swathi Gundlakunta, Dr Shio Priye,
Dr Durga Prasad Reddy
PERIOPERATIVE MANAGEMENT OF CONGENITAL HEART DISEASE WITH

NEAR SYSTEMIC PULMONARY ARTERY PRESSURE
Muthu Vijayasankar, Anuradha Mahender, Gopal Karunanidhi Jaikaran,

Kasinadhan, Arunkumar.
344
LECTURES
IACTACON
Chennai 2016
ALBUMIN IN CARDIAC SURGERY

CURRENT STATUS
I
A
C
T
A
C
O
N
Dr. D. I. Sujatha,
Senior Consultant, Cardiac Anesthesia,
The Madras Medical Mission, Chennai
Human Albumin (HA) is the most common plasma protein synthesized by the liver.
It accounts to about 50-60% of total protein content of plasma and is responsible for
about 80% of intravascular colloid oncotic pressure [COP]. The albumin concentration
in plasma in healthy humans ranges between 3.3 and 5.2gm/dl. Albumin levels less
than 3gm/dl is considered to be hypoalbuminemia. The COP in healthy adults is about
25mmHg. The main physiological actions of albumin is the maintenance of COP,
vascular barrier function, binding and transport of substances in the blood (bilirubin,
drugs, toxins), free radical scavenger, platelet inhibition and antithrombotic effects. HA
is prepared from pooled human plasma by the process of fractionation, varying the
temperature, ethanol concentration, PH as shown in fig (1), we get different components
of plasma. The last fraction to be obtained is HA.
(Fig 1)
IACTACON 2016
HA is pasteurized at 60 C for 10 hours and disinfected. HA can be transfused to all patients independent of the blood
group. HA is available as 5%, 20% and 25%, 5% is iso oncotic. 20% and 25% are hyperosmotic. 5% HA is ideal
for volume replacement. 20% and 25% increase the oncotic pressure 4 and 5 fold of normal plasma albumin levels.
HA was first used in the World War II for 7 Navy Sailors who were badly burnt in pearl Harbour bombing. HA is a
physiological plasma volume expander, because of cost containment and limited availability it is essential to use HA
appropriately.
Indications for Albumin usage

Appropriate
Occasionally appropriate
1. Paracentesis
1. Volume replacement in cardiac surgery as last

choice after using crystalloids and non-protein colloids
2. Major surgery
2. Therapeutic plasmapheresis
3. Cirrhosis of liver with refractory ascites
3. Spontaneous bacterial peritonitis
4. Contraindications to the use of non-protein

colloids.
5. Hepato renal syndrome
6. Nephrotic syndrome
The formula used for HA supplementation:

Dose (gm) = [Desired albumin concentration (2.5 gm/dl)Actual albumin concentration (gm/dl)]
x Plasma volume (0.8 x kg)

How does albumin work?
Movement of fluids between intravascular and extravascular compartment is no more dependent on older concept
of vascular permeability based on Ernest Starling principle 1896.
Trans capillary Exchange Starling principle
(Fig 2)
32
LECTURE
Starlings equation:
F / A / T = HC x [(PC PIF) (P IF)]
F / A / T Net filtration per unit area per time to be driven by the hydrostatic pressure difference between the
vascular lumen and the interstitial space (PC PIF) and limited by the opposing oncotic pressure within the vascular
lumen, suctioning fluid from the protein-low interstitial compartment (P IF), the effective fluid flux resulting from
these 2 opposing forces is determined by hydraulic conductivity (HC), a primary property of the vascular barrier
(30).
The Timely Model of Vascular Barrier Function

The newer concept is based on the Timely Model of Vascular Barrier function which emphasizes an important
structure called Endothelial Glycocalyx (EGL) as a key determinant for movement of fluid between intra and
extravascular compartment.
Role of Endothelial Glycocalyx
( Fig 3)
Endothelial Glycocalyx is an important filament like structure attached to the endothelial surface layer. It consists of
proteoglycons and glycosaminoglycons carrying negatively charged side chains which has strong affinity to albumin.
Albumin with EGL form the endothelial surface layer functioning as a vascular barrier. Fig 3 shows the normal
and injured EGL
33
IACTACON 2016
Modified Starlings Model

Endothelial Glycocalyx Vascular barrier function
(Fig 4)
Fig 4, shows the schematic view of the Modified Starlings Model, The Endothelial Glycocalyx forming a vascular
barrier with Albumin(Adapted from Beckel et al, 31). There is strong attractive forces for Albumin on endothelial
glycocalyx. Albumin adheres to EGL forming a layer inside the vascular lumen called Endothelial Surface Layer.
There is a space below the endothelial surface layer which is protein free space, allowing an inward oncotic force
at the luminal side of the endothelial cell line (dark gray arrow). This modified starlings model explains that the
hydrostatic pressure within the vascular lumen (light gray arrow) pushes the fluid out while this is counteracted
by the inward oncotic pressure exerted by Albumin forming a vascular barrier with endothelial glycocalyx The
Endothelial glycocalyx with Albumin plays a important role as vascular barrier against capillary permeability.(31) The
EGL is degraded during ischemic reperfusion injury on CPB, by inflammatory mediators released on CPB, sepsis,
stress, hyperglycemia, trauma, diabetes.
EGL degradation and protection

(Fig 5)
34
LECTURE
Figure 5 shows A- normal EGL, B degraded EGL, C Albumin pretreated coronary grafts.
Pre-treatment of the coronary grafts with antithrombin, albumin, Corticosteroids protects the glycocalyx from
degradation (1). Studies have shown that the usage of 0.9%. Saline have damaged EGL when compared with colloids
and there was more cardiac interstitial edema in saline group vs colloid group which might be due to damage to EGL
and disruption of vascular barrier (2, 3, 4)
Role of pre operative and post operative albumin levels:

Low pre operative levels of pre Albumin and Albumin less than 3 gm/dl both in adults and paediatric cardiac surgical
patients are associated with increased risk of post surgical infection, increased incidence of morbidity, mortality
and increase in the duration of ICU and hospital stay (5, 6, 7, 8). Interestingly post operative hypoalbuminemia
immediately after off-pump coronary artery bypass surgery is associated with adverse outcomes (9). Immediate post
surgical hypoalbuminemia may be used as a prognostic indicator of adverse surgical outcomes in these patients.
Role of Albumin for volume therapy in cardiac surgery

Fluid Management in cardiac surgery should be goal directed therapy. The distribution of fluids between the
intravascular and extravascular compartment depends on the integrity of the EGL. Both on on-pump and off-pump
surgeries may cause systemic inflammatory response syndrome (SIRS) more so on CPB surgeries.
The choice of fluid therapy in cardiac surgery is controversial. The ultimate goal of fluid therapy in cardiac surgery
is to improve organ perfusion, both micro and macro circulation and reduce inflammatory response. Crystalloid vs
colloid for fluid resuscitation controversy still continues (27, 28). After the 2 sensational studies 6S study (Scandinavian
starch for severe sepsis) and CHEST study (crystalloid versus Hydroxyethyl starch trial) which compared the third
generation modern hydroxyl ethyl starch (130/0.4) with ringers acetate and 0.9% saline in severe sepsis patients
and critically ill , showed increased incidence of adverse renal effects, renal replacement therapy (RRT) and 90 days
mortality in patients receiving colloids. After these 2 trials US FDA and EMA (European Medicines Agency) have
boxed warning and concluded that Hydoxyethyl starch( HES) must no longer be used to treat patients with sepsis,
or critically ill patients. CHEST study included surgical patients which can be implied to cardiac surgical patients also
(10, 11).
Similarly people who debate against crystalloids say that physiologically unbalanced crystalloids especially 0.9% saline
is known to cause Acute Kidney Injury (AKI) and increase the incidence of mortality. This is due to the high chloride
content in the saline causing profound renal vasoconstriction and AKI.(17). On reviewing these literature on Colloids
and Crystalloids, Physiologically balanced solutions (plasmalyte , Normasal) are preferable in cardiac surgery (27).
The role of albumin for volume expansion in cardiac surgery has been recommended as occasionally appropriate
(12). Albumin may be used for volume expansion as last choice of treatment after using crystalloids and non-protein
colloids, when they have not shown any improvement. According to a study conducted in United States comparing
the patients receiving either Albumin or Non protein Colloids for volume expansion during Coronary Artery Bypass
Grafting showed decreased incidence of Mortality in patients receiving Albumin(32). In SAFE study(29) outcomes
were similar in both Albumin and Saline Group when used in ICU patients for volume therapy. Majority of the
studies which showed superiority of human Albumin over Hydroxyethyl Starch (HES) were compared with older
HES (13,14,15,16), They reported increased incidence of impaired coagulation after cardiac surgery and risk of
bleeding complications requiring blood product transfusion in the post operative period. Similarly there are studies
which favour the usage of modern HES (18, 19) and there are studies which question the safety of modern HES
(130/0.4) in cardiac surgery (20, 21, 22).
After analyzing so many studies, usage of colloids should be in moderation and it is better to use balanced crystalloid
solutions in cardiac surgery due to impairment of vascular barrier following CPB.
ALBUMIN IN CPB PRIME

Albumin usage in paediatric cardiac surgery for priming the cardiopulmonary bypass (CPB) circuit is Grade 2C
recommendation (12) (weakly recommended).
In paediatric cardiac surgical patients CPB priming volume causes significant haemodilation because of small body
surface area of the Neonates and Infants. The reduction in the Colloid Oncotic Pressure can be corrected by adding
35
IACTACON 2016
Either Fresh Frozen Plasma (FFP) or Albumin in the CPB prime. There are 2 schools of thought regarding adding
FFP or Albumin in the CPB prime. Theoretically adding FFP increases fibrinogen levels in the prime. These fibrinogen
adhere to the CPB circuit, attract platelets to fibrinogen via glycoprotein IIb/IIa receptor and there is consumption
of platelets and fibrinogen thereby increasing thrombin generation necessitating more heparin. According to this
strategy there may be consumption of coagulation factors by the addition of FFP (30) while in the 2nd strategy addition
of albumin in the prime coats the CPB circuit and causes less activation of coagulation pathway and reduction in the
consumption of coagulation factors. Albumin also prevents platelet adhesion causing a better platelet preservation
effect (23, 24).This explains the better platelet counts and coagulation profile in albumin supplemented patients
(26). Blood loss and transfusion requirements were less in albumin group. Apart from maintaining colloid oncotic
pressure (COP), Albumin in the CPB circuit also prevents complement cascade activation thus preserving endothelial
glycocalyx (EGL) and prevents the breakdown of vascular barrier. Attenuation of compliment cascade activation
and maintaining COP reduces tissue injury and 3rd spacing, thereby reducing myocardial edema, pulmonary edema,
interstitial edema and improving the outcome in paediatric cardiac surgical patients (25)
Conclusion:
Even though the debate for crystalloids vs colloids continues, volume therapy in cardiac surgery should be goal
directed. The distribution of albumin and synthetic colloids depends on integrity of the endothelial glycocalyx
(EGL) so even albumin can leak into interstitial space following systemic inflammatory response (SIRS) which should
make us think and restrict its usage in critically ill patients following cardiac surgery where balanced crystalloid
solutions will be a better option. Albumin should be used as a safe alternative in renal failure, coagulopathy and fluid
overloaded patients.
Worldwide albumin is used for priming CPB circuit in paediatric cardiac surgery because of following
reasons like
(1) Albumin protects endothelial glycocalyx and maintains endothelial vascular integrity
(2) Maintains colloid oncotic pressure
(3) Reduces 3rd spacing thereby improving cardiac performance, ventilation and reducing morbidity, mortality,
ICU and hospital stay.
(4) Reduces compliment cascade activation on CPB
(5) Coats the CPB circuit thereby preventing activation of coagulation pathway
(6) Albumin also has better platelet preservation effect improving coagulation profile thereby reducing blood
loss and transfusion requirements in the post operative period
Most of the times Albumin usage in many hospitals is based on practices and preferences of the physicians than on
the recommendations. It should be remembered that Albumin is a human blood product associated with the risk of
transmitting Prions (proteinaceous infectious particles) and rarely Anaphylaxis. Because of limited availability and
cost containment Albumin usage should be restricted.
References:
1. Antithrombin reduces shedding of the endothelial glycocalyx following ischemia reperfusion - Daniel
Chappell et al. D Cardiovasc Res 2009;83:388-396
2. Contrasting effects of colloids and crystalloid. Resuscitation fluids on cardiac vascular permeability Jacob
Mathew et al. Anesthesiology 2006;104:1223-1231
3. The impact of crystalloidal and colloidal infusion preparations on coronary vascular integrity, interstitial
oedema and cardiac performance in isolated hearts Zausig et al. Critical care 2013;17:203.
4. Plasma volume expansion of 5% Albumin, 4% gelatin, 6% HES 130/0.4, and normal saline in the rat under
increased microvascular permeability Dubniks et al. Int care med 2007;33:293-298
5. Serum albumin and clinical outcome in paediatric cardiac surgery Heitor pon et al. Nutrition 21(2005);553558
6. Pre-operative serum albumin concentration as a predictor of mortality and morbility following cardiac
surgery M Koertzem et al. Perfusion 28(5);390-394
36
LECTURE
7. Albumin is a better predictor of outcomes than body mass index following coronary artery bypass grafting
Castigliano et al. Surgery 2011,150;4:626-634
8. Impact of pre albumin on outcomes after cardiac surgery Medical devices and surgical technology
2015;27:401
9. Post operative hypoalbuminemia is associated with adverse outcome in patients undergoing off-pump
coronary artery bypass graft surgery Eun Ho Lee et al. JCTVA 2011;25,3:462-468
10. Hydroxyethyl starch 130/0.42 versus Ringers acetate in severe sepsis Anders Pernere et al. NEJ Med
2012;367:124-34
11. Hydroxyethyl starch or saline for fluid resuscitation in intensive care - John A Myburgh et al. N Engl J
Med 2012; 367:1901-11
12. Recommendations for the use of albumin and immunoglobulins - Gian Carlo Liumbruno et al. Blood
Transfusion 2009;7(3):216-234
13. Hetastarch and bleeding complications after coronary artery surgery - Avorn J. Patel M
2003;124:1437-42
et al. Chest
14. Use of intraoperative hetastarch priming during coronary bypass - Canver CC et al. Chest 2000;118:1616-20
15. Does intraoperative hetastarch and administration increase blood loss and transfusion requirements after
cardiac surgery - Anesth Analg 200;90:801-7
16. Hydroxyethyl starch and gelatin impair blood coagulation after cardiac surgery - Scharmko et al . BJA 2010
17. A clinical score to predict acute renal failure after cardiac surgery - J Am Soc Nephrol 2005;16(1):162-8
18. The pharmacokinetics and tolerability of an intravenous infusion of the new hydroxyl ethyl starch 130/0.4
(6% 500ml) in mild to severe renal impairment - Anaesth Analg 2002;96:1453-1459
19. Six percent hydroxylethyl starch 130/0.4 (Voluven) versus 5% Human serum Albumin for volume
replacement therapy during Elective open heart surgery in pediatric patient - Philippe et al. Anesthesiology
2013;119:1296-309
20. A systemic review of third generation hydroxyethyl starch (HES 130/0.4) in resuscitation safety not
adequately addressed - Hartig et al. Anaesth Anaes 2011.
21. Safety of modern starches used during surgery - Vander linden et al. Anes Analg 2013
22. Rapidly degradable hydroxyethy starch solution impair blood coagulation after cardiac surgery Schramko
et al. Anaesth Analg 2009
23. Albumin versus crystalloid for pump priming in cardiac surgery: Meta-analysis of controlled trials - JCTVA
2004;18:429-437
24. Does priming implementation with low dose albumin reduce postoperative bleeding following
cardiopulmonary bypass? - On Orati F et al. Int J Artif organs.2003;26:211-216
25. Albumin Vs Crystalloid for pump priming in cardiac surgery. James et al. JCTVA 2004
26. Blood loss in infants and children for open heart operations: Albumin 5% versus Fresh frozen plasma in the
prime - William C. Oliver et al. Ann Thorac surgery 2003;75:1506-12
27. Fluid management in cardiac surgery crystalloid or colloid - Andrew shaw et al. Anaesthesiology clinics
31(2013);269-280
28. Volume therapy in cardiac surgery - J. Boldt et al. Annals of cardiac anesthesia
2005;8:104-116.
29. A comparison of albumin and saline for fluid resuscitation in the intensive care unit - Simon Finfer et al.
NEJM 2004;350:2247-56
30. Albumin Beyon fluid replacement in cardiopulmonary bypass surgery: Why, How and When? - Enrique et
al. Car.thor.vas Anaes 2014:1-8
31. Endothelial glycocalyx and coronary vascular permeability: the fringe benefit - Becker
Cardiol 2010;105:687-701.
et al. Basic Res
32. Volume expansion with Albumin decreases mortality after coronary Artery Bypass Graft Surgrey Artyom
Sedrakyan et al Chest 2003;123(6):185,3-57
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IACTACON 2016
Anaesthetic challenges in patients with

multi-valvular heart disease coming for a
double valve replacement
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Dr Praveen Kumar Neema, MD, PDCC

Professor and Head Anaesthesiology,
AIIMS Raipur (CG),
E-mail: praveenneema@gmail.com
Multivalvular involvement is caused most frequently by rheumatic fever, Marfan
syndrome and other connective tissue disorders, and degeneration of aortic valve
associated with degenerative mitral annular calcification causing mitral stenosis (MS)
and aortic regurgitation (AR). Different pathological conditions can affect two valves
in the same patient such as infective endocarditis of the aortic valve causing AR and
myocardial ischaemia causing MR. Similarly, the development of pulmonary and tricuspid
regurgitation can be secondary to pulmonary hypertension after mitral or aortic valve
disease. The rationale management in such patients depends on systemic analysis of the
determinants of hemodynamic functions. The presence of combined valvular lesions
results in varied pathophysiological changes and clinical manifestations that depend on
the severity, nature and the position of the lesion. In general, the clinical manifestations
depend on the relative severities of each of the lesions and relates to the valve affected
more severely (dominant lesion). If the two lesions are of approximately equal severity,
clinical manifestations produced by the lesion of the proximal valve are more prominent
as compared to those produced by the lesion of the distal valve (i.e., the mitral valve in
patients with combined mitral and aortic valvular disease and the tricuspid valve in patients
with combined tricuspid and mitral valvular disease). In general, the proximal lesion tends
to mask the distal lesions and it may be difficult to estimate the severity of each lesion by
clinical examination or noninvasive testing. For this reason, to evaluate true extent of the
disease left and right-sided cardiac catheterization and angiography should be considered.
It is important to recognize multivalvular involvement preoperatively because failure to
correct all significant valvular lesions simultaneously results in considerably increased
mortality. If there is any question regarding the presence of significant AS in a patient
undergoing mitral valve surgery, the aortic valve should be inspected; similarly it is useful
to palpate/examine the tricuspid valve at the time of mitral valve surgery.\
Combined valvular lesions:

1. Aortic stenosis with Mitral stenosis
2. Mitral stenosis with Aortic regurgitation
3. Aortic stenosis with Mitral regurgitation
4. Aortic regurgitation with Mitral regurgitation
Apart from the above combination of valvular lesions, chronic dysfunction of the
mitral and aortic valve invariably results in pulmonary artery hypertension and tricuspid
and pulmonary valve regurgitation. As discussed earlier, in such situations clinical
manifestations of the proximal valvular lesions predominate and the severity of the distal
valvular lesion may be underestimated.
38
LECTURE
1. Aortic stenosis with mitral stenosis:

The left ventricle (LV) in such a situation is usually small, stiff and hypertrophied. The cardiac output tends to be
reduced more than in patients with isolated AS. The reduced cardiac output lowers transaortic pressure gradient and
the LV systolic pressure that retards the development of aortic valvular calcification and LV hypertrophy and in turn
results in diminished incidence of angina. However, the clinical manifestations associated with MS such as pulmonary
congestion, edema, atrial fibrillation, and systemic embolization, occur more frequently. In a patient of MS scheduled
to undergo balloon mitral valvotomy, it is vital to know the presence of hemodynamically significant AS because
relief from MS can impose sudden load on the LV and may lead to acute pulmonary edema.
Anaesthetic management:
The goals are prevention of pulmonary congestion and edema, and maintenance of LV output. The LV output
depends on its preload, myocardial contractility, diastolic time period and timed atrial kick. LV failure can further
exaggerate transmitral gradient. The perfusion of the hypertrophied myocardium depends on diastolic pressure and
diastolic period that depends on cardiac output, systemic vascular resistance (SVR) and the heart rate. Myocardial
depression, tachycardia, surge in the sympathetic activity, all can result in significant increase in transmitral pressure
gradient, pulmonary congestion and edema. The goals are best achieved by preservation of myocardial contractility,
sinus rhythm, SVR and normal heart rate. It follows that for the safe conduct of anaesthesia in this situation,
myocardial depression and tachycardia should be avoided while SVR should be preserved. However, systemic
vasodilatation invariably follows induction of anaesthesia and can potentially compromise myocardial perfusion.
Systemic hypotension during induction or prebypass period can best be avoided by careful induction and by reducing
the depth of anaesthesia or by administration of a titrated dose of an inotrope with vasoconstrictor properties.
Concomitant rapid administration of fluid and a potent peripheral vasoconstrictor (phenylephrine) may result in
pulmonary congestion and edema.
The technique of anaesthesia can be narcotic based, and the undesirable sympathetic responses can be effectively
controlled by the judicious use of inhalation anesthetic agent like sevoflurane or isoflurane. Monitoring methods
are routine. The use of pulmonary artery catheter to assess LV filling pressure may not be helpful because of the
presence of transmitral pressure gradient and pulmonary artery hypertension. Conduct of cardiopulmonary bypass
(CPB) is routine. Adrenaline may be an appropriate inotrope in the post-bypass period as it ensures peripheral
vasoconstriction and enhances myocardial contractility. Although, hypertrophied myocardium needs adequate filling,
aggressive volume resuscitation can cause severe hypertension in the post bypass and postoperative period which
is troublesome. Transesophageal echocardiography (TEE) can provide valuable input on preload of LV apart from
evaluation of implanted valves and myocardial contractility.
Mitral stenosis
Aortic stenosis
Aortic & Mitral stenosis
Prevent tachycardia
Prevent tachycardia
Prevent tachycardia
Maintain LV preload
Adequate diastolic interval
Maintain sinus rhythm
Maintain LV preload
Adequate volume
Maintain myocardial contractility
Maintain LV preload
Maintain myocardial contractility
Prevent pulmonary edema
Suppress sympathetic surge
Avoid volume overload
Avoid volume overload
Avoid
Avoid
Avoid
Vasodilatation
Vasodilatation
Vasodilatation
Myocardial depressants
Treatment of hypotension
Inotropic support
Volume & inotrope with peripheral
vasoconstriction
39
Inotrope with
peripheral
vasoconstriction
IACTACON 2016
2. Mitral stenosis with Aortic regurgitation:

The diagnosis of MS in presence of AR is confusing. The AR results in Austin-flint diastolic murmur that can
easily be confused with the murmur of MS. However, the presence of accentuated S1, opening snap, early dyspnea,
pulmonary edema, hemoptysis, or systemic emboli, strongly indicate the diagnosis of MS. Approximately 10% of
patients with rheumatic MS have severe AR, that can be recognized by the usual signs of AR such as widened pulse
pressure, LV dilation and increased wall motion on echocardiography. In keeping with the general observations, the
clinical manifestations of the proximal valvular lesions predominate and the severity of the distal valvular lesion may
be underestimated. Echocardiography, particularly pulsed Doppler echocardiography is decisive in detecting MS.
The hemodynamic goals of the two lesions are conflicting. Mild tachycardia and systemic vasodilatation is preferred
in presence of AR, as it decreases the regurgitant fraction and reduces the LV size thereby reduces LV wall stress and
O2 requirement. In presence of MS mild bradycardia is recommended to ensure adequate filling of the LV, a low
transmitral gradient and for the prevention of pulmonary venous hypertension and pulmonary edema. Theoretically,
a low heart rate, by increasing the regurgitant fraction, can directly increase the LV diastolic pressure and indirectly the
transmitral pressure gradient. Though, the goals are not described, it appears that in this situation a mild tachycardia
(heart rate of 80-90), maintenance of normal myocardial contractility; and a low normal SVR are the optimal
hemodynamic goals. To treat hypotension, volume augmentation can result in pulmonary edema; hence, inotropic
support appears appropriate.
The technique of anaesthesia can be narcotic based, isoflurane is the inhalation anaesthetic of choice to control
sympathetic responses. Monitoring methods are similar to the previous combination (MS+AS). The utility of PAC is
questionable in view of mitral stenosis and pulmonary artery hypertension. Conduct of CPB is complicated because
of the presence of AR. Slowing of the heart results in left ventricular distention. Left heart venting can decompress
the LV, but can result in systemic hypotension and reduced cerebral perfusion. The only effective way to prevent
distention and to maintain perfusion of the various organs is to apply aortic cross clamp soon after initiation of CPB.
Significant hypertension in the post bypass and postoperative period is common. Dobutamine appears appropriate
inotrope if a support is required. TEE helps evaluating LV preload.
Mitral stenosis
Aortic regurgitation
Mitral stenosis with Aortic regurgitation
Prevent tachycardia
Mild tachycardia
Reduced regurgitant fraction
Smaller LVEDV
Mild tachycardia (80-90 beats/min)

Smaller LVEDV
Low Transmitral gradient
Preserve afterload
Reduced afterload
Reduced afterload
Maintain LV preload
Avoid myocardial depression

Maintain Sinus rhythm
Suppress Sympathetic surge
Avoid Volume overload

Volume overload
Prevent hypotension
Inotropic support
Inotropic support
Volume resuscitation
40
Inotropic support
LECTURE
3. Aortic regurgitation with Mitral regurgitation:

This combination of valvular heart disease is due to rheumatic heart disease, due to myxomatous degeneration of
both the aortic and mitral valves causing prolapse and regurgitation, and by dilatation of both annuli in patients with
connective tissue disorder. The LV is greatly dilated. The normal mitral valve limits the volume of regurgitation by its
premature closure in presence of AR. With combined valvular lesions, blood may reflux from the aorta through both
chambers of the left side of the heart into the pulmonary veins. The relative severity of each lesion can be assessed
by Doppler echocardiography and contrast angiography.
The forward cardiac output is dependent on myocardial contractility, LV size, heart rate and afterload. Mild tachycardia
and peripheral vasodilatation favors forward flow. Maintained inotropy results in smaller LV size and a small mitral
annulus for regurgitation. A sudden and significant rise in SVR can catastrophically increase mitral regurgitation and
result in precipitous rise in left atrial pressure, pulmonary artery pressure and right ventricular pressure overload with
sequels like bulging of the interventricular septum towards LV and compromise of LV size and filling. Logically the
goals are a mild tachycardia, reduced afterload, and preserved myocardial contractility. However, it should be realized
that a significant diastolic hypotension can drastically reduce myocardial perfusion.
Mitral regurgitation
Aortic regurgitation
Mitral and Aortic regurgitation
Mild tachycardia
Smaller LVEDV
Mild tachycardia
Smaller LVEDV
Mild tachycardia (80-90 beats/min)

Smaller LVEDV
Low Transmitral gradient
Reduced afterload
Reduced afterload
Reduced afterload

Prevent vasoconstriction
Inotropic support
Volume resuscitation
Inotropic support

Inotropic support
The technique of anaesthesia is narcotic based; isoflurane is favored because of its peripheral vasodilating properties
and is useful in suppressing sympathetic surges associated with intense surgical stimulation. PAC in conjunction with
systemic arterial pressure monitoring is useful in titrating vasodilators. Conduct of CPB is complicated because of
the presence of AR. Slowing of the heart result in LV distention. Left heart venting can decompress the LV, but
can result in systemic hypotension and reduced cerebral perfusion. The only effective way to prevent distention and
to maintain perfusion of the various organs is to apply aortic cross clamp soon after initiation of CPB. Significant
hypertension in the post bypass and postoperative period is common. Dobutamine is the preferred inotrope if
required. TEE helps deciding LV preload and most appropriate monitor.
4. Aortic stenosis with mitral regurgitation:

Fortunately this combination is very uncommon. This combination of lesions is usually caused by rheumatic heart
disease although AS may be congenital and the regurgitation may be due to mitral valve prolapse. Maintenance of
LV preload and timed atrial kick are the important mechanisms that maintains the stroke volume in presence of AS.
Obstruction to the LV outflow, AS, increases the volume of mitral regurgitation and the presence of MR reduces the
LV preload necessary for the maintenance of LV stroke volume. The result is a reduced forward cardiac output and
marked left atrial and pulmonary venous hypertension. The development of atrial fibrillation can further compromise
the hemodynamics.
41
IACTACON 2016
The combination can pose significant problems during anaesthesia. Theoretically the optimum management would
be the preservation of SVR to maintain myocardial perfusion. A normal heart rate and preservation of timed atrial
kick are the useful hemodynamic goals. The best course is to minimize induction and prebypass period. In the event
of significant hypotension, inotrope with peripheral vasoconstrictor property is a useful choice. In the situation of
severe or critical AS, provision of percutaneous CPB or emergent bypass could be life-saving.
Aortic stenosis
Mitral regurgitation
Aortic
stenosis
regurgitation
with
Mitral
Prevent tachycardia
Sinus rhythm
Mild tachycardia
Smaller LVEDV
Maintain Normal heart rate (70-80

beats/min)
Prevent vasodilatation
Reduced afterload
Maintain afterload
Avoid
myocardial
depression
Maintain LV preload
Adequate volume
Sinus rhythm
Prevent hypotension
Volume & inotrope with peripheral
vasoconstriction
Prevent hypotension
Inotropic support
Inotrope with
peripheral
vasoconstriction
In addition to the described combined valvular lesions, the patient can have concomitant involvement of tricuspid
valve also. Complex lesions and combinations such as MS, MR and AS, AR can further complicate the Pathophysiology
in the same patient. In general, the clinical manifestations are related to the more dominant lesion; in situations when
both the lesions (e.g. AR and MR) are equally severe, the clinical manifestations relate to the proximal lesion (MR).
Further, the proximal lesion tends to mask the distal lesion; therefore, the diagnosis of the distal valvular lesion may
not be straightforward on the basis of clinical features and noninvasive investigations.
The hemodynamic goals during the anaesthetic management are generally aimed according to the dominant lesion.
However, from the preceding discussion, it is clear that when both the lesions are equally severe, the anesthetic
management strategy directed to achieve favorable hemodynamic goals for the distal lesion is beneficial for the
proximal lesion also (e.g. In presence of AS with MS, hemodynamic goals that improve flow across the aortic valve,
improve the flow across the mitral valve also. The same also holds true for other combinations.

A few generalizations can be made. In the presence of combined valvular heart disease, the clinical
manifestations are either related to the proximal lesion (if both the valvular lesions are equally severe) or to the
dominant lesion. In general the anaesthetic management is aimed to attain the hemodynamic goals that benefit the
dominant lesion. In situations when both the valvular lesions are of equal severity, the anesthetic management should
be directed to benefit the distal lesion. However, the measures that prevent worsening of the hemodynamics because
of the, proximal lesion should also be followed (e.g. Volume overloading should be avoided in presence of severe MS;
irrespective of the presence of any other associated lesion of any other valve).
Suggested Readings:
1. Bonow RO, Braunwald E: Valvular Heart Diseases, In: A Text Book of Cardiovascular Diseases (Heart
Diseases). Zipes DP, Libby P, Bonow RO, Braunwald E (Ed). Elsevier, Philadelphia, 2005 pp 1553
42
LECTURE
2. Dinardo JA: Anesthesia for valve replacements in patients with acquired valvular heart disease, In Anesthesia
for Cardiac Surgery, Dinardo JA: (Ed), Appleton and Lange, Stamford, Connecticut, 1998 pp 109
3. Jackson JM, Thomas SJ: Valvular heart diseases, in Kaplan JA (Ed): Cardiac Anesthesia. Philadelphia, PA.
Saunders, 1993, pp 629-680
4. Jack Shanwise and Carl C Hug: Anesthesia for Adult Cardiac Surgery, In Anesthesia, Gucchiara RF, Miller
ED, Reeves JG, Roizen MF, Sevarese JJ (ed), Philadelphia, Churchill-Livingstone, 2000 pp 1753
5. John A Parkos: Combined Valvular disease, In Valvular Heart Disease, Alpert JS, Dalen JE, Rahimtoola SH
(ed), Philadelphia, Lippincot-Williams Wilkins, 2000 pp 291
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IACTACON 2016
Aortic Arch SurgeryDr Vijay Shetty,

Head of Department of Anaesthesia , Fortis Mulund ,Mumbai.
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Thoracic aortic aneurysm is a frequently encountered condition with a potential to cause

lethal complications and morbidity. When dissection or rupture occurs as complication
of a thoracic aneurysm, emergency surgical treatment is most often the only available
option to save a patients life. Thoracic aortic operations were performed increasingly
during a 40-year time period. Early mortality decreased and late survival increased
significantly in all patient groups. A significant proportion of patients required multiple
operations. Large studies have shown a shift from 70% emergency/urgent operations to
70% elective surgeries, and a shift from predominantly descending aortic operations to
increasing number of ascending aortic or aortic arch operations. The better understanding
of inherited conditions has led to further recommendations for early intervention at even
minimally abnormal aortic diameters in patients with specific gene mutations and might
play an additional role in the increase of the number of operations performed. Deep
Hypothermic Circulatory Arrest (DHCA) is frequently required in major arch surgeries.
Davies and colleagues estimate the yearly rate of rupture, dissection, or death to be 6%
for aneurysms 5.0 to 5.9 cm and 15% for aneurysms >6 cm. They found the 5-year
survival of non-operated patients to be 54%, which is clearly inferior than the survival of
operated patients. This information can be used in advising patients with asymptomatic
aneurysms and may be used to lower the threshold for elective aortic replacement. Aortic
disease may be present in multiple segments of the aorta, especially in patients with
Marfan disease or other genetic aortic diseases.
The risk factors for aneurysm expansion (predicted at least 0.1cm/year) include a history
of hypertension, male sex, age older than 70 years, history of smoking, and initial
aneurysm diameter more than 5 cm at diagnosis were independent predictors of rapid
expansion
Age, body mass index, New York Heart Association classification(III-IV), preoperative serum
creatinine, creatinine clearance, myocardial ischemia time, and fresh-frozen plasma
transfused intraoperatively were important factors with emergency surgery, inotropes and
prolonged cardiopulmonary bypass duration emerging as factors significantly associated with
prolonged ICU stay.
44
LECTURE
Conduct of Anaesthesia for Arch RepairTwo arterial monitoring lines, transesophageal ECHO(TEE),cerebral monitoring choices including EEG,BIS,Cerebral
oximetry etc..are also part of the standard cardiac anaesthesia monitoring .Aortic arch surgery using DHCA plus
Selective Antegrade Cerebral perfusion (SACP) through right axillary arterial cannulation has been a standard procedure
in many centres. All operations are performed through a median sternotomy. The right axillary artery is isolated
before sternotomy. After standard dose anticoagulation with heparin to maintain an activated coagulation time more
than 480 seconds, CPB is instituted using right axillary arterial cannulation and right atrial venous cannulation. During
DHCA, the brachiocephalic trunk is clamped, and selective antegrade cerebral perfusion through right axillary arterial
cannulation is instituted. Alternately, an Ascending Aortic site may be chosen for cannulation (Epiaortic ECHO may
be useful) and selective cannulation of the Arch vessels with balloon tipped catheters may be used to perfuse and
protect the brain even without significant hypothermia. In most cases however, Nasopharynx temperature is allowed
to plateau to approximately 15C for total aortic arch replacement and 20C during partial aortic arch replacement.
After the distal anastomosis for aortic arch repair, the aortic graft is cannulated and proximally clamped to recover
circulation. The proximal end of the prosthetic graft is then anastomosed to the ascending aorta. The neuroprotective
drugs administered in CPB included the following: methylprednisolone, 30 mg/kg; magnesium sulfate, 1 g;Thiopental
Sodium 10mg/kg; and Mannitol, 0.5 g/kg. Standard Antegrade cold cardioplegia is used for myocardial protection.
Heparin is reversed with protamine at a 1:1.5 ratio on weaning from CPB. Blood components including packed
red blood cells, fresh-frozen plasma, and platelets are infused to maintain the post-CPB hematocrit and correct the
coagulopathy and are often guided by the point of care systems.
The challenges of Anaesthesia in managing Aortic arch repairs can be estimated at the time of assessment and
subsequent team discussion where the surgical steps are discussed and specific roles requiring the inputs from the
anaesthesiologists and perfusionists are sought. Based on the collective experience of the team, a strategy is agreed
upon to tackle the most vexing problem in arch surgeries-Cerebral protection. The best strategy for protecting the
brain from irreversible ischaemic damage during the period of circulatory arrest remains controversial. Patients
present with diverse aortic pathologies and this may dictate different cerebral protection methods that are tailored for
the circumstances of each individual case.
Deep Hypothermic Circulatory ArrestDHCA has been in clinical practice for over 4 decades and removes the need for a distal clamp, allows a clear
and dry view of the anatomy and assists greatly in performance of a dependable distal anastomosis. The most
important requirement of using this as a sole technique is time. The time allowed for the all-important circulatory
arrest is a function of the core temperature. A rough estimate is around 20 min for temperature of 18 C. With
profound hypothermia(less than 10C),the time of TCA may be stretched to 40 minutes. Recent studies have clearly
demonstrated, however that the cerebral isoelectricity is a myth and upto 17 % of electrical activity present even at a
properly conducted TCA at 15C.The initiation and subsequent reversal of TCA should be gradual with a temperature
gradient of not more than 10C between the perfusate and core temperature. A duration of circulatory arrest of 25
minutes is reported to be associated with an increased risk of transient neurological, memory and fine motor deficits.
The advantages of DHCA include:
*A bloodless and motionless operative field
*Avoidance of clamping and manipulation of the aorta with reduced risk for brain embolism
*Simplicity and no need for additional perfusion equipment.
The disadvantages of DHCA include:
*Limited safe time of circulatory arrest
*Prolonged cardiopulmonary bypass (CPB) time required to cool down and rewarm patients, which may result in an
increased occurrence of pulmonary, renal, cardiac and endothelial dysfunction
*Reperfusion injury
*Coagulopathy.
DHCA may therefore be recommended as a sole technique in arch surgery for only the briefest possible arrest
periods.
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IACTACON 2016
Retrograde cerebral perfusionRetrograde Cerebral perfusion (RCP) is usually performed through a superior vena cava cannula with snaring of the
caval cannula to prevent cardiac distention.
Evidence has been presented for the RCP being instrumental in
*Cerebral metabolic support
*Expelling atheromatous and gaseous emboli from the cerebral vasculature
*Maintaining cerebral hypothermia.
Disadvantages*Cerebral edema
*Requirements of perfusion pressures of more than 30 mm Hg to overcome the resistance of the venous valves
and venous capacitance vessels and allow arterial flow reversal.
RCP is chosen in high risk for stroke patients but its routine application is still not a popular choice but it is certainly
superior than DHCA alone.
Selective antegrade cerebral perfusionSACP is a more effective tool for cerebral protection. Perfusion of the cerebral artery/arteries reduces the dependency
on Hypothermia and provides effective safety without the complications of Hypothermia.
SACP provides several advantages:*The circulatory arrest time can safely be extended up to 90 minutes allowing more complex aortic repairs to be
performed
*Moderate (nasopharyngeal, 25 ) instead of profound hypothermia can be used with reduced coagulative and
systemic complications.
Disadvantages- Technical complexity
*Reduced surgical visibility
*Requirement of repeatedly manipulating the aortic arch and arch vessels.
Current evidence backs SACP to effect superior neurological outcome but the impact on surgical outcome and
prognosis is less impressive.
Role of Nuerological Monitoring

Various Neurophysiological monitoring may be utilized including the
*EEG based to confirm EEG silence
*Transcranial Doppler to confirm blood flow/flow reversal as well as monitor for emboli
*Devices like NIRS(Near InfraRed Spectroscopy) which provide an input about the oxygenation status of the
cerebral tissue. Here Regional readings are extrapolated to supposedly reflect global wellbeing and that may be a big
assumption.
Any monitoring device needs to be backed with a good algorithm of interventions in case of reading abnormality.
For example a unilateral fall in NIRS may indicate kinking or hypoperfusion of that sided carotid circulation. A
bilateral fall may be a signal to up the protective steps like-Increasing flow/lowering temperature /correcting low
paCO2/Increasing MAP etc..
The Anaesthesiologist will be a key player in the treatment of Arch repair right from helping choose the best strategy
on Brain protection, maintaining vigilance at times of significant physiological turmoil as well as bringing together the
surgical and interventional teams when a cohesive plan needs to be tailored for vexing arch anatomies.
Further Reading46
LECTURE
1. Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE Jr, et al. 2010 ACCF/AHA/AATS/
ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with
thoracic aortic disease: a report of the American College of Cardiology Foundation/American Heart
Association Task Force ,Circulation. 2010;121:e266-369
2. Thoracic aortic surgery: An overview of 40 years clinical practice-Jos A. Bekkers, MD et al-. (J Thorac
Cardiovasc Surg 2014;147:332-43
3. Preoperative and Intraoperative Risk Factors for Prolonged Intensive Care Unit Stay After Aortic Arch
Surgery-Qian Lei et al Journal of Cardiothoracic and Vascular Anesthesia, Vol 23, No 6 (December), 2009:
pp 789-794,
4. Cerebral protection in hemi-aortic arch surgery-Mohamad Bashiret al- Ann Cardiothorac Surg 2013;2(2):239244
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Acute Intermittent Hypoxia (AIH) As

Therapy For Incomplete Spinal Cord Injury:
Exploratory Findings
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William Z Rymer MD PhD

Rehabilitation Institute of Chicago
Northwestern University
Chicago, Illinois, USA
Introduction
Currently, the treatment of incomplete spinal cord injury relies on two broadly different
strategies. The first of these, called motor learning, seeks to restore function as close to
normal as possible using the framework of neural plasticity. This is a change in structure
and function of neural tissue linked to training induced structural changes in neural
circuits and in neuronal function. This approach is preferred if it can be implemented,
because it may be able to restore neural function to a level closer to that which existed
prior to the injury.
The second approach, neural compensation, teaches spinal cord injured persons to learn
ways in which to perform a task differently by using different limb movements and
different sets of muscles, and sometimes additional approaches such as the tenodesis grip
to assist with grasping by extending the wrist. This approach is practical but often less
desirable because it may increase joint loading, or demand high levels of co-contraction
of muscles around the joint, requiring more energy consumption. Because position and
movement trajectories are different, there may also be loading of joints inappropriately,
giving rise potentially to long-term discomfort and joint or muscle and tendon damage.
Application of Hypoxia as a mediator of Neural Plasticity

It has become evident over the last 10 years that intermittent hypoxia, used at moderate
level can be used to drive neural plasticity and to augment neural rehabilitation, especially
in patients with incomplete spinal cord injury.
To illustrate briefly, we have known for more than 50 years that animal models with
damage to phrenic nerve on one side and to spinal white matter on the other in the
spinal cord, may at first appear to succumb to their injury, but then exhibit rescue
mechanisms by which descending pathways to phrenic nuclei can be opened triggered
by the declining levels of oxygen in the tissues. Although these rescue mechanisms have
been most extensively studied in the respiratory system, it has also become evident
that these neural plasticity pathways are equally well developed in limb motor neurons
and limb neural circuits. It is now evident, based on further studies in both animal and
human preparations, that modest levels of acute intermittent hypoxia can enhance neural
plasticity in spinal cord injury.
Accordingly, this presentation will review the evidence derived from respiratory control
that hypoxia can induce neural plasticity in the respiratory and segmental motor systems
system. It will also confirm that the structural synaptic mechanisms linked to hypoxia
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are present in cervical and lumbar enlargements where limb neural circuitry resides. I will summarize evidence for
plasticity induction in motor circuits following acute intermittent hypoxia. Finally, I will review the opposing effects
induced by concurrent neural inflammation and describe briefly pilot data showing that in some patients, concurrent
anti-inflammatory drug interventions such as non-steroidal anti-inflammatory agents (NSAIDs) and corticosteroids,
can serve to augment plasticity in the presence of inflammation.
Our slide affirms that cervical hemi-section of the spinal cord in a rat or other quadruped model, such as in studies
undertaken by Professor Goshgarian and colleagues in Detroit, Michigan (United States), confirm that in the presence
of progressive hypoxia following such neural lesions, that the animal is able to rapidly open alternative descending
pathways from the contralateral brainstem to activate phrenic nuclei on the hemi-sected side. This effect is sufficient
to allow the animal to restore oxygen saturation to safer levels. These effects, which are described as long-term
facilitation, are quite long lasting. Short-term episodes of hypoxia in which oxygen intake is reduced to 11% will
induce augmented discharge of phrenic motor neurons for more than 60 minutes.
A number of investigators in different countries have begun to utilize these features to examine potential therapeutic
benefits from such hypoxia interventions. Much of the work has been done by Professor Gordon Mitchell during
many years of research at the University of Wisconsin in Madison. And this network is being continued in the
University of Florida in Gainesville. If an animal is subjected to a C-2 hemi-section for example, and then exposed to
repeated episodes of acute intermittent hypoxia over a week, the performance in motor tasks such as ladder climbing
is greatly enhanced in those animals that were exposed to hypoxia when compared to controls.
These effects have now been demonstrated in multiple systems, including respiration (using the crossed phrenic
spinal hemi-sected model), in contusion or cervical injuries of the cord at C-8 or C-6 (T-1 in the rat model) where
intermittent hypoxia improves both grasping and locomotion, and more recently in man from our group where
patients with lumbo-sacral injuries at L-4 to S-4 segments have been shown to demonstrate substantial increases in
voluntary ankle strength measured using plantar flexion testing.
We also know a great deal about the different biochemical pathways that are being activated by the hypoxia. These
effects appear to depend on the presence of serotine that acts on synthetic pathways in the cord to induce synthesis
and release of Brain Derived Neurotrophic Factor (BDNF). This BDNF acts on TrkB receptors to induce changes
in synaptic efficacy in excitatory synaptic pathways.
The evidence for the role of BDNF in serotine is also quite strong, and these agents appear to be pivotal to the
development of neural plasticity following acute intermittent hypoxia. There are, multiple pathways emerging that can
play a useful role in this neural plasticity, and they appear to be hierarchically organized in that the degree of hypoxia
can induce neural rescue in several alternative pathways, allowing for greater chance for life preservation.
I will next review briefly several of our studies in man showing that acute intermittent hypoxia can produce changes
in muscle strength in the lower extremity, and that such changes, if used as part of a continuing protocol in which
hypoxia is coupled with locomotor training, can induce increases in walking speed and endurance (Trumbower, et al,
2012). Our slide illustrates a typical protocol in which a subject sits in a stable chair (Biodex) with back, chest, and
proximal limb strapped to minimize spurious contributions to forces recorded at the ankle.
Our slide illustrates the patient position as well as the positioning of the load cell at the ankle and the appropriate
recording systems (blood pressure, pulse oximetry, and electromyographic activity from plantar flexors and extensors
of the ankle). The patient is given a mask and oxygen at normal atmospheric concentration, and this is alternated
quietly with hypoxia with oxygen intake dropping to 9.5%, approximately half of that normally available at sea level.
Episodes are brief, lasting 90 seconds, and are followed by 60 seconds of normoxia, and this sequence is repeated 15
times. There is then typically a prolonged break, and the whole sequence is then repeated several times.
Our slide shows a progressive increase in key features including strength and muscle activation of the ankle. For
example, there is a significant increase in plantar flexion torque recorded at the ankle at 30 minutes after the hypoxia
sequence is completed, and there is a further increase recorded at 60 minutes. If the person is given sham hypoxia
through the mask, there are no comparable changes recorded. We do not yet know the length of time where these
hypoxia effects persist, but it seems to be for at least several hours.
Similar results are visible during walking when hypoxia is followed by a period of training when supported with an
overhead harness. If the 10-meter walk, which is a measure of gait speed, is recorded over successive days of training,
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there is a progressive reduction in elapsed time and an associated increase in walking speed, again not visible in sham
exposed patients. In short, combining acute intermittent hypoxia together with gait training produces a substantially
greater increase in both walking speed and in endurance (as measured by the 6-minute walk) than exposure to training
alone.
While these effects were visible in 60-70% of patients, there is a significant minority that did not respond well to
acute intermittent hypoxia. We do not know why this happens. One possibility is that many patients, including our
hypoxia resistant group, are self-medicating by exposing their nervous system to hypoxia in the course of nocturnal
sleep apnea. This is common in intact persons, but appears to be even more prevalent in persons with spinal cord
injury. Although we do not have data with sleep studies on these people currently, we do plan to explore the potential
association between sleep apnea and resistance to additional hypoxia therapy.
A second potential mechanism that could interfere with hypoxia as an agent inducing neural plasticity is the
presence of concurrent inflammation, either existing within the central nervous system or induced by tissue damage
elsewhere. Presence of spinal cord injury often has concurrent musculoskeletal damage as well as concurrent lowgrade pneumonia, pressure sores, urinary tract infection, and other ongoing inflammation. To combat concurrent
inflammation, we repeated our studies of ankle strength by pre-treating patients with a large dose of non-steroidal
anti-inflammatory agent (Ibuprofen) administered an hour before hypoxia testing. In roughly half of the subjects
there was a substantial increase in voluntary force recorded at the same time-points as that done in our earlier study.
We do not know currently which inflammatory pathways are active and which ones are being affected by the oral
non-steroidal agent, but this work is currently ongoing.
Finally, more recently we have begun to explore the potential impact of high-dose corticosteroids (in this case,
Prednisolone) as a broadly acting anti-inflammatory agent. This drug is again given 90 minutes before testing of lower
extremity function, and in more than half of the patients examined so far there is a striking increase in plantar-flexion
torque at the ankle.
While results are very promising, we do not yet know if this treatment will turn out to be an effective and safe therapy.
Although there have been extensive studies performed in animal models demonstrating no adverse effects to date,
it is difficult to establish that long-term neurological sequelae are not likely to happen. Accordingly, we plan to do
continued safety studies of the effect of acute intermittent hypoxia over the next few months.
In spite of the need for caution, we do believe that this is a very promising therapy for improving neural plasticity
following neurological injury and anticipate that we may be ready for more extensive trials in the future, including
potentially other kinds of injuries such as stroke, ALS, multiple sclerosis, and even more rare illnesses such as
hereditary spastic paraplegia.
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Predictors of Failures in
Fast Track cardiac Surgery
Dr.K.Nedumaran
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Definition
A fast track approach to cardiac surgery can be defined as a perioperative process
involving rapid progress from preoperative preparation through surgery and discharge
from the hospital. Although highly individualized among the various heart surgery
centers, the fast-track process is a team activity. It requires a team of health care providers
to interact with the patient at various phases, from admission to discharge. The necessary
elements of the fast-track program are choice and the titration of short-acting anesthetic
drugs, standardized surgical procedures, early extubation, rewarming and sustained
postoperative normothermia, postoperative pain control, early ambulation, alimentation
and discharge, and follow-up after discharge.(1)
The aim of fast track anesthesia in cardiac surgery patients is to shorten ventilation time,
length of stay in intensive care unit and total hospital length of stay and thereby reducing
the cost (2, 3).
The definition of fast track cardiac surgery extend from immediate extubation in the
operation room to extubation within 10 hours after the end of the operation(4), whereas
extubation in the operation room is often called ultra-fast track (5).Kogan and colleagues
have published their results of fast track in the elderly population. In that study, the fast
track pathways was described as extubation within 10 hours, ICU stay of less than 24
hours and total length of stay in hospital of less than 6 postoperative days (6).
The multiplicity of possible approaches embodied in different fast-track concepts
substantially impedes comparison of the different publications in the literature.
Outcomes of Fast Track

In a study by Joerg Ender, The Fast-track Concept where postanesthestic care unit
(PACU), staffed by anesthesiologists and anesthetic nurses trained in the methods of
early extubation,directly admits postoperative cardiac surgery patients in PACU.In that
study,they have found significantly shorter intubation times and lengths of stay in the
fast-track group, despite a similar risk profile. In addition, they found a decreased rate of
postoperative low cardiac output syndrome and mortality in the fast-track group. shorter
intubation and ventilation times may be one important reason for the observed lower
mortality in the fast-track group. Patients in the fast-track group may have been at lower
risk for ventilator-related infections and sepsis (7).
Fast-track end-points
The Fast-track pathway was considered successful when the patient was transferred to
the ward the same day of the operation (within 24 hours), and there was no admission to
the ICU, no take-back to the operation room for exploration and no operative mortality
or morbidity (8).
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The postoperative morbidity can be cardiac and non-cardiac; the following complications were subsumed under the
heading of postoperative cardiac morbidity: new myocardial infarction, low cardiac output syndrome, multiorgan
failure, cardiopulmonary resuscitation, implantation of an intra-aortic balloon pump (IABP). The concept of
postoperative non-cardiac morbidity is defined by the following complications: intubation period longer than 24hours,
total reintubations, pneumonia, adult respiratory distress syndrome (ARDS), cerebrovascular stroke, postoperative
renal failure, total rethoracotamies, sternal infection, sepsis(9).
Predictors for fast-track failure

Different independent risk factors have been reported to predict failure of a fast-track process after cardiac surgery.
Constantinides et al. have identified eight independent predictors for fast-track failure: impaired left ventricular
function, acute coronary syndrome within 30 days of surgery, reoperative surgery, peripheral vascular disease,
preoperative intraaortic balloon pump, raised serum Creatinine, operative urgency, and complex surgery(10).
ASA class of >3,Chronic obstructive pulmonary disease (COPD) GOLD class 2.,Body mass index (BMI) of
35kgm2.,Surgical complications necessitating prolonged cardiopulmonary bypass time (CPB) (>150min).(11)
The ASA>3, NYHA class>3 and operation time >267minutes are independent predictors of fast track protocol
failure. Therefore, parameters should be used more strictly in fast track patient selection and fast track termination.
(12)
Predictors of failure were reduced renal function, hypertension, age, Euro SCORE, cardiopulmonary bypass time,
first lactate or base deficit after surgery and cross-clamp time. The study showed that the strongest predictor of
failure was glomerular filtration rate (GFR)<65 mL/min/BSA (sensitivity, 54%; specificity, 61% ) (13)
Advanced age should not be a contraindication for fast track treatment, although it is associated with a higher failure
rate as compared to younger patients. The author, J Ender, further stated that not the age itself, but the type of
surgery and comorbidities are important factors for failed fast track treatment Careful selection of the patients who
undergo fast track treatment is very important for successful outcome(14)
Ways to overcome fast track failure

There are important contributory factors to help the success of fast-track cardiac surgery.
1.Patient selection.
Precise preoperative screening and patient selection are critical.
2.Fast track Anesthetic technique(customized)

3.Surgical strategy
The surgeon should minimize the surgical trauma in order to promote early extubation and fast recovery
Isolated procedure (CABG, AVR, MVR, myxoma)

Easy combined (i.e. AVR + 1 CABG)

OPCAB
Selected minimal invasive valve/TAVI procedures
Selected hybrid procedures
4.Perfusionist strategy

Normothermia-based setting
Short CPB time (fast surgeon, suture less valves)
Delnido cardioplegia

Use of mini-CPB
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Close circuit, no hemodilution (RAP)

Less inflammatory response
Less risk of postop vasoplegia
5.The PACU protocol

Patients were extubated on the PACU after normalization of the body temperature (rectal temperature >36.5C),
and adequate stabilization of their haemodynamic and respiratory conditions. In addition, careful monitoring within
the first 24h postoperatively and the availability of experienced and highly trained nurses on the ward are essential.
Communication between the dedicated nursing staff on the ward and the responsible physicians is mandatory for the
success of this protocol.
Conclusions:
In selected patients, fast-track cardiac surgery guarantees short intubation time and ICU length of stay.
It is a team activity and the cardiac anaesthetist plays the role of perioperative physician and team leader.
Minimal invasive surgery, hybrid suites and new technologies minimize the surgical trauma and guarantee fast and
reliable clinical results.
References
1. Heart Surg Forum.2003; 6(4):244-8.
2. Cheng DC. Fast-track cardiac surgery: economic implications in postoperative care. J Cardiothorac Vasc Anesth
1998; 12:72-9.
3. Cheng DC. Fast track cardiac surgery pathways: early extubation, process of care, and cost containment.
Anesthesiology 1998; 88:1429-33.
4. Wong DT, Cheng DC, Kustra R, et al. Risk factors of delayed extubation, prolonged length of stay in the intensive
care unit, and mortality in patients undergoing coronary artery bypass graft with fast-track cardiac anesthesia: a
new cardiac risk score. Anesthesiology 1999;91:936-44.
5. Djaiani GN, Ali M, Heinrich L, et al. Ultra-fast-track anesthetic technique facilitates operating room extubation in
patients undergoing off-pump coronary revascularization surgery. J Cardiothorac Vasc Anesth 2001;15:152-7.
6. Kogan A, Ghosh P, Preisman S, et al. Risk factors for failed fast-tracking after cardiac surgery in patients older
than 70 years. J Cardiothorac Vasc Anesth 2008;22:530-5.
7. Anesthesiology 2008; 109:616
8. Marco C. Haanschotena,b,Fast-track practice in cardiac surgery: results and predictors of outcome. Interact
CardioVasc Thorac Surg 2012
9. http://www.cardiothoracicsurgery.org/content/8/1/47
10. Constantinides VA, Tekkis PP, Fazil A, Kaur K, Leonard R, Platt M, Casula R, Stanbridge R, Darzi A, Athanasiou
T: Fast-track failure after cardiac surgery:Development of a prediction model. Crit Care Med 2006; 34:287582
11. Heart Surg Forum.2003;6(4):244-8.
12. Arndt H Kiessling,Risk factor analysis for fast track protocol failure Journal of Cardiothoracic
Surgery2013,8:47
13. http://dx.doi.org/10.1053/j.jvca.2015.07.002 {December 2015,Volume 29, Issue 6, Pages14661471}
14. Fast- track Cardiac Anesthesia in the Elderly by J Ender www.csarim.cz/Public/csarim/doc/perioperativecare/6_Ender.pdf
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Post cardiac surgery hemodynamic

monitoring: how to interpret the data?
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Dr. Madan Mohan Maddali, MD

Senior Consultant
Department of Cardiac Anesthesia
National Heart Center
Royal Hospital, Muscat, Oman
Email: madanmaddali@hotmail.com
Introduction:
The basic principles of the postoperative management of cardiac surgical patients involve
hemodynamic monitoring and cardiocirculatory management with adequate volume,
positive inotropic drugs and vasopressors based on the data obtained from monitoring.
This review deals with:
1. An appraisal of the available monitoring methods
2. Cardiocirculatory therapy based on the data that is derived from the hemodynamic
monitoring
1. Available monitoring modalities:

The available monitoring methods can be broadly classified as:
A. Basic monitoring
B. Advanced hemodynamic monitoring
A. Basic monitoring: This involves continuous monitoring of ECG, pulse oxymetry,
continuous invasive arterial and central venous pressures, fluid balance, arterial and
venous blood gas analysis. Evidence based recommendations for basic monitoring are
shown in Table-1.
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The grade of recommendations are classified as a) should for strong recommendation, b) might for intermediate
recommendation and c) can for open recommendation throughout this review.
B. Advanced hemodynamic monitoring:

The most popular advanced hemodynamic monitoring modalities are:
a. Echocardiography [Transthoracic (TTE), Transesophageal (TEE)]
b. Transpulmonary thermodilution and calibrated pulse contour analysis[PiCCO,LiDCO,
Doppler method]
esophageal
c. Pulmonary artery catheter
a. Echocardiography
Transesophageal echocardiography (TEE) provides additional information (between 13 and 45% more) compared
to other advanced monitoring methods and can influence therapy in 1052% of cases. Echocardiography provides
guidance in volume and catecholamine therapies, and can influence surgical decision making. TEE has the advantage
of a relatively short period of time required to perform it. The disadvantage of TEE is not providing continuous
hemodynamic monitoring, the need for expensive equipment and the dependency on operator training and
availability. TEE has a complication rate up to 1.2% for severe gastrointestinal complications. The recommendations
for echocardiography in the postoperative set up are summarized in Table-2.
Table 2: Evidence based recommendations for advanced hemodynamic monitoring by echocardiography1
Advanced hemodynamic monitoring: echocardiography
Echocardiography is recommended for establishing diagnosis in the perioperative
period in patients who show acute persistent hemodynamic disturbances, do not
respond to initial therapies, and demonstrate unclear ventricular dysfunction
Grade of
recommendation
might be done
TEE in comparison with TTE is preferred as it has diagnostic advantages

particularly in ventilated post operative patients
can be done
TEE in the perioperative period can improve clinical outcome in patients at increased
risk of MI
can be done
Assessing cardiac output with echocardiography by Doppler method is as reliable as

the thermodilution techniques and is recommended to be used as an alternative to
measuring CO discontinuously.
might be done
The TTE or TEE examination should be documented.
should be done
b. Transpulmonary thermodilution and calibrated pulse contour analysis:

Pulse contour analysis by whatever technique is inaccurate in patients with significant aortic insufficiency, peripheral
vascular disease, cardiac arrhythmias and intra-aortic counter pulsations[IABP]. Dynamic variables like volume
variation (SVV) and pulse pressure variation (PPV) involve cardiopulmonary interaction and is possible under full
mechanical ventilation. Table-3 highlights the recommendations
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Table 3: Evidence based recommendations for transpulmonary thermodilution and pulse contour analysis1
Extended hemodynamic monitoring: transpulmonary thermodilution and
pulse contour analysis
The pulse contour analysis in post operative cardiac surgery
patients shows good correlation with thermodilution
Grade of
recommendation
might be
monitored
Measurement of ITBV seems to be superior to the CVP and the PAOP for the
appraisal of cardiac preload.
can be monitored
SVV and PPV are superior to the CVP and PAOP for predicting volume responsiveness.
SVV and PPV therefore might be used as helpful supplement to hemodynamic
diagnostics.
might be
monitored
c. Pulmonary artery catheter [PAC]:

The use of a PAC in cardiac surgery patients with a low perioperative risk is not considered necessary. Use of PAC is
justified in a) high risk patients for complex cardiac surgery interventions, b) in severe low cardiac output syndrome
[LCOS], c) pulmonary hypertension and d) for the differentiation between severe right or left ventricular dysfunction.
The PAC is unique in that it can be used to measure mixed venous oxygen saturation(SvO2). SvO2 allows assessment
of the global balance between oxygen supply and consumption. A SvO2 orientated therapy has been shown to be
relevant in regard to morbidity and hospital length of stay in postoperative cardiac surgery patients2 Table for show
recommendations for PAC use in cardiac surgery
Table 4: Evidence based recommendations for pulmonary artery catheter1
Extended hemodynamic monitoring: pulmonary artery
catheter
The PAC in cardiac surgical patients with low perioperative risks
might not be used
The PAC can be used:
For determining the cause and guiding therapy in severe
LCOS
For differentiating between left or right ventricular
dysfunction
For diagnosis and therapy of Pulmonary hypertension
In high risk cardiac surgery patients undergoing complex
interventions
Grade of recommendation
Recommendation might be
considered
can be monitored
2. Hemodynamic data interpretation and cardiocirculatory therapy:

The goal of fluid as well as positive inotropic and vasoactive drug management is to ensure sufficient tissue perfusion
and a normalization of oxidative metabolism. Cardiac output and O2-supply are dependent on adequate intravascular
volume and cardiac function. The following parameters are recommended as goals for postoperative cardiovascular
therapies.

ScvO2 >70% or SvO2 >65%
MAP (mean arterial pressure) >65 mmHg
Cardiac Index >2.0 l/min/m2
CVP 812 mmHg (dependent on ventilation mode)
LV-EDAI 69 cm2/m2
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ITBVI 8501000 ml/m2
GEDVI 640800 ml/m2
PAOP 1215 mmHg
Diuresis >0.5 ml/kgBW/h
Lactate <3 mmol/l
The success of the intervention depends on the time to initiation aimed at optimizing the parameters in a goal
directed fashion. Following surrogate parameters are possible indicators of a cardiocirculatory failure1:

ScvO2 <60% with SaO2 98%
Mean arterial pressure <60 mmHg
Urine output <0.5 ml/h, existing for longer than an hour
Plasma lactate >2.0 mmol/l
Peripheral vasoconstriction with delayed capillary refill, respectively cool extremities corresponding to
centralization.
In case of suspected post-operative cardiovascular dysfunction:

1. Optimization of cardiac frequency and rhythm are the first-line tasks.
2. A rough initial assessment of volume status by means of central venous pressure should be performed.
i.
The hemodynamic reaction to volume administration should first be estimated with

autotransfusion by means of passive leg raising3,4.
ii.
Then fluid challenge with the administration of a maximum of 10 ml/kg body weight of

colloid or crystalloid solution should be performed.
3. If a preload increase does not lead to hemodynamic stabilization, an echocardiogram is indicated.
4. A 12 lead ECG to rule out an acute ischemia in unstable patients
5. Scvo2 and lactate concentration should be obtained
6. Fluid balance should be carefully controlled
Management of specific postoperative conditions based on hemodynamic data

The two of the most often encountered hemodynamically compromising postoperative conditions are left and right
heart failure. Management of these two conditions based on hemodynamic data is enumerated below.
A. Management of left heart failure

a.
Preload optimization is the basic prerequisite for management of left heart failure.

b.
Where preload optimization is not sufficient to achieve the targeted hemodynamic goals, treatment

with positive inotropes is indicated.

Left heart failure generally results in one of 4 broad clinical situations:
Clinical situation 1:
Hypovolemic patients are tachycardic and show inadequate ventricular filling. In the presence of a left ventricular end
diastolic area index <5 cm2/m2, or a pulmonary artery occlusion pressure (PAOP) <5 mmHg or an intrathoracic
blood volume index <750 ml/m2, the initial therapeutic approach should be preload optimization.
In smaller volume deficiencies (left ventricular end diastolic area index <7 cm2/m2, or pulmonary artery occlusion
pressure (PAOP) <10 mmHg or an intrathoracic blood volume index <850 ml/m2) a cautious fluid challenge should
be given. If a marked increase in preload parameters does not result in an adequate improvement in cardiac output
or systemic blood pressure, fluid administration should be ceased.
In addition to preload optimization inotropic support of the left ventricle should be started with Dobutamine when
the MAP is <60 mmHg and a PDE III inhibitor or levosimendan is recommended when the MAP is >60 mmHg.
In the case of systemic hypotension it may be essential to additionally use a vasopressor. The use of epinephrine
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is indicated if these therapeutic approaches fail to stabilize the hemodynamic situation or if critical hypotension is
present.
In patients with an adequate preload, a left ventricular end-diastolic area index >9 cm2/m2, a pulmonary artery
occlusion pressure (PAOP) >15 mmHg, or an intrathoracic blood volume index >1000 ml/m2, dobutamine or a PDE
III inhibitor can be used. Norepinephrine should be considered for the contra-regulation of systematic hypotension
and to increase coronary perfusion. Initial treatment with epinephrine is indicated when serious hypotension is
present. In cases where a LCOS does not improve significantly upon the administration of dobutamine or PDE III
inhibitors, supplemental inotropic support with epinephrine is warranted. If down-regulation of -adrenoreceptors is
suspected, the combination of epinephrine and a PDE III inhibitor or levosimendan seems reasonable. If the patient
has undergone a CABG operation, the implantation of an IABP is indicated.
In a hypervolemic patient with a clearly increased preload (left ventricular end diastolic area index >11cm2/m2, a
pulmonary artery occlusion pressure (PAOP) >20 mmHg, or an intrathoracic blood volume index >1200 ml/m2)
volume removal should be the primary goal and the circulation should be supported pharmacologically. Hemofiltration
or hemodialysis can be used as adjuvant therapies. Hemodynamic instability should be treated with dobutamine or
a PDE III inhibitor. Under certain circumstances the additional administration of epinephrine, a combination of
epinephrine and a PDE III inhibitor or levosimendan may be indicated.
Once an adequate arterial pressure has been achieved and the hemodynamic situation has become stable, consideration
can be given to decreasing of pre- and afterload. Total peripheral resistance should be modulated to minimize the
work of the heart, while maintaining an adequate perfusion pressure at the same time. To achieve this treatment goal,
vasodilators such as nitroglycerine [NTG] or sodium nitroprusside and vasopressors such as norepinephrine are
recommended
B. Management of right heart failure:

Clinical manifestations of right ventricular failure occur in 0.041% of patients after cardiac surgery5, and are an
indication for invasive monitoring. The diagnostic instrument of choice is echocardiography. The combination of a
small, well contracting left ventricle and a large akinetic right ventricle is pathognomonic for acute right heart failure.
Assessment of right ventricular preload is typically made by measuring the central venous pressures (CVP) or less
frequently the right ventricular end-diastolic pressure (RVEDP). Values above 10 cmH20 are considered to reflect
adequate ventricular filling.
Assessment of right ventricular after load is reflected by mean pulmonary artery pressure (MPAP). Pulmonary
vascular resistance (PVR) is the next most commonly used indirect measure of right ventricular after load. A decrease
in CO caused by a decrease in contractility will result in an increase in PVR (MPAP = PVR x CO), without any change
in tension in the wall of the right ventricle.
Measurement of right ventricular ejection fraction using the fast-response thermodilution technique is not an ideal
measure of right ventricular contractility. An increase in preload commonly causes an increase in ejection fraction
without any change in contractility. Conversely an increase in right ventricular after load will result in a decreased
ejection fraction. The ejection fraction only reflects right ventricular contractility under conditions of constant preand after load.
In a practical approach, the treatment of right heart failure should begin with three starting points:
1. Where TEE demonstrates a low right ventricular filling volume or where the PAOP to CVP ratio is >1, cautious
volume loading should be the first line treatment. In normotensive patients, treatment with vasodilators is justified.
When this therapeutic approach fails, treatment with inotropes is indicated.
2. In normotensive patients (a MAP between 70 and 80 mmHg), where TEE shows right ventricular volume overload
with signs of right ventricular dilation or where the PAOP to CVP ratio is <1, or where this ratio is rapidly
increasing, dobutamine and/or a PDE III inhibitor should be used to increase inotropy. If the combination of
dobutamine with NTG and/or a PDE III inhibitor is not effective, epinephrine should be used. Epinephrine can,
if necessary, be given in combination with nitroglycerine and/or a PDE III inhibitor.
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Pre-existing pulmonary hypertension and/or therapy resistant right heart failure can be treated with inhalative
prostanoids or NO in addition to positive inotropes. The treatment goal should not be to minimize PAP or PVR
but rather to optimize the PVR to SVR ratio, while maintaining contractility of the right ventricle, myocardial O2
supply and blood pressure (MAP >60 mmHg).
3. Hypotensive patients with a MAP <70 mmHg and high right ventricular preload are by definition in decompensated
right heart failure. Initially therapy consists of dobutamine and a PDE III inhibitor, in combination with
norepinephrine. When this approach fails to sufficiently stabilize hemodynamics, epinephrine should be used.
Depending on the peripheral resistance, nitroglycerine can be additionally used. When pulmonary hypertension is
present, inhaled prostacyclin or NO can be used.
Intra-aortic balloon counterpulsation

The classic indications for the implantation of an IABP include a persistent or worsening LCOS, despite treatment
with high dose inotropes or vasoactive substances, ST elevation or new hypokinesia in the TEE, where surgical or
interventional reversal is not possible and/or where surgical anastomoses are known to be problematic and coronary
revascularization was not complete.
A systematic review has demonstrated that the use of IABP improves long-term survival in cardiac surgical patients6.
A cardiac index-guided goal-directed therapy strategy using fluids, inotropes, and blood transfusion reduced the
composite endpoint of 30-day mortality and major complications and resulted in a shorter ICU and hospital length
of stay in high-risk patients [with European System for Cardiac Operative Risk Evaluation score equal to or greater
than 6] after cardiac surgery7. Implementing preemptive goal directed therapy in moderate to High-Risk Surgery has
shown significant clinical and economic benefits, including 23 to 56% morbidity, and reduced length of hospital stay
by 1 to 2 days8,8,10.
In conclusion, proper data interpretation of hemodynamic data and implementing goal directed therapies, there is
enough evidence to show that postoperative outcome could be increased in cardiac surgery.
References
1. Carl M, Alms A, Braun J et al: S3 guidelines for intensive care in cardiac surgery patients: hemodynamic
monitoring and cardiocirculary system. Ger Med Sci. 2010 Jun 15;8:Doc12.
2. Plnen P, Ruokonen E, Hippelinen M, Pyhnen M, Takala J. A prospective, randomized study of goaloriented hemodynamic therapy in cardiac surgical patients. Anesth Analg. 2000;90:1052-9.
3. Boulain T, Achard JM, Teboul JL et al: Changes in BP induced by passive leg rising predict response to
fluid loading in critically ill patients. Chest. 2002;121:1245.
4. Lafanechre A, Pne F, Goulenok C et al: Changes in aortic blood flow induced by passive leg raising
predict fluid responsiveness in critically ill patients. Crit Care. 2006;10:R132.
5. Kaul TK, Fields BL. Postoperative acute refractory right ventricular failure: incidence, pathogenesis,
management and prognosis. Cardiovasc Surg. 2000;8:1-9.
6. Baskett RJ, Ghali WA, Maitland A et al: The intraaortic balloon pump in cardiac surgery. Ann Thorac Surg.
2002;74:1276-87.
7. Osawa EA, Rhodes A, Landoni G et al: Effect of Perioperative Goal-Directed Hemodynamic
Resuscitation Therapy on Outcomes Following Cardiac Surgery: A Randomized Clinical Trial and
Systematic Review. Crit Care Med. 2015 Dec 7.
8. Hamilton M, Cecconi M, Rhodes A. A systematic review and meta-analysis on the use of preemptive
hemodynamic intervention to improve postoperative outcomes in moderate and high-risk surgical patients.
Anesth Analg 2011;112:1392-1402.
9. Grocott M, Dushianthan A, Hamilton M, et al. Perioperative increase in global blood flow to explicit
defined goals and outcomes after surgery: a Cochrane Systematic Review. BJA 2013;111:535-548.
10. Pearse R. Harrison D, MacDonald N, et al. Effect of a Perioperative, Cardiac Output-Guided
Hemodynamic Therapy Algorithm on Outcomes Following Major Gastrointestinal Surgery: A Randomized
Clinical Trial and Systematic Review. JAMA 2014; 311:2181-90
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undergoing vascular surgery (CON)
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MBBS, MD, DNB, PDCC, FTEE, FIACTA,American National Board of Echocardiography fellowship in Advanced Perioperative TEE,Consultant Cardiac
Anesthesiologist, Apollo Hospitals, Chennai
Why there is no widespread use of cell salvage?

Surgeon feels - operative field is wet after cell saver blood. Heparin rebound
happens. No consensus how much heparin to use.
Anesthesiologist feels- Processing time of salvage procedure when you use

more number of cycles to wash cells is more. Washed cells are lesser in volume
also. You need at least 250ml to 600ml of blood loss before washing cycle can
be triggered.
Perfusionist feels- Disposables are not freely available and leukocyte depletion filters (LDF) are not available in India. (LDFs are used during the processing of donated blood to remove white blood cells. So they should be available
in Blood banks.
Sudden or Expected sudden loss of blood in major cardiovascular surgeries trigger OT

personnel to order and keep adequate allogenic blood inside OT. We feel more safe
when you see PRCs in hand in such situations. Finally we end up giving equal amount
of allogenic blood as we have not used cell saver. Routinely for all cases we dont use
due to cost and expected blood loss is less than a litre. In emergency sudden bleeding
getting allogenic blood is more faster than assembling cell saver.So after a while we
feel like cell saver is not really helpful and it does not come to our mind when it is
really warranted.Risk of transmission of HIV and Hepatitis are negligible with allogeneic
blood transfusion due to improvement in blood bank standards.
Why should we use cell savers?

Allogeneic blood transfusion has been associated with increased risk of tumour
recurrence, postoperative infection, acute lung injury, perioperative myocardial infarction,
postoperative low-output cardiac failure, and increased mortality.So we should better
use autologous blood. Methods of autologous blood transfusion- Preoperative blood
donation, Acutenormovolemichemodilution and intraoperative cell salvage (ICS)
Intraoperative cell salvage1

One type the red blood cell (RBC) washing type collects the shed blood, washes and
centrifugally separates out the RBCs, and then reinfuses them. RBC washingdevices can
theoretically remove any toxic byproducts in the scavenged blood; however, they also
remove platelets and clotting factors. The RBC washing devices are of variable capacity
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and design (e.g. continuous or discontinuous flow) and yield RBC concentrates with different characteristics and
quality. (Hemonetics and Medtronic).
The second major type of autotransfusion device hemofiltration only devices just collects the blood, filters it,
and reinfuses it. These devices return all of the blood elements, including the platelets and the clotting factors, but
they do not remove potentially harmful debris and contaminants.
Complications of cell salvage2

There are many potential complications associated with cell salvage, such as non-immune haemolysis, air embolus,
febrile non-haemolytic transfusion reactions, mistransfusion, coagulopathy, contamination with drugs, cleansing
solutions and infectious agents, and incomplete washing leading to contamination with activated leucocytes, cytokines,
and other microaggregates.Prolonged use of cell salvage with large-volume autotransfusion may be associated with
dilution of clotting factors and thrombocytopenia, and regular laboratory or near-patient monitoring is required, along
with appropriate blood product use.Suctioning of RBCs may cause sheer stress injury, which can result in haemolysis
and therefore reduction in return of RBCs.RBC loss in swabs has been shown to account for 30 50% of intraoperative
blood loss. Cell salvage in obstetrics has been controversial because of the theoretical risk of precipitating amniotic
uid embolus (AFE) based on the concern that amniotic uid mixed with the salvaged RBCs may not be completely
removed by the washing process and subsequently re-infused. Same way cell salvage is controversial with oncological
surgeries.The use of cell salvage in patients with sickle-cell disease has generally been avoided because the hypoxic
environment of the reservoir was thought to result in RBC sickling and re-infusion of this blood may precipitate
a sickle cell crisis.During sterile procedures, the incidence of microbiological contamination of salvaged blood
ranges from 12.7% to 33.3%.The most common source of contamination is thought to be skin and environmental
contamination. Cell salvage with an LDF resulted in signicant reductions in bacterial contamination.
Vascular cases2
Cell salvage has been used for many years in elective and emergency vascular surgery. It has been demonstrated to
be safe, but its efciency at reducing the need for allogeneic blood transfusion and cost-effectiveness has not yet
been proven.A systematic review of ve randomized controlled trials (RCTs) in 2004 concluded that there was not
enough evidence to recommend the routine use of cell salvage during elective abdominal aortic aneurysm (AAA) or
aorto femoral bypass surgery.Cell salvage was more cost-effective in cardiac and orthopaedic surgery than in vascular
surgery.
Orthopaedic, Pediatric and cardiac cases2

Orthopaedic - The majority of available evidence is grade 2/3 and consists of non-randomized, retrospective studies where the use of cell salvage is at the surgeons discretion.
Pediatric - At least 250 to 600 ml volume of blood that has to be collected before processing. So it may not be practical in pediatric surgeries.
Cardiac - It may not be cost effective in low-risk cases, such as primary coronary surgery or isolated valve replacement or repair.
Review of literature
Mannova et al (2014) Review Article3
In the starting of the article they have written like, we may say that both autotransfusion techniques (ANH and ICS)
can be used in elective infra renal aortic surgery. Both techniques can potentially save allogeneic blood and money but
the positive result depends on the amount of blood loss during the surgery, which is frequently higher in abdominal
aortic aneurysm surgery.
Clagett et al (1999)4
Clagett et al published a randomized trial of intraoperative transfusion during aortic surgery. In this study, 100 patients
who underwent AAA repair or aortofemoral bypass for occlusive disease were randomized to ICS (cell salvage) and
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control group. No significant differences were found in estimated blood loss, allogeneic blood transfusion (unit
administered intraoperatively, postoperatively, and total), proportion of patients not receiving allogeneic blood (34%
of patients randomized to ICS and 28% in control patients), postoperative haemoglobin levels and complications
(cardiac, septic, stroke, venous thromboembolism, gastro-intestinal bleeding, pancreatitis, death. The authors found
no benefit of intraoperative autotransfusion (cell-salvage technique) in patients undergoing elective infrarenal aortic
surgery.
Spark et al (1997)5
Spark et al published another prospective randomized study in which they assessed the postoperative outcomes of
patients in elective infrarenal abdominal surgery. Autologous (n=23) and homologous blood transfusion (n=27)
groups were compared. In the autologous group the cell salvage autotransfusion device was used. There was no
difference in perioperative mortality, postoperative development of SIRS and chest sepsis.
Mercer et al (2004)6
In contrast to the studies mentioned above, the results of the study by Mercer were positive for the cell salvage technique.
Significantly fewer patients in the intraoperative autotransfusion group received homologous autotransfusion, 21 vs.
31 (p=0.038), and the median blood requirement per patient was 2 units lower (p=0.012) in the autotransfusion
group. There was a higher incidence of chest infection (12 vs. 5 patients, p=0.049) and SIRS (20 vs. 9 patients,
p=0.020) in the homologous blood transfusion group.
Tawfick et al (2008)7
Tawfick et al. [14] published a retrospective cohort study with 187 patients who underwent open repair of AAA.
One group of patients received an autotransfusion system (cell salvage) and the second group allogeneic transfusion.
61% in the autologous group required 2 or less units of allogeneic blood and all the control patients received 3 or
more units of allogeneic blood. Allogeneic transfusion in the autotransfusion group patients decreased significantly
(p<0.0001). In this study the cell salvage technique markedly reduced the amount of allogeneic blood and was
associated with the reduced intensive care and postoperative hospital stay.
Quriel K et al (1993)8
Quriel et al used an autotransfusion device that administers unwashed, filtered blood (200 patients undergoing
aortic reconstructive surgery). The authors found that using it was safe and efficacious, served as an alternative to
homologous blood transfusion, and diminished the need for additional homologous blood transfusion.
Kelley- Patteson and colleagues [1993]9

Kelley- Patteson and colleagues concluded that routine set up and use of the Cell Saver Autotransfusion Device is
not necessary in those patients undergoing any type of elective aortic surgery, whether for occlusive disease or for
aneurysmal disease, because the use of homologous blood was not altered.
Huber TS et al (1997)10
Huber et al. included 173 cases in their study. No difference was seen in the blood transfusion requirement between
patients with aneurysm and those with aortoiliac occlusive disease. Even if the Cell Saver was used, 73.8% of patients
required homologous blood transfusion with a mean of 3.0 3.1 units being transfused during the hospital stay.
The use of the Cell Saver proved not to be cost-effective in either abdominal aneurysm repair or aortoiliac occlusive
disease patients. The cost was increased by US$263.75 in the aneurysm patients, but only 0.00218 QALYs (Quality
Adjusted Life Year) were added (US$120 794 per QALY). For aortoiliac occlusive disease the cost was US$356.68
and 0.00062 QALYs were added (US$528 275 per QALY). Cost-effectiveness was achieved only if the incidence of
hepatitisC was 10-fold higher and if blood loss routinely was more than 5units in the aneurysm patients and 6units
in the aortoiliac occlusive disease patients.
Goodnough LT et al (1996)11
Goodnough and colleagues followed 184 patients who underwent elective AAA repair to evaluate the costeffectiveness of the cell salvage technique. Blood loss on average was 1748 1236 ml in these patients. Thirty-two
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(89%) of the 36 patients, who did not receive any Cell Saver blood, required transfusions. Of the patients who had
Cell Saver blood salvaged a similar percentage (67%) required homologous transfusions. Cost savings could only be
demonstrated in 22% of the patients who underwent surgery. The investigators concluded that intraoperative cell
salvage was beneficial for patients who had intraoperative blood losses of 1000 ml or more and Cell Saver volumes
returned of 750 ml or more.

Based on the results of these papers, only one study among the randomized studies confirmed the convincing
benefit of using the cell salvage technique (Mercer et al) and only 2 non-randomized studies (Quriel et al)-unwashed
filtered blood, Tawfick et al) provided similar results. In comparison with the other three randomized studies the
specificity of this study was that Mercer and colleagues assessed only a subpopulation of patients in infrarenal
aortic surgery, i.e. those who underwent abdominal aortic aneurysm repair where blood loss is usually more than
the aorto occlusive disease.The advantage of the retrospective non-randomized studies was that the amount of
patients who were estimated was higher but their results were similarly controversial. Quriel et al. found a positive
benefit of ICS in saving both allogeneic blood and money, however, the autotransfusion device, used in this study,
administered unwashed filtered blood in contrast to the other non-randomized studies in which the second major
type of autotransfusion device (RBC washing device) was used.
Freischlag et al (2004) Review Article1

In 2004, Freischlag published a review dedicated to intraoperative blood salvage in vascular surgery. The studies,
mentioned in this work, are a mixture of prospective and retrospective evaluations of cell salvage techniques (KelleyPatterson et al., Quriel et al., Goodnough et al., Huber et al.). The author summarized that the use of cell salvage
techniques in vascular surgery had the potential to prevent the use of homologous blood transfusions, but in reality
that does not appear to occur. The risk of transmitting diseases by blood transfusions is sufficiently low and the use
of the Cell Saver does not appear to have an impact on the individual patients. Cost savings only occur when there is
a high blood loss. Economically, the set up for both types of devices has been shown to be cost-effective only when
2 or more units are recovered from the surgical field during the operation and then transfused back into the patient.
Cell saver techniques often do not prevent the need for transfusions, nor are they very cost-effective; therefore, their
use should be considered on a case-by-case basis.
Alvarez et al (2004)12
In the same year, 2004, Alvarez et al assessed only randomized controlled trials involving cell salvage and vascular
surgery with similar results. The authors identified five randomized trials in MEDLINE, EMBASE and the Cochrane
library (Clagett et al., Spark et al., Kelley-Patterson et al.). These studies compared the cell salvage group and the
control group in abdominal vascular surgical procedures. In this meta-analysis of randomized controlled trials the
authors were unable to demonstrate that cell salvage decreased exposure to allogeneic red cells.
Takagi et al (2007)13
In 2007 Tagaki et al identified 4 randomized controlled trials including data for 292 patients (Spark et al. Clagett
et al. Wong et al. Mercer et al.). Two out of 4 sensitivity analyses demonstrated statistically non-significant results
favouring intraoperative autotransfusion.Pooled analysisshowed a statistically significant 37% reduction in the risk of
allogeneic blood transfusion with intraoperative autotransfusion compared with control group (risk ratio, 0.63; 95%
confidence interval, 0.41-0.95; p=0.03). Based on this a meta-analysis of randomized controlled trials in AAA surgery,
intraoperative autotransfusion reduces the risk of allogeneic blood transfusion in elective infrarenal AAA repair.
Tavare et al (2011)14
Later, in 2011, Tavare et al. [18] did another meta-analysis of randomized controlled trials with the aim of assessing
the improvement of clinical outcomes.The authors found that the use of intraoperative cell salvage did not cause
an increase in morbidity or mortality when compared with the standard practice of transfusion of allogeneic blood
and may actually improve some clinical outcomes: shorter stay in ICU, shorter hospital stay, reduction in chest sepsis,
occurrence of SIRS in elective AAA surgery.According to these authors intraoperative cell salvage is a useful and safe
strategy.
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Shantikumar S et al (2011)15
The authors identified 23 studies in order to delineate the role of cell salvage in reducing allogeneic blood use in open
AAA repairs. As the authors wrote, even if some data were conflicting, cell salvage appeared to reduce the overall use
and exposure allogeneic blood, and reduced the length of ICU and hospital stay after elective AAA repairs.
Ashworth et al (2010) Review Article2

Cell salvage reduces the requirement for allogenic blood transfusion. It should be considered for surgery with an
anticipated blood loss of 1000 ml. There is still a need for large prospective randomized controlled trials

In conclusion we may say that the results of single studies are full of contradictions, and meta-analyses of these
studies have brought no solution to the dispute over the efficiency of the cell salvage technique in vascular surgery.
Only a few of the studies showed the Cell Saver device to be beneficial. Some papers seem to suggest that the only
purpose of setting up the Cell Saver Autotransfusion Device is to provide the surgeon with peace of mind in the
event of sudden and unforeseen blood loss, such as when the aorta, vena cava, or renal vein is injured. On the other
hand, it should be said that the use of cell salvage techniques in vascular surgery can have the potential to prevent
the use of allogeneic blood transfusions and bring cost savings. It depends on the amount of blood loss during the
operation.In terms of AAA repair, blood losses are mostly higher than 1000 ml, and administering of Cell Saver
device is better justified. The cost effectiveness of the cell salvage technique depends on what type of device is used.
The cost of the RBC no-washing type is lower and savings are more evident in this case (Quriel et al). And what is
more, economically, the set-up for both types of the device has been shown to be cost-effective only when 2 or more
units are recovered from the surgical field during the operation and then transfused back into the patient.
Conclusion
The use of cell salvage techniques in vascular surgery has the potential to prevent the use of homologous blood
transfusions, but in reality that does not appear to occur.1The risk for transmission of disease by blood transfusions
is sufficiently low that the use of the Cell Saver does not appear to have an impact on the individual patient.1Cost
savings only occur when there is a high blood loss and a high RBC salvage rate.1Expertise regarding operation of
cell savers and leucocyte depletion fitters is not freely available to recommend its use in all cases in present
scenario.
References
1. Freischlag et al, Critical Care 2004, 8(Suppl 2):S53-S56 (DOI 10.1186/cc2409) Intraoperative blood salvage
in vascular surgery worth the effort?
2. A. Ashworth and A. A. Klein et al, British Journal of Anaesthesia 105 (4): 40116 (2010) Advance Access
publication 28 August 2010 . doi:10.1093/bja/aeq244, Cell salvage as part of a blood conservation strategy
in anaesthesia.
3. Mannova J et al, Blood Transfusion Strategies in Elective Vascular Surgery, Mannova et al., J Blood Disorders Transf 2014, 5:6 A Review Article
4. Clagett GP, Valentine RJ, Jackson MR, Mathison C, Kakish HB, et al. (1999) A randomized trial of intraoperative autotransfusion during aortic surgery. J Vasc Surg 29: 22-30.
5. Spark JI, Chetter IC, Kester RC, Scott DJ (1997) Allogeneic versus autologous blood during abdominal
aortic aneurysm surgery. Eur J Vasc Endovasc Surg 14: 482-486.
6. Mercer KG, Spark JI, Berridge DC, Kent PJ, Scott DJ (2004) Randomized clinical trial of intraoperative
autotransfusion in surgery for abdominal aortic aneurysm. Br J Surg 91: 1443-1448.
7. Tawfick WA, O`Connor M, Hynes N, Sultan S (2008) Implementation of the ContinousAutoTransfusion
System (C.A.T.S.) in open abdominal aortic aneurysm repair: an observational comparative cohort study.
Vasc Endovascular Surg 42: 32-33.
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8. Quriel K, Shortell CK, Green RM, DeWeese JA (1993) Intraoperative autotransfusion in aortic surgery. J
Vasc Surg 18: 16-22.
9. Kelley-Patteson C, Ammar AD, Kelley H: Should the Cell Saver Autotransfusion Device be used routinely
in all infrarenal abdominal aortic bypass operations? J Vasc Surg 1993, 18: 261-265
10. Huber TS, Carlton LC, Irwin PB, Flug RR, Harward TRS, Flynn TC, Seeger JM: Intraoperative autologous
transfusion during elective infrarenal aortic reconstruction. J Surg Res 1997, 67:14-20
11. Goodnough LT, Monk TG, Sicard G, Satterfield SA, Allen B, Anderson CB, Thompson RW, Flye W, Martin K: Intraoperative salvage in patients undergoing elective abdominal aortic aneurysm repair: an analysis
of cost and benefit. J Vasc Surg 1996, 24:213-218.
12. Alvarez GG, Fergusson DA, Neilipovitz DT, Hbert PC (2004) Cell salvage does not minimize perioperative allogeneic blood transfusion in abdominal vascular surgery: a systematic review. Can J Anaesth 51:
425-431.
13. Takagi H, Sekino S, Kato T, Matsuno Y, Umemoto T (2007) Intraoperative autotransfusion in abdominal
aortic aneurysm surgery: meta-analysis of randomized controlled trials. Arch Surg 142: 1098-1101.
14. Tavare AN, Parvizi N (2011) Does use of intraoperative cell-salvage delay recovery in patients undergoing
elective abdominal aortic surgery? Interact CardiovascThorac Surg 12: 1028-1032
15. Shantikumar S, Patel S, Handa A (2011) The role of cell salvage autotransfusion in abdominal aortic aneurysm surgery. Eur J Vasc Endovasc Surg 42: 577-584.
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undergoing vascular surgery (PRO)
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DNB MNAMS PDCC PGHM
Senior Consultant (Cardiac Anesthesiology)
Medanta- The Medicity
Gurgaon (Haryana)
Introduction
Cell salvage is the process by which blood from the surgical field is collected, filtered and
washed to produce autologous blood for transfusion back to the patient. It consists of
scavenging the blood from the operative field or wound for reinfusion into the patient,
typically after noncellular matter is reduced by centrifugation, a process termed as washing.
History1,2
1818- 1st recorded use of cell salvage and autologous transfusion when a gynaecologist (Blundell) treated patients with post-partum haemorrhage. Blood
soaked swabs were washed in saline & mixture was re-infused. However it was
associated with high mortality.
1931- Blood salvaged from a haemothorax was directly re-infused.
1943- Arnold Griswald- 1st cell salvage autotransfusion device. Suctioned blood
was collected in a bottle and then strained through a cheese cloth before being
re-infused. This formed the basic principles for modern cell salvage devices.
1960s- Number of commercial devices became available
1970s-1st modern cell saver
Type of devices3
RBC Washing type- Collects the shed blood, washes and centrifugally separates out the RBCs and then returns them back. During this process, platelets
and clotting factors are also removed
Hemofiltration only- Collects the blood, filters it, and re-infuses it. These devices return all of the blood elements, do not remove any potentially harmful
debris and contaminants
Risk of Allogenic transfusion4

Risk of tumour recurrence
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Postoperative infection
Acute lung injury
Perioperative myocardial infarction
Postoperative low-output cardiac failure
Morbidity
5 year mortality
Indications of Cell salvage5

Anticipated intraoperative blood loss >1litre or >20% of blood volume

Preoperative anemia or increased risk of beeding
Patient with Rare blood group or antibodies
Patient refusal to receive allogenic blood transfusion (Jehovahs witness)
American Association of Blood Bank- would ordinary be arranged or where >10% of patients undergoing
the procedure require transfusion
Advantages of Cell salvage6

Mean erythrocyte viability as high as 88%
2,3-disphosphoglycerate (2,3-DPG) & adenosine triphosphate (ATP) levels
Salvaged RBCs maintain their normal biconcave disc shape, but allogeneic blood assumes an echinocyte
shape after 14 days that impairs its ability to cross the capillary bed.
Improved oxygen-carrying capacity and tissue oxygen delivery
Cell Salvage in vascular surgery

Vascular surgery particularly aortic aneurysm repairs (elective & ruptured) involves blood loss (>1000ml) due to
opening of aneurysm sac or back bleeding from lumbar arteries. Massive blood loss may lead to bowel ischemia,
multiorgan failure and thereby increase morbidity & mortality.7
Review of literature revealed cell salvage as a reliable method to replace lost blood products without significant deleterious side effects and significantly reduces allogeneic blood requirements. A multicentre, prospective, randomized
study also revealed that cell salvage in combination with acute normovolaemic haemodilution (ANH) decreased the
exposure to allogeneic blood transfusion from 80.0% to 33.7%. Some authors also showed decreased length of stay
in intensive care and hospital.8-10
Conclusion
Cell salvage is an important modality in vascular surgery particularly aneusysm and complex repairs. The main aim is
to reduce overall blood product use and to reduce the proportion of patients exposed to allogeneic blood. There is
an initial cost of the set-up, disposables, and staff training, however, it may be cost-effective when compared with the
cost and scarcity of allogeneic blood. Its use should be encouraged in all major vascular procedures with anticipated
blood loss >1000ml. However, larger prospective RCT are required to further prove its efficacy.
References
1. Blundell J. Experiments on the transfusion of blood by the syringe. Med Chir Trans 1818; 9: 5692
2. Brown AL, Debenham MW. Autotransfusion: use of blood from hemothorax. J Am Med Assoc 1931; 96:
12235
3. Serrick CJ, Scholz M, Melo A, Singh O, Noel D: Quality of redblood cells using autotransfusion devices: a
comparativeanalysis. J Extra Corpor Technol 2003, 35:28-34
4. Duffy G, Neal KR. Differences in post-operative infection rates between patients receiving autologous and
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allogenic blood transfusion: a meta-analysis of published randomized and nonrandomized studies. Transfus
Med 1996; 6: 3258
5. The Association of Anaesthetists of Great Britain and Ireland (AAGBI) Safety GuidelineBlood Transfusion and the Anaesthetist: Intra-operative Cell Salvage. 2009. http://aagbi.org/publications/guidelines/
docs/cell%20_salvage_2009_amened.pdf
6. Schmidt H, Kongsgaard U, Kofstad J, Geiran O, Refsum HE. Autotransfusion after open heart surgery: the
oxygen delivery capacity of shed mediastinal blood is maintained.
Acta Anaesthesiol Scand 1995; 39: 7548
7. Ouriel K, Shortell CK, Green RM, DeWeese JA. Intraoperative autotransfusion in aortic surgery. J Vasc Surg
1993;18(1):16e22
8. Maarkovic M; et al. Intraoperative cell salvage versus allogeneic transfusion during abdominal aortic surgery:
clinical and financial outcomes.Vascular 2009; 17: 8392
9. Healy CF; et al. Transfusion requirements and outcomes in patients undergoing abdominal aortic surgery
using intra-operative cell salvage. Ir J Med Sci 2007; 176: 336
10. Wong JC; et al. Autologous versus allogeneic transfusion in aortic surgery: a multicenter randomized clinical
trial. Ann Surg 2002; 235: 14551
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Diastolic Function
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Justiaan LC Swanevelder, Francois Roodt

University Department of Anaesthesia
Groote Schuur and Red Cross War Memorial Childrens Hospitals
University of Cape Town, South Africa
The Diastolic phase of the cardiac cycle has only recently become appropriately
recognized as an independent component of overall cardiac function. It is defined as
the phase where the ventricle relaxes and fills in preparation for the next contraction (fig
1). The filling of the left ventricle depends on a complex interaction between ventricular
relaxation, compliance, systolic function, as well as an important late diastolic contribution
from atria contraction.
Physiology of Diastole
The diastolic phase of the cardiac cycle can be divided into four distinct phases from
aortic valve closure (AVC) to mitral valve closure (MVC) (Fig 1). Phase 1, isovolumic
relaxation, begins with AV closure. Once pressure in the left ventricle (LV) falls below
left atrial (LA) pressure, phase 2, rapid ventricular filling begins with opening of the
mitral valve. This early rapid LV filling is dependant upon LV elastic recoil, energy
dependant relaxation, compliance and the LA-LV pressure gradient. As this pressure
gradient equilibrates phase 3, diastasis, begins resulting in minimal flow between the
two chambers. Atrial contraction then takes place, representing phase 4 resulting in an
increased LA pressure and therefore contributing 10-20% of LV filling in a healthy adult.
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Diastolic Dysfunction
Normal diastolic function is required for optimal cardiac performance. Prolonged, slowed, incomplete or uncoordinated
diastolic processes of relaxtion and/or filling leads to diastolic dysfunction. Increased LV filling pressure is the final
pathway of these abnormalities, leading to symptoms and risk of heart failure.
Doppler echocardiography has helped to establish diastolic dysfunction as a major pathophysiological component
of many cardiac disorders. It has been used to predict functional class and prognosis in congestive heart failure(1).
Echocardiographic studies have also suggested that diastolic dysfunction may contribute to perioperative
hemodynamic instability and adverse outcomes following cardiac surgery (2) and 30-70% of cardiac surgical patients
have diastolic dysfunction pre-operatively. Identifying high risk patients pre-operatively and monitoring diastolic
function intra-operatively may direct therapeutic intervention to facilitate weaning from cardiopulmonary bypass
and reduce perioperative mortality. Nearly half of patients with Heart Failure have diastolic dysfunction and a near
normal ejection fraction (HFNEF or HF with Normal EF)(3).
Diastolic dysfunction may be present in the absence of heart failure, with normal filling pressures, and is also
commonly present in patients with systolic LV dysfunction. It increases with age, especially elderly women with
hypertensive heart disease. It is also present in coronary artery disease, cardiomyopathies, constrictive pericarditis
and valvular heart disease.
Echocardiographic evaluation of Diastolic Function

The gold standards for diagnosing diastolic dysfunction, is the time constant of relaxation () correlating to the rate
of cardiac relaxation, and pressure volume curves obtained by direct measurement to assess chamber compliance.
These are research tools in the majority of patients.
Two dimensional (2-D) echocardiography can be used to infer diastolic dysfunction by assessing ventricular wall
thickness, contractility, pericardial thickness, dilatation of inferior vena cava and hepatic veins and heart valve function.
As a rule of thumb left atrial enlargement and left ventricular hypertrophy is indictive of diastolic dysfunction, untill
proven other wise.
Doppler echocardiography has emerged as the principal clinical tool for the assessment of left ventricular diastolic
function. Doppler mitral inflow velocity derived variables is the most widely used method of diastolic evaluation.
Pulmonary venous Doppler flow indices (atrial filling) provide additional information. Unfortunately these two
methods are influenced by several physiological factors, especially acute changes in preload. More recently colour M
mode and tissue Doppler imaging have emerged as new modalities that are less affected by loading conditions.
Mitral Valve Inflow

The normal Doppler recording of ventricular inflow should ideally be obtained with the pulse wave Doppler sample
volume placed at the tips of the mitral valve leaflets.
Doppler inflow pattern into the ventricle
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Following isovolumic relaxation blood flow accelerates from the atrium to the ventricle accounting for the initial
E-wave velocity (0.6-0.8 m/s) corresponding to the maximum LA-LV pressure gradient. The LA-LV pressure
gradient falls causing a deceleration in blood flow down to minimal flow during diastasis as the chamber pressures
equilibrate. LA pressure then increases during atrial contraction giving rise to a second velocity peak, the A-wave (0.20.35m/s). The four useful variables from mitral flow interrogation are peak early diastolic transmitral flow velocity
(E), peak late diastolic transmitral flow velocity (A), early filling deceleration time (DT), and A-wave duration (Adur).
Normal mitral flow velocity curves vary with loading conditions, age, and heart rate. Normal aging results in slowing
of relaxation and therefore the gradual decrease of E and increase of A, and they become approximately equal in the
sixth decade of life. A normal E/A ratio is between 0.75 and 1.5. Early filling DT reflects LV compliance in early
diastole and is normally less than 220 milliseconds.
There are three patterns of progressive abnormal LV filling consistent with diastolic dysfunction: (1) impaired
relaxation, (2) pseudonormal pattern and (3) a restrictive pattern associated with abnormal LV compliance.
Impaired relaxation produces a delayed drop in LV pressure and a decreased early transmitral gradient resulting in a
prolonged IVRT and a decrease in the peak E velocity. The reduced early filling delays equilibration of the transmitral
gradient and prolongs DT. The resulting compensatory increase in late filling from atrial contraction produces an
increase in peak A-wave velocity. Impaired relaxation occurs in LV hypertrophy, myocardial ischemia, and early
cardiomyopathies.
In the restrictive defect of diastolic function relaxation is still impaired but occurs together with decreased LV
compliance and elevated LA pressure. This results in a much-increased E-wave velocity and a short IVRT. The
transmitral pressure gradient equilibrates very quickly producing a short deceleration time <150 msec. The A-wave is
reduced because LV pressure is relatively high during atrial contraction resulting in early mitral valve closure.
As the transition from impaired relaxation to restrictive physiology takes place, the ventricular filling pattern undergoes
pseudonormalization. The E and A velocities, DT, and IVRT tend to fall in the normal range. This is due to the
moderately raised LA pressure, which compensates for the impaired relaxation. Performing a Valsava maneuver,
unmask this by reducing the preload, reveals an impaired relaxation pattern of Doppler indices.
Left Atrial Filling Pulmonary venous flow

Doppler interrogation of the pulmonary veins (PV) can be useful in evaluating ventricular diastolic function. Normal
PV velocity consists of an antegrade systolic velocity (PVS), which may be monophasic or biphasic during atrial
relaxation and mitral valve closure. A second antegrade velocity occurs in diastole (PVD) following opening of the
mitral valve, as the LA becomes a conduit between the PV and LV. Atrial contraction accounts for the retrograde
flow velocity (PVA) in late diastole. Impaired relaxation typically shows decreased PVD that parallels reduced
transmitral E-wave velocity and a compensatory increase in the PVS. Conversely, restrictive physiology, consistent
with decreased compliance, results in the reverse situation. As the compliance continues to worsen the velocity of the
retrograde PVA may increase and its duration may exceed the duration of the mitral inflow A velocity.
Both mitral inflow and pulmonary vein flow velocities are altered by several factors and can therefore be inconclusive.
Recently, colour M-mode (CMM) and Doppler tissue imaging (DTI) have emerged as new modalities that are less
affected by loading conditions and provide strong complementary role in the assessment of diastolic function
Colour M-Mode Propagation Velocity

Early diastolic flow propagation velocity by CMM (Vp) displays velocity information along a scan line from the mitral
valve to the LV apex in the 4 chamber view. The advantage is CMM provides superior temporal, spatial and velocity
resolution. VP is the velocity that blood travels from the mitral annulus to the apex of the ventricle. A slope should
be drawn from the mitral valve at the first aliasing velocity during early filling to 4 cm distally into the LV cavity. A
velocity of less than 45cm/s is consistent with diastolic dysfunction in patients more than 30 years old. Also a ratio
of the mitral E velocity to VP correlates well to LV filling pressures and a E/VP ratio > 1.5 is associated with increased
LA pressures. A Vp < 50cm/s has also been shown to identify patients with diastolic dysfunction during coronary
artery bypass graft surgery
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DTI of the Mitral Annulus

The lateral mitral annulus velocity in the 4 chamber view is recorded by DTI to evaluate diastolic function. There is
a positive systolic signal (peak systolic myocardial velocity) and a negative signal in early (Ea) and late diastole (peak
diastolic myocardial velocity during atrial contraction). An Ea value of less than 8cm/s is consistent with diastolic
dysfunction. The main limitation of DTI is the extrapolation of this regional annular motion to global diastolic
function. This load independence of this modality has been questioned although it is much less in worsening
ventricular relaxation.
Newer modalities of Deformation Imaging with Speckle Tracking as well as Global Diastolic Strain and Strain Rate
shows promise in assesing for Diastolic Dysfunction. It has been derived from DTI with the following advantages
(1) global diastolic dysfunction isnt base on measurement of a few segments, (2) tethering and translational motion
does not affect it, (3) nor is it angle dependant. The later has a closer correlation with TAU than Ea, with a very good
predictive value.
Diastolic dysfunction poses a clinical important and relevant cahallange to perioperative management. Routine
evaluation of diastolic dysfunction should be done on every patient presenting with congestive heart failure. All
modalities of echocardiography should be used beginning with a detailed 2D anatomical scan as well as the above
methods described.
Ideally a cause for any diastolic dysfunction should be sought so that it can be treated. There is no pharmacological
intervention that specifically targets the molecular mechanism of diastolic dysfunction at the moment but evaluation
can provide important prognostic information.
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Dr.R.Satish
Pulmonary hypertension (PHT) often complicates patient care in the surgical units and
intensive care units. Severe acute pulmonary hypertension may produce right ventricular
(RV) failure.
Pulmonary hypertension and RV failure may reduce left ventricular (LV) filling, decrease
cardiac output, and lead to systemic hypotension. Decreased arterial blood pressure may
compromise RV coronary perfusion at a time when RV end- diastolic pressures and RV
myocardial oxygen consumption are increased as a result of increased RV wall tension,
thereby leading to RV ischemia. RV ischemia will exacerbate RV failure, causing a further
reduction in cardiac output and blood pressure.This vicious cycle may continue unless the
pulmonary artery pressure (PAP) is reduced, permitting an increased RV ejection fraction.
Unfortunately, treatment of pulmonary hypertension with intravenous vasodilators may
worsen the systemic hypotension.
KEY SIGNALLING PATHWAYS IN PAH

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A selective pulmonary vasodilator should decrease pulmonary artery pressure (PAP) and pulmonary vascular resistance
(PVR), without affecting systemic arterial pressure and potentially improve oxygenation by redistributing pulmonary
blood flow to ventilated areas of lung1. Inhaled Nitric oxide possesses these properties.
Prior to the discovery of selective pulmonary vasodilators for the treatment of PHT, clinicians were faced with
the difficult task of finding the precise dose of a given systemic vasodilator that produced the greatest decrease
in pulmonary arterial pressure for the smallest decrease in systemic arterial pressure. The number of systemic
vasodilators that have been evaluated for the treatment of PHT testifies to the difficulty of achieving this balance and
of treating this condition.
The introduction of inhaled vasodilators with the ability to produce selective pulmonary vasodilation was a major
advance in the treatment of PHT.
In 1991, Frostell and colleagues demonstrated a therapeutic potential for inhaled NO to act as a selective pulmonary
vasodilator. NO rapidly binds to haemoglobin (Hb) with a high affinity and the vasodilatory effect of inhaled NO is
limited to the lung, unlike the intravenously infused vasodilators.
Inhaled NO (iNO) increases blood flow to well-ventilated lung areas, which may, in some cases, have an increased
vasomotor tone. This inhaled vasodilatory effect is in marked contrast to the effect of intravenously administered
vasodilators, which produce diffuse dilation of the pulmonary vasculature, thereby increasing blood flow to areas of
non ventilated lung and increasing intrapulmonary shunting and reducing the PaO2. In contrast, inhaled NO should
selectively improve the perfusion of ventilated regions, thereby reducing intrapulmonary shunting and improving
arterial oxygenation. These beneficial effects of inhaled NO on intrapulmonary shunting and oxygenation have been
demonstrated in some adult and paediatric patients with acute respiratory distress syndrome (ARDS)2. Unfortunately,
this effect can, at times, be transient.
Use of iNO is limited by the potential for toxicity and high cost. NO forms methemoglobin and nitrate upon exposure
to oxyhemoglobin in the pulmonary circulation3. In humans without methemoglobin reductase deficiency, doses <40
ppm do not cause methemoglobinemia, and animal data suggests that long term administration at comparable doses
are nontoxic. In addition to methemoglobinemia, lung injury may occur if excessive amounts of NO are oxidized
to nitrogen dioxide (NO2), a pulmonary irritant that can cause bronchospasm and pulmonary edema. Modern iNO
delivery systems include monitoring for NO and NO2 levels. The hourly cost for use of iNO is estimated to be $117
in 2012 in the United states4.
Although inhaled NO therapy results in a temporary increase in oxygenation in patients with acute respiratory distress
syndrome (ARDS), it has not been shown to improve survival. This factor, combined with its potential toxicity,
difficulties in administration and cost (a major consideration), has prompted the search for alternative selective
pulmonary vasodilators.
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ALTERNATIVES TO NITRIC OXIDE:

NO donors:
Inhaled sodium nitroprusside
Inhaled nitroglycerine
Prostaglandins:
Epoprostenol
Iloprost
Treprostinol
PGE1
Phosphodiesterase Inhibitors:
Sildenafil
Milrinone
Adrenomedullin
Nitric Oxide Donor Drugs:
A number of synthetic agents release nitric oxide (NO) either spontaneously or after enzymatic cleavage and thereby
provide a means of delivering NO to its site of action in a form other than as a gas.
Sodium Nitroprusside (SNP)
Inhaled SNP has been evaluated in animal models of PH. It has been shown to produce dose-dependent pulmonary
vasodilation in isolated perfused rabbit lungs with thromboxane-induced PH. When administered through a nebulizer
connected to the inspiratory limb of the breathing circuit, SNP has been shown to be a selective pulmonary vasodilator5.
In a study on cardiopulmonary effects of nebulized sodium nitroprusside in term infants with hypoxic respiratory
failure6, 22 newborn term infants with hypoxia (PaO2 <100 mm Hg) during mechanical ventilation (FiO2 =1.0) were
nebulised (neb) with sodium nitroprusside (5 mg followed by 25 mg) into the inspiratory arm of the ventilator circuit.
PaO2 increased significantly with 5 mg neb SNP ( P=0.04) and with 25 mg neb SNP (P=0.009). Differences between
mean PaO2 at 5 mg versus 25 mg neb-SNP were also statistically significant (P=0.03). When comparing the effect of
neb-SNP to iNO, the treatment-induced increases in PaO2 were similar. Thus nebulised sodium nitroprusside causes
a dose-dependent increase in oxygenation in term infants with hypoxic respiratory failure, similar in magnitude to
iNO (inhaled Nitric Oxide).
SNP administration is however limited by its short duration of action necessitating continuous administration and
also by the potential cyanide/thiocyanate toxicity and methemoglobinemia.
Nitroglycerin(NTG)
Nitroglycerin produced dose-dependent pulmonary vasodilation, which was noted to be significantly less efficacious
than the other agents tested, including SNP.
Mandal et al7 in their study comparing the acute hemodynamic effects of inhaled nitroglycerine (iNTG), intravenous
nitroglycerine (IV NTG) alone and their combination with intravenous dobutamine (IV DOB) during the early
postoperative period, in patients with PAH concluded that only iNTG produced selective pulmonary vasodilatation,
while IV NTG and its combination with IV dobutamine had a significant concomitant systemic vasodilatory effect.
Administation of a dose of 2.5 g/kg/min of inhaled nitroglycerin produced significant decreases in pulmonary
arterial pressure, pulmonary vascular resistance and intrapulmonary shunting without affecting systemic arterial
pressures8.
However inhaled NTG is limited by its short duration of action and the need for continuous or repeated
nebulisation.
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Nitric OxideNucleophile Adducts:

Compounds formed by reacting NO with various nucleophiles release Nitric oxide spontaneously in physiologic
solutions, are stable as solids, are highly soluble in aqueous media, and have the potential to function as an aqueous
slow-release form of NO. Jacobs et al9. demonstrated that an inhaled NONOate [2-(dimethylamino) ethylputreanine
NO] improved oxygenation and reduced PVR, without affecting systemic hemodynamics, in a porcine model4.
However the NONOate decreased both pulmonary and systemic vascular resistances, implying a non selective action.
There are currently no clinical investigations describing the use of these novel NO donor drugs.
Phosphodiesterase (PDE) Inhibitors:

Nitric oxide exerts its biologic properties by increasing intracellular concentrations of cyclic guanosine monophosphate
(cGMP). Cyclic guanosine monophosphate is rapidly metabolized by phosphodiesterases, thereby terminating the
effect of NO. Both cGMP and cAMP are metabolized by PDEs. While cGMP is metabolized predominantly by
type 5 PDEs, cAMP is metabolized mainly by type 3 PDEs. Type 5 PDEs are expressed in relatively high amounts
in the pulmonary vasculature and animal models suggest that type 5 PDE inhibitors are more effective at decreasing
pulmonary arterial pressures than type 3 PDE inhibitors.
Milrinone:
A study by Hentschel et al10 on the role of Inhaled milrinone on congestive heart failure in animal model revealed
that while intravenous infusion of milrinone reduced both pulmonary and systemic arterial blood pressure, inhalation
of milrinone predominantly dilated pulmonary blood vessels, resulting in a reduced pulmonary-to-systemic vascular
resistance ratio.
Repeated milrinone inhalations in 20 minute intervals caused a stable reduction of pulmonary artery pressure. Inhaled
vasodilators may potentially circumvent these detrimental effects by acting predominantly in the pulmonary circulation
with little or no vasodilatory effect in systemic blood vessels. Inhalation of 1 mg/ml milrinone reduced PAP more
effectively than the maximal intravenous dose of 1 g/kg/min, but without exerting systemic hemodynamic effects.
Haraldsson et al11. recently demonstrated that inhaled milrinone caused selective pulmonary vasodilation in cardiac
surgical patients with postoperative PHT without systemic effects in cardiac surgical patients with pulmonary
hypertension. Furthermore, inhaled milrinone appears to potentiate and prolong the pulmonary selective vasodilatory
effect of iPGI2. Inhaled milrinone alone or combined with iPGI2 maybe an important therapeutic option in the
treatment of patients with pulmonary hypertension and right ventricular failure.
Sildenafil:
Sildenafil is a selective PDE5 inhibitor commonly used in the treatment of erectile dysfunction. Sildenafil by virtue
of its action of slowing the degradation of cGMP, has been extensively used in the management of PHT in its oral
and intravenous formulations. Though inhaled sildenafil is postulated to be of benefit, there are not many studies
except on animal models12.
Prostaglandins:
Intravenous PGI2 (ivPGI2) is an established treatment for primary PH, and has also been studied in more acute
conditions such as ARDS. Disadvantages of ivPGI2 include the need for long-term intravenous access, the lack
of pulmonary selectivity, resulting in systemic side effects, and the potential for causing increased intrapulmonary
shunting (in patients with lung injury).
In contrast, inhaled PGI2 produces selective pulmonary vasodilation, can potentially improve oxygenation and does
not cause the systemic side effects associated with the intravenous route.
Inhaled PGI2 and iNO have been compared in animal models of PH and in several clinical studies. Inhaled PGI2
produces comparable effects to iNO, with a trend (in both animal and clinical studies) for inhaled PGI2 to produce
greater decreases in pulmonary vascular resistance while iNO produces greater improvements in oxygenation. In
patient with ARDS, inhaled PGI2 was shown to produce selective pulmonary vasodilation and increases in PaO2
comparable to those obtained with iNO. Approximately 53% of patients with ARDS respond to inhaled PGI2 with
an increase of >10% in the PaO2/FiO2 ratio, which is again comparable to that produced by iNO therapy13.
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Epoprostenol:
Epoprostenol was discovered in 1976 and was the first FDA-approved therapy for the treatment of PAH as
intravenous administration. It is the only FDA-approved agent shown to reduce mortality in prospective, randomized
clinical trials. PGI2 acts through cyclic adenosine monophosphate (cAMP) whereas NO acts through cyclic guanosine
monophosphate (cGMP).
It causes vasodilation of the intra-acinar pulmonary arteries that tightly surround the alveolar surfaces decreasing the
pulmonary vasculature resistance and improving oxygenation.
Several studies demonstrate that inhaled epoprostenol is effective in the management of acute pulmonary hypertension
and produces comparable decreases in pulmonary artery pressure as does iNO.
Inhaled Epoprostenol is associated with fewer systemic effects due to the low blood concentrations of epoprostenol.
Side effects include pulmonary edema, headaches, jaw pain, diarrhoea, anti-platelet effects
It spontaneously hydrolyzes to 6-ketoprostaglandin F1alpha (inactive metabolite) which localizes its effects to
ventilated lung.. It has a serum half-life of 3-6 minutes and is less expensive than iNO ($135/hour vs ~$220/day)
Epoprostenol lacks the toxic effects/metabolites of nitric oxide and therefore does not need a complicated delivery
system. However it needs the use of a mini heart nebulizer attached to the inhalational limb of the breathing circuit.
Iloprost:
Iloprost is a stable analogue of prostacyclin that can be administered by inhalation, avoiding the systemic side-effects
associated with i.v. administration. Administration of iloprost by inhalation also causes selective vasodilation of wellventilated regions of the lung (intrapulmonary selectivity), ensuring optimal gas exchange.
It has a half-life of 20-30 minutes (compared with only 3 minute for PGI2). The pulmonary vasodilator effect of
inhaled iloprost is approximately 2060 min. Clinical studies have demonstrated that inhaled iloprost has comparable
pulmonary hemodynamic effects to iNO and PGI2.
It has been shown to produce selective pulmonary vasodilation in patients with primary PH, producing a 30%
decrease in pulmonary vascular resistance which was greater than that produced by 40 ppm INO14.
In a review of 28 studies (including 195 children), Mulligan et al15 summarised that inhaled iloprost showed acute
effects similar to those of inhaled NO and might have a role in the short-term treatment of paediatric PHT, including
in neonates. This application of inhaled Iloprost is useful especially in countries where inhaled NO may not be
available.
Repeated daily nebulizations of inhaled iloprost have also been used for the long-term management of PH and were
shown to improve pulmonary arterial pressures and increase exercise capacity16.
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Unlike epoprostenol, iloprost does not require continuous nebulization because its half life is longer, but the
frequency of administration must be 69 times during waking hours.
However, not all patients with primary PHT respond to inhaled iloprost and non responders require transfer back to
an intravenous formulation to achieve therapeutic benefit.
The long-acting analogues of PGI2 are treprostinol and beraprost. Treprostinol can be administered by either the
intravenous or the subcutaneous route.
Inhaled Treprostinil:
Treprostinil is a tricyclic benzindene prostacyclin analog with pharmacologic actions similar to those of epoprostenol.
It is stable at room temperature and has an elimination half-life of 4.6 hours.
Treprostinil is administered 4 times daily with a ultrasonic nebulizer- Optineb, at maximum of nine breaths (each of
6 microgram) four times a day17.
Initial open label studies with inhaled treprostinil have demonstrated favourable effects in terms of exercise capacity
and hemodynamic status.
The TRIUMPH [TReprostinil Sodium Inhalation Used in the Management of Pulmonary Arterial Hypertension]
assessed the efficacy and safety of inhaled treprostinil or placebo in PAH patients receiving therapy with either
bosentan or sildenafil. This trial demonstrates that, among PAH patients who remain symptomatic on bosentan or
sildenafil, inhaled treprostinil improves exercise capacity and quality of life and is safe and well-tolerated.
Inhaled treprostinil was safe and well-tolerated. The most common adverse event was cough, which occurred in 54%
and 29% of the treprostinil and placebo groups, respectively. Other commonly reported adverse events included
headache, nausea, dizziness, and flushingall common side effects of prostanoid therapy.
The complicated delivery system and potential side effects associated with parenteral prostanoids have deterred some
patients and caregivers from instituting this effective class of agents early. The ease of delivery of inhaled treprostinil,
combined with the clinical benefits as demonstrated here, might expand the prostanoid treatment options for PAH
patients.
Adrenomedullin:
Adrenomedullin is a long-lasting vasodilator peptide that was originally isolated from human pheochromocytoma.
There are multiple binding sites for adrenomedullin within the lung and plasma levels increase in proportion to
the severity of PH. The vasodilatory effects of adrenomedullin are mediated by both cAMP- and NO-dependent
mechanisms. In animal models of PH, repeated inhalation of adrenomedullin decreased pulmonary arterial pressures
and significantly improved survival18.
REFERENCES:
1. M. Lowson. Inhaled Alternatives to Nitric Oxide Stuart. Anesthesiology
2002;96:1504-1513
2. Ronald D. Miller, Lars I. Eriksson,et al. Millers Anesthesia 8th Edition 2014;087-3088
3. Griffiths MJ, Evans TW. Inhaled nitric oxide therapy in adults. N Engl J Med 2005;353:2683-95
4. Prostacyclin May Be a Cost-Effective Option to Nitric Oxide. Medscape. Oct 31, 2012
5. Meadow W, Rudinsky B, Bell A, Hipps R. Effects of nebulized nitroprusside on pulmonary and systemic
hemodynamics during pulmonary hypertension in piglets. Pediatr Res 1998;44:181-6
6. Mestan KK1, Carlson AD et al. Cardiopulmonary effects of nebulized sodium nitroprusside in term infants with
hypoxic respiratory failure. J Pediatr.2003 Nov;143(5):640-3
7. Mandal B1 et al. Acute hemodynamic effects of inhaled nitroglycerine, intravenous nitroglycerine, and their
combination with intravenous dobutamine in patients with secondary pulmonary hypertension.Ann Card
Anaesth.2010 May-Aug;13(2):138-44
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8. Yurtseven N, Karaca P, Kaplan M, et al. Effect of nitroglycerin inhalation on patientswith pulmonary hypertension
undergoing mitral valve replacement surgery. Anesthesiology 2003;99:855858
9. Jacobs B et al.Aerosolized soluble nitric oxide donor improves oxygenation and pulmonary hypertension in acute
lung injury. Am J Respir Crit Care Med 1998; 158: 153642
10. Hentschel T et al. Inhalation of the phosphodiesterase-3 inhibitor milrinone attenuates pulmonary hypertension
in a rat model of congestive heart failure. Anesthesiology. 2007 Jan;106(1):124-31.
11. Haraldsson A, Kieler-Jensen N, Ricksten S. The additive pulmonary vasoldilatory effects of inhaled prostacyclin
and inhaled milrinone in postcardiac surgical patients with pulmonary hypertension. Anesth Analg 2001;93:1439
45
12. CA Thunberg, ST Morozowich, Harish Ramakrishna. Inhaled therapy for the management of perioperative
pulmonary hypertension. Ann Card Anaesth 2015 Jul-Sep;18(3):394-402
13. Stuart M. Lowson. Alternatives to nitric oxide. Br Med Bull 2004;70(1):119-131
14. Hoeper M, Olschewski H, Ghofrani H, et al. A comparison of the acute hemodynamic effects of inhaled nitric
oxide and aerosolized iloprost in primary pulmonary hypertension.J Am Coll Cardiol,2000;35:176182.
15. Mulligan C, Beghetti M. Inhaled iloprost for the control of acute pulmonary hypertension in children: A systematic
review. Pediatr Crit Care Med 2012;13:472-80
16. Olschewski H, Simmoneau G, Sitbon O, et al. Inhaled iloprost in severe pulmonary hypertension. N Engl J
Med,2002;347,322329
17. Usha krishnan et al. Effectiveness and Safety of Inhaled Treprostinil for the Treatment of Pulmonary Arterial
Hypertension in Children. Am J Cardiol. 2012 Dec 1; 110(11): 17041709.
18. Nagaya N, Okumura H, Uematsu M, et al.Repeated inhalation of adrenomedullin ameliorates pulmonary
hypertension and survival in monocrotaline rats. Am J Physiol. 2003;285:H2125H2131
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TIVA Vs. Inhalational Anesthesia in Cardiac

Surgery: Con
Dr. Deepak Borde, MD, DNB, FCA, FTEE.

Cardiac Anesthesiologist, Ozone Anesthesia Group, Aurangabad, Maharashtra, India.
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Introduction:
In the first landmark experimental evidence, Bland and Lowenstein reported in 1976 that
administration of halothane (0.75 minimum alveolar concentration [MAC]) significantly
(p < 0.001) attenuated ST-segment elevation caused by brief coronary artery occlusion in
six anesthetized dogs, demonstrating anti-ischemic effects of inhalational anesthetics[1].
Since this, several studies provided further evidence that volatile anesthetics protected
myocardium against reversible and irreversible ischemic injury. Considering this large
body of accumulated evidence, it should not be particularly surprising that volatile
anesthetics also protect human myocardium against ischemic damage in laboratory
settings in ways that are virtually indistinguishable from those described in experimental
animals[2].
Mechanisms of Myocardial Protection by Inhalational Anesthetics:

Ischemic preconditioning is characterized by attenuation of infarct size after sustained
ischemia, if this period of sustained ischemia is preceded by a period of brief ischemia.
This ischemic preconditioning can be triggered by events other than ischemia; cellular
stress of various forms, pharmacologic agonists and most importantly inhalational
anesthetics. In general terms, alterations in G proteincoupled receptor activity, ion
channel function, intracellular signaling kinases, regulation of apoptosis, reactive oxygen
and nitrogen species production, gene expression, and mitochondrial physiology have
been shown to play important roles in volatile anesthetic-induced myocardial protection
against ischemic injury[3].
Drug Delivery: Inhalational Vs. TIVA

Administering volatile anesthetics through the lung via a calibrated vaporizer affords
several fundamental advantages compared with intravenous delivery. These advantages
are primarily a function of gaining access to the circulation indirectly through the lung.
Because uptake of inhaled anesthetic progressively diminishes as equilibrium between
alveolar and pulmonary capillary partial pressures is approached, the vaporizer setting
is a proportional reflection of the anesthetic concentration in the blood and therefore
at the site of drug action at steady state. This enables accurate administration of the
inhaled drug to a target concentration; the anesthesiologist can set an upper limit above
which the partial pressure cannot rise. Moreover, the expired concentration of the
inhaled agent can be measured and confirmed by respiratory gas monitoring, ensuring
that the targeted concentration has been achieved. When access to the circulation for
drug delivery is obtained directly as with all intravenous techniques, there is nothing
to prevent indefinite uptake of the drug (ie, there is no equilibration process as with
inhalation drug delivery). Therefore, without the aid of a pharmacokinetic model, the
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infusion rate of an intravenous anesthetic does not reveal much about the temporal profile of drug concentration in
the blood, preventing administration targeted to a designated concentration. Chief among TIVA advances are more
suitable drugs like remifentanil, Target Control Infusion technology, and sophisticated PK/PD concepts[4]. But these
newer techniques remain far from present cardiac anesthesia practice in India.
Evidence for myocardial protection by Inhalational Anesthetics:

A recent international consensus conference indicated that volatile anesthetics are among the few drugs, techniques,
strategies that might be associated with mortality reduction[5]. In a meta-analysis of 22 studies, demonstrated that both
desflurane and sevoflurane significantly decreased the rate of myocardial infarction and death in patients undergoing
cardiac surgery[6]. Another meta-analysis performed on isoflurane demonstrated a trend (P=0.05) towards a reduction
in mortality in a subgroup of high-quality studies comparing isoflurane vs propofol in cardiac surgery[7].
Recently a Bayesian network meta-analysis (which allows indirect comparisons of drugs not otherwise compared
in head-to-head trials) of 38 studies enrolling 3996 patients, including 1648 (41%) receiving TIVA and 2348 (59%)
receiving volatile agents showed that sevoflurane (OR=0.31, 95% credible interval 0.140.64) and desflurane
(OR=0.43, 95% credible interval 0.210.82) were individually associated with a reduction in mortality when compared
with TIVA. The authors were unable to identify whether there is a best or a worst volatile agent according to survival.
This Bayesian network meta-analyses showed that conducting cardiac anesthesia with propofol-based TIVA, seems
to increase mortality, especially when the comparator is desflurane or sevoflurane. The authors of this meta-analysis
recommended that cardiac anesthesiologists, cardiac surgeons, and perfusionists should be aware that inhalational
anesthetics have pharmacological properties that go beyond the pharmacodynamic or pharmacokinetic properties
and that the anesthetic plan should take into account the effect of these drugs on survival[8].
A longitudinal, risk- adjusted analysis of 64 cardiac surgery centers in Italy examined whether there was a correlation
between the use of volatile anesthetics and a decline in 30-day mortality in 34,310 patients undergoing CABG.The
authors concluded that the use of a volatile anesthetic was weakly (r2 = 0.07; p = 0.035) correlated with a decline in
30-day mortality[9]. A second, uncontrolled, retrospective study of 10,535 patients also suggested that sevoflurane
anesthesia was associated with lower 30-day mortality in patients who did not have unstable angina (which mimics
the beneficial effects of IPC) or recent myocardial infarction compared with a propofol-based anesthetic technique
(2.28% v 3.14%; p = 0.015)[10].
In another meta-analysis by Cai et al explored whether volatile anesthetics could provide renal protection to patients
undergoing cardiac surgery. 10 trials with a total of 1600 participants were eligible. 6trials were performed on patients
undergoing coronary surgery, and the other 4 studies on patients undergoing aortic or mitral valve surgery. Compared
with controls, volatile anesthetics significantly reduced AKI incidence [relative risk (RR): 0.65, 95% CI: 0.43 to 0.97;
p=0.04)][11].
There is some evidence also suggesting equivocal results with inhalational Vs. TIVA. Most notable among this is
multicenter RCT study of 100 patients which did not demonstrate any difference between sevoflurane anesthesia and
propofol TIVA on the composite endpoint of prolonged ICU stay, mortality at 30 days and one year, or both in patients
undergoing high risk cardiac surgery[12]. In largest RCT ever performed, comparing volatile anesthesia versus TIVA
in OPCAB surgery by Suryaprakash et al also, did not find any difference in postoperative levels of cardiac troponin
(cTn) among the three study groups receiving sevoflurane, desflurane, or propofol[13]. Another recent, adequately
powered, multicenter RCT demonstrated that sevoflurane did not reduce the incidence of myocardial ischemia in
high-risk patients undergoing major non-cardiac surgery. No difference was noted in postoperative release of cTn,
N-terminal prohormone of brain natriuretic peptide, major adverse cardiac events, and survival at one year[14].
The total amount of myocardium at risk for ischemic injury and the relatively low incidence of perioperative
myocardial infarction are probably the most important explanations to this phenomenon. The intentional production
of severe ischemia-reperfusion injury and the observation of its pathologic consequences without intervention to
treat them are characteristic features of virtually all laboratory studies. In contrast, substantially less myocardium
may be at risk for ischemia during elective cardiac surgery, and the incidence of more severe myocardial damage
is relatively low unless an unanticipated intraoperative coronary artery occlusion occurs or myocardial protection
efforts are grossly inadequate. In high-risk patients, the mechanisms of cardiac damage might only in part be due to
ischemia/reperfusion injury.
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Conclusions:
There is large body of laboratory and clinical evidence for myocardial protection and improved mortality with
Inhalational Anesthetics!
Inhalational Anesthetic should be part of Anesthesia Plan in Cardiac Surgery
The results in high-risk patients (where one expects maximum protection!) are equivocal.
References:
1. Bland JHL, Lowenstein E: Halothane-induced decrease in experimental myocardial ischemia in the non-failing
canine heart. Anesthesiology 45:287-293, 1976.
2. Pagel PS. Myocardial Protection by Volatile Anesthetics in Patients Undergoing Cardiac Surgery: A Critical Review
of the Laboratory and Clinical Evidence. Journal of Cardiothoracic and Vascular Anesthesia, 27; 972982. 2013
3. In Kaplans Cardiac Anesthesia, Sixth Edition 2011.
4. Egan TD. Total Intravenous Anesthesia Versus Inhalation Anesthesia: A Drug Delivery Perspective. Journal of
Cardiothoracic and Vascular Anesthesia, Vol 29, No S1 (June), 2015: pp S3S6.
5. Landoni G, Rodseth RN, Santini F, et al. Randomized evidence for reduction of perioperative mortality. J
CardiothoracVascAnesth 2012; 26: 76472
6. Landoni G, Biondi-Zoccai GG, Zangrillo A, Bignami E, D'Avolio S, Marchetti C, et al. Desflurane and sevoflurane
in cardiac surgery: a meta-analysis of randomized clinical trials. J CardiothoracVascAnesth 2007;21:502-11.
7. BignamiE,GrecoT,BarileL,etal.The effect of isoflurane on survival and myocardial infarction. A meta-analysis of
randomized controlled studies. J CardiothoracVascAnesth 2013; 27: 50 8
8. LandoniG,GrecoT,Biondi-ZoccaiG,etal.Anestheticdrugsandsur- vival. A Bayesian network meta-analysis of
randomized trials in cardiac surgery. Br J Anaesth 2013; 111: 88696
9. Bignami E, Biondi-Zoccai G, Landoni G, et al. Volatile anesthetics reduce mortality in cardiac surgery. J
CardiothoracVascAnesth 2009; 23: 5949
10. Jakobsen CJ, Berg H, Hindsholm KB, et al: The influence of propofol versus sevoflurane anesthesia on outcome
in 10,535 cardiac surgical procedures. J CardiothoracVascAnesth 21:664-671, 2007.
11. Cai J, Xu R, Yu X et al. Volatile anesthetics in preventing acute kidney injury after cardiac surgery: A systematic
review and meta-analysis. J ThoracCardiovascSurg 2014;148:3127-36.
12. Landoni G, Guarracino F, Cariello C et al. Volatile compared with total intravenous anaesthesiain patients
undergoing high-risk cardiac surgery: a randomized multicentre study. British Journal of Anaesthesia 113 (6):
95563 (2014)
13. Suryaprakash S, Chakravarthy M, Muniraju G, Pandey S, Mitra S, Shivalingappa B, et al. Myocardial protection
during off pump coronary artery bypass surgery: A comparison of inhalational anesthesia with sevoflurane or
desflurane and total intravenous anesthesia. Ann Card Anaesth 2013;16:4-8.
14. LuratiBuse GA, Schumacher P, Seeberger E, Studer W, Schuman RM, Fassl J, et al. Randomized comparison
of sevoflurane versus propofol to reduce perioperative myocardial ischemia in patients undergoing noncardiac
surgery. Circulation 2012;126:2696-704.
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Liberal v/s restrictive use of transfusion in

cardiac surgery: Pro
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Dr. Rajesh Arya,

Consultant Cardiac Aanaesthesiologist,
Hero DMC Heart Institute, Ludhiana (Pb.)
Perioperative anemia is common after cardiac surgery and is associated with significant
increases in morbidity and mortality1-3. More than 50% of patients receive a perioperative
transfusion4,5. Threshold for perioperative transfusion is an issue of debate for a long
time. There are always one group in favor of going for liberal transfusion and try to
maintain the circulation blood as near to physiology as possible. Contrary to this, another
group would be very conservative about it and would be cautious about the complications
related to transfusion. My opinion is to go liberal with transfusion anddont let the Hb fall
too much. A proactive and liberal approach will help to prevent complications related to
anemia during perioperative period in cardiac surgery.
Transfusion and cardiac surgery:

Transfusion in cardiac surgery is an important issue because a lot of hemodynamic changes
are expected during surgical procedure. Most of cardiac patients have compromised
pump function of heart and any change in oxygen carrying capacity of circulating blood
will result in extra burden on heart; forcing it to work more to improve cardiac output
and oxygen delivery to tissues. In such a scenario, any factor mainly anemia, will reduce
oxygen carrying capacity of blood and will be very detrimental.
Let us discuss why transfusion in cardiac surgery deserves more attention:
Blood loss during cardiac surgery: Cardiac surgery is a major surgery in view of the
size of dissection, duration of surgery and hemodynamic variations that occur during
the procedure.
Pre-operative medications: Most of cardia surgery patients are on some or other
anticoagulants preoperatively. This presence of deranged bleeding profile makes
them to bleed more during the perioperative period, thus requiring more transfusion
as compared to non-cardiac surgery.
Handling of blood vessels and opening of circulating blood channels is obvious in
cardiac surgery and this results in more blood loss and thus requirements.
Almost all cardiac surgical procedure require induced anticoagulation during the
surgery. Mostly heparin is given as anticoagulant and at the end, it is reversed with
protamine. There are always chances of heparin rebound and bleeding.
On pump cardiac surgery causes haemodilution due to prime solution of pump. This
not only reduces the hematocrit but also dilutes the coagulation factors. So apart from
maintaining hematocrit, we require transfusion for improving coagulation factors as
well which requires transfusion of whole blood or components.
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Anemia and red blood cell efficacy

Anemia has long been associated with adverse patient outcomes. With respect to correlative data, anemia in older
people has been well documented as being an independent risk factor for increased mortality, functional dependence,
impaired cognition, re-admission to hospital, and falls6-8.
The physiological utility of oxygen delivery via RBC transfusion cannot be ignored and remains a salient issue. At
rest, myocardial energy demands are high, with coronary extraction of oxygen approaching 90%, with virtually no
measurable increase during conditions of ischemia9. During anemic states (Hb <10 g/dl), systemic oxygen delivery
is maintained via initial increases in stroke volume and then heart rate, which leads to early sub-endocardial ischemia
when coronary sinus oxygen supply is diminished. Such conditions of energy imbalance are further increased in
patients with atherosclerotic or valvular disease9.
Problems with blood storage:

An important RBC storage lesion often discussed is depletion of 2,3-diphosphoglycerate, whose level is inversely
proportional to the affinity of Hb for oxygen10. Despite an increase in Hb following a transfusion, left-shifting
the Hb disassociation curve may theoretically not improve tissue delivery of oxygen. However, there are ample
clinical data during correction of anemia in both stable and critically ill patients that support an acute increase
in oxygen delivery and functional organ tissue benefit following RBC transfusion11,12. This effect also appears
independent of the storage duration of the transfused red cells. It has been hypothesized that oxygen delivery is
reduced less than predicted because the oxygen affinity of Hb is affected also by temperature, pH, and base excess,
and it is the local in vivo environment with respect to these variables that may reduce the impact of the decreased
2,3-diphosphoglycerate11.
Transfusion and adverse events:

Transfusion is not free of complications; which mainly include acute and chronic reactions. In acute reactions, it is
mainly because of mismatched transfusion or allergic reactions whereas chronic complications are mainly infection
related issues. There are reports of acute kidney injury or acute lung injury after blood transfusion or even volume
overload (especially in pediatric patients or patients with poor LV functions).
To overcome these complications, hematological services have improved greatly over the time. Any unit of blood
or blood product passes through a tough series of investigations and screening before it is finally transfused thus
reducing the risk of these complications to a great extent.Carlson et al has reported in randomized, controlled
trials of red-cell transfusion with restrictive thresholds versus more liberal thresholds in a range of acute care and
surgical settings that no significant differences between the two approaches with respect to adverse events or 30-day
mortality.13
Anemia and cardiology intervention:

Studies have shown that even in the absence of acute hemorrhage, the sole presence of anemia during the period
of PCI represents an independent risk for poor outcome14. In a more recent study involving review of adverse
cardiovascular events through 30 days in 39,922 patients enrolled in clinical trials of acute coronary syndromes, when
Hb was the fixed variable not transfusion cardiovascular mortality increased as Hb levels fell below 14 g/dl15. To
further this point, in the recent Integrilin and Enoxaparin Randomized Assessment of Acute Coronary Syndrome
Treatment trial, the corresponding rates of recurrent ischemia were 39.1%, 22.0%, 15.6%, and 11.9% in patient
cohorts that had base Hb levels of <12.0 g/dl, 12.0 to 13.9 g/dl, 14.0 to 15.9 g/dl, and >16.0 g/dl16.
Transfusion Indication Threshold Reduction (TITRe2) trial:

To address the issue of liberal v/s restricted transfusion but most of them lacked adequate statistical power,17-21 and
most trials involved non cardiac surgery which should not be implemented in cardiac surgical setup22. To overcome
these drawbacks, another TITre2 trial was conducted in UK which was a multicenter randomized controlled trial. In
this trial, patients with Hb less than 9gm% were included and group where transfusion was started when Hb fell to
7gm% was labelled as restrictive group whereas the other group was called liberal group where transfusion was given
when Hb fell below 9gm%. Primary outcome i.e. serious infection or myocardial ischemia were same in both groups.
There were significantly more deaths in the restrictive-threshold group than in the liberal-threshold group (4.2%
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vs. 2.6%; mortality at 30 days was 2.6% in the restrictive group and 1.9% in the liberal group. Incidence of acute
kidney injury was observed higher in the restrictive group than in the liberal group. Overall 3 moth duration cost to
healthcare system was similar in both groups.
The results of TITRe2 trial seem to support a hypothesis that the use of a more liberal hemoglobin threshold may be
beneficial in patients with a hemoglobin level of less than 9 g per deciliter after cardiac surgery.
The only contemporary trial we could find that showed restrictive transfusion to be beneficial, a trial that assessed
transfusion thresholds in patients with acute upper gastrointestinal bleeding23. In contrast, a large trial involving
patients with hip fracture24, in which 63% of the participants had cardiovascular disease, showed no benefit from
restrictive transfusion, and a more recent feasibility trial of transfusion thresholds in patients with unstable coronary
disease (myocardial infarction) showed a reduced risk of death among patients who received transfusions at a more
liberal hemoglobin threshold25.This trial stresses that patients with cardiovascular disease may represent a specific
high-risk group for which more liberal transfusion thresholds are to be recommended. Therefore, patients undergoing
cardiac surgery are often at the limits of their cardiovascular reserve and may benefit from higher hemoglobin levels.
Recommendations:
As per current guideline by American Association of Blood Banks (AABB) for RBC transfusion were published
in 2012 26. The AABB does not make recommendations for or against a liberal or restrictive transfusion threshold
for hospitalized, hemodynamically stable patients with an acute coronary syndrome, and weakly recommends that
transfusion decisions be influenced by symptoms as well as Hb concentration.In a paper published by Marek A et al
in Critcal Care journal in 2015 27, interestingly, inspection of the RCTs themselves reveals that, with the exception
of TACO, liberal RBC transfusion practices have not been readily associated with increased rates of transfusionrelated complications28-31. Similarly in Transfusion Requirements in Critical Care (TRICC) trial, it was observed that
restrictive RBC transfusion was associated with reduced mortality in younger but not in older study participants (age
<55) and in those with less severe acute illness.
Future direction
At an academic level, a multidisciplinary think-tank from the National Heart, Lung, and Blood Institute32 convened
and agreed to the need for three adult trials evaluating RBC transfusion trigger strategies to improve overall outcome
and to validate the following hypotheses:
Higher Hb levels resulting from a liberal transfusion strategy during cardiopulmonary bypass surgery will lead to
lower incidence of 30-day all-cause mortality, recurrent myocardial infarction, infection, and other complications
as compared with a restrictive transfusion threshold.
In patients with acute coronary syndrome or coronary artery disease undergoing cardiac catheterization, a liberal
transfusion strategy will be associated with a lower incidence of composite outcome of all-cause mortality at 30
days, recurrent myocardial infarction, emergent percutaneous intervention (angioplasty or stent insertion), or
coronary artery bypass graft surgery within 30 days of enrollment when compared with a restrictive transfusion
strategy.
In hemodynamically stable patients in the ICU with a history of ischemic heart disease, multiple organ dysfunction
scores will be improved by maintaining Hb >10 g/dl.
Conclusion
Current evidence suggests that though in many clinical settings a restrictive RBC transfusion strategy is cost-effective,
reduces the risk of adverse events specific to transfusion BUT in bleeding patients or those at high risk for
hemorrhage restrictive therapy may be hazardous. In patients with ischemic brain, spinal cord, or myocardium, or
in debilitated patients requiring prolonged functional recovery, the optimal Hb transfusion trigger remains unknown,
but may be higher than for a severe, restrictive algorithm. So I would recommend that in a cardiac surgical setup
where cardiac functions are already compromised, we should follow a liberal strategy for perioperative transfusion
and improve safety margins for patient benefit.
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References:
1. Habib RH, Zacharias A, Schwann TA, et al. Role of hemodilutional anemia and transfusion during cardiopulmonary
bypass in renal injury after coronary revascularization: implications on operative outcome. Crit Care Med
2005;33:1749-1756
2. Murphy GJ, Reeves BC, Rogers CA et al. Increased mortality, postoperative morbidity, and cost after red blood
cell transfusion in patients having cardiac surgery. Circulation 2007;116:2544-2552
3. Karkouti K, Wijeysundera DN, Beattie WS. Risk associated with preoperative anemia in cardiac surgery: a
multicenter cohort study. Circulation 2008;117:478-484
4. Bennett-Guerrero E, Zhao Y, OBrien SM, et al. Variation in use of blood transfusion in coronary artery bypass
graft surgery. JAMA 2010;304:1568-1575
5. Murphy MF, Murphy GJ, Gill R, Herbertson M, et al. National comparative audit of blood transfusion: 2011 audit
of blood transfusion in adult cardiac surgery. Birmingham, United Kingdom: National Health Service, 2013.
6. Balducci L. Anemia, fatigue and aging. TransfusClin Biol. 2010;17:37581.
7. Terekeci HM, Kucukardali Y, Onem Y, et al. Relationship between anaemia and cognitive functions in elderly
people. Eur J Intern Med. 2010;21:8790.
8. Chaves PH, Xue QL, Guralnik JM et al. What constitutes normal hemoglobin concentration in community
dwelling disabled older women? J Am Ger Soc. 2004;52:18116.
9. Levy PS, Kim SJ, Eckel PK, et al. Limit to cardiac compensation during acute isovolemichemodilution: influence
of coronary stenosis. Am J Physiol.1993;265:H3409.
10. Chaplin Jr H, Beutler E, Collins JA et al. Current status of red-cell preservation and availability in relation to the
developing national blood policy. N Engl J Med. 1974;291:6874.
11. Weiskopf RB, Feiner J, Hopf H, et al. Fresh blood and aged stored blood are equally efficacious in immediately
reversing anemia-induced brain oxygenation deficits in humans. Anesthesiology. 2006;104:91120.
12. Walsh T, McArdle F, McLellan SA, et al. Does the storage time of transfused red blood cells influence regional or
global indexes of tissue oxygenation in anemic critically ill patients? Crit Care Med. 2004;32:36471.
13. Carson JL, Carless PA, Hebert PC. Transfusion thresholds and other strategies for guiding allogeneic red blood
cell transfusion. Cochrane Database Syst Rev 2012;4
14. Correia LC, Souza AC, Sabino M, et al. Hemoglobin level adds prognostic value to the global registry of acute
coronary events score in non-ST elevation acute coronary syndromes. Cardiology. 2012;121:2139.
15. Sabatine MS, Morrow DA, Giugliano RP, et al. Association of hemoglobin levels with clinical outcomes in acute
coronary syndromes. Circulation. 2005;111:20429.
16. Rousseau M, Yan RT, Tan M, et al. Relation between hemoglobin level and recurrent myocardial ischemia in acute
coronary syndromes detected by continuous electrocardiographic monitoring. Am J Cardiol. 2010;106:141722.
17. Johnson RG, Thurer RL, Kruskall MS, et al. Comparison of two transfusion strategies after elective operations for
myocardial revascularization. J ThoracCardiovasc Surg1992;104:307-314
18. Hajjar LA, Vincent JL, Galas FR, et al. Transfusion requirements after cardiac surgery: the TRACS randomized
controlled trial. JAMA 2010;304:1559-1567
19. Murphy GJ, Rizvi SI, Battaglia F, et al. A pilot randomized controlled trial of the effect of transfusion- threshold
reduction on transfusion rates and morbidity after cardiac surgery.TransfusAlternTransfus Med 2007;9:Suppl
1:41-42
20. Hajjar LA, Vincent JL, Galas FR, et al. Transfusion requirements after cardiac surgery: the TRACS randomized
controlled trial. JAMA 2010;304:1559-1567
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21. Shehata N, Burns LA, Nathan H, et al. A randomized controlled pilot study of adherence to transfusion strategies
in cardiac surgery. Transfusion 2012;52:91-99
22. Carson JL, Carless PA, Hbert PC. Outcomes using lower vs higher hemoglobin thresholds for red blood cell
transfusion. JAMA 2013;309:83-84
23. Villanueva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl
J Med 2013;368:11-21
24. Carson JL, Terrin ML, Noveck H, et al. Liberal or restrictive transfusion in high-risk patients after hip surgery. N
Engl J Med 2011;365:2453-2462
25. Carson JL, Brooks MM, Abbott JD, et al. Liberal versus restrictive transfusion thresholds for patients with
symptomatic coronary artery disease. Am Heart J 2013;165:964-971
26. Carson JL, Grossman BJ, Kleinman S, Tinmouth AT, Marques MB, Fung MK, et al. Red blood cell transfusion: a
clinical practice guideline from the AABB. Ann Intern Med. 2012;157:4958.
27. Marek A M, Steven M F, Daryl J K, Jean-Louis V, David R H Jr; Restrictive and liberal red cell transfusion
strategies in adult patients: reconciling clinical data with best practice. Critical Care201519:202
28. Hbert PC, Wells G, Blajchman MA, Marshall J, Martin C, Pagliarello G, et al. A multicenter, randomized, controlled
clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators,
Canadian Critical Care Trials Group. N Engl J Med. 1999;340:40917.
29. Bracey AW, Radovancevic R, Riggs SA, Houston S, Cozart H, Vaughn WK, et al. Lowering the hemoglobin threshold
for transfusion in coronary artery bypass procedures: effect on patient outcome. Transfusion. 1999;39:10707.
30. Cooper HA, Rao SV, Greenberg MD, Rumsey MP, McKenzie M, Alcorn KW, et al. Conservative versus liberal red
cell transfusion in acute myocardial infarction (the CRIT Randomized Pilot Study). Am J Cardiol. 2011;108:1108
11.
31. Villanueva C, Colomo A, Bosch A, Concepcin M, Hernandez-Gea V, Aracil C, et al. Transfusion strategies for
acute upper gastrointestinal bleeding. N Engl J Med. 2013;368:1121.
32. Josephson CD, Glynn SA, Kleinman SH. State-of-the Science Symposium Transfusion Medicine Committee. A
multidisciplinary think tank: the top 10 clinical trial opportunities in transfusion medicine from the National
Heart, Lung, and Blood Institute-sponsored 2009 state-of-the-science symposium. Transfusion. 2011;51:82841.
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CARDIAC BIOMARKERS
Dr. Vishwas Malik, Dr. ArunSubramanium
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Introduction
What is a biomarker? A biomarker is defined asa characteristic that is objectively
measured and evaluated as an indicator of normal biological processes, pathogenic
processes, or pharmacologic responses to a therapeutic intervention.
Cardiac biomarkers are protein components of cell structures that are released into
circulation when myocardial injury occurs. They play a pivotal role in thediagnosis, risk
stratification, and treatment of patients.
Regardless of the intended use, it is important to remember that biomarkers that do not
change disease management cannot affect patient outcome and therefore are unlikely to
be cost-effective
The features of an ideal cardiac marker would be:

High sensitivity and specificity
Rise and fall rapidly after ischemia
Able to perform reliably and uniformly
Be simple to perform
Have turnaround time <60 min
Not influenced by functioning of other organs, in particular, functioning of

kidney.
Active investigation has brought forward an increasingly large number of novel
candidate markers but few have withstood the test of time and become integrated into
contemporary clinical care because of their readily apparent diagnostic, prognostic, and/
or therapeutic utility.
Cardiac surgery with the cardiac bypass machine causes an acute inflammatory response
through activation of inflammatory cells, complement cascade, and secretion of
cytokines and chemokines.
Protein biomarkers
A major biomarker in the heart is serum cardio-specific troponin T. Although typically
present at low levels in the heart, its levels rise after cardiac surgery, before returning
to baseline levels. Recently, a new highly sensitive and specific immunoassay to detect
cardiac troponin T in the serum was introduced. A promising and potential application
for this marker is better prediction of patient outcome and a clearer understanding of
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the extent of cardiac damage . In addition to Troponin T and IL-6, cardiac troponin I (CTn1), myoglobin, creatine
kinase (CK) and its isoenzyme creatine kinase-myocardial band (CK-MB), which is specific to the heart, are all
involved in cardiac inflammation.
B-type natriuretic peptide (BNP), a protein commonly used to evaluate heart failure, is a polypeptide secreted by
the ventricles of the heart in response to excessive stretching of cardiac myocytes. Measuring BNP is an indirect
way to evaluateventricular function and identify patients at risk that may be asymptomatic.Especially in patients
with a history of CAD, increased BNP levels are associated with an increased rate of myocardial infarction and
cardiovascular death during mid-term follow-up. In contrast to BNP, higher NT-proBNP levels are associated with
female gender, impaired renal function, and older age.
Cytokine biomarkers
Certain cytokines have been discovered to be closely related to the inflammatory cascade and also can be used as
biomarkers to trend response to cardiac stress. While patients are on the CPB machine, pro-inflammatory cytokines
such as tumor necrosis factor alpha (TNF-) and interleukins (IL) 1, 6 and 8 are released and mediate the systemic
inflammatory response syndrome (SIRS), which is believed to play an essential role in myocardial ischemia and
reperfusion injury. Comparing the extent of elevation of these markers among patients will help ascertain those that
are more at risk for reperfusion injury after the procedure.
Breath biomarkers
While a variety of hematological markers are used to monitor pre-op and post-op status, less invasive techniques
have also been utilized. Numerous studies have demonstrated a close correlation between clinical conditions and
the exhalation of volatile biomarkers. Some of these volatile substances are excreted into breath within minutes of
their formation in tissues. Exhaled concentrations of these compounds can, therefore, be used to detect pathological
conditions in the body at an early stage. As breath tests are completely non invasive they can be performed repeatedly
or continuously without any burden to the patient. An excellent study performed by Pabst et al. determined that
oxidative and metabolic stress during cardiac surgery could be monitored by breath biomarkers. They assessed acetone,
isoprene, and pentane, and found that acetone release was an indicator of stress and isoprene levels correlated with
cardiac output. There is a positive relationship between exhaled acetone levels and post-operative troponin T, as well
as pre-op CRP and exhaled acetone levels. Exhaled pentane concentrations measured immediately after termination
of extracorporeal circulation correlated with the CK:CKMB ratio measured a few hours later, suggesting that exhaled
pentane might serve as a fast and direct biomarker for early recognition of oxidative stress and ischemic reperfusion
injury.
Biomarkers in outcomes studies

Numerous studies have investigated pre-operative and post-operative variables that influence the outcome of CABG
patients. Evaluating factors such as co-morbidities, family history, and diet can help anticipate problems that may
ensue during the procedure or obstacles that might impede recovery time.
Eikvar et al. compared post-CABG levels of cardiac markers in groups of patients that suffered from postoperative
MI and those that did not. The first postoperative day patients with postoperative myocardial infarction (POMI) had
higher levels of serum troponin T and CK-MB compared to those that did not suffer from a POMI.
A study performed by Morimoto et al. found that plasma levels of BNP are markedly elevated in the acute phase after
cardiac surgery requiring bypass and reflect the left ventricular function at the same time. Furthermore, myocardial
damage due to ischemia may participate in the mechanism of synthesis and secretion of BNP. Wazni et al. found that
patients with atrial fibrillation following cardiac surgery exhibited higher BNP levels than patients who remained in
sinus rhythm throughout the post-operative course.. Based on converging results, BNP cut-off value is likely around
2030 pg/mL and NT-proBNP cut-off value is likely around 125 pg/mL for preoperative screening purposes in
moderate to high-risk patients .(Tepper D, Harris S, Ip R. The role of N-terminal pro-brain natriuretic peptide and
echocardiography for screening asymptomatic left ventricular dysfunction in a population at high risk for heart
failure: the PROBE-HF study. Congest Heart Fail 2009;15:296) and (Betti I, Castelli G, Barchielli A, et al. The
role of N-terminal PRO-brain natriuretic peptide and echocardiography for screening ssymptomatic left ventricular
dysfunction in a population at high risk for heart failure. The PROBE-HF study. J Card Fail 2009;15:37784).Hutfless
et al demonstrated that apreoperative BNP levels >385 pg/ml predict the postoperative complications and one-year
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mortality after heart surgery with a sensitivity of 80-85% and a specificity of 90%. Postoperatively, elevated peak
BNP levels and elevated change to peak BNP levels were associated with prolonged hospital stay and mortality within
one year. Schachner et al. determined the influence of preoperative serum NT-proBNP on postoperative outcome
and mid- term survival in patients undergoing CABG. Patients with NT-proBNP levels greater than 502 ng/l had
more co-morbidities than those with NT- proBNP levels less than 502 ng/l. Postoperatively, those patients had a
significantly longer time of ventialtion, a longer ICU stay, a higher rate of renal failure requiring hemofiltration, a
higher rate of IABPs, and a higher rate of postoperative atrial fibrillation
Consensus guidlelines for cardiac troponin testing

For patients with normal baseline cTn values, elevations above the 99th percentile upper reference limit (essentially
any measurable cTn) are indicative of peri-procedural myocardial necrosis.
A type 5 MI is defined as:

Increases of cTn greater than five times the 99th percentile upper reference limit, plus
New pathological Q waves/new left bundle branch block or
Angiographically documented new graft or native coronary artery occlusion or imaging evidence of new
loss of viable myocardium.
Marker
cTnT
cTnI
Cut off point

0.46 pg/ml
0.80 pg/ml
1.0 pg/ml
13 pg/ml
13 pg/ml
14 pg/ml
Reference
Lehrke et al
Nesher et al
Brown et al
Lasocki et al
Papparella et al
Hashemzadeh et al
Table 1: Recently reported optimal cTn cut-points for prediction of risk following cardiac surgery.
In a prospectively gathered cohort of patients undergoing a wide range of surgical procedures, the optimal cut-point
for cTnT to predict adverse outcomes was 1.58 ng/mL (Januzzi JL et al. A comparison of cardiac troponin T and
creatine kinase-MB for patient evaluation after cardiac surgery. J Am Coll Cardiol 2002; 39: 1518-1523) this cut-point,
more than 10 times above the currently endorsed upper reference limit for cardiac surgery, was recently validated
among a larger group of more than 800 subjects undergoing CABG (Mohammed AA, Agnihotri AK, van Kimmenade RR, et al. Prospective, Comprehensive Assessment of Cardiac Troponin T Testing Following Coronary Artery
Bypass Graft Surgery. Circulation 2009). The relation between troponin release and adverse events has been decribed
by Fellahi et al and Ailenklan et al. Y van Geene et al. showed that a shows a cTnI-level > 4.25 mg/l, one hour after
surgery is associated with an increased risk for hospital mortality. It is difficult to compare this cut-off point with
other studies because there are many manufacturers who produce assays for measuring cTnI, all resulting in different
variations of cTnI concentrations. Lim et al. subsequently reported that the cardiac troponin I (cTnI) test at 1h after
CABG could potentially differentiate patients with significant revascularization injury; a cutoff of cTnI exceeding
5g/L at 1h had 67% sensitivity and 79% specificity for detecting new late gadolinium enhancement in cardiac
magnetic resonance image as confirmatory. Omar et al reported when patients fulfill diagnoses of PMI, ROC analysis
reported that the highly sensitive (hs) TnT level of 3466ng/L or above is associated with 90% sensitivity and 90%
specificity for diagnosis of PMI, where the level of 2309ng/L is associated with 80% sensitivity and 86% specificity
for an equivalent level of CKMB, which would be suspicious of myocardial injury.
Conclusion
Our objective was to examine the literature on cardiac biomarkers and identify associations regarding outcome from
the current published data. A knowledge of the cut off values in cardiac surgery will help us in identifying pateints
at risk of MACE and initiate appropriate care if applicable. The use of biomarkers is fairly well established in other
fields of medicine, such as oncology, however is not well explored in predicting cardiac patient prognosis. Our hope
is that biomarkers will become routinely used in this field and will help to improve patient outcome.
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HEART BRAIN CROSS TALK: WHAT DO WE

NEED TO KNOW
DR.R.GOPINATH
NIMS, HYDRABAD
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Neurocardiology has many dimensions, but it may beconceptualized as divided into 3

major categories: thehearts effects on the brain (eg, cardiac source embolicstroke), the
brains effects on the heart (eg, neurogenic heartdisease), and neurocardiac syndromes
(eg, Friedreich disease).The concept of visceral organ dysfunction that occurs as a result
of neurological stimuli can be traced to Ivan Pavlov.
History of Learning the Nature of theBrainHeart Connection

In 1942, Dr.WalterB. Cannon, Professor of Physiology at Harvard Medical School,
published a paper entitled VoodooDeath, in which he recounted anecdotal
experiences,largely from the anthropology literature, of death from fright.He postulated
that death was caused by a lasting and intense action of the sympathico-adrenal system.
Neurogenic Heart Disease

A wide variety of changes in the ECG is seen in the context of neurological disease. Two
major categories of change areregularly noted: arrhythmias and repolarization changes.
It is likely that the life-threatening arrhythmias found in patients with acute neurological
diseases are due to repolarization change, andresult in ventricular tachycardia and/or
ventricularfibrillation.
ECG, changes are seen in the ST segment and T wave, which reflect abnormalities in
repolarization. Most often, the changes are seen best in the anterolateral or inferolateral
leads. The electrocardiographic abnormalities usuallyimprove, often dramatically, with
death by brain criteria. Myofibrillar degeneration (also known as coagulativemyocytolysis
and contraction band necrosis) is an easily recognizable form of cardiac injury. In
myofibrillar degeneration the cells die in a hypercontracted state with prominent
contraction bands.
Nervous System Stimulation

Nervous system stimulation produces cardiac lesions that are histologically indistinguishable
from those described forstress and catecholamine-induced cardiac damage. Stimulation
of the lateral hypothalamus produces hypertension and/or electrocardiographic changes
reminiscent of those seen in patients with central nervous system damage. Other
methods to produce cardiac lesions of this type include stimulation of the limbic cortex,
the mesencephalic reticular formation, the stellate ganglion, and regions known to elicit
cardiac reflexes such as the aortic arch.
NEUROGENIC STRESS CARDIOMYOPATHY (NSC)

Neurogenic stunned myocardium, also called Neurogenic Stress Cardiomyopathy
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(NSC),is a syndrome that can occur after severe acute neurologic injury, such as subarachnoid hemorrhage
(SAH),traumatic brain injury,ischaemic or hemorrhagic stroke,central nervous system infections,epileptic
seizures,oranysuddenstressful event.
The cardiac involvement is expressed either in terms of electrocardiographic (ECG) signs with Q-T interval
prolongation, long Q-T syndrome and torsade de pointes, S-T-segment depression, T-wave inversion, and ventricular
and supraventricular arrhythmias, or intheformof leftventricular (LV)wallmotionabnormalities, myocardial necrosis
enzyme release, and increased B-type natriuretic peptide (BNP).
ECG abnormalities occur in 2575% of SAH patients and arrhythmias are present in almost 100% of patients.
Serummarkers of cardiac injury are increased in 2030% of patients with the most severe grades of SAH and wall
motion abnormalities occur in 813% of patients with regional or global kinetic patterns.
Neurocardiogenic injury is associated with an increased risk of all-cause mortality cardiac mortality and heart failure.
Neurocardiogenic injury is less common in other forms of acute brain injury.
Despite high morbidity and mortality, NSC management is mainly supportive and symptomatic, based on thetreatment
of life-threatening events.
The anaesthetic challenges of the neurologically critically ill patient presenting with NSC, the possible occurrenceof
myocardial stunning during anaesthesia, and the impact of anaesthesia on the autonomic nervous system (ANS)
during the perioperative period have not been fully explored.
Pathophysiology/Mechanisms
The Cardiac component of the problem
Cardiac innervation abnormalities are described in several pathologies, including cardiac amyloidosis,dilated
cardiomyopathy, Parkinsonsdisease,and Lewy body dementia.
NSC is secondary to structural or functional brain damage and part of the stress-related cardiomyopathy syndrome
spectrum,including the Takotsubo syndromewith its typical apical and mid-ventricular dysfunction and significant
overlap with NSC in clinical appearance, underlyingpathophysiology and reversibility.
The term NSC reflects the underlying pathophysiology of myocardial dysfunction related to the stress of catecholamine
excess, triggered by an acute neurological injury. Takotsubo cardiomyopathy, in contrast, relates to the primary form
of stress-related cardiomyopathy.
Many theories for stress-related cardiomyopathy syndrome have been described: (i) transient multi-vessel coronary
artery spasm; (ii) microvascular dysfunction; (iii) aborted myocardial infarction with spontaneous coronary thrombus
lysis;and (iv) the catecholamine hypothesis.
The mammalian left ventricle contains apical-basal gradients of beta adrenergic receptors (beta ARs) and sympathetic
innervation, with the apex characterized by highest beta AR and lowest sympathetic nerve density. This pattern results
in increased apical responsiveness to circulating catecholamines, predominantly epinephrine from the adrenal glands,
as a compensatory mechanism for the sparse apical sympathetic innervation, to ensure optimal ventricular ejection
during times of stress.
Epinephrine, at high levels, can act as a negative inotrope via ligand-mediated trafficking of the beta 2AR from
stimulatory G protein to inhibitory G protein subcellular signaling pathways. The beta 2AR is widely reported as
being pleiotropic, having the potential to couple through Gs-adenylate cyclase-cAMP (like the beta 1AR) but also
though Gi beta, Gbeta, and nonG-protein pathways.
At high epinephrine concentrations, the beta 2AR switches its coupling from Gs protein to an inhibitory Gi protein,
a process described as ligand- or stimulus-directed trafficking, or biased agonism. This switch would be favored in
conditions of high catecholamine stress because it depends on beta 2AR phosphorylation by both protein kinase A
(PKA) and G-protein receptorcoupled kinases (GRKs).
Norepinephrine has 20-fold lower affinity for the beta 2AR compared to the beta 1AR, with much weaker beta 2AR
stimulus trafficking to the Gi pathway. Although this negative inotropy is detrimental from a mechanical perspective,
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the Gs-to-Gi switch is potentially both antiapoptotic and antiarrhythmic and may represent a cardioprotective
mechanism against beta 1AR-catecholamine cardiotoxicity.
Polymorphisms of adrenergic receptors

Cardiac responsiveness to catecholamines is affected by genetic polymorphisms of the adrenoceptors.Single
adrenoceptor polymorphisms were associated with a three- to five-fold increase in the risk of cardiac dysfunction,
whereas patients with combinations of two of these polymorphisms had a 10-to 15-fold increased risk of cardiac
injury after SAH.
In patients with LVapical ballooning syndrome, a correlation was found with a polymorphism of G protein-coupled
receptor kinase 5 (GRK5), a protein involved in post-receptor signal transduction.
EFFECTS OF HIGH CATECHOLAMINE LEVELS

High myocardial interstitial concentrations of norepinephrine result in myocyte calcium overload and cell deathcausing
cardiac dysfunction free radical production, and adenosine triphosphate depletion, with resulting ECG changes,
failure of myocardial contraction, and possible cell death.
With extreme sympathetic discharge, a specific tissue lesion called myocardial contraction band necrosishas been
described, characterized by hypercontraction of sarcomericmyofibrils, eosinophilic transverse bands, and interstitial
mononuclear infiltration.
With ischaemic disease, cells die in a relaxed state with a polymorphonuclear cell response and necrosis in the
compromised vascular territory; in NSC, cells die in a hyper-contracted state with contraction bands and early
calcification and myofibrillar lesions, which are visible within minutes of onset, appearing close to cardiac nerves.
Furthermore, in NSC, the regional wall motion abnormalities extend beyond a single epicardial vascular distributionand
are reversible.
ROLE OF INFLAMMATION
The role for inflammation among the mechanisms contributing to themyocardial injury of NSC has also been
proposed.While acetylcholine inhibits the release of pro-inflammatory cytokines, parasympathetic dysfunction may
facilitate uncontrolled inflammation, causing myocardial damage.Furthermore, elevated levels of cytokines have been
described in the cerebrospinal fluid and serum of SAH patients, contributing to neurocardiogenic damage.
A combined evaluation of myocardial sympathetic innervation, myocardial perfusion, and LVsystolic function in
patients with SAH can provide a more comprehensive assessment of LV dysfunction.
The insular cortex and cardiovascular system
The classical literature on neurocardiology has focused mainly on the subcortical regions of the central autonomic
nervous system. However, recent studies have supported the notion that the cardiovascular system is regulated by
cortical modulation. Modern neuroimaging data, including positron emission tomography and functional magnetic
resonance imaging, have revealed that a network consisting of the insular cortex, anterior cingulate gyrus, and
amygdala plays a crucial role in the regulation of central autonomic nervous system.
Because the insular cortex is located in the region of the middle cerebral arteries, its structure tends to be exposed to
a higher risk of cerebrovascular disease.
The insular cortex damage has been associated with arrhythmia, diurnal blood pressure variation disruption (eg, a
non-dipper or riser pattern), myocardial injury, and sleep disordered breathing, as well as higher plasma levels of brain
natriuretic peptide, catecholamine, and glucose.
The hypothalamic-pituitary-adrenocortical and sympatho-adrenomedullary axes are the main biological systems
activated during the stress response. Lateralization for cardiovascular function, with sympathetic tone predominantly
regulated in the right insular region and parasympathetic effects situated in the left insula, is supported by several
studies. Bradycardia or a depressant effect (on diastolic arterial pressure)was more frequent with stimulation of the
left insular cortex, whereas tachycardia or a pressor effect was elicited if the right insula was stimulated.
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The mechanism of NSC after acute brain injury may be related to disinhibition of the right insular cortex and a
resulting augmentation of sympathetic tone.
Associations between Heart Rate Variability and specific brain regions including the amygdala and ventromedial
prefrontal cortex, thus further supporting a structural and functional link between the brain and the heart.To
maintainadequate cerebral blood flow, baroceptors send afferent signals to the brain,which in turn sends efferent
outputs to regulate changes in arterial pressure.
Monitoring for NSC

All SAH patients should be screened on admission with a fullcardiac evaluation including a complete clinical history,
a12-lead ECG, a chest X-ray, cardiac enzyme profile, pro-BNP level, lipid profile, and electrolyte panel.
A baseline assessment of cardiac function with, troponin levels, serial enzymes, ECG, and echocardiography may be
beneficial, especially if any sign of myocardial dysfunction is present and that cardiac output should be monitored in
those patients with myocardial dysfunction or hemodynamic instability.
An ejection fraction of <40% and troponin I <2.8 ng/ ml are predictive of NSC rather than acute myocardial
infarction.
Elevated BNP levels also occur after SAH. A two- to three-fold increase in BNP levels in plasma but not in
cerebrospinal fluid supports the heart as the source of increased BNP levels after SAH.
Cardiac catheterization and cardiac MRI may be considered in patients to differentiate an acute coronary syndrome.
Indexes of sympathetic activity

1. Tissue, plasma and urine catecholamine levels
2. Heart-rate variability: represents the beat-to-beat oscillation of heart rate. Power spectral analysis of sequence
of500 RR intervals can detect two major bands: LF is the expression of baroceptor-mediated regulation and
occurs because of the contribution of parasympathetic and mainly sympathetic discharge, and HF reflects
the modulation of vagus nerve discharge caused by respiration. LF%, LF/HF and Hunt and Hess class are
independent predictors of in hospital mortality in patients with SAH.
3. Baroreflex sensitivity: a measure of the reflex response (both vagal and sympathetic) to the stimulation of the
baroceptors induced by arterial pressure changes. It can be measured by infusion of vasoactive drugs or noninvasively through spontaneous variations in arterial pressure and RR intervals
4. Cardiac MIBG scintigraphy: detection of the uptake of a specific tracer showing the activity of sympathetic
post-synaptic fibers. MIBG bears a structural resemblance to norepinephrine, and the uptake of MIBG in various
tissues closely parallels that of norepinephrine. MIBG is used to assess human cardiac sympathetic nervous
viability and function.
5. Microneurography MNSA, SSA, RNSA (muscle, skin, and renal sympathetic nerve activity): direct recording of
the activity of the vasoconstrictive sympathetic fibers at muscle, skin, and renal levels.
Proposed treatment for NSC

Anaesthetic challenges of the neurologically critically ill patient presenting with NSC, the possible occurrence of
myocardial stunning during anaesthesia, and the impact of anaesthesia on the autonomic nervous system (ANS)
during the perioperative period have not been fully explored.
Hemodynamic instability, arrhythmias, cardiogenic shock, pulmonary edema, and sudden cardiac death are the main
concerns with a clinical presentation similar to Myocardial infarction.
With high indices of sympathetic activity, there is a strong physiological role for beta blockade. In a large prospective
study in stroke patients, b-blocker use was associated with less severe stroke on presentation, correlated with lower
cardiac sympatho-vagal tone, and exerted its protective effect through sympatholytic action, inhibition of thrombin
generation, reduced inflammation and may also protect cardiac myocytes from norepinephrine-stimulated apoptosis.
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Although controversial, neurogenic stunned myocardium may benefit from inotropic medication to maintain
equilibrium between myocardial oxygen supply and demand. Epinephrine-mediated stunning is recognized as a
causative factor for NSC; administration of epinephrine may worsen negative inotropism further increasing the
switch from Gs protein signaling to Gi protein signaling.
Levosimendan theoretically may be the inotrope of choice in Takotsubo cardiomyopathy-related shock; it increases
myocardial systolic performance, improves coronary perfusion, has an anti-apoptotic and an anti-stunning effect.
Sympathomimetic drugs should be used with caution.
In limited cases of life-threatening acute LV failure, intra-aortic balloon pump and ventricular assist devices mayalso
be necessary.
The role of estrogen in the pathogenesis of NSC has recently been investigated. In a retrospective analysis, SAH
grading, increased plasma norepinephrine, and decreased plasma estradiol levels were independently associated with
wallmotion abnormalities. Based on these results, the administration of estradiol to postmenopausalfemale patients
with SAH complicated by severe wall motion abnormalities could be considered a possible therapeutic option.
The presence of a thrombus in the LV may require anticoagulation to prevent systemic embolization if not
contraindicated.
Potential organ donors who have been treated aggressively with steroids, insulin, vasopressin and thyroxine should
be allowed to recover from NSC.
Takotsubo cardiomyopathy
This is a stress-related cardiomyopathy syndrome mimicking an acute coronary event.
There is, as yet, no consensus on the diagnostic criteria for takotsubo cardiomyopathy. Researchers at the Mayo
Clinic proposed diagnostic criteria in 2004, which have been modified recently: (1) transient hypokinesis, akinesis, or
dyskinesis in the left ventricular mid segments with or without apical involvement; regional wall motion abnormalities
that extend beyond a single epicardial vascular distribution; and frequently, but not always, a stressful trigger; (2) the
absence of obstructive coronary disease or angiographic evidence of acute plaque rupture; (3) new ECG abnormalities
(ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin; and (4) the absence of
pheochromocytoma and myocarditis.
This syndrome shares common pathophysiological mechanisms with NSC. The switch of b2-receptors from Gs to
Gi signaling causes stimulation of the cardio-protective PI3K/AKT signaling pathway, explaining the modest and
patchy presence of myocardial cell death in Takotsubo.
Reversibility of ventricular function occurs once the surge in epinephrine levels has cleared and the b2AR switch back
to Gs protein, enabling the inotropic function of the cardiomyocytes to recover.
Under anaesthesia, the stress of tracheal intubation and the consequent sympathetic reflex stimulation may explain
the occurrence of Takotsubo at induction. It may also occurbecause of anaphylaxis, meperidine-induced histamine
release,transfusion reaction as a result of histamine release, activation of the so-called histamine-adrenergic
crosstalk,and the infusion of adrenergic drugs.
Regional anaesthesia provides optimal postoperative pain control but Takotsubo syndrome has also been described
during spinal anaesthesia and in response to uncontrolled pain.
Any potential triggering event that could result in a catecholamine surge and consequent cardiac dysfunction is
avoided during the entire perioperative period.
Opioids and the central a2-inhibitor, dexmedetomidine, both of which target the locus coeruleus, the important
supraspinal sympathetic centre that regulates the reflex response to stress, may be the most appropriatedrugs.
Dexmedetomidine may also protect against psychological stress by depressing the activity of the amygdala related to
anxiety.
Magnesium, involved in several fundamental processes including gating of calcium channels, regulation of adenylate
cyclase, cardiac excitability, control of vasomotor tone, and neurotransmitter release,has also been proposed as a
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potential drug to attenuate the stress response.
CONCLUSION
Intense brainheart crosstalk is increasingly recognized in the acute phase after severe brain injury, NSC being the
best known clinical life-threatening expression. Establishment of a Registry of perioperative Takotsubo casesmay
play an important role in identifying the real scale of the problem. Identifying patients at risk at an early stage
and monitoring cardiovascular status at admission should be considered. A more complete understanding of the
pathogenesis of the syndrome requires further research. Vigilance and a high index of suspicion are essential to
avoid misdiagnosis or delayed recognition, and the entire surgical team should be educated in the recognition of this
potentially life-threatening syndrome.
REFERENCES
1. Samuels MA. The brain-heart connection. Circulation 2007; 116: 7784.
2. Zaroff JG, Leong J, Kim H, et al. Cardiovascular predictors of longterm outcomes after non-traumatic
subarachnoid hemorrhage. Neurocrit Care 2012; 17: 37481
3. Steptoe A, Kivimaki M. Stress and cardiovascular disease. Nat Rev Cardiol 2012; 9: 36070.
4. Paur H, Wright PT, Sikkel MB, et al. High levels of circulating epinephrine trigger apical cardiodepression in a
beta2- adrenergic receptor/Gi-dependent manner: a new model of Takotsubo cardiomyopathy. Circulation 2012;
126: 697706
5. Heart Disease in Asia. Takotsubo Cardiomyopathy:A New Form of Acute, Reversible Heart Failure Yoshihiro J.
Akashi, et alCirculation; Volume 118(25):2754-2762 December 16, 2008
6. Nagai M, Hoshide S, Kario K. The insular cortex and cardiovascular system:anewinsight into the brain-heart axis.
JAmSocHypertens 2010; 4: 17482.
7. Liu S, Dhamee MS. Perioperative transient left ventricular apical ballooning syndrome: Takotsubo cardiomyopathy:
a review.J Clin Anesth 2010; 22: 6470.
8. Sugimoto K, Inamasu J, Hirose Y, et al. The role of norepinephrineand estradiol in the pathogenesis of cardiac
wall motion abnormalityassociated with subarachnoid hemorrhage. Stroke 2012;43: 1897903.
9. Bybee KA, Prasad A. Stress-related cardiomyopathy syndromes. Circulation 2008; 118: 397409.
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PERIOPERATIVE MANAGEMENT OF
INTERRUPTED AORTIC ARCH (IAA)
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Dr.Kamlesh Tailor
Consultant & Chief
Pediatric cardiac Anesthesiologist & Intensivist
Kokilaben Ambani Hopsital, Mumbai
DEFINITION:
Interrupted aortic arch is a complete luminal and anatomic discontinuity
between two segments of the aortic arch.
It can be an extreme form of Coarctation in which the aortic arch is atretic or
a segment of the arch is absent.
HISTORICAL NOTE :
In 1778- By Steidele-First described Interrupted aortic arch
In 1818- By Siedel-Described the Absent segment between LCA & LCCA
In 1948- By Kesten- Described the Absent segment between LCCA and
Brachiocephalic arteries
In 1959- Celoria and Patton-classified according to the site of obstruction into
types A, B, and C
INCIDENCE :
A rare form of CHD.
Overall incidence-1% of all CHD.
Usually occurs in association with a nonrestrictiveventricular septal
defect(>95%) and less commonly, with a large AP window ortruncus
arteriosus.(1)
CLASSIFICATION :
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TYPE OF INTERRUPTION
TYPE A
TYPE B
TYPE C
SITE OF INTERRUPTION
DISTAL TO LSA
BETWEEN LCCA & LSA
BETWEEN INNOMINATE
ARTERY & LCCA
INCIDENCE
40 %
> 50 %
<5%
ASSOCIATED ABNORMALITIES:
IAA &CHARGE Syndrome:
C-coloboma,
H-heart disease,
A-atresia choanae,
R-retarded growth and development,
G-genital hypoplasia, and
E-ear anomalies
which is usually caused by mutations inCHD7on chromosome 8q12.1(2)
IAA & DeGeorge SYNDROME:

Deletion of Chromosome 22q11.2
-Defective development of 3rd and 4th pharyngeal pouches
Absence of Thymus
-Therefore Low or absent T cells
-No B cell abnormalities except in more severe form
Associated anomalies
-Conotruncal cardiac defects like VSD, TOF, or IAA
-Parathyroid Hypoplasia cause Low Calcium and Tetany
EMBRYOLOGY:

Proximal segment of the aortic arch develop from aortic sac.

Middle segment of the aortic arch develop from Left 4th aortic arch
Distal segment of the aortic arch develop from Left dorsal aortic segment.
Specifically, Interrupted aortic arch is caused by obliteration of the fourth aortic arch on the left side.
Pathophysiology of IAA :
In IAA, Due to absence in the continuity between proximal and distal aorta, the source of blood supply
to the descending aorta will be totally dependent on Patent Ductus arteriosus(PDA) flow, and hence it is
called duct dependent systemic circulation. In more than 95% cases Ventricular septal defect is present in
association with IAA and due to which there will be mixing of blood at ventricular level.
Due to closuring Duct/small duct, LV is suddenly exposed to very high afterload and invariably become
dysfunctional. RV also has to face high resistance due to duct closure (In Presence of VSD) and also due
to high neonatal PVR and soon RV failure also set in.
Presenting sign/symptoms in IAA :

Almost all neonate present as critically ill.
Tachypnea, poor feeding, lethargy- presenting symptoms
Before ductus arteriosus closure: differential oxygen saturation between the right arm (normal saturation)
and the legs (decreased)
After ductus arteriosus closure: severe congestive heart failure, lower extremity hypoperfusion, Acidosis,
anuria, and shock
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Arm and leg oxygen saturation commonly used as a screening test

In IAA, with the ductus shunting, the expected differential cyanosis between arms and legs is usually not
visible, partly because the intracardiac bidirectional shunt minimizes oxygen saturation differences between
ascending and descending aorta.
Reverse differential cyanosis may present in IAA with TGA
X-Ray findings in IAA:

Cardiomegaly
Increased PV markings, Pulmonary Venous congestion or pulmonary edema
Narrow upper mediastinum or decrease cardio-thymic silhouette: due to absence of the thymus
ECG findings in IAA:

Right ventricular hypertrophy
ST-T wave abnormalities
QT prolong(CATCH22 syndrome related hypocalcemia)
Echocardigraphy for IAA:

The ascending aorta follows a straight course to its branches without the normal continuous curvature to
the descending aorta.
The V sign: type B -IAA. The W sign: type A-IAA.
CT/MRI for IAA:

CT or MRI is one of the confirmatory investigation for IAA and is been done in most of the congenital
heart centre as a routine. It helps in various ways like
To decide about the Plan of Surgery
Differentiate between Severe CoA Vs IAA
Site of interruption
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Deficient length of Arch

Additional information like aberrant vessels etc.
PREOPERATIVE STABILISATION
Fetal Diagnosis help to plan delivery at tertiary care centre where the facilities to handle such neonates
available.
Transfer to tertiary care center as soon as diagnosis confirmed.
Avoid using high FiO2- because it can cause or fasten the duct closure
Treatment for Acidosis/ shock
Prostaglandin E1 infusion (maintain the patency of ductus arteriosus)
Intubation and mechanical ventilatory support
diuretic and inotropic agents
Monitoring and correction of abnormal blood gases and electrolytes
Role of PGE1

Effect: Direct vasodilatation action on the ductus arteriosus and vascular smooth muscle
Dose- 0.02 mics/kg/min- 0.15 mics/kg/min
Adverse effect: Apnea,fever, hypotension, tachycardia, pulmonary overcirculation, generalized edema
High chance of apnea and requirement of intubation with higher dose of PGE1.
Preoperative preparation :

Rule out Other system Abnormalities

Difficult Airways Assessment
Low Calcium may require IV calcium Correction
Coagulopathy- Due to Liver dysfunction with Low calcium and Vit K supplement will help to correct it to
some extent.
Reserved Irradiated Blood product- To reduce Lymphocyte Load as such neonates are low on immunity
and CPB run also make then further immune-compromised.
Rule out Sepsis before taking such neonates for complex cardiac surgery.
Multi-Disciplinary-Team Meeting:
Such group discussion will help each team member to know about the plan of surgery, what will be the
best period/Time for surgery, conduct of CPB and various other minute details.
Surgical Timing
Type of Surgery- Single Stage Vs Stage Repair
Approach of CPB- Arterial Cannulation
Use of Low Flow Vs DHCA CPB approach
Cooling Temperature on pump
Parents counseling is very important aspect before taking neonates for such complex cardiac procedure.
Anesthesia Induction:
Anesthesiologist should be extra cautious in inducing such subset neonates as these patients are with
biventricular dysfunction with very delicately balanced circulation. Small judicious dose of sedation with
muscle relaxant should be used to induce such patients.
Opioids Based induction-we follows
Oral/Nasal Intubation- depend on institutes practices
Cuffed/ Uncuffed ET tube- no proven benefit one over other.
Avoid using High FiO2- Chances of PDA closure and can cause sudden cardiac arrest
Avoid Using excess sedatives- as already High LV afterload with ventricular dysfunction
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Inotrope as and when require before or after induction

PGE1 infusion is lifeline for such duct dependent systemic circulation neonates and hence should not be
stopped or reduce during or after induction.
Use of Steriod (15-30mg/kg- Methylprednisolone-Our protocol) - its role is not established for the benefit
of reducing SIRS or CNS insult or Ventilation or ICU time.
Intraoperative monitoring:
ECG with Chest Lead,
ETCO2- Mainstream-our protocol as it is more sensitive and not affect the delivered tidal value in tiny
neonates.
Invasive Arterial & Venous Access- very important for the conduct and established proper surgical repair.
In all the cases Two invasive arterial line- one in Right Radial and one in any Femoral artery is must. One
of the IJV cannulation for the central venous access is fine either by blind technique or under USG guided
depend on the expertise available.
Temperature monitoring- central and peripheral temperature monitoring with two probe- Naso-Pharyngeal
& Rectal is utmost important for the uniform cooling and rewarming during the CPB run.
Use of NIRS ( Near Infrared Spectroscopy) for such kind of complex procedure is mandatory. Any
fluctuation in NIRS reading during or after induction should be tackle appropriately with either optimizing
the oxygenation or cardiac output.
Urine output
Surgical management:
This uncommon anomaly is highly lethal If surgically uncorrected, with median age of death 4 to 10 days;
75% of such babies die within 1 month of birth.
Early surgical repair is recommended.
Single-staged complete repair with primary anastomosis of the interruption should be the surgical goal.
Single stage repair is now a routine practice in most well established pediatric surgical units. One stage
repair through median sternotomy has been demonstrated to offer an improved prognosis when compared
to 2-stage repair since 1990s.
Some of the units are still in favor of two stage repair where the first stage will be repair of interrupted
aortic segment with PA band to restrict pulmonary blood flow.
Cerebral Protection during IAA repair:

Newborn brain are vulnerable to any subtle changes in cerebral blood flow and hence as I mentioned in
previous heading NIRS monitoring is utmost important.
Surgeon should take all measures to avoid the use of Total circulatory arrest (TCA) and if that is required
then should take all measure to shorten the TCA period.
To avoid TCA and maintain adequate CNS blood flow various technique is been described like the use
Regional Flow Cannula to perfuse selective Cerebral vessel with low flow during pump run.
Cooling the patient sometime upto 200-240 C to reduce the CMRO2 and hence to protect the brain against
the low flow is one the widely acceptable technique. The most important aspect to use such method is
that there has to be slow and uniform cooling and rewarming with the help of agent like SNP or NTG and
there has to be minimal gradient between core to peripheral temperature.
Use of extracranial cooling is also adds to the benefit of reducing CMRO2.
Use of High dose steroid as to protect brain injury is as I mentioned not established but some center use it
as a part of protocol.
Rewarming of such patient has to restrict till 35.5-36 0 C as hyperthermia in perioperative phase reported
high incidence of brain injuries.
Use of Thiopentone during the Cooling or Before Initiation of TCA has some evidence as a role for CNS
protection.
Use of pH stat Vs Alfa stat strategies for the patient with use of TCA or Extreme low temperature is still
debatable. Use of pH stat strategies during very low temperature has definitely theoretical benefit.
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Myocardial Protection in IAA case:

Preoperative sick LV and RV myocardium require extreme care before and during CPB so wean off bypass
become easy.
Reducing overall neonates body temperature and in addition use topical ice slush over myocardium can
have dual benefit in reducing myocardial tissue demand.
Use of blood cardioplegia at an adequate interval (We use Del-Nido Cardioplegia with interval of 30-40
min) will minimize the myocardial dysfunction.
Reducing selective low flow perfusion time, TCA time (if used) and Aortic cross clamp time is universally
accepted method to minimize the myocardial injuries for any neonatal cardiac surgeries.
Use of Ultrafiltration during and after CPB run is also showing benefits for this kind of complex
procedure.
Use cold light source, switching off overhead lights to prevent unwarranted rewarming of myocardial
surface during hypothermia and cross clamp period though looks minute measure but have unproven
benefits for tiny heart and we follow it as a part of our unit protocol.
Managing Coagulopathy in IAA case:

Mechanism of Coagulopathy Preoperative Altered LFT due ventricular dyfunction and shock
Dilutional Coagulopathy due to long pump volume
Consumptive coagualopathy due to exposure to comparatively larger external surface for neonates
SIR induced Bleeding
Measures to manage coagulopathy Use of miniaturized pump circuit to reduce pump prime volume and reduce requirement of blood
transfusion.
To reduce further prime volume by Reduce the length of arterial and venous tubing by positioning pump
head as near as possible
Use of heparinized circuit with addition of albumin and FFP in prime volume which reduces coagulation
factor consumption.
Use of preoperative Vit K and correct Low calcium level
Use of point of care coagulation monitoring and replace it with specific blood product helps to reduce
bleeding
Choice of Inotropes for IAA :

Catecholamine : Adrenaline- may require high dose due to preoperative biventricular dysfunction ,CPB
related myocardial dysfunction and dilutional effect on intrinsic catecholamines
Inodilator: Milrinone- ideal with adrenaline as preoperative PAH and postoperative ventricular diastolic
dysfunction require- PVR and SVR reduction agent.
Calcium : use as effective as any other inotropes. It improves ventricular contractility, maintain adequate
serum calcium level in case of Degeorge syndrome. Multiple transfusions also need the calcium
supplement in form of infusion/boluses.
Open sternum vs Primary Closure:

Keeping the sternum open is use as a one of the proven & effective postoperative management strategies
for IAA postoperative neonate.
Indication in case of IAA Complex Neonatal Surgery with Long CPB Run
Severe Bi-Ventricular Dysfunction
Coagulopathy-Generalized Bleeding
High airway Pressure on Ventilator
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Expected ICU Problems:

As covering all postoperative problems of IAA in details is not a part of this topic, I am highlighting heading of
ICU problems.
Low cardiac output Phase- common in such complex lesion. Early recognition and treatment provide
better outcome.
Bleeding and Coagulopathy- point of care management is the answer for it.
Decrease UOP- use of PD catheter helps to manage such phase.
Low threshold for TPN- nutrition plays important role in overall outcome of such cases.
Non-Invasive Ventilation (NIV) - early extubation is possible with elective NIV.
Sepsis- predisposing factor like Neonatal age, Preoperative sick condition, Open sternum, Prolong
Ventilation & Prolong ICU Course
Diaphragm Palsy
Chylothorax
REFERENCE :
1. Gruber PJ, Epstein JA. Development gone awry: congenital heart disease.Circ Res. 2004 Feb 20. 94(3):27383.
2. Jongmans MC, Admiraal RJ, van der Donk KP, Vissers LE, Baas AF, Kapusta L. CHARGE syndrome: the
phenotypic spectrum of mutations in the CHD7 gene.J Med Genet. 2006 Apr. 43(4):306-14
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Renal Protection in Cardiac Surgery: An

overview
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Madhav Swaminathan, MD, FASE, FAHA

Professor of Anesthesiology
Duke University Health System
Durham, NC, USA
Introduction
Acute kidney injury (AKI) is a significant cause of morbidity and mortality among
hospitalized patients, especially in the postoperative setting. In addition, it remains a
significant complication of cardiac surgery throughout the world.1-5 Consequences of
AKI include an increase in mortality risk which can exceed 60% among patients requiring
dialysis.3 Even when serum creatinine values remain within the normal range, modest
increases from baseline values are associated with increased odds of death and end-stage
renal disease, as well as longer hospital stays and increased costs.2,5,6 In general, there
have neither been any associated improvements in incidence nor mortality despite many
recent advances in our understanding of the etiology and pathophysiology of AKI.7
Incidence
Nearly 500,000 coronary artery bypass graft (CABG) surgeries are performed each year
in the US.8 AKI is a common complication following cardiac surgery that appears to be
increasing in frequency independent of increasing severity of patient case-mix, perhaps
related to changing diagnostic criteria (Figure 1).9 Common risk factors include age,
Figure 1: Trends in acute renal failure (ARF) and a subset requiring

concurrent dialysis (ARF-D). Unadjusted values over an estimated US
population of 7.4 million CABG cases over 16 years from 1988-2003.
(Swaminathan, M, et al. Crit Care Med. 2007 Oct;35(10):2286-91)
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diabetes, hypertension, and metabolic syndrome, and chronic kidney disease. In addition to the substantial increase
in short-term mortality associated with AKI following cardiac surgery, long-term mortality may be mediated by
persistent chronic kidney disease among AKI survivors.10
Pathophysiology
Perioperative AKI is the net result of several possible insults. Common to all AKI though, are tubular and vascular
cell dysfunction, necrosis, and apoptosis. Although details of the trigger mechanisms for AKI are unclear, there is
better understanding of some insults specific to cardiac surgery, the field in which it has been comprehensively studied.
Cardiac surgery is an ideal model for studying the AKI phenomenon a non-physiological insult and exposure to a
pro-inflammatory, frequently hypothermic and ischemic cardiopulmonary bypass (CPB) circulation in a patient with
cardiovascular disease already at risk for renal injury.
Inflammation
Circulating proinflammatory cytokines are part of the systemic inflammatory response to surgical trauma and CPB.
Additionally, local release of cytokines related to renal ischemia/reperfusion is mediated by nuclear factor kappa
B (NF-B) activation. Renal dysfunction also influences the inflammatory responses since filtration is a primary
clearance mechanism for many cytokines.
Ischemia Reperfusion
Embolism, low-output syndrome, and exogenous catecholamines can all contribute to renal ischemia/reperfusion
during cardiac surgery, leading to phosphate depletion, calcium accumulation, oxygen free radical generation, local
leukocyte activation, and NF-B activation. These changes cause necrosis, and apoptotic cell death through caspase
activation. Experimentally, caspase or NF-B inhibition attenuates ischemia-reperfusion mediated AKI.11
Embolism
Renal atheroembolism can be a major cause of postoperative AKI. Aortic atheroma burden and intraoperative
emboli counts predict AKI. Aortic plaque disruption due to intra-aortic balloon pump counterpulsation is likely
also a significant contributor to AKI. Anti-atheroembolism strategies have been widely adopted into the conduct of
cardiac surgery, including aortic avoidance and use of devices that limit aortic manipulation, but none have proved
effective tools at preventing postoperative AKI.
Nephrotoxins
Nephrotoxic agents blamed in the pathogenesis of AKI include pigments and drugs such as antifibrinolytics.
Myoglobin and hemoglobin avidly bind nitric oxide, causing AKI through direct cytotoxicity, vasoconstrictor effects,
and tubular obstruction. Leg ischemia from femoral artery cannulation has been blamed for myoglobinuric AKI.
Although statins have been associated with myopathy, they have not been associated with increased renal risk in
vascular and major non-cardiac surgery patients.
While both aprotinin and the lysine analogues (tranexamic acid, epsilon aminocaproic acid) are freely filtered by the
glomerulus and attach to the same brush border receptors in the proximal tubule (megalin/cubilin), understanding
of subsequent metabolism of these agents is incomplete. Aprotinin is taken up into proximal tubular cells, where it
remains for many hours. In contrast, epsilon aminocaproic acid and tranexamic acid, both of which resemble amino
acids in size, block these same receptors, causing minor tubular proteinuria. While proteinuria would normally be
evidence of tubular injury, this type can also be elicited by doses of lysine or arginine, and completely resolves 15
minutes after the agent is discontinued.
A single retrospective analysis of epsilon aminocaproic acid in 1502 patients did not find an increase in AKI.12
Controversial retrospective studies comparing renal and other consequences of aprotinin, tranexamic acid, and epsilon
aminocaproic acid in large cardiac surgery populations found increased AKI and mortality with aprotinin.13,14Concerns
persist that a bias towards sicker patients receiving aprotinin cannot be adequately addressed by statistical methods in
these studies. Other studies on AKI have also used exposure to aprotinin as models of investigating better creatinine
profiles for AKI prediction.15
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Biomarkers
Given the limitations of using serum creatinine and urine output for detecting AKI, there is a need for better
biomarkers that can more reliably help diagnose AKI that is specifically caused by acute tubular necrosis, the most
common renal injury among post-cardiac surgery patients. If such a diagnosis could be accurately detected early after
the injury, then the window of opportunity for effective therapies may shift dramatically (figure 2). In addition,
earlier and more reliable detection of AKI would facilitate better risk stratification. Examples of outcomes that could
be estimated include the degree of AKI including dialysis requirement, duration of AKI, subsequent chronic kidney
disease, or mortality.
Several new biomarkers have been identified while those previously known have been more intensely studied.
Although there have been over 20 unique biomarkers of AKI identified or under investigation, most of the current
interest has focused on a handful of promising biomarkers: neutrophil gelatinase-associated lipocalin, cystatin C,
interleukin-18, and kidney injury molecule1.16
Figure 2: The difference between a creatinine-based biomarker and novel

early biomarker-based diagnostic approach for postoperative AKI. (Hudson,
C et al. SeminCardiothoracVascAnesth. 2008 Dec;12(4):320-30.)
In the setting of cardiac surgery, NGAL has been demonstrated to be a highly sensitive and specific biomarker of
postoperative AKI. Its gene is one of the earliest and the most upregulated in the kidney after ischemic injury.17 In
a study of 81 adult cardiac patients, 20% of the patients developed postoperative AKI. NGAL was higher in patients
with AKI at 1 hour, 3 hours, and 18 hours post-CPB when compared with their non-AKI counterparts. A more
recent study found that the use of aprotinin versus epsilon amino-caproic acid in patients undergoing cardiac surgery
resulted in a two-fold incidence of AKI in the aprotinin group. Urinary NGAL was significantly higher at both 0 and
3 hours post CPB in patients receiving aprotinin.18
Interleukin-18 (IL-18) is a proinflammatory cytokine that belongs to the IL-1 superfamily, and has been shown
to be both a mediator and biomarker of ischemic AKI. Kidney injury molecule-1 (KIM-1) is an immunoglobulin
superfamily transmembrane protein normally present at low levels in proximal renal tubular cells that dramatically
increases in expression following acute ischemic or nephrotoxic insult. Several studies among non-cardiac patients
have demonstrated that KIM-1 is a very sensitive indicator of AKI. However, fewer studies exist in the cardiac
surgery literature.
It has been suggested that cystatin C is an ideal molecule for measuring GFR because it is freely filtrated by the
glomerulus, completely reabsorbed by the proximal convoluted tubules, and is not secreted. Unlike creatinine, it
is not affected by age, gender, sex, or body mass. There have only been a few studies to date that have explored
cystatin C as a biomarker for AKI post-cardiac surgery. In one prospective study, both serum cystatin C and NGAL
were measured in 129 pediatric patients following CPB for corrective congenital heart surgery.19 Both cystatin C
and NGAL were very strong independent predictors of AKI when compared to creatinine. In the 41 patients who
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developed AKI, NGAL levels were elevated 2 hours postoperatively while cystatin C levels were elevated at 12 hours
postoperatively.
In the largest cardiac surgery AKI biomarker study performed so far, the Translational Research Investigating
Biomarker Endpoints (TRIBE) AKI consortium gathered detailed plasma and urinary biomarker data in 1,219 adults
undergoing cardiac surgery at high risk for postoperative AKI.20 These investigators found that the highest quintiles
of plasma NGAL and urinary IL-18 were associated with 6.8 and 5 fold greater odds of developing AKI, in addition
to being at higher risk for dialysis, longer hospital stay and overall mortality. The addition of these novel biomarkers
significantly improved the AKI risk predictive capability of conventional models inclusive of only clinical variables.20
Renal Protective Strategies

Advances in identifying individuals at-risk for AKI early are of limited value if they cannot be used to meaningfully
improve patient outcomes. To date, attempts to prevent and attenuate renal injury have met with limited success.
Current renal protective strategies involve optimization of renal perfusion, avoidance of nephrotoxic agents, and
the use of several pharmaceutical agents. Despite decades of trying to mitigate the severity of renal injury, none of
these strategies have shown a consistent benefit in improving outcomes such as reduced incidence of AKI requiring
dialysis or death.
Although these biomarkers are still early in the process of being validated, several are likely to be used in clinical
trials. Some current trials are revisiting previously tested renal protective agents while others are testing newer ones.
Nonetheless, there are several exciting trials under way in post-cardiac surgical AKI. For example, erythropoeitin
has been shown to have diverse effects on nonhematopoeitic tissues that may be beneficial in the prevention of
AKI. Another promising treatment currently under investigation for the prevention of AKI is minocyline. A second
generation tetracycline, this antibiotic has both anti-inflammatory and antiapoptotic properties. It has been shown
in rat models to reduce nephrogenic inflammation and cell death. Currently, there is a randomized, double-blind
placebo control study under way to evaluate its efficacy preoperatively in patients with pre-existing renal insufficiency
undergoing cardiac surgery.21
Intrarenal infusion of medication is another emerging therapy proposed to improve efficacy and decrease the systemic
effects of renal protective therapies. For instance, while systemic administration of a vasodilator may be detrimental
in a hypotensive post-surgical patient, selective renal vasodilation via intrarenal catheter infusion may be beneficial in
preventing AKI. Other therapies being investigated or revisited in AKI post cardiac surgery are sodium bicarbonate,
N-acetylcysteine, and tight glucose control.
Figure 3: The association between early recovery of renal function as

characterized by the percentage decrease in creatinine 24 hours after
its peak value (PD24) and long-term adverse outcome. Significant
differences exist in event-free survival among patients grouped according to magnitude of early recovery, with superior survival among
those with a higher PD24. (Swaminathan, M et al. Ann Thorac Surg.
2010) Apr;89(4):1098-104.)
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Another phenomenon that is appears promising for management of AKI is recovery of renal function.22 We have
recently shown that patients that recover renal function early after AKI may have reduced risk of mortality compared
to those who do not recover as well, given the same magnitude of injury (figure 3).22 The repair and regenerative
potential of the kidneys may therefore be crucial to overall survival. With our failure to significantly prevent
postoperative AKI, salvage of renal function by targeting regenerative potential may the interventional strategy that
should be assessed next.
Summary
Acute kidney injury in the postoperative cardiac surgery population remains a significant cause of perioperative
morbidity and mortality. Despite extensive research in the prediction and treatment of this disease, there has been
limited success in altering patient outcomes. With advances in our understanding of underlying clinical and genetic
risk, as well as the development of more sensitive and specific biomarkers, we may be on the cusp of a new era of
AKI treatment. Once promising therapies are identified, customized approaches would harness information from
individuals own genetic profiles and biomarker responses following cardiac surgery in order to identify specific
personalized interventions. For example, preoperative evaluation may include a genetic panel that stratifies patients
into categories of risk and targets them for preventive therapies. For some high-risk patients, this may also assist with
the decision whether to proceed with surgery or to use more conservative medical management for their cardiovascular
Figure 4: A suggested strategy for post-AKI targeted intervention

stratified using a combination of biomarkers and genomic methods
to stratify those at risk of adverse outcome. (Hudson, C et al. SeminCardiothoracVascAnesth. 2008 Dec;12(4):320-30.)
disease. During the perioperative period, urinary and serum biomarkers could be used to detect AKI in the earliest
stages, confirm the appropriate phenotype warranting intervention, and discern anticipated responses to available
agents in order to deliver tailored therapy to each individual patient (figure 4). Targeting renal salvage to reduce
mortality risk may offer hope in those already affected by AKI. Although such a future hinges on many advances
from the current state, we believe that this multifaceted, individualized approach will finally lead to meaningful
improvements in postoperative AKI.
References
1. Conlon PJ, Stafford-Smith M, White WD, et al. Acute renal failure following cardiac surgery. Nephrol Dial Transplant.
1999;14(5):1158-1162.
2. Mangano CM, Diamondstone LS, Ramsay JG, Aggarwal A, Herskowitz A, Mangano DT. Renal dysfunction after
myocardial revascularization: risk factors, adverse outcomes, and hospital resource utilization. The Multicenter
Study of Perioperative Ischemia Research Group. Ann Intern Med. 1998;128(3):194-203.
3. Chertow GM, Lazarus JM, Christiansen CL, et al. Preoperative renal risk stratification. Circulation. 1997;95(4):878884.
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4. Loef BG, Epema AH, Smilde TD, et al. Immediate postoperative renal function deterioration in cardiac surgical
patients predicts in-hospital mortality and long-term survival. J Am Soc Nephrol. Jan 2005;16(1):195-200.
5. Chertow GM, Burdick E, Honour M, Bonventre JV, Bates DW. Acute kidney injury, mortality, length of stay, and
costs in hospitalized patients. J Am Soc Nephrol. Nov 2005;16(11):3365-3370.
6. Praught ML, Shlipak MG. Are small changes in serum creatinine an important risk factor? Current opinion in
nephrology and hypertension. May 2005;14(3):265-270.
7. Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis. May 2002;39(5):930-936.
8. Thom T, Haase N, Rosamond W, et al. Heart disease and stroke statistics--2006 update: a report from the American
Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. Feb 14 2006;113(6):e85151.
9. Swaminathan M, Shaw AD, Phillips-Bute BG, et al. Trends in acute renal failure associated with coronary artery
bypass graft surgery in the United States. Crit Care Med. Oct 2007;35(10):2286-2291.
10. Bhandari S, Turney JH. Survivors of acute renal failure who do not recover renal function. QJM. Jun 1996;89(6):415421.
11. Daemen MA, van de Ven MW, Heineman E, Buurman WA. Involvement of endogenous interleukin-10 and
tumor necrosis factor-alpha in renal ischemia-reperfusion injury. Transplantation. Mar 27 1999;67(6):792-800.
12. Stafford-Smith M, Phillips-Bute B, Reddan DN, Black J, Newman MF. The association of epsilon-aminocaproic
acid with postoperative decrease in creatinine clearance in 1502 coronary bypass patients. Anesth Analg.
2000;91(5):1085-1090.
13. Mangano DT, Tudor IC, Dietzel C. The risk associated with aprotinin in cardiac surgery. N Engl J Med. Jan 26
2006;354(4):353-365.
14. Shaw AD, Stafford-Smith M, White WD, et al. The effect of aprotinin on outcome after coronary-artery bypass
grafting. N Engl J Med. Feb 21 2008;358(8):784-793.
15. Brown JR, Kramer RS, Coca SG, Parikh CR. The prognostic value of using the duration of acute kidney injury in
cardiac surgery: an example using two antifibrinolytics. The Journal of extra-corporeal technology. Dec 2011;43(4):227231.
16. Edelstein CL. Biomarkers of acute kidney injury. Adv Chronic Kidney Dis. Jul 2008;15(3):222-234.
17. Mishra J, Dent C, Tarabishi R, et al. Neutrophil gelatinase-associated lipocalin (NGAL) as a biomarker for acute
renal injury after cardiac surgery. Lancet. Apr 2-8 2005;365(9466):1231-1238.
18. Wagener G, Gubitosa G, Wang S, Borregaard N, Kim M, Lee HT. Increased incidence of acute kidney injury with
aprotinin use during cardiac surgery detected with urinary NGAL. Am J Nephrol. 2008;28(4):576-582.
19. VandeVoorde RG, Katlman TI, Ma Q, et al. Serum NGAL and cystatin C as predictive biomarkers for acute
kidney injury. J Am Soc Nephrol. 2006;17:404A.
20. Parikh CR, Coca SG, Thiessen-Philbrook H, et al. Postoperative biomarkers predict acute kidney injury and poor
outcomes after adult cardiac surgery. J Am Soc Nephrol. Sep 2011;22(9):1748-1757.
21. http://clinicaltrials.gov/ct2/show/NCT00556491. Minocycline to Prevent Acute Kidney Injury After Cardiac Surgery.
Clinicaltrials.gov 2008; http://clinicaltrials.gov/ct2/show/NCT00556491, 2008.
22. Swaminathan M, Hudson CC, Phillips-Bute BG, et al. Impact of early renal recovery on survival after cardiac
surgery-associated acute kidney injury. Ann Thorac Surg. Apr 2010;89(4):1098-1104.
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Antiplatelet agents and cardiac

anaesthesia: quo vadis
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Dr Manjula Sarkar
Professor & Head Cardiac anesthesia
GSMC & KEM hospital
Mumbai
Introduction
In the era of modern cardiac anesthesia, role of antiplatelet agents are challenging for
all of us. We should know all the antiplatelet agents in detail to provide safe anesthesia.
Definition:
Antiplatelet agents (platelet inhibitors) are the drugs, capable of inhibiting platelet
function, in particular platelet activation and aggregation (1).
Indications:
Acute myocardial infarction ,
Acute coronary syndrome (unstable angina and/or infarction without Q wave).
Stable angina.
Percutaneous transluminal coronary angioplasty (PTCA) with stent implantation.
Secondary preventive measure (after myocardial infarction, cerebrovascular
accident [CVA] or arteritis).
Primary prophylactic strategy against the risk of death and myocardial infarction.
Anticoagulant therapy is contraindicated or cannot be monitored.
Young patients with atrial fibrillation.
Patients with valvular prostheses with previous incidence of embolic events.
Prevention of coronary angioplasty complications.
Classification of antiplatelet agent

Classification based on its site of action,
1. Arachidonic acid pathway inhibitors e.g aspirin
2. Phosphodiesterase inhibitors e.g. dipyridamol Recent drug: cilastazol
3. ADP pathway inhibitors.

Ticlopidine- Clopidogrel
Recent drug: Prasugrel,
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4. Glycoprotein IIb/IIIa inhibitors.

Abciximab, tirofiban, eptifibatide
Chart showing site of action of different drugs.
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Management of patients on preoperative antiplatelet agents

If a patient at increased risk of thrombotic complications is undergoing an operation associated with a low risk of
bleeding - antiplatelet therapy should be continued.
If a patient is at low risk of thrombosis undergoing a procedure with high blood loss, then treatment can be suspended.
The problem arises when patients with an increased risk of thrombosis present for surgery with a moderate-high risk
of bleeding.
Monitoring platelet function

All the pt. on antiplatelet agents should be biologically assessed in the form of platelet counts performed after
initiation of treatment
Platelet counts performed 2 to 4 then 24 hours after initiation of treatment with intravenous glycoprotein IIb/IIIa
antagonists.
Polynuclear neutrophil counts every 15 days during the first 3 months of treatment with Ticlopidine.
All patients receiving platelet inhibitors must be considered to have drug-induced altered platelet function.
At present, there is no suitable bioassay test sophisticated enough to be used routinely for the monitoring of side
effects associated with platelet inhibitors.
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Antiplatelet agents increase the perioperative surgical risk of bleeding?

In cardiac surgery, NSAIDs and aspirin administered in the preoperative period moderately increase postoperative
bleeding without significantly affecting transfusion requirements (evidence levels II to IV).
When used continuously or within a few hours prior to emergency cardiac surgery, abciximab seems to increase the
risk of hemorrhage and transfusion exposure.
The risk appears to be lower with glycoprotein IIb/IIIa antagonists that have a short half-life (tirofiban, eptifibatide),
but has yet to be evaluated.
In cardiac surgery, increased risk of bleeding is a cause for serious concern in patients treated preoperatively with
thienopyridines.
Peripheral block and Central neural blockade can be given to patients those are on antiplatelet agents.
There is nothing in the medical literature on the risk of hemorrhage associated with antiplatelet agents in peripheral
regional anesthesia of the limbs (limb nerve block).
Aspirin and NSAIDs likely carry a very small or negligible risk (grade D).
Discontinuation of antiplatelet agents should be evaluated by mechanism of action, duration, type of surgical
procedure and risk of haemorrhage.
The risk of an epidural/spinal hematoma in patients treated with aspirin or NSAIDs seems to be very small.
Perioperative bleeding complications induced by certain antiplatelet agents are avoided?

Steroids to reduce or eliminate any possible increase in perioperative blood loss are not recommended in patients on
antiplatelet therapy (grade E).
Prophylactic platelet transfusions to reduce or eliminate any possible increase in perioperative blood loss are not
recommended in patients on antiplatelet therapy. Platelets must, however, be readily available.
Perioperative management of antiplatelet therapy

Continue dual antiplatelet thearpy during and after surgery.
Discontinue clopidogrel but bridge the patient to surgery with Glycoprotein IIb/IIIa inhibitor or an
antithrombin, and restart clopidogrel as soon as possible after surgery.
Discontinue clopidogrel before surgery and restart it as soon as possible after surgery
Chart showing
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2014 ACC/AHA Guidelines

Class I
1. Urgent Non Cardiac Surgery 4-6 weeks after BMS or DES

Continue DAPT unless RR of bleeding outweighs benefit of preventing stent thrombosis.
2. Patient with coronary stent & surgical procedure mandates discontinuation of P2Y12 platelet receptor inhibitor,

Continue aspirin perioperatively, re-start P2Y12 platelet receptor inhibitor ASAP after surgery.
3. Obtain a consensus between surgeon, anesthesiologist, cardiologist & patient to weigh RR of bleeding versus
preventing stent thrombosis when deciding, perioperative antiplatelet management.
Class IIb
Non-emergent/Non-urgent, Non Cardiac surgery:

If patients have not had previous stenting, continue aspirin perioperatively when the risk of potential
increased cardiac events outweighs the risk of bleeding.
Postoperative management of antiplatelet drugs

Non- specific method to reduce blood loss

Tight hemodynamic control
Use of beta blockers
Good HR control
Good BP control
Decrease sympathetic outflow and therefore decrease platelet activation
use of tranexamic acid or aprotinin or desmopressin
Assess qualitative and quantitative function of platelets and transfuse platelet concentrate as needed.
Class I Recommendation
a. For stable nonbleeding patients, aspirin should be given within 6 to 24 hours of CABG to optimize vein graft
patency. (Level of evidence A)
b. For patients undergoing CABG after ACS, guideline indicated dual antiplatelet drugs should be restarted when
bleeding risk is diminished to decrease intermediate- term major adverse cardiovascular outcomes. That may have the
secondary benefit of increasing early vein graft patency. (Level of evidence A)
Newer and recent update about Antiplatelet Therapy

Mechanism
Route
Elimination
Cangrelor
Reversible
IV
Half-Life
36 minutes
Elinogrel
Competitive ADP
P2Y12 receptor
IV/Oral
1112 hours
antagonist
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Recovery
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Cangrelor a parenteral, reversible direct P2Y12 inhibitor

Half-life of 59 min allows 100% recovery of platelet function 1 h after the infusion is discontinued
4 mcg/kg/min infusions achieve complete platelet inhibition when measured at 4 min.
AZD6140 is an oral, reversible direct P2Y12 receptor antagonist with a half-life of 12 hrs.
Chart showing Newer Drugs as per there site of action ,
Recent guidelines for pt. having stent
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Recent literature
Prasugrel in combination with aspirin is indicated: Based on the TRITON-TIMI 38 trial

When immediate percutaneous coronary intervention (PCI) is necessary to treat an ST segment- elevation
myocardial infarction
When immediate PCI is necessary to treat a non-ST-segment-elevation myocardial infarction in patients with
diabetes
When stent occlusion occurs whilst the patient is taking clopidogrel
Triton-TIMI 38: efficacy and safety of Prasugrel and clopidogrel

13,608 patients with moderate to high-risk acute coronary syndromes with scheduled PCI
Randomized to Prasugrel (60 mg loading dose and a 10 mg daily maintenance dose) or clopidogrel (300 mg
loading dose and a 75 mg daily maintenance dose) for 6-15 months.
Graph showing
Graph showing ,
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NICE recommendations of dual antiplatelet therapy
Conclusion
More and more patients are coming to surgery while on antiplatelet drugs. Anesthesiologists should be aware of the
indications, potential complications and means of substitution of these agents. They also should be convicted that
preoperative antiplatelet withdrawal is not always the best solution and could be harmful. Finally, the ways to control
perioperative bleeding complications in close relationship with antiplatelet treatments should be considered.
References
1. Patrono C, Coller B, Dalen JE, FitzGerald GA, Fuster V, Gent M, Hirsh J, Roth G . Platelet-active drugs : the
relationships among dose,effectiveness, and side effects. Chest 2001;119 :39S-63S.
2. Bennett JS, Mousa S. Platelet Function Inhibitors in the year 2000. Thromb Haemost 2001 ; 85 : 395-400.
3. Bertrand M, Rupprecht HJ, Urban Ph, Gershlik AH, for the CLASSICS Investigators. Double-blind study of the
safety of clopidogrel with and without a loading dose in combination with aspirin compared with ticlopidine in
combination with aspirin after coronary stenting. The Clopidogrel Aspirin Stent International Cooperative Study
(CLASSICS). Circulation 2000; 102: 624-9.
4. Topol EJ, Moliterno DJ, Herrmann HC, Powers ER, Grines CL, Cohen DJ, Cohen EA, Bertrand M, Neumann FJ,
Stone GW, DiBattiste PM, Demopoulos L. Comparison of two platelet glycoprotein IIb/IIIa inhibitors, tirofiban
and abciximab, for the prevention of ischemic events with percutaneous coronary revascularization. N Engl J Med
2001; 34: 1888-94.
5. International Stroke Trial Collaborative Group. The International Stroke Trial (IST): a randomised trial of aspirin,
subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. Lancet 1997; 349:15691581..
6. Collaborative overview of randomised trials of antiplatelet therapy-III. Reduction in venous thrombosis and
pulmonary embolism by antiplatelet prophylaxis among surgical and medical patients. Br Med J 1994 ;308 :23546..
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7. Lasne D, Fiemeyer A, Chatellier G, Chammas C, Baron JF, Aiach M. A study of platelet functions with a new
analyzer using high shear stress (PFA100) in patients undergoing coronary artery bypass graft. Thromb Haemost
2000 ; 84 : 794-9 .
8. Steinhubl SR, Talley D, Braden GA, Tcheng JE, Casterella PJ, Moliterno DJ et al. Point-of-care measured platelet
inhibition correlates with a reduced risk of an adverse cardiac event after percutaneous coronary intervention.
Results of the GOLD (AUAssessing Ultrega) multicenter study. Circulation. 2001 ; 103 : 2572-8 .
9. Gammie JS, Zenati M, Kormos RL, Hattler BG, et al.: Abciximab and excessive bleeding in patients undergoing
emergency cardiac operations. Ann Thorac Surg 1998; 65: 465-9..
10. Urmey WF, Rowlingson J : Do antiplatelet agents contribute to the development of perioperative spinal hematoma?
Reg Anest Pain Med 1998 ; 23 (S2) : 146-51 .
11. Rodgers A, Walker N, Schug S, McKee A, Kehlet H, van Zundert A, Sage D, Futter M, Saville G, Clark T,
MacMahon S. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: results
from overview of randomised
12. Collet JP, Himbert D, Steg PG. Myocardial infarction after aspirin cessation in withdrawal. International J Cardiol
2000 ;76 :257-8 21.
13. Kaluza GL, Joseph J, Lee JR, Raizner ME, et al.: Catastrophic outcomes of noncardiac surgery soon after coronary
stenting. J Am Coll Cardiol 2000; 35: 1288-94..
14. Brochier ML. Evaluation of flurbiprofen for prevention of reinfarction and reocclusion after successful
thrombolysis or angioplasty in acute myocardial infarction. Eur Heart J 1993 ; 14 : 951-7..
15. Murkin JM, Lux J, Shannon NA, Guiraudon GM, Menkis AH, McKenzie FN, Novick RJ . Aprotinin significantly
decreases bleeding and transfusion requirements in patients receiving aspirin and undergoing cardiac operations.
J Thorac Cardiovasc Surgery 1994 ; 107 : 554-61.
16. Casati V, Bellotti F, Gerli C, Franco A , Oppizzi M, Cossolini M, Calori G, Benussi S, Alfieri O, Torri G. Tranexamic
acid administration after cardiac surgery, a prospective, randomized, double-blind, placebo-controlled study.
Anesthesiology 2001 ; 94 : 8-14.
17. Alderman EL, Levy JH, Rich JB, Nili M, Vidne B, Schaff G, Uretzky G, Pettersson G, Thiis JJ, Hantler CB,
Chaitman B, Nadel A. Analyses of coronary graft patency after aprotinine use : results from the International
Multicenter Aprotinin Graft Patency 22 Experience (IMAGE) trial. J Thorac Cardiovasc Surg 1998 ; 116 : 716-30
18. Beck KH, Mohr P, Bleckmann U, Schweer H, Kretschmer V, Desmopressin effect on acetylsalicylic acid impaired
platelet function Semin Thromb Hemost 1995 ; 21 Suppl 2 : 32-9.
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POINT OF CARE COAGULATION WHICH

TEST AND WHEN? DR SANDEEP MUTHA
(PACPL PUNE)
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In our day to day management of patients undergoing Cardiac Surgery, Perioperative

Bleeding or Coagulation management always puts you in a dilemma. Management of
bleeding patients is a challenge for the Anaesthesiologists and intensive care physician.
What to give?
When to give?
How much is good?
Coagulopathy is a major concern in cardiac surgery due to multiple systemic problems,
anti-platelets, anti-coagulants, Cardiopulmonary bypass and surgery itself. These factors
increase bleeding, increases transfusion of blood products and also morbidity. Because
of the lag time in obtaining results from lab, many decisions of initial transfusion of
blood products depend on clinical judgement. To prevent the problems due to bleeding
we require rapidly identifying the culprit factors and correcting them.
Specific target oriented care i.e. Point of care (POC) management is necessary for rapid
and efficient control of hemostasis. POC devices into treatment algorithms make it
possible to reduce transfusion requirement and cost of treatment.
Perioperative Coagulopathy during cardiac surgery was categorised by Despotis in 1999
as:

Hemodilution: Crystalloids and colloids in CPB>> dilution of coagulation factors

and platelets.
Activation: Anti-platelets and Anti-coagulants in Perioperative period
Consumptive Coagulopathy:
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So if we get a bedside , POC, rapid, accurate, effective diagnostic tool which pin points the root of bleeding will
improve hemostasis, reduce blood transfusion and cost.
Coagulation monitoring methods:

1. Activated Partial Thromboplastin time: aPTT : It gives overall integrity of intrinsic pathway and coagulation. It
is affected by Factors- II, V, VIII, IX, XI, XII, temperature, Ph, heparin and oral anticoagulants. It doesnot pin
point coagulation deficiency.
2. Prothrombin time: PT: It gives integrity of intrinsic and common pathway. It is affected by factors: II, V, VII, X
3. INR: International normalisation ratio: POC INR is shown to be safe and effective to monitor effect of oral
anticoagulants like Warfarin ( coumarin)
4. Qualitative Platelet count: it is not bedside POC monitoring technique.
5. Platelet functional assay: used for patients on anti-platelets like Aspirin.
6. Multielectrode aggregometry: it is more accurate platelet function assay. It calculates electrical resistance between
electrodes due to platelet plug formation.
7. Platelet mapping assay: Assessing aspirin or clopidogrel bleeding. It is a modification of TEG.
8. Fibrinogen assay:
9. Activated clotting time: ACT: It is one of the first and most widely used POC coagulation monitoring tools in
cardiac surgery. ACT is mainstay in monitoring heparin status. ACT assesses the time taken by whole blood to
clot in presence of activators like Kaolin or Celite (normal 100-150sec). It is a sensitive test but not specific.
Variation is seen due to quality of blood sample, inter or intra individual variation and presence of drug activator.
10. Verify now Assay: Assess degree of platelet reactivity in patients on medication.
11. Sonoclot: It is to test visco-elastic property of blood like TEG.
12. Thromboelastography (TEG), Rotational thromboelastometry (ROTEM): It records the viscoelastic property of
blood clot by measuring and mapping mechanical impedance and related changes during clot formation and lysis.
TEG or ROTEM rapidly assess the whole blood coagulation status, concentration of clotting factors, influence
of platelets, fibrinogen levels, effect of heparin and fibrinolysis. It is a bedside tool, takes shorter time and points
out the deficiency in coagulation, POC.
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The thromboelastograph uses whole blood in an oscillating cuvette into which a piston is
lowered.
L. J. Enriquez, and L. Shore-Lesserson Br. J. Anaesth.

2009;103:i14-i22
The Author [2009]. Published by Oxford University Press on behalf of the British Journal of
Anaesthesia. All rights reserved. For Permissions, please email:
journals.permissions@oxfordjournal.org
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TEG and ROTEM monitors clot formation to fibrinolysis. The graph is divided into different parts wrt. Clot
formation.
1. Clot initiation: Reaction time r sec or Clotting time CT sec . from no clot to amplitude of 2mm which depends
on thrombin generation.
2. Clot formation: k sec or clot formation time CFT sec. 2mm to 20mm amplitude. Alpha angle is tangent of slope
between 2mm to 20mm. It depends on fibrin strength and platelet function.
3. Clot strengthening: Maximum amplitude MAmm or Maximum clot firmness MCFmm. This depends on rate
of polymerisation of fibrin and platelet aggregation. It is also called clot rigidity (G) or maximum clot elasticity
(MCE).
4. Clot stability or Lysis index: LY30 or LI30. It is reduction in clot strength after achieving MA/MCF. LY30 or
LI30 is percentage of clot strength after 30 min of MA. Maximum lysis ML% is maximum percentage decrease
in amplitude. Decreased LY30 or increased ML indicates hyperfibrinolysis.
ROTEM consists of 5 different testd depending on reagent:

INTEM (ellagic acid) intrinsic coag. Pathway

EXTEM (tissue factor) extrinsic pathway
FIBTEM (cytochalasin D) fibrinogen binding to glycoprotein GP IIb/IIIa
HEPTEM ( heparinise) Residual heparin
APTEM effect of aprotinin
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Clotting Parameters
Clot initiation
Clot formation
TEG
Reaction time r sec
Alpha angle
ROTEM
Clotting time CT sec
Clot formation time - CFT
Alpha angle
Clot strengthening
Maximum amplitude MA
Amplitude
Maximum clot formation MCF mm
Fibrinolysis
Lysis at 30 min LY30 %
Maximum lysis
Lysis at 30 min LI30%
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TPCH CARDIAC SURGERY ALGORITHM
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STEP WISE ALGORITHM BASED APPROACH TO COAGULATION Goal directed Coagulation

management in Perioperative period of Cardiac surgery
Faroani etal.
Journal of Cardiothoracic and Vascular Anesthesia- Oct 2013
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1. IDENTIFICATION OF RISK PATIENTS: history of bleeding tendency, family history of bleeding,

anti-platelet, anti-coagulation medication, H/O hepatic disease, anaemia, thrombocytopenia etc.
Correct the correctable factors like anaemia, stopping anticoagulants, stopping anti platelets maintain hydration and tissue oxygenation.
Conventional screening- aPTT, PT, INR , platelet assay(1C)
Platelet functional assay, platelet mapping for patients on medication like aspirin and clopidogrel.
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PRO/CON - Liberal versus restrictive

strategy of blood transfusion (CON)
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Consultant and Head
Department of Cardiac Anaesthesia
Nayati Multi-Superspeciality Healthcare Hospital and Research Centre
Mathura, UP.
Circulation was discovered as early as 1600s, and the next two decades saw a sluggish
move towards the first human transfusion in 1800s. Cardiac surgical procedures consume
20% of all transfusion in the US. Only in the latter half of twentieth century were the
deleterious effects of transfusion studied and opened the era of restricting transfusions,
searching targets of transfusion and minimising blood exposure in perioperative period.
Cardiac surgery has seen a paradigm shift in literature from a dominant very restrictive
transfusion strategy in the early part of the century to a more liberal strategy over the
last few years.Most evidence in favour of restrictive transfusion came from retrospective
analysis of large cohorts (cumulative data of 30000 to 50000 patients).
Restrictive and liberal transfusion triggers have varied across studies. Most restrictive
triggers have haemoglobin of more than 7gms/dl as triggers and liberal trigger has been
haemoglobin more than 9gms/dl. Though not defined very well, these definitions are
more of consensus.
Van Straten in a study of 10,425 CABG patients observed that RBC transfusion was an
independent risk factor for early mortality. In another study of 3,024 CABG procedures,
Kuduvalli et al observed an increased 30-day and 1-year mortality in blood transfused
patients. Murphy et al found a significant negative impact of perioperative transfusions
even after exclusion of 1st year outcomes, suggesting the long term deleterious effects
persisted.
The age of transfused RBCs also generated interest, RBCs more than 2 weeks duration
having more deleterious effect than the fresh once. Tough most recent studies do not
substantiate this view. Most awaited are the results of the ongoing trial, the Red Cell
Storage Duration Study (RECESS) randomising patients exposure to RBCs <10 days
versus >21 days with primary outcome being change in Multiple Organ Dysfunction
Score by day 7.
Perioperative RBC transfusion have been independent risk factors for postoperative
Atrial Fibrillation (AF). There has been an increased rate of infections, sternal woundinfections, clostridium-difficile associated diarrhoea and bacteraemia in patents transfused
with RBCs during cardiac surgery. Higher risk-adjusted rates of postoperative respiratory
distress, respiratory failure, acute respiratory distress syndrome, and reintubation, and
longer times on the ventilator, have been demonstrated in patients undergoing transfusion.
Karkouti et al in 2011 observed that Acute Kidney Injury increased proportionately
with the number of RBC units transfused in 12,388 patients undergoing cardiac surgical
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procedures. Similar observations were made by Koch et al in 11,963 CABG procedures. A propensity matching
of 322 Jeovah witness patients with 48986 non-jeovah witness undergoing cardiac surgery at Cleveland Clinic also
witnessed lower acute complications including MI, prolonged ventilation, lesser re-operations and shorter length of
hospital stay in them.
Liberal transfusion strategies have been compared with the conventional restrictive transfusion strategies in cardiac
surgical practice. Two prominent RCTs have been conducted in last few years throwing more light. Both TRACS
(Transfusion requirements After Cardiac Surgery) and TITRe2 (Transfusion Indication Threshold Reduction study)
trials have looked for non-inferiority of liberal transfusion versus restrictive strategy in cardiac surgical patients
been randomised to Liberal (hb>9) and restrictive (Hb>7) strategy limbs. TRACS trial randomised 502 patients
undergoing cardiac procedures with CPB, with comparable primary outcomes of 30-day mortality and in-hospital
major morbidity between the two strategies. Restrictive group had 60% reductions in RBCs transfused and also RBC
transfusion was found to be an independent risk factor for mortality. For every unit of RBC transfused, the risk of
occurrence increased for cardiac complications (OR 1.27), renal complications (OR 1.26), infectious complications
(OR 1.2), and 30-day mortality (OR 1.25).
TITRe2 trial by Murphy et al is the latest multi-centre trial which randomised patients undergoing cardiac surgery into
liberal (Hb<9gm/dl) and restrictive (Hb<7gm/dl) transfusion strategies. Restrictive transfusion strategy was found
not superior to liberal strategy with respect to morbidity or health-care costs. Close to 50% of consentedpatients
were not randomised raising concerns of bias.Significantly high proportions of patients with severe non-adherence
and lower proportion with any nonadherence in the restrictive limb may have confounded the results. There was
a very high rate of blood and product use before randomisation, high transfusion rates after randomisation (63%
in restrictive and 94% in liberal) and the mean difference in haemoglobin nadir being 1gm/dl. These factors may
suggest a huge similarity among the groups and hence making the comparison questionable.Indicators of adequacy
of oxygen delivery to tissues (ScVO2) were not monitored for and neither plausible explanations for the differences
in outcomes discussed.
Also the above mentioned studies fail to consider the usual course of haemoglobin drift that occurs after a cardiac
surgery. A usual trend is represented by a gradual fall in haemoglobin in postoperative period with a nadir fall by third
to fourth day (average fall of 2-3gms/dl as compared to preopHb level) and return to 7080% of baseline by 7-10
days. Most transfusions made in TRACS trial were on third and fourth post-operative days.
Borde et al studied the impact of anaemia and transfusion on all-cause in-hospital mortality in Rheumatic heart
disease undergoing cardiac surgery. Transfused patients had an odds ratio of 2.28 towards the composite end point.
They also observed a significantly low Hb in the first three post-operative days in the transfused patients, probablya
suggesting that RBC transfusion is not the only modality to deal with preoperative anaemia. They also further reemphasize the additional impact anaemia and transfusion have in a worse perioperative outcome.
The rationale for implementing a restrictive transfusion strategy is based on such many studies (30000-40000
retrospective analysed cohorts and a few thousand prospective analysed patients) that have shown a lack of benefit
and, at the same time, substantially increased costs and adverse effects associated with RBC transfusion. These
findings also suggest that the primary strategy in patients undergoing cardiac surgery should be to avoid giving RBC
transfusion solely to correct low haemoglobin levels.
Till more robust RCT consider the comparison of different strategies of RBC transfusion after cardiac surgery,
the current practices considering clinical and bio-chemical markers of oxygen delivery to tissues and avoiding unwarranted can be continued.
REFERENCES
1. Murphy GJ, Pike K, Rogers CA et al.TITRe2 Investigators.Liberal or restrictive transfusion after cardiac surgery.N
Engl J Med. 2015 Mar 12;372(11):997-1008.
2. Hajjar LA1, Vincent JL, Galas FR et al. Transfusion requirements after cardiac surgery: the TRACS randomized
controlled trial.JAMA. 2010 Oct 13;304(14):1559-67.
3. Arman K, G.J.R. Whitman et al. Blood Transfusions in Cardiac Surgery:Indications, Risks, and Conservation
Strategies. Ann ThoracSurg2014;97:72634
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4. George TJ, Beaty CA, Kilic A, et al. Hemoglobin drift aftercardiac surgery. Ann ThoracSurg2012;94:7039.
5. van Straten AH, Bekker MW, Soliman Hamad MA, et al.Transfusion of red blood cells: the impact on short-term
andlong-term survival after coronary artery bypass grafting, aten-year follow-up. Interact CardiovascThoracSurg
2010;10:3742.
6. Karkouti K, Wijeysundera DN, Yau TM, et al. Influence oferythrocyte transfusion on the risk of acute kidney
injuryafter cardiac surgery differs in anemic and nonanemicpatients. Anesthesiology2011;115:52330.
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Monitoring Cerebral Blood Flow during

cardiopulmonary bypass
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Prof. Srinivas Rao G

Chief Cardiac Anesthesiologist
NRI Medical College & Heart Centre
Guntur, A.P.
1. Introduction
Ischemic brain injury is a significant area of concern during cardiopulmonary
bypass (CPB). Efforts to reduce the risk of such neurological complications
include searching for causal mechanisms, making improvements to the surgery,
anesthesia and CPB techniques, and refining the CPB equipment. The
complications range from minor cognitive disorders of a temporary nature to
irreversible cerebral lesions, and the incidence increases up to 16% as surgery
becomes more complex. The presence of proximal atherosclerosis has been
shown to five-fold the risk. The incidence is also associated with predisposing
factors such as age, vascular diseases, diabetes.
2. Cerebral blood flow, metabolism and ischemia
Cerebral blood flow (CBF) in the resting adult human is on average 45-55 ml/100 g
brain tissue/min, corresponding to 12-15% of the total cardiac output flow. The flow is
determined by several factors, e.g. the mean arterial blood pressure (MAP), the arterial
carbon dioxide partial pressure (PaCO2), the hem-atocrit, the blood temperature, and
the cerebral perfusion pressure (CPP). A significant difference exists between CBF in
grey matter (70 ml/100 g/min) and in white matter (34 ml/100 g/min).
3. Blood Supply
The main arterial blood supply to the brain emanates from the two common
carotid arteries, which origin from the aortic arch on the left, and from the
brachiocephalic trunk on the right side in humans. The carotid arteries form the
anterior cerebral circulation, while the vertebral arteries, originating from the
subclavian artery bilaterally form the posterior cerebral circulation. (Fig-ure
1) The carotid arteries divide into an internal and an external carotid branch, of
which the internal supplies the frontal brain regions, and the external supplies the face
and neck. Together, the vertebral arteries form the basilar artery that supplies the rear
brain regions and the brain stem.
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Figure 1. Schematic overview of the brains arterial blood supply routes. The main vessels for cerebral blood supply
are the left and right internal carotid arteries and the left and right vertebral arteries.
The internal carotid arteries and the basilar artery connect in the Circle of Wil-lis, an anastomosis that allows flow
distribution to both hemispheres of the brain in the event of unilateral proximal disturbances. (Figure 2) Although
this vascular ring structure may be critically important in some cases, 54% of all individuals and 79% of patients
presenting with clinical signs of neural dys-functions do not have a fully developed Circle of Willis.(1
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Figure 2. Schematic overview of the Circle of Willis, as seen from below. The bas-ilar artery, which is an extension
of the two conjoined vertebral arteries, connects to the two internal carotid arteries via the posterior communicating
arteries. A func-tional blood vessel circle is completed with the connection of the anterior cerebral arteries to the
anterior communicating artery, thus ensuring blood supply to both brain hemispheres in the event of a unilateral
blood flow obstruction.
The brains venous vascular system consists of two main routes. One is the superior sagittal sinus, a superficial
longitudinal folding of the dura mater that extends from the frontal to the occipital skull. The other includes the
inferior sagittal sinus, which together with the superior sagittal sinus form the trans-verse sinuses and subsequently
the jugular veins which in turn form the bra-chiocephalic veins that eventually drains into the superior vena cava
(SVC) and the right atrium. (Figure 3)
Figure 3. Principal overview of the of the cerebral venous blood system. The two main routes for the intracranial
venous blood flow are the superior and the inferior sagittal sinuses, which are conjoined in the occipital region. From
there, the venous blood passes through the two transverse sinuses which will eventually form the in-ternal jugular
veins that leads the blood to the superior vena cava.
4. Metabolism
The brain metabolism depends largely on an uninterrupted supply of oxygen and glucose, and the capacity for
anaerobic metabolism is low. A reduction of the CBF below approximately 0.10-0.15 ml/g/min leads to loss of
the trans-membrane ion balance. The energy reserves are limited to small amounts of glycogen in the astrocytes.
During aerobic metabolism in neurons and the astrocytes, glucose-derived pyruvate enters the citric acid cycle, where
it is transformed into energy in form of adenosine triphosphate (ATP). The py-ruvate metabolism also creates
nicotinamide adenine dinucleotide (NADH) which enters the mitochondrial respiratory chain to supply additional
ATP. During anaerobic conditions, the respiratory chain is blocked, and pyruvate and NADH are accumulated.
Pyruvate then interacts with NADH and lactate dehydrogenase (LDH), forming lactate. Thus, oxygen shortage will
increase lactate and decrease pyruvate concentrations. The relationship between the lactate and pyruvate concentration
levels, the L/P ratio, is considered to indi-cate ischemia when >25-30.
The pathogenesis of ischemic brain injuries includes three elements; a de-polarization, a bio-chemical cascade, and
a reperfusion injury. Lactic acidosis disturbs the transmembrane ion gradients, allowing an excessive inflow of calcium ions (Ca2+) into the cytosol. The altered Ca2+ balance triggers a release of neurotoxic glutamate, the neuronal
recycling of which is blocked by ische-mia. The accumulation of glutamate disables glutamate-operated membrane
ion channels, which further enhances the Ca2+ inflow. The increased Ca2+ con-centrations and the acidosis trigger
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the release of oxygen radicals, thereby in-ducing neuron damage and cell death by proteolysis and lipolysis. The
cascades also result in a reperfusion injury involving intravascular accumula-tion of leukocytes that impairs the microcirculation and leads to further re-lease of oxygen radicals.
Autoregulation
The CBF is driven by the cerebral perfusion pressure (CPP), and as a result of the restrictive nature of the skull,
elevations in intracranial pressure (ICP) may affect the CBF. Limited cerebral drainage can produce increases in ICP.
The CPP is commonly defined as MAP - ICP, but in case the ICP is not available, other definitions can be used.
During CPB, the CPP can be esti-mated as the MAP - CVP, under the assumption that there is no focal intracra-nial
problem. A CPP of <30 mm Hg has been shown to result in ischemic metabolism in normothermic pigs.
The brain is able to autoregulate its blood flow in order to enable physio-logical metabolism within certain limits. This
autoregulation is believed to be governed by metabolic, neurogenic, and myogenic components.
Figure 4. Relationship between mean arterial pressure (MAP) and mean cerebral blood flow (CBF). The dotted lines represent the upper and lower pressure limits for functional cerebral blood flow autoregulation.
Cardiopulmonary bypass (CPB)

Cardiac surgery usually relies on a CPB system where the IVC and SVC blood is diverted from the body through
plastic cannulas inserted proximal to the right atrium. Thereby, the diverted blood escapes the pulmonary circulation
and is pumped from the venous reservoir through an oxygenator where gase-ous exchange takes place across a semipermeable membrane for gas diffu-sion.
There are two main types of CPB pump; the centrifugal pump and the roller pump. In a centrifugal pump the blood
is directed into the center of a pump chamber where a rapidly rotating impeller or a set of stacked plastic cones
transfers its kinetic energy to the blood, creating a vortex. The blood is then transferred out to the CPB tubing system
via a pump chamber periphery outlet. The roller pump is a pos-itive displacement pump constituted of an outer
housing, which contains a runway for the CPB tubing. The tubing enters and exits the housing on the same side,
where the pump tubing segment is connected to the rest of the CPB tubing system. In the center of the housing is a
rotor with peripherally placed rollers, which press the tubing against the housing inner wall. A finite amount of blood
is thus enclosed between the rollers, and the rotor movement trans-ports the blood forward.
In the oxygenator, gases such as oxygen and anesthetics enters the blood, and carbon dioxide is removed. Venous
drainage through the CPB tubing is usually achieved by the gravity siphonage generated by the level difference
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between the patient and the venous reservoir. The oxygenated blood is re-transfused to the patients blood circulation
through the CPB tubing and via a cannula, commonly inserted into the aortic arch or a femoral artery.
When stable hemodynamics are obtained, the aortic arch can be cross-clamped and protection during cardiac arrest
can be provided through intra - coronary infusion of a cardioplegic solution, typically containing potassium.
The CPB system is usually equipped with a heat exchanger to regulate the patients body temperature, suctions to
retrieve heparinized blood from the surgical wound and pumps to deliver cardioplegic solution.
Figure 5. Schematic presentation of the principle for cardiopulmonary bypass. Ve-nous blood flow is deviated before it
enters the heart, and is led to a venous reser-voir, from which it is transported by means of a pump to the oxygenator
and then onward to the aorta. In the oxygenator, oxygen is added to the blood and excess car-bon dioxide is removed.
Venous drainage
Venous drainage is typically maintained using a dual stage venous cannula that is inserted into the IVC through the
right atrial auricle. The cannula has distal end openings for IVC drainage, and lateral for the SVC. Alternatively, the
SVC and the IVC can be separately cannulated (bi-caval). (Figure 6) The SVC and IVC cannulas are connected to a
Y-piece outside the patient and then connected to the CPB tubing. The positions of the cannulas can be exam-ined by
trans-esophageal ultrasound to confirm that the IVC cannula has not unintentionally entered the hepatic vein instead
of the IVC, a position associ-ated with inadequate drainage.
The venous CPB drainage is based on gravity and the siphon effect, and is therefore basically passive. Drainage may
be improved by applying a negative pressure to the venous blood reservoir, adding a vacuum effect to the venous
tubing.
Obstruction of the blood flow in a dual stage or SVC cannula may lead to congestion in the superior territory, and to
elevated CVP that is propagated into the cerebral vasculature. Consequently, increased ICP can occur and reduce the
CPP with impaired cerebral perfusion as a result.
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SVC
IVC
SVC
IVC
Figure 6. Schematic presentation of common venous cannulation alternatives for cardiopulmonary bypass. A; bicaval cannulation. Cannulas are separately inserted into the superior vena cava (SVC) and the inferior vena cava (IVC),
and then inter-connected to lead the venous blood to the heart-lung machine reservoir. The respec-tive cannulas
are snared to avoid redundant blood flow to the heart. B; a dual stage venous cannula is inserted into the IVC, and
positioned so that the SVC is drained via side wall openings in the cannula. IVC = inferior vena cava, SVC = superior
vena cava.
Arterial blood flow and pressure

In contemporary practice, the arterial CPB blood flow is commonly 2.2-2.5 l/min/m2 body surface area. Commercially
available oxygenators are typically designed for blood flows up to about 7 l/min, which covers the re-quirements for
adult CPB in most cases. It is common that heart-lung ma-chines offer the user a choice between pulsatile and nonpulsatile blood flows, and switching between them to achieve optimal organ perfusion is uncontro-versial.
Arterial blood pressure during CPB is usually lower than normal blood pressure at equal blood flow, which to
some extent can be explained by de-creased vascular resistance caused by hematocrit reduction, reduced catecholamine levels, the initial transient low oxygen tension and low pH of the CPB crystalloid priming fluid. The levels
of empirically accepted MAP may range from 50 to 95 mm Hg, and while hypotension may be desir-able in some
situations in order to reduce surgical blood loss, it may also lead to cerebral hypoperfusion, which forms a practical
dilemma.
Clinical problems
There are a number of potential risk factors associated with CPB that have significance for the development of
cerebral injury, and understanding such risk factors is essential for ensuring safe perfusion during cardiac surgery.
Examples
Venous drainage issues
Unsatisfactory positioning of cannulas, inadvertent kinking or dislocation of venous cannulas and CPB tubing,
imprecision or malfunction of monitoring or CPB equipment, as well as human errors, are all examples of factors
that may contribute to significant hypoperfusion. This was illustrated by one of our animal experiments, in which
accidental superior vena cava congestion lead to a fatal outcome, despite the fact that conventional monitoring did
not reveal any apparent abnormalities. In that case, the CVP, the mixed venous oxygen saturation (SvO2), and MAP
were all within normal ranges, but sim-ultaneous magnetic resonance imaging (MRI) scanning revealed the absence
of cerebral circulation.
To explore the properties of cerebral venous congestion due to SVC obstruc-tion, some authors foccused on cerebral
oxygen saturation and metabolism during controlled stepwise occlusion of the SVC cannula in increments of 25%
until total occlusion. Based on the aforementioned interaction between the CVP, ICP and CPP, the situation allowed
us to apply different strategies to preserve the CPP after SVC obstruction.
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Ensuring regional perfusion

A substantial proportion of patients undergoing cardiac surgery also suffer from vascular disease, which may have
implications for the arterial supply for the brain in case the cerebral vessels are affected. The CPB flow mode profiles
can be adjusted, and such optimization of the CPB can readily be performed by the perfusionist. Hypothetically, poststenotic perfusion might benefit from the pressure peaks generated by pulsatile blood flow.
Organ protection during circulatory arrest

When the CPB needs to be interrupted for surgical reasons, mainly during aortic surgery, patient safety relies on
rapid surgical management and certain protective strategies. The principal strategy is circulatory arrest in deep hypothermia (HCA), which can be accompanied by selective cerebral perfusion
using the CPB system. Both alternatives offer exsanguinated surgical fields in order to facilitate the rapidness and
effectiveness of the surgery.
Selective cerebral perfusion can be performed either with antegrade tech-nique (selective antegrade cerebral perfusion,
SACP) via the carotid arteries, or retrograde technique (retrograde cerebral perfusion, RCP) via the venous SVC
cannula. Signs of is-chemia could be seen below 6 ml/kg/min in terms of regional increases in lactate concentrations.
Aetiology
Atheromatous emboli from aorta manipulation
Lipid microemboli from recirculation of unwashed cardiotomy suction
Gaseous microemboli from air leakage and cavitation
Cerebral hypoperfusion or hyperperfusion
Cerebral hyperthermia
Cerebral dysoxygenation
To identify the problems in cardiopulmonary bypass (Cerebral perfusions). Many techniques came into practice
Real-time neurologic monitoring should be an integral part of neuroprotective strategies .
Several monitoring modalities are available.
1.
2.
3.
4.
5.
6.
7.
EEG (Electroencephalogram
BIS (The Bispectral Index)
NIRS (Near Infrared Spectroscopy)
TCD (Transcranial Doppler)
JUGLAR VENOUS OXYMETRY
TOI (Tissue Oxynation Index)
Positrom-emission tomography (PET)
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Anterior mediastinal masses,

Anaesthesiologists nightmare
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Dr. Thomas Koshy,

Professor, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum,
Kerala
Anterior mediastinal masses though uncommon, when they present at surgery for
diagnostic or therapeutic procedures, can pose serious challenges for the anaesthesiologist
in the perioperative period. Tumors of the mediastinum include lymphoma, thymoma,
metastasis, teratoma, cystic hygroma, bronchogenic cyst, and intra thoracic thyroid
tumors (figure 1).
Figure 1: Chest radiograph of an adult

patient with an anterior mediastinal
mass (lymphoma).

The anatomical location of these tumors can produce compression of three important
structures of the mediastinum: (a) trachea and main bronchi (b) large vessels particularly
superior vena cava (c) heart. Total occlusion of the airway and cardiovascular collapse are
well-recognized complications during general anesthesia even in asymptomatic patients.
These complications can occur while placing the patient in supine position, at the
induction of anesthesia, at extubation, and in the post operative period. It is important
to notice that airway compression usually occurs distal to the endotracheal tube (ETT) at
the time of induction of anesthesia, when voluntary control of airway is lost, and it is not
possible to forcibly pass the ETT through the airway once it has collapsed. Several studies
have found an incidence of anesthesia- related life-threatening respiratory complications
of up to 20% in such patients, which includes death of the patient.
Management of these patients should focus on three aspects: (a) Cardiorespiratory signs
and symptoms at presentation (b) Estimate the presence and degree of obstruction of
the trachea-bronchial tree and major vessels (c) Serious consideration to be given to avoid
GA in certain cases; for e.g. tissue biopsy can be obtained under local anesthesia.
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History and Physical examination

In the history, symptoms of airway obstruction and compression of heart & great vessels should be sought. Minimal
to moderate cardiopulmonary symptoms include cough, dyspnea on exertion, chest pain, fatigue and vocal cord
paralysis. Severe cardiorespiratory findings are orthopnea, stridor, cyanosis, jugular venous distension or superior
vena cava syndrome. An effort should be made to asses the presence of either dysponea or noisy breathing at rest,
on exertion and in different positions particularly supine position. During physical examination, stridor, rhonchi, and
decreased breath sounds should be carefully looked for again with the patient in different positions. A history of
supine dyspnea or cough should alert the anesthesiologist to the possibility of airway obstruction on induction of
anesthesia. Symptoms of supine presyncope suggest vascular compression (figure 2).
Figure 2: Contrast CT scan of an adult

with thymoma having symptoms of
supine presyncope. Main pulm artery
(Main PA) is partially compressed and
Left pulm artery (Left PA) is almost
completely occluded
Life-threatening complications may occur in the absence of symptoms especially in children. The adult population
carries a lesser risk of intraoperative respiratory problems. This could be explained by the fact that the airways of
infants and small children are more compressible than adults.
In a large study by Bechard et al, it was observed that a higher perioperative complication rate occurred for patients
with severe cardiorespiratory symptoms (stridor, orthopnea, cyanosis, jugular distension, and superior vena cava
syndrome). It seems prudent to avoid general anesthesia if possible, whenever severe cardiorespiratory symptoms
are encountered.
Superior vena cava syndrome is the result of progressive enlargement of a mediastinal mass and compression of
mediastinal structures, particularly the vena cava. The caval compression produces venous engorgement and edema
of the head, neck, and arms. Direct mechanical compression as well as mucosal edema severely compromise airflow
in the trachea.
Pulmonary Function Tests

Though Benumof had recommended recording of flow volume loop in upright and supine in asymptomatic or
minimally symptomatic patients during preoperative evaluation other authors have questioned its utility in predicting
perioperative complications. According to them this recommendation is based on anecdotal data and upright and
supine spirometry may not be any better than symptoms and CT scanning. However Betchard et al had reported
that peak expiratory flow rate of 40% or less and a mixed restrictive and obstructive pattern was associated with a
significantly increased risk of postoperative respiratory complications like reintubation, bronchoscopy and pneumonia.
Chest X-ray and CT scan

It is crucial to assess the patency of both trachea and bronchi. Chest radiographs (PA view) allow measurement of
the tracheal diameter / tracheal compression in the coronal plane in addition to showing the mass (figure 3). A lateral
view will show the compression of the trachea in the antero-posterior direction.
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Figure 3: Chest X-ray of an adult with an

anterior mediastinal mass. There is no
lateral compression on the trachea
A CT scan of the chest will again show the compression of the trachea and bronchi in addition to confirming the
diagnosis of mediastinal mass. Scan also will demonstrate presence of atelectasis, pleural and pericardial effusions,
and superior vena cava compression. Significant tracheal compression is defined (Shamberger et al) as greater than
50% diminution of tracheal cross-sectional area and such patients have a very high chance of near total/total airway
obstruction during induction or emergence from anesthesia (figure 4).
Figure 4: CT scan of the patient in figure

3 showing >50% narrowing of distal
trachea by the mass. This patient had
life-threatening distal airway collapse on
induction at the authors institute.
When tracheal compression was greater than 50%, a sevenfold increase in the risk of postoperative respiratory
complications was observed by Bechard et al in a study of 98 patients.
Echocardiography
Transthoracic echocardiography is indicated for patients with vascular compression symptoms. Cardiac
output may be severely depressed due to impeded venous return from the upper body, direct mechanical
compression of the heart, and (with malignancies) pericardial invasion. An echocardiogram is useful in
evaluating cardiac function and detecting pericardial fluid. Patients with significant pericardial fluid can
develop cardiovascular collapse on initiation of positive pressure ventilation. Preoperative pericardial
drainage or institution of CPB is an option in such cases.
General Anesthesia vs Local Anesthesia
Fatal or near-fatal cardiopulmonary arrest in the course of anesthesia for diagnostic or therapeutic surgical procedures
in patients with a mediastinal mass has been reported many times. Unexpected and often total airway obstruction
occurs on induction of anesthesia and conventional techniques like intubation with ETT or tracheostomy will prove
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futile as the obstruction is at the carina or bronchi. Securing the airway by passing a double lumen endobronchial tube
may also fail in such circumstances. Newman has given three mechanisms for the dangers of GA i.e., exacerbation of
extrinsic intrathoracic airway compression.
1. Lung volume is reduced to around 500-1500 ml under GA
2. GA relaxes bronchial smooth muscles leading to greater compressibility of the airway by the overlying tumor
3. The loss of spontaneous diaphragmatic movement with muscle paralysis decreases the normal transpleural
pressure gradient which dilates the airway, thus enhancing the effect of extrinsic compression.
Management of these patients is guided by a grading based on their symptoms and finding on the CT scan (table
1&2).
Table 1: Grading Scale for Symptoms
Asymptomatic
Mild: Can lie supine with some cough/pressure sensation
Moderate: Can lie supine for short periods but not indefinitely
Severe: Cannot tolerate supine position
Table2: Stratification of Patients with Mediastinal Masses Regarding Safety for General Anesthesia
Safe
(I)
Asymptomatic adult, CT minimum tracheobronchial diameter > 50% of normal
Unsafe
(I)
Severely symptomatic adult or child
(II)
Children with CT tracheobronchial diameter < 50% of normal, regardless of symptoms
Uncertain
(I)
Mild/moderate symptomatic child with CT tracheobronchial diameter > 50%of normal
(II)
Mild/moderate symptomatic adult with CT tracheobronchial diameter < 50% of normal
(III) Adult or child unable to give history
Patients with uncertain airways should have diagnostic procedures performed under local or regional anesthesia whenever possible. When
GA has to be used in such patients, spontaneous respiration with avoidance of muscle paralysis would maintain airway
patency. These patients are premedicated with anticholinergic drugs only and sedative & narcotic premedications
are avoided. If there is a concomitant superior vena cava obstruction, a large bore peripheral intravenous cannula
should be placed in the lower extremity. Inhalational induction with sevoflurane or titrated amount of propofol
with or without ketamine maintaining spontaneous ventilation until the airway is definitely secured or the procedure
is completed is the preferred method. If muscle relaxants are required, ventilation should first be gradually taken
over manually to ensure that positive pressure ventilation is possible and only then a short-acting muscle relaxant
be administered. If the CT scan shows an area of non-compressed distal trachea, then an awake intubation using
fiberoptic bronchoscope to position the ETT to distal non-compressed trachea is another option. Those who undergo
debulking procedure should have little difficulty with extubation. All other patients should be extubated wide awake.
Management of airway or vascular compression occurring during GA

The options before the anesthesiologists are
1. Awaken the patient as rapidly as possible
2. If life threatening airway collapse takes place: (a) Reposition the patient to a position (determined during
preanesthetic evaluation) that causes less compression and fewer symptoms OR (b) Rigid bronchoscopy and
ventilation distal to the obstruction
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The rigid bronchoscope can be passed into one of the bronchus during resuscitation for oxygenation. Once
adequate oxygenation has been restored, an airway exchange catheter is positioned using it, over which a
flexometallic ETT is threaded to distal trachea or one of the principal bronchi.
Role of Femoro-femoral CPB

There are insufficient data in the literature to permit prediction of which patient will develop near or total airway
obstruction. Goh MH et al recommend cannulation of femoral vessels under local anesthesia in patients with more
than 50% reduction of cross-sectional area of trachea before induction of anesthesia. Institution of femoro-femoral
CPB is a possibility for some adult patients who are considered unsafe at stratification. The concept of CPB
standby during attempted induction of anesthesia is fraught with danger of hypoxic cerebral injury because of the
time taken to establish CPB.
Options in unsafe patients

Biopsy of the mediastinal mass (CT guided) or another node (e.g., supraclavicular) under local anesthesia
Preoperative radiotherapy to shrink the mass with a nonirradiated window for subsequent biopsy
Preoperative chemotherapy or short-course corticosteroids
Airway compromise in children with mediastinal mass

Life-threatening respiratory complications under GA were mostly reported in the pediatric population. The predictors
in this age group are given in table 3.
Table 3: Predictors of Airway compromise in children with mediastinal mass
Anterior location
Histologic diagnosis of lymphoma
Superior vena cava syndrome
Radiologic evidence of major vessel compression or displacement
Pericardial or pleural effusion
Summary and Conclusion
Adult with anterior mediastinal mass seem less at risk of perioperative complications than children. Patients at high risk
of complications can be identified by the presence of significant cardiorespiratory symptoms and signs and tracheal
compression of > 50% or pericardial effusion. Tissue biopsy should preferably be done under local anesthesia. When
GA has to be used maintenance of spontaneous respiration would maintain airway patency. If life-threatening airway
collapse occurs, it is best managed with rigid bronchoscopy. A small subset of high risk patient may benefit from early
institution of femoro-femoral CPB.
REFERENCES
1. Shamberger RC, Holzman RS, Griscom NT, Tarbell NJ, Weinstein HJ: CT quantitation of tracheal cross-sectional
area as a guide to the surgical and anesthetic management of children with anterior mediastinal masses. J Pediatr
Surg1991; 26:13842
2. Shamberger RC, Holzman RS, Griscom NT, Tarbell NJ, Weinstein HJ, WohlME: Prospective evaluation by
computed tomography and pulmonary function tests of children with mediastinal masses. Surgery 1995;
118:46871
3. Bchard P, Ltourneau L, Lacasse Y, et al: Perioperative cardiorespiratory complications in adults with mediastinal
mass, incidence and risk factors Anesthesiology 2004; 100:82634
4. Goh MH, Liu XY, Goh YS: Anterior mediastinal masses: an anesthetic challenge. Anaesthesia 1999;54:670-682
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5. Millers Anesthesia 7 ed, Chapter 59

6. Neuman GG, Weingarten AE, Abramowitz RM et al: The anesthetic management of the patient with an anterior
mediastinal mass. Anesthesiology 1984;60:144-147
7. Levin H, Bursztein S, Heifetz M: Cardiac arrest in a child with an anterior mediastinal mass. Anesth Analg 1985;
64:112930
8. Benumof JL: Anesthesia for Thoracic Surgery, 2nd edition. Philadelphia,
Saunders, 1995, pp 570
9. Azizkhan RG, Dudgeon DL, Buck JR, Colombani PM, Yaster M, Nichols D, Civin C,
Kramer SS, Haller JA: Life-threatening airway obstruction as a complication to the
management of mediastinal masses in children. J Pediatr Surg 1985; 20:81622
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Anaesthesia for robotic cardiac surgery
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Dr Yatin Mehta
MD, MNAMS, FRCA, FAMS, FICCM,FIACTA
Chairman, Medanta Institute Of Critical Care & Anesthesiology
Medanta- The Medicity, Delhi NCR, India
DheerajArora,
DNB MNAMS PDCC PGHM
Senior Consultant, Medanta Institute of Critical Care and Anaesthesiology
Medanta the Medicity, Sector 38, Gurgaon, Haryana
The image of cardiac surgery has been changed with evolution of computerized telemicromanipulator so called Robot, which is the resulting transformation of the minimally
invasive surgical evolution. Robotic devices allow unprecedented control and precision
of surgical instruments in minimally invasive procedures. The anticipated benefits
of robotic surgery to the patient include less pain and trauma, shorter hospital stays,
quicker recovery, and a better cosmetic result. With these technologic innovations, new
anaesthetic implications for patient care are being discovered. As surgery evolves into the
robotic era, anaesthesiologists must keep abreast of these changes and their impact on
patient care and safety.
History
The first group of robots consisted of assisting tool that were used for holding and
positioning the endoscope during surgery. The second group of robots comprises
telemanipulators that were originally invented to facilitate working under remote or
hazardous conditions, such as nuclear plants. Telemanipulators are under the constant
control of an operator who works at a console using commands or motions to direct the
manipulators. The operator (surgeons) and the manipulator (robot) can be connected
mechanically or electronically by a control panel. There is motion dawn scaling of 4:1
to 10:1. the 4:1 motion dawn scaling means when surgeon`s hand move 4 cm robotic
arm will move only 1 cm. similarly 10:1 ration means when surgeon`s hand move 10
cm robotic hand will move only 1 cm. the use of robotic devices also reduces tremors
of surgeon hand. These Tremor filtering and motion dawn scaling support dexterous
manipulations in confined spaces by ports or trocars and we can work in a miniature
area. Two telemanipulation systems that are currently in use for cardiac surgery are the da
Vinci Robotic System (Intuitive Surgical Inc, Mountain View, CA) and the ZEUS Robotic
System (Computer Motion Inc, Goleta, CA).
The advantage of the da Vinci system include integrated three-dimensional visualization
and a robotic wrist at the end of the instruments that provide articulated motions with
7 of freedom (DOF) of movement inside the chest cavity. The ZEUS system lacks an
articulated wrist allowing only 4-5 DOF inside the chest cavity. Internal mammary artery
harvesting was successfully performed thoracoscopically in 1997 by Nataf . In 1998,
Loulmet and colleagues reported the first totally endoscopic coronary artery bypass
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surgery. In 1998, Carpentier et al and Falk et al independently reported the first mitral valve repair using the da Vinci
robotic system through a 4-7 cm minithoracotomy using separate ports for surgical instrumentation.
Laborde et al published the first series of total endoscopic patent ductusarteriosus (PDA) closure using the ZEUS
robotic system achieving not only better cosmetic results, but also reducing pain in the postoperative period. Dogan
et al were the first to report a successful case of totally endoscopic ASD closure using the da Vinci system. Now a
cardiothoracic application of robotically assisted surgery have expanded and includes atrial septal defect closures,
mitral valve repairs, patent ductusarteriosus ligations, and totally endoscopic coronary artery bypass grafting.
The da Vinci telemanipulation system is used in our institute. It consists of a master console for remote control of
the microinstruments, surgical cart for monitor and CO2 insufflation unit and robot withit`s four arms. The middle
arm carries a stereo endoscope. It takes images of surgical field and transfers it to console and to the monitor. The left
and right arm serves as endothoracic end effectors for remote tissue manipulation using microinstruments resembling
the human wrist. Fourth arm is used to stabilize tissue structure. An additional video cart carries the light source, a
carbon dioxide insufflator, an image processor, and a conventional 2-dimensional screen. A surgical assistant places
the ports. The surgeon is seated at the master console and controls the endoscopic instruments, as well as the camera
mounted on the slave unit. The image from the stereo endoscope is transferred to the master console, magnified (10
x) and projected as a 3-dimensional image for optimal visualization of the surgical field.
Limitations
There are few restriction set by the use of robotic device. it`s arms are large and there are chances of collision
among it`s arm with patient, OT personals, and surrounding OT equipments. Its large size also invade anaesthetic
working place and make access to the patient difficult. The detection of endotracheal tube and its dislodgment or
cardiopulmonary resuscitation becomes difficult. Moreover repositioning of the patient after arm placement is very
difficult so proper positioning in the first instance is essential. Any movement of patient or OT table with the arm in
situ may cause serious harm to the patient.
Robotic assisted cardiac surgical procedures

Atrial septal defect

Mitral valve repair
Aortic valve repair or replacement
Internal mammary artery harvesting
Ablation of atrial fibrillation
Intra cardiac tumour resection
Pleura pericardial window
Ligation of PDA
Trans atrial repair of Fallot`s tetralogy
Epicardial lead placement of cardiac synchronization
Facilitated adhesiolysis for reoperative cardiac surgery
Robotic assisted surgical procedures

Urology- Radical prostatectomy, Pyeloplasty, Radical cystectomy, Cyst decortication
Thoracic surgery- Lobectomy, Thymectomy
Gynecology-Hysterectomy, Prolapse repair, Tubal reversals, Fistula repair, Myomectomy
General- Gastric bypass, Cholecystectomy
Robotic surgery- Contraindication

Contraindication for one lung ventilation (Corpulmonale, COPD, TB, asthma)
Severe PAH
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Dense pleural adhesion (TB, pleural infection)

Recent myocardial infarction, unstable CAD
Emergency surgery
Small calcified or intramyocardial vessel
Left superior vena cava (for atrial septal defect closure)
Sever atherosclerosis precluding peripheral and endovascular cannulation
Robotic surgery- problems

Video system dysfunction

Patient robot conflicts
Emergency conversion to thoracotomy or sternotomy
Emergency cardiopulmonary resuscitation with robot arms in situ
Vascular injury and dissection from endoaortic cannula
Incomplete de-airing
Protamine reaction in closed chest
Anaesthetic management
The anaesthesiologist should have good knowledge of cardiac and thoracic anaesthesia, TEE and should be able to
manage non sternotomy CPB. While making anaesthetic plan one must keep in mind primary cardiac disease of the
patient, restriction set by robot, implication of OLV in cardiac disease patient, prolonged percutaneous CPB and
management of many complication which may arise.
Proper patient selection is important for optimal result. The robotic surgery involves multiple small incisions that
extend over several dermatomal segments, induced peumothorax, prolonged OLV, postoperative pain management.
Adequate patient size to allow insertion of robotic instruments with adequate movements of robotic arm is important.
The ability of patient to tolerate OLV should be tested prior to actual commencement of the surgery. Airways and
chest anatomy should be suitable for insertion of a double lumen tube to facilitate OLV. A patient with difficult
intubation, major scoliosis, or emphysematous chest may be identified in the postoperative clinic as unsuitable for this
type of surgery. Patients with severe chronic obstructive pulmonary disease or asthma will also be poor candidates
for prolonged OLV. CPB may be needed in these patients if OLV is not tolerated. Condition such as chronic renal
failure, hepatic failure, coagulopathy or previous neurological events as stroke which may not allow prolonged CPB
should be screened for. All patients are evaluated preoperatively by TEE to exclude the possibility of persistent
left SVC or patent foramen ovale. The iliac and femoral arteries should also be evaluated for their size by Doppler
ultrasonography.
The proper position of patient is the key to comfortably perform robotic cardiac surgery. Proper position allows
robotic arm movements without obstruction and allows easy initiation of percutaneous CPB if needed for the
procedure. Patients are draped with the thorax, abdomen, both groins, and one lower limb exposed for surgical
access. This leaves only the right arm for arterial pressure monitoring and intravenous access. Access to the patient
chest and airways is nearly impossible after putting of robotic arm into position, so precautions should be taken to
confirm position of DLT with the help of fibreoptic bronchoscope.
In most of cases patient position is supine. Arm is hanged over the edge of the table with the help of a sling to allow
proper space for port placement. If arms are not carefully positioned, brachial plexus injury may result. Additional
care should be taken to avoid neurological injury. Pads are put below chest to elevate this hemithorax by 25-30 to
allow port placement in triangular fashion. The thoracic landmarks such as jugulum, xiphoid and ribs are marked for
external orientation and port placement. External defibrillation pads and ECG stickers should be placed away from
port placement. Patient should be painted and draped for emergency sternotomy if required.
OLV is required for the procedure. The ipsilateral lung is collapsed to facilitate access and to avoid movements
induced by respiratory excursions. Active peumothorax is induced with CO2 insufflations to facilitate surgery but
it may causes respiratory embarrassment, ventilation perfusion mismatch, increase in the shunt flow, large alveolar
arterial oxygen gradient and low oxygen tension and increase in closing volume. The airway is narrowed with use of
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DLT, which result in distension of alveoli which further compress adjacent ducts and other alveoli. Few alveoli are
over inflated and damaged due to high inspiratory pressure resulting in alveolar oedema. Capnothorax worsen the
respiratory dysfunction. It also causes obstruction to other systems, decrease venous return resulting in hemodynamic
instability. Rise in intrathoracic pressure result in reduced cardiac output, increase in CVP, mean PAP, PCWP, and
decrease in mixed venous saturation. There is moderate rise in arterial CO2 tension during OLV and marked rise in
PaCO2 during CO2 insufflation which is a cause of concern as it can cause coronary vasoconstriction. Exaggerated
response is seen in chronic smoker, obese, and patient with CHF. Maintaining insufflation with CO2 at 2-3 liters per
min and avoiding intrapleural pressure above 10 mm of Hg reduces chances of cardiopulmonary compromise. After
deflation of one lung the camera is placed bluntly to avoid left ventricular injury. Usually fifth intercostal space close
to the anterior axillary line is identified and the chest is insufflated with warm CO2. After insertion of endoscope
two ports are placed under visual control to accommodate the two robot arms usually in third and seventh intercostal
space. Any bleeding point is cauterized with means of low energy cautery.
Preparation

Betabloker , calcium channel blocker, nitrate should be continued
ACE inhibitor omitted to avoid unexpected hypotension during intra-operative period
Antiplatelet drug should be stopped 5-7 days before surgery
Smoking should be stopped, bronchodilators and incentive spirometry used to enhance lung function and as
a part of patient training for respiratory exercise.
Premedication
Anxiolytic: Benzodiazepine to allay anxiety of the patient
Monitoring
ECG, ETCO2, SPO2, CVP, BIS, nasopharyngeal temp, urine output, PAC, TEE, right and left radial artery pressure.
Monitoring of the right radial artery pressure tracing is imperative when using an endovascular balloon-occlusion.
The proximal dislodgement of the endovascular device can be detected with dampening of redial artery trace.
Induction and maintenance of anaesthesia- Standard drugs should be used forinduction and maintenance.
Appropriate sized DLT in used for one lung ventilation, it`s position is ascertained by a fibreoptic bronchoscope.
The correct position of this tube should be again checked after making the position of patient on the table. Since the
access to the patient is difficult due to large robotic arms, so once surgery is started it is very difficult to reposition
DLT. A TEE probe is placed in all patients after intubation. External defibrillation patches are applied in all the cases.
Any movement of the patient or table with robotic arm inside chest may cause injury to the internal parts of the
patient. Care should be taken to avoid movement of table. Hemodynamic disturbances due to raised intrathoracic
pressure are countered by intravenous fluid and inotropic/vasopressor. There is chance of hypothermia due to
prolonged surgery, use of cold intravenous saline, respiratory gases, and CO2 insuflation. Adequate measures should
be taken to avoid hypothermia.
CPB management
Arterial access: femoral arterial cannulation, 15-19 Fr
Venous access: Venous cannula is longer. Trans-femoral cannula cannot empty the ventricle completely so it may
require additional cannulation of superior vena cava via IJV.
TEE is helpful for placement of guide wire and cannula, positioning of SVC and IVCcannulae. 100unit/Kg heparin
is given before CS manipulation to prevent thrombosis. When cardiopulmonary bypass is anticipated, the left femoral
artery is cannulated with a 17- or 21-Fr Remote Access Perfusion (RAP) catheter with an aortic occlusion balloon.
This catheter allows anterograde flow of 4 or 5 L/min, respectively. The cannula has a separate lumen for delivering
cardioplegia to the aortic root beyond the occlusion of the balloon. The aortic cannula is positioned in the ascending
aorta, 2 cm above the aortic valve, with TEE guidance. The endovascular balloon is inflated with a volume equal to the
diameter of the sinotubular junction of the aorta. A balloon pressure above 300 mm Hg usually provides complete
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occlusion of the aorta. Residual flow around the balloon can be seen and monitored with colour flow on TEE. The
use of bilateral radial artery lines is useful in detecting the migration of the occlusion balloon toward the innominate
artery. Proximal migration of the balloon can most easily be seen with TEE, preventing balloon herniation through
the aortic valve. After full cannulation and being poised for cardiopulmonary bypass, the right lung is allowed to
collapse, and left lung ventilation is begun. The ventilator is adjusted to provide an end-tidal carbon dioxide pressure
of 35 to 40 mm Hg. Ports can be safely placed after the right-sided pneumothorax has formed. Carbon dioxide is
insufflated into the right hemithorax and continued at a pressure of 5 to 10 mm Hg. This allows the affected lung
to collapse further and provides a larger visual field.
Endoaortic balloon is inflated at 250-300 mm Hg pressure after TEE guided position is checked, to produce an internal
cross clamp. Decompression of the heart may be aided by the PA catheter vent. Cardioplegia can be administered
antegrade through a distal port in the endovascular aortic canula. Cardioplegia can be given retrograde through CS
canulla. We can also perform transthoracic clamping with a soft clamp which can be placed through transthoracic
approach on the aorta
Dearing and weaning: We cannot directly access heart. Moreover due to slight lateral tilt of the table, air tends
to retain along dorsal interventricular septum and right pulmonary veins. So dearing of heart is difficult in robotic
cardiac surgery. Hand ventilation is used to displace air from the pulmonary vein. Weaning from CPB is done similar
to standard practice as with conventional CPB. Protamine is given slowly to prevent any hemodynamic instability.
After the procedure DLT is changed with single lumen tube.
Robotic assisted thoracic surgery (RATS)

Nowadays RATS is becoming increasingly popular technique particularly lobectomy or thymectomy or procedures
related to pleural cavity. Main anaesthetic concerns are patient positioning, lung isolation, OLV, monitoring
of hemodynamic & ventilatory parameters. Hemodynamic compromise involves decreased venous return and
acutecardiovascular collapse. Internal retractors may compress cardiac or major vascular structures that may lead to
hemodynamic instability.
CO2 insufflation pressure should be 8-10mmHg at a slower rate of 1l/min. Insufflation of CO2 in the chest
increases airway pressure. Venous return and compliance of the heart decreases and may results in hypotension and
hemodynamic instability.
Proper positioning of the patient is also important. Commonly used position is incomplete lateral decubitus position
(30 side up) and another is supine position with slight support with back and ipsilateral upper limb is abducted,
extended and externally rotated. There may be possibility of neurovascular compression / nerve injury of the
ipsilateral side
Main concerns are sharing of airway, OLV, elderly patients with co morbid states and need for post op ICU stay
& ventilation. Pulmonary function testing should be done and patients should be reported high risk if FVC<50%,
FEV1 <2L, FEV1/FVC <50%, diffusing capacity <50% predicted and PaCO2 >45 mmHg. Postoperatively analgesia
should be with intrapleuralpleural catheter, need for post op ventilation. Chest tube drainage & suction should be
checked in the postoperative area on a regular basis.
Conclusion
Robotic system is an important tool for minimally invasive cardiac surgery. It may eventually make surgical sternotomy
obsolete; however surgeons must still be trained and prepared to convert to an open sternotomy if the need arises.
The anaesthesiologist is also confronted with a multitude of situations requiring multiple management skills. The
anaesthesiologist should be versed in cardiac and thoracic anaesthesia and must possess the skills required for TEE
and nonsternotomy CPB.
Nowadays, role of robotic system in thoracic surgery is emerging with encouraging results. RATS is commonly used
thymectomy, lobectomy and procedures relate to pleural cavity.
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(www.theiaforum.org) 2003(2)
2. Trehan N, Mishar YK, Sharma M, Bazaz S, Mehta Y, Sharma KK, Shrivastava S. Robotically controlled video
assisted port access mitral valve surgery. Asian CardiovascThorac Ann 2002; 10: 133-136
3. Mishra YK, Wasir HS, Sharma M, Mehta Y, Trehan N. Robotically enhanced coronary artery bypass surgery.
Indian Heart J 2004; 56:622-627
4. Mehta Y, Arora D, Sharma KK, Mishra Y, Wasir H, Trehan N. Comparison of continuos thoracic epidural
and paravertebral block for postoperative analgesia alter robotic-assisted coronary artery bypass surgery.
Annals of Cardiac Anaesthesia 11:2; 90-95, 2008
5. Chauhan S, Subin S. Anesthesia for robotic cardiac surgery: An amalgam of technology and skill. Ann Card
Anaesth 2010;13:169-75
6. Boehm DH, Reichenspurner H, Gulbins H et al. Early experience with robotic technology for coronary
artery surgery. Ann ThoracSurg, 68:1542-1546, 1999 .
7. Czibik G, DAncona G, Donais H, et al. Robotic cardiac surgery: present and future applications. J CardiothoracVascAnesth 16:502-507,2002.
8. Carpentier A, Loulmet D, Aupecle B, et al. Computer assisted cardiac surgery. Lancet 353:379-380, 1999
9. Falk V, Walther T, Autschbach R, et al. Robot-assisted minimally invasive solo mitral valve operation. J ThoracCardiovascSurg 115:470-471, 1998.
10. Dogan S, Wimmer-Greinecker G, Andressen E, et al. Totally endoscopic coronary artery bypass (TECAB)
grafting and closure of an atrial septal defect using the da Vinci system. ThoracCardiovascSurg 48;21, 2000
(suppl 1)
11. Dogan S, Aybek T, Andreben E. Totally endoscopic coronary artery bypass grafting on cardiopulmonary
bypass with robotically enhanced telemanipulation: Report of forty five cases. J ThoracCardiovascSurg
123:1125-1131, 2002.
12. Byhalin C, Mierde S, Meinenger D, Wimmer-Greinecker G etal. Hemodynamics and gas exchange during
carbon dioxide insufflation for totally endoscopic coronary artery bypass grafting. Ann ThoracSurg 72:14961501;2001.
13. DAttellis N, Loulmet D, Carpentier A, et al. Robotic-assisted cardiac surgery: anesthetic and postoperative
considerations. J CardiothoracVascAnesth 16:397-400, 2002
14. Garg R et al. Brachial plexus inj in thymectomy JCVA, 2009,23,584-87
15. Jellish W S et al. Methods to reduce brachial plxinj, Anasth- Analg; 1997,84,260-65
16. Pandey et al. Robot assisted thymectomy: Perianaesthestic concerns. Eur. J. Anaesth, 2010,27(5), 473-7
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TIVA Vs Inhalational Anesthesia in Cardiac

Surgery
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Dr. Rahul Guhabiswas,

Consultant, Anesthesia and Intensive Care,
NH Rabindranath Tagore International Institute of Cardiac Sciences,
Kolkata.
Cardioprotective effects of inhalational anesthetics have been demonstrated in multiple
animal experiments and clinical studies 1. The possible reasons of cardio-protection has
been attributed to myocardial protection due to pharmacological cardiac preconditioning
and protection from myocardial reperfusion injury. However the effect of volatile
anesthetics on actual clinical outcomes in patients undergoing cardiac surgery still
remains unclear. Contrarian studies, showing non-superiority of volatile agents over Total
Intravenous Anesthesia (TIVA) based anesthetic management, are fewer but available on
review of literature 2. Additionally, a recent meta-analysis has shown that these these
cardioprotective effects are evident only in single center, low risk Coronary Artery Bypass
Grafting (CABG) patients 1. Evidence is also contradictory in valve replacement surgery
3
. Other limitations in studies on inhalational agents include small population size, lack
of power and risk of bias in randomized control trials included in various meta-analysis.4
Inadequacy of sample size is a major area of concern. For instance, in order to prove that
the cardioprotective effects of inhalational agents are capable of reducing major adverse
cardiac event by 50% (assuming a 2% incidence in current cardiac surgical practice with a
power of 0.8 and P value < 0.05), a total of 5030 patients will be necessary to accurately
answer the question.
Naturally, proof of true benefits of volatile anesthetics in improving clinical outcomes in
cardiac surgery via-a-vis TIVA await the conduct of a large multi-center trial. Recently this
intention has been achieved, in a multi-center, randomized , parallel group prospective
trial 1. The authors of this study found no superiority of volatiles over TIVA in a subset
of patients undergoing high risk cardiac surgery, a fact of life in contemporary clinical
practice. In fact, in this study, there was a five percent reduction in the composite outcome
of death during the first hospital stay and/or prolonged ICU stay in the propofol group,
although this did not reach statistical significance. Interestingly, an earlier study which
failed to find superiority of volatiles in myocardial protection had half of the patients
with moderate to severely impaired ventricular function, unstable angina, indication for
re-operation and recent myocardial infarction in the study sample.2 Here also, the time
to extubation was significantly shorter in the propofol group (P=0.006), other outcomes
being similar in the two groups. To sum up, the supposed benefits of volatile agents
disappear when the full spectrum of cardiac operations are brought into the picture.
A recent editorial has commented on the possible reason for this discrepancy in research
findings 5. The editors commented that one of the possibilities to consider in the previous
studies showing superiority of volatiles, is an erroneous false positive interpretation .
This phenomenon of a high incidence of false positive conclusion is not uncommon in
even the highest impact journals 6.
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There are other unresolved issues in trying to determine the efficacy of inhalational agents in cardioprotection.
We still do not know the optimal dose and timing needed for adequate perioperative organ protection. We need to
remember that phase IV trials for effective dosing of volatile agents were done solely for assessing their anesthetic
effect. Cardioprotective effects of volatiles were discovered much later and naturally standardized tests for effective
dose and timing of administration to achieve desired clinical outcomes are yet to be studied.
There are several limitations of using inhalational anesthetics in cardiac surgery. Unlike Total Intravenous Anesthesia,
Total Inhalational Anesthesia is not possible as the need for potent intravenous analgesics and neuromuscular
blockers still remain.
The monitoring of anesthetic depth by measuring anesthetic gas concentrations in the exhaust of the oxygenator
remains at least as contentious as Bispectral index monitoring during cardiopulmonary bypass. Thirdly, in the
postoperative period, patients have to be shifted to the cardiovascular intensive care unit under intravenous sedation
which inserts a potential bias to outcome studies comparing intravenous versus inhalational techniques.
References:
1. Landoni G et al. BJA 2014; 113 (6): 955-63.
2. Myles PS et al. Anesth Analg 1997; 84:12-9.
3. Cromheecke S et al. Anesth Analg 2006;103:289-296.
4. Landoni G et al. BJA 2013; 111 (6): 886-96.
5. Editorial. BJA 2015; 114 (1): 3-5.
6. Jager LR et al. Biostatistics 2014; 15: 112.
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PRO/CON - Liberal versus restrictive

strategy of blood transfusion (CON)
Dr SHREEDHAR S JOSHI
MD., DM
Consultant and Head

Department of Cardiac Anaesthesia
Nayati Multi-Superspeciality Healthcare Hospital and Research Centre
Mathura, UP.
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Circulation was discovered as early as 1600s, and the next two decades saw a sluggish
move towards the first human transfusion in 1800s. Cardiac surgical procedures consume
20% of all transfusion in the US. Only in the latter half of twentieth century were the
deleterious effects of transfusion studied and opened the era of restricting transfusions,
searching targets of transfusion and minimising blood exposure in perioperative period.
Cardiac surgery has seen a paradigm shift in literature from a dominant very restrictive
transfusion strategy in the early part of the century to a more liberal strategy over the
last few years.Most evidence in favour of restrictive transfusion came from retrospective
analysis of large cohorts (cumulative data of 30000 to 50000 patients).
Restrictive and liberal transfusion triggers have varied across studies. Most restrictive
triggers have haemoglobin of more than 7gms/dl as triggers and liberal trigger has been
haemoglobin more than 9gms/dl. Though not defined very well, these definitions are
more of consensus.
Van Straten in a study of 10,425 CABG patients observed that RBC transfusion was an
independent risk factor for early mortality. In another study of 3,024 CABG procedures,
Kuduvalli et al observed an increased 30-day and 1-year mortality in blood transfused
patients. Murphy et al found a significant negative impact of perioperative transfusions
even after exclusion of 1st year outcomes, suggesting the long term deleterious effects
persisted.
The age of transfused RBCs also generated interest, RBCs more than 2 weeks duration
having more deleterious effect than the fresh once. Tough most recent studies do not
substantiate this view. Most awaited are the results of the ongoing trial, the Red Cell
Storage Duration Study (RECESS) randomising patients exposure to RBCs <10 days
versus >21 days with primary outcome being change in Multiple Organ Dysfunction
Score by day 7.
Perioperative RBC transfusion have been independent risk factors for postoperative
Atrial Fibrillation (AF). There has been an increased rate of infections, sternal woundinfections, clostridium-difficile associated diarrhoea and bacteraemia in patents transfused
with RBCs during cardiac surgery. Higher risk-adjusted rates of postoperative respiratory
distress, respiratory failure, acute respiratory distress syndrome, and reintubation, and
longer times on the ventilator, have been demonstrated in patients undergoing transfusion.
Karkouti et al in 2011 observed that Acute Kidney Injury increased proportionately
with the number of RBC units transfused in 12,388 patients undergoing cardiac surgical
procedures. Similar observations were made by Koch et al in 11,963 CABG procedures.
A propensity matching of 322 Jeovah witness patients with 48986 non-jeovah witness
undergoing cardiac surgery at Cleveland Clinic also witnessed lower acute complications
including MI, prolonged ventilation, lesser re-operations and shorter length of hospital
stay in them.
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Liberal transfusion strategies have been compared with the conventional restrictive transfusion strategies in cardiac
surgical practice. Two prominent RCTs have been conducted in last few years throwing more light. Both TRACS
(Transfusion requirements After Cardiac Surgery) and TITRe2 (Transfusion Indication Threshold Reduction study)
trials have looked for non-inferiority of liberal transfusion versus restrictive strategy in cardiac surgical patients
been randomised to Liberal (hb>9) and restrictive (Hb>7) strategy limbs. TRACS trial randomised 502 patients
undergoing cardiac procedures with CPB, with comparable primary outcomes of 30-day mortality and in-hospital
major morbidity between the two strategies. Restrictive group had 60% reductions in RBCs transfused and also RBC
transfusion was found to be an independent risk factor for mortality. For every unit of RBC transfused, the risk of
occurrence increased for cardiac complications (OR 1.27), renal complications (OR 1.26), infectious complications
(OR 1.2), and 30-day mortality (OR 1.25).
TITRe2 trial by Murphy et al is the latest multi-centre trial which randomised patients undergoing cardiac surgery into
liberal (Hb<9gm/dl) and restrictive (Hb<7gm/dl) transfusion strategies. Restrictive transfusion strategy was found
not superior to liberal strategy with respect to morbidity or health-care costs. Close to 50% of consentedpatients
were not randomised raising concerns of bias.Significantly high proportions of patients with severe non-adherence
and lower proportion with any nonadherence in the restrictive limb may have confounded the results. There was
a very high rate of blood and product use before randomisation, high transfusion rates after randomisation (63%
in restrictive and 94% in liberal) and the mean difference in haemoglobin nadir being 1gm/dl. These factors may
suggest a huge similarity among the groups and hence making the comparison questionable.Indicators of adequacy
of oxygen delivery to tissues (ScVO2) were not monitored for and neither plausible explanations for the differences
in outcomes discussed.
Also the above mentioned studies fail to consider the usual course of haemoglobin drift that occurs after a cardiac
surgery. A usual trend is represented by a gradual fall in haemoglobin in postoperative period with a nadir fall by third
to fourth day (average fall of 2-3gms/dl as compared to preopHb level) and return to 7080% of baseline by 7-10
days. Most transfusions made in TRACS trial were on third and fourth post-operative days.
Borde et al studied the impact of anaemia and transfusion on all-cause in-hospital mortality in Rheumatic heart
disease undergoing cardiac surgery. Transfused patients had an odds ratio of 2.28 towards the composite end point.
They also observed a significantly low Hb in the first three post-operative days in the transfused patients, probablya
suggesting that RBC transfusion is not the only modality to deal with preoperative anaemia. They also further reemphasize the additional impact anaemia and transfusion have in a worse perioperative outcome.
The rationale for implementing a restrictive transfusion strategy is based on such many studies (30000-40000
retrospective analysed cohorts and a few thousand prospective analysed patients) that have shown a lack of benefit
and, at the same time, substantially increased costs and adverse effects associated with RBC transfusion. These
findings also suggest that the primary strategy in patients undergoing cardiac surgery should be to avoid giving RBC
transfusion solely to correct low haemoglobin levels.
Till more robust RCT consider the comparison of different strategies of RBC transfusion after cardiac surgery,
the current practices considering clinical and bio-chemical markers of oxygen delivery to tissues and avoiding unwarranted can be continued.
REFERENCES
1. Murphy GJ, Pike K, Rogers CA et al.TITRe2 Investigators.Liberal or restrictive transfusion after cardiac
surgery.N Engl J Med.2015 Mar 12;372(11):997-1008.
2. Hajjar LA1,Vincent JL,Galas FR et al. Transfusion requirements after cardiac surgery: theTRACSrandomized
controlledtrial.JAMA.2010 Oct 13;304(14):1559-67.
3. Arman K, G.J.R. Whitman et al. Blood Transfusions in Cardiac Surgery:Indications, Risks, and Conservation
Strategies. Ann ThoracSurg2014;97:72634
4. George TJ, Beaty CA, Kilic A, et al. Hemoglobin drift aftercardiac surgery. Ann ThoracSurg2012;94:7039.
5. van Straten AH, Bekker MW, Soliman Hamad MA, et al.Transfusion of red blood cells: the impact on short-term
andlong-term survival after coronary artery bypass grafting, aten-year follow-up. Interact CardiovascThoracSurg
2010;10:3742.
6. Karkouti K, Wijeysundera DN, Yau TM, et al. Influence oferythrocyte transfusion on the risk of acute kidney
injuryafter cardiac surgery differs in anemic and nonanemicpatients. Anesthesiology2011;115:52330.
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Low Tidal Volume Ventillation in ARD

Dr Jacob Abraham
Chief Cardiac Anaesthesiolgist
Lisie Heart Institute,Kochi
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Mechanical ventilation is a cornerstone in the management of patients with acute

respiratory distress syndrome(ARDS).Mechanical ventilation per se can aggravate
lung injry,a process referred to as ventilator induced lung injury(VILI),through several
mechanisms including volutrauma,barotrauma and biotrauma.Dynamic lung distension
and repeated opening and closing of recruitable lung units are considered the two main
mechanisms contributing to lung injury.The lung protective ventilation strategy using
low tidal volume and limiting plateau pressure has been proven to improve survival in
patients with ARDS.Currentresearch suggests that further reducing ventilator associated
or induced lung injury is the main avenue to further reduce mortality in this syndrome.
Identification of patients at risk of developing ARDS and implementation of preventive
strategies is an important approach for critically ill patients admitted to ICUs particularly
patients receiving mechanical ventilation. ARDS is not frequently present at the time of
admission and it frequently occurs over hours to days following the clinical insult. Many
clinical factors are associated with the development of ARDS such as sepsis, shock,
pneumonia, pancreatitis, aspiration, high risk trauma and surgery and multiple blood
transfusions. Mant studies demonstrated that inadequate antimicrobial therapy, medical
and surgical adverse events, hospital acquired aspiration,ventilation with high tidal
volumes and multiple blood transfution were significantly associated with the secondary
development of ARDS.
A lung protective ventilation strategy using low tidal volume and limiting Pplat is
now proposed in patients with ARDS. Potentially injurious ventillatory settings might
also be associated with secondary development of ARDS in mechanically ventilated
patients without ARDS at the onset. Observational studies demonstrated that high tidal
volume and Pplat are the major risk factors for the secondary development of ARDS.
Thus lung protective ventilation strategy may also prevent lung injury in mechanically
ventilated patients without ARDS.A randomized controlled study comparing low versus
conventional tidal volumes(6 versus 10 mL.kg-1 predicted body weight(PBW) in critically
ill patients without acute lung injury at the onset of mechanical ventilation found that
the level of systemic inflammatory cytokines decreased significantly in the low tidal
volume group and development of lung injury was higher in the conventional tidal
volume group. A recent meta analyses suggested that using lower tidal volumes(<6 versus
>10ml/kgPBW)in patients without ARDS was associated with better clinical outcomes,
including development of ARDS, mortality and duration of mechanical ventilation.
Application of appropriate PEEP level may be needed in patients requiring mechanical
ventilation in whom it is expected to be required for >48hrs.
How to Use Low Tidal Volume Ventilation in ARDS

The protocol from the ARMA trial can serve as a guideto performing low tidal volume ventilation for mechanically ventilated patients with ARDS:

Start in any ventilator mode with initialtidal volumes of 8 mL/kg predictedbody weight in kg, calculated by:[2.3 *(height ininches - 60) + 45.5 for
women or + 50 for men].
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Set the respiratory rate up to 35 breaths/minto deliver theexpected minute ventilation requirement
(generally,7-9 L /min)
Set positive end-expiratory pressure (PEEP) to at least 5 cm H2O (but much higher is probably better),
and FiO2to maintain an arterial oxygen saturation (SaO2) of 88-95% (paO2 55-80 mm Hg). Titrate
FiO2 to below 70%when feasible (though ARDSNet does not specify this).
Over a period of less than 4 hours, reduce tidal volumes to 7 mL/kg, and then to 6 mL/kg.
Ventilator adjustments are then made with the primary goal of keeping plateau pressure (measured during an
inspiratory hold of 0.5 sec) less than 30 cm H2O, and preferably as low as possible, while keeping blood gas parameters
compatible with life. High plateau pressures vastly elevate the risk for harmful alveolar distension (a.k.a. ventilatorassociated lung injury, volutrauma).If plateau pressures remain elevated after following the above protocol, further
strategies should be tried:
Further reduce tidal volume, to as low as 4 mL/kg by 1 mL/kg stepwise increments.
Sedate the patient (heavily, if necessary) to minimize ventilator-patient dyssynchrony.
Considerother mechanismsfor the increased plateau pressure besidesthe stiff, noncompliant lungs of ARDS.
As a last resort, neuromuscular blockade can be employed to reduce plateau pressure by eliminating patient effort,
muscle tone and dyssynchrony. However, this approach has unquantified risks of long-term neuromuscular weakness
and disability.
Permissive Hypercapnia in ARDS

Achieving these low plateau pressuresusually requirestidal volumes low enough to result inhypoventilation,with
resulting elevations in pCO2 and respiratory acidemia that can be severe and to the treating physician, anxietyprovoking. This approach, permissive hypercapnia, represents a paradigm shift from previous eras, in which
achieving normal blood gas values was the main goal of mechanical ventilation.
How permissive can one be?Mechanically ventilated patients with ARDSappear to tolerate very low blood pH and
very high pCO2s without any adverse sequelae (defying physicians anxietiesbased onintuition, training and medical
lore):

Current consensus suggests it is safe to allow pH to fall to at least 7.20.
The actual pCO2 is of little importance.
When pH falls below 7.20, many physicians choose to administer sodium bicarbonate, Carbicarb, or
THAM to maintain blood pH between 7.15 - 7.20.
However, it is unknown whether such correction of acidemia is helpful, harmful, or neither (good evidence
is lacking for any of these hypotheses).
Conditions in which permissive hypercapnia for ARDS could theoretically be harmful include cerebral edema, mass
lesions or seizures; active coronary artery disease; arrhythmias; hypovolemia; GI bleeding, and possibly others. These
are hypothetical harms based on pathophysiology and not outcomes data, while the harm of ventilator induced
lung injury and the benefits of a protective ventilator strategy in ARDS are real and known. The potential risks of
hypercapnia in such patients must be weighed against the risks of ARDS, and therapy individualized.
Major advances have been made in our understanding of the pathophysiological abnormalities present at different
stages of ARDS.We have evidence for the benefits of using low tidal volume and high PEEP but also understand that
it needs to be basd on a individual response.
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ANAESTHESIA FOR ENDOVASCULAR AORTIC

ANEURYSM REPAIR (EVAR)
ANAESTHESIA TUTORIAL OF THE WEEK 303
27TH JANUARY 2014

Dr Gagan Atwal, Dr Sandi Wylie
Royal Free University Hospital, UK
Correspondence to gaganatwal@hotmail.com

QUESTIONS
Before continuing, try to answer the following questions. The answers can be found in the body of the
text.
1.
Answer True or False:

a. EVAR is a low risk procedure as it is minimally invasive
b. EVAR carries a lower operative risk than an open AAA repair
c. EVAR is advocated for older, less fit patients and open repairs for younger patients
d. EVAR is associated with fewer long term complications and re-interventions than
open AAA repair
2.

a. Surgery is considered when the AAA is greater than 5.5cm in diameter
b. EVAR requires yearly radiological surveillance of the graft
c. Significant blood loss can occur with EVAR
d. Emergency EVAR should never be done under LA
3.

a. An increasing size of AAA is associated with an increased risk of rupture
b. There is a greater risk of spinal cord ischaemia with infra-renal EVARs compared to
supra-renal EVARs
c. Neuraxial block is contra-indicated due to the use of heparin intra-operatively
d. There is a 10% conversion rate to an open procedure
4.
The risk of renal impairment is increased with:

a. The use of carbon dioxide contrast
b. Increasing number of graft fenestrations
c. The use of sodium bicarbonate solution
d. Supra-renal EVAR compared to infra-renal EVAR

INTRODUCTION

Endovascular Aortic Aneursym Repair (EVAR) is increasingly being used for repair of Abodminal
Aortic Aneurysms (AAA). It is the most common method of treatment for AAA in the USA (>70%
elective AAA repairs) (1). As technology improves and surgeons and interventional radiologists are
becoming more experienced, endovascular repair is being increasingly used for more complex juxtarenal and supra-renal AAA repairs, AAA ruptures and for repair of thoracic aneurysm and dissections.
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This work is licensed under the Creative Commons Attribution-NonCommercial 3.0 Unported License. To view a copy of this license, visit
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IACTACON 2016
ABDOMINAL AORTIC ANEURYSMS

The normal diameter of the aorta is 2cm and it is considered to be aneurysmal when it reaches 3cm in
diameter. The prevalence of AAA in the UK is approximately 4% in males aged 65-74. Risk factors
include age >60years, male gender (6 times more common than in females) and smoking (lifelong
smokers are at 4 times greater risk than non-smokers). Other risk factors include hypertension,
hypercholesterolaemia, family history and inherited connective tissue diseases such as Marfans or
Ehlers Danlos (type IV).
The risk of rupture increases with increasing size of the aneurysm:
Table 1. Annual risk of rupture with size of aneurysm
SIZE OF ANEURYSM
ANNUAL RISK OF RUPTURE
4 - 4.9 cm
0.5 - 5%
5 - 5.9 cm
3 - 15%
6 - 6.9 cm
10 - 20%
7 - 7.9cm
20 - 40%
With approximately 5% mortality rate following elective open AAA repair, elective surgery is usually
only considered in AAA greater than 5.5cm or if is rapidly growing (>5mm in 6 months) (Nice
guidelines EVAR 2009)
Surgical Procedure
Technique
A distinction should be made between anaesthesia and surgery for simple infra-renal aneurysm repairs
and that for more complex infra-renal, para-renal and suprarenal aneurysms.
Repair of a simple infra-renal AAA is a minimally invasive surgical technique which involves
catheterising the femoral or iliac arteries and passing one or more expandable grafts into the abdominal
aorta under fluoroscopic guidance. The stent is deployed across the aneurysm thus preventing blood
flow into the aneurysmal sac, which will eventually thrombose. Additional trouser grafts can be
inserted into the common iliac arteries, overlapping the main graft. Infra-renal aneurysms which have
an inadequate infra-renal neck to support the graft can be stabilised by using a stent graft which has a
bare metal portion (known as a crown of thorns) extending above the renal artery ostia. It has been
proven that these bare metal stents do not impede blood flow to the renal arteries.
Juxta-renal and supra-renal aneursyms can be treated with fenestrated grafts which have orifices for the
coeliac, superior mesenteric and renal arteries as required. Once in place, further covered stents can be
deployed via the orifices into the arteries. These fenestrated grafts are purpose-made, specific to the
patients anatomy which is determined by 3D reconstruction CT approximately 6 weeks prior to
surgery and therefore they can only be used in elective cases. For more expedient surgery, standard
chimney grafts can be inserted into the visceral or renal arteries and a main stent deployed over these
into the aorta.
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Figure 1. Stent graft with scallop for the superior mesenteric artery and fenestrations for the
renal arteries. Crown of thorns extending up from the graft.
In some cases it may be required to insert the stents from above and the surgeons will cannulate a
brachial or subclavian artery to achieve this. This possibility should be discussed with the surgeon
before deciding on the site for arterial line placement.
The use of more complex grafts and an increasing number of fenestrations increases the skill required
from the operator, and can increase the procedural time significantly. The fluoroscopy time and hence
the dose of iodinated contrast used is also likely to be higher, increasing the risk of renal impairment.
The use of carbon dioxide as a contrast agent is possible in patients with high risk of renal impairment
however it carries the risk of localised accumulation and significant gas embolism. It also results in
poorer images and requires a higher radiation dose per image so is not used routinely.
Figure 2. 3D CT reconstruction of complex EVAR graft

Blood Loss
Blood loss during a simple infra-renal EVAR is usually minimal approximately 200ml, and
intraoperative transfusion is rare. Prolonged procedures will have on-going blood loss from the access
vessels and complex EVARs can result in significant blood loss. Use of cell salvage is prudent in
complex EVARs and consideration should be given to the use of a rapid infusion device in high risk
cases. With all EVARs there should be a high index of suspicion for occult blood loss from damage to
the aorta, iliac, femoral or other access arteries and there should be a low threshold to carry out an
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angiographic assessment to identify any bleeding point. The highest risk period for acute rupture of the
aneurysm is during stent deployment.
Risk of conversion to an open procedure is 2% per annum, with female patients and patients with a
small body habitus having a higher incidence of abandoned procedures.
EVAR vs Open surgery
Potential benefits of EVAR over the conventional open surgical procedure are: less physiological
disturbance, reduced blood loss, less pain, reduced length of ICU and hospital stay. For infra-renal
aneurysms additional benefits include reduced procedural time and avoidance of general anaesthesia.
Disadvantages of EVAR include potential conversion to GA in a patient deemed unfit for GA,
increased long-term complications such as endoleak and graft migration and the requirement of
lifelong yearly surveillance by CT scan or duplex ultrasound.
Two UK multicentre studies looked at outcomes between open and endovascular AAA repair from
1999 to 2003.
The EVAR 1 study showed that EVAR reduces the operative mortality (30 day mortality) compared to
open surgery by a third and medium term aneurysm-related mortality, but offered no decrease in longterm all-cause mortality at 4 years. EVAR is also associated with increased re-interventions and
complications but has the same health related quality of life as open procedures.
The EVAR 2 study concluded there was no long-term survival benefit of EVAR versus surveillance in
patients deemed unfit for open repair and showed that there was considerable 30 day operative
mortality with EVAR in these patients (9% mortality). The study recommended focusing on increasing
patients physiological fitness. A number of patients in the surveillance group however, crossed over
into EVAR group so potentially skewing results. The most recent NICE guidelines state that there is
uncertain benefit of EVAR over surveillance in patients who are unfit for open repair.
Since these studies, increasingly complex aneurysms are being treated with EVAR and in patients who
would otherwise be deemed unfit for open surgery. Also, technological improvements in stent design
and operator experience have increased so studies and longer term follow-up is required to determine
the long-term risks and benefits of EVAR.
Suitability for EVAR

Location and Expertise
Evidence shows a reduced mortality from elective AAA repair in centres which carry out more than 32
cases per year. In recent years there has been a reconfiguration of vascular surgery services in the UK
to create fewer specialist centres with a greater concentration of resources and experience in the field.
The Vascular Society of Great Britain and Ireland state that all patients undergoing elective AAA
repair should be discussed by a multidisciplinary team consisting of vascular surgeons, interventional
radiologists and anaesthetist with an interest in vascular surgery. A joint decision should be made,
weighing up factors such as technical issues, physiological fitness and life expectancy of the patient,
short and long-term benefits and risks of the procedure and the patients wishes.
Technical Suitability
Suitability of the aneurysm for endovascular repair depends on its morphological features and is
formally assessed by 3D reconstruction CT. Features of the aneurysm assessed include: the proximal
neck (length, diameter, presence of thrombus, angle), Distal landing zone (length, diameter), the
calibre, tortuosity and presence of aneurysms or thrombus in the Iliac arteries and access vessels.
Preoperative assessment
Patients having EVAR should undergo the same thorough preoperative assessment and workup as for
an open procedure. The incidence of major cardiorespiratory disease, hypertension, diabetes and stroke
is increased in this group of patients. 70% of patients with AAA also have coronary artery disease. The
American College of Cardiology and American Heart Association (ACC/AHA)) joint guidelines are a
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useful tool for the evaluation and care of cardiac patients undergoing non-cardiac surgery. According
to the guidelines infra-renal EVAR is an intermediate risk procedure. Complex EVARs should be
considered high risk procedures.
In addition to standard tests of cardio-respiratory fitness, the Vascular Anaesthesia Society of Great
Britain and Ireland (VASGBI) recommend that an objective assessment of the patients functional
status should be made with cardiopulmonary exercise testing performed if it is available. Medication
should be reviewed and optimised all patients should be on low-dose aspirin and a statin unless there
are specific contraindications. Consideration should be made to stopping non-steroidal antiinflammatory drugs.
Particular attention should be paid to the preoperative renal function as these patients are at high risk
for acute kidney injury (AKI) postoperatively for a number of reasons including the use of IV contrast
and para-renal stents. Strategies for minimising renal impairment such as maintaining adequate
hydration, limiting contrast load and omitting nephrotoxic drugs should be considered and planned for.
Current guidelines by the UK Renal Association on prevention of contrast induced nephropathy
recommend that pre-procedural volume expansion with 0.9% sodium chloride or isotonic sodium
bicarbonate should be used in patients at risk. There is conflicting evidence of benefit of one solution
over the other. Meta-analyses have not shown compelling evidence for the use of N-Acetyl cysteine in
the prevention of contrast induced AKI.
In general, younger, fitter patients undergo open AAA repair as they are more likely to cope with the
physiological demands of open surgery and will avoid the longer-term complications and yearly
surveillance associated with EVAR. EVAR is usually advocated for older patients with more
significant co-morbidities who are deemed unfit for open repair as there is a reduced operative
mortality compared with an open procedure.
Objective functional assessment of cardiovascular fitness

should be made (eg. CPEX)
High risk of renal impairment:
- Stop nephrotoxic drugs
- Ensure adequate hydration
- Limit contrast dose
Intraoperative Management
Site and Setup
All EVARs should be carried out in a hybrid theatre with appropriate imaging facilities and the ability
to convert to an open procedure if required.
Some hybrid theatres are not within the main theatre complex, so attention must be paid to the issues of
remote-site anaesthesia. Protection from ionising radiation is important and additional mobile lead
shielding should be placed between the patient and theatre staff, and an adequate distance from the xray tube should be maintained. This can make access to the patient more difficult so all IV lines and
monitoring cables should be of sufficient length.
Monitoring
In addition to AAGBI minimum monitoring, an arterial line should be placed prior to induction of
anaesthesia on the contralateral side to any surgical upper limb access site. Large bore IV access
should be gained as there is potential for significant blood loss if converted to an open procedure.
Central venous access should be inserted in complex or lengthy procedures and cardiac output should
be monitored where appropriate. Temperature and hourly urine output should be monitored.
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General vs Regional Anaesthesia
The use of general anaesthesia or neuraxial block is acceptable for EVAR. Short, infra-renal
procedures have also been performed under local anaesthetic with sedation. Robust evidence of
mortality or morbidity benefit of one technique over another is lacking. Factors to consider when
making a decision include patient co-morbidities, use of antiplatelet or anticoagulant drugs, duration of
surgery, the ability to lay flat and patient preference. The use of intraoperative heparin is not a
contraindication to inserting an epidural however consideration should be given to the timing of
removal post-operatively when the patient may still be significantly anti-coagulated. During prolonged
procedures awake patients can become restless, requiring sedation or even conversion to GA.
Prolonged femoral and internal iliac artery occlusion can cause ischaemic pain in the legs and buttocks
respectively. Short periods of apnoea during the procedure are required to improve the image quality
in digital subtraction angiography, so the ability of the patient to perform a breath-hold should also be
considered. Other risks and benefits of regional versus general anaesthesia are documented elsewhere.
In open AAA repair, heparin is given to prevent thrombosis associated with stasis distal to the aortic
cross-clamp. There is a lack of trial data regarding the use of heparin in EVAR, however experience
with open vascular procedures means that most surgeons will apply the same practice and request
systemic heparinisation routinely - given after the access vessels are cannulated. In centres where the
activated clotting time (ACT) can be measured the aim is to maintain an ACT of 2-2.5 times the
baseline (approximately 200-250 seconds). The surgeons may request reversal with protamine at the
end of the procedure.
Complications of EVAR
Complications of EVAR can be divided into immediate and long term complications (see table 2).
Table 2. Complications of EVAR
Immediate and Short term
Long Term
Failed deployment conversion to GA (2%)
Endoleak
Arterial rupture
Infection
Arterial dissection
Graft migration
Embolisation
Delayed AAA rupture
Ischaemia of:
- spinal cord
- kidneys
- bowel
- buttocks/legs
Endoleak
The reported incidence of secondary procedures in EVAR varies from 10-30% with the most common
indication being endoleak.
The types of endoleak are classified as follows:
Type I At sites of graft attachment
Type II At sites of branches (i.e. back bleeding into the aneurysmal sac)
Type III Graft defect eg. Hole in the graft
Type IV Graft wall porosity
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LECTURE
Type I and II leaks can cause on-going bleeding into the aneurysm leading to rupture. Endoleaks can be
managed in a number of ways including conservative management with increased surveillance, coil
embolisation, placement of graft cuffs, ligation of feeding collateral arteries, open repair and redoEVAR.
Spinal Cord Ischaemia
Spinal cord ischaemia (SCI) following infra-renal EVAR is rare: 0.21%, however the risk of SCI in
complex, supra-renal abdominal EVARs is increased due to a number of factors. Long stent grafts will
occlude more of the thoracic and lumbar collateral arteries to the spinal cord. The largest collateral
artery, the artery of Adamkeiwicz arises directly from the aorta anywhere from T5 L5 (although most
commonly from T9-T12) so it is more at risk from occlusion with stent grafts which extend suprarenally. Collaterals to the spinal cord also arise from the internal iliac, inferior mesenteric (IMA) and
middle sacral arteries caudally. The IMA is invariably occluded during infra-renal EVAR.
Hypoperfusion, thrombosis and microembolism of atheromatous material into the collateral arteries are
also thought to be contributory factors to SCI in abdominal EVARs. Factors increasing the risk of
microembolism include a prolonged procedural time, extensive manipulation of the intravascular
catheters and perioperative embolisation the lumbar arteries. Patients who have had previous AAA
repair are also at greater risk of SCI.
Spinal drainage of CSF can be used to prevent or treat SCI, by increasing the perfusion pressure to the
spinal cord (perfusion pressure = MAP CSF pressure). Pre-operative spinal drains are occasionally
inserted for complex abdominal EVARs if the patient is thought to be at particularly high risk of SCI.
A high index of suspicion should be maintained in all patients post-operatively and a spinal drain
inserted if neurology develops.
Emergency EVAR
An increasing number of ruptured AAAs are being treated with EVAR. Several case series have
suggested a lower mortality with EVAR compared with open repair in ruptured AAA however this
may be due to selection bias with more stable patients undergoing EVAR. (A multi-centre randomised
controlled trial is currently underway looking at this (IMPROVE trial).
There is a risk of conversion to an open procedure, so preparation should be as for an emergency open
repair. The anaesthetic perioperative management for open ruptured AAA repair is well covered
elsewhere in the literature.
In brief, the preoperative anaesthetic management should include a rapid, targeted assessment, large
bore IV access, cross-match and hypotensive resuscitation. Equipment for large volume, rapid blood
transfusion and cell salvage should be prepared, as well as infusions of inotropes and vasodilators.
Arterial access should be gained if possible before the start of the procedure.
Smooth co-ordination and communication between the anaesthetic, surgical, radiology and theatre
teams is vital to ensure minimal delay and optimal outcome in this group of patients. In stable patients
a pre-operative CT scan is acquired and a joint decision is made between the surgeons and radiologists
as to the suitability of the aneurysm for endovascular repair.
The first surgical step is often to cannulate the access vessels and insert an expandable aortic balloon
into the supracoeliac aorta under local anaesthesia. The balloon acts as a cross-clamp which can be
deployed to gain haemorrhage control if required. After this the procedure can continue under local
anaesthesia with judicious use of sedation, or general anaesthesia. Neuraxial anaesthesia is not
appropriate for ruptured AAA repair.
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Emergency EVARs can be carried out solely under local anaesthesia and some studies have suggested
improved outcomes with local anaesthesia alone, however a number of factors may prevent the patient
tolerating the procedure, including:
Abdominal pain from expanding haematoma

Respiratory insufficiency from increased intra-abdominal pressure
Ischaemic pain in legs and buttocks
Agitation from hypotension and metabolic disturbance.
Induction of anaesthesia causes loss of abdominal tone and can lead to loss of tamponade of the
aneurysm with catastrophic bleeding ensuing. If general anaesthesia is required, it must not be induced
until the surgical team is prepared to deploy the aortic balloon or open the abdomen rapidly and apply
an aortic cross-clamp.
Post operatively the patient should be nursed in an intensive care or high dependency care
environment.
Excellent teamwork and communication is vital in EVAR for

ruptured AAA
Prepare for an open procedure
Consider local anaesthesia alone in appropriate patients until
haemorrhage control is gained
Summary
Patients undergoing endovascular AAA repair have a greater incidence of major comorbidities and
should undergo thorough preoperative assessment and optimisation within a multidisciplinary setting.
A distinction should be made between simple infra-renal EVAR and complex supra-renal EVARs
which can carry a greater perioperative risk.
Anaesthetic preparation should be carried out with the awareness that there is a risk of major
haemorrhage and conversion to an open procedure can occur.
Good team-work and communication is essential when carrying out EVARs and this is even more vital
during emergency EVARs.
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ANSWERS TO QUESTIONS
1. FTTF, 2. TTTF, 3.TFFF, 4. FTTT

WEBLINKS AND FURTHER READING

1.
NICE: Abdominal Aortic Aneurysm endovascular stent grafts: guidance.

http://guidance.nice.org.uk/TA167/Guidance/pdf/English
2. ACC/AHA 2007 Guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery. Anesth Analg. 2008 Mar;106(3):685-712
3. The Vascular Anaesthesia Society of Great Britain and Ireland
4. http://www.vasgbi.com/
5. Endovascular Aneurysm repair trials. http://www.evartrials.org/
6. Abdominal Aortic Aneurysm Quality Improvement Project
7. http://www.aaaqip.com/aaaqip/index.html
8. Clinical Practice Guidelines for endovascular Abdominal Aortic Aneurysm repair: Written by
the Standards of Practice committee for the Society of Interventional Radiology, and Endorsed
by the Cardiovascular and interventional radiological society of Europe and the Canadian
Interventional Radiology Association. http://www.sirweb.org/clinical/quality.shtml
9. Endovascular aneurysm repair versus open repair in patients with abdominal aortic aneurysm
(EVAR trial 1): randomised controlled trial. Lancet. 2005 Jun 25-Jul 1;365(9478):2179-86
10. Endovascular aneurysm repair and outcome in patients unfit for open repair of abdominal
aortic aneurysm (EVAR trial 2): randomised controlled trial. Lancet. 2005 Jun 25-Jul
1;365(9478):2187-92.
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IACTACON 2016
Myocardial protection by inhalational agents
Dr A. Syama Sundar,
Assistant professor, Nizams institute of medical sciences, Hyderabad.
Abstract
Cardiac surgery and some noncardiac procedures are associated with a significant risk of perioperative cardiac morbid
events. Experimental data indicate that clinical concentrations of volatile general anesthetics protect the myocardium
from ischemia and reperfusion injury, as shown by decreased infarct size and a more rapid recovery of contractile
function on reperfusion. These anesthetics may also mediate protective effects in other organs, such as the brain
and kidney. Recently, a number of reports have indicated that these experimentally observed protective effects may
also have clinical implications in cardiac surgery. However, the impact of the use of volatile anesthetics on outcome
measures, such as postoperative mortality and recovery in cardiac and noncardiac surgery, is yet to be determined.
Introduction
Myocardial ischaemiareperfusion injury, which commonly occurs during and after cardiac surgery, can lead to
marked myocardial dysfunction and, possibly, myocardial infarction (MI) and prolonged hospitalization. Strategies
that reduce these events should therefore improve overall outcomes. The concept of pharmacologically protecting
the myocardium to prevent this type of injury is an attractive concept.
A growing body of evidence indicates that volatile anesthetics protect myocardium against reversible and irreversible
ischemic injury. Identifying the mechanisms by which volatile agents mediate these anti-ischemic actions is the subject
of intense research. This objective has been difficult to accomplish because volatile anesthetics also profoundly
affect cardiovascular function. Volatile agents reduce arterial and coronary perfusion pressure, cause dose-related
depression of myocardial contractility, produce coronary vasodilation, affect electrophysiologic function, and modify
autonomic nervous system activity to varying degrees. Therefore, the anti-ischemic effects of volatile anesthetics may
be mediated, at least in part, by favorable alterations in myocardial oxygen supply-demand relations, preservation of
energy-dependent cellular functions, and increased coronary blood flow. However, it seems unlikely that changes in
myocardial metabolism and coronary perfusion caused by volatile anesthetics are solely responsible for protection
against ischemic damage. Instead, several endogenous signal transduction pathways, acting through the adenosine
triphosphate (ATP) sensitive potassium (KATP) channel and involving the generation of reactive oxygen species
(ROS), have been implicated in mediating the anti-ischemic actions of volatile anesthetics. The experimental and
clinical findings documenting the phenomenon of volatile anesthetic preconditioning against ischemic injury of
myocardium are evaluated. Recent findings in vitro and in vivo that seek to define the intracellular mechanisms
responsible for these beneficial actions are also summarized.
Historical Perspective
The anti-ischemic effects of volatile anesthetics were initially proposed more than 30 yr ago. Since 1985, when
Freedman and colleagues reported that enflurane could improve postischaemic myocardial recovery in the isolated
rat heart, there has been a body of research into the potential benefits of anaesthetic myocardial protection in both
animal and human models.(1) Lowenstein et al. demonstrated that halothane reduced ST segment elevation in a
canine model of brief coronary artery occlusion.(2) These data were consistent with the hypothesis that exposure
to halothane reduced acute ischemic injury.(2) A subsequent study by this research group also demonstrated that
halothane reduced myocardial infarct size when administered before prolonged coronary artery occlusion in dogs.
(3) Lactate production was decreased in the presence as compared with the absence of enflurane during demandinduced ischemia produced by a critical coronary artery stenosis and ventricular pacing when coronary perfusion
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pressure was maintained.(4)These results suggested that myocardial metabolism may be improved by administration
of a volatile agent during an ischemic episode independent of alterations in hemodynamics. The relative importance
of these early findings was initially overshadowedby a series(5) of reports published in the mid-1980s(6, 7)suggesting
that isoflurane may be capable of producing an abnormal redistribution of coronary blood flow away from ischemic
toward normal myocardium. This coronary steal phenomenon was attributed to the coronary vasodilating properties
of isoflurane that are known to occur primarily in arterioles of less than 100 m in diameter. Isoflurane was thought
to be capable of directly producing myocardial ischemia in susceptible patients with steal-prone coronary artery
anatomy under certain hemodynamic conditionsin a fashion similar to that of potent coronary vasodilators (e.g.,
adenosine, chromonar, dipyridamole).(8)
The implication that isoflurane might produce myocardial ischemia through such a steal mechanism was subsequently
dispelled by several investigations conducted in animal models(9-11)and humans with coronary artery disease.For
example, isoflurane did not selectively redistribute blood flow away from the collateral-dependent region in a
chronically instrumented canine model of multivessel coronary artery disease.(12)In contrast, adenosine produced
marked coronary steal by preferentially shunting blood flow away from collateral-dependent myocardium in this
model.Other studies(11, 13, 14)also suggested that isoflurane-induced hypotension may reduce myocardial perfusion,
but true coronary steal did not occur when coronary perfusion pressure was maintained. Subsequent investigations
with the newer volatile anesthetics sevoflurane(14) and desflurane(15)showed that these drugs also did not reduce
or abnormally redistribute coronary collateral blood flow. Therefore, despite initial concerns, volatile anesthetics were
subsequently shown to be relatively weak coronary vasodilators that are incapable of causing coronary steal under the
vast majority of clinical conditions.(16)
Contrary to the hypothesis that the use of volatile anesthetics may be potentially deleterious in some patients with
coronary artery disease, many laboratory and clinical investigations conducted since the resolution of the coronary
steal controversy have convincingly shown that volatile anestheticsprotect the heart against ischemia and reperfusion
injury. In addition to previously cited studies suggesting that halothane(2, 3, 16)and enfluraneexerted anti-ischemic
effects, halothane was also shown to preserve contractile function and ultrastructural integrity during cardioplegic
arrest.(17) This latter study was of considerable interest because these data indicated that halothane was capable of
exerting a cardioprotective effect completely independent of improvements in myocardial oxygen supply-demand
balance. In addition, halothane,enflurane,desflurane,and sevofluranehave been shown to reduce myocardial damage
when administered during reperfusion after prolonged coronary occlusion or cardioplegic arrest.
The precise mechanisms responsible for volatile anesthetic-induced protection against ischemic injury remain unclear
despite extensive study. Although it is clear that volatile anesthetics may indirectly improve myocardial oxygen
supply-demand relations or enhance coronary collateral perfusion, it is equally clear that these actions are not entirely
responsible for the anti-ischemic effects of these agents. This contention is emphasized by findings showing that
volatile anesthetics conferred protection during cardioplegic arrest (17)and during reperfusion,conditions in which
myocardial oxygen supply-demand relations play little if any role. Similarly, isoflurane and sevoflurane increased the
viability of isolated cardiac myocytes,and sevofluraneand desflurane improved contractility of isolated cardiac muscle
exposed to simulated ischemia.(18, 19) These results were initially attributed to reductions in excessive intracellular
Ca2+concentrations during ischemia and reperfusion produced by partial inhibition of Ca2+channel activity.
However, this relatively generic Ca2+hypothesis did not address the precise mechanisms or provide deeper insight into
the intracellular processes by which volatile anesthetics exert protective effects in the intact heart. Knowledge about
the mechanisms of ischemia reperfusion injury and ischemic preconditioning is essential to understand inhalational
anesthetic induced myocardial protection.
Mechanisms of ischemic-reperfusion injury

Ischemia precludes adequate oxygen supply, which rapidly results in depletion of ATP. This inhibits ATP-driven
Na+-K+ pumps, increasing [Na+]. [H+] is increased due to poor washout of metabolites and inhibition of mitochondrial
oxidation of NADH2. Increased [H+] enhances Na+-H+ exchange to retain normal pH, leading to increased [Na+].
Accordingly, [Ca2+] is augumented via Na+-Ca2+ exchange . High [Ca2+] degrades proteins and phospholipids. Onset
of ischemia increased the production of free radicals derived mainly from neutrophils and mitochondria. When
coronary arteries are damaged, ischemia-related injury prevents swift gas exchange by swollen endothelial cells.
Vessels with malfunctioning endothelium and smooth muscle cannot dilate when necessary. Moreover, neutrophils/
platelets aggregating in the lumen decrease adequate coronary flow. malfunctioning endothelium and smooth muscle
cannot dilate when necessary. Moreover, neutrophils/platelets aggregating in the lumen decrease adequate coronary
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flow. Neutrophils release oxygen free radicals, cytokines and other proinflammatory substances, which injure the
endothelium, vascular smooth muscle and myocardium. A pathway for neutrophil sequestration is the specific
interaction of adhesion molecules whose expression is promoted by ischemia-reperfusion. Adhesion molecules, for
example, intercellular adhesion molecule-1 (ICAM-1), L-selectin and CD11b/CD18 are expressed on neutrophils
and endothelium. On reperfusion, [H+] outside the cell is rapidly decreased to normal levels because of wash-out.
This results in an increase in [Ca2+] due enhanced Na+-H+ and Na+-Ca2+ exchange. Reperfusion also results in a
burst of free radical generation because oxygen abundantly supplied. Both increased [Ca2+] and free radicals harm
the myocardium during reperfusion. Damage of the vascular system is more prominent during reperfusion than
ischemia. Infarction is one of the major events of ischemia-reperfusion injury during anesthesia. Another major
event is myocardial stunning, which is defined as reversible myocardial dysfunction that persists after reperfusion.
Mechanisms of early preconditioning

Preconditioning is a treatment before an ischemic event while ischemia-reperfusion injury is developed during
and after an ischemic period. The signals were generated by short period of ischemia in ischemic preconditioning.
Ischemic preconditioning is mediated via several sacrolemmal receptors, which are mostly linked to inhibitory G
(Gi)-protein), namely adenosine (A-1, A-3), purinoceptors (P2Y), endothelin (ET1), acetylcholine (M2), 1- and
-adrenergic, angiotensin II (AT2), bradykinin (B2) and opioid ( 1,) receptors, which couple to a highly complex
network of kinases. The involvement of many receptors or triggers in mediating preconditioning reflects the biological
redundancy in this life-saving signal transduction pathway. Figure 1 shows the main signaling steps and components
of early and delayed preconditioning (20). G-proteins link the initial stimulus from the individual receptors to
phospholipase C and D. They have several additional functions such as inhibition of Ca2+ influx during ischemia,
regulation of cellular metabolism and activation of KATP channels, the putative main end-effectors of preconditioning.
Activation of phospholipase C and D introduces formation of inositol triphosphate (IP3) for the release of Ca2+ from
the sarcoplasmic reticulum via the IP3 receptor, and production of diacylglycerol (DAG). DAG activates different
isoforms of protein kinase C (PKC). PKC is activated by a large number of phosphorylating enzymes, including Giproteins, phosphlipids, DAG, increased intracellular [Ca2+], and nitric oxide (NO), which is derived from intracellular
constitutively active NO synthsae (NOS) or from extracellular sources. PKC can be activated by reactive oxygen
species (ROS) derived from mitochondria either during the short ischemic or the subsequent repetitive reperfusion
episodes. Activation of this key enzyme leads to isoform-specific and cytoskeletonmediated translocation of cytosolic
PKC, inducing phosphorylation and thus activation of the sacrolemnal and mitochondrial KATP channels. After only
10 min of ischemic preconditioning, PKC activity in the cytosol reduces, whereas PKC in the particulate fraction
(i.e., nuclei, mitochondria and membranes) increases.(21) PKC-translocation seems to be responsible for activating
mitochondrial KATP channels and PKC-translocation for the establishment of late preconditioning by phosphorylating
nuclear targets.
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LECTURE
Fig 1: Signalling for cardiac preconditioning. The signalling components depicted illustrate current knowledge regarding
the mechanisms of early (left of dashed line) and delayed (right of dashed line) cardiac preconditioning. m=inner
mitochondrial membrane potential; AlRed=aldose reductase; Bcl2=antiapoptotic protein; Ca=sarcolemmal voltage
dependent Ca2+ channels; DAG=diacylglycerol; COX2=cyclooxygenase type 2; eNOS=endothelial NO synthase; G
proteins=heterotrimeric Gproteins; HSP27 and HSP70=heat shock proteins; iNOS=inducible NO synthase; IP3=inositol
triphosphate; IP3R=inositol triphosphate receptor; K=sarcolemmal and mitochondrial KATP channels; MnSOD=manganese
superoxide dismutase; NFB=nuclear factorB; NO=nitric oxide; PIP2=phosphatidylinositol bisphosphate;
PKC=protein kinase C; PLC/PLD=phospholipases C and D; ROS=reactive oxygen species; RYR=ryanodine

Ca2+release channel; SERCA2=Ca2+ pump of the SR; SR=sarcoplasmic reticulum.
However, the observation that PKC inhibition may not completely block the preconditioning stimulus (22) supports
the concept that additional intracellular kinases downstream, upstream or in parallel to PKC signaling contribute to
the amplification and establishment of the preconditioned state.
Recent studies suggested that mitochondrial KATP channels play a greater role than sacrolemmal KATP channels (23,
24). Mitochondrial KATP channels regulate mitochondrial volume state, mitochondrial membrane potential, formation
of ROS and energy production. Toyoda et al. (25) suggested differential role of sarcolemmal and mitochondrial
KATP channels in preconditioning. Reduction of myocardial infarct size is mediated largely by mitochondrial KATP
channels, but functional recovery is mediated by sarcolemmal KATP channels. Mitochondrial KATP channels also play
an important role in the prevention of cardiomyocyte apoptosis and in late preconditioning protection. A lot of
experimental studies indicate the mitochondrial KATP channels as the main end-effector of preconditioning, but role
of sarcolemmal KATP channels cannot be dismissed totally.
Sarcolemmal KATP channels may modulate myocardial infarct size by reducing Ca2+ enterance into the myocytes from
outside and by attenuating Ca2+ overload. There are three possible explanations about reduction of infarct size by
mitochondrial KATP channels. First, the decreased mitochondrial Ca2+ overload during ischemia may prevent opening
of the mitochondrial permeability transition pores and guarantee optimal conditions for ATP production. Second,
Garlid and Pancek (26)proposed that opening of the mitochondrial KATP channel decreases the ischemia-induced
swelling of the mitochondrial interspace, which would preserve functional coupling between adenosine nucleotide
translocase and mitochondrial creatine kinase (prevention of structure/function). This secures the transport of newly
synthesized ATP from the site of production by ATP synthase on the inner mitochondrial membrane to the cytosol.
Thus, high-energy phosphate substrates are supplied continuously from the mitochondria to the sites of energy
consumption. Third, mitochondrial KATP channels may elicit protection in basis of the observation of increased
formation of ROS. ROS would stimulate the activation of multiple transcriptional factors (NF- B, activator protein1, protein kinases, protein phosphatase, etc.), ultimately leading to cardioprotection.
ROS, important intracellular signaling molecules derived from mitochondria, are increased during sublethal oxidative
stress (preconditioning stimulus) and play a pivotal role in triggering early and delayed cardioprotection. ROS activate
phospholipase C and PKC, which, in turn, amplify the preconditioning stimulus. Generation of ROS during the
initiation of preconditioning represents an essential trigger for early and delayed cardioprotection. NO can induce
a cardioprotective effect against myocardial stunning and infarction. Recent studies revealed direct evidence of
enhanced biosynthesis of NO in the myocardium subjected to brief episodes of ischemia and reperfusion, probably
via increased NOS activity. Although NO is not necessary for ischemia-induced early preconditioning, exogenous
or pharmacologically increased endogenous NO production elicits an early preconditioning effect, that is, NO is
sufficient but no necessary for early preconditioning. Conversely, NO has an obligatory role in late preconditioning.
Mechanisms of late preconditioning

Late preconditioning requires NO formation and increased synthesis of protective proteins. PKC and multiple
kinases are involved in the signaling cascade, leading to activation of several transcription factors, such as nuclear
factor- B (NF- B), which leads to the sustained expression of a number of proteins considered to be responsible
for the delayed protection phase. Disruption of the inducible NOS (iNOS) gene completely abolished the delayed
infarct-sparing effect, which indicates the obligatory role of iNOS in the cardioprotection afforded by delayed
preconditioning. The most likely cardioprotective effects of NO in late preconditioning are: i) inhibition of Ca2+
influx; ii) antagonism of -adrenergic stimulation; iii) reduced contractility and myocardial oxygen consumption; iv)
opening of KATP channels; v) antioxidant actions; and vi) activation of COX-2 with the synthesis of prostanoids.
Activation of KATP channels also plays a role in delayed protection.
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Pharmacological preconditioning
Many characteristics of preconditioning by volatile anesthetics are similar to those of ischemic preconditioning.
These involve activation of A1 adenosine receptors, PKC and KATP channels. Ischemic preconditioning and anesthetic
preconditioning similarly reduce Ca2+ loading, augment post-ischemic contractile responsiveness to Ca2+ and decrease
infarct size. The main routes of activation by volatile anesthetics involve the Gi protein-coupled adenosine receptor
and the production of NO, probably by modulation of NOS activity. These two signaling pathways converged at
the level of PKC, although alternative routes for NO could be operative as well. Finally volatile anesthetics activate
mitochondrial and sarcolemmal KATP channels, thereby providing cardioprotection. As previously discussed there is
a question of whether the sarcolemmal KATP channel or mitochondrial KATP channel is more important in mediating
volatile anesthetic-induced preconditioning. Although several experimental studies have addressed this question (27,
28), it is important to note that considerable cross-talk is documented between sarcolemmal and mitochondrial KATP
channels and the importance of the individual KATP channels may vary among experimental approaches and species
differences. Sato et al. pro(29)posed the concept of channel priming (including the sarcolemmal and mitochondrial
KATP channels) by volatile anesthetics. The primed channel state allows easy and rapid opening at the initiation of
ischemia. On the other hand, volatile anesthetics mediate their protection by selectively enhancing mitochondrial
KATP channels through the triggering of multiple PKC-coupled signalling pathways, namely NO and adenosine/Gi
signaling pathway(27). Biosynthesis of NO plays a pivotal role in reducing ischemic damage in heart tissue. Moreover,
NO and cGMP may be major players in volatile anesthetic-induced cardioprotection. Both NO/cGMP signaling
and basal NOS activity play a fundamental role in pacing associated preconditioning. Volatile anesthetics may
differentially modulate the activity of the various isoenzymes of NOS (nNOS, eNOS, iNOS), which are ubiquitous
but heterogeneously distributed in myocytes. The observation that isoflurane-induced preconditioning is inhibited by
free radical scavengers supports the concept that generation of radicals, either by means of altered NO synthesis or
by enhanced formation of ROS/NO (possibly by opening mitochondrial KATP channels), is important (30). These
results show that the preconditioning effects of volatile anesthetics are triggered by multiple signaling cascades
and mediated mainly by mitochondrial KATP channels, but sarcolemmal KATP channels may also contribute to the
protection induced by volatile anesthetics. Volatile anesthetics can elicit coronary protection through an ischemic
(pharmacological) preconditioning-like effect. Ischemic preconditioning is known to reduce ICAM-1 production and
neutrophil entrapment, and to preserve the response to vasodilators. Treatment with volatile anesthetics decreased
neutrophil adhesion on the endothelium and expression of CD11b, which forms an integrin with CD18, while the
anesthetic did not affect endothelial cell actibation vis--vis neutrophils. Inhibition of neutrophil activation by volatile
anesthetics decreases adhesion to cultured human endothelial cells.(31) These findings supports that administration
of volatile anesthetics prior to reperfusion maintains coronary vasculature.
Evidence of preconditioning in humans

Only recently research has turned to clinical implementation of preconditioning, and experimental protocols have
been turned into clinical ones. APC has indeed been demonstrated in randomised clinical trials conducted in patients
undergoing cardiac surgery - mostly coronary artery bypass graft. Myocardial ischaemia is an integral part of this type
of surgery, allowing transposition of a preconditioning/ischaemia/reperfusion sequence into a clinical protocol. The
first clinical study (32) using a preconditioning protocol with an anaesthetic agent was published in 1999 and showed
that administration of isoflurane prior to aortic cross-clamping resulted in smaller postoperative release of creatine
kinase MB (CK-MB) and cTn even if this reduction in cardiac biomarkers did not reach a statistic significance due to
the small sample of studied patients.
A key question is whether the cardioprotective effects of volatile anaesthetics are clinically applicable and associated
with improved cardiac function, ultimately resulting in a better outcome in patients with coronary artery disease. This
is especially of interest since it was commonly believed that the choice of the primary anaesthetic agent does not
result in a different outcome. The first study to suggest that the use of halogenated anaesthetics might have relevant
clinical advantages was conducted in 2002. (33) It appeared from this study that the use of sevoflurane was associated
with a preservation of global haemodynamic and left ventricular function with a significant lower postoperative
release of cTnI compared with the TIVA regimen. Two recent RCTs confirmed these protective properties in terms
of cTnI release and also demonstrated that the use of desflurane during coronary surgery is associated with shorter
ICU and overall LOS and a faster weaning from mechanical ventilation. (34, 35)
De Hert et al. also showed that the cardioprotective effects (lower postoperative cTnI release and preservation of
postoperative cardiac function) of an anaesthetic regimen with sevoflurane are most apparent when the volatile
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anaesthetic is administered throughout the entire surgical procedure as compared to administration only before or
after cardiopulmonary bypass (CPB). (36) These data support the idea that the cardioprotective effects of anaesthetic
agents depend upon an interaction of factors such as the administration protocols, the choice of a specific agent, the
concomitant use of other drugs, and the variables used to assess myocardial function.
A recent meta-analysis showed that desflurane and sevoflurane reduce postoperative mortality and incidence of
myocardial infarction (MI) following cardiac surgery with significant advantages in terms of postoperative cardiac
troponin (cTn) release, need for inotropic support, time on mechanical ventilation, intensive care unit (ICU) and
overall hospital stay.(37) Specifically, volatile anaesthetics reduced the risk of myocardial infarction (MI) (24/979
[2.4%] in the volatile anaesthetics group vs 45/874 [5.1%] in the control arm, odds ratio (OR) = 0.51 [0.32-0.84], p
for effect = 0.008, p for heterogeneity = 0.77, I 2 = 0%) and all-cause mortality (4/977 [0.4%] vs 14/872 [1.6%], OR
= 0.31 [0.12-0.80], p for effect = 0.02, p for heterogeneity = 0.88, I 2 = 0%). Beside increasing in-hospital survival,
use of volatile anaesthetics was also associated with a significant reduction in cTnI peak release and need for inotropic
support. Furthermore, the use of desflurane and sevoflurane was associated with shorter ICU stay, time to hospital
discharge and time on mechanical ventilation.
Multicentre, randomised clinical trials (RCT) had previously demonstrated that the use of desflurane can reduce
the postoperative release of cardiac troponin I (cTnI), the need for inotropic support, and the number of patients
requiring prolonged hospitalisation following coronary artery bypass graft (CABG) surgery either with (34) and
without (35) cardiopulmonary bypass.
Nonetheless, whether volatile anaesthetics improve the outcome of cardiac surgical patients is still matter of debate.
In a retrospective, non-randomised study including more than 10,000 cardiac surgical patients, Jakobsen et al . (38)
compared sevoflurane and a total intravenous anaesthesia (TIVA). The authors found no difference in postoperative
mortality and myocardial infarction rate; patients without preoperative unstable angina or recent myocardial infarction,
however, showed a lower postoperative mortality after sevoflurane anaesthesia. Although this study carries some
others limitations in its design - such as the fact that cardioprotective strategies and surgical and anaesthetic teams
varied across the three participant centres - it yields some interesting evidence over a very large number of patients.
Evidence in non-coronary surgical settings is even more contradictory. Landoni et al . found no advantage in using a
preconditioning protocol with volatile anaesthetics in patients undergoing coronary mitral surgery. (37) Interestingly,
patients undergoing mitral surgery with concomitant coronary artery disease showed a marked decrease in
postoperative cTnI release when preconditioned with desflurane. (37) In another study on a small group of patients
undergoing aortic valvular replacement,(39) Cromheecke et al . found that sevoflurane-based anaesthesia reduced
postoperative cTnI dismissal. They also observed that patients anaesthetised with sevoflurane had an advantage in
terms of minor clinical outcomes, such as the incidence of atrial fibrillation and ICU stay.
Clinical Evidence in Non-Cardiac Surgery

Recent American College of Cardiology/American Heart Association Guidelines (40) recommended volatile
anaesthetic agents during non-cardiac surgery for the maintenance of general anaesthesia in patients at risk for MI
(class IIa, level of Evidence B), but whether halogenated anaesthetics also have cardioprotective properties in noncardiac surgery settings is controversial.(41)
A recent meta-analysis (42) included 79 studies, involving 6219 patients (2768 received TIVA and 3451 received
desflurane or sevoflurane in their anaesthesia plan) undergoing non-cardiac surgery. Inclusion criteria were random
allocation to treatment, comparison of a TIVA regimen vs an anaesthesia plan including desflurane or sevoflurane,
performed on adult, non-cardiosurgical patients. All authors administered volatile or intravenous anaesthetics
throughout the procedure. Volatile anaesthetic dosage varied across studies, ranging 0.33-2 MAC in the 609 patients
receiving desflurane and 0.25-2 MAC in the 2842 patients receiving sevoflurane. No MI or deaths were observed in
any of the examined studies. No author reported any postoperative MI or death among the study population nor any
significant cardiac adverse event.
Conclusions:
This review summarizes recent knowledge about the key cellular events involved in ischemic and pharmacological
preconditioning. The cellular mechanisms responsible for such protection are not fully understood yet, but many
studies have indirectly evidenced that this preconditioning property indeed translates into clinically evident cardiac
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IACTACON 2016
protection in patients undergoing cardiac surgery.Many characteristics of anesthetic-induced preconditioning are

similar to ischemic preconditioning. However, there may be fundamental differences in terms of signal intensity and
the potential to concomitantly injured cardiac tissue. Of many anesthetics, volatile anesthetics are arguably the most
promising agents as cardiopro-tectors. They demonstrated the beneficial effect against ischemic-reperfusion injury
better than any other anesthetic. Volatile anesthetics provide cardioprotection at clinically relevant concentrations
and morphine has also been to be protective at clinical concentrations. Therefore, volatile anesthetics might be good
choice for the patients at risk of myocardial ischemia.
1.
Freedman MDBruceM, Hamm MDDavidP, Everson MDCharlesT, Wechsler MDAndrewS, Christian

MDPDCharlesM. Enflurane Enhances Postischemic Functional Recovery in the Isolated Rat Heart. Anesthesiology. 1985;62(1):29-33.
2.
Bland JH, Lowenstein E. Halothane-induced decrease in experimental myocardial ischemia in the non-failing canine heart. Anesthesiology. 1976;45(3):287-93.
3.
Davis RF, DeBoer LW, Rude RE, Lowenstein E, Maroko PR. The effect of halothane anesthesia on myocardial necrosis, hemodynamic performance, and regional myocardial blood flow in dogs following coronary artery occlusion. Anesthesiology. 1983;59(5):402-11.
4.
van Ackern K, Vetter HO, Bruckner UB, Madler C, Mittman U, Peter K. Effects of enflurane on myocardial ischaemia in the dog. Br J Anaesth. 1985;57(5):497-504.
5.
Warltier DC, Kersten JR, Pagel PS, Gross GJ. Editorial view: anesthetic preconditioning: serendipity and
science. Anesthesiology. 2002;97(1):1-3.
6.
Becker LC. Is isoflurane dangerous for the patient with coronary artery disease?: Anesthesiology. 1987 Mar;66(3):25961.
7.
Buffington CW, Romson JL, Levine A, Duttlinger NC, Huang AH. Isoflurane induces coronary steal in a
canine model of chronic coronary occlusion. Anesthesiology. 1987;66(3):280-92.
8.
Buffington CW, Davis KB, Gillispie S, Pettinger M. The prevalence of steal-prone coronary anatomy in
patients with coronary artery disease: an analysis of the Coronary Artery Surgery Study Registry. Anesthesiology. 1988;69(5):721-7.
9.
Moore PG, Kien ND, Reitan JA, White DA, Safwat AM. No evidence for blood flow redistribution with
isoflurane or halothane during acute coronary artery occlusion in fentanyl-anesthetized dogs. Anesthesiology. 1991;75(5):854-65.
10.
Hartman JC, Kampine JP, Schmeling WT, Warltier DC. Actions of isoflurane on myocardial perfusion in
chronically instrumented dogs with poor, moderate, or well-developed coronary collaterals. J Cardiothorac
Anesth. 1990;4(6):715-25.
11.
Pulley DD, Kirvassilis GV, Kelermenos N, Kater K, Barzilai B, Genton RE, et al. Regional and global myocardial circulatory and metabolic effects of isoflurane and halothane in patients with steal-prone coronary
anatomy. Anesthesiology. 1991;75(5):756-66.
12.
Hartman JC, Kampine JP, Schmeling WT, Warltier DC. Steal-prone coronary circulation in chronically
instrumented dogs: isoflurane versus adenosine. Anesthesiology. 1991;74(4):744-56.
13.
Hartman JC, Kampine JP, Schmeling WT, Warltier DC. Alterations in collateral blood flow produced by
isoflurane in a chronically instrumented canine model of multivessel coronary artery disease. Anesthesiology. 1991;74(1):120-33.
14.
Leung JM, Goehner P, OKelly BF, Hollenberg M, Pineda N, Cason BA, et al. Isoflurane anesthesia and
myocardial ischemia: comparative risk versus sufentanil anesthesia in patients undergoing coronary artery bypass graft surgery. The SPI (Study of Perioperative Ischemia) Research Group. Anesthesiology.
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1991;74(5):838-47.
15.
Hartman JC, Pagel PS, Kampine JP, Schmeling WT, Warltier DC. Influence of desflurane on regional
distribution of coronary blood flow in a chronically instrumented canine model of multivessel coronary
artery obstruction. Anesth Analg. 1991;72(3):289-99.
16.
Kenny D, Coughlan MG, Kampine JP, Montgomery RR, Bosnjak ZJ, Warltier DC. Cultured endothelial
cells restore vasodilator responses to coronary arteries with impaired endothelial function and alter the
response to a nitric oxide donor. Pharmacology. 1994;49(4):249-56.
17.
Lochner A, Harper IS, Salie R, Genade S, Coetzee AR. Halothane protects the isolated rat myocardium
against excessive total intracellular calcium and structural damage during ischemia and reperfusion. Anesth
Analg. 1994;79(2):226-33.
18. Yvon A, Hanouz JL, Haelewyn B, Terrien X, Massetti M, Babatasi G, et al. Mechanisms of sevoflurane-induced myocardial preconditioning in isolated human right atria in vitro. Anesthesiology. 2003;99(1):27-33.
19.
Hanouz JL, Yvon A, Massetti M, Lepage O, Babatasi G, Khayat A, et al. Mechanisms of desflurane-induced preconditioning in isolated human right atria in vitro. Anesthesiology. 2002;97(1):33-41.
20.
Zaugg M, Lucchinetti E, Uecker M, Pasch T, Schaub MC. Anaesthetics and cardiac preconditioning. Part I.
Signalling and cytoprotective mechanisms. Br J Anaesth. 2003;91(4):551-65.
21.
Strasser RH, Braun-Dullaeus R, Walendzik H, Marquetant R. Alpha 1-receptor-independent activation of

protein kinase C in acute myocardial ischemia. Mechanisms for sensitization of the adenylyl cyclase system.
Circ Res. 1992;70(6):1304-12.
22.
Vahlhaus C, Schulz R, Post H, Onallah R, Heusch G. No prevention of ischemic preconditioning by the

protein kinase C inhibitor staurosporine in swine. Circ Res. 1996;79(3):407-14.
23.
Nakano A, Cohen MV, Downey JM. Ischemic preconditioning: from basic mechanisms to clinical applications. Pharmacol Ther. 2000;86(3):263-75.
24.
Rubino A, Yellon DM. Ischaemic preconditioning of the vasculature: an overlooked phenomenon for protecting the heart? Trends in Pharmacological Sciences;21(6):225-30.
25.
Toyoda Y, Friehs I, Parker RA, Levitsky S, McCully JD. Differential role of sarcolemmal and mitochondrial
KATP channels in adenosine-enhanced ischemic preconditioning. American Journal of Physiology - Heart
and Circulatory Physiology. 2000;279(6):H2694-H703.
26.
Garlid KD, Paucek P. Mitochondrial potassium transport: the K(+) cycle. Biochim Biophys Acta.
2003;30:1-3.
27.
Zaugg M, Lucchinetti E, Spahn DR, Pasch T, Schaub MC. Volatile anesthetics mimic cardiac preconditioning by priming the activation of mitochondrial K(ATP) channels via multiple signaling pathways. Anesthesiology. 2002;97(1):4-14.
28.
Toller WG, Gross ER, Kersten JR, Pagel PS, Gross GJ, Warltier DC. Sarcolemmal and mitochondrial adenosine triphosphate- dependent potassium channels: mechanism of desflurane-induced cardioprotection.
Anesthesiology. 2000;92(6):1731-9.
29.
Sato T, Sasaki N, ORourke B, Marban E. Adenosine primes the opening of mitochondrial ATP-sensitive
potassium channels: a key step in ischemic preconditioning? Circulation. 2000;102(7):800-5.
30.
Mullenheim J, Ebel D, Frassdorf J, Preckel B, Thamer V, Schlack W. Isoflurane preconditions myocardium

against infarction via release of free radicals. Anesthesiology. 2002;96(4):934-40.
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31.
Mobert J, Zahler S, Becker BF, Conzen PF. Inhibition of neutrophil activation by volatile anesthetics decreases adhesion to cultured human endothelial cells. Anesthesiology. 1999;90(5):1372-81.
32.
Belhomme D, Peynet J, Louzy M, Launay JM, Kitakaze M, Menasche P. Evidence for preconditioning by
isoflurane in coronary artery bypass graft surgery. Circulation. 1999;100(19 Suppl):II340-4.
33.
De Hert SG, ten Broecke PW, Mertens E, Van Sommeren EW, De Blier IG, Stockman BA, et al. Sevoflurane but not propofol preserves myocardial function in coronary surgery patients. Anesthesiology.
2002;97(1):42-9.
34.
Tritapepe L, Landoni G, Guarracino F, Pompei F, Crivellari M, Maselli D, et al. Cardiac protection by volatile anaesthetics: a multicentre randomized controlled study in patients undergoing coronary artery bypass
grafting with cardiopulmonary bypass. Eur J Anaesthesiol. 2007;24(4):323-31.
35.
Guarracino F, Landoni G, Tritapepe L, Pompei F, Leoni A, Aletti G, et al. Myocardial damage prevented by volatile anesthetics: a multicenter randomized controlled study. J Cardiothorac Vasc Anesth.
2006;20(4):477-83.
36.
De Hert SG, Van der Linden PJ, Cromheecke S, Meeus R, Nelis A, Van Reeth V, et al. Cardioprotective
properties of sevoflurane in patients undergoing coronary surgery with cardiopulmonary bypass are related
to the modalities of its administration. Anesthesiology. 2004;101(2):299-310.
37.
Landoni G, Biondi-Zoccai GG, Zangrillo A, Bignami E, DAvolio S, Marchetti C, et al. Desflurane and
sevoflurane in cardiac surgery: a meta-analysis of randomized clinical trials. J Cardiothorac Vasc Anesth.
2007;21(4):502-11.
38. Jakobsen CJ, Berg H, Hindsholm KB, Faddy N, Sloth E. The influence of propofol versus sevoflurane anesthesia on outcome in 10,535 cardiac surgical procedures. J Cardiothorac Vasc Anesth. 2007;21(5):664-71.
39.
Cromheecke S, Pepermans V, Hendrickx E, Lorsomradee S, Ten Broecke PW, Stockman BA, et al. Cardioprotective properties of sevoflurane in patients undergoing aortic valve replacement with cardiopulmonary
bypass. Anesth Analg. 2006;103(2):289-96.
40.
Fleisher LA, Beckman JA, Brown KA, Calkins H, Chaikof EL, Fleischmann KE, et al. ACC/AHA 2007
Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: Executive
Summary: A Report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular
Evaluation for Noncardiac Surgery) Developed in Collaboration With the American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and
Biology, and Society for Vascular Surgery. J Am Coll Cardiol. 2007;50(17):1707-32.
41.
Landoni G, Fochi O, Zangrillo A. Cardioprotection by volatile anesthetics in noncardiac surgery? No, not yet at least: J
Am Coll Cardiol. 2008 Apr 1;51(13):1321; author reply 1321-2. doi: 10.1016/j.jacc.2007.12.020.
42.
Fochi O BE, Landoni G, Pappalardo F, Calabr MG, Giardina G. Cardiac protection by volatile anesthetics
in non-cardiac surgery: A meta-analysis. Minerva Anestesiol 2007;73:26.
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CPB DISASTERS - SUDDEN UNEXPECTED AORTIC

DISSECTION
Dr.M.Vijayasankar., M.D.
Aortic dissection is a rare ,catastrophic complication of cardiopulmonary bypass. In most reported cases of aortic
dissection during cardiac surgery, the site of arterial cannulation is the origin of dissection. Though there are number
of complications related with CPB, aortic dissection carries the high mortality but with less incidence.
The incidence of acute aortic dissection ranges from0.08-0.35% (average 0.21% ) and associated with mortality of
15-50% (average 25%). The incidence of arterial cannula associated with dissection is about 0.06-0.09% for ascending
aortic cannulation, 0.7% with axillary artery cannulation and about 0.2-1.3% with femoral cannulation.
The dissection can be due to direct trauma or indirect trauma. The site of origin most commonly is the arterial
cannulation, other sites arein decreasing frequency the aortic cross clamp,antegrade cardioplegia cannula, partial
clamp,proximal anastomosis of coronary graft and aortatomy. The arterial cannula dissection typically presents
shortly after initiating CPB but can occur anytime including late postoperatively.
Clues to its occurrence include hypotension, loss of venous return and perfusate, increase arterial line pressure,
evidence of impaired organ perfusion, blue discoloration or distension of the cannulation site. And bleeding from
the needle holes, arterial incisions and cannulation sites can be obvious. Best way to establish the diagnosis is by TEE
or epiaortic scanning.
Risk factors include location of cannula, old age, chronic hypertension, diseased or dilated aorta, atherosclerotic
peripheral vessels, cystic medial necrosis, high arterial pressure at the time of cannulation, decannulation and
application and removal of aortic clamps and type of purse-string suture and cannulation technique.
For early diagnosis, pay attention to and evaluating all possible causes of hypotension during initiation of bypass,
frequent visual inspection of the cannulation site and TEE monitoring of the aorta are recommended. Care should
be given to monitor the cardioplegia pressure. When femoral cannulation is used, TEE monitoring of the descending
thoracic aorta during initiation of CPB and frequently during CPB is advisable.
Management of this catastrophe is influenced by the type of cannulation, the stage of the cardiac surgery, and the
extent of the dissection. When it occurs at the initiation of the CPB via femoral cannulation, discontinue CPB
immediately and re-establishment of circulation by the patients own heart, if feasible , may resolve the situation.
Then re-institute CPB via an alternate arterial cannulation (ascending aorta, subclavian or axillary) and continue with
the planned cardiac procedure with or without repairing the aorta.
When the ascending aorta is the cannulation site, CPB should be stopped immediately and flow re-initiated via
peripheral cannulation ( femoral, subclavian or innominate ), into the true lumen of aortic arch through the flap or
by trans apical cannulation.
Initiating deep hypothermia in anticipation of need for circulatory arrest to repair the ascending aortic dissection
is advocated. Adjunct cerebral protective techniques including selective cerebral perfusion may also be necessary if
the dissection is extensive and involves the arch vessels. Depending upon the extent of the dissection, this may be
repaired by closed exclusion suturing, insertion of a patch or graft replacement of the ascending aorta, but usually
graft replacement is recommended and has given the best results.
Proposals to minimize its occurrence include lowering arterial pressure during cannulation, decannulation and
applicationand removal of aortic clamps, care with the insertion of cannulae, checking for pulstility and pressure in
the arterial line after cannulation, and checking impedence/resistance/line pressure with a test infusion before going
on full CPB. Use of high pressure audible alarm with pump shut off of the perfusion inflow line may limit the extent
of the injury.
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1/30/16!
Perioperative Transfusion Therapy!

Local & Global Perspective!
Im an Academic Anesthesiologist,
Internist, &Intensive Care Physician"
Douglas B. Coursin, MD!
Professor of Anesthesiology & Medicine

University of Wisconsin - Madison !
School of Medicine & Public Health!
dcoursin@wisc.edu!
Full Disclosure, I Am Not An"

OR!
CT Anaesthetist"
Take Away Messages"

OR/CT Surg ICU pts sometimes chronically anemic
(& occasionally coagulopathic)!
Routinely become acutely anemic & often
coagulopathic!
Little clear cut benet to most transfusions!
May harm > immune, infectious, volume, etc.!
TACO & TRALI underappreciated !
Tx triggers -> RBCs, FFP, Platelets -> lack data!
Evolving data on Liberal vs. Conservative tx triggers!
Individualize tx > clinical situation, co-morbidity, R/B!

No good blood substitutes, yet!
Cardiac surgery is the largest consumer of

blood products in medicine; although
believed life saving, transfusion carries
substantial adverse risks.!
CT surgery uses 10% to 15% of US blood supply"

(on rise 2nd to increased operative complexity)!
of CT surgical pts receive blood products!
Horvath AR, et al. Blood Transfusion & Infection After !
Cardiac Surgery Ann Thorac Surg 2013; 95: 21942201.!
doi: 10.1016/j.athoracsur.2012.11.078!
Anesthesiologists & Intensivists"

Transfuse 50 65% of all blood products in
America"
I continue to alter my transfusion practices
& continue to have many questions about
who, what, when, & how much to transfuse"
My practice & patient population vs. yours
& other CT anesthesiologists/intensivists"
1!
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1/30/16!
Why Are CT Patients Anemic?!
Anesthesiology January 2015!
Either !
Lose blood!
CT surg!
Retained in pump!
Post op drains/suture deciency

Periop Coagulopathy
Breakdown blood!
Valve pts!
Device pts!
COMBINATIONS!
!!
THEREOF!
Dont make blood!

Acute or chronic!
How Do ICU Patients Lose Blood?"

Often !
Hit, shot, knifed, fell or collided !

Operated on or had invasive procedures!
Phlebotomized excessively!
Why Dont Some ICU Pts Make Blood?"

Bone marrow turned off!
Diffuse depression (pancytopenia)!
Chest 1995; 108:767-771 !

Crit Care Med 2000; 28:2773-2778!
JAMA 2002; 288:1499-1507!
Drug, toxin, other!

Replacement with tumor, abnormal cell line, brosis!
Anticoagulated!
Substrate deciency - Fe, Folate, B12 - (9-10%)!
Sometimes on purpose, sometimes not!
Relative or absolute of erythropoietin (EPO) !
Have overt or occult blood loss!
Renal insufciency/failure!
GI bleed, during CPB, dialysis, pheresis!

Coagulopathic, bleeding diathesis!
Other, particularly inammatory processes!
Abnormal Erythropoiesis!
Crit Care Med 2000; 28:3098-99 "
Blunted EPO Response in the Critically Ill!
ICU pts frequently have !
Low Fe, TIBC, Fe/TIBC ratios, transferrin levels,

& increased ferritin!
Low or inadequate EPO levels!
Inammatory mediators (IL-1, IFN,

TNF, TGF) directly inhibit!
EPO gene transcription in renal JGA cells !

RBC production by the bone marrow!
Erythroid precursor cell response to EPO!
So, we have an acute anemia of acute disease!

Similar to the anemia of chronic disease!"
181
Inammatory mediators indirectly limit

Fe2+ availability by increasing Fe2+
sequestration in macrophages!
2!
1/30/16!
IACTACON 2016
Anemic benets -2"
Teleologic Reason for ICU Anemia?"
Advantage over the bugs !
Yes!!
Micro-organisms need Fe to reproduce !
Efciency !
Limits deleterious Fe driven processes !
Use energy & resources elsewhere!
Fenton & Haber-Weiss reactions !
Occur when Fe & 02 in close proximity!

Generate reactive 02 species - 02., H202, 0H., etc !
Lipid peroxidation, DNA injury, Sulfhydrylenzyme inhibition!
May exacerbate reperfusion ischemic injury !
Decrease viscosity!
Aids microcirculation, limits sludging!
Alters coagulation cascade!
May act as an anti-inammatory mechanism !

Limits thrombosis of acute disease!
May limit excessive pro-inam cascade"
Effects of Anemia in Normals"
Is Anemia Bad?"
Sometimes!
Decreased viscosity!
How do we tell when it is bad?!
CO, SV , may HR & myocardial V02 !
Thats the BIG & KEY question!
Are all pts vulnerable at same level of anemia?!
Tx pts with cerebrovascular or CV disease earlier?!
Young ASD pt vs. ACS vs. elderly CABG/Valve?!

Septic? COPD? TBI, Burn, other!
Improved microcirculation!
If so, who, when,, how much, with what? !
Alters blood clotting & platelet function !
O2 extraction ratio!
Tx -> Benet? !
Tolerance to Anemia - JAMA 1998; 279:217-221!
Should Anyone Be Transfused?"
ANH in 31 resting, healthy pts & volunteers!!!

Hemoglobin
CI
!
!
HR !
!
SVRI
!
D02 !
!
V02 !
!
No lactic acidosis!
ECG changes
!13.1
!3.05
!58
!2372
!13.5
!3.07
!
!
!
!
!
!
!
!5.0 g/dL!
!5.71 L/min/m2!
!92 bpm!
!1001dyn.s.cm-5.m2!
!10.7 ml/kg/min!
!3.42 ml/kg/min!
Evolving practices!
Recognize benecial outcome data

when tx limited - > not inferior, but
not consistent across populations!
Benets of anemia > risks of tx?!
1 patient (? rate-related)!
For all pts?!
Anesthesiology 2000; 92:1646-52 !
Dont cognate as well at a Hgb of 5 g/dL!
Cognition recovers if 02 supplemented to Pa02 >350!
Blind spots?!
Anesthesiology 2002; 96; 871-7!
182
3!
LECTURE
1/30/16!
Why Transfuse RBCs in the ICU?"
Why Transfuse?"
Corwin, et al. Chest 1995; 108:767-71 "
Increase O2 delivery (D02) !
Indications!
Increase cell mass/blood volume!
40% - no indication for transfusion !

25% low Hgb, 20% low output or suspected ischemia!
More transfusion !
Correct coagulation abnormalities/stop

bleeding!
longer ICU stay, ventilation, mortality!
Hebert PC, et al. Tx requirements in critical care:

a pilot study. JAMA 1995;273:1439-44 !
Make patient better!

Improve outcome short & long-term!
Multicenter - precursor to the multicenter TRICC trial!

35% txed for bleeding
25% to increase D02
Historical Tx Guidelines"
How Often Tx in ICU?"
Expert Opinion on Tx trigger"
Groeger, et al. Crit Care Med 1993; 21:279-291 !
NIH Consensus Conference - JAMA 1988!

Magic Hgb - 7, except CV disease!
1/7 medical patients/d receive a tx!
ACP - Ann Intern Med 116:403, 1992!
1/5 surgical patients/d receive a tx!
ABC trial. JAMA 2002; 288:1499-1507 - EUROPE !

47% of pts receive a tx during their ICU course!
TX on a unit-by-unit basis to relieve symptoms in acute blood

loss only after volume repletion with crystalloid!
Consider EPO for anemia of chronic disease!
ASA - Anesthesiology 1996; 84:732-42 & 2006:105: 198-208 !
CRIT trial. Crit Care Med 2004; 32:39-52 - US!
Hgb > 8, usually dont need, Hgb < 6, almost always need!
37% transfused during ICU course!
50% of ICU pts txed, if there > wk, get 5 u!
Transfusion Trigger Controversy"
ASP - Arch Pathol Lab Med 1998; 122:130!
In acute anemia almost always Tx for Hgb < 6 or for > 30 - 40%
blood loss, ideally use invasive monitoring to decide!
Blood Transfusion in the ICU"
Tx trigger Hgb/Hct value where risks of

decreased O2 carrying capacity exceed the
risks of tx!
Transfusion Requirement in Critical Care (TRICC)!

Hebert PC et al. Multicenter, PRCT of tx requirements
in critical care. TRICC Trials Group. N Engl J Med 1999;
340:409!
Empiric # not a lot of scientic basis!

Historically 10/30!
One trigger probably does not t all patients!
Randomized to !
Liberal (hgb >10) or !

Conservative (hgb 7-9) transfusion trigger!
Outcome: number & amount of tx,

complications, length of stay , & survival!
The tx trigger may not be the same as the

optimal hematocrit!
183
4!
1/30/16!
IACTACON 2016
Others report conservative tx approach ok!

(at least non-inferior)"
More HISTORY - TRICC Trial Results!

Hgb in restrictive (8.5) vs. liberal(10.7) tx!
Blood txs in restrictive pts!
2.6 vs. 5.6 units (54%), none in 1/3 restricted!

All results favored restrictive strategy!
Trend towards !
30 day mortality (19% vs. 23%)!
hospital mortality (22% vs. 28%)!
ICU mortality (14% vs. 16%)!
organ failure score (8.3 vs. 8.8)!
FOCUS - Carson J, et al (2011) Liberal or restrictive

tx in high-risk patients after hip surgery. NEJM
365:245362 !
Older with Hx of CV disease, but no prolonged Hgb < 9 !
TRISS - Holst LB, et al (2014) Lower vs higher hgb

threshold for tx in septic shock. NEJM 371:138191 !
Few CT/CVM pts!
Am J Med 2014;127:124-31.e3. !
Meta-analysis 2500 pts 3 trials less CV,

rebleed, infection!
Survival if <55 y/o & less ill & tranfused!

Subsequent subgroup analyses!
TRISS - Time to Death & Relative Risk of Death at 90 Days!
Transfusion Guidelines"
Practice Guidelines for Perioperative Blood Rx: An
Updated Report by the ASA Task Force on Periop Blood
Management. Anesthesiology 2015;122:241-75!
Use adjunct medications to prevent &/or Rx bleeding!
Greater use of pharmacologic therapies to minimize
blood txs, EPO for anemia, PCC for urgent reversal of
warfarin, & intraop TXA for selected cardiac/
noncardiac procedures with high risk bleeding!
Advocates use of Tx algorithms, especially TEG,
blood ordering schedules, & restrictive transfusion
strategies !!
Holst LB et al. N Engl J Med 2014;371:1381-1391."
STS Transfusion Guidelines!
Recognize Preop Risk Factors for

Periop/Post op Tx in CT Patients"
Ann Thorac Surg 2011;91:944-82. doi: 10.1016/

j.athoracsur.2010.11.078"
1) Advanced age!
2) Low RBC volume (preop anemia or low BMI) !
3) Preop anticoagulation or antiplatelet rx!
4) Urgent or emergent operation!
5) Anticipated prolonged duration CP bypass!
6) Certain co-morbidities -> CHF, COPD, CKD!
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1/30/16!
2011 STS Guidelines Emphasize Teamwork

in Blood Management & the Following"
STS Guidelines"
1) Management of preop dual anti-platelet Rx!

2) Use of drugs to augment RBC volume/limit loss !
Number of units transfused in CT

surgerical patients increasing despite
conservative practices!
3) Use of blood derivatives FFP, Factor XIII,

leukoreduced RBCs, platelet plasmapheresis,
rFactor VII, AT III, & Factor IX concentrates !
Especially reops, AVRs, VADs!
4) Enhanced blood salvage!
On pump pts receive more blood than off!
5) Use of minimally invasive procedures as able!
6) Enhanced blood conservation in ECMO & CPB!

7) Use of topical hemostatic agents!
Lancet Haematol 2015: 2: e54353!
Complications of Transfusions"
Infection!
Immune modulation!
Volume Overload!
Anaphylaxis!
Storage defects!
Clerical errors!
Murphy G, et al. Liberal or restrictive tx after cardiac surgery. NEJM 2015;372:997-1008!
Infection"
Huge driving force with onset of AIDS
epidemic!
15 m RBC, 5-7 m Pl, 2 m FFP!
Viral, bacterial, parasitic, other!

Immune modulation lymphocyte/WBC!
Able to make blood supply v. safe, but costly!

Donor screening/selection!
NAT!
Other!
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IACTACON 2016
VOLUME - Transfusion-Associated"
Circulatory Overload (TACO)"
Transfusion-Associated !
Acute Respiratory Failure"
TACO!
Cardiogenic pulmonary edema!
TRALI!
Occurs < 6 hr after transfusion (FFP)!

Occurs after 1-8% of blood transfusions!
Anaphylaxis!
Severity: mild to life-threatening (20%)!
Blood borne sepsis (contamination)!
Increased ICU and hospital LOS!
Hemolytic transfusion reaction (mismatch)!
TACO Risk Factors"
Cardiac Volume Sensitivity"

Pre-existing uid overload!
Infusion of multiple blood products!
Age > 70 yrs, female gender, small staure!

Severe decompensated anemia!
High total volume infused (relative)!
LV failure, CHF!
Rapid rate of infusion (300-900 mL/hr)!
Chronic kidney disease (CKD)!
Cardiac volume sensitivity (tipping point)!
CV instability on vasopressors!
Criteria for TACO!
CDC National Healthcare Safety Network!

Any 3 of the following!
Acute Respiratory Distress!
Occurs 3 6 h after transfusion!
Positive uid balance!
Elevated CVP!
Elevated BNP > 1200 pg.mL!
Pulmonary edema on CXR!
Prevention & Treatment of TACO"

Awareness of risk factors!
Close evaluation of uid status!
Restrictive uid volume administration!
Restrictive volume infusion rate/use of infusers!
Management is supportive as for cardiogenic
edema + judicious use of diuresis!
Transfus Med Rev 2013;27:105-12. !
doi: 10.1016/j.tmrv.2013.02.001. !
Signs of Left heart failure!
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Immune & Non-Immune"
Transfusion Related Acute Lung Injury (TRALI)"

Non-cardiogenic pulmonary edema!
1/30/16!
Triulzi DJ. Transfusion-related acute lung injury

(TRALI) current concepts for the clinician.!
Anesth Analg 2009; 108:770-6"
Most common major tx reaction !
Occurs 1-2 hr after transfusion!
1/3 of tx related deaths!
Under-recognized like TACO!
1/500 - 1/5,000 units, any tx, most often RBCs/platelets!
Relatively high mortality!
Thought rare (0.04 0.1%), but ICU tx pts -> 5 8%!

ALI with SIRS!
Hypoxia & bilateral pulmonary edema occurring

during or within 6 h of a tx in absence of CHF or
TACO!
Mechanism(s)!
Leukocyte antibody!
!- hypotension, low CVP, fever, leukocytosis!
Double hit model!
May occur simultaneously with TACO!
5 - 10 % mortality!
+/- prior history of transfusion reaction!
The Neutrophil & TRALI"
TRALI Risk Factors"

Cellular blood products (RBC, platelets)!
Older blood products!
Sepsis!
Cardiac disease!
Hematologic malignancy!
Liver transplant patients!
Thrombotic thrombocytopenia purpura (TTP)!
TRALI: Prevention"
TRALI: Work up"
FFP from male or nulliparous females!
Identify blood components transfused!
multiparous females have highest antibody titer!
Notify blood bank/transfusion service!
Leukoreduction of RBCs, platelets!
Obtain blood samples!
removal of white cells!
HNA / HLA type & cross match!

Screen for antibodies in donor, recipient!
Pool FFP from multiple donors!
Should not again donate!
Administer platelets within 3-5 days!

Avoid prolonged storage of blood products!
dilute HLA / HNA antibodies present!
Inform donor if antibodies identied!
accumulation of bioactive lipids!
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IACTACON 2016
Presentation!
TRALI: Treatment"
TACO!
TRALI!
Temperature!
Usually normal!
1/3 febrile!
BP!
Often elevated!
NL or low!
Respiratory status!
Acute Dyspnea!
Acute Dyspnea!
Auscultation !
Rales + S3!
Rales !
Chest x-ray!
Diffuse bilateral inltrates! Diffuse bilateral inltrates!
Ejection fraction!
Usually decreased!
Normal!
PAOP!
Elevated!
< 18 mm Hg!
Invasive vs. non-invasive ventilation!
Pulmonary edema uid!
Transudate!
Exudate!
Fluid balance!
Net positive!
Usually negative or neutral!
Judicious volume since often

hypovolemic and hypotensive!
Response to diuretics!
Marked improvement !
Inconsistent!
White blood cell count!
Unchanged!
BNP!
> 1200 pg/mL!
Transient leukopenia may

be present!
Again supportive as for other causes of

ALI/ARDS!
Steroids no specic role!
< 250 mg/mL!
Modied from Robert Sladen, MD presentation and Up-to-Date!
Addl points of interest with RBCs"

TACO!
TRALI!
1 8%!
Variable!
3 6 h!
1 2 h!
Pathogenesis!
Volume overload!
Cardiac echo!
Volume overload!
ALI immune & nonimmune mechanisms !
Systemic
inammation!
Absent!
Incidence!
Onset!
Impact of age of blood !

RECESS !
Steiner ME, et al. ,Effects of red-cell storage

duration on pts undergoing cardiac surgery. NEJM
2015; 372:1419-29. doi: 10.1056/NEJMoa1414219.!
US, CTS pts, <7 d, 2 4 weeks, none > 5 weeks!
Underlled!
ABLE"
Prominent!
Lacroix J, et al. Age of Transfused Blood in

Critically Il Adults N Engl J Med 2015;372:1410-8
DOI: 10.1056/NEJMoa1500704!
Canada& Europe 64 cts, < 8 d vs. standard!
Addl Points"
Methods to reduce ICU transfusions"
Massive Transfusions"
Holcomb J, et al. Transfusion of plasma, platelets,

& RBCs in a 1:1:1 vs a 1:1:2 ratio & mortality in
patients with severe trauma: the PROPPR
randomized clinical trial. JAMA 2015;313:471-82.
doi: 10.1001/jama.2015.12.!
Reduce blood sample size (point of care)!

Return dead space blood loss!
Reduce number of indwelling catheters!
Eliminate standing orders for blood tests!
No diff in 1:1:1 vs 1:1:2!
The Trauma- Formula-Driven Vs. Lab-Guided Study

(TRFL Study) Study on 1:1:1 therapy!
Tolerate anemia!
rHuEPO??!
Myocardial Ischemia & Transfusion (MINT) trial!

Am Heart J 2013;165:964-71 Feasibility study 110 pts!
Suggested benet to liberal tx, need follow up!
O2 carrying solutions??!
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1/30/16!
So, what about alternatives"

HuR(EPO)!
Anemia acute & 2nd to

EPO & RBC
production.!
Why not use EPO?!
NEJM 2007; 357:965-76!
Benet only trauma pts!

thrombotic risk!
CMAJ 2007;177: 725-34!
Blood substitutes / Hgb

based 02 carriers (HBOC)!
Colloid/other that carries 02!

Unlimited supply!
No immune/infectious risk !
Easy to store!
Close, but no cigar!
Limits !
Meta-analysis - no benet!
Non RBC transfusions"
Short life!
NO binding!
Other, none approved!
HBOCs : indications &

future. Applications. Br J
Hosp Med 2015 76:78-83. "
Fresh Frozen Plasma (FFP)"

Whats in it?!
What is FFP S/D?!
When should we administer FFP?!
Factor! Name!
1/2 life! Synthesis! Vit K dep!
I!
1 - 6 d!
Fibrinogen!
II!
Prothrombin!
II!
Bleeding with INR/aPTT? !
Tissue factor!
IV!
Calcium!
VII!
Proconvertin!
V!
Invasive procedure with INR/aPTT? !
Proaccelerin!
VIII!
Reverse anticoagulant - warfarin?!
IX!
Correct bleeding from diffuse deciency of

multiple coag factors (DIC, liver disease,
dilutional)?!
X!
XI!
XII!
Reverse vitamin K deciency?!
XIII!
Plasma exchange for TTP/HUS, other?!
Antihemophilic!
Christmas!
Stuart-Prower!
Thromboplastin!
Hageman!
Fibrin stabilizer!
12-24h!
????!
12-24h!
1-5h!
9-18h!
15-24h!
2-9h!
40-80h!
48-52h!
5-12h!
L!
L!
N!
Y!
Endothelial! N!
L!
L!
RES!
L!
L!
L!
L!
L!
N!
Y!
N!
Y!
Y!
N!
N!
N!
Evidence-based guidelines for FFP.

Transfusion 2010;50:1227-39. Epub 3/19."
FFP - 3rd most often TX product"
FFP tx to pts requiring massive tx !
> 1/3 of FFP infused to correct an INR/PT!

NO PRCT to support this !
Just assume!
INR/PT grt bleeding!

Prophylactic FFP corrects INR/PT!
Assume transfusion reduces bleeding!
No rec for or against tx of plasma at a FFP : RBC ratio

of 1:3 or more!
Couldnt recommend for or against FFP tx to pts

undergoing surgery in absence of massive tx !
FFP tx in pts with warfarin therapyrelated
intracranial hemorrhage!
Not recommend for or against FFP transfusion of
plasma to reverse warfarin anticoagulation in pts
without intracranial hemorrhage. !
Suggested against FFP for other selected pt

groups!
Holland LL, BrookJP. Am J Clin Path 2006;126:1-7!
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10!
IACTACON 2016
Improper use of FFP"
1/30/16!
Platelets 2nd Most Commonly Tx Product"

Thrombocytopenia!
As a volume expander!
As a nutritional source!
Enhance immune function/healing!
Increased use/destruction!
Decreased production!
Sequestration/dilution!
Not suitable as replacement for

hypogammglobulinemia!
Thrombocytopathy!
Medication!
To replace mild to moderately

prolonged INR/PT/aPTT prior to
invasive procedures!
Platelet transfusion"
2nd to disease!
Therapeutic !
Pump/CV procedure related"
Summary!
Anemia frequent in CT surgery/critically ill pts !
Blood loss !
Limit the iatrogenic component -- - > phlebotomy !
Bleeding with low platelets (surgical

bleeding rarely occurs if pl ct > 50k)!
High risk for bleeding from low platelets
(spontaneous bleeding risk increases when
pl ct is < 10k)!
Surviving sepsis campaign advise Tx if < 5,000!
Look for occult loss CT surg related!
Dilution!
Lack of production !
Primary process - anemia of inammatory disease!
Hemolysis!
Anemia well-tolerated in majority of pts !

Optimal Hgb unknown!
Selected thrombocytopathies!
Appropriate transfusion trigger unknown !
Avoid if HUS/TTP"
Does need to tx differ between pts & disease states?!
Summary (II)!
Tx common in OR/ICU!
1/3 - 1/2 of ICU pts, indications often unclear!
Longer ICU stay - tx, mech vent & mortality!
Txs in critically ill may not improve outcome, may

be harmful!
Tx mediated infection, immune modulation, volume
overload, transfusion reaction, etc!
rHuEPO can the need for RBC txs in some

settings, including SICU, doesnt improve survival!
Use products on individualized basis!
Difcult to dene & apply universally

accepted guideline!
Susceptibility of pts to anemia is as
individual as the pt & complicated by the
pts comorbidity!
Unlikely that a value or number, be it
Hgb or DO2, universally applicable to all!
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LECTURE
Tx Practice in the ICU"
Final Thoughts"
No clear data that tx improves outcome

with ALI/ARDS or enhances weaning!
Human error remains greatest risk

to recipients of blood!
No data improves outcome in sepsis!
Hemovigilance!
1/30/16!
Similar to medication/surg site error!

Use of newer technologies!
Team approach!
Bar coding, other!
Use in ACS/MI still under evaluation!
Indian Society of Blood Transfusion &

Immunohaematology (ISBTI)"
Safe blood should be waiting for
the patient not the patient
should be waiting for the safe
blood!
191
12!
IACTACON 2016
Peter H Norman BSc MD FRCPC
Professor of Anesthesiology and Perioperative Medicine

Professor of Thoracic and Cardiovascular Surgery
UT MD Anderson Cancer Center
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LECTURE
}
}
}
Current Literature Review and Recommendations

BLS, ACLS
A few cases from over the years
}
}
Bilateral pneumothorax
Repeated respiratory arrest
What is the rhythm?
Hypertensive crisis
Amiodarone?
VT or SVT+Aberrancy?
Post Pneumonectomy Syndrome

IMHO
193
IACTACON 2016
6382 postop CPR in 1.3 million surgeries

} 1:203 cases
}
1:2174 0 comorbidity
1:699 1 comorbidity
1:95
2+ comorbidities
Overall 30 day mortality 1.7%, if CPR 71.6%

} 9% of intraoperative arrests had postop CPR
} Mortality intraoperative arrest 61.1%
} 37% of intraoperative arrests discharged alive
} 17% of postoperative arrests discharged alive
}
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LECTURE
195
IACTACON 2016
2 cases of postoperative CVICU arrest

} Both ECP initiated after 60 minutes
} 1st case postop arrest in CVICU, open
massage to OR, OM occluded. Regrafted.
} 2nd case VF and catheterization + IABP. 3
hours later refractory VF. To OR urgent
bypass. LAD + OM + ECMO
} Both discharged home neurologically intact.
}
COPD patient intubated and sent to ICU

} Coughing on ventilator
} Physician-on-call unaware of admission
} Suddenly no BP and unable to ventilate
} Physician called and arrives in 2 minutes
} Diagnosis?
}
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LECTURE
18 year old male after syringomyelia repair

} Postoperative ventilation
} Extubated at 24 hours, good mechanics
} Respiratory arrest 3 days later
} Reintubated, full recovery in hours, extubated
} Respiratory arrest 3 days later
} Several more cycles
} What is the diagnosis?
}
Failure of Autonomic control

} Congenital Central Hypoventilation Syndrome
} Usually fatal
} Acquired Central Hypoventilation Syndrome
}
Following trauma or surgery

Cuirass ventilator?
The 72 hrs. is how long you can stay awake.
Cardiac mapping for recurrent arrythmias

} Unusual rhythm postoperative day 1
} Cardiac surgeon present. Upset
} Many 12-lead EKGs
} Two cardiac electrophysiologists present
} More 12-lead EKGs
} Much wailing and gnashing of teeth
} Colleague stopped it cold
}
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IACTACON 2016
Colleague suggested turning off the

temporary transthoracic pacer..
Does suggest when all else fails to examine
the patient
Postoperative AVR in CVICU

} Being admitted
} Blood pressure 210/120..will the aorta hold?
} Beta blockade and nitroprusside not working
} Surgeon having a canary
} Yelling at anesthesiologist who did the case
} Anesthesiologist yelling back
}
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LECTURE
End Stage Cardiac Disease on amiodarone

} Cardiac transplant
} Initially does well
} Heart rate maintained by isoproterenol
} Gradual HR slowing and decreased output
} Epinephrine added
} Norepinephrine added
} Dies POD #3
} No autopsy
}
I listened to the patients chest

} No air entry
} Ventilator had not been turned on
} A flick of the switch and no BP problem
}
Cardiac Surgeon:
Missed CAD in transplanted heart

Ultrarapid rejection
Or would it be possible for amiodarone to

leach out from tissues and poison the
transplanted heart?
199
IACTACON 2016
Postoperative CABG
} Arrives in CVICU on dopamine, balloon pump
} BP adequate, HR 120
} Wide complex rhythm, regular
} Anes: SVT + aberrancy
} Me: VT + synchronized balloon pump
} 12-lead EKG done
}
VPB
early
compensatory pause
bizarre
retrograde P
LAD when in VT
concordance (V1=V6)
pause when converts
Aberrancy
P wave
RBBB
same initial deflection as nsr
triphasic V1, V6
Ashmans (as RR, aberrancy)
discordant (V1V6)
no pause when converts
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LECTURE
57 year old male right pneumonectomy 2011

} Active until late 2015
} Intermittent respiratory failure
} Ventilated with difficulty removing CO2
} Planned thoracotomy for saline implants
} Difficult surgery due to anatomy
} Despite 2X normal ventilation pCO2 in the 70s
} Ventilated postoperatively
} Further thoracotomy, tracheostomy
} Died 3 weeks postoperatively, ? hemorrhage
}
Described in 1978 in a child with bronchial

compression after pneumonectomy
} 1:640 pneumonectomies
} Median onset 7.5 years (1.1 to 54.8)
} Both right and left
} Torsion/compression of mediastinum
} Saline implants or other volume therapy?
}
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IACTACON 2016
Arrest either cardiac or other is unusual

} BLS or ACLS is not helpful
} Norepinephrine and octreotide are helpful
} Need to know the immediate past history
} Physical examination is essential
} Also examine the surroundings
}
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LECTURE
Shen KR, Wain JC, Wright CD, Grillo HC, Methisen DJ.
Postpneumonectomy syndrome: Surgical management and
long-term results.
J Thorac Cardiovasc Surg 2008;135:1210-9
Bdard ELR, Uy K, Keshavjee S. Postpneumonectomy
Syndrome: A Spectrum of Clinical Presentations
Ann Thorac Surg 2007;83:1185 8
Shamji FM, Deslauriers J, Daniel TM, Matzinger FR, Mehran R,
Todd TRJ. Postpneumonectomy Syndrome With an Ipsilateral
Aortic Arch After Left Pneumonectomy
Ann Thorac Surg1996;62:1627-31
203
IACTACON 2016
JANAK MEHTA AWARD PAPERS
IACTACON
Chennai 2016
204
janak mehta AWARD PAPERS
COMPARISON BETWEEN NON INVASIVE MEASUREMENT

OF CENTRAL VENOUS PRESSURE USING NEAR INFRARED
SPECTROSCOPY WITH AN INVASIVE CENTRAL VENOUS
PRESSURE MONITORING IN CARDIAC SURGICAL ICU.
Dr N. Sathish, Dr Nagaraja P S, Dr Naveen G Singh, Dr. Sarala B M , Dr Manjunath N
Department of Cardiac Anaesthesiology,
Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bangalore
Abstract:
Introduction:
Central venous pressure (CVP) measurement is essential in management of clinical situations, including cardiac
failure, volume overload and sepsis. CVP measurement requires catheterization of central vein which is invasive &
leads to complications. Aim the study was to evaluate the accuracy of measurement of CVP using a new non invasive
method based on near infrared spectroscopy (NIRS) in a group of cardiac surgical intensive care unit (ICU) patients.
Methodology:
Thirty patients in cardiac surgical ICU were enrolled in the study who had in situ central venous catheter (CVC). Sixty
measurements were recorded in one hour in each patient. A total of 1800 values were compared between non invasive
CVP (CVPn) obtained from Mespere Venus 2000 CVP System and invasive CVP (CVPi) obtained from CVC.
Result:
Strong positive correlation was found between CVPi and CVPn (R=0.9272,p<0.0001). Linear regression equation
- CVPi=0.5404+ 0.8875 X CVPn (r2=0.86, p<0.001) Bland-Altman bias plots showed mean difference SD and
LOA: -0.311.36 and 2.99 to +2.37. (CVPi CVPn).
Conclusion:
Non invasive assessment of the central venous pressure based on NIRS yields readings consistently close to those
measured invasively. Non invasive CVP may be a clinically useful substitute for invasive CVP measurements which is
also simple and continuous. It is a promising tool for early management of acute states where in knowledge of CVP
is helpful.
Key words:
Central venous pressure, near infrared spectroscopy, cardiac Preload
Introduction:
Central venous pressure (CVP) measurement is essential for assessment of preload and volume status 1
in peri operative management of cardiac patients and intensive care unit (ICU). CVP estimation guides
in the management of critical ill patients with congestive cardiac failure, cardiogenic shock, sepsis and
others.2,3 Clinical estimation of CVP may not be reliable when compared with invasive monitoring of CVP
using a catheter in superior vena cava (SVC) and right atrium (RA) junction though internal jugular vein
(IJV) or subclavian vein (SCV) approach.4 Invasive placement of CVP catheter is time consuming and
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IACTACON 2016
complications associated with it are not uncommon.5 Hence a quick and reliable tool for measuring CVP
without central venous access might be helpful.
Previous studies have reported the use of non invasive and minimal invasive methods to assess CVP. But
non invasive methods lack the accuracy and precision for routine use and minimal invasive techniques
which include cannulating peripheral limb veins, external jugular vein (EJV) have shown mixed results when
compared with invasive CVP.6-15
In the present era of ultra fast tracking in cardiac surgery, there is a need for a reliable non invasive CVP
monitor mostly in high dependency units where the patients are not with in-situ invasive CVP catheters.
Hence the purpose of the present study was to evaluate the correlation, accuracy and agreement for
measuring CVP using a new non invasive method - Mespere Venus 2000 CVP System, based on near
infrared spectroscopy (NIRS) in a group of cardiac surgical intensive care unit patients.
Methodology:
After obtaining institutional ethics committee clearance 30 patients who were admitted in post operative cardiac
surgical intensive care unit (ICU) were enrolled in the study. Informed consent was obtained from these patients
before the procedure. Inclusion criteria were patients above 18 yrs of age who had an indwelling central venous
catheter (CVC) placed either in IJV or SCV, during peri operative period of cardiac surgery. Exclusion criteria were low cardiac output patients, allergic to medical grade adhesive tape and EJV thrombosis.
CVC was placed in each patient after induction of anaesthesia into either IJV or SCV (CVPi), which was used for
continuous monitoring during peri operative period. CVC was connected to a transducer that was calibrated at the
level of the patients right atrium. The tubing and transducer were inspected to ensure that there were no technical
issues or air bubbles that could cause erroneous recordings.
Mespere VENUS 2000 central venous pressure system (CVPn) consists of 5 components CVP sensor, CVP
sensor patch, reference patch, docking station and a display monitor (Figure 1A & 1B). CVP Sensor consists of light
emitting diode / photo detector (LED/PD), sensor tube with a stopcock cap and connecting cables. It is to be placed
superficially on EJV with help of sensor patch. Reference patch holder is used to connect reference patch to sensor
tube of the VENUS 2000 CVP sensor. Reference patch is placed on reference point (zero reference) i.e. phlebostatic
axis (PA) or sternal angle of Louis. Phlebostatic Axis is used to estimate the position of SVC-RA. It is commonly
used as the zero reference point when using a CVP catheter which is at the intersection of the 4th intercostal space and
the mid axillary line. Docking station consists of two points required for the calibration of the CVP sensor. Display
monitor displays CVP either in cms of H20 or mmHg, pulse strength index (P.I) which should be greater than one,
plethysmographic waveform and trend display area.
After calibration of the VENUS CVP sensor, it was placed on EJV with patient inclined between 150 to 300 with
head slightly tilted to left. Meniscus of the liquid present in the sensor tube should be between the two clips of the
reference patch holder. This reference patch holder was later stuck on to reference patch at the PA. Care to be taken
to see that stopcock present at the end of sensor tube is kept open during measurement of CVP. Later sensor was
connected using cables to the display monitor. Display monitor was switched on, which displayed the CVP number
and plethysmographic waveform.
Simultaneous CVP measurements were obtained from CVC placed invasively (CVPi) and from Mespere VENUS
2000 central venous pressure system (CVPn) from 30 patients. Total of 60 values were recorded per patient over a
period of 60 mins. No clinical decision was made on the values obtained from CVPn.
Statistical analysis was done using MedCalc version 11.3.0.0. CVPi and CVPn values were analyzed by Pearson
test of correlation (R) to determine the strength of relationship between the values. Correlation co-efficient values
range from negatively correlated (1) to uncorrelated (0) to positively correlated (+1). (0.0 is no association, +0.2
is weakly positive, +0.5 is moderately positive, +0.8 is strongly positive, +1.0 is perfectly positive).
Linear regression analysis was used to calculate the regression equation between CVPi and CVPn. The coefficient
of determination (r2) is the proportion of variation in the dependent variable explained by a linear regression
model using the independent variable. For all analysis, P < 0.05 was considered statistically significant.
206
BlandAltman analysis16 was used to find the agreement between CVPi and CVPn . The (CVPi CVPn) difference
versus the average value ([CVPi + CPVn]/2) was plotted. Means, standard deviations (SDs), and 95% prediction
intervals (limits of agreement) were evaluated. The limit of agreement (LOA) was calculated as a bias +2SD.
Results:
A total of 30 patients (22 males and 8 females) were included in the study. The average age being 43+/-17 yrs (range
from 18-73 yrs). Out of 30 patients, 3 patients were post-operative closure of atrial septal defect, five aortic valve
replacement(AVR), ten coronary artery bypass surgery(CABG), 8 mitral valve replacement (MVR) and 4 patients
were pre operative moderate to severe (two each) tricuspid regurgitation patients with mitral valve involvement.
Total of 1800 values were analyzed (i.e. 60 values per subject). Invasive CVP value ranged from 2 to 19 mmHg.
A strong positive correlation was found between CVPi and CVPn with R value = 0.9272 (C.I 0.92 to 0.93) and
was statistically significant (p<0.0001). Linear regression equation was derived to estimate CVPi values from CVPn
values i.e. CVPi = 0.5404+ 0.8875 X CVPn (r2=0.86, p<0.001) (Figure 2A). Bland-Altman bias plots showed mean
difference SD and LOA: -0.311.36 and 2.99 to +2.37. (CVPi CVPn). This means that there is 95% chance of
predicted CVPi value to lie within LOA of CVPn value (Figure 2B)
Discussion:
The principle of NIRS has been widely used in various monitoring devices during cardiac surgery like Swan Ganz
monitoring catheter, Spo2 plethysmograph and CNAP (Continuous non invasive arterial pressure) smart pod17.
Mespere VENUS 2000 central venous pressure system which is used in the present study to monitor non invasive
CVP is also based on NIRS technology. It uses single wavelength LED and photo detectors to detect changes in the
blood volume. It detects the jugular venous pulse (JVP) in the neck and the height of the JVP column relative to
the superior vena cava which requires that the patient sits at a proper inclination angle so the top of JVP pulse
lies in the range of the Sensor.
The ability to non-invasively, reliably and continuously measure CVP to assess the preload status in post operative
cardiac patients could lead to the promising role of non invasive CVP in the development of novel protocols for
the treatment of patients with fluid sensitive conditions. The majority of other non-invasive measures of CVP,
such as ultrasound of the inferior vena cava or the passive leg raise technique are not continuous measures and
dependent on the clinician skill and are subjective. However, there are methods to monitor CVP continuously
but are invasive. In the present study, non invasive CVP monitor is simple, continuous, and reproducible.
Estimation of CVP by physical examination of visible JVP pulse is mostly done by an experienced clinician.
Certain conditions like tricuspid regurgitation, atrial fibrillation where in wave forms of JVP are altered
could mislead the clinician for an accurate measurement of CVP.18
Recent few studies have shown good correlation between invasively measured peripheral venous pressures (PVP) and
CVP.19-21 However there are conflicting results exhibited between PVP and CVP. Study by Kumar et al22 showed poor
correlation (R=0.092 at baseline and R=0.038 at passive leg raise) and unacceptable limits of agreement (1.57111.780 at base line and 3.180-11.35 at passive leg raise) between invasive PVP and CVP, in group of patients where
CVP was less than 10 mmHg. Thalhammer et al14 showed acceptable correlation (R=0.85) and acceptable bias (-0.7)
and LOA (-8.7 to 8.7) between non invasive PVP and invasive CVP measured at heart level. In the present study mean
difference and LOA were -0.31 and 2.99 to +2.37 respectively. Peripheral measurement might be inappropriate in
patients who have inadequate visible veins or as a result of multiple venous punctures. It is also non continuous with
possibility of observers bias when measured using sonographic technique.
Ward KR et al23 has studied impedance based technique for the assessment of CVP and showed that mean difference
of -0.26mmHg, LOA of -2.7 to 2.2, with correlation value of 0.95 which is similar to the present study which is non
invasive and continuous. CVP measurement by impedance method is non invasive but is not continuous.
A clinically acceptable LOA was defined as 4cm of H2o (or 3mm Hg) between CVP and PVP which was comparable
with the present study.20 PVP measured at cephalic, basilic and brachial veins had a good correlation with SVC due
to low resistance to venous return.13 In a similar manner EJV is in continuity with SVC and also reflects the SVC
pressure.
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Xing et al24 reported a new method for non invasive quantification of CVP, where centre of the right atrium and both
collapse points of IJV were located using ultrasound. Their study showed bias of 0.22 mmHg with LOA of -2.16 to
2.59 during preoperative measurement which was comparable to the present study.
Non invasive continuous monitoring of CVP could dictate the management strategy in HDU where invasive lines are
not available. Since it adopts NIRS technology it does not require much expertise to interpret the values.
Conclusion:
Non-invasive CVP based on NIRS technology is simple, continuous, reliable and reproducible method to estimate
CVP in post operative cardiac surgical patients.
References:
1. Magder S. Central venous pressure monitoring. Curr Opin Crit Care 2006;12:21927.
2. Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, et al. Surviving Sepsis Campaign: international
guidelines for management of severe sepsis and septic shock. Crit Care Med 2008; 36:296-327.
3. Stevenson LW, Perloff JK. The limited reliability of physical signs for estimating hemodynamics in chronic heart
failure. JAMA 1989; 261:884-8.
4. McGee SR. Physical examination of venous pressure: a critical review. Am Heart J 1998;136:108.
5. Schroeder RA, Barbeito A, Bar Yosef S, Mark JB. Millers Anesthesia. 7th ed. New York: Churchill Livingstone
Inc.; 2009.
6. Baumann UA, Marquis C, Stoupis C, Willenberg TA, Takala J, Jakob SM. Estimation of central venous pressure
by ultrasound. Resuscitation 2005;64: 193-9.
7. Charalambous C, Barker TA, Zipitis CS, Siddique I, Swindell R, Jackson R, et al. Comparison of peripheral and
central venous pressures in critically Ill patients. Anaesth Intensive Care 2003; 31:34-9.
8. Marcelino P, Fernandes AP, Marum S, Ribeiro JP. Non-invasive evaluation of central venous pressure by
echocardiography. Rev Port Cardiol 2002; 21:125-33.
9. Ritter S, Tani LY, Shaddy RE, Day RW, Orsmond GS, Pagotto LT et al. Can Doppler systemic venous flow
indices predict central venous pressure in children? Echocardiography 2000;17:127-32.
10. Bloch KE, Krieger BP, Sackner MA. Noninvasive measurement of central venous pressure by neck inductive
plethysmography. Chest 1991;100:371-5.
11. Jue J, Chung W, Schiller NB. Does inferior vena cava size predict right atrial pressures in patients receiving
mechanical ventilation? J Am Soc Echocardiogr 1992;5:613-9.
12. Lipton B. Estimation of central venous pressure by ultrasound of the internal jugular vein. Am J Emerg Med
2000; 18:432-4.
13. Ricksten SE, Medegard A, Curelaru I, Gustavsson B, Linder LE. Estimation of central venous pressure by
measurement of proximal axillary venous pressure using a half-way catheter. Acta Anaesthesiol Scand 1986;
30:13-7.
14. Thalhammer C, Aschwanden M, Odermatt A, Baumann UA, Imfeld S, Bilecen D, et al. Noninvasive central
venous pressure measurement by controlled compression sonography at the forearm. J Am Coll Cardiol 2007;
50: 1584-9.
15. Briscoe CE. A comparison of jugular and central venous pressure measurements during anaesthesia. Br J Anaesth
1973; 45:173-8.
16. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement.
Lancet 1986; 1:30710.
208
17. Jagadeesh AM, Singh NG, Mahankali S. A comparison of a continuous noninvasive arterial pressure (CNAP)
monitor with an invasive arterial blood pressure monitor in the cardiac surgical ICU. Ann Card Anaesth
2012;15:1804.
18. Rizkallah J, Jack M, Saeed M, Shafer LA, Vo M, Tam J. Non-invasive bedside assessment of central venous
pressure: scanning into the future. PLoS One 2014;9:e109215.
19. Amar D, Melendez JA, Zhang H, Dobres C, Leung DH, Padilla RE. Correlation of peripheral venous pressure
and central venous pressure in surgical patients. J Cardiothorac Vasc Anesth 2001;15:40 3.
20. Desjardins R,Denault AY,Blisle S,Carrier M,Babin D,Lvesque S, et al. Can peripheral venous pressure be
interchangeable with central venous pressure in patients undergoing cardiac surgery? Intensive Care Med 2004;
30:62732.
21. Tobias JD, Johnson JO. Measurement of central venous pressure from a peripheral vein in infants and children.
Pediatr Emerg Care 2003;19: 42830.
22. Kumar D, Ahmed SM, Ali S, Ray U, Varshney A, Doley K. Correlation between central venous pressure and
peripheral venous pressure with passive leg raise in patients on mechanical ventilation. Indian J Crit Care Med
2015; 19:648-54.
23. Ward KR,Tiba MH,Draucker GT,Proffitt EK,Barbee RW,Gunnerson KJ, et al. A novel noninvasive impedancebased technique for central venous pressure measurement. Shock 2010; 33:269-73.
24. XingCY,Liu YL,Zhao ML,Yang RJ,Duan YY,Zhang LH, et al. New method for noninvasive quantification of
central venous pressure by ultrasound. Circ Cardiovasc Imaging 2015;8:e003085.
Figure 1A: A- Sensor, B- Reference patch and holder, Sensor tube with a stopcock cap, C- Connecting
cables from CVP sensor to display monitor.
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Figure 1B: Non invasive CVP (Mespere VENUS 2000) display monitor and Invasive CVP display monitor.
Figure2: A- Linear regression analysis & B- Bland Altman analysis between CVPi and CVPn
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FEASIBILITY OF MEASURING SUPERIOR MESENTERIC

ARTERY BLOOD FLOW DURING CARDIAC SURGERY
UNDER HYPOTHERMIC CARDIOPULMONARY BYPASS
USING TRANS ESOPHAGEAL ECHOCARDIOGRAPHY AN
OBSERVATIONAL STUDY.
Dr Nagaraja P S, Dr Naveen G Singh, Dr Divya Gopal, Dr Manjunath N
Abstract:
Background: Abdominal complications being rare but results in a high mortality, commonly due to splanchnic organ
hypoperfussion during peri operative period of cardiac surgery. There are no feasible methods to monitor intra
operative superior mesenteric artery blood flow (SAMBF). Hence aim of the study was to evaluate the feasibility
and to measure SAMBF using trans esophageal echocardiography (TEE) during cardiac surgery under hypothermic
cardio pulmonary bypass (CPB).
Methods:
Thirty five patients undergoing elective cardiac surgery under CPB were enrolled. Heart rate, Mean arterial pressure
(MAP), cardiac output (CO), and SMABF, superior mesenteric artery (SMA) diameter, SMA/CO ratio and arterial
blood lactates were recorded at three time intervals. T0: before sternotomy, T1: 30 mins after initiation of CPB & T2:
after sternal closure.
Results:
SMA was demonstrated in 32 patients. SMABF, diameter, SMA/CO, MAP & CO - decreased significantly (p<0.0001)
between T0 & T1, increased (p=/<0.001) between T1 & T2 & no significant change (p>0.05) between T0 & T2.
Lactates increased progressively from T0 to T2.
Conclusion:
Study shows that there is decrease in SMABF during CPB and returns to baseline after CPB. Hence it is feasible
to measure SMABF using TEE in patients undergoing cardiac surgery under hypothermic CPB. TEE can be a
promising tool in detecting & preventing splanchnic hypoperfussion during perioperative period.
Key word:
Superior mesenteric artery, cardiopulmonary bypass, trans esophageal echocardiography.
Introduction:
Gastrointestinal complications are reported to be <1% in cardiac surgical patients, but these carry a very high mortality
of 14%. Acute mesenteric ischemia (AMI) accounts to majority of these complications around 10 67% with a case
fatality rate of 70-100%.1 Blood supply to gastro intestinal (GI) tract is by splanchnic circulation which includes
celiac trunk, superior mesenteric artery (SMA) and inferior mesenteric artery (IMA). Cardio pulmonary bypass (CPB)
induces regional hypoperfussion commonly involving splanchnic circulation2 leading to GI complications. SMA
supplies majority of small and large intestine and monitoring the SMA blood flow during cardiac surgery would help
in early diagnosis of mesenteric ischemia. There are various invasive and non invasive modalities to image SMA,
gold standard being angiography. Altered liver and renal function with unstable haemodynamics limits the use of
angiography in acute mesenteric ischemia (AMI).3 Other non invasive methods like CT and abdominal ultrasound
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can diagnose SMA ischemia but lacks sensitivity and specificity.1 However none of the methods are feasible in
operating room.
Trans esophageal echocardiography (TEE) has been routinely used during cardiac surgery for monitoring ventricular
and valvular function. Demonstration of Branches of abdominal aorta using TEE has been reported.4 This study
was conducted for the feasibility of SMA visualisation and quantification of SMA blood flow in - on pump cardiac
surgical patients using TEE.
Methodology:
After obtaining institutional ethics committee clearance and informed consent from each patient, 35 adult patients
scheduled for elective on pump cardiac surgery were enrolled in the study. Exclusion criteria included acute myocardial
infarction (< 7 days), preoperative hemodynamic instability, preoperative or intraoperative intra aortic balloon
pulsation, Doppler angle > 20 degree and contraindication for insertion of TEE probe.
All patients were premedicated with Inj midazolam 0.05mg/kg intravenously. Radial artery was cannulated under local
anaesthesia for invasive monitoring. General anaesthesia was induced with Inj fentanyl 5mcg/kg, titrated doses of Inj
propofol and Inj vecuronium 0.1mg/kg to facilitate muscle relaxation. Following endotracheal intubation, patients
were mechanically ventilated and maintained with Inj fentanyl, midazolam and vecuronium. A 5MHz Biplane TEE
probe (Philips En Visor CHD, Bothell, Washington, USA 98041) was inserted after induction of anaesthesia. A triple
lumen central venous catheter in right internal jugular vein and femoral arterial catheter were inserted for invasive
monitoring.
Heparin sulphate 4 mg/kg was administered prior to CPB to maintain an activated clotting time (ACT) of at least 480
sec. CPB was conducted with roller pump using a membrane oxygenator and non-pulsatile perfusion (at a flow rate of
2 to 2.4 L/min/m2). Antegrade intermittent warm blood cardioplegia was used for myocardial protection. Systemic
temperature was maintained between 280 320C. Mean arterial pressure was kept at 50 to 80 mmHg. Anaesthesia
during cardiopulmonary bypass was maintained using inj midazolam, fentanyl and vecuronium. Heparin sulphate was
reversed with a corresponding dose of protamine sulphate at the end of surgery.
SMA was visualised by TEE starting from mid esophageal descending aortic short axis view and by advancing the
probe into the stomach, with appropriate rotation and anteflexion to keep the image of the aorta at the centre
of the screen. The 1st branched vessel was visualized at 10 clock position - celiac trunk. (Figure 1A, Video1) The
colour Doppler signal detection scale was lowered to get a clear vision of the vessel and the blood flow signal. The
distinguishing feature of the celiac trunk was its distal bifurcation. The probe was further advanced until the 2nd
branched vessel at 30 clock position appeared on the screen i.e superior mesenteric artery. (Figure 1B, Video 2)
SMA velocities i.e. Vs (peak systolic velocity), Vd (end diastolic velocity) and VTI (velocity time integral) were
measured using pulse wave Doppler (PWD) and tracing the outer contour of Doppler curve accordingly. Diameter
of SMA was measured in M-mode by inner edge to inner edge method at the peak of R wave ECG (Figure 2).
Diameter and VTI were averaged over 3 consecutive cardiac cycles in normal sinus rhythm patients and 5 consecutive
cardiac cycles in patients who had arrhythmias. Resistive index (R.I) of SMA was calculated using formula: Vs Vd/
Vs which reflects the vascular resistance. SMA blood flow (ml/min) was calculated using the formula:- (d/2)2 X
VTI X HR during off pump (Figure 3A) and (d/2)2 X Vm X 60 during CPB. (d = diameter, HR= heart rate, Vm
= Mean velocity) (Figure 3B).
HR, Mean arterial pressure (MAP), cardiac output (CO), SMA blood flow (Vs, Vd, VTI, Diameter) and lactates
(ABG) were recorded at three time intervals. T0: before sternotomy, T1: 30 mins after initiation of CPB. T2: after
sternal closure.
During CPB MAP was replaced by perfusion pressure, CO by pump flow rate, SMA blood flow was calculated using
Vm and diameter.
Patient was followed up for 48 hrs post operatively for any adverse events.
Statistical Analysis:
Haemodynamic and echocardiographic variables were compared by means of Students ttest for paired data on
pump and off pump. A two tailed probability level of less than 0.05 was considered significant. All results were
212
expressed as mean standard deviation. Statistical analysis was performed using MedCalc software version 12.2.1.
Results:
Thirty five patients were enrolled in the study protocol. SMA was successfully demonstrated in 32 patients with a
success rate of 91.4% and three patients were excluded as they could not complete the study. Two patients had a
Doppler angle correction >200, hence were excluded. There were 16 female patients and 19 male patients with age
ranging from 20 yrs to 54 yrs. Average CPB time were 66+/-18 mins. There were 8 patients who underwent mitral
valve replacement (MVR), 13 patients aortic valve replacement, 2 patients atrial septal defect closure, 3 patients
for coronary artery bypass surgery with MVR, 1 patient for tetrology of fallot correction and 8 patients for mitral
valve repair. Statistical analysis was done for 30 patients only. All patients required inotrope or vasoconstrictor while
weaning from CPB.
There was statistically significant decrease (p <0.0001) in SMABF, SMA diameter, MAP, CO, SMA/CO ratio between
T0 (Before sternotomy) and T1 (30 mins after CPB). In similar manner there was statistically significant increase
in SMABF (p <0.0001), SMA diameter (p <0.0001), MAP (p=0.001), CO (p <0.0001), SMA/CO ratio (p=0.0002)
between T1 (30 mins after CPB) and T2 (after sternal closure). (Table 1)
There was no significant change in SMABF (p=0.25), SMA diameter (p=0.18), MAP (p=0.21), CO (p=0.19), SMA/
CO ratio (p=0.14) and R.I (p=0.58) between T0 and T2. (Table 1)
There was a progressive, significant increase in lactate levels over time (p=/<0.0001) from T0 till T2. (Table 1)
T0
T1
T2
MAP (mm Hg)
73.53+/-12.86
58.27+/-10.59
70.37+/-11.94
CO (l/min)
5.24+/-0.66
3.95+/-0.44
5.13+/-0.65
R.I
0.78+/-0.06
------------------------
0.79+/-0.07
SMABF (ml/min)
343.10+/-204.50
170.80+/-117.46
325.50+/-200.18
SMA diameter (cms)
0.51+/-0.18
0.37+/-0.15
0.49+/-0.16
SMA/CO (%)
6.56+/-3.82
4.25+/-2.71
6.22+/-3.86
1.13+/-0.42
2.83+/-0.88
3.47+/-1.24
Arterial
(mmol/l)
lactates
Table 1:- Intra operative haemodynamic parameters and superior mesenteric artery blood flow data.
(MAP - Mean arterial pressure, CO - Cardiac output, R.I - Resistivity index, SMABF - Superior mesenteric artery
blood flow, T0- before sternotomy, T1-30mins after initiation of CPB. T2 - after sternal closure)
There was no post operative gastrointestinal complication or mortality observed in the study patients with
maximum post operative intensive care unit (ICU) stay being 2 days.
Discussion:
SMA being demonstrated in 91.4% of the patients, present study showed it is feasible to visualize and quantify SMABF
intra operatively by trans esophageal approach of abdominal arteries using duplex ultrasound. This technique is simple
and reproducible by an experienced operator.5 Accurate velocity measurement can be obtained when there is correct
estimation of the vessel diameter, proper Doppler interrogation using two dimensional mode and recommended
Doppler angle. In the present study patients with Doppler angle >200 were excluded and the insonation angle was
kept same during T0, T1 and T2 VTI measurements.
Abdominal complication following cardiac surgery is rare but results in high mortality which are due to Ischemia/
reperfusion of splanchnic organs.6,7 Splanchnic ischemia causes damage of the mucosal barrier resulting in gut
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translocation of endotoxin leading to systemic inflammatory response and later multi organ failure in cardiac
surgical patients.6,8 Acute mesenteric ischemia (AMI) is due to - arterial embolus, arterial thrombosis, splanchnic
vasoconstriction, known as non-occlusive mesenteric ischemia (NOMI) and venous thrombosis. NOMI is the most
common cause of AMI following CPB.9,10,11
Results of present study shows significant decrease in SMABF (170.80+/-117.46 ml/min) after 30mins of initiation
of CPB (T1) as compared to baseline (343.10+/-204.50 ml/min) (T0). There was significant decrease in CO, MAP
and diameter (p <0.0001) during CPB which may have resulted in decrease in SMABF. Splanchnic hypoperfusion
involving mesenteric arterial trunk (which has adrenergic innervations)12 is due to regional vasoconstriction caused
by catecholamine, sympathetic and renin angiotensin stimulation,13 and hypothermia during CPB. This can result in
increased resistance,14 decrease diameter and hence decreased flow in SMA.
SMABF reduced to a greater extent than CO T0 vs T1 (50.21% vs 24.62%), with a decrease in fractional output
flowing through SMA from 6.56+/-3.82% to 4.25+/-2.71%, p<0.0001 (T0 vs T1). During stages of shock there
is less amount of CO directed to splanchnic organs, with greater reduction in visceral organ perfusion compared
to CO.15 Blood flow to heart and central nervous system is maintained by decreasing blood flow to visceral organ
microcirculation.16
There was an increase in SMABF at T2 (325.50+/-200.18) as compared to T1, and insignificant change as compared
to T0 (343.10+/-204.50 ml/min). This could be due to increase in CO, MAP and SMA diameter (p>0.05) between
T0 and T2. (Table 1) Previous studies have shown sudden reactive hyperaemia after sustained reduction in mesenteric
artery blood flow which is due to stimulation of constrictor fibres or mechanical occlusion.17,18
But in the present study increase in SMABF and diameter may have been because of return of CO, MAP and
resistivity index (0.78+/-0.06 vs 0.79+/-0.07) close to baseline value (T0). T2 values were obtained on an average
after 1 to 1.5 hours weaning from CPB, where reactive hyperaemia causing increase in SMABF is unlikely. All patients
were weaned from CPB with inj Dopamine or Dobutamine or a vasodilator which are known to dilate the mesenteric
bed. Only 3 patients had a vasoconstrictor (inj adrenaline).
Splanchnic circulation which supplies gastrointestinal tract includes celiac trunk (gastric, hepatic, pancreatic), SMA
and IMA. There are many methods to measure splanchnic blood flow like by using Ficks principle, laser Doppler
flowmetry and hepatic venous oxygen saturation. Gastric tonometry, splanchnic lactate extraction, and D-dimer can
be used to detect splanchnic ischemia. But among all these methods only few are feasible intra operatively. Hepatic vein
blood flow (HBF) has been demonstrated using TEE during cardiac surgery with CPB. The authors have concluded
that there is decrease in HBF during hypothermic CPB and not in normothermic CPB as compared to baseline with
increase in HBF 4hrs after termination of CPB.19 Previously TEE has been used to demonstrate SMABF20,21 but there
is limited literature on use of TEE to asses SMABF during hypothermic CPB. Doppler recordings from the TEE
give us the advantage of obtaining the data that is almost an online picture of changes in SMABF. Study by Fiore
et al 21 demonstrated SMA using TEE in off pump CABG patients and concluded that there is decrease in SMABF
during decrease in CO which occurred while revascularization of obtuse marginal and right coronary artery. SMABF
increased at the end of surgery after normalization of CO. Another study by Straub et al22 demonstrated increase
in resistive and pulsatility index after CPB indicating rigidity in mesenteric vascular bed with decrease in perfusion.
But in their study measurements were done using Doppler sonography 30 mins after induction of anaesthesia and
60 mins after end of the surgery. They concluded that increase in resistivity index was due to systemic inflammatory
response due to CPB. But in the present study SMABF measurement was done using TEE intraoperatively.
Lactates showed a progressive increase from T0 to T1 which could be accounted for a poor splanchnic perfusion
with normal physiological CPB pump flows and perfusion pressures. There is decrease in hepatic clearance leading
to pyruvate accumulation resulting in increase lactate23 or increased intestinal production of lactate secondary to
transient intestinal ischemia24 during and after CPB which could have lead to progressive increase in lactate from T1
to T2.
Limitations of the present study were that - SMABF obtained by TEE was not compared with SMA angiography and
mucosal microcirculation was also not assessed.
Conclusion:
This study demonstrated that TEE is feasible to monitor SMABF during hypothermic CPB. SMABF decreased
214
during CPB as compared to baseline value, which returned to near baseline value after CPB. Hypo perfusion although
transient might result in sub clinical ischemia causing gastro intestinal complication. Further studies are required to
compare SMABF between hypothermic and normothermic CPB and if an intervention could treat non occlusive
mesenteric ischemia caused due to mesenteric hypo perfusion during CPB.
References:
1. Abboud B,Daher R,Boujaoude J. Acute mesenteric ischemia after cardio-pulmonary bypass surgery. World J
Gastroenterol 2008;14:5361-70.
2. Lazenby WD,Ko W,Zelano JA,Lebowitz N,Shin YT,Isom OW,et al. Effects of temperature and flow rate on
regional blood flow and metabolism during cardiopulmonary bypass. Ann Thorac Surg 1992;53:957 64.
3. Trompeter M, Brazda T, Remy CT, Vestring T, Reimer P. Non-occlusive mesenteric ischemia: etiology, diagnosis,
and interventional therapy. Eur Radiol 2002; 12: 1179-87.
4. Orihashi K,Matsuura Y,Sueda T,Shikata H,Morita S,Hirai S,et al. Abdominal aorta and visceral arteries
visualized with transesophageal echocardiography during operations on the aorta. J Thorac Cardiovasc Surg
1998; 115:9457.
5. Fujimura J, Camilleri M, Low PhA, Novak V, Novak P, Opfer-Gehrking TL. Effect of perturbations and a meal
on superior mesenteric artery flow in patients with orthostatic hypotension. J Auton Nerv Syst 1997; 67:1523.
6. Hessel E. Abdominal organ injury after cardiac surgery. Seminars in Cardiothoracic and Vascular Anesthesia
2004; 8: 243-63.
7. Khan JH,Lambert AM,Habib JH,Broce M,Emmett MS,Davis EA. Abdominal complications after heart
surgery. Ann Thorac Surg 2006; 82:1796-1801.
8. Warltier D. The Systemic Inflammatory Response to Cardiac Surgery: Implications for the Anesthesiologist.
Anesthesiology 2002; 97:215-52.
9. Pinson CW, Alberty RE. General surgical complications after cardiopulmonary bypass surgery. Am J Surg 1983;
146: 133-7.
10. Wilson C, Gupta R, Gilmour DG, Imrie CW. Acute superior mesenteric ischaemia. Br J Surg 1987; 74: 279-81.
11. Hasan S, Ratnatunga C, Lewis CT, Pillai R. Gut ischaemia following cardiac surgery. Interact Cardiovasc Thorac
Surg 2004; 3: 475-8.
12. Gelman S, Mushlin PhS. Catecholamine-induced changes in the splanchnic circulation affecting systemic
hemodynamics. Anesthesiology 2004;100:434 9.
13. Jakob SM. Splanchnic blood flow in low-flow states. Anesth Analg 2003;96:1129 38.
14. Texter EC, Merrill S, Schwartz M, Van derStappen G, Haddy FJ. Relationship of blood flow to pressure in the
intestinal vascular bed of the dog. Am J Physiol 1962;202:253 6.
15. Vatner SF. Effects of hemorrhage on regional blood flow distribution in dogs and primates. J Clin Invest
1974;54:22535.
16. Takala J. Determinants of splanchnic blood flow. Br J Anaesth 1996;77:508.
17. Granger DN, Richardson PDI, Kvietys PR, Mortillaro NA. Intestinal blood flow. Gastroenterology 1980;78:837
63.
18. Fatehi-Hassanabad Z, Parratt JR, Furman BL. Endotoxininduced inhibition of mesenteric vasodilator responses
to acetylcholine, bradykinin, and post-occlusion hyperemia in anesthetized rats. Shock 1996;5:371 6.
19. Gardeback M, Settergren G, Brodin LA. Hepatic blood flow and right ventricular function during cardiac
surgery assessed by transesophageal echocardiography. J Cardiothorac Vasc Anesth1996;10:318-22.
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20. Orihashi K, Sueda T, Okada K, Imai K. Perioperative diagnosis of mesenteric ischemia in acute aortic
dissection by transesophageal echocardiography. Eur J Cardiothorac Surg 2005;28:871-6.
21. Fiore G,Brienza N,Cicala P,Tunzi P,Marraudino N,Schinosa Lde L, et al. Superior mesenteric artery blood flow
modifications during off-pump coronary surgery. Ann Thorac Surg 2006;82:627.
22. Straub U,Winning J,Greilach P,Isringhaus H,Kalweit G,Huwer H. Alterations of mesenteric blood flow
after cardiopulmonary bypass: a Doppler sonographic study. J Cardiothorac Vasc Anesth 2004;18:731-3.
23. Manthous CA,Schumacker PT,Pohlman A,Schmidt GA,Hall JB,Samsel RW, et al. Absence of supply dependence
of oxygen consumption in patients with septic shock. J Crit Care 1993; 8:203-11.
24. Landow L. Splanchnic lactate production in cardiac surgery patients. Crit Care Med 1993;21:S81-S94.
B
Figure 1: TEE demonstration of A - Celiac artery (CA), B - Superior mesenteric artery (SMA), Ao- Aorta
216
Figure 2: M-Mode estimation of diameter of SMA.
B
Figure 3: A - Colour wave Doppler of SMA before and after CPB,
B Colour wave Doppler of SMA during CPB.
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IACTACON 2016
EFFECT OF DEXMEDETOMIDINE ON CORONARY

VESSEL DIAMETER AND MYOCARDIAL PROTECTION IN
PERCUTANEOUS CORONARY INTERVENTIONAL PATIENTS
Dr Tanveer Singh Kundra, Dr Nagaraja P.S, Dr Naveen G Singh, Dr Manjunatha.N
ABSTRACT:
Introduction:
Dexmedetomidine is an alpha-2 agonist used for conscious sedation. It has also been shown to have a myocardial
protective effect in off-pump coronary artery bypass (OPCAB) patients. The aim of our study was to assess the effect
of dexmedetomidine for myocardial protection in percutaneous coronary interventional patients.
Methodology:
A total of 60 patients(Group dexmedetomidine n = 30, Group normal saline n = 30) were enrolled in the study.
Dexmedetomidine infusion (1mcg/kg) over 15 minutes was given as a loading dose after coronary angiography in
group dexmedetomidine(D) while normal saline was given in the control group(C) and then maintainance infusion
was started at 0.5mcg/kg/hour in both the groups. Coronary vessel diameter was noted before (T0) and after (T1)
loading dose of dexmedetomidine/saline in each group. Troponin T values were noted at baseline (T0), 6hours (T2),
12hours (T3) and 24hours (T4) after starting the loading dose. Hemodynamic variables(heart rate(HR), mean blood
pressure(MAP)) were monitored at T0,T1 and at regular intervals till 2 hours post procedure.
Results:
Coronary vessel Diameter and HR significantly decreased in group D as compared to control group (p<0.05) whereas
the decrease in Troponin T at 6hours, 12hours and 24hours was not statistically significant between the two groups.
Conclusion:
Dexmedetomidine decreases the coronary vessel diameter, but maintains the myocardial oxygen demand-supply ratio
by decreasing the heart rate. The decrease in Troponin T is statistically insignificant at the doses used.
Key words :
Dexmedetomidine, percutaneous coronary intervention, troponin
INTRODUCTION:
Myocardial injury in acute myocardial infarction is due to both ischemic as well as reperfusion injury. Reperfusion
can cause hyperkalemia,1 arrhythmias and a rise in cardiac enzymes (Troponin I & T and CPK-MB). A number
of strategies have been used to prevent lethal myocardial reperfusion injury in patients undergoing percutaneous
coronary interventional procedures(PCI). Mechanical interventions include Remote Ischaemic preconditioning,
Therapeutic hypothermia and Therapeutic hyperoxemia whereas Pharmacological Interventions include Adenosine,
Anti-inflammatory agents, Atrial Natriuretic Peptide, Atorvastatin, Erythropoietin, GIK Therapy and Sodium Nitrite2.
Dexmedetomidine is a selective alpha-2 agonist which may shrink the coronary arteries and reduce coronary blood
flow.3,4 But at the same time, dexmedetomidine reduces heart rate and consequently the myocardial oxygen demand.
Hence, we postulate that dexmedetomidine should maintain the myocardial oxygen demand-supply ratio. Also,
dexmedetomidine results in sympathetic blockade, as it affects the alpha2 receptors in the central nervous system and
restrains the release of central sympathetic neurotransmitter (predominantly norepinehrine).5 Patients undergoing
218
PCI have a lot of stress response and hence dexmedetomidine may be useful to alleviate anxiety which can also
decrease the oxygen demand and improve the oxygen demand-supply ratio.
Dexmedetomidine has been shown to have a protective effect on myocardial ischemia-reperfusion(I/R) injury in
rats6,7 and decreases the incidence of arrhythmias. However, there is limited literature on effect of dexmedetomidine
during I/R injury in PCI patients.
Hence the aim of the study was to assess the effect of dexmedetomidine on coronary vessel diameter and myocardial
protective effect in patients undergoing PCI.
METHODOLOGY:
After institutional ethics committee approval, a prospective double-blind randomized controlled trial was conducted.
60 patients were randomized into group D (Dexmedetomidine) n=30 and group C (control) n=30 undergoing PCI for
single vessel disease. Patients above the age of 70 years, Ejection fraction(EF) of less than 40%, in cardiogenic shock
were excluded from the study. Patients were randomized on the basis of computer generated randomization table.
The randomization scheme was generated by using the Web site Randomization.com http://www.randomization.
com. The computer generated group number (D or C) was put in a closed opaque envelope. A person not related
to study was asked to open the closed envelope containing computer generated group number. The groups were as
under:
Group D: Injection Dexmedetomidine 1mcg/kg was administered over 15 minutes as a loading dose and then
0.5mcg/kg/hr as maintenance infusion.
Group C: Injection 0.9%NaCl (started and maintained at the same rate as calculated for group D).
Immediately after coronary angiogram (T0), a baseline troponin T(Trop T) was sent and coronary vessel diameter was
measured. Then dexmedetomidine or 0.9%NaCl infusion was started. After the loading dose and before initiation
of coronary angioplasty (T1), coronary diameter was again measured to see the effect of dexmedetomidine on the
coronary diameter. The infusion of dexmedetomidine was continued until 30 minutes post-procedure. Trop T was
sent at 6hours (T2), 12 hours (T3) and 24 hours (T4) after starting the loading dose.
Heart rate(HR) and blood pressure(BP) were monitored every 5 minutes during the procedure and every 10 minutes
post procedure for 2 hours.
ECG was done pre-procedure, post-procedure, at 24 hours and 72 hours for arrhythmias and new ECG changes.
Statistical analysis was performed using Medcal 11.3.0. Intra group analysis were done using paired student t test and
unpaired student t test was done for analysis between the two groups. Hemodynamic variables and trop T values were
expressed as mean SD. A p value < 0.05 was considered significant.
RESULTS:
30 patients were included in each of the two groups. In group D, there were 18 males and 12 females, whereas
in group C there were 16 males and 14 females. All the patients were aged between 40 to 60 years. In Group D, 25
patients had EF between 40-50% and 5 patients had EF between 51-60%. In Group C, 23 patients had EF between
40-50% and 7 patients had EF between 51-60%.
The diameter of the coronary vessel decreased significantly after loading dose of dexmedetomidine infusion (p=0.000)
whereas no such significant change was observed in the control group (p=0.25) (Table 1).
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Mean Standard Deviation

Diameter before
dexmedetomidine (T0)
p value
2.79 0.396
0.000
Diameter after loading dose of

Diameter before NS (T0)
Diameter after loading dose of
NS (T1)
2.39 0.455
2.63 0.384
0.252
2.61 0.388
Table 1- Diameter of the coronary vessel before and after administration of dexmedetomidine/NS
Heart rate also decreased significantly after loading dose of dexmedetomidine infusion (p=0.000), while the change
in heart rate was not significant in the control group (p=0.59) (Table 2).
Heart rate before
Heart rate after loading dose of
Heart rate before NS (T0)
Heart rate after loading dose of
NS (T1)
p value
86.77 18.522
0.000
75.17 18.607
89.50 6.857
88.73 9.770
0.593
Table 2- Heart rate before and after administration of dexmedetomidine/NS

There was a statistically significant decrease in SBP and DBP after giving loading dose of dexmedetomidine but no
such decrease was observed in the control group.(Table 3A and 3B)
220

SBP before dexmedetomidine
(T0)
p value
137.83 26.95
0.000
SBP after loading dose of
117.67 17.31
SBP before NS (T0)
129.617.63
SBP after loading of NS (T1)
129.317.23
0.36
Table 3A : Systolic blood pressures(SBP) before and after administration of dexmedetomidine/NS
DBP before dexmedetomidine
(T0)
p value
76.83 15.86
0.000
DBP after loading dose of
66.33 13.11
DBP before NS (T0)
75.510.25
DBP after loading of NS (T1)
75.810.38
0.46
Table 3B : Diastolic blood pressures(SBP) before and after administration of dexmedetomidine/NS
There was no statistically significant difference in the Trop T values at baseline(T0), 6hours(T2) ,12hours(T3) and at
24hours(T4) between dexmedetomidine group and control group(Table 4).
Dexmedetomidine
group
Control group
p value
T0
1.38 2.86
2.02 2.29
0.34
T2
1.49 2.61
1.79 1.35
0.58
T3
1.21 1.95
1.29 0.87
0.85
T4
0.81 1.34
1.12 1.10
0.31
Table 4- Trop T values at baseline, 6hours, 12hours, 24hours after initiation of the drug.
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Three patients in the control group had arrhythmias during the procedure and post-procedure, while none in the
dexmedetomidine group had arrhythmias.
DISCUSSION:
Reperfusion injury is defined as damage to the tissue caused when blood supply is restored to the ischemic or hypoxic
area after a certain period. Similar type of injury occurs in the myocardium after acute myocardial infarction treated
with percutaneous coronary intervention or fibrinolytic therapy. 8-10
Reperfusion is associated with microvascular injury, particularly due to increased permeability of capillaries and
arterioles. Activated endothelial cells produce more reactive oxygen radicals but less nitric oxide after reperfusion.
This imbalance causes an inflammatory response which is partially responsible for the damage caused by reperfusion
injury.11 White blood cells(WBC) are carried to the reperfused area by restoration of blood flow which causes a
release of inflammatory factors such as interleukins and free radicals.12 These cause damage to the cellular proteins,
DNA, and the plasma membrane which may cause further release of more free radicals. These mediators may also
act indirectly in redox signaling to initiate apoptosis. WBC may also obstruct the small capillaries by binding to their
endothelium worsening the ischemia.12 Also the ischemic tissue has decreased free radical scavengers, which results
in further tissue damage after reperfusion.
Hyperkalemia,1 arrhythmias and rise in cardiac enzymes (Trop I & T and CPK-MB) may help us in recognizing this
reperfusion injury.
Dexmedetomidine being a selective alpha-2 agonist may cause coronary vasoconstriction. Yoshitomi et al13 and
Okada et al14 showed that dexmedetomidine has direct dose-dependent cardioprotective effect on reperfusion injury
and high dose of dexmedetomidine had favourable subendocardial-to-subepicardial blood flow ratio resulting in
better functional recovery from myocardial stunning.
Dexmedetomidine is an ideal sedative agent in cardiac patients as it is a sympatholytic, reduces heart rate and
consequently the myocardial oxygen demand. In the present study the SBP and DBP has shown a statistically
significant decrease in group D. This can be attributed to sympatholysis and anxiolysis. However the decrease in blood
pressure was never less than 20% of the baseline. It causes conscious sedation in which the patient can be woken up
easily when stimulated. Hence it is beneficial to use dexmedetomidine for sedating the anxious cardiac PCI patients.
In the present study, there was a significant decrease in the coronary vessel diameter. But there was no significant
change in the levels of Trop T. This infers that myocardial damage has not occurred with the decrease in coronary
diameter in the dexmedetomidine group. Although the blood flow has decreased due to coronary vasoconstriction,
at the same time the demand has also decreased by a significant decrease in heart rate caused by dexmedetomidine.
Hence our hypothesis is proved that dexmedetomidine maintains the demand-supply ratio inspite of decreasing the
coronary vessel diameter.
In the present study, three patients of control group had arrhythmias during the procedure and post-procedure,
while none in the dexmedetomidine group had arrhythmias. There is a probability that dexmedetomidine could have
prevented arrhythmias caused by I/R in the study group.
Chi X et al15 found that dexmedetomidine reduces myocardial damage in patients undergoing off-pump coronary
artery bypass graft surgery as noted by a decrease in the myocardial enzymes in the dexmedetomidine group as
compared to the control group. In the present study, there was no significant decrease in Trop T levels in patients who
were given the same dose of dexmedetomidine as in the above study. This could be due to various reasons. Firstly,
the dosage of dexmedetomidine used was based on previous studies done in cardiac surgical patients. The dosage
required in PCI patients may be different because of shorter duration of the procedure. The total duration and
dosage of dexmedetomidine was lesser in the present study as compared to the cardiac surgical patients.15 Secondly,
the extent of myocardial damage is lesser in PCI patients as compared to cardiac surgical patients. The myocardial
damage caused by surgical handling is more due to the duration of surgery, increased inflammation, vasopressors and
surgical stress. Thirdly, the sample size was calculated based on previous surgical studies. Maybe a larger sample size
is required in PCI patients. Further study with a different dose and/or duration with larger sample size is required to
validate the myocardial protective effect in ischemia reperfusion injury.
222
CONCLUSION:
Dexmedetomidine decreases the coronary vessel diameter, but it maintains the oxygen demand-supply ratio by
decreasing heart rate.
REFERENCES:
1. John L. Atlee. Complications in anesthesia. 2nd edition. Elsevier Health Sciences:2007.p.55.
2. Derek J. Hausenloy, Derek M. Yellon. Myocardial ischemia-reperfusion injury: a neglected therapeutic target. J
Clin Invest. 2013;123(1):92-100.
3. Willigers HM, Prinzen FW and Roekaerts PM: Comparison of the effects of dexmedetomidine and esmolol on
myocardial oxygen consumption in dogs. Eur J Anaesthesiol 2004;21: 95766.
4. Snapir A, Posti J, Kentala E, et al: Effects of low and high plasma concentrations of dexmedetomidine on
myocardial perfusion and cardiac function in healthy male subjects. Anesthesiolog 2006;105: 90210.
5. Penttila J, Helminen A, Anttila M, Hinkka S, Scheinin H. Cardiovascular and parasympathetic effects of
dexmedetomidine in healthy subjects. Can J Physiol Pharmacol 2004; 82: 359-62.
6. Kocoglu H et al. Preconditioning effects of dexmedetomidine on myocardial ischaemia/reperfusion injury in
rats. Current Therapeutic Research 2008; 69: 150-58.
7. Kip G et al. Dexmedetomidine protects from post-myocardial ischaemia reperfusion lung damage in diabetic
rats. Libyan Journal of Medicine 2015; 10: 27828- http://dx.doi.org/10.3402/ljm.v10.27828
8. Simoons ML, Serruys PW, van den Brand M, et al. Early thrombolysis in acute myocardial infarction: limitation
of infarct size and improved survival. J Am Coll Cardiol 1986; 7:717.
9. White HD, Norris RM, Brown MA, et al. Effect of intravenous streptokinase on left ventricular function and
early survival after acute myocardial infarction. N Engl J Med 1987; 317:850.
10. Sheehan FH, Doerr R, Schmidt WG, et al. Early recovery of left ventricular function after thrombolytic therapy
for acute myocardial infarction: an important determinant of survival. J Am Coll Cardiol 1988; 12:289.
11. Carden DL, Granger DN .Pathophysiology of ischaemia-reperfusion injury. The Journal of pathology 2000; 190:
25566.
12. Clark, Wayne M. Reperfusion injury in stroke.2005; eMedicine: WebMD.
13. Yoshitomi O, Cho S, Hara T et al. Direct protective effects of dexmedetomidine against myocardial ischemiareperfusion injury in anesthetized pigs. Shock 2012; 38: 92-7.
14. Okada H, Kurita T, Mochizuki T et al. The cardioprotective effect of dexmedetomidine on global ischaemia in
isolated rat hearts. Resuscitation 2007; 74: 538-45.
15. Chi X, Liao M, Chen X et al. Dexmedetomidine attenuates myocardial injury in off-pump coronary artery bypass
graft surgery. Journal of Cardiothoracic and Vascular Anaesthesia. Article in press.
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IACTACON 2016
THE ROLE OF NEUTROPHIL GELATINASE ASSOCIATED

LIPOCALIN (NGAL) IN PREDICTING ACUTE KIDNEY
DISEASE IN PATIENTS UNDERGOING OPCABG: A PILOT
STUDY
Introduction
Acute kidney Injury (AKI) is not uncommon after cardiac surgery and is associated with increased morbidity and
mortality. Up to one third of the patients undergoing cardiac surgery can develop some form of AKI, and 1-5% of
these patients may go on to develop severe form of kidney injury, requiring dialysis. [1, 2, 3]
There is increasing evidence that AKI is associated with increased risk of both short-term and long-term risk of
death, as well as risk of progressive renal failure. Even a subtle increase in serum creatinine levels resulting from
a mild AKI can increase the risk of 30 day mortality to 3 folds and larger serum creatinine increases are associated
with a more than 18 fold elevation. [4, 5]
There are a number of preoperative risk factors which are associated with increased likelihood of developing AKI
after cardiac surgery. Prominent amongst those include female gender, reduced left ventricular function, history
of congestive heart failure, diabetes requiring insulin, preoperative use of an intra-aortic balloon pump(IABP),
chronic obstructive pulmonary disease (COPD), the need for emergent surgery, and an elevated preoperative
serum creatinine. Valve replacement surgeries have higher incidence of AKI as compared to coronary artery
bypass graft surgery (CABG). [6-10]
Another controversial risk factor is cardiopulmonary bypass (CPB) i.e. conventional CABG (CCABG) versus
Off-pump CABG (OPCAB). Most of the studies have shown that OPCAB is associated with lower incidence of
AKI postoperatively as compared to CCABG. Patients undergoing OPCAB have a significantly lesser increase
in inflammatory markers as compared with those who undergo CCABG. Nigwekar et al reported a significant
reduction in overall AKI [odds ratio (OR) 0.57, 95% confidence interval (CI) 0.43-0.76] and AKI- requiring
renal replacement therapy (RRT) (OR 0.55, 95% CI 0.43-0.71) in OPCAB cases compared from CCABG.[11,12] A
meta-analysis of 22 randomized controlled trials suggested that OPCAB performed in a relatively heterogeneous
patient population with coronary artery disease was associated with a reduction in the incidence of AKI but had
no effect on dialysis requirement or all-cause mortality. [13]
Serum creatinine is a degradation product of muscle cells and represents a surrogate for the efficiency of
glomerular filtration. It has poor predictive accuracy for kidney injury, particularly in the early stages of AKI. [14]
Neutrophil gelatinase-associated lipocalin (NGAL) is 25kDa iron-transporting glycoprotein which accumulates
in the kidney tubules and urine after nephrotoxic and ischemic insults. Human NGAL was originally isolated
from the supernatant of activated neutrophils. It has been proposed as an early, sensitive, non-invasive biomarker
for AKI. [15-21]. We conducted a pilot study to assess the role of NGAL in predicting AKI in patients undergoing
OPCAB who were at increased risk of developing AKI.
Material and Method

This was a prospective Cohort study, conducted at our tertiary care hospital after taking permission from the
institutional review board. 80 patients posted for OPCAB with an increased risk of developing AKI defined as having
a Cleveland Clinic Foundation Acute renal failure scoring System score of 6 were included in the study. Venous
blood samples were collected on the day of admission for routine investigations including renal function tests. A
baseline urine NGAL level before the start of surgery was assessed and another urine NGAL level was assessed at 4
hrs post surgery. Renal function tests were assessed on the day of surgery (4 hrs post surgery) and on the next three
days.
All the patients underwent OPCAB using a standard technique as per the institution protocol. All patients were
224
premedicated with lorazepam 2mg and pantaprazole 40 mg orally a night before and on the morning of surgery.
Anaesthesia was induced with thiopentone sodium 2-4 mg/kg, fentanyl 4-5 microgram/kg and midazolam 0.030.04mg/kg intravenously (IV). Neuromuscular Blockade was achieved with vecuronium bromide (0.1mg/kg)
and following tracheal intubation, anaesthesia was maintained with isoflurane and intermittent doses of fentanyl,
midazolam and vecuronium. A median sternotomy was performed and heparinisation was done to keep activated
clotting time (ACT) greater than 300 s. Heparin sulphate was reversed with protamine after the completion of
revascularization. Patients were shifted to ICU immediately after the surgery and were managed as per protocol.
Inclusion Criteria
- Age group: 18- 85 yrs.
- Patients with increased risk of AKI postoperatively, defined as having a Cleveland Clinic Foundation Acute renal
failure scoring System score of 6.
- Patients giving valid written informed consent.
- Patients planned for elective OPCAB.
Exclusion Criteria
- Preoperative Hematocrit < 25 %.
- Leukocyte rich blood transfusion < 30 days before surgery.
- Coronary Angiography (CAG) within 48 hrs prior to surgery
- Pre-existing AKI
- Preoperative RRT.
- CKD stage 5
- Post renal transplant
Patients scheduled for OPCAB were examined a day before the procedure and all the baseline investigations were
noted. Demographic data (age, sex, height, and weight), preoperative risk factors and perioperative surgical and
anaesthetic management were recorded for all the patients. Urine sample for baseline NGAL levels were taken before
the start of surgery. Patients were shifted to ICU after surgery and urine sample for NGAL was taken 4 hrs post
surgery. Renal functions tests were assessed on the day of surgery at 4 hrs post surgery and for the next three days.
Diagnostic Criteria for defining AKI was taken from AKIN criteria i.e. an AKI with a Rapid time course (less than
48 hours), reduction of kidney function with an absolute increase in serum creatinine of 0.3mg/dl (26.4 mol/l)
or a percentage increase in serum creatinine of 50% and a reduction in urine output, defined as <0.5 ml/kg/hr for
more than 6 hours.
Statistical methods
All the values are expressed as in terms of means and standard deviation. Qualitative/categorical data are expressed
in terms of absolute number and percentages. Diagrams and charts are given wherever necessary to substantiate
the important findings. All statistical tests were two tailed. Mann-Whitney U Test was used for comparision and a p
< 0.05 was considered statistically significant. Statistical analysis was performed in SPSS version 18.0 (IBM, SPSS
statistics).
Results
Eighty patients who were planned to undergo OPCAB at our centre were enrolled in this prospective study. Baseline
demographics are shown in table 1. Mean age of the patients in our study was 64.188.88 years with 90% male
patients and 10% of patients being female. All the patients had a preoperative left ventricular ejection fraction of
30%. All the patients had IABP inserted at least one day prior to the surgery. In addition to that, all the patients in the
study were diabetics. Five patients had history of COPD and four surgeries in the study were redo surgeries.
Seven patients (8.75%) developed AKI as defined by AKIN and RIFLE criteria for AKI [Table 2]. Six patients who
developed AKI had stage one AKI according to AKIN criteria, while one patient had stage 2 AKI. One patient had
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IACTACON 2016
very high value of NGAL both preoperatively and 4-hrs after the surgery, suggesting that the patient already had
developed AKI before the surgery and was therefore excluded from the study. Mean baseline NGAL value in patients
who developed AKI, although higher but was comparable to those who did not develop AKI (20.05 ng/ml v/s
15.14 ng/ml respectively) [Table 3, Figure 1]. NGAL value at 4 hrs in patients who developed AKI was 385.58 ng/
ml, which was significantly higher as compared to patients who did not develop AKI (35.42 ng/ml, p<0.05) . Serum
creatinine levels at baseline and at 4 hrs postoperatively were comparable in patients who develop AKI and those
who did not develop AKI (p>0.05). However, serum creatinine levels at 24 hrs, 48 hrs and 72 hrs were significantly
higher in patients who developed AKI as compared to those who did not develop AKI [Table 3, Figure 2]. None
of the patient who developed AKI required dialysis. There was no mortality in the seven day postoperative period.
Discussion
Serum creatinine has long been used as a marker of renal function in spite of it being an unreliable and delayed
indicator of renal injury. Serum creatinine in a setting of AKI, may take several hours to days to reach a steady
state. Also, serum creatinine level is influenced by several non-renal factors, such as age, gender, muscle mass,
muscle metabolism, medications, and hydration status.
Availability of early biomarkers in predicting AKI in cardiac surgery may enable the physicians to perform
timely interventions to prevent further deterioration of kidney functions. A number of biomarkers have recently
been investigated as possible biomarkers for early and accurate identification of AKI. These include a plasma
biomarkers such as NGAL and cystatin C and urine biomarkers like NGAL, Interleukin-18, and Kidney Injury
Molecule (KIM-1). [22-24]
NGAL is one such novel biomarker, which is primarily a marker of renal tubular injury There is a marked up
regulation of NGAL mRNA in the thick ascending limb of Henles and the collecting ducts [25], with resultant
synthesis of NGAL protein in the distal nephron and secretion into the urine where it comprises the major fraction
of urinary NGAL.
We found a significant relationship between a rise in urine NGAL levels at 4 hrs postoperatively to occurrence of
AKI, although it was not clear whether the degree of rise in NGAL levels was associated with more severe form
of AKI or not. This was because of the reason that six out of seven patients in our study who developed AKI had
only stage one AKI. Also the rise in urine NGAL levels at 4 hrs in these paients was not uniform. One patient
who developed AKI had hundred fold rise in urine NGAL levels at 4 hrs while the other six had lesser degree of
elevation of urine NGAL at 4 hrs. Six patients who developed AKI had a normal serum creatinine value at 4 hours
post operatively. Serum creatinine levels rose only at 24 hours or more in all these six patients. However, urine
NGAL levels were significantly high in these patients at 4 hours suggesting that urine NGAL rises much earlier
than serum creatinine levels and is an early biomarker of AKI. One patient who developed AKI had high urine
NGAL levels at 4 hours as well as raised serum creatinine levels at 4 hours post operatively.
Since none of patient in our study who developed AKI had grade 3 AKI and neither of the patient had dialysis
requirement, the diagnostic utility of NGAL may be better assessed by determining its predictive utility for
clinical outcomes such as mortality or progression to dialysis-dependent renal failure.
One of the strengths of our study was that all the patients who were selected in the study had a high risk for
developing AKI postoperatively. Various studies and scoring systems for predicting AKI in patients undergoing
cardiac surgery have shown that patients with poor left ventricular function and diabetes mellitus are at increased
risk of developing AKI after cardiac surgery. The effect of diabetes mellitus on postoperative renal dysfunction
may be the result of renal parenchymal disease, such as glomerulonephritis or glomerulosclerosis. Renal artery
stenosis in diabetic patients may further compromise renal function. Also, perioperative IABP is an independent
predictor of perioperative AKI and in-hospital mortality. Wijeysundera et al. also demonstrated that the preoperative placement of an IABP significantly increased the risk for AKI in a heterogeneous group of cardiac
surgical patients. [26]
Our study is in agreement with other similar studies which have found that NGAL is an early biomarker of AKI.
Bennett et al. in a prospective uncontrolled cohort study concluded that NGAL predicts AKI, mortality and
morbidity after pediatric cardiac surgery [27]. Several other studies have reported NGAL as a sensitive and specific
predictor of AKI after cardiac surgery. [28, 29]
226
It also supports the fact that OPCAB may have a protective effect as far as postoperative renal dysfunction is
concerned as compared to CCABG, as only 7.14% of patients had AKI in our study which is consistent with the
findings in other studies which showed that risk of AKI was much more in CCABG. [30]. Loef and associates found
significantly less changes in microalbuminuria, free hemoglobin, fractional excretion of sodium, and free water
clearance as well as N-acetyl-D glucosaminidase as a marker for tubular function and damage, respectively,
in patients undergoing OPCAB as compared with CCABG patients. Patients with concomitant diseases or risk
factors seem to benefit from the beating heart approach as compared to CCABG. [31, 32]
Limitations
One of the important limitation of our study is that only a small study group (n=80) was included in the study. Large
randomized prospective trials are needed to validate the diagnostic utility of urine NGAL in predicting AKI.
Another limitation of the study is that the urine NGAL levels were observed for upto only 4 hrs postoperatively
which is a relatively short period of observation. But earlier studies have indicated that AKI and a rise in urine NGAL
levels occur mostly within this period.
Although all the subjects in the study had normal serum creatinine measurements before surgery, an estimation of
GFR to document normal kidney function was not made.
Role of perioperative diuretics in influencing the urine NGAL levels was not considered in the study. Patients without
AKI who received diuretics may have a marked diuresis thereby diluting urinary NGAL, whereas patients with
evolving AKI may have a blunted response to diuretics with less urinary dilution, thus enhancing the discriminant
ability of urinary NGAL for AKI.
Conclusion
In our study, we found a definite relationship between a rising urine NGAL level and AKI after OPCAB. Further
larger studies are required to confirm the potential role and limitations of NGAL as an acute kidney injury biomarker.
Also, our study reaffirms the lesser effect of OPCAB on renal function as compared to CCABG, which may be due
to the biological effects of CPB and the activation of inflammatory system by CPB.
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5) Thakar CV, Worley S, Arrigain S, Yared J-P, Paganini EP: Influence of renal dysfunction on mortality after cardiac
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6) Mehta RH, Grab JD, OBrien SM, Bridges CR, Gammie JS, Haan CK, Ferguson TB, Peterson ED; Society of
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7) Thakar CV, Arrigain S, Worley S, Yared J-P, Paganini EP: A clinical score to predict acute renal failure after cardiac
surgery. J Am Soc Nephrol 16: 162168, 2005.
8) Tuttle KR, Worrall NK, Dahlstrom LR, Nandagopal R, Kausz AT, Davis CL: Predictors of ARF after cardiac
surgical procedures. Am J Kidney Dis 41: 7683, 2003.
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9) Demirjian S, Schold JD, Navia J, Mastracci TM, Paganini EP, Yared JP, Bashour CA: Predictive models for acute
kidney injury following cardiac surgery. Am J Kidney Dis 2012, 59:382-389.
10) Grayson AD, Khater M, Jackson M, Fox MA: Valvular heart operation is an independent risk factor for acute renal
failure. Ann Thorac Surg 75: 18291835, 2003.
11) Garg AX, Devereaux PJ, Yusuf S, et al; CORONARY Investigators. Coronary Artery Bypass Grafting Surgery
Off- or On-pump Revascularisation Study (CORONARY): kidney substudy analytic protocol of an international
randomised controlled trial. BMJ Open. 2012;2(2).
12) Nigwekar SU, Kandula P, Hix JK, Thakar CV. Off-pump coronary artery bypass surgery and acute kidney
injury: a meta-analysis of randomized and observational studies. Am J Kidney Dis. 2009;54(3):413-423.
13) Victor F. Seabra, Sami Alobaidi, Ethan M. Balk, Alan H. Poon, Bertrand L. Jaber: Off-Pump Coronary Artery
Bypass Surgery and Acute Kidney Injury: A Meta-Analysis of Randomized Controlled Trials. CJASN October
2010 vol. 5 no. 10 1734-1744.
14) Waikar SS, Betensky RA, Bonventre JV. Creatinine as the gold standard for kidney injury biomarker studies?
Nephrol Dial Transplant. 2009;24:32633265.
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novel urinary biomarker for ischemic injury. J Am Soc Nephrol 4: 25342543, 2003.
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novel urinary biomarker for cisplatin nephrotoxicity. Am J Nephrol 24: 307315, 2004.
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renal injury by NGAL. J Am Soc Nephrol 15: 3073 3082, 2004.
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Cheema FH, Markowitz G, Suganami T, Sawai K, Mukoyama M, Kunis C, DAgati V, Devarajan P, Barasch J:
Endocytic delivery of lipocalin-siderophore-iron complex rescues the kidney from ischemia. J Clin Invest 115:
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19) Devarajan P: Emerging biomarkers of acute kidney injury. Contrib Nephrol 156: 203212, 2007.
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acute injury following transplantation. Pediatr Nephrol 21: 856863, 2006.
21) Sargentini V, Mariani PM, DAlessandro M, et al. Assessment of NGAL as an early biomarker of acute kidney
injury in adult cardiac surgery patients. J Biol Regul Homeost Agents 26:48593.2012.
22) Siew ED, Ware LB, Ikizler TA. (2011). Biological markers of acute kidney injury. J Am Soc Nephrol 22:81020.
23) de Geus HR, Betjes MG, Bakker J. Biomarkers for the prediction of acute kidney injury: a narrative review on
current status and future challenges. Clin Kidney J. 2012; 5 (2): 102-108.
24) Xin C, Yulong X, Yu C, et al. (2008). Urine neutrophil gelatinase associated lipocalin and interleukin-18 predict
acute kidney injury after cardiac surgery. Ren Fail 30:90413.
25) Kuwabara T, Mori K, Mukoyama M, et al. (2009). Urinary neutrophil gelatinase-associated lipocalin levels reflect
damage to glomeruli, proximal tubules, and distal nephrons. Kidney Int 75:28594.
26) Wijeysundera DN, Karkouti K, Dupuis JY, Rao V, Chan CT, Granton JT, Beattie WS. Derivation and validation
of a simplified predictive index for renal replacement therapy after cardiac surgery. JAMA. 2007;297:18011809.
27) Michael Bennett,Catherine L. Dent,Qing Ma,Sudha Dastrala,Frank Grenier, Ryan Workman et al. Urine NGAL
Predicts Severity of Acute Kidney Injury After Cardiac Surgery: A Prospective Study. Clin J Am Soc Nephrol.2008
May;3(3): 665673.
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29) Mishra J, Dent C, Tarabishi R, et al. (2005). Neutrophil gelatinase associated lipocalin (NGAL) as a biomarker for
acute renal injury after cardiac surgery. Lancet 365:12318.
30) Celik JB, Gormus N, Topal A, Okesli S, Solak H: Effect of off-pump and on-pump coronary artery bypass
grafting on renal function. Ren Fail 27: 183188, 2005.
31) Jan Bucerius, Jan F. Gummert, Thomas Walther, Dierk V. Schmitt, Nicolas Doll, Volkmar Falk et al: On-Pump
Versus Off-Pump Coronary Artery Bypass Grafting: Impact on Postoperative Renal Failure Requiring Renal
Replacement Therapy. Ann Thorac Surg 2004;77:1250-1256.
32) Loef BG, Epema AH, Navis G, Ebels T, van Oeveren W, Henning RH. Off-pump coronary revascularization
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IACTACON 2016
Monitoring diastolic function using a simplified algorithm

in patients undergoing off pump coronary artery bypass
grafting (OPCABG) surgery
Deepak Borde
Context:
Left Ventricle Diastolic Dysfunction (LVDD) is gaining importanceas useful marker of mortality and morbidity
in cardiac surgical patients. Different algorithmshave been proposed for the intraoperative grading of diastolic
dysfunction. Knowledge of the particular stage of DD has clinical implications with the potential to modify
therapybut there is paucity of literature on the role of diastolic function evaluation during OPCABG surgery.
Aims:
The aim of the present study was to monitor changes in LVDD using simplified algorithm proposed by
Swaminathan et al in patients undergoing OPCABG.
Settings and design:
Tertiary care level hospital.
Prospective observational study.
Methods and material:
Fifty consecutive patients undergoing OPCABG were enrolled. Hemodynamic and echo parameters were
measured at 6 stages in every patient viz;after anesthetic induction (Baseline), during LIMA to LAD grafting
(LIMA LAD), SVG to OM grafting (SVG OM), SVG to PDA grafting (SVGPDA), during proximal
anastomosis of SVG to aorta and post protamine. The patients were classified in grades of diastolic dysfunction
as per simplified algorithm proposed by Swaminathan et alusing only intra operatively measured E and E.
Statistical Analysis:
Results:
The success rate of measurement and classification of diastolic dysfunction was 98.92% (277 out of 280 measurements).
The grades of diastolic dysfunction varied significantly as per surgical steps with maximum downgrading occurring
during OM and LAD grafting. During OM grafting, none of the patient had normal diastolic function, while 29%
patients exhibited restrictive pattern (Grade 3 LVDD). Patients with normal baseline LV diastolic function also
exhibited downgrading during OM and LAD grafting. Post protamine 37% patients with normal baseline diastolic
function continued to exhibit some degree of diastolic dysfunction.
Conclusion:
The LVDD changes dynamically during various stages of OPCABG, which can be successfully monitored with
simplified algorithm.
Introduction:
Left Ventricle Diastolic dysfunction (LVDD) refers to an abnormality of ventricular relaxation, compliance,
or filling that results in the requirement for an elevated left atrial pressure to achieve left ventricular filling[1].
Echocardiographically identified diastolic dysfunction has been reported to be an independent predictor of morbidity
mortality in variety of surgeries [2-8]. As per ASE/EAE recommendations, LVDD is assessed by the integrated use of
multiple echocardiographic parameters including spectral Doppler analysis of mitral inflow and pulmonary venous
flow, propagation velocity of mitral inflow, and tissue Doppler indices of mitral annular motion[1].
230
To date, at least 5 different algorithms have been proposed for the intraoperative grading of diastolic dysfunction[1,
9-12].
Swaminathan et al have proposed highly simplified algorithmusing only intraoperatively measured E and E. It was
observed that increasingly severe grades of diastolic dysfunction were significantly associated with reduced long-term
freedom from a composite endpoint of major adverse cardiac events (MACE) in 905 patients undergoing isolated
CABG surgery [9].
Hemodynamic management of patients undergoing OPCABG is challenging. TEE is extremely important monitoring
tool[13]. Knowledge of the particular stage of DD has clinical implications with the potential to modify therapy[10].
But, the role of diastolic function evaluation during OPCABG surgery has not been well reported.
The aim of the present study was to monitor changes in LVDD using simplified algorithm proposed by Swaminathan
et alin patients undergoing OPCABG.
Methods:
Fifty-oneconsecutive patients undergoing OPCABG were enrolled in this study. One patient was converted to on
pump CABG in view of hemodynamic instability while doing obtuse marginal (OM) grafting. Final analysis included
50 patients. The review board approved this study with waiver off to take separate consent. All patients underwent
surgery by midline sternotomy. Standardized anesthesia protocol consisted of general anesthesia with midazolam,
fentanyl and propofol. Vecuronium was used as muscle relaxant. Anesthesia was maintained with boluses of fentanyl,
midazolam and isoflurane as inhalational agent. Monitoring consisted of arterial blood pressure measured by femoral
arterial catheter, pulmonary artery (PA) catheter inserted by right internal jugular vein before induction. Surgical steps
consisted of midline sternotomy, harvesting of left internal mammary (LIMA) and saphenous vein grafts (SVG),
adequate heparinization (target activated clotting time>300 sec),LIMA to left anterior descending (LAD) grafting,
then as per severity of the coronary artery lesion remaining grafts on OM and posterior descending artery (PDA).
After the grafting heparin was reversed with protamine, hemostasis was achieved and wound was closed in layers. A
single surgical team performed all surgeries.
A TEE probe was gently inserted after induction and TEE images acquired and stored in Acuson X 500 Siemens Echo
Machine.Hemodynamic and echo parameters were measured at 6 stages in every patient viz;after anesthetic induction
(Baseline), during LIMA to LAD grafting (LIMA LAD), SVG to OM grafting (SVG OM), SVG to PDA grafting
(SVGPDA), during proximal anastomosis of SVG to aorta and post protamine. All the measurements were made
after hemodynamic stability was achieved, for example the measurements were made after passing intracoronary
shunt when the distal anastomosis were performed.When more than one grafts were performed in a territory the
values were averaged. All measurements were made in real-time and stored for analysis.
The details of echo measurements are as follows: Transmitral Doppler consisted of measurement of E-wave velocity,
A-wave velocity, E/A ratio, and Deceleration Time (DT) performed in the mid-esophageal 4-chamber view. A PW
Doppler sample volume was placed at the mitral leaflet tips. Spectral recordings were made at end expiration, when
feasible, at a sweep speed of 50 to 100 mm/s depending on heart rate. Measurements were not averaged over several
cycles, but the most representative waves were chosen for measurements. To ensure proper alignment, color flow
Doppler was performed prior to PW Doppler interrogation, to visualize the direction of blood flow, since the direction
of mitral inflow may vary depending on the underlying pathology and varying position of the heart. Mitral annular
motion was assessed in the mid-esophageal 4-chamber view with the Doppler beam aligned as parallel as possible to
the axis of motion of the cardiac tissue being measured. A sample volume was placed on the lateral annulus within 1
cm of the mitral leaflet insertion sites. The velocity scale was reduced to 20 cm/s from baseline, and the sweep speed
is adjusted to approximately 50 to 100 mm/s, most representative waves were chosen for measurements.
The patients were classified in grades of diastolic dysfunction as per simplified algorithm proposed by Swaminathan
et al as shown in Figure 1.
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IACTACON 2016
Results:
Baseline characteristics of 50 patients are as shown in Table 1.
Parameter
Mean age (years)
Female (%)
Mean Height (Cm)
Mean Weight (Kg)
Hypertension
Diabetes Mellitus
Mean Creatinine (mg%)
Mean ejection Fraction %
H/o myocardial infarction (%)
Mean No of coronary arteries diseased
Mean grafts performed
Values
59
6 (12%)
164
65
34 (68%)
17 (34%)
1.01
51
13 (26%)
2.74
3.29
An Echo measurement for diastolic dysfunction by simplified algorithm at baseline was possible in all 50 patients.
In 49 patients undergoing LIMA LAD echo measurement was possible in all patients; in 43 patients OM and
in 41 PDA grafting was done and echo measurement was possible in 42 and 40 patients respectively; in one
patients echo measurement was not possible at proximal grafting; echo measurementwas successfully done in all
50 patients post protamine. Thus the success rate of measurement and classification of diastolic dysfunctionwas
98.92% (277 out of 280 measurements). The main reason for unsuccessful measurement was inability to obtain
good mitral annular motion.
232
The hemodynamic parameters at various stages of surgery are as shown in Table 2.

Baseline
HR
SBP
DBP
SPAP
DPAP
Inotrope use
(%)
78
114
65
21
10
0 (0%)
L I M A
LAD
79
104
60
25
13
12 (24.4%)
SVG OM SVG
PDA
85
82
99
106
58
62
26
22
13
11
16 (37.4%) 10 (24.3%)
Proximal
anastomosis
81
98
54
18
7
9
Post Protamine
85
105
58
21
10
9
(18.36%)
(18%)
HR= mean heart rate (/min); SBP= mean systolic blood pressure (mm of Hg); DBP= Mean diastolic blood
pressure (mm of Hg); SPAP = mean systolic pulmonary artery pressure (mm of Hg); DPAP= mean diastolic pulmonary artery pressure (mm of Hg).
The echo parameters at various stages of surgery are as shown in Table 3.
Baseline
L I M A
SVG OM
LAD
SVG PDA
P r o x i m a l Post
anastomosis
mine
59
52
51
50
51
54
55
58
61
60
54
56
E/A
1.1
0.95
0.93
0.87
0.97
1.02
9.58
6.55
5.23
7.17
8.14
8.18
7.92
6.67
5.21
7.77
8.28
8.04
7.96
6.55
5.97
6.99
7.44
7.24
6.42
8.31
10.23
7.23
6.60
6.97
E/E
Prota-
The patients grades of diastolic dysfunction as per various stages of surgery are as shown in Table 4 or figure 2.
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IACTACON 2016
Grade
Baseline (n= L I M A SVG OM

50)
LAD (n=49) (n= 42)
Post
ProtaSVG PDA P r o x i m a l
Anastomosis mine
(n= 40)
(n= 49)
(n= 50)
40
19 (38%)
01 (2%)
00
05 (12%)
13 (26%)
15 (30%)
21 (42%)
20 (41%)
12 (29%)
21 (53%)
26 (53%)
22 (44%)
10 (20%)
27 (55%)
18 (42%)
14 (35%)
10 (21%)
13 (26%)
00
01 (2%)
12 (29%)
00
00
00
The grades of diastolic dysfunction varied significantly as per surgical steps with maximum downgrading occurring
during OM and LAD grafting. During OM grafting, none of the patient had normal diastolic function, while 29%
patients exhibited restrictive pattern (Grade 3 LVDD).
Patients with normal baseline LV diastolic function also exhibited downgrading during OM and LAD grafting.
Post protamine 37% patients with normal baseline diastolic function continued to exhibit some degree of diastolic
dysfunction as shown in figure 3.
234
A representative patients Trans Mitral PW Doppler and TDI are shown in Figure 4-15.
Figure 4- Trans Mitral PW Doppler at baseline
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IACTACON 2016
Figure 5- TDI at Baseline
Figure 6- Trans Mitral PW Doppler at LIMA LAD
236
Figure 7- TDI at LIMA LAD
Figure 8- Trans Mitral PW at SVG OM
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IACTACON 2016
Figure 9- TDI at SVG OM
Figure 10- Trans Mitral PW Doppler SVG PDA
238
Figure 11- TDI at SVG PDA
Figure 12- Trans Mitral PW Doppler at Proximal Anastomosis
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IACTACON 2016
Figure 13- TDI at Proximal Anastomosis
Figure 14- Trans Mitral Doppler post protamine
240
Figure 15- TDI at Post Protamine.
Discussion:
The main findings of this observational study are: LVDD changes dynamically in patients undergoing OPCABG as
per surgical stages with maximum downgrading occurring during OM and LAD grafting. This can be successfully
classified with the help of a simplified algorithm proposed by Swaminathan et al in 98.92% (277 out of 280)
measurements. Even in patients with normal baseline diastolic function there is downgrading of LVDD particularly
during OM grafting, around one third of patients with normal baseline diastolic function continued to exhibit some
degree of DD post protamine.
It is now well established that diastolic function, just as systolic function, has clinical, therapeutic, and prognostic
implications. In an observational study by Afilalo et al documented that preoperative diastolic dysfunction as
evidenced by restrictive filling was a strong predictor of mortality with odds ratio of 2.96[2]. Brenard et al reported
that abnormal diastolic filling patterns were frequently observed particularly in patients with altered LV function. DD
present before CPB was associated with an increased risk of difficulty in separation from CPB and vasoactive support
in the ICU[3]. Same group of investigators from Montreal, Canada in another study reported that moderate and
severe LVDD and Right ventricular DD could be identified with very good reproducibility, and both degrees
of diastolic dysfunction were associated with difficulty in separation from CPB[12].New or worsened DD after
CABG surgery is associated with an increased incidence of postoperative AF[4]. There is evidence suggesting that
moderate to severe diastolic dysfunction in patients with aortic stenosis is an independent predictor of late mortality
after valve replacement[5].The presence of perioperative diastolic dysfunction as assessed with Vp is an independent
predictor of postoperative CHF and prolonged length of stay after major vascular surgery[6].Despite this, a recent
multinational survey on TEE suggests that only 46% of academic centers currently perform an assessment of
diastolic function routinely during cardiac surgery [14].
There is evidence supporting that preoperative diastolic dysfunction is associated with poor outcome in patients
undergoing OPCABG. In a large study of 1048 patients undergoing OPCABG the authors evaluated the prognostic
implications of preoperative estimated LV filling pressure, assessed by E/E ratio which was an independent
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IACTACON 2016
predictor of 30-day and 1-yr MACE. The recommended that measurements of E/E may assist in preoperative risk
stratification of these patients[15].In another study, E/e ratio >15 was a significant predictor of composite endpoints
of postoperative morbidity[16]. Another study suggested that even in patients with preserved systolic LV function,
patients with E/E>15 were more prone to undergo a significant decrease in cardiac output during OPCAB, which
did not return to baseline level after completion of grafting[17]. In contrast to preoperative dysfunction, our study
has evaluated intraoperative stage wise changes in diastolic dysfunction in patients undergoing OPCABG. About
one third of patients with normal baseline function did not return to normal; but whether these changes in diastolic
dysfunction is associated with poor outcome remains to be evaluated.
Knowledge of the particular stage of DD has clinical implications with the potential to modify therapy[10, 18,19].During
the impaired relaxation phase, the mainstay of treatment is increasing preload and reducing heart rate to allow for
adequate LV filling. Patients in the decreased compliance stage have an increased LA pressure at baseline, i.e., preload
intolerant, thus requiring a careful perioperative fluid management and the judicious use of diuretics. Also, they may
require a higher aortic pressure to increase the coronary perfusion pressure owing to an increased LVEDP. The
appreciation of these fine differences between the stages of DD can further optimize perioperative management and
possibly improve outcome.
To date, at least 5 different algorithms have been proposed for the intraoperative grading of diastolic dysfunction[1,
9-12]
. Some of these algorithms are very complex to be used in busy environment of operating rooms; some are not
validated while using some of these guidelines result in inability to classify a large proportion of patients.A simplified
approach is highly desirable intraoperatively owing to the limited time frame for TEE examination. However, any
grading system, regardless of simplicity, is irrelevant unless it provides prognostic information by identifying those at
risk of adverse outcomes.
The simplified algorithm suggested by Swaminathan et al [9] fulfills most of these criteria. It is simple, can be rapidly
used in intraoperative period, and is validated in cardiac surgical population. Using the highly simplified algorithm
using only intraoperatively measured E and e, increasingly severe grades of diastolic dysfunction were significantly
associated with reduced long-term freedom from a composite endpoint of major adverse cardiac events (MACE)
in 905 patients undergoing isolated CABG surgery[9]. In contrast, strict application of a comprehensive algorithm
in keeping with ASE guidelines to grade diastolic dysfunction provided no clear association between grade of
dysfunction and MACE-free survival. In our study also we could assign a particular grade of diastolic dysfunction to
around 98% patients during all stages of OPCABG.
The hemodynamic management during OPCABG
is challenging.It is advocated that TEE should be used in all
[21]
patients undergoing OPCBAG [13,20]. Gurbuz et al looked at the effect of intraoperative TEE on OPCAB patients
specifically. Seven hundred forty-four OPCAB patients who had intraoperative TEE were retrospectively studied.
They found that TEE revealed previously undiagnosed intracardiac pathology in 1.3% of patients, with major
modification in surgical procedure. An IABP was placed in 3.2% of patients at the start of the procedure after
intraoperative TEE revealed severe left ventricular dysfunction that had previously been underappreciated. Severe
aortic atheromatous disease was found in 4.1% of patients, and all of these patients had a change in surgical plan
to a no-touch aorta technique with complete arterial revascularization. In another series of 500 patients undergoing
OPCABG Mishra et al[22], observed that was development of new regional wall motion abnormalities in 59.2%
and a decrease in global left ventricular functions in 61.2%. Obstruction of the right ventricular outflow tract was
observed on TEE at various stages during vertical displacement of the heart. The authors concluded that the use of
intraoperative TEE was valuable in enhancing the safety of the procedure.
However, intraoperative patterns of change in echocardiographic patterns of diastolic function, as well as their
clinical significance, remain poorly defined. We could describe a particular pattern of diastolic dysfunction using this
simplified algorithm. Maximum diastolic dysfunction occurred during OM and LAD grafting. None of the patients
had normal diastolic function during OM grafting. Two third of patients with normal baseline function returned
to normal values post protamine. It remains to be ascertained whether applying particular therapy can improve
outcomes depending on grade of diastolic dysfunction.
There can be various explanations to these changes. Tachycardia and rhythm disturbances may occur due to
hypovolemia, anemia, or electrolyte imbalances and may impair left ventricular filling[19]. Patients may develop mitral
regurgitation due to positioning of the heart particularly while performing OM grafting[23]. Diastolic dysfunction
can be an early marker of ischemia. Myocardial ischemia affects the processes underlying systolic inactivation, that
242
is, calcium extrusion from the cytosol and cross-bridge detachment, and will result in delayed relaxation. Adequate
relaxation depends on systolic events such as timing, velocity and synchronicity of contraction; increased left
ventricular afterload and wall stress and left ventricular dyssynchronous contraction result in delayed and incomplete
relaxation[19].
The present study has some notable limitations. The study is limited to only intraoperative period; we dont have similar
preoperative data orpostoperative follow up. A study with postoperative follow up with larger patient population
undergoing OPCABG is highly desirable. This study consisted of limited number of patients operated by a single
surgical team, varying results are highly possible with different patients population and expertise.
References:
1. Nagueh SF, Appleton CP, Gillebert TC, et al: Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echo 2009; 22:107.
2. Afilalo J, Flynn AW, Shimony A et al; Incremental Value of the Preoperative Echocardiogram to Predict
Mortality and Major Morbidity in Coronary Artery Bypass Surgery. Circulation 2013;127:356.
3. Bernard F, Denault A, Babin D, et al: Diastolic dysfunction is predictive of difficult weaning from cardiopulmonary bypass. AnesthAnalg2001; 92:291.
4. Ashes CM, Yu M, Meineri M, et al: Diastolic dysfunction, cardiopulmonary bypass, and atrial fibrillation after
coronary artery bypass graft surgery. Br J Anaesth2014;113:815.
5. Gjertsson P, Caidahl K, Farasati M, et al: Preoperative moderate to severe diastolic dysfunction: A novel
Doppler echocardiographic long-term prognostic factor in patients with severe aortic stenosis. J ThoracCardiovascSurg2005; 129:890.
6. Matyal R, Hess PE, Subramaniam B, et al: Perioperative diastolic dysfunction during vascular surgery and its
association with postoperative outcome. J VascSurg2009; 50:70.
7. Lee EH , Yun SC, Chin JH et al. Prognostic Implications of Preoperative E/e Ratio in Patients with Offpump Coronary Artery Surgery. Anesthesiology 2012; 116:362.
8. Jun NH, Shim JK, Kim JC, et al: Prognostic value of a tissue Doppler-derived index of left ventricular filling
pressure on composite morbidity after off-pump coronary artery bypass surgery. Br J Anaesth 2011; 107:519.
9. Swaminathan M, Nicoara A, Phillips-Bute BG, et al: Utility of a simple algorithm to grade diastolic dysfunction and predict outcome after coronary artery bypass graft surgery. Ann ThoracSurg 2011; 91: 1844.
10. Mahmood F, Jainandunsing J, Matyal R: A practical approach to echocardiographic assessment of perioperative diastolic dysfunction. J CardiothoracVascAnesth 2012; 26:1115.
11. Matyal R, Skubas NJ, Shernan SK, et al: Perioperative assessment of diastolic dysfunction. AnesthAnalg2011;
113:449.
12. Denault A Y, Couture P, Buithieu J, et al: Left and right ventricular diastolic dysfunction as predictors of
difficult separation from cardiopulmonary bypass. Can J Anesth2006; 53: 1020.
13. Kapoor PM, Chowdhury U, Mandal B, Kiran U, Karnatak R. Trans-esophageal echocardiography in offpump coronary artery bypass. Ann Card Anaesth 2009; 12: 174.
14. Dobbs HA, Bennett-Guerrero E, White W, et al: Multinational institutional survey on patterns of intraoperative transesophageal echocardiography use in adult cardiac surgery. J CardiothoracVascAnesth2014; 28:54.
15. Lee EH, Yun SC, Chin JH, Choi DK, Son HJ, Kim WC et al. Prognostic Implications of Preoperative E/e
Ratio in Patients with Off-pump Coronary Artery Surgery. Anesthesiology 2012; 116: 362.
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16. Jun NH, Shim JK, Kim JC, et al: Prognostic value of a tissue Doppler-derived index of left ventricular filling
pressure on composite morbidity after off-pump coronary artery bypass surgery. Br J Anaesth2011; 107:519.
17. Shim JK, Choi YS,Chun DH et al. Relationship between echocardiographic index of ventricular filling pressure and intraoperative haemodynamic changes during off-pump coronary bypass surgery. British Journal
of Anaesthesia2009; 102: 316.
18. McIlroy D, Lin E, Durkin C: Intraoperative transesophageal echocardiography: A critical appraisal of its
current role in the assessment of diastolic dysfunction. J Cardiothorac Vasc Anesth 2015; 29:1033.
19. Nicoara A, Whitener G, Swaminathan M: Perioperative diastolic dysfunction: A comprehensive approach to
assessment by transesophageal echocardiography. SeminCardiothoracVascAnesth2013; 18: 218.
20. Morganstern J, Kanchuger M. Pro: All Off-Pump Coronary Artery Bypass Graft Surgeries Should Include
Intraoperative Transesophageal Echocardiography Assessment. J Cardio Vasc Anesthesia; 2008: 625.
21. Gurbuz AT, Hecht ML, Arslan AH, et al: Intraoperative transesophagial echocardiography modifies strategy
in off-pump coronary artery bypass grafting. Ann Thorac Surg 2007; 83:1035.
22. Mishra M, Malhotra R, Mishra A, Meharwal ZS, Trehan N. Hemodynamic Changes During Displacement
of the Beating Heart Using Epicardial Stabilization for Off-Pump Coronary Artery Bypass Graft Surgery. J
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EFFECT OF VITAMIN C ON ADRENAL

SUPPRESSION BY ETOMIDATE INDUCTION IN
PATIENTS UNDERGOING CARDIAC SURGERY:
A RANDOMISED CONTROLLED TRIAL
Introduction:
I
A
C
T
A
C
O
N
Etomidate is a short acting hypnotic anaesthetic agent usually used as induction agent in
cardiac patients. It is preferred over other induction agents in patients with heart disease
due to its relative cardiovascular stability.[1] But etomidate inhibits cortisol synthesis due
to reversible adrenal suppression.[2]. This limits the use of etomidate as an induction
agent despite having so many fovourable effects on hemodynamics in cardiac patients as
compared to other conventional agents for induction of anaesthesia.
It has been proved that etomidate causes a dose-dependent inhibition of the enzyme
11-hydroxylase which converts 11-deoxycortisol to cortisol, thereby decreasing cortisol
level. It is well known that even a single dose of etomidate can suppress adrenal function
for up to 24 hours[3] and can decrease serum cortisol level even after cardiac surgery
which provides high level of stimulation to release endogenous stress hormones.[4]
Now for safe use of etomidate, a drug is to be searched for which will prevent this
reversible adrenal insufficiency so that etomidate can be used as an induction agent mainly
in cardiac compromised patient without its undesired side effects on the adrenal gland.
It is very important in cardiac compromised patients with poor cardiopulmonary reserve
where smooth induction is the prime goal to all cardiac anaesthesiologists. Moreover
adrenal dysfunction associated with etomidate may contribute to acute respiratory
distress syndrome (ARDS).[5]
Vitamin C (ascorbic acid) is a water-soluble vitamin that has a role in the synthesis of
cortisol. This drug can inhibit the suppression of cortisol formation after etomidate
injection. Vitamin C helps to maintain a normal adrenal function and helps in formation
of cortisol specifically in the terminal step of the conversion of 11-deoxycortisol to
cortisol.[6] Boidin et al. introduce vitamin C as a treatment option to decrease Etomidate
induced adrenal insufficiency. But many studies reported a controversial result whether
vitamin C can promote cortisol formation in patient having etomidate induced cortical
suppression.[7] There is paucity of evidence which has kept this area sill under research.
This study has been proposed to observe the effect of vitamin C on adrenal suppression
after etomidate induction in patients undergoing cardiac surgery.
We hypothesize that after etomidate induction, adrenocortical suppression will be less
in patients pretreated with vitamin C as compared to those not receiving the drug
preoperatively.
Materials and methods:

After obtaining the institutional ethical committee clearance and written informed consent from all patients, the study was conducted.
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IACTACON 2016
Inclusion criteria:
Patients of either sex, free of any endocrine disease, aged 25 60 years with NYHA status <IV, scheduled for
elective cardiac surgery were included.
Exclusion criteria:
Patients with Parsonnet score >10, on steroid, with history of DM, alcohol abuse, smoker, pregnant, suffering from
epilepsy, haematological disease, impaired hepatic and renal function, patients having hypersensitivity to any of the
study drugs and a patient requiring cross clamp time of more than 2 hours were excluded from the study.
During pre anaesthetic check up all patients were explained the procedure and informed written consent were
obtained. Angiotensin-converting enzyme inhibitors were stopped 24 hours before surgery. However, calciumchannel antagonists and -adrenergic blocking drugs were continued till the day of surgery. Group I received oral
vitamin C (500mg) twice daily and Group II received Antacid tablet as placebo (aluminium hydroxide and magnesium
hydroxide) twice daily instead of vitamin C for 7 consecutive days prior to surgery till morning of surgery. The
drug was administered according to a computer-generated randomization chart by an anesthesiologist who was not
involved in the study.
After proper pre-anaesthetic optimization, all patients were examined again the day before surgery. Patients of both
the groups were premedicated with lorazepam 1 mg, ranitidine 150 mg, and metoclopramide 10 mg orally, the night
before surgery. Patients were wheeled into operating room and standard ASA monitors (pulse oxymeter, NIBP till
the IBP were done, ECG) were attached. An intravenous line was inserted in all patients in right dorsum or forearm.
Left Radial arterial cannulation was done after local anaesthesia. All patients received intravenous (i.v.) piperacillin
and tazobactum (4.5 gm).
Induction of anaesthesia was performed with inj midazolam (0.01 mg/kg), fentanyl (2-3g/kg) and etomidate (0.10.3 mg/kg) till loss of consciousness. Neuromuscular blockade was achieved by 1 mg/kg of rocuronium to facilitate
endotracheal intubation. Intraoperatively, neuromuscular relaxation was maintained with rocuronium. The lungs were
ventilated with nitrous oxide in oxygen (50:50). End-tidal CO2 was maintained between 35 and 45 mmHg. Anaesthesia
was maintained with isoflurane at 0.8 1.0 minimal alveolar concentration. Pulmonary artery catheterization and
central venous cannulation were performed thereafter and surgery was started. All the drugs were diluted/dissolved
in normal saline. In both groups serum cortisol and lactate level were checked preoperatively 10 minutes before
induction and was evaluated 3 minutes after laryngoscopy, after sternotomy, at 1 hour of induction, after cross
clamp application and after cross clamp release and then at 6th,12th and 24th hour after induction. Arterial blood
gas analysis (ABG) was done hourly to check acid base imbalance and electrolytes and was corrected accordingly.
Blood glucose was estimated hourly and insulin infusion was started to maintain <180 mg/dl in the intraoperative
and postoperative period. Hemodynamic parameters were monitored continuously and recorded at different point
of time. Urine output was monitored. Data were collected by a resident blinded to the study. Heparin (400 units/
kg) was administered before placement of aortic cannulation to achieve an activated clotting time of >480s. The
CPB circuit was primed with lactated Ringers solution, sodium bicarbonate, mannitol, and heparin. Hematocrit
was maintained at 21-28% during CPB. Myocardial protection was achieved by antegrade cold cardioplegia (at 4C,
St. Thomas solution-based crystalloid-blood cardioplegic solution PLEGIOCARD as 1:4 ratio) after aortic cross
clamp and the cardioplagia was repeated every 20 minutes. The cardiac repair or valve replacement was carried
out under CPB with mild hypothermia using standard extracorporeal techniques. Nitroglycerine infusion 0.5g/
kg/min, adrenaline 0.05 g/kg/min and dopamine 5 g/kg/min were started at the onset of rewarming as per
the institutional protocol. Infusion of milrinone, noradrenaline and amiodarone was also initiated according to the
need to maintain mean arterial pressure >70mmHg, pulmonary artery pressure below 30mmHg and normal sinus
rhythm. All the patients were rewarmed to 37C. Serum potassium levels were optimized to 4-4.5 mEq/L throughout
surgery. Ventricular fibrillation (VF) or ventricular tachycardia (VT) was treated with Xylocard, MgSO4, amiodarone
as appropriate and in cases refractory to medical management internal defibrillation with 20-50 J was administered.
Intravenous protamine sulphate 1.3 times the heparin dose was used to reverse the effect of heparin when patient
was weaned off CPB support to return the activated clotting time to within 20% of the preoperative value. In all
cases Epsilon-aminocaproic acid (EACA) was administered before going on pump, on pump and post pump at the
dose of 100mg/kg.
After surgical closure, all patients were transferred to postoperative intensive care unit where they were monitored
closely for the first few postoperative days. Any adverse events like new onset arrhythmia, hypo/hyperglycaemia,
electrolyte imbalance, bleeding, infections, acute renal failure in the perioperative period were recorded and treated
accordingly.
246
Statistics
For the purpose of sample size calculation, serum cortisol level at 1hour following etomidate administration was
taken as the primary outcome measure. It is calculated that 35 subjects will be required per group in order to detect
the difference of 0.5g/dl in serum cortisol level between the two groups with 80% power and 5% probability of
Type I error. This calculation assumes two sided testing and 0.75g/dl as a SD for serum cortisol level. We enrolled
total 78 patients considering dropout. Patients were randomised by a computerized randomization chart on the day
of first pre anaesthetic checkup, into two groups; group I (n=35) and group II (n=35) to receive either oral vitamin
C (500 mg) twice daily and Antacid tablet (aluminium hydroxide and magnesium hydroxide) as placebo twice daily
instead of vitamin C for 7 cosequitive days prior to surgery, respectively.
In this study multivariate regression model specially a difference in difference (DID) method has been used to figure
out whether there is any difference of cortisol secretion between individuals belonging in the group I and the group
II. Other numerical variables were compared between groups by Students unpaired t-test if normally distributed or
a Mann-Whitney U-test as appropriate. Fishers exact test was employed for inter group comparison of categorical
variables. A two-tailed P value <0.05 was considered as statistically significant.
Results
A total of 78 patients were assessed initially for eligibility for inclusion in this prospective parallel group double
blinded randomized controlled trial. In the beginning, 6 patients were excluded as they refused to participate. The
study was started with 72 patients, who were randomized to be divided into two groups (n=36) equal in numbers
as per a computerized randomization chart. During operation 2 patients one from each group were excluded from
the study as the aortic cross clamp was applied more than 2 hours. So, data of 35 patients of each group was finally
analyzed.
Cortisol level at different points of time in between the two groups was assessed and it shows clearly that cortisol
level is much lower in group II (27.744.72) as compared to group I (69.517.65] in the first post induction hour
(P=0.000)[Table1] (fig 1). It has been also strongly established that cortisol suppression in group 2 is significantly
higher as compared to group I. In group II cortisol level is lower not only at the first post induction hour but
throughout the first 24 post induction hour. On the contrary patients of group I have higher cortisol level throughout
the first 24 post induction hour indicating the positive effect of vitamin C.
Figure 1: Difference in cortisol secretion at different points of time in between two groups.
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IACTACON 2016
Eight different regression equation has been used here to calculate the difference in cortisol level at 8 different points
of time (considering the first observation t=0). The regression equation for time point t is..
Xt is the vector of controls. is a time specific dummy variable which takes values 1 if time is t and 0 for the initial
time point. The coefficient vector captures the effect of control. We have considered proxies of stress variable in
X. is the error term, following the usual classical linear regression model assumption (Woldridge 2005). Now at time
point 0 (first observation) the difference in average cortisol secretion between group I and II captured the differences
of inter-person differences.
Table 1: Difference in difference estimators before and after treatments
time 1
time 2
time 3
time 4
time 5
time 6
time 7
time 8
1.t
1.69
(1.22)
0.40
(0.18)
0.07
(0.02)
5.98
(1.87)
-1.16
(-0.39)
-3.03
(-0.83)
-5.98
(-1.54)
10.81***
(3.40)
1.D
-0.59
(-0.54)
-0.58
(-0.56)
-0.58
(-0.46)
-0.59
(-0.52)
-0.58
(-0.51)
-0.58
(-0.56)
-0.58
(-0.57)
-0.59
(-0.51)
delta
14.88***
(9.42)
19.14***
(11.97)
42.15***
(16.30)
48.39***
(19.05)
51.16***
(17.49)
44.03***
(15.60)
38.11***
(16.78)
13.87***
(7.16)
lactate
-3.14
(-1.67)
-0.08
(-0.06)
0.17
(0.11)
-2.16
(-1.57)
0.19
(0.21)
0.39
(0.40)
1.55
(1.44)
-2.42
(-1.59)
Constant
30.58***
(14.71)
27.43***
(17.36)
27.18***
(14.39)
29.57***
(18.21)
27.16***
(22.63)
26.95***
(21.89)
25.77***
(19.58)
29.84***
(16.95)
Observations
140
140
140
140
140
140
140
140
R2
0.65
0.79
0.93
0.95
0.96
0.95
0.94
0.71
0.643
0.781
0.923
0.946
0.956
0.949
0.943
0.699
Adjusted R
t statistics in parentheses
p < 0.05, ** p < 0.01, *** p < 0.001
Table 2. shows the result of the model corresponding to the regression equation. We have estimated the model
separately with or without including controls for the lactate. It is clearly observable that the results remain consistent
with the previous finding i.e that of Table 1.
Table 2: Difference in difference estimators in a panel data framework
1.t
2.t
3.t
4.t
Cortisol
Cortisol
0.289
0.309
(0.23)
(0.24)
0.283
0.351
(0.23)
(0.24)
0.386
0.469
(0.31)
(0.30)
1.289
1.387
(1.04)
(0.83)
248
5.t
6.t
7.t
8.t
1.D
time 1
-0.574
-0.430
(-0.46)
(-0.21)
-1.623
-1.457
(-1.31)
(-0.65)
-0.591
-0.432
(-0.48)
(-0.20)
6.080
6.169***
***
(4.90)
(3.86)
-0.583
-0.583
(-0.47)
(-0.47)
14.45
14.45***
***
(8.23)
time 2
time 3
time 4
time 5
time 6
time 7
time 8
(8.22)
***
19.11
19.13***
(10.88)
(10.78)
***
42.35
42.40***
(24.12)
(22.86)
***
45.29
45.36***
(25.80)
(23.80)
***
51.68
51.81***
(29.44)
(22.75)
***
45.00
45.11***
(25.63)
(20.68)
***
40.64
40.72***
(23.15)
(20.89)
12.20
12.23***
***
(6.95)
lactate
(6.82)
-0.0456
(-0.09)
Constant
27.35
Observations
R
Adjusted R
***
27.40***
(31.16)
(26.72)
630
630
0.932
0.932
0.930
0.930
*
**
***
t statistics in parentheses
p < 0.05, p < 0.01, p < 0.001
Total requirement of adrenaline is higher in group II as compared to group I [Table 3]. Though noradrenaline dose
was higher in group II as compared to group I, it is not statistically significant though it has a positive impact on the
study result.
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Table 3 Requirements of infusion of cardiac drugs

P Value
Total requirement of
P value
3.41.09
0.047*
Noradrenaline
455.00
-1.850
0.064
169.4340.36
159.4338.26
0.291
Milrinone
609.50
-0.035
0.972
31.3413.29
30.0312.42
0.670
Amiodarone
580.50
-0.375
0.707
Total require- Group I

ment of
(n=35)
Group II
Adrenaline
2.81.27
Dopamune
NTG
(n=35)
Students
unpaired t
test has been
done
Mann-Whitney
U test has been
done
= Values represent mean Standard deviation; *P< 0.05 = Statistically significant

Data analysis in table 4 reported the demographic parameters and patient profiles as well as perioperative events
which did not show any statistically significant difference between the two groups.
Figure 2: No difference in blood glucose level at different points of time in between the two groups
Table 4. Patient profile and perioperative events

Parameters
Group I (n=35)
Group II(n=35)
P value
Age (year)
48.146.46
45.2311.47
0.195
Mean arterial pressure (mmHg)
65.094.93
66.034.96
0.428
Ejection fraction (%)
56.175.86
56.146.15
0.984
Duration of surgery (hour)
6.831.45
6.471.26
0.280
CPB Time (minute)
93.6319.03
93.6022.20
0.995
Duration of aortic cross clamp (minute)
71.4620.36
65.5223.53
0.263
250
NYHA(II/III)
22/13
20/15
0.808
History of previous cardiac intervension (yes/no)
4/31
2/33
0.673
Incidence of hypoglycaemia(Yes/No)
4/31
3/32
1.000
Incidence of Atrial Fibrillation(Yes/No)
5/30
7/28
0.752
Incidence of Ventricuar tachycardia(Yes/No)
3/32
5/30
0.710
Incidence of ectopic beats(Yes/No)
6/29
3/32
0.477
30 days mortality(Yes/No)
2/33
1/34
1.000
Incidence of reintubation(Yes/No)
4/31
5/30
1.000
Incidence of pre operative MI(Yes/No)
3/32
2/33
1.000
Incidence of sepsis(Yes/No)
2/33
3/32
1.000
= Values represent mean Standard deviation; P < 0.05 is statistically significant; NYHA = New York Heart
Associationfunctional classification, CCF = Congestive cardiac failure, CVP= Central venous pressure, COPD=
Chronic obstructive pulmonary disease, ETT=Endotracheal tube, MI=Myocardial ischemia.
Discussion
The properties of etomidate include hemodynamic stability, minimal respiratory depression, cerebral protection,
and pharmacokinetics enabling rapid recovery after a single dose. In cardiac patients etomidate results in very
stable hemodynamics with almost no change in heart rate, mean arterial pressure, mean pulmonary artery pressure,
pulmonary capillary wedge pressure, central venous pressure, stroke volume, cardiac index or pulmonary and
systemic vascular resistance.[8] In cardiac surgery where all patients are suffering from poor cardiac function thereby
compromised cardiac reserve where now a days etomidate is increasingly used. A recent study of etomidate in
pediatric patients with intracardiac shunt lesions showed that induction with 0.3 mg/kg produced minimal changes
in hemodynamics or shunt fraction.[9] Though many studies have reported its advantages over other induction agent
in cardiac compromised patients, its safe use is still controversial rather restricted due its unwanted adverse effect on
adrenal gland. It is already well established that etomidate causes reversible adrenal insufficiency for at least 24 hours
even after a single bolus dose.[10]
To overcome such problem this study has evaluated the effect of vitamin C on etomidate induced adrenal suppression
in patients undergoing cardiac surgery under cardiopulmonary bypass.
In present study, adrenal suppression by etomidate was significantly less in group I as compared to group II which is
reflected by a higher level of cortisol in patients who received vitamin C.. This is statistically significant throughout
the first 24 post induction hour. The total requirement of adrenaline dose were also significantly higher in group II
(3.401.09) than group I (2.831.27) with P =0.047 that also signifies the positive correlation of inhibitory effect of
vitamin C on adrenal suppression by etomidate.
Etomidate inhibits 11-hydroxylase (CYP11B1), 11- and 18-hydroxylase (CYP11B2) and cholesterol side-chain
cleavage enzyme system (CYP11A) with decreasing effectiveness. Decreased CYP11B1 activity will lead to lower
levels of cortisol and increased levels of the upstream precursor 11-deoxycortisol. Decreased CYP11B2 will lead
to lower aldosterone and higher 11-deoxycorticosterone levels, whereas decreased CYP11A will lead to generally
decreased steroidogenesis.[11][12]
Supplementation with ascorbic acid, a major source of NADPH, inhibits adrenal suppression by etomidate by
promoting the turnover rate of 11-beta-hydroxylase, thereby increasing the cortisol formation. The blockade of
11-hydroxylase seems to be related to the free imidazole radical of Etomidate-binding cytochrome P-450.[13] This
results in inhibition of ascorbic acid re-synthesis, which is required for steroid production in humans. Blockade of the
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cytochrome P-450 dependent enzyme 11-hydroxylase results in decreased mineralocorticoid production in critically
ill patients.[14] Therefore, vitamin C supplementation restores cortisol levels to normal after the use of Etomidate.
Duthie and his colleagues showed that patients undergoing minor peripheral surgery, plasma cortisol levels were
slightly depressed from the pre-induction levels for 1 hour postoperatively and the nadir of mean cortisol levels did
not fall out of the normal range.[15] However, high-stress surgery can induce a clinically significant level of cortisol
deficiency and adrenocortical suppression. Other studies showed no evidence of a clinically relevant attenuating
effect of ascorbic acid or xylitol on Etomidate-induced adrenocortical suppression.[16][17][18]
In this study oral vitamin C rather than intravenous was selected as it is less invasive and easy with effective blood
concentration when taken 500 mg twice daily. Daily dose is recommended as maintaining optimal levels of vitamin
C is difficult because it is water soluble and cannot be stored in the body especially with regard to chronic illness.[19]
Iribarren et al examined a prospective cohort of 120 patients and found etomidate to be a risk factor for relative
adrenal insufficiency and higher vasopressor requirements after surgery up to 4 h of ICU admission.[20] In the present
study total requirement of adrenaline was significantly higher in patients who did not receive vit C that indicates
adrenal suppression is significant. Though noradrenaline dose were similar in both the groups in this study. This may
be due to variation in type of surgery. There are few studies which showed no difference in vasopressor requirements
in between groups with or without etomidate. This variation may be due to different in patient population and
different stress response to various cardiac surgery.
The perioperative adverse events like arrhythmia, ventricular fibrillation, ventricular tachycardia, blood loss and
incidence of blood transfusion were consistent in both the groups.
In this study there is no clinically or statistiacally significant difference in length of ICU stay, 30 days mortality
or incidence of infection rates in between the two groups though relative adrenal insufficiency is associated with
increased mortality and mobidity in seriously hemodynamic compromised patients. The retrospective analysis of the
Corticosteroid Therapy of Septic Shock study suggested that etomidate use was associated with a 1.8-fold increased
risk of mortality although the 95% CI ranged from 0.5 to 6.4.[20],[21] The CORTICUS cohort suggest that patients
receiving etomidate before enrollment had 28 day mortality significantly higher than other patients in the trial.[21][22][23]
No large studies have evaluated the effect of etomidate use on prolonged mechanical ventilation or hospital length
of stay. Present study suggests that vit C administration provided no added advantage in length of ICU stay and
early extubation. Though it is an indirect evidence that lower requirements of inotropes in the perioperative period
in group I enhances early recovery but there is no ststistically significant difference in extubation time and length of
ICU stay in between the two groups. This finding is consistent with one of the largest retrospective studies in sepsis
patients where etomidate use not associated with longer mechanical ventilation or hospital length of stay.[24]
The present study did not show any significant difference in total dose of insulin required to maintain blood glucose
level <200 mg/dl throughout the study period. Though a recent study has shown that oral vitamin C 1000 mg daily
decreases HbA1c in diabetic patient.[25] This contrary is probably due to selection of nondiabetic patients in our study
and further research is still needed.
To avoid the confounding effect of circadian rhythm on hormone levels, all operations were performed in the
morning between 8:30 and 9:00 am. We have used the advanced statistics (Multivariate regression model) so that an
unmeasured variable can not influence the evidence of relation between etomidate use with vitamine C pretreatment
and perioperative outcomes.
Limitation of the study:

We did not assess adrenal function preoperatively rather just clically excuded any endocrinal disease. A large study
sample would be better to evaluate the exact result. This result may not be similar in peadiatric population. So, further
research is needed.
Conclusion:
Oral Vitamin C 500 mg twice daily for 7 days preoperatively can inhibit adrenal suppression by etomidate induction
in cardiac patients who are posted for elective cardiac surgery under cardiopulmonary bypass. So, etomidate may be
an acceptable option for the induction of anesthesia in cardiac compromised patients with pretreatment of vitamin C.
252
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ABSTRACTS
IACTACON
Chennai 2016
258
ABSTRACTS
EuroSCORE II, STS and ACEF Scoring systems fail to

predict outcome after Minimally Invasive Direct
Coronary Artery Bypass graft surgeries in Asian patients.
Dept. of Anesthesiology, Fortis Hospital, B.G. Road, Bengaluru, India
ABSTRACT
Introduction
Risk stratification models perform well in development cohort, but need to be revalidated and recalibrated in new
populations. This study aim to assess the performance of EuroSCORE II (European System for Cardiac Operative
Risk Evaluation II), STS Society of Thoracic surgeons risk score for mortality) and ACEF (Age, Creatinine and
Ejection Fraction) scores in predicting outcomes after minimally invasive direct coronary artery bypass graft
(MIDCAB) surgeries.
Methods
We reviewed all MIDCAB patients from March 2013 to December 2015 at Fortis hospital, Bengaluru. IEC approval
was obtained, data collected and scores calculated.
Statistical Analysis
Associations of survival to scores were tested using Cox proportional hazard (Cox PH) regression. Survival
distributions between high and low score categories were compared using Kaplan-Meier (KM) method. Areas under
time dependent receiver operator characteristic curves were used to compare scoring systems at different time points.
Bootstrapping was done. R and SPSS for Windows were used. All tests were two-sided, and P < 0.05 was considered
to indicate statistical significance.
Results
Cohort size was 56 patients who underwent isolated MIDCAB. EuroSCORE II, STS score and ACEF scores were
1.44 1.06, 0.80 0.82 and 1.09 0.33, respectively. There were 9 MACCEs during follow-up. Cox PH regression
resulted in hazard ratios of 0.662 (p=0.4), 0.591 (p=0.45) and 1.906 (p=0.35) for ESII, STS score and ACEF score,
respectively. Comparing between high and low risk categories in each scoring system, the difference noted was
statistically insignificant (Mantel-Cox Log rank test p of 0.55, 0.4 and 0.077, for ESII, STS score and ACEF score,
respectively). Timed ROC curve analysis also failed to demonstrate a significant difference.
Conclusion
In MIDCAB patients, ESII, STS score and ACEF scores fail to predict long term survival.
259
IACTACON 2016
2 mg/kg heparin is non-inferior to 3mg/kg in off-pump

coronary artery bypass surgeries: randomized, single
center, blinded, noninferiority study
Dept. of Anesthesiology, Fortis Hospital, B.G. Road, Bengaluru, India

Introduction
Off pump coronary artery bypass surgery (OPCAB) is considered hyper-coagulable state; there are no
guidelines regarding dosage of heparin during OPCAB. Some clinicians use 2 mg/kg while others 3 mg/kg.
We wished to study the effects of two different doses of heparin during OPCAB on activated coagulation
times, bleeding and postoperative outcome.
Materials and Methods
62 consecutive patients undergoing OPCABG were randomized into 2 mg/kg (N=36) and 3 mg/kg (N=26)
regimen of heparin. Preoperative demographics, laboratory values, intra-operative ACT, blood loss and
complications were noted.
Results
The groups were comparable except in terms of history of platelet count, Clotting time and INR. ACT after
heparin was significantly higher (386.83 vs. 485.04 seconds) in 3 mg/kg group, but was similar after protamine
(137.6 vs. 142.96 seconds). There was no difference in requirement for extra protamine. Perioperative ECG
changes, arrhythmias, need for CPB conversion and IABP insertion were similar. Intra and postoperative
blood loss (685.56 vs. 671.15 ml, p= 0.82 and 1906.29 vs. 1793.65 ml, p= 0.49, respectively) and need for
blood products were similar.
Conclusion
Heparin dosing of 2 mg/kg does not differ from 3mg/kg.
260
ABSTRACTS
TRANSCATHETER AORTIC VALVE IMPLANTATION OUR

EXPERIENCE.
DR ASHUTOSH V. SHARMA,
DEPT OF ANESTHESIOLOGY, FORTIS ESCORTS HEART INSTITUTE, NEW DELHI, INDIA.
INTRODUCTION
Transcatheter aortic valve implantation (TAVI) is an emergent technique for treating elderly patients with symptomatic
severe aortic valve stenosis who are poor candidates for surgical AVR.We present anesthetic management of 15 cases
who underwent TAVI at Fortis Escorts Heart Institute, New Delhi during the period Feb 2012 to June 2015.
METHODS
Prior approval from hospital ethical committee & informed consent from the patients were taken.A total of 15 cases
received self expanding Corevalve (Medtronics Inc.) using transfemoral arterial approach except one which was done
via right subclavian artery.All patients had severe calcific aortic stenosis with a mean Euroscore of 16 (range 4 35).
Age of patients ranged from 59 84 yrs (mean 75.46 yrs ) 9 were male & 6 female.Nine patients had previous CABG
& three had received coronary stent in the past.Five patients had LV dysfunction (EF 35 45%) & four patients had
S.Creatinine more than 1.5mg%.
GA with TEE was used in 13 cases. Two patients who were high risk for GA were done under LA
& MAC. One patient had retrosternal thyroid compressing the trachea & the other had ILD with room air SpO2 of
84%.All GA cases except one were extubated within 4 hrs in the recovery. Discharge from the hospital ranged from
4 20 days (mean 8 days) after the procedure.
RESULTS
There was no anesthetic complication under GA or LA & the valve was successfully implanted in all 15 cases.In one
patient the valve got malpositioned during partial deployment. It was retrieved, reloaded & placed successfully.Two
patients developed CHB during the hospital stay & needed permanent pacemaker implantation.
CONCLUSION
TAVI is a promising technique for elderly symptomatic patients with severe aortic stenosis in whom surgical AVR is a
high risk. Success of the procedure depends on a HEART TEAM comprising of interventional cardiologist, cardiac
surgeon, cardiac anesthetist, radiologist, perfusionist & paramedical staff. It can be safely performed under both GA
& LA.
261
IACTACON 2016
HEMODYNAMIC EFFECTS OF PERIOPERATIVE

DEXMEDETOMIDINE THERAPY IN VALVULAR HEART
SURGERIES A RANDOMIZED CONTROL TRIAL
Sambhunath Das, Neeti Makhija, Balram Airan, Gautam Sharma
Department of Cardiac Anaesthesia, CTVS and Cardiology, AIIMS, New Delhi
Introduction:
The association of arrhythmia and ventricular dysfunctions produce trouble shooting postoperative recovery
in valvular heart diseases. Surgery, anaesthesia and cardiopulmonary bypass (CPB) generate tremendous stress,
inflammation and hemodynamic alterations. This results in increased morbidity, mortality and cost. Dexmedetomidine
is a new alpha-2 adrenergic agonist proved to reduce stress, tachyarrhythmia, inflammation, adrenergic stimulation
and myocardial dysfunction. Hence this prospective randomized control trial was designed to study hemodynamic
effects of perioperative dexmedetomidine therapy in valve surgery.
Method:
110 patients were recruited to the study. Patients were distributed randomly into control (Group-1; n=55) and
dexmedetomidine (group-2; n=55). In group 2 dexmedetomidine 0.5g/kg was administered slowly over 10min as
bolus and followed by 0.5 g/kg/h throughout the surgery and in ICU. In group 1 a similar infusion of normal saline
was continued. Heart rate, MAP and cardiac index were recorded at baseline, after induction, 30 min after CPB, after
8h and 24h of surgery. Cardiac Holter recorded for 24h to detect ECG changes.
Result:
Patients were similar in demographic parameters. Group 2 had significant lower HR (p=0.01 0.007). Other than
base line, MAP in group 2 patients was higher than control but statistically non-significant (p= 0.17- 0.51). Higher
cardiac index detected in group2 (p=0.001). Significantly lower requirement of fentanyl and midazolam, extubation
time, ICU stay and hospital stay was observed in group 2. Post-operative atrial fibrillation was less in group 2. Lower
inotrope requirement needed in group 2 but non-significant (p=0.8)
Discussion:
Perioperative dexmedetomidine reduced heart rate and improved blood pressure and cardiac index. The incidence
of AF, requirement of inotrope, ICU stay and hospital stay was less in dexmedetomidine treated patients. The study
indicates that dexmedetomidine is beneficial in valve surgery.
Conclusion:
Perioperative dexmedetomidine therapy improved hemodynamic parameters in valvular heart surgery. Further study
needed to establish beneficial effect of dexmedetomidine.
262
ABSTRACTS
APPLICATION OF BLOOD CONSERVATION STRATEGY IN A

RARE BLOOD GROUP PATIENT - CHALLENGES FACED IN
PERIPHERAL CENTRES
Dr Satwik Telkar,Dr Madhuprakash,S C.Dr Manjunatha B N,Dr Srinivas Kulkarni
Consultant cardiac anaesthesiologist, Cauvery heart hospital, Mysore, Karnataka
Abstract
Middle aged male patient, with severe AR and MR presented with NHYA class III symptoms. DVR was planned for
him and he was subjected to routine investigations, during which he was found to have a rare subtype of O -ve blood
group, BOMBAY BLOOD group. Blood compatible with his group was not available in any centre, in Mysore.
Hence usage of blood conservation strategy was planned for him , after explaning to him about the risks involved
and consent was obtained.Patient was started on erythropoietin and hematenics, 2 pints of blood were collected
over a period of 2 weeks and 1 pint of blood was collected on the day of surgery by ANH technique.Intra operative
blood loss was significantly reduced by meticulous surgery and usage of drugs like tranexamic acid, EACA.The
main challenge in managing this case was to conduct such a major surgery on a very rare blood group patient , in a
peripheral centre with limited resources, which we managed efficiently.
263
IACTACON 2016
MITRAL VALVE REPLACEMENT USING CHITRA HEART

VALVE PROSTHESIS: INTRAOPERATIVE TRANSESOPHAGEAL
ECHOCARDIOGRAPHY EVALUATION
INTRODUCTION:
Dr Shrinivas Gadhinglajkar, Dr Jagadeesh N Vaggar, Dr Neelam Aggarwal, Dr Rupa
Sreedhar.
Sree Chitra Tirunal Institute For Medical Sciences and Technology, Trivandrum, Kerala, India
Objective
TTK Chitra heart valve prosthesis is a tilting disc artificial heart valve which is commonly used for aortic and mitral
valve replacement. Although, postoperative studies depicting echocardiographic characteristics of Chitra heart
prosthesis at mitral position are available in the literature, intraoperative studies are lacking. We present our experience
on intraoperative transesophageal echocardiography evaluation of Chitra heart valve prosthesis at mitral position.
METHODS:
45 consecutive patients operated for mitral valve replacement using Chitra prosthesis were prospectively evaluated
using intraoperative TEE. Echocardiographic evaluation was performed before establishment of cardiopulmonary
bypass and after weaning from bypass. Hemodynamic parameters, inotropes, pacing requirement were noted. Chitra
prosthesis was evaluated using 2D echocardiography, color and spectral Doppler imaging. Statistical analysis was
performed using windows SPSS version 16 and Microsoft excel version 2010.
RESULTS:
Various sizes of replaced valves were 23,25,27,29 and 31 mm in 9, 16, 9, 6 and 5 number of patients respectively.
On 2D evaluation, CHVP was found normally functioning in all patients with less than mild MR on color Doppler
evaluation. The Peak velocity and mean gradients were inversely related to the size of the prosthesis, whereas effective
orifice area calculated by PHT and CE were in direct correlation with the valve size. DVI and mean velocities did not
have any significant correlation with the size of the valve implanted.
CONCLUSION:
Chitra heart valve prosthesis implanted at mitral position meets the guidelines published by American society of
echocardiography pertaining to echocardiographic evaluation of heart valve prosthesis.
REFERENCES:
1) Recommendations for evaluation of prosthetic valves with echocardiography
and doppler ultrasound: a report From the American Society of
Echocardiographys Guidelines and Standards Committee and the Task Force on
Prosthetic Valves. J Am Soc Echocardiogr. 2009 Sep; 22(9):975-1014
264
ABSTRACTS
LA Aneurysm A case report
Dr Yogesh Z , Dr Amol T , Dr V.R. Shrotey

Dept of Anesthesia Govt Medical College & Super Specialty Hospital Nagpur.
We are presenting rare case of girl undergoing surgery for giant left atrial aneurysm.
15 yr old girl had history of sudden collapse at school, she was taken to hospital where she was Found to have left
hemiparesis, ECG revealed atrial fibrillation which was refractory. On echo it was found that she was having huge LA
aneurysm with LA clot. She was referred to our centre for surgical management. She underwent LA aneurysmectomy.
Perioperative course was uneventful. She was discharged after 2 weeks.
265
IACTACON 2016
Minimizing blood and blood product usage in

open heart surgery by simple approach of blood
conservation.
Dr. Sachin K. Nachane et al
ABSTRACT
Surgical procedures account for the transfusion of nearly 15 million units of red blood cells and 1.5 million platelet
(PLT) transfusions per year in the United States. Although the risk for transmission of viral diseases with transfusion
decreased with the advent of improved screening of blood for pathogens, other adverse effects remain. These include
transfusion reactions, immunomodulation, acute lung injury, fluid overload, and, in some cases, mortality. In the
current environment of health care, in which cost containment has become of utmost importance, any intervention
that will reduce perioperative bleeding and transfusion should be welcome.
This is an audit of the use of homologous blood and blood products in patients who underwent open-heart surgery
by a single surgical team that follows an in-house protocol for blood conservation.
Consecutive 2284 patients undergoing open-heart surgery over a period from Jan 2002 to November 2014 were
retrospectively reviewed to assess the comprehensive blood and blood product usage. This series included adult
as well as pediatric patients (Age 6months to 86 years). All types of cases were included (routine & emergency,
coronaries, valves and congenital). Homologous blood and blood product usage during and after surgery, in the
intensive care unit and up to hospital discharge was analyzed. Different statistical tests were used to analyze this data
including the sub-group analysis.
73.2% patients did not receive any blood or blood products. Average unit usage of blood, FFP and platelets per
patient were 0.62, 0.15 and 0.18 respectively. The sub-group analysis was done for adult Vs pediatric group, CABG
groups (On Vs Off pump). Mean hemoglobin at the time of discharge was 9.5 Gm% (7.913.5 Gm%). Factors were
identified which would increase the need for transfusion. The results of these tests and the measures used to reduce
blood and blood product usage will be discussed.
Simple standardized multidisciplinary approach of blood conservation in cardiac surgery, decreases bleeding and
transfusion requirements in a safe and cost effective manner.
266
ABSTRACTS
Experience of an anaesthetist in a HYBRID operating room.
Dr.KARUPPIAH.R, Dr. Mrugesh Prajapati

UNMICRC, B.J.Medical College, Ahmedabad
INTRODUCTIONThoracic, abdominal and thoraco-abdominal aortic pathologies have highest mortality and morbidity causing
pathologies in cardiovascular surgery. Co-existing diseases and age significantly increase risk of anaesthesia and
mortality rate in treatment of these patients. Endovascular techniques are used increasingly due to minimally invasive
approach, decreased anaesthesia risk during implementation, reduced length of hospital stay, and low mortality
and morbidity rates. The aim of this case report is focused on anaesthetic experiences in endovascular techniques
performed at our center.
CASE REPORT50 years old lady following a Bentall procedure presented with abdominal pain on evaluation found to have Stanford
type B aortic dissection( dissection flap seen extending from arch up to bifurcation of aorta with celiac trunk and
left renal artery arising from false lumen and right renal artery from true lumen. No evidence of anastomotic leak
or pseudo aneurysm formation seen at anastomotic site). The patient was posted for TEVAR procedure in a hybrid
operating room. After establishing standard monitors under General Anaesthesia (anticipating the duration of
the procedure and cooperation of the patient) with invasive monitoring, anaesthesia maintained with sevoflurane,
vecuronium and fentanyl under controlled ventilation. During Intraoperative period Blood pressure was controlled
with Nitroglycerine and Propofol infusion and titrated accordingly to maintain mean arterial BP of 80-90mmHg.
At the beginning of the procedure heparin 100U/Kg i.v was administered to achieve a activated clotting time in the
level twice as high of normal. Procedure went uneventful and shifted to PACU where she was extubated and shifted
to ward on the same day. Rest of the hospital stay was uneventful and started to mobilize on third postoperative day.
DISCUSSIONEVAR should be considered as a beneficial alternative treatment option for high-risk and inoperable, elderly patients.
Postoperatively, the rate of being intubated and the length of stay in intensive care unit were found significantly lower
in endovascular aortic repair (EVAR). Anaesthesia approach to be selected in these patients may be affected not only
by general condition and cooperation of the patient, but also by the location of the pathology and duration of the
process. Thus, the anaesthesiologists should be prepared to face issues related to the patients safety both during the
administration of anaesthesia and in the postoperative period.
267
IACTACON 2016
COMPARATIVE STUDY BETWEEN EFFECTS OF TRANEXAMIC

ACID AND EPSILON AMINO CAPROIC ACID IN ADULT
VALVULAR HEART SURGERIES- RAMDOMIZED CONTROL
TRIAL
DR ISHA SAMADHIYA
DEPARTMENT OF ANAESTHESIA AND CRITICAL CARE,SRI SATHYA SAI INSTITUTE OF HIGHER
MEDICAL SCIENCES, WHITEFIELD, BANGALORE, KARNATAKA,INDIA
INTRODUCTIONExcessive blood loss after cardiac surgery continues to be a major problem after surgeries performed on a
cardiopulmonary bypass(CPB) ,which alters the hemostatic balance and predisposes the patients to an increased risk
of microvascular bleeding. Thus prophylactic antifibrinolytic therapy has its importance here which prevents primary
fibrinolysis and preserve platelet function. We review here a Randomized control trial study done on 90 patients
undergoing valvular heart surgery at SSSIHMS ,Prashantigram, Puttaparthi from Dec 2011- Dec 2013
METHODS90 patients undergoing Valvular heart surgeries were randomly divided into 3 groups. Group A received Normal
saline (placebo), Group B received Epsilon Amino Caproic Acid (EACA) 100 mg/kg pre CPB, on CPB and post
CPB, and Group C received Tranexamic Acid (TXA) 10mg/kg similarly. Intraoperatively the sternal closure time, and
postoperaively-24 hour chest tube drainage,blood product requirement ,Activated clotting time, platelet count at 6
hours and reexploration rates were observed and assessed.
RESULTSThe 3 groups were comparable in terms of age, sex and CPB time. Chest closure time was significantly longer in the
control group A, (P<0.05 vs groups B and C), while the difference between groups B and C was not significantly
different.
Postoperative data shows that cumulative blood loss was significantly greater (P<0.05) in the control group A, as
compared to group B and C. The increased postoperative blood loss in group A was reflected in the increased
requirement of blood transfusion in the control group, compared to the groups B and . Blood samples taken at 6
hours postoperatively revealed preserved platelet count in all three groups. There were no re-explorations in our study
in any group.
CONCLUSIONThe use of lysine analogues- EACA and Tranexamic acid lead to decreased postoperative bleeding in adult patients
undergoing Valvular heart surgeries on CPB , and hence much lesser requirement of transfusion of blood and blood
products, thus preventing numerous transfusion related complications.
REFEENCESChauhan, S. (2004). A Comparison of Aminocaproic Acid and Tranexamic Acid in Adult Cardiac Surgery. Annals of
Cardiac Anaesthesia 2004; 7: 4043 .
Robert S. Brown, M. B. (1997). Tranexamic Acid Is Effective in Decreasing Postoperative Bleeding and Transfusions in
Primary Coronary Artery Bypass Operations: A Double-Blind, Randomized,Placebo-Controlled Trial. International
Anesthesia Research Society . Anesth Analg 1997;85:963-70)
Craig A. Umscheid, B. A. (2007). Antifibrinolytic use in adult cardiac surgery. Curr Opin Hematol 14:455467. 2007
Lippincott Williams & Wilkins
268
ABSTRACTS
MINIMALLY INVASIVE MITRAL VALVE REPAIR IN

POST RENAL TRANSPLANT PATIENT-PERIOPERATIVE
MANAGEMENT
Dr. Jigisha Pujara, Dr. Nirav Parikh, Dr. Alpesh Sarvaiya
U. N. Mehta Institute of Cardiology and Research Center (affiliated to BJ medical college, Ahmedabad),
India.
Abstarct
Several studies have reported the impact of cardiac surgical operation on morbidity and mortality in
renal transplant recipient, on renal graft function, safety and effect of immunosuppressant. Very few
data available about risk and immunosuppressant medication in patient who underwent on pump mitral
valve surgery by minimally invasive technique.
This case study serves important insight into the perioperative management in view of immunosuppressive
medications, antibiotic protocols, perioperative fluid balance, analgesic plan etc. for a patient of
minimally invasive mitral repair after renal transplantation.
Key words: Minimally invasive mitral valve repair, renal transplantation, immunosuppressive medication
Reference:
Mu Junsheng, Zhou Fan, Li Xianshuai, et al. Cardiac surgical operation after renal transplantation.
Chinese Medical Journal, 127(10), 1990-1991.
269
IACTACON 2016
INTRA-OPERATIVE AUTOLOGOUS DONATION REGULATES

INCREASE IN THORACIC FLUID CONTENT IN PATIENTS
UNDERGOING HEART VALVE REPLACEMENT ON
CARDIOPULMONARY BYPASS
Jitin Narula, Usha Kiran, Poonam Malhotra Kapoor, Minati Choudhury, Ujjwal Kumar
Chowdhary,
All India Institute of Medical Sciences, New Delhi, India
Introduction
Intra-operative autologous donation(IAD) decreases the circulatory overload being handled by the compromised
ventricles, in volume loaded patients with pulmonary hypertension (PH) secondary to left heart disease (LHD).
Electrical cardiometry (EC) has recently been shown to provide accurate, noninvasive, continuous, measurements
ofcardiac output (CO) and thoracic fluid content (TFC).This study was designed to evaluate the effect of volume
shifts induced by IAD by measuring changes in EC derived TFC and hemodynamics in patients with PH-LHD.
Methods:
Prospective randomized controlled trial conducted in 50 patients undergoing heart valve replacement. IAD performed
in the test group was simultaneously replaced with 1:1 colloid. TFC, hemodynamic and EC data were recorded at
T1- Baseline (post induction) and T2- 20 minutes post IAD.
Results:
Withdrawal of 15% of blood volume in the IAD group caused a significant reduction in TFC -10.1% (-15.0 to -6.1),
right atrial pressure -23% (-26.6 to -17.6), mean arterial pressure -12.6% (-22.2 to -3.8), airway pressures; peak -6.2%
(-11.7 to -2.8) and mean -15.4% (-25.0to-8.3) and oxygenation index (OI) -10.34%(-16.4 to -4.8). Linear regression
analysis showed good correlation between the amount of autologous blood removed and percentage change in TFC,
RAP, peak and mean airway pressures and OI.
Discussion:
Therapeutic benefits derived from IAD by decreasing TFC and decongesting volume loaded patients further warrant
its routine use in patients with PH-LHD. Even though EC derived parameters predict fluid and hemodynamic status
during IAD and help to execute an early patient specific goal directed therapy, their implementation into decision
making requires further trials.
270
ABSTRACTS
An innovative way to reinsert dislodged Arndt blocker

using urological glide wire
Melvin Alex Abraham, Rahul Pillai, Sneha Ann Ancheri, Sathish Kumar, Raj Sahajanandan*
Department of Anesthesia, Christian Medical College, Vellore
Abstract
Bronchial blockers have found its place in thoracic surgery especially in cases with abnormal airway anatomy,
anticipated difficult intubation, critically ill patients and in children. The Arndt blocker is positioned using a wire loop
to piggyback the blocker on the fiber-optic bronchoscope (FOB). The wire loop once removed cannot be reinserted
in 5F and 7F blockers making repositioning of the blocker difficult.
A 34 year patient was planned for left thoracotomy followed by laparoscopic cholecystectomy. The left lung was
isolated with a 7F Arndt bronchial blocker. During one lung ventilation in right lateral decubitus position the wire
loop was removed for oxygen insufflation to treat hypoxia. There was loss of lung isolation during the procedure
and dislodgement of the blocker was confirmed by FOB. The initial attempts to reintroduce the blocker into the
left main bronchus failed. A straight 0.032 inch zebra glide wire was introduced through the accessory port of the
paediatric FOB (4 mm Karl Storz). The bronchoscope was then introduced through the endobronchial blocker port
of the Arndt multiport adaptor and advanced into left upper lobar bronchus. The glide wire was advanced into the
left upper lobe under vision. The FOB was withdrawn leaving the glide wire in place. The proximal end of the glide
wire was introduced into the lumen of the Arndt bronchial blocker and the blocker was rail-roaded over it into the
left main bronchus under fiber-optic (through FOB port) guidance . The blocker balloon was inflated under vision
and isolation was confirmed. The 0.032 inch zebra glide wire may be effectively used to reposition a dislodged 7 fr
Arndt blocker if the wire loop has been removed.
271
IACTACON 2016
CARDIAC TUBERCULOSIS AN UNUSUAL PRESENTATION
Dr.Naresh Kumar T, GKNM hospital, Coimbatore

Cardiac tuberculosis usually involves the pericardium. Myocardial involvement is rare and described only in 0.3% of
patients with extrapulmonary tuberculosis. Myocardial tuberculosis can present with rhythm disturbances, cardiac
failure, ventricular aneurysm, coronary involvement, venacaval obstruction and pulmonary embolism. We present
here a case of 57 years old male with history of TIA and sinus bradycardia. On evaluation he was diagnosed to have
right atrial mass which was surgically excised. Mass was sent for histopathology which turned out to be caseating
tuberculosis of right atrium. Patient was discharged with anti tubercular treatment. Although cardiac tuberculosis is
rare, they should be suspected in patient with intra cardiac masses.
272
ABSTRACTS
LEARNING EXPERIENCES OF TRANS-CATHETER AORTIC

VALVE IMPLANTATION AT MEDANTA: A CASE SERIES OF
SIXTEEN PATIENTS
Dr Neeraj Kumar Sharma, Dr Rajeev Juneja, Dr Yatin Mehta, Dr Anand Kumar, Dr Ravindra
Sawhney, Dr Nagendra Chouhan, Dr Praveen Chandra, Dr Naresh Trehan, Medanta,
The Medicity, Gurgaon, Haryana, India
Objective:
Trans-catheter aortic valve implantation (TAVI) is an alternative therapy for surgical aortic valve replacement in
patients with symptomatic severe aortic stenosis considered to be at high risk for surgery. The aim of this study was
to describe the anaesthetic implications and short-term results of TAVI.
Materials and Methods:

Sixteen patients treated by TAVI through trans-femoral access between 2012 and 2015, were included. General
anesthesia (GA) was administered with etomidate, midazolam, fentanyl, oxygenair mixture with isoflurane in
14 patients while 2 patients were performed under monitored anaesthesia care (MAC) with dexmedetomidine,
midazolam, fentanyl.
Monitoring in all patients under GA included direct arterial pressure (DAP), pulmonary arterial catheter, transesophgeal
echocardiography (TEE) and under MAC were monitored with central venous pressure, DAP, transthoracic
echocardiography apart from standard monitoring.
Results:
The median age of the patients was 73 years. The median Euroscore and Society of Thoracic Surgeons score of
patients were 31% (24%42%) and 15% (10%20%), respectively. The mean aortic valve pressure gradient was 48
(4473) mm Hg before treatment and 16 (1224) mm Hg after treatment (p=0.003). The mean aortic valve area was
0.65 (0.30.80) cm2 before treatment and 1.8 (1.62.0) cm2 after treatment. The functional status of the patients
improved from NYHA class 3-4 to class 1-2. Intra-procedural mortality was not observed, and the overall 6-month
mortality was 6%. 2 patients required permanent pacemaker implantation for intermittent complete heart block. One
patient developed LBBB under MAC and one required inotropic support in GA. In one patient the aortic valve frame
was obstructing movement of anterior mitral leaflet, which was reshaped on cardiopulomonary bypass. One patient
with dialysis dependent chronic kidney disease died due to sepsis. No patient required blood transfusion. Moderate
and mild para-valvular aortic regurgitation occurred in one and six patients, which remained clinically insignificant
at 6 month follow up.
Conclusion:
The short term outcomes are acceptable with minimal complications. There was no significant difference in outcomes
using either MAC or GA in our case series.
273
IACTACON 2016
IMPACT OF RETROGRADE AUTOLOGOUS PRIMING OF

THE CARDIOPULMONARY BYPASS CIRCUIT ON POST
OPERATIVE HEMODILUTION AND BLOOD TRANSFUSION
REQUIREMENTS
Prashant A Biradar , C Ganesan, Krishnanand Pai, P R Murugesan, M S Murugan,
PSG Institute of Medical Sciences and Research, Coimbatore
Introduction:
Approximately 60% of patients undergoing cardiac surgeries on cardiopulmonary bypass (CPB) require blood and/or
blood products transfusion1. However, blood transfusion during cardiac surgery is associated with increased risk of
Deep Sternal Wound Infection [DSWI] and Renal Impairment in the immediate post-operative period and poor long
term outcomes in terms of survival and graft patency after coronary artery bypass grafting (CABG)2,3.Retrograde
Autologous Priming (RAP) of the CPB circuit has the potential to be part of an effective blood conservation strategy.
Methods:In a prospective, randomized single blinded study, we compared the degree of hemodilution and transfusion
requirement in patients in whom RAP was used (Group A) with those patients in whom RAP was not used (Group
B) intraoperatively during first-time CABG. Primary end-point was intraoperative and postoperative haematocrit
between the two groups. The secondary outcomes measured were total blood loss during and after surgery, total
number of blood and blood products transfused in the postoperative period, inotropic requirement, need for reexploration, number of days of ICU and hospital stay and major outcomes and any postoperative complications.
Results/Discussion :
Statistical analysis is being done at the present and the results will be discussed during the conference
References:
1. Blood Transfusions in Cardiac Surgery:Indications, Risks, and Conservation Strategies. Kilic A,Whitman GJR.
Ann ThoracSurg 2014;97:72634
2. Shaw RE, Johnson CK, Ferrari G, Brizzio ME, Sayles K, Rioux N, et al. Blood transfusion in cardiac surgery does
increase the risk of 5-year mortality: Results from a contemporary series of 1714 propensity-matched patients.
Transfusion 2014;54:1106-13.
3. Bhaskar B, Dulhunty J, Mullany DV, Fraser JF. Impact of blood product transfusion on short and long-term
survival after cardiac surgery: More evidence. Ann Thorac Surg 2012;94:460-7.
274
ABSTRACTS
CATASTROPHIC CORONARY STENT THROMBOSIS

SECONDARY TO REVERSAL OF DUAL ANTI-PLATELET
THERAPY WITH PLATELETS.
Dr.RAJASEKAR.A
Department of Surgical ICU, Christian Medical College,Vellore.
INTRODUCTION:
A 55-year-old known hypertensive gentleman with previous history of anterior STEMI and left ventricular dysfunction
underwent sirolimous eluting stenting of the left anterior descending and right coronary arteries. He was receiving
combined aspirin and clopidogrel prophylaxis. Approximately 10-months after the stent implantation, he sustained
an accident and presented with open fractures involving the femur and tibia. He was posted for emergency fracture
fixation under general anaesthesia.
METHOD:
Cardiologist advised to withhold clopidogrel and to continue aspirin. Anticipating excessive blood loss, the concerned
surgeons obtained hematologist's opinion and transfused five units of platelets preoperatively. Anaesthetic induction
was performed cautiously, the entire anaesthetic course was unremarkable except for the requirement of vasopressors
to maintain the perfusion pressures. The surgical fixation involved 6-hours and resulted in 500ml of blood loss.
Post-operatively he was transferred to ICU, his inotropic requirements increased in association with elevated cardiac
enzymes, new ST-T segment changes and anterior wall akinesia. The patient was immediately shifted for emergency
coronary angiography and the LAD stent was found to be completely thrombosed. Repeated efforts at recannulation
was unsuccessful and he succumbed to refractory ventricular fibrillation during the angiography.
DISCUSSION:
Perioperative care of emergency lifesaving surgeries in the presence of coronary stents is an intricate circumstance in
terms of decision making. Given the uncertainty regarding the management of patients presenting within the optimal
period of dual antiplatelet therapy, it was left to the clinicians discretion to contemplate the benefits of coronary
protection versus the risks of haemorrhage (1). Even though the literature has suggested platelet transfusion as one
of the measures to reverse anti-platelets action (2), doing so prophylactically might result in disastrous consequences.
Since, coronary thrombosis carries a very high mortality (3), until conclusive recommendations are available, it would
be prudent to treat the bleeding rather than precautious transfusions.
REFERENCES:
1. Fleisher LA, Fleischmann KE, Auerbach AD, Barnason SA, Beckman JA, Bozkurt B, et al. 2014 ACC/AHA
Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac
SurgeryA Report of the American College of Cardiology/American Heart Association Task Force on Practice
Guidelines. J Am Coll Cardiol. 2014 Dec 9; 64(22):e77137.
2. Li C, Hirsh J, Xie C, Johnston MA, Eikelboom JW. Reversal of the anti-platelet effects of aspirin and clopidogrel.
J Thromb Haemost JTH. 2012 Apr; 10(4):5218.
3. Nasser M, Kapeliovich M, Markiewicz W. Late thrombosis of sirolimus-eluting stents following noncardiac
surgery. Catheter Cardiovasc Interv. 2005 Aug 1; 65(4):5169.
275
IACTACON 2016
Early extubation in cases of septuagenarian and

octagenarians undergoing on pump CABG. A 2 yr single
centre prospective study .
Dr Rakhi.K.R, Dr Nikhil,Dr Sunil Agarwal, Dr Gee Varghese, Dr Sajiv
St Gregorios cardiovascular centre, Parumala, Pathinamthitta, Kerala
Introduction: Early extubations are a dream especially in cases concerning geriatric age group and especially so
in patients undergoing on pump CABG.As on pump CABGs usually involve patients with worse coronary artery
profile than the usual and lower ejection fractions including associated medical co-morbidities, ability to successfully
extubate geriatric patients during the early 6 hours after surgery involves a lot of jugglery with opiods and anesthetic
drugs.
Aim of the study: This was an endeavor to prove that fast tracking is possible in on pump CABGs in septua and
octogenarians .
Material and methods: The patient group involved all those who were in the age group above 70 yr old between 2014
Jan and 2015 Dec who had underwent CABG on pump. Both males and females were included. All patients with co
morbidities like diabetes and hypertension and severe LV dysfunction were also included. The only exception was
patients on IABP in whom the early extubation was not considered clinically possible. All patients were induced
with fentanyl 100mic and propofol i.v titrated to maintain vital hemodynamics. The maximum dose of Fentanyl
did not exceed 6micrograms/kg during the duration of the CABG. Sedative and relaxant used was Midazolam and
Pancuronium respectively. Over the span of 2 years we have successfully extubated within the first 6 hrs around 56
patients in this age group who had underwent on pump CABG.
Conclusion: It is possible to curtail the duration of ventilation and ICU stay in on pump CABG cases in this vulnerable
group of patients. . We have endeavoured to successfully combine low dose opiods and sedatives to achieve this feat
of early extubations in our patients who are from rural kerala.
276
ABSTRACTS
QUANTIFYING THE PROPOSED BENEFITS FOLLOWING

GOAL-DIRECTED THERAPY (GDT) IN HIGH RISK CARDIAC
PATIENTS UNDERGOING CORONARY ARTERY BYPASS
GRAFTING: A CLINICAL OUTCOME & BIOMARKER BASED
STUDY
Dr.Rohan Magoon
Department of Cardiac Anesthesiology,All India Institute of Medical Sciences, New Delhi, India
With regards to the beneficial aspects of the EGDT in high risk cardiac surgical patients, we have begun from where
we had left in our previous study. EGDT encompasses guidance of intravenous fluid and vasopressor/ inotropic
therapy by cardiac output or similar parameters to help in early recognition and management for better outcomes.
With the aim of quantifying the proposed benefits of EGDT using robust clinical and biochemical outcomes,
we conducted the present study. This mulicentre study included 210 patients of either sex, with EuroSCORE
3 undergoing coronary artery bypass grafting with no absolute contraindications for an offpump grafting. The
patients were divided into three groups based on the therapy and type of surgery as, control (conventional therapy
on an off pump basis or using cardiopulmonary bypass), EGDT group on an off pump basis, EGDT group using
cardiopulmonary bypass. All the subjects received standardized care; arterial pressure was monitored through radial
artery, central venous pressure through a triple lumen in the right internal jugular vein, electrocardiogram, oxygen
saturation, temperature, urine output per hour and frequent arterial blood gas analysis. In addition, cardiac index
monitoring using FloTrac and continuous central venous oxygen saturation using PreSep was used in patients
in the EGTD group. Our aim was to maintain the cardiac index at 2.5-4.2 l/min/m2, stroke volume index 30-65
ml/beat/m2, systemic vascular resistance index 1500-2500 dynes/s/cm5/m2, oxygen delivery index 450-600 ml/
min/m2, continuous central venous oximetry more than 70%, stroke volume variation less than 10%; in addition
to the control group parameters such as central venous pressure 6-8 mmHg, mean arterial pressure 90-105 mmHg,
normal arterial blood gas analysis values, pulse oximetry, hematocrit value above 30% and urine output more than
1 ml/kg/h. The aims were achieved by altering the administration of intravenous fluids and doses of inotropic or
vasodilator agents. The data of 70 patients in the three groups was analyzed. The average duration of ventilation
(13.8 3.2 and 13.2 3.1 v/s 17.6 8.2 h), number of adjustments of inotropic agents (3.1 1.1 and 3.3 1.3
v/s 0.8 0.6), ICU stay (2.57 0.70 and 2.52 0.77 v/s 3.55 0.98 d) and overall mortality were significantly less
in the EGDT group, compared to those in the control group with a p value < 0.001. The extra volume used (322
134 and 342 140 v/s 288 82 ml,P= 0.031) days of use of inotropic agents (1.9 0.95 and 1.6 0.6 v/s 2.2
1.8 d, P= 0.016), hospital stay (6.07 3 and 5.52 2.3 v/s 6.86 + 3.2 d, P=0.033) were also significantly less in the
EGDT group. The pattern of biomarkers like BNP, HSCRP, NGAL had a higher rise in levels at T2 and T6 in the
control group as compared to the EGDT group. This study is conclusive with regard to the beneficial aspects of the
early goal-directed therapy in cardiac surgery patients. At the same time, considering the fact that the off pump GDT
group had better clinical and biomarker profile out of the three groups in the study, the study is expected to open the
new area of interest so as to which subset benefits the most with the advent of EGDT in cardiac clinical practice.
Keywords:
Cardiac surgery, early goal-directed therapy, haemodynamic monitoring, outcome measures(clinical and biomarker)
277
IACTACON 2016
MINIMALLY INVASIVE APPROACH FOR REDO VALVE

SURGERY-A CASE SERIES
SSSIHMS, WHITEFIELD, BANGALORE
Introduction
Redo cardiac surgery represents a clinical challenge due to a higher rate of perioperative morbidity and mortality.
Re-sternotomy may also be complicated in patients with vascular structures (brachiocephalic vein, ascending aorta,
right ventricle) that lie directly behind the sternum or in patients who had previous sternal wound infections or chest
radiotherapy In these cases, a minimally invasive surgical approach through a right-sided mini-thoracotomy is a valid
alternative to a repeated conventional median sternotomy
Case Reports
We review 2 cases of minimally invasive approaches for redo valve surgery-a 44 year male post ASD closure, mitral
repair and mitral annuloplasty for MVR -a 38 year lady post MVR for TVR
Cardiac CT in both patients revealed proximity of cardiovascular structures to sternum, hence making MACS
through anterolateral minithoracotomy a safer option. Percutaneous SVC cannulation was done by anesthesiologist
under ultrasound and TEE guidance. IVC and aorta were cannulated under TEE guidance through femoral route.
Chitwood cross clamp was inserted through separate incision for the MVR. The TVR was done on beating heart.
After valve replacement and confirmation by TEE, the patients were weaned off CPB. Both patients were given 500
mg tranexamic acid before incision and post bypass. Intraoperative blood product requirement was minimal. While
the TVR did not require any products, the MVR was given 1 unit FFP post bypass. The post operative recovery was
faster compared to redo sternotomy cases.
Discussion
The greatest potential benefit of a right mini-thoracotomy is the avoidance of sternal re-entry and limited dissection of
adhesions, avoiding the risk of injury to cardiac structures or patent grafts, and limiting the amount of postoperative
bleeding . This consistently translates into reduced blood loss, less transfusions and faster recovery. Minimally invasive
procedures with an unclamped aorta have the potential to combine the benefits of minimally invasive access and
continuous myocardial perfusion. . Redo valve surgeries can be safely and effectively performed by a minimally
invasive approach through right mini thoracotomy.
References
1. Botta L, Cannata A, Bruschi G, Fratto P, Taglieri C, Russo CF, Martinelli L. Minimally invasive approach for redo
mitral valve surgery. J Thorac Dis 2013;5(S6):S686-S693.
2. Nakamura et al.: Beating heart mitral valve repair for a patient with previous coronary bypass: a case report and
review of the literature. Journal of Cardiothoracic Surgery 2013 8:187.
Declaration of consent for publication and assignation of copyright:
1. I declare that the study was conducted according to the protocol approved by the institutional or local committee
on ethics in human participation.
2. I confirm that I previewed this abstract and that all information is correct. I accept that the content of the
abstract cannot be modified or corrected after final submission and I am aware that it will be published exactly as
submitted.
3. I declare that the submission of the abstract constitutes my consent to publication.
278
ABSTRACTS
PHLEGMASIA CERULEA DOLENS FOLLOWING HEPARIN

INDUCED THROMBOCYTOPENIA {HIT} A CASE REPORT
Dr.Shilpa bhojraj, Simin Mehta, Aliasgar Behranwalla,
Saifee hospital, Mumbai
We report a 49 year old female patient posted for emergency on pump coronary artery bypass grafting who developed
heparin induced thrombocytopenia on postoperative day six.
Patient received 25,000 units of unfractionated heparin during the course of surgery.Surgery was uneventful and she
was extubated on second postoperative day.She was started on Enoxaparin . Her platelet count steadily decreased
from 96,000 to 23,000 over six days.
On the sixth postoperative day, patient was observed to have a cold, cyanosed right lower limb with loss of pulsations.
Venous Doppler revealed a thrombus in the common femoral vein extending to the great saphenous vein. Enoxaparin
was discontinued and fondaparinux was started on clinical suspicion of HIT.
She also developed a clot in the left ventricle on day 12, She was treated with warfarin for the same.On day 23, patient
became breathless, developed gangrene in both upper and lower limbs. She underwent amputation of the right
forefoot and was discharged on 47 th day
HIT is a life threatening complication of exposure to heparin and occurs as a result of autoantibodies against platelet
factor 4.Laboratory tests may take time to prove the diagnosis, thus clinical suspicion is very important .The 4T s
score is an easy to use score and should be used as a guide by clinicians.
In the event of HIT, heparin in all forms should be immediately discontinued and alternative anticoagulants like
thrombin inhibitors should be used
279
IACTACON 2016
LUTEMBACHER SYNDROME: DILEMMA OF DOING A

TRICUSPID ANNULOPLASTY
Varsha A V, Gladdy George, Raj Sahajanandan
Department of Anaesthesiology, Christian Medical College, Vellore, Tamil Nadu
ABSTRACT
Introduction: Lutembacher syndrome is a rare clinical condition characterized by the presence of a congenital
atrial septal defect (ASD) and acquired mitral stenosis(MS) (commonly of rheumatic origin). The left to right shunt
secondary to the MS and ASD results in right ventricular overload, consequent dilatation of tricuspid annulus and
a functional tricuspid regurgitation (TR). There is limited data regarding the optimal treatment of functional TR in
this disorder1.
Methods:
We describe the case of a 24 year old woman with Lutembacher syndrome who underwent surgical closure of ASD
and mitral valve replacement without tricuspid annuloplasty despite a severe TR on preoperative echocardiogram.
Results:
Preoperative transthoracic echocardiogram revealed a large ostium secondum ASD 29mm with left to right shunt,
severe MS (MVA 0.9cm2 and mean transmitral gradient of 10 mmHg), severely dilated RA and RV, severe TR with
tricuspid annulus of 5.8 cm, PAH with TV max PG 73.8 mmHg and mild RV dysfunction. 31mm St Jude Mitral valve
was placed. ASD was closed with a large dacron patch. Post bypass echocardiogram showed a tricuspid annulus of
4.7 cm. considering the mobile valve leaflets with good coaptation and good right ventricular function; it was decided
against a tricuspid annuloplasty despite the severe TR in the preoperative echocardiogram. An echocardiogram done
on post operative day 5 showed that the TR was only mild.
Discussion:
Recent guidelines recommend surgical correction of moderate functional TR (with annular diameter > 4cm) during
cardiac surgery especially involving left sided lesions2. In this case, the MS was augmenting the shunt through the large
ASD. The correction of MS and ASD aided in reducing the right ventricular overload and TR, eventually obviating
the need for tricuspid annuloplasty. The case also emphasizes the role of perioperative echocardiography.
References
1. Bashi VV, Ravikumar E, Jairaj PS, Krishnaswamy S, John S. Coexistent mitral valve disease with left-to-right shunt
at the atrial level: clinical profile, hemodynamics, and surgical considerations in 67 consecutive patients. Am Heart
J 1987;114:1406-14
2. Nishimura R.A., Otto C.M., Bonow R.O., et al;2014 AHA/ACC guideline for the management of patients
with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines.JAm Coll Cardiol. 2014; 63:e57-e185.
280
ABSTRACTS
TITLE: ANESTHETIC MANAGEMNT OF PULMONARY

EMBOLISM-A CASE SERIES OF TEN PATIENTS
Dr Dhawal Wadaskar, Dr Bharati Tendolkar,Dr Shakuntala Basantwani
Department of anaesthesiology, LTMGH & LTMMC, Sion, Mumbai
INTRODUCTION:
Anesthetizing a patient with acute pulmonary embolism (PE) for embolectomy or endartectomy could be nightmare
for an anaesthesiologist. Previously perioperative mortality used to be as high as 59% but it has decreased up to 20%
with early interventions and management 1, 2. We present a data of ten patients, undergone emergency pulmonary
embolectomy during 2013 to 2015.
METHODS:
All ten patients were symptomatic and admitted on emergency basis. None underwent thrombolysis; instead they
were started on I.V. heparin 5000 units 6 hourly. Hemodynamic instability, hypoxemia, signs of right ventricular
failure and no improvement of symptoms were indications to stop conservative management and post patient for
surgery. None of the patient had cardiovascular collapsed during induction of anaesthesia. Three patients needed
preoperative inotropic support, of which two required ventilator support as well. Postoperatively we used milrinone
plus adrenaline combination for all patients which was tapered over 24 hours. They required ventilator support
for 12 to 48 hours postoperatively till their arterial blood gas improved. Except for one who died within 24 hours
postoperatively, all were discharged by 7th postoperative day.
DISCUSSION
Traditionally in PE surgical intervention has been reserved for patients with contraindications for thrombolysis. None
of the patient was thrombolysed in our study instead they were posted for surgery within 6 hours of admission. With
earlier intervention mortality with PE is decreasing now1, 2, 3. Noradrenaline is preferred inotrope preoperatively as
many of the patients are hypotensive on admission. We used milrinone plus adrenaline combination postoperatively
which worked very well in decreasing RV afterload. Anticoagulation should be initiated as early as possible, preferably
with heparin or heparin plus fibrinolysis4. We recommend early surgical intervention in massive or sub-massive
pulmonary embolism.
References:
1. Stein PD, Alnas M, Beemath A, Patel NR; Outcome of pulmonary embolectomy. Am J Cardiol, 2007 feb
1:99(3):421-3
2. Douglas Kopcke, Ondyna harryman, Emyr W Benbow, Charles Hay, Nicholas Chalmers; Mortality from
pulmonary embolism is decreasing in hospital patients. J R Soc Med. 2011 Aug; 104(8):327-331
3. B Sareyyupoglu, K L Greason, RK Suri, MT Keegan, JA Dearani, TM Sundt; More aggressive approach to
emergency embolectomy for acute pulmonary embolism. Mayo Clin Proc. 2010 Sep ;85(9):785-790
4. Micheal R Jaff, M Sean McMurtry, Stefen L Archer, May Cushman, Neil Goldenberg, Samuel Z Goldhaber,
Stefen Jenkins, Jeffery A Line. Management of massive and submassive pulmonary embolism, illeofemoral deep
vein thrombosis, and chronic thromboembolic pulmonary hypertention. Circulation. 2011;123;1788-1830.
281
IACTACON 2016
Asias first heart and liver en bloc transplant case

report
Dr Minal Vora, Dr Disha Khanpara, Dr Bhaskaran K,
Apollo Hospital, Chennai
Combined heart and liver en bloc transplant for a patient with right ventricular endomyocardial fibrosis and
end stage cardiac cirrhosis. It is a procedure carried out to replace both heart and liver connected together
via inferior vena cava and required opening of both chest and abdominal cavity at the same time.
Endomyocardial fibrosis (EMF) is a neglected tropical cardiomyopathy that is common in certain tropical
areas. Endocardial fibrosis is the hallmark of this restrictive cardiomyopathy leading to restriction to diastolic
filling of the ventricles with severe atrial dilatation.
We report the combined heart liver en bloc transplant in a 29 years old male with end stage heart and liver
disease. He had cirrhotic transformation of liver with fibrous obliteration of hepatic vein. As a routine
investigation cardiac evaluation was done this revealed severely dilated right atrium with ejection fraction
(EF) of 65% and right ventricle EMF along with mild displacement of septal bicuspid leaflet.
On availability of a suitable donor combined heart liver en bloc transplant was done. He came off pump
and remained haemodynamically stable with very minimal inotropes. Trans esophageal echocardiogram
revealed good ventricular function (EF66%). Periodic doppler showed good blood flow in the hepatic
arterial and portal venous system. He was extubated on 1st post operative day (POD). He maintained good
urine output throughout. He was discharged on 8th POD with stable haemodynamics.
Conclusion proper evaluation and crucial decision making requires a multi speciality approach for such
complex cases. This is the first successful heart liver en bloc transplant in Asia.
282
ABSTRACTS
DIFFICULTY IN WEANING OFF CPB IN A CASE OF WILLIAMS

SYNDROME WITH SUPRAVALVULAR AORTIC STENOSIS
SSSIHMS,WHITEFIELD,BANGALORE
Introduction
Patients with congenital supravalvular aortic stenosis and associated peripheral pulmonary artery stenoses, the
majority of whom have Williams-Beuren syndrome, are inherently at risk for development of myocardial ischemia.
The biventricular hypertrophy that accompanies these lesions increases myocardial oxygen consumption and
compromises oxygen delivery.
Several case reports have documented an increased incidence of anesthesia-related cardiac arrest in these patients.
The cause of cardiac arrest in most cases was suspected to be myocardial ischemia caused by reduced coronary artery
blood flow
Case Report
A 10 year old boy diagnosed as Williams syndrome with Supravalvular Aortic stenosis (SVAS) came for corrective
surgery. Anesthetic induction was done smoothly with opiod-benzodiazepene combination. The patient went on
CPB and Broms Aortoplasty was done.
The patient was weaned off CPB with Dobutamine 5 mics/kg/min and Adrenaline 0.05 mics/kg/min. While
attempting to come off CPB, the patient developed hypotension, significant ST depression and TEE showed globally
hypokinetic LV with EF of 25%. The patient was put back on CPB and the heart rested for 1 hour. To improve the
coronary perfusion pressure, Adrenaline was increased to 0.2 mic/kg/min and Nor adrenaline
0.05 mic/kg/min. , The patient again developed ST depression and hypotension. After the 2nd failed attempt at
weaning from CPB, Dobutamine was replaced with Vasopressin .0009 IU/kg/min and Adrenaline and Nor adrenaline
doses were increased. The increased systemic pressure increased coronary perfusion and the patient was slowly
weaned off CPB.
Post operatively, vasopressin was weaned off on 1st post operative day and patient had an uneventful recovery
Discussion
The presence of LVH increases myocardial oxygen demand. Conversely, there is impaired coronary blood flow if the
CPP or SVR falls post CPB as as the coronaries are exposed to higher perfusion pressures pre operatively due to the
high prestenotic pressure and will require a high coronary perfusion pressure post operatively as well.
Vasopressors such as phenylephrine and vasopressin should be used as first-line agents to treat hypotension and ST-T
wave changes indicative of myocardial ischemia. Drugs which reduce SVR should be avoided in patients with SVAS.
References
Thomas M. Burch, Francis X. McGowan, Jr., Barry D. Kussman, Andrew J. Powell, James A. DiNardo, Congenital
Supravalvular Aortic Stenosis and Sudden Death Associated with Anesthesia: Whats the Mystery? Anesth Analg
2008;107:1848 54
Andrew J. Matisoff, Laura Olivieri, Jamie M. Schwartz, Nina Deutsch, Risk assessment and anesthetic management
of patients with Williams syndrome: a comprehensive review Pediatric Anesthesia Dec 2015, Volume 25, Issue 12,
120715

2. I confirm that I previewed this abstract and that all information is correct. I accept that the content of the
abstract cannot be modified or corrected after final submission and I am aware that it will be published exactly as
submitted.
283
IACTACON 2016
TRACHEAL INJURY FOLLOWING DOUBLE LUMEN

ENDOTRACHEAL INTUBATION A CASE REPORT
Dr. Subha C.P, ,Dr.Minal Vora, Dr.Bhaskaran .K,
Department of Cardiothoracic Anaesthesia,APOLLO HOSPITALS,Chennai
INTRODUCTION
Tracheobronchial disruption is an uncommon but severe complication of double lumen endotracheal tube placement.
Both conservative and surgical therapy have been advocated, but the condition is uncommon and data concerning
results are sparse
CASE REPORT
54 yr old hypertensive female was admitted for surgical removal of cavernous hemangioma of left lung.After
induction of general anaesthesia and right sided 35 Fr double lumen endotracheal intubation surgical emphysema
was noted in the right side of neck with positive pressure ventilation. Mucosal tear with air leak was suspected and
DLT was changed to 7mm single lumen endotracheal tube immediately .Bronchoscopy done revealed no obvious
abnormality. Surgery commenced in right lateral position with left lateral thoracotomy in 5th ICS. Intraoperatively
patient desaturated secondary to right pneumothorax and right tube thoracostomy done in 2nd MCL.After surgical
removal of the tumour and chest closure with drains patient extubated inside the operating room and shifted to ICU.
Postoperative period was uneventful until 4th POD when she developed a massive right pneumothorax which
required ICD insertion.Subsequent bronchoscopy revealed a tracheal tear 2cm long in the posterior wall of trachea
3 cm proximal to carina with no significant air leak.Tracheal tear was managed conservatively with serial X rays
demonstrating no air leak with full lung expansion and patient was discharged on 12th post op day in stable conditions.
DISCUSSION
A tracheal rupture after intubation with a double lumen endotracheal tube during an operation is very rare. Prompt
recognition and repair are important to optimal patient outcome and prevention of further endobronchial as well as
systemic complications.
REFERENCES
1. Liu H, Jahr JS, Sullivan E, Waters PF. Tracheobronchial rupture after double-Lumen endotracheal intubation.
Journal of Cardiothoracic and Vascular Anesthesia.2004;18(2):228233.
2. Iatrogenic Left Main Bronchus Injury following Atraumatic Double Lumen Endotracheal Tube Placement
.William R. Hartman,* Michael Brown, and James Hannon.Case Rep Anesthesiol. 2013; 2013: 524348.
284
ABSTRACTS
Posterior aortic root widening during aortic valve

replacement : Role of intraoperative transesophageal
echocardiography
Dr Neelam Aggarwal ,Dr Srinivas Gadhinglajkar ,Dr Rupa Sreedhar
Department of cardiac anesthesia,SCTIMST, Trivandrum
Introduction
Patient prosthesis mismatch is a complication of aortic valve replacement. PPM is considered when EOAI <0.85cm2/
m2. Before cardiopulmonary bypass, the appropriate size of prosthesis can be selected to achieve the desired EOAI
by using normograms. In case of narrow aortic root, its widening may be required to accommodate the prostheis.
Aortic root measurements can be performed effectively using transesophageal echocardiography. We report two
patients of aortic stenosis operated for AVR in whom pre-CPB TEE helped in surgical decisions.
Methodolgy
Two ladies of age 58 years (BSA -1.72 m2) and 69 years (BSA- 1.4 m2) with severe aortic stenosis were operated
for AVR. Pre- CPB aortic root dimenssions were measured by TEE. The desired EOA to prevent PPM were 1.46
cm2 and 1.2 cm2 which corresponded with 21mm and 19mm Perimount bioprosthetic valve respectively. In the first
patient, after placing 19mm Perimount prosthesis, surgeon noticed valve obstructing the coronary ostia. Posterior
root augmentation was performed using bovine pericardial patch to accommodate the prosthesis. Posterior root
widening was performed electively in second patient in view of narrow aortic root. Both the patients were weaned
from CPB using minimal ionotropic support and were examined using transthoracic echocardiography before their
discharge.
Results
The post-CPB TEE revealed acceptable Doppler parameters in both the patients. First patient had mean transvalvular
pressure gradient of 26 mmHg and DVI of 0.5. Her mean gradient reduced to 19 mmHg on subsequent TTE
examination. In second patient, peak velocity and mean gradient were 1.8 cm/s and 6 mmHg. The indexed EOA in
both the patients were 0.82 cm2/m2 and 0.89 cm2/m2 respectively.
Conclusion
Posterior root widening enable the surgeon to place a large valve size to avoid PPM. Intraoperative TEE reliably
predicts the prostheis size and the need for root enlargement in pre-CPB period.
References
1. Pibarot P, Dumesnil JG, Lemieux M, Cartier P, Metras J, Durand LG. Impact of prosthesis-patient mismatch on
hemodynamic and symptomatic status, morbidity and mortality after aortic valve replacement with bioprosthetic
heart valve. J Heart Valve Dis 1998;7:211-218.
2. Dumesnil JG, Honos GN, Lemieux M, Beauchemin J. Validation and applications of indexed aortic prosthetic
valve areas calculated by Doppler echocardiography. J Am Coll Cardiol 1990;16:637 43.
3. Kulik A, Al-Saigh M, Chan V, Masters RG, Bdard P, Lam BK, Rubens FD. Enlargement of the Small Aortic Root
During Aortic Valve Replacement: Is There a Benefit? Ann Thorac Surg 2008;85:94 101.
4. Nunez L, Aguado MG, Pinto AG, Larzea JL. Enlargement of the aortic annulus by resecting the commissure
between the left and noncoronary cusps. Texas Heart Institute J 1983;10:301-303.
5. Manougian S, Seybold-Epting W. Patch enlargement of the aortic valve ring by extending the aortic incision into
the anterior mitral leaflet. J Thorac Cardiovasc Surg 1979;78:402-412.
6. Nicks R, Cartmill T, Bernstein L. Hypoplasia of the aortic root. The problem of aortic valve replacement. Thorax
1970;25:339-346.
285
IACTACON 2016
ULTRASOUND GUIDED SYMPATHETIC BLOCK AS A

TREATMENT MODALITY FOR ACUTE AS WELL AS CHRONIC
ISCHEMIA OF THE UPPER LIMB
Dr. Rupa Sreedhar,Dr.Shrinivas Vitthal Gadhiglajkar
Sree Chitra Tirunal Institute for Medical Sciences & Technology,
Thiruvananthapuram, Kerala State, India,
INTRODUCTION:
The objective is to report the use of stellate ganglion block in, 1) a patient who received inadvertent intravascular
injection of Diclofenac and, 2) a patient who has peripheral vascular disease of upper limb
METHODS:
A 52 year old lady doctor presented with pain on volar aspect of left forearm and pain as well as discolouration of
thumb, index and middle fingers of left hand following inadvertent intra-arterial injection of diclofenac sodium at
the left elbow. She was found to have bluish discolouration of 3 fingers and pain score of 5/10 in the left arm. We
administered left stellate ganglion block under ultrasound guidance using 7 mL of 0.25% bupivacaine.
A 37-year old smoker presented with severe right upper limb pain (1 year) and non-healing ulcers in right middle and
index fingers (3 months). CT angiogram revealed narrowing of radial and ulnar artery in distal and mid-right forearm.
We administered right stellate ganglion block with 6 mL of 0.25% bupivacaine and 2 ml (80 mg) of Depomedrol
under ultrasound guidance.
RESULTS:
Stellate ganglion block resulted in immediate total relief of pain and disappearence of discolouration within 12 hours
in the patient who received intra-arterial diclofenac injection and in marked reduction of pain (8/10 to 2/10 for last
3 months) in the patient who has peripheral vascular disease of upper limb.
DISCUSSION:
Stellate ganglion block relieves pain caused by ischemia of upper limb. During ischaemia, timely intervention is
important, to prevent gangrene and amputation.
REFERENCES:
Kapil Dev Soni, Chhavi Sawhney, Manpreet Kaur, Sarita Ramchandani, and Maneesh Singhal. Stellate ganglion block
as a limb salvaging technique. Indian J Anaesth. 2012 May-Jun; 56(3): 307308.
Tran DQ, Finlayson RJ. Use of stellate ganglion block to salvage an ischemic hand caused by the extravasation of
vasopressors. Reg Anesth Pain Med. 2005;30:4058.
286
ABSTRACTS
Mechanical circulatory support as a bridge to

transplant: Our experience
Dr. Ajay Aravind, Dr. Murali Krishna, Dr. Suresh Rao K G,
Dr. K R Balakrishnan
Department of Cardiac Sciences,Fortis Malar Hospital, Chennai
Introduction:
Heart transplant remains the definitive treatment for end-stage heart failure. These patients are highly unstable and
have high mortality rates while being wait-listed awaiting a donor organ. Our strategy for pre-transplant patients is to
maintain them on minimal inotropes, escalate inotropes serially and then use IABP, V-A ECMO (Femoro-femoral)
and LVAD (Thoratec Centrimag) support in an escalating manner. We present our experience of using mechanical
circulatory support (MCS) as bridge to transplant in these critically ill patients.
Data & Discussion:

A total of 74 patients underwent heart transplantation at our institute over the past four years. Prior to transplant,
they were managed with escalating inotropes. Out of the 70, 19 patients were supported on IABP for up to four
weeks. Of these, seven patients could not be stabilized with IABP and inotropes, and had to be put on V-A ECMO.
Two of these patients were later converted to LVAD using Centrimag. All these patients later underwent a heart
transplant. Thirteen of the nineteen patients were successfully discharged after transplant. With appropriate patient
selection and management, even highly unstable heart failure patients can be successfully bridged to transplant with
modern mechanical circulatory support.
287
IACTACON 2016
Role of Transesophageal echocardiography during

repair of Double Chambered Right Ventricle (DCRV)
Amit Mathew, Melvin Alex Abraham, Raj Sahajanandan
Christian Medical College, Vellore
Double chambered right ventricle (DCRV) is a rare congenital anomaly in which the right ventricle is divided into a
high pressure proximal chamber and a low pressure distal chamber by an anomalous muscle bundle. DCRV may be
associated with other congenital anomalies, most commonly with perimembranous VSD.
A 10 year old boy was posted for intracardiac repair of Double chambered right ventricle (DCRV). His preoperative
Echocardiogram revealed Double chambered right ventricle, gradient inside RV of 76 mm Hg across subpulmonic
membrane and single vegetation on pulmonic valve, Echo did not reveal any intracardiac shunts. Intraoperative TOE
confirmed the preoperative findings, revealed a muscle bundle obstructing RVOT causing turbulent flow normal
pulmonary valve and a sub aortic VSD. A modified deep transgastric RVOT view showed a gradient of 51.8 mm
Hg. Surgical findings confirmed TOE diagnosis and RVOT was widened with a piece of pericardium and the
VSD was closed. A post bypass examination revealed widened RVOT with a gradient of 4.07 mmHg. Since VSD is
the most common associated congenital anomaly you should have a high index of suspicion for detection of this
condition. Elevated right ventricular pressures in right ventricle can minimize the flow across the defect and lead to
non detection of this defect in prebypass examination. A high index of suspicion, knowledge about the associated
anomalies and multiple views specifically looking for associated pathologies are crucial.
We conclude that use of Transesophageal echocardiography proved to be a valuable tool for detection of associated
congenital anomaly and monitoring the adequacy of repair.
288
ABSTRACTS
BRIDGING BRONCHUS IN ASSOCIATION WITH

CONGENITAL HEART DEFECT IN A 2 MONTH OLD
INTERESTING CASE REPORT.
Dr.Anupama Mallappa, Dr .Shivanand Nandimiti, Dr.Gangadhar Tagada Basavaiah,
Dr Devananda Nijagal Shivanna
Manipal heart Institute, Bangalore, Karnataka.
A two month old baby was referred to our unit with a provisional diagnosis of severe pulmonary arterial hypertension
.On evaluation the baby was found to have a large secundum atrial septal defect and a large ductus arteriosus
,abnormal course of the left pulmonary artery resulting in the obstruction to the left main bronchus and anomalous
origin of the right lower lobe bronchus from the left main bronchus (bridging bronchus ,left pulmonary artery sling
).The baby successfully underwent re-implantation of the left pulmonary artery and closure of atrial septal defect and
division of ductus on cardiopulmonary bypass. Post op recovery was uneventful , The baby is doing well at ONE
month follow up
289
IACTACON 2016
EFFICACY OF CONTINUOUS LOCAL ANAESTHETIC

INFILTRATION AT STERNAL WOUND SITE FOR
POSTOPERATIVE ANALGESIA IN PATIENTS UNDERGOING
CARDIAC SURGERY BY MEDIAN STERNOTOMY
Banerjee Anusua, Sen Dasgupta Chaitali, Goswami Anupam
Institute of Postgraduate Medical Education and research, Kolkata
Background
Most of the cardiac surgeries are performed through median sternotomy and associated with severe pain which if
not relieved, leads to stress response with detrimental effects on major organ systems with increased postoperative
morbidity and mortality.

Eightyfour patients (18 and 75 years), with modified Parsonnet score< 10 posted for cardiac surgery were included.
Two multi holed, epidural catheters were placed by surgeon, one in sub-fascial plane just above sternum and another
just below skin after sternal closure. Through each catheter, Group I patients received 0.25% levobupivacaine and
Group II patients received 0.25% levobupivacaine and 2 mcg/ml of clonidine at 2 ml per hour in ICU via elastomeric
pumps for patient controlled analgesia.
Results:
The pain (VAS at 24 hours) was significantly lower in Group II than Group I (2.7381 + 0.7005 vs 4.0238 + 0.8968).
The total morphine requirement in 48 hours was significantly higher in Group I than Group II (11.2262 + 1.7455
vs 4.8714 + 2.4111mg) . Duration of tracheal intubation and time for mobilisation were similar in both groups.
Serum lactate and cortisol levels at 48 post-operative hours were significantly lower Group II than Group I (Lactate
1.39 + 0.613 vs 1.8 + 1.073; Cortisol 22.07 + 9.048 vs 30.73 + 15.666). Patient satisfaction scores in Group II were
significantly higher than Group I(78.3095 + 8.4637 vs 72.5238 + 5.2277).
Conclusion
Clonidine as an adjuvant in levobupivacaine infusion at sternal wound site significantly decreases postoperative pain
in cardiac patients.
Key Words
Continuous infusion, levobupivacaine and clonidine, median sternotomy
290
ABSTRACTS
ASD closure in postpneumonectomy patientAnaesthesia management

Dr Dhawal Wadaskar,Dr Bharati Tendolkar,Dr Shakuntala Basantwani
Department of anaesthesiology, LTMGH & LTMMC, Sion, Mumbai
Introduction
Fewer data is available on cardiac surgery in post-pneumonectomy patients. There is no reported case of sinus
venosus and OS-ASD (ostium secondum-atrial septal defect) surgical closure in post-pneumonectomy patient in
literature.1 Cardiac surgery itself predisposes patient to postoperative pulmonary dysfunction due to intraoperative
atelectasis and CPB related complications. We report a challenging case for anaesthesiologist, where we anesthetized
post-pneumonectomy patient for surgical ASD closure.
Methods
10-year old male child who had undergone left pneumonectomy 14 months back for non-functioning left lung, now
posted for ASD closure. Most probably the cause of non-functioning left lung was repeated pneumonia due to ASD.
He was having SVC type sinus venosus and OS ASD with mild pulmonary artery hypertension. Preoperative postpneumonectomy pulmonary function test (PFT) showed FVC of 1.09 L (93% of predicted), FEV1 of 0.92 L (89%
of predicted), and FEV1/FVC of 99% predicted. We used intravenous general anaesthesia with single lumen tube
avoiding elective endobronchial intubation on right. Volume control mode of ventilation used with VT 5 ml/kg along
with respiratory rate between 20-25/min. Sinus venosus ASD was closed using autologous pericardial patch and OS
ASD closed directly. Patient weaned off ventilator gradually in ICU and extubated 12 hours after surgery, Discharged
on 6th postoperative day.
Discussion
Postpneumonectomy patients undergo various anatomical and physiological changes over a period of time.2 In
left pneumonectomized patient right lung gets compensatory hyperinflation and heart deviates counterclockwise
in left side of chest. One has to be careful while doing sternotomy as it can cause trauma to hyperinflated lung.
Hyperventilation is necessary many a times to maintain normal acid-base balance. One can encounter difficulty in
Internal jugular cannulation for central venous access and fluid management.3 Early ASD closure can be advisable in
postpneumonectomy patients safely.
References
1. Coronary artery bypass grafting and/orvalvular surgery in patients with previous pneumonectomy. Alexander
Fragkidis, Alexander Dimitrios, Dimitrios Dougenis; Journal of cardiothoracic surgery, 7:110, 2012.
2. S.E. Kopec, R.S. Irwin, C.B. Umali-Torres, J.P. Balikian, A.A. Conlan; The postpneumonectomy state Chest,
vol.114, no.4, pp 1158-1184, 1998
3. Cardiac surgery in patients with previous pneumonectomy; Sanjay V Ghotkar, Vikram Aerra, Neeraj Mediratta;
journal of cardiothoracic surgery, 2008, 3:11
291
IACTACON 2016
IMMEDIATE AND LONG-TERM OUTCOMES AFTER REPAIR

OF ANOMALOUS ORIGIN OF LEFT CORONARY ARTERY
FROM PULMONARY ARTERY: RESULTS FROM A LARGE
SINGLE CENTER EXPERIENCE FROM A LIMITED RESOURCE
ENVIRONMENT
Dr Jessin P Jayashankar, Dr Sunil GS, Dr Rakhi Balachandran, Dr Amitabh C Sen,
Dr Abraham Cherian , Dr Raman Krishnakumar
Amrita Institute of Medical Sciences and Research Centre, Kochi, Kerala, India
Background:
We describe immediate and long-term results following repair of anomalous origin of left coronary artery from
pulmonary artery in a low resource setting where delayed presentation is common and left ventricular assist devices
and extracorporeal membrane oxygenators are generally unavailable.
Methods:
We reviewed records of 101 consecutive patients who underwent surgical correction for anomalous left coronary
artery from pulmonary artery between Nov 1998- Feb 2015 at our institution. Patient characteristics included: median
age 4.0 months (1month-55 years), 55% females, heart failure at presentation in 65(64.4%), myocardial infarction
in 77 (76.2%), significant mitral regurgitation in 52(51.5%), and moderate or severe left ventricular dysfunction in
87 (86.1%). Anomalous left coronary artery originated from the posterior facing sinus of the pulmonary artery in
90(89.1%)patients. Operations included aortic re-implantation (n=93), Takeuchi repair (n=2), coronary artery bypass
grafting with left coronary artery interruption (n=5) and ligation (n=1). Mitral valve repair was undertaken in 5.
Results:
Early outcomes included in-hospital mortality: 8.9%, ventilation duration: 87(12-994) hours, intensive care unit stay:
7 (1-120) days and hospital stay: 18(4-150) days. The mean follow up was 6.0 4.18 years. Time related survival
was 89.1 % at 16 years. There were two late deaths. Restoration to normal ventricular function was noted in 67/73
(88.4%) patients with moderate or severe LV dysfunction. Significant mitral regurgitation persisted in13.3% of the
entire cohort.
Conclusions:
Notwithstanding the constraints of limited resource environment, it is possible to obtain satisfactory long-term
results after repair of anomalous origin of left coronary artery from pulmonary artery.
292
ABSTRACTS
ANESTHETIC MANAGEMENT OF A 3.2 Kg JEHOVAHS

WITNESS PATIENT FOR SURGICAL REPAIR OF TRUNCUS
ARTERIOSUS - A CASE REPORT
Dr. Kaushik Jothinath, Dr. Vindhya Kumar, Dr. Shivananda Nadiminti, Dr. Anupama
Mallappa, Dr.Thirumuruga Pandian, Dr. Greeshma Prabhakar Gowdar, Mr. Elayaraja, Ms.
Vedasree Satyanarayana, Dr.Gangadhar, Dr. Devananda
Department of Cardiac Anesthesia,Manipal hospitals,Bangalore,Karnataka,India
INTRODUCTION:
The management of cardiac surgery in Jehovahs witness patients presents several challenges to the cardiac
anesthesiologist.
CASE PRESENTATION:
A two month old female baby, belonging to Jehovahs witness faith, born to a non-consanguinously married couple
by Caesarean section, was detected to have a heart defect on day 1 of life. She presented to our hospital for further
management.
On examination, saturation was 86-90% on room air and hyperdynamic precordium with grade III ejection systolic
murmur was noted. Blood evaluation showed preoperative hemoglobin of 16.8 g%.
ECHO findings:
Type II truncus arteriosus, quadricuspid truncal valve with moderate regurgitation, large sub-truncal VSD and severe
pulmonary arterial hypertension.
The child was taken up for surgical repair after obtaining a detailed, informed consent. After intravenous induction,
invasive arterial and central venous access was obtained. VSD closure was done and a 15 mm cryopreserved pulmonary
homograft was used for RVOT-PA conduit. Truncal valve was repaired by plicating the tip of the non-coronary cusp
of truncal valve.
Measures taken to minimize blood loss intraoperatively were Minimized Perfusion Circuits, Retrograde Autologous
Priming, syringe administration of cardioplegia, meticulous hemostasis, use of tranexemic acid infusion and Factor
VII concentrates, minimal blood sampling and double dilution of inotropes. Rapid and skillful surgical technique,
with a cross clamp time of 157 minutes and total CPB time of 218 minutes helped in further minimizing blood loss.
Postoperative hemoglobin was 8 g%. The baby was ventilated with inhaled nitric oxide and high inotropic supports in
the immediate postoperative period. She was slowly weaned off the ventilator and extubated on the tenth postoperative
day. Oral iron therapy, along with recombinant erythropoeitin was given postoperatively, to improve the hemoglobin.
She was discharged in a stable condition on the twenty third postoperative day. Pre-discharge hemoglobin was 10.3
g/dL and saturation on room air was 96%.
CONCLUSION:
Detailed discussion between the surgeon, anesthesiologist, perfusionist, pediatrician and hematologist, about the
management strategies led to the development of a detailed plan, which contributed significantly towards the
successful outcome of this case.
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IACTACON 2016
Effect of induction with etomidate and thiopentone on

hemodynamic responses in patients with left ventricular
dysfunction due to coronary artery disease undergoing
coronary artery bypass graft surgery a pilot study
Arindam Choudhury, Agarwal SMilind Hote,Chauhan U,Kiran U
All India Institute of Medical Sciences, New delhi
Introduction
The cardiovascular system of an individual with a normal healthy heart has a large reserve. In contrast, patients with
severe left ventricular (LV) dysfunction, function at the very limit of their cardiac reserve. With the increasing trend
of supporting failing hearts with left ventricular assist device (LVAD) implantation and heart transplantation etc,
development of a safe anaesthesia induction and maintenance protocol for this subset of population is very much
essential. Considering the gravity of the matter, we planned to study the haemodynamic effect of induction with
the novel induction agent etomidate vis--vis thiopentone sodium in patients with left ventricular dysfunction (LV
ejection fraction < 40%) who underwent coronary artery bypass graft suegry (CABG).
Methods
After obtaining approval from the ethics committee of AIIMS and written informed consent, patients were
randomized into two groups after fulfilling the inclusion criteria. A 8 Fr introducer sheath was inserted using aseptic
techniques and a 7 Fr four lumen Swan-Ganz catheter was floated into the pulmonary artery before induction. Cardiac
output was estimated using intermittent cold saline boluses by thermodilution method before and after anaesthesia
induction. Group one received inj etomidate 0.3 mg/kg and group two received inj thiopentone sodium 3 mg/kg for
induction respectively. Haemodynamic data were noted at 1, 2, 3 and 5 minutes after induction and computed.
Results
Along with demographic parameters, the LVEF values in both groups were statistically identical. Cardiac output
values over different time points are statistically significant (p = 0.04) in group 2, whereas in group 1, these overall
changes are not found to be significant. Systemic vascular resistance (SVR and SVRI) values are significantly different
in all time points in group 1 but in group 2 they are significant only at 10 and 20 minutes.
Conclusion
Etomidate is a safe drug for inducing anaesthesia in patients with poor LV function for it maintains a steady cardiac
output after a single bolus dose.
294
ABSTRACTS
Transesophageal Pacing in a Neonate with Sick Sinus

Syndrome Posted for Emergency Laparotomy
Gladdy George, Varsha A.V, Raj Sahajanandan
Department of Anaesthesia, Christian Medical College, Vellore
Case Report
Neonates are unique and are essentially different from adults. Sick sinus syndrome in a neonate is a rare entity. When
such a patient is posted for emergency laparotomy, it is an anaesthetic challenge.
We describe a case of a 48 hours old 2.7 kilogram preterm neonate with sick sinus syndrome who had repeated
episodes of bradycardia since birth posted for emergency laparotomy. In view of the risk symptomatic bradycardia
during induction of anaesthesia, use of opioids, and certain surgical manipulations ,it was decided to insert a temporary
pacemaker on the morning of surgery. Transesophageal pacemaker(TEP) was selected since it was least invasive,
can be quickly inserted, and suitable size was available. A 5 french bipolar pacemaker with platinum electrode was
inserted through the nostril into the esophagus and fixed at the depth at which there was sustained adequate pacing
(14 cm). The pacing mode was AAI at 117 b/m with output of 20 mA. After a stable rapid sequence induction and
intubation, a single shot caudal block was given. Anaesthesia was maintained on isoflurane, air, oxygen, atracurium
and fentanyl. For most of the surgery the child was paced but the childs own intrinsic heart rate of 140-150 b/m
appeared occasionally during which the pacing stopped.
Discussion
The proximity of the esophagus to the left atrium is the basis for using esophageal elecrodes to deliver electrical
stimuli to the left atria. In neonates, the cardiac output is rate dependent, hence they are intolerant to both bradycardia
or severe tachycardia. The TEP delivered a fixed rate when the child had bradycardia and consequently provided
haemodynamic stability. Transesophageal pacing is a versatile therapeutic and diagnostic tool.
295
IACTACON 2016
MINIMAL ACCESS ATRIAL SEPTAL DEFECT CLOSURE- A

SINGLE INSTITUTIONAL RETROSPECTIVE REVIEW OF 56
CASES
DR ISHA SAMADHIYA
DEPARTMENT OF ANAESTHESIA AND CRITICAL CARE, SRI SATHYA SAI INSTITUTE OF HIGHER
MEDICAL SCIENCES, WHITEFIELD, BANGALORE, KARNATAKA,INDIA
INTRODUCTION Cardiac surgery typically involves large incisions with complete access to the heart and great vessels. The introduction
of Minimal Access Cardiac Surgery (MACS) has revolutionised the field of cardiac surgery with its well established
benefits thereby avoiding the complications of open sternotomy.
We review 56 cases of MACS-Atrial Septal Defect done in our institute SSSIHMS, Whitefield, Bangalore from
August 2014-Dec 2015.
METHODS56 patients of ASA-2 and NYHA-2 with Ostium Secondum- ASD (OS-ASD) were chosen for undergoing MACSASD closure on Cardiopulmonary bypass (CPB). They were induced using benzodiazepine-opioid and muscle relaxant
combination, and maintained on Oxygen-air with Isoflurane. Analgesic technique was either epidural, paravertebral
block or intercoastal block (ICB). Percutaneous Superior venacava cannulation and open Inferior venacava and Aortic
cannulation was done through femoral vein and artery respectively, under Transesophageal echocardiography(TEE)
and Ultrasound (USG) guidance. Intraoperatively the anesthesia and analgesia technique, Incision size, total CPB
time, Cross Clamp time, total surgical time, complications and requirement of conversion to open sternotomy was
noted. Postoperatively time of extubation, time of first rescue analgesia, total analgesic requirement, 24 hour chest
tube drainage, blood product transfusion, re-exploration rate, time of ICU Stay and discharge from hospital were
observed and assessed.
RESULTS:
Average age of patients 23 yrs
Diagnosis- OS-ASD
Incision size- 4-5 cm
IV induction as technique of choice
Mean CPB time- 90 min
Mean Cross Clamp time- 39 min
Number of reconversion to open in ASD - 1
Average Surgical time- 240 min
Analgesic Technique- ICB
Average time of Extubation- within 2 hrs
Average time for Rescue Analgesia- 6-10 hrs
Average Drainage- <50 ml, minimal blood product requirements
Re-explorations- 1
Average Discharge from ICU- 1st POD
Average Discharge from Hospital- 2nd POD
Mortality- Nil
296
ABSTRACTS
CONCLUSION :
MACS offers a less invasive approach as compared to conventional ASD closure. Although there is a learning curve
but the long term benefits cannot be overlooked. MACS can offer Minimal stay in ICU and Hospital, Minimal scar
thus better cosmetic appearance, avoidance of re-do sternotomy if required at a later date, and Maximal comfort to
the patient.
REFERENCES:
Abdel-Rahman U, Wimmer-Greinecker G, Matheis G, et al. 2001. Correction of simple congenital heart defects
in infants and children through a minithoracotomy. Ann Thorac Surg 72:1645-9.
Ak K, Aybek T, Wimmer-Greinecker G, et al. 2007. Evolution of surgical techniques for atrial septal defect repair
in adults: a 10-year singleinstitution experience. J Thorac Cardiovasc Surg 134:757-64.
Barbero-Marcial M, Tanamati C, Jatene MB, Atik E, Jatene AD. 1998. Transxiphoid approach without median
sternotomy for the repair of atrial septal defects. Ann Thorac Surg 65:771
297
IACTACON 2016
PERIOPERATIVE VARIATIONS IN SERUM ALBUMIN PREDICT

ADVERSE OUTCOME AFTER CARDIAC SURGERY FOR
TETRALOGY OF FALLOT REPAIR.
Jitin Narula, Poonam Malhotra Kapoor,Ujjwal Kumar Chowdhury, Sameer Taneja
Associate Consultant, Cardiac Anesthesiology, Max Super Speciality Hospital, Patparganj, New Delhi
Abstract
Introduction:
Serum albumin concentration has been shown to predict surgical outcome and is a low cost alternative to cardiac
biomarkers. Cardiopulmonary bypass (CPB) associated immune response and low flow states induce a host of
morbidities in cyanotic heart disease patients with low serum albumin levels.
Methods:
150 patients, Group 1 18 years (n=75, 42males) and Group 2 >18 years (n=75, 48 males) were included in this
prospective observational non blinded study. Albumin levels were measured preoperatively (T1), after termination
of CPB (T2) and 48 hours post CPB (T3). Primary parameters (mortality, duration of post-operative ventilation,
duration of inotropes and duration of ICU stay) and secondary parameters (urine output, oliguria, arrythmias and
hemodynamic parameters) were recorded.
Results:
The albumin levels in Group 1 at T1, T2 and T3 were 4.710.49, 4.260.44 and 3.790.42; in Group 2 were 4.700.50,
4.240.46 and 3.850.41 respectively, showed no statistical difference between the two groups(p value>0.05). Intra
group analysis with respect to time showed significant decrease in albumin concentration (p<0.01). 11 patients
expired during the study period. Receiver operating characteristic (ROC) curve showed that a cut off value of 3.3 g/
dL predicts mortality with a positive predictive value 47.6% and a negative predictive value of 99.2% (p value <0.05).
A positive correlation was seen between Albumin levels and duration of CPB (r2=0.6321), ICU stay (r2=0.7447) and
oliguria (r2=0.8803).
Conclusions:
The study demonstrated a fall in albumin concentration in TOF patients undergoing intra cardiac repair on CPB,
which correlates well with adverse clinical outcomes, more commonly in younger patients.
298
ABSTRACTS
ELECTRICAL CARDIOMETRY: A RELIABLE SOLUTION

TO CARDIAC OUTPUT ESTIMATION IN CHILDREN WITH
STRUCTURAL HEART DISEASE.
Jitin Narula, Sandeep Chauhan, Saurabh Gupta, M Ramakrishnan
Dept of Cardiac Anesthesiology, Max Super Speciality Hospital, Patparganj, Department of Cardiac Anesthesiology,
Department of Cardiology, All India Institute of Medical Sciences, New Delhi, India
Introduction:
In the modern era of evidence based medicine, cardiac output (CO) estimation plays center-stage to the concept of
goal-directed therapy. Avoiding the nuances of pulmonary artery catheterization (PAC) and still obtaining reliable
cardiac output is now possible with reasonable accuracy in adult population using electrical cardiometry (EC).
Evidence however still lacks in pediatric population where validation studies in newer technologies have either not
been conducted or have shown poor correlation with invasively derived catheterization data. Aim off the study was
comparison of cardiac output obtained by non-invasive electrical cardiometry with pulmonary artery catheterization.
Methods
Prospective observational study in fifty pediatric patients with congenital heart disease undergoing cardiac
catheterization and intervention procedures under sedation/ general anesthesia in cardiac catheterization laboratory
of a tertiary care hospital. EC cardiometry derived CO was measured by cardiometry device (ICON; Osypka
Medical, Berlin, Germany). Cardiac output data triplets were obtained simultaneously from both techniques at
predefined time points: (1) baseline; 5 minutes after arterial and venous cannulation (2) T2, 5 min post procedure,
generating 50 data triplets and average of the three readings was taken for analysis. Intraclass correlation coefficient
(ICC), limits of agreement and mean bias were calculated and Bland-Altman Analysis was done to determine the
accuracy of the CO measured with different methods.
Results
EC-cardiac index (CI) 4.22 (3.84-4.60) Lmin-1 and PAC-CI 4.26 (3.67-4.67) Lmin-1 measured were statistically
insignificant (p value <0.05) at T1. The BlandAltman analysis revealed a mean bias of 0.0051 and precision limits
of 0.4927 Lmin-1. The ICC was 0.789 and Cronbachs alpha was 0.652 showing strong agreement and reliability.
Post catheterization analysis also revealed good reproducibility and internal consistency between the two techniques
[EC-CI 4.29 (3.99-4.73) Lmin-1 and PAC-CI 4.38 (3.95-4.76) Lmin-1, p value <0.05, mean bias -0.015, limits of
agreement 0.0340 Lmin-1, ICC 0.907 and Cronbachs alpha 0.830]. Intraclass correlation coefficient and Bland
Altman analysis also showed a good agreement between the stroke volume derived from EC and PAC.
Discussion:
Our preliminary data demonstrates that cardiac output measurement in children using the EC based ICON (Osypka
Medical, Berlin, Germany) reliably represents absolute CO values as compared to PAC in children with congenital
heart diseases. Whether electrical cardiometry can be used as a CO trend monitor has to be assessed by further
investigations with larger samples sizes.
299
IACTACON 2016
Outcomes of Midcab Vs Conventional CABG

DR. JITUMONI BAISHYA , DR. MURALI CHAKRAVARTHY
FORTIS HOSPITAL, B.G. ROAD, BENGALURU, INDIA
ABSTRACT
Minimally invasive cardiac surgery is a rapidly advancing surgery all over the world, and more so in India, especially
Minimally invasive direct coronary artery bypass surgery (MIDCAB). The anesthetic & surgical techniques are varied
in MIDCAB surgeries, We aimed to compare the outcome of minimally invasive to conventional approach for
Coronary Artery Bypass Graft surgery (CABG) on beating heart surgery in this study.
Methods:
The prospective, comparative study was conducted at Fortis Hospitals Bangalore, Institutional Ethical board approved
the study .All patients who underwent coronary artery bypass graft (CABG) surgery via minimally invasive approach
( via left anterior thoracotomy or via partial sternotomy or via subxiphoid approach) on beating heart from July 2015
to December 2015 were enrolled in MICAS group. Same number of EuroSCORE II matched patients undergoing
CABG through conventional mid-sternotomy approach were selected (CCABG group). Various intra-operative and
post-operative variables were collected. Sample size was 25 per group.
Results:
In MICAS group, Duration of the surgery was significantly longer (p = 0.029). intra-operatively blood loss lesser
(P= 0.002), shorter duration of ventilation (, p=0.002), shorter ICU stay (p=0.004), shorter hospital stay (p=0.003),
lesser postoperative analgesic requirements (p =0.027), and lower VAS scores on day of surgery (p = 0.032) and first
postoperative day (p=0.025). no significant difference in postoperative blood loss, blood transfusion or duration of
inotrope requirement observed
DISCUSSION:
Though the duration of surgery was longer in MICAS group, there was no conversion to mid-sternotomy in any
patients, 8% patients had desaturation intraoperatively, there was no operative mortality. Duration of ventilation was
shorter , with lesser pain postoperatively & overall shorter ICU & hospital stay.
Conclusion:
MICAS on beating heart is associated with lesser intraoperative blood loss, better analgesia and faster recovery.
Introduction:
Coronary artery bypass surgery (CABG) is the most durable and complete therapy of ischemic heart disease.
Conventional coronary artery bypass surgery via midsternotomy approach (CCABG) is more popular, though with
inherent drawbacks. To overcome these, Minimally Invasive Coronary artery surgery (MICAS) has been suggested
as a safer alternative. They have gained acceptance, probably due to patient demand (less trauma and cosmesis) and
economic demand (faster recovery and shorter hospital stay) 1. There have been multiple studies comparing minimally
invasive to conventional approaches to CABG 24, but none in the Indian scenario 5. There could be a reasonably steep
learning curve affecting the outcome. We wished to study the effect of the learning curve on the outcome.
Methods:
Patient population:
The prospective, observational, comparative study was conducted at Fortis hospitals, Bangalore, a tertiary level
cardiac centre. Institutional Ethical committee clearance was taken with waiver of patient consent. All patients who
300
ABSTRACTS
underwent CABG from July 2015 to Dec 2015, via anterolateral thoracotomy and subxiphoid approaches were
enrolled (MICAS group). All the patients were operated by a single surgeon. These patients were selected by the
operating surgeon and patients informed consent was taken before the procedure.
Operative procedure:
In MICAS group, patients were intubated with double lumen tube or bronchial blocker. The position confirmed by
fibre-optic bronchoscope. Injury to the airway if any was noted down. Patient was positioned with 15-30 degree
Right lateral tilt for MIDCAB and a wedge was placed under the chest for subxiphoid surgery. One-lung ventilation
was initiated during internal mammary artery harvesting.
Proximal and distal anastomoses were performed using standard techniques.
Intraoperative inotropes and blood transfusion were standardized. Hypotension (defined as mean arterial pressure
decrease of more than 30% of preoperative value) was treated using a combination of either intravenous lactated
Ringers solution, and/ or Trendelenburgs position and/ or intravenous infusion of noradrenaline (0.01 to 0.05
mcg/kg/min.) . Intraoperative events such as conversion to midsternotomy or institution of cardiopulmonary bypass,
blood or product transfusion were also made note of.
Post-operative management:
Postoperative management was similar in both groups. Pain relief was administered using thrice daily regimen of 5
mg subcutaneous morphine and breakthrough pain was treated with aliquots of 1 mg. Patients were followed-up till
discharge from hospital. Patients who underwent subxiphoid coronary artery bypass graft surgery underwent graft
study by angiography.
Statistical analysis:
Continuous data were described as Mean Standard Deviation (SD) and categorical data as number (%). Comparisons
of means were done using independent sample t-test. P value of < 0.05 was considered statistically significant. SPSS
for windows 16.0.0 for windows (SPSS Inc., Chicago, IL, USA) was used for analysis. Sample size calculated was
16, assuming an alpha error and beta error of 5% and 80% respectively, based on duration of hospital stay in study
published by Poston et al6 .
Results:
25 patients who underwent MICAS were enrolled (16 via anterolateral thoracotomy approach and 9 via subxiphoid
approach). From 112 patients who underwent CCABG, operated by the same surgical team, 25 EuroSCORE II
matched patients were selected. (Figure 1)
The comparison between intraoperative and postoperative variables is analyzed in Table 2.
In MICAS group, there was no incidence of airway injury or conversion to mid-sternotomy. 8% patients had
desaturation during one-lung ventilation and 1 patient needed change from one-lung to two-lung ventilation. There
was no intraoperative mortality. Duration of the surgery was significantly longer in MICAS group (334.4 76.12
vs. 292.8 52.5, p = 0.029). MICAS group had significantly lesser intra-operatively blood loss (365.92 156.84 vs.
519.44 171.86, P= 0.002), shorter duration of ventilation (240 193.68 vs. 495 333.4, p=0.002), shorter ICU stay
(1.72 0.54 vs. 2.24 0.66, p=0.004), shorter hospital stay (4.52 1.27 vs. 5.72 1.4, p=0.003), lesser postoperative
analgesic requirements (97.22 25.57 vs. 123.91 47.36,p =0.027), and lower VAS scores on day of surgery (3.08
1.15 vs. 3.79 1.1, p = 0.032) and first postoperative day ( 2.04 1.10 vs. 2.72 0.98, p=0.025). There was no
significant difference in postoperative blood loss, blood transfusion or duration of inotrope infusion.
Discussion:
In this study MICAS group had significantly longer duration of the surgery, lesser intra-operatively blood loss, shorter
duration of ventilation, shorter ICU stay, shorter hospital stay, lesser postoperative analgesic requirements, and lower
VAS scores on day of surgery and first postoperative day. There was no significant difference in postoperative blood
loss, allogenic blood transfusion or duration of inotrope infusion.
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IACTACON 2016
Rogers et al in a randomised study (STET trial) of 93 elective CABG patients undergoing off pump revascularisation
via median sternotomy and anterolateral thoracotomy approaches. They noted a longer duration of surgery (median,
4.1 vs. 3.3 hours), shorter intubation time (256 vs. 321 minutes) and similar ICU stay (22.4 vs. 23 hours) in thoracotomy
group. Pain scores were similar, though thoracotomy group need more analgesics. In our study, duration of surgery
was longer in the MICAS group (5.3 vs. 4.5 hrs), but duration of intubation (240 vs. 495 minutes), length of ICU
(1.72 vs. 2.24 days) and hospital stay (4.52 vs. 5.72 days) were shorter. Analgesic requirements were lesser in MICAS
group (97.22 vs. 123.91 mcg of fentanyl), and VAS scores (3.08 vs. 3.79 on day 0, and 2.04 vs. 2.72 on day 1) were
lower 2.
Lichtenberg et al in a study comparing MIDCAB to Conventional CABG, noted shorter operation time (140 vs. 189
minutes) and duration of ventilation (300 vs. 840 minutes) in MIDCAB group. Postoperative pain scores were higher
in MIDCAB group (5.5 vs. 3.6 on day 1 and 4 vs. 2.9 on day 3) 3. In our study, MICAS group had longer operating
time (334 vs. 292 minutes), but had shorter duration of ventilation (240 vs. 495 minutes). Contrary to their findings
VAS scores were lower in MIDCAB group in our cohort as noted earlier.
Poston et al in a comparison of 100 consecutive minimally invasive CABG cases to traditional sternotomy CABGs,
concluded that intubation times (4.8 vs. 12.24 hours), hospital stay (3.77 vs. 6.38 das) were shorter in minimally
invasive group. Similarly, in our study the intubation times as well as hospital stay was shorter 6.
In a study by Lapierre et al, comparing 150 sternotomy Off-pump coronary artery bypass grafting (OPCABG) to
MICAS, after matching patients according to age, gender, LV function, and number of distal anastomoses, found
hospital stay (5.4 vs. 7.2 days) was lower in MICAS group 7. The trend is similar in our study, though the ICU stay was
shorter even in the conventional group.
In another study, Rabindranauth et al studied 130 MICAS patients who were 2:1 matched to traditional OPCABG
patients. Mean postoperative length of stay in MICS group was 4 days vs. 5 days in conventional group. They
concluded that MICS was safe and reasonable alternative to conventional CABG 8. Results of our study indicate a
similar trend.
In a study by Birla et al which compared MIDCAB and off pump coronary artery bypass graft (OPCAB) surgeries,
they noted 6(8.6%) conversion to sternotomy, higher transfusion requirements (1.6 vs. 3.2 units) in MIDCAB group.
MIDCAB group had shorter duration of ventilation (5.04 hours vs. 5.35 hours) and ICU stay (38.36 hours vs. 47.87
hours) 9. There was no incidence of conversion in our cohort, and transfusion requirements were similar in both
groups. Duration of ventilation and ICU stay were shorter, as explained earlier.
In a comparative study of MIDCAB and OPCAB Karpuzoglu et al noted shorter duration of mechanical ventilation
6.8 vs. 8.3 hours) and total hospital stay(4.5 vs. 5.2 days), which is similar to our findings 10.
In a prospective trial of 65 consecutive MIDCAB patients using anterolateral thoracotomy approach, off-pump
technique and 95 matched patients who underwent conventional CABG with CPB, postoperative pain was higher in
after MIDCAB on POD 1, but they had better pain relief during subsequent days 11. In our cohort, postoperative pain
was consistently lower from the day of surgery into the postoperative period.
The intraoperative blood loss in MI group was significantly lesser (365.92 vs. 519.44 ml), but transfusion requirements
were similar in the group. The data on intraoperative transfusion was not collected.
Limitation
Patient selection was not randomised, thus selection bias may exist in MICAS group, as low risk patients may have
been favoured for undergoing MICAS. We have tried to control by EuroSCORE II based 1:1 matching of patients
undergoing conventional approach CABG. Long term follow up was not done. Thus issues related to graft patency
and long term event free survival have not been studied, although the entire subxiphoid surgical cohort underwent
post operative graft angiography.
Conclusion:
MICAS compared to CCABG on beating heart is associated with lesser operative blood loss, better analgesia and
faster recovery.
302
ABSTRACTS
References:
1. Reser D, Holubec T, Caliskan E, Guidotti A, Maisano F. Left anterior small thoracotomy for minimally invasive
coronary artery bypass grafting. Multimed Man Cardio-Thorac Surg. 2015 Jan 1;2015:mmv022.
2. Rogers CA, Pike K, Angelini GD, Reeves BC, Glauber M, Ferrarini M, et al. An open randomized controlled trial
of median sternotomy versus anterolateral left thoracotomy on morbidity and health care resource use in patients
having off-pump coronary artery bypass surgery: the Sternotomy Versus Thoracotomy (STET) trial. J Thorac
Cardiovasc Surg. 2013 ;146:30616.
3. Lichtenberg A, Hagl C, Harringer W, Klima U, Haverich A. Effects of minimal invasive coronary artery bypass on
pulmonary function and postoperative pain. Ann Thorac Surg. 2000;70:4615.
4. Ohkado A, Nakano K, Nakatani H, Gomi A, Sugiyama N, Saegusa N. The superiority of pulmonary function
after minimally invasive direct coronary artery bypass. Jpn J Thorac Cardiovasc Surg Off Publ Jpn Assoc Thorac
Surg Nihon Kybu Geka Gakkai Zasshi. 2002;50:669.
5. Pande S, Agarwal SK, Gupta D, Mohanty S, Kapoor A, Tewari S, et al. Early and mid-term results of minimally
invasive coronary artery bypass grafting. Indian Heart J. 2014;66:1936.
6. Poston RS, Tran R, Collins M, Reynolds M, Connerney I, Reicher B, et al. Comparison of economic and patient
outcomes with minimally invasive versus traditional off-pump coronary artery bypass grafting techniques. Ann
Surg. 2008;248:63846.
7. Lapierre H, Chan V, Sohmer B, Mesana TG, Ruel M. Minimally invasive coronary artery bypass grafting via a small
thoracotomy versus off-pump: a case-matched study. Eur J Cardio-Thorac Surg Off J Eur Assoc Cardio-Thorac
Surg. 2011;40:80410.
8. Rabindranauth P, Burns JG, Vessey TT, Mathiason MA, Kallies KJ, Paramesh V. Minimally invasive coronary
artery bypass grafting is associated with improved clinical outcomes. Innov Phila Pa. 2014;9:4216.
9. Birla R, Patel P, Aresu G, Asimakopoulos G. Minimally invasive direct coronary artery bypass versus off-pump
coronary surgery through sternotomy. Ann R Coll Surg Engl. 2013 Oct 1;95(7):4815.
10. Karpuzoglu OE, Ozay B, Sener T, Aydin NB, Ketenci B, Aksu T, et al. Comparison of minimally invasive direct
coronary artery bypass and off-pump coronary artery bypass in single-vessel disease. Heart Surg Forum. 2009
Jan;12(1):E3943.
11. Diegeler A, Walther T, Metz S, Falk V, Krakor R, Autschbach R, et al. Comparison of MIDCAP versus conventional
CABG surgery regarding pain and quality of life. Heart Surg Forum. 1999;2(4):2905; discussion 2956.
Figure 1 Anterolateral approach to MICAS
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IACTACON 2016
Table 1- Comparison of EuroSCORE II between the groups
EuroSCORE II
MICAS (N=25)
Standard
Mean
Deviation
1.48
.48
CCABG (N=25)
Standard
Mean
Deviation
1.32
0.39
P value
0.21
Table 2-Descriptive Statistics

CATEGORY
MICAS (N=25)
Standard
Mean
Deviation
DURATION OF
SURGERY
INTRAOPERATIVE
INOTROPES
INTRAOPERATIVE
BLOODLOSS
POST OPERATIVE
BLOOD LOSS
BLOOD PRODUCTS
USED
DURATION
OF INOTROPE
INFUSION
DURATION OF
VENTILATION
ICU LENGTH OF
STAY
TIME TO
MOBILISE
HOSPITAL LENGTH
OF STAY
DURATION OF OLV
POSTOPERATIVE
FENTANYL
POSTOPERATIVE
PARACETAMOL
POSTOPERATIVE
MORPHINE
VAS SCORE DAY 0
VAS SCORE DAY 1
VAS SCORE DAY 2
P value
CCABG (N=25)
Standard
Mean
Deviation
334.40
76.12
292.80
52.50
.06
.04
.06
.03
365.92
156.84
519.44
171.86
326.25
184.72
328.28
218.40
314.20
220.98
362.40
324.91
240.00
193.68
495.00
333.44
1.72
.54
2.24
.66
17.12
3.40
18.44
5.15
4.52
1.27
5.72
1.4
189.67
52.15
97.22
25.57
123.91
47.36
1.40
.71
1.60
.76
5.00
8.80
6.69
3.08
2.04
1.40
1.15
1.10
1.15
3.79
2.72
1.72
1.10
.98
.84
304
0.029
0.759
0.002
0.972
0.54
0.002
0.004
0.290
0.003
0.027
0.341
0.631
0.032
0.025
0.269
ABSTRACTS
Table 2-Descriptive Statistics

CATEGORY
MICAS (N=25)
Standard
Mean
Deviation
DURATION OF
SURGERY
INTRAOPERATIVE
INOTROPES
INTRAOPERATIVE
BLOODLOSS
POST OPERATIVE
BLOOD LOSS
BLOOD PRODUCTS
USED
DURATION
OF INOTROPE
INFUSION
DURATION OF
VENTILATION
ICU LENGTH OF
STAY
TIME TO
MOBILISE
HOSPITAL LENGTH
OF STAY
DURATION OF OLV
P value
CCABG (N=25)
Standard
Mean
Deviation
334.40
76.12
292.80
52.50
.06
.04
.06
.03
365.92
156.84
519.44
171.86
326.25
184.72
328.28
218.40
314.20
220.98
362.40
324.91
240.00
193.68
495.00
333.44
1.72
.54
2.24
.66
17.12
3.40
18.44
5.15
4.52
1.27
5.72
1.4
189.67
52.15
305
0.029
0.759
0.002
0.972
0.54
0.002
0.004
0.290
0.003
IACTACON 2016
POSTOPERATIVE
FENTANYL
POSTOPERATIVE
PARACETAMOL
POSTOPERATIVE
MORPHINE
VAS SCORE DAY 0
VAS SCORE DAY 1
VAS SCORE DAY 2
97.22
25.57
123.91
47.36
1.40
.71
1.60
.76
5.00
8.80
6.69
3.08
2.04
1.40
1.15
1.10
1.15
3.79
2.72
1.72
1.10
.98
.84
306
0.027
0.341
0.631
0.032
0.025
0.269
ABSTRACTS
307
IACTACON 2016
EMPIRICAL TRANSFUSION OF BLOOD PRODUCTS IN

CARDIAC SURGERY. CAN YOU TRUST YOUR CLINICAL
JUDGEMENT? AN AUDIT
Joseph Punnoose Paarel , Sathish Kumar D, Raj Sahajanandan
Department of Anesthesia, Christian Medical College and Hospital, Vellore,India
INTRODUCTION:
Transfusion of blood and blood products is associated with increased morbidity and mortality in cardiac surgery.
Point-of-care (POC) coagulation tests coupled to algorithm based management have shown to decrease transfusion
requirements in cardiac surgery.
METHODOLOGY:
After IRB approval all consenting adult patients who is undergoing elective cardiac surgery except elective CABG,
patients with known coagulation abnormalities were recruited into the study. Patients who did not need transfusion
were excluded from the study. Anesthesia and perfusion techniques were standardised. An ACT of 480 sec was
aimed on CPB. After the completion of repair/ graft and discontinuation of CPB, protamine was given to get the
ACT < 140 sec. If the surgeon feels that there is coagulopathy, blood sample is send for haemoglobin, Platelet Count,
PT, aPTT, fibrinogen and Thromboelastograph (TEG). Blood product transfusion will be carried out as per surgical
judgement while keeping an Hb > 8g/dl.
Prophylactic tranexamic acid (bolus 20mg/kg, followed by 5mg/kg) was used in all cases.
RESULTS:
Of the 25 patients who received transfusion, 64% of patients had normal coagulation parameters and TEG values
prior to transfusion.
DISCUSSION:
Clinicians decision to transfuse blood products is often influenced by factors like continuation of antiplatelet therapy
or heparin therapy. Studies have shown that experience of surgeon and the CPB time as risk factors for transfusion.
A transfusion algorithm based on Point-of-Care testing would have significantly reduced transfusion requirements in
cardiac surgical patients.
BIBLIOGRAPHY:
1. Nuttall GAMD, Oliver WCMD, Santrach PJMD, Bryant SMS, Dearani JAMD, Schaff HVMD, et al. Efficacy of a
Simple Intraoperative Transfusion Algorithm for Nonerythrocyte Component Utilization after Cardiopulmonary
Bypass. Anesthesiol May 2001. 2001;94(5):77381.
2. Efficacy of a Simple Intraoperative Transfusion Algorithm fo...: Anesthesiology [Internet]. [cited 2014 Nov
13]. Available from: http://journals.lww.com/anesthesiology/Fulltext/2001/05000/Efficacy_of_a_Simple_
Intraoperative_Transfusion.14.aspx
3. Rady MY, Ryan T, Starr NJ. Perioperative determinants of morbidity and mortality in elderly patients undergoing
cardiac surgery. Crit Care Med Febr 1998. 1998;26(2):22535.
4. Despotis G j., Grishaber J e., Goodnough L t. The effect of an intraoperative treatment algorithm on physicians
transfusion practice in cardiac surgery. Transfusion (Paris). 1994 Apr 1;34(4):2906.
5. Anderson L, Quasim I, Soutar R, Steven M, Macfie A, Korte W. An audit of red cell and blood product use after
the institution of thromboelastometry in a cardiac intensive care unit. Transfus Med. 2006 Feb;16(1):319.
308
ABSTRACTS
TITLE - A RARE CASE OF ADULT TOTAL ANOMALOUS

PULMONARY VENOUS RETURN (SUPRA CARDIAC TYPE)
INTERESTING TRANSESOPHAGEAL ECHOCARDIOGRAPHIC
VIDEOS AND IMAGE
Dr. KARTHIK N, Dr. PARIMALA P SIMHA, Dr. MANJUNATHA N, Dr. LAKSHMI
DEPARTMENT OF CARDIAC ANAESTHESIA
SRI JAYADEVA INSTITUTE OF CARDIOVASCULAR SCIENCES AND RESEARCH BANGALORE,INDIA
TAPVC accounts for approximately 2 % of all congenital heart diseases. The condition leads to symptoms in neonatal
period and infancy and 50% of unrepaired infants die within the 1st 3 months of life with mortality approaching
approximately 80% by end of 1st year. However a few patients are known to survive beyond infancy into adulthood.
Our patient aged 34 years female presented with history of cyanosis, palpitations and easy featiguability. She was
diagnosed to have supracardiac TAPVC with severe pulmonary arterial hypertension. She underwent re-routing
of pulmonary veins to the left atrium and closure of ASD. Her recovery was uneventful in the post operative
period. Transesophageal echocardiography was an important tool for the diagnosis and delineation of anatomy of
TAPVC preoperatively and also helped us in monitoring adequacy of post operative repair in terms of ASD closure,
obstruction at the pulmonary venous anastamosis, pulmonary artery pressure and adequacy of right ventricular
function. The purpose of this report is to present interesting transesophageal echocardiographic videos and images
of adult supracardiac TAPVC preoperatively and after complete correction.
309
IACTACON 2016
SURGERY FOR TRUNCUS AND HEMITRUNCUS ARTERIOSUS:

ANESTHESIA AND ECHOCARDIOGRAP
Dr.Keerthi Chigurupati, Dr.Shrinivas Gadhinglajkar, Dr.Rupa Sreedhar,
Sree Chitra Tirunal Institute of Medical Sciences and Technolog Trivandrum,Kerala.
BACKGROUND:
TRUNCUS ARTERIOSUS accounts for 1% of congenital heart diseases and is characterized by persistent single
arterial outlet and a common valve for both ventricles. Hemitruncus is a variant of Truncus arteriosus which is
associated with an abnormal origin of a single pulmonary artery with normal relationship of the remaining PA to
the right ventricle. Babies with truncus arteriosus present in the neonatal period with symptoms of high pulmonary
artery pressure and biventricular failure. Surgical repair is the treatment of choice. Anesthesia and perioperative care
in these cases is associated with high-risk. Intraoperative transesophageal echocardiography has an important role
in the complex congenital surgery. We present anesthesia and perioperative management in two patients, one with
truncus arteriosus and another with hemitruncus highlighting the echocardiographic features in both of them.
MATERIALS AND METHODS:

Both patients with truncus arteriosus and hemitruncus were scheduled for elective surgical correction. The 1year
7month old child with truncus arteriosus presented with features of cardiac failure. The hemitruncus patient was
28-days-old at the time of surgery. Anesthesia in both patients was induced using sevoflurane. A balanced anesthesia
technique was followed in both the patients for maintenance. Cardiac examination was performed using a microTEE
probe (I/E 33, Philips Medical Systems) throughout the surgery focusing on diagnostic and monitoring aspects. Both
patients were transferred to ICU for postoperative ventilation at the end of surgery.
OBSERVATIONS:
Both patients maintained stable hemodynamic parameters before CPB. In Truncus arteriosus patient TEE could
guide the surgeon regarding morphology of truncal valve, coronary artery anatomy, location and number of VSD
and function of both ventricles. Epicardial echocardiography was used in addition to evaluate the pulmonary artery
flow in post-CPB period. The hemitruncus patient, showed an abnormal origin of RPA from aorta and LPA is
originated as a continuation of MPA. Tricuspid reguirgitation was noted with an organic pathology requiring valve
repair. TEE showed satisfactory surgical results in post-CPB period. Both patients maintained stable hemodynamic
condition with minimum inotropic support.
CONCLUSION :
Truncus arteriosus surgery can be performed safely under balanced anesthesia technique. Intraoperative
transesophageal echocardiography is a useful monitoring tool for assessment of the features of truncus arteriosus,
to guide the surgeon for surgical correction, to evaluate the surgical results in post-CPB period and to monitor the
hemodynamic parameters in the intraoperative period.
310
ABSTRACTS
Use of Methylprednisolone In Neonatal Cardiac SurgeryA Randomized Control Single Centre Trial
Leena V. Chaudhari, Kamlesh B. Tailor, Shankar V. Kadam, Smrutiranjan R. Mohanty,
Suresh G. RaO
Introduction :
Corticosteroids are commonly used in pediatric cardiac surgery to reduce the cardiopulmonary bypass induced
inflammatory response but their potential effects on clinical outcomes has not been well studied.
Methods:
A prospective randomized double blind trial conducted between June - November 2015 comparing outcomes between
a steroid receiving group and a no steroid group. Clinical outcomes like perioperative glycemic values, inotrope score,
cumulative fluid balance, laboratory markers for infection, duration of ventilation, icu and hospital stay were studied
for both the group.
Results:
A total of 50 cases were studied, 25 neonates in each group. In univariate analysis, intraoperative use of
methylprednisolone was associated with hyperglycemia during the intraoperative and postoperative period (p=0.01,
p=0.004, p=0.001). Clinical sepsis was found to be statistically insignificant but the biochemical markers for infection
came positive in the steroid receiving group (p=0.048). The steroid group showed high inotrope score 48 hours after
surgery(p=0.01). The study noted a negative fluid balance achieved in the steroid subset over 120 hours of surgery
(p=0.047). Steroids were not associated with reduction in hospital stay (p=0.75), icu stay (p=0.85) or duration of
mechanical ventilation (p=0.64).
Conclusion:
Use of steroid was associated with the benefit of achieving more negative fluid balance but this did not reflect in
terms of postoperative morbidity outcomes. Contrary, use of steroid was associated with poor glycemic control and
raised markers of infection perioperatively.
Key words :
Neonates, Congenital heart surgery, Methylprednisolone
311
IACTACON 2016
Comparison of USG guided Internal Jugular Vein

Cannulation with traditional landmark technique in
paediatric patients for Cardiac Surgery.
Dr Munir Ahmad Khan, Dr Devashish Chakravarty, Dr Milan Pendse.
Department of Cardiac Anaesthesiology1, Chirayu Medical College and Hospital, Bhopal, M.P., India.
Introduction :
Central venous cannulation for patients undergoing Cardiac surgery has been in routine practise since ages, however
the art of practising the traditional landmark technique requires ages to perfect and cannulating a paediatric patient
undergoing cardiac surgery stays to be a challenge. With the evolution of ultrasonography securing an access under
direct vision is possible with lesser/no complications.
Method:
100 paediatric patients from new born to 18 years of age undergoing Cardiac surgeries were recruited and were allotted
random computer generated groups. After sterile preparation internal jugular vein cannulation was done in group I
using traditional landmark guided technique, while in group II by ultrasound guidance using high frequency linear
array probe once access was secured a triple lumen central venous catheter was placed using Seldingers technique, and
central venous pressure was measured.
Result:
The result analysis was done using IBM Spss ver 20 and the two groups were found to be statistically similar
demographically, it was observer that there was a lesser frequency of arterial puncture and hematoma formation in
group II patients were as in group I the incidence of higher number of pricks and accidental puncture was observed.
Discussion:
USG guided vascular access is a novel technique where in the venous access is secured under direct vision, there is
reduced incidence of accidental carotid artery puncture. This technique though under tight scrutiny due to PCPNDT
act on use of USG, has the potential advantage over age old methods and can become a gold standard technique.
312
ABSTRACTS
Pediatric heart transplant our experience
Murali Krishna.T, Ajay Aravind, Suresh Rao.K.G. , K.R. Bala Krishnan

Fortis Malar Hospital, Chennai.
Introduction
Heart transplant is the treatment of choice for the patients with end stage heart failure refractory to medical therapy.
Keeping these patients fit and alive till the availability of the suitable donor organ is challenging. The options of
mechanical circulatory support are limited in pediatric age group when compared to adults.
Data and discussion

Out of the total 74 heart transplants at our centre 14 patients were pediatric age groups (up to 18 years). The age
group varied from 2 years to 16 years. Dilated cardiomyopathy was the most common cause followed by restrictive
cardiomyopathy. Preoperatively ten of the fourteen patients were on inotopes, six of these ten required more than
one inotrope to treat low cardiac output. One patient had cardiac arrest due to poor ventricular function, she was
resuscitated and had to be put on ECMO to support the circulation. The age of the donor varied from 2 years to
adults. The ratio of the donor to recipient weight was from 1:1 to 1:3.5. Postoperatively all the patients were weaned
off bypass except one who had left ventricular dysfunction requiring continuation of ECMO. Subsequently the
patient was successfully weaned from ECMO. Two patients had right ventricular dysfunction that was managed with
inotropes, right ventricle recovered completely over the next few days. Two patients had big heart syndrome secondary
to the high donor to recipient weight ratio, both of them recovered well. There was one death in the entire group of
fourteen; the cause of death in that patient was sepsis. Immunosuppression protocol included induction therapy and
maintenance therapy with triple drug regimen. All the thirteen patients were discharged in a stable condition.
Conclusion
Heart transplant remains treatment of choice for end stage heart failure. Managing these patients in the preoperative,
intraoperative and postoperative period is challenging. Cardiac Anesthesiologist plays a vital role in association with
surgical team during the entire perioperative course in the ICU and operating room.
313
IACTACON 2016
Pretreatment with Methylprednisolone versus lidocaine

for attenuating propofol injection pain: a randomized
controlled trial.
Dr.Shivaprakash, Dr.Shiopriye , Dr.Satya Narayana Jagannath
Vydehi institute of medical science and research centre
Abstract
Background
Propofol (2,6-di-isopropylphenol) used for the induction of anesthesia often causes mild to severe pain or discomfort
on injection, for which various methods have been tried, but with conflicting results. We designed this double-blind,
placebo-controlled study to compare the efficacy of methylprednisolone and lidocaine in reducing the pain of
propofol injection in patients scheduled for cardiac surgery.
Methods
One hundred sixty five adult patients(38 women, 127 men), scheduled for elective cardiac surgery, were divided into 3
groups: saline (Group S, n = 55), lidocaine 20mg (Group L, n = 55), and methylprednisolone 125mg diluted into 2ml
of distilled water (Group MP, n=55).Drugs were administered after tourniquet application and occlusion was released
after 1 min and 1/4th of the total dose of propofol (2mg/kg) was administered at the rate of 0.5ml per second. Pain
on propofol injection was evaluated by four point verbal rating scale.
Results
Demographic variables were similar among groups. The overall incidence of pain was 70.9% in the saline group,
30.9% in the lidocaine group, and 36.4% in the methyl prednisolone group. Pain intensity was significantly less in
patients receiving drugs for pretreatment than those receiving saline (P<0.05). Adverse effects at the injection site
were not observed in any patient in the 24 hours post-surgery.
Conclusions
Pretreatment with intravenous methylprednisolone was found to be as effective as lidocaine in reducing propofol
injection-induced pain.
Key words:
intravenous anaesthesia, propofol, pain, lidocaine, methylprednisolone, dexamethasone, venous occlusion.
314
ABSTRACTS
Conscious sedation using dexmedetomidine for

percutaneous transcatheter closure of atrial septal
defects: A single centre experience
Pushkar M Desai, Dr Manjula Sarkar, Dr Sanjeeta Umbarkar
Seth GSMC & KEM Hospital, Mumbai
SUMMARY
Percutaneous transcatheter closure of atrial septal defect offers numerous advantages over surgical closure in terms
of minimally invasive nature, better cosmesis, shorter hospital stay and avoiding complications of open heart surgery
using cardiopulmonary bypass. We report our experience of percutaneous ASD closure using Amplatzer device
(between Jan 2014 to June 2015) under conscious sedation without any complications. Total 43 cases (36 females
and 7 males including adults and adolescents) were performed. Mean age was 31.56 + 13.74 years (range 12 to 56
years). The mean ASD diameter measured by transesophageal echocardiography was 22.34 + 5.15 mm. The mean
device size implanted was 27 + 4.87mm. Mean recovery time was 7.64 + 3.01 minutes. Procedure was successful
in 40 of 43 patients (93.02%). Three patients were denied procedure due to inadequate rims around ASD. Four
patients developed atrial fibrillation following procedure which responded to pharmacological treatment and DC
cardioversion. No major complications were observed. All patients and cardiologist were satisfied with the quality of
anesthesia.
Conclusion:
Conscious sedation using Dexmeditomidine is also a safe and effective anesthetic technique for percutaneous ASD
closure.
315
IACTACON 2016
Efficacy of Clonidine, as adjuvant,to 0.75% Ropivacaine

for potentiation of postoperative analgesia, when
added in Supraclavicular Brachial plexus blocks for
upper limb vascular surgery
Rahul maria*, Ritesh Shah , M.H Parmar, Vaishali Sarvariya
Department of Cardiac Anesthesiology,U.N.Mehta Institute of Cardiology & Research Centre,Affliated to B.J.Medical
College,Ahmedabad,Gujarat
Aims & Objectives

To compare onset of action (both sensory & motor)
Hemodynamic changes intraoperatively
Total duration of analgesia
To note side effects/complications if any.
To evaluate the safety
Material & Method

Prospective,randomized,control, double blind study for vascular surgeries of arm and forearm. After written
informed consent -60 patients aged 18-65Yrs , irrespective of sex, were divided into two equal groups Group R
received 35 ml of 0.75% ropivacaine with 1 ml of saline.Group C received 35 ml of 0.75% ropivacaine with 2 g/kg
of clonidine.Premedication-inj. Midazolam 20 g/kg and were preloaded with- crystalloid at 4ml/kg/hr.Vitals were
monitored with the help of multi para monitor.
Result:

Does not alter the onset of action.
Mild short lived sedation in two pts.
No significant change in Haemodynamic parameters in both groups
Longer duration of analgesia observed in Group C compound to Group R.
316
ABSTRACTS
RED BULL IN PEDIATRIC CARDIAC INTENSIVE CARE UNIT
Dr.Rahul Norawat, Dr.Deepa Sarkar, Dr.Reetesh Gupta, Dr.Jothi Muthu.

Department of Cardiac Anaesthesia, Pediatric cardiac surgery and Pediatric cardiac care unit, Indraprastha Apollo
Hospital, New Delhi, India
Introduction:
Patients in pediatric cardiac ICU with prolong inotrope requirement secondary to persisting myocardial dysfunction
are a difficult substrate to treat. In our settings these comprise patients presenting late with congenital heart disease,
complex anatomy and cardiomyopathies. Carnitine is an essential co-factor of fatty acid metabolism in heart, liver,
and skeletal muscle. Carnitine is amino acid, mainly used in adult patients with low EF following MI and pediatric
patients with dilated cardiomyopathy. We discuss, a case that had improved myocardial function after carnitine
supplementation in a late presenting tetralogy of fallot.
Case summary:
11 years old, polycythemic child, diagnosed case of TOF. On evaluation patient had TOF physiology with hypoplastic
pulmonary annulus with adequate PA branches. Child underwent total correction with trans-annular patch repair. She
had significant RV dysfunction post operatively and was supported with ventilator and inotropes. She was extubated
but had persisting low output state secondary to RV dysfunction evidenced by tachycardia, borderline pressures
and cold extremities. Digoxin was started but inotropes could not be weaned till 7th POD. After discussion she was
started on syrup carnisure and within 48 hrs her low output state improved dramatically. She was later weaned of
inotropes successfully and discharged.
Discussion:
Many experimental studies have shown that levo-carnitine reduces myocardial injury after ischemia and reperfusion
by counteracting the toxic effect of high free fatty acids levels, which occur in ischemia. It increases rate of fatty
acid transport into mitochondria and improves carbohydrate metabolism. Supplementation of myocardium with
levocarnitine, increases tissue carnitine content, prevent loss of high-energy phosphate stores, ischemic injury and
improved heart recovery. There are no studies about its use in postoperative pediatric cardiac surgery patients. Few
of our patients especially a substrate with inotrope dependence have benefited from the supplementation. If proven
beneficial in pediatric cardiac patients, it will be equivalent to red bull invention.
References:
1. Ferrari R, Merli E, Cicchitelli G, Mele D, Fucili A, Ceconi C. Therapeutic effects of L-carnitine and propionyl-Lcarnitine on cardiovascular diseases: a review. Ann N Y Acad Sci. 2004 Nov;1033:79-91.
2. Oliver Niebur. Mayo Clinic review links L-Carnitine to multiple heart health benefits. (cited on 20th November
2014).
3. Y. Suzuki,Y. Masumura,A. Kobayashi,N. Yamazaki,Y. Harada,M. Osawa. Myocardial carnitine deficiency in
chronic heart failure. The Lancet,Vol 319, Issue 8263:116-120.
317
IACTACON 2016
ABRUPT CARDIOVASCULAR COLLAPSE ON PARALYSIS

IN A CHILD WITH TRAUMATIC LEFT DIAPHRAGMATIC
HERNIATION OF ABDOMINAL VISCERA.
Dr.Rajasekar A.
Department of Surgical ICU, Christian Medical College, Vellore
INTRODUCTION:
A 7-year-old girl sustained blunt trauma to the chest, abdomen and pelvis in a road traffic accident and was referred
with breathlessness and desaturation. Initial bedside imaging revealed left pneumothorax with right-sided mediastinal
shift due to herniation of abdominal contents. Needle thoracostomy was performed immediately, subsequent CT
thorax identified left diaphragmatic rupture with the stomach, spleen and intestine herniating into the left hemithorax. In addition the child had undisplaced pelvic fracture with concealed retroperitoneal hematoma. With the
resuscitation in progress, the child was transferred for an exploratory laparotomy.
METHOD:
Prior to induction, a radial arterial line and additional intravenous access were secured in the right upper extremity.
Nasogastric tube was suctioned and the child was preloaded adequately. Pre-oxygenation and induction were performed
cautiously using sevoflurane, ketamine and fentanyl. Under optimal anaesthetic plane, with the thoracostomy needle
in position, intubation was achieved with 5.5mm cuffed ETT maintaining spontaneous respiration. Atracurium was
administered to preclude childs respiratory efforts from hampering the surgical incision. Approximately 90 seconds
after paralyzing, she developed sudden electro-mechanical dissociation. CPR was initiated instantly and adrenaline
was administered. Re-expansion of the pre-existing pneumothorax was excluded and the cardiac output resumed
immediately after positioning in the left lateral position. Laparotomy was performed promptly, the thorax was
decompressed and the diaphragm was repaired uneventfully. After intercostal drain insertion, she was transferred to
PICU for elective ventilation.
DISCUSSION:
Diaphragmatic hernia can have multitude of effects on the cardiorespiratory system. The intrathoracic visceral
herniation limits lung expansion and causes mediastinal displacement (1). In our case, the loss of diaphragmatic
tone associated with paralysis might have resulted in severe compressive effect resulting in cardiac arrest, which
got corrected with repositioning. Hence, anticipation of expected complications along with vigilant monitoring is
imperative. Spontaneous respiration should therefore be preserved until the thorax is decompressed (2).
REFERENCES:
1. Loehning R W., Takaori Masuhiko,. Safar Peter. Circulatory collapse from Anesthesia for Diaphragmatic Hernia.
Arch Surg. 1965; 90(1):109-114.
2. Lobb T. R., Butlin G. R. Anaesthesia and traumatic diaphragmatic hernia. Canadian Anaesthetists Society Journal
March 1974, Volume 21, Issue 2, pp 173-180.
318
ABSTRACTS
Diarrhea in a post heart transplant patient: Challenging

as always
Dr. Rohit, Dr. Vidya Devarajan, Dr. Murali Krishna, Dr. Suresh Rao, Dr. K.R. Bala Krishnan
Fortis Malar hospital, Chennai
Background:
Diarrhea in a post organ transplant is a frequent complication with myriad etiologies including the immunosuppressive
agents themselves contributing to it. It always remains a diagnostic challenge.
Case details:
Sixty six year old gentleman post heart transplant on 8/10/2015 for dilated cardiomyopathy presented with abdominal
distension preceded by diarrhea of two weeks duration. The diarrheal stool was greenish watery had no blood
or mucus. He had history of tenesmus .Prior to presentation at our centre patient had abdominal distention. He
had no history of fever. Although there was history of weight loss and loss of appetite. On clinical examination
he was afebrile,haemodynamically stable.Examination of the gastrointestinal system revealed a mildly distended
abdomen ,diffuse tenderness and sluggish bowel sounds .Examination of the hernial orifices and PR examination
was noncontributory.There were no visible peristalisis.Examination of the other systems were non contributory.He
was on the following immunosuppressantss- steroids ,Mycofenolate mofetil and tacrolimus
He had received induction therapy with Basiliximab and Methyl prednisolone.He had also received prophylactic
antibiotics at the time of transplant. He was on co trimoxazole and valgancylovir prophylaxis.His immediate post
transplant period was uneventful.
Differentials considered at this juncture were CMV colitis Vs MMF induced Diarhoea Vs CDifficile vs other
opportunistic infections due to T cell mediated immune suppression like mycobacterial disease of the GI tract.
Basic lab data showed a total count of 3100.S Creatinine was 2.2mg/dl. CT abdomen revealed dilated fluid filled
large bowel loops.Stool routine showed pus cells no RBC culture was negative,Stool for OVA cyst and parasites were
negative.
It was decided to do a colonoscopy for therapeutic(colonoscopic decompression) and diagnostic purposes
.Colonoscopy showed ulcers involving the descending colon .The biopsy of the ulcer confirmed pseudomembranous
colitis .There were no CMV inclusions or granulomas . Stool for C Diff PCR was positive He was treated with oral
Vancomycin and IV metronidazole for a total of two weeks with which he made a remarkable recovery.
Conclusion:
Diarrhoea in a post transplant setting continues to be a diagnostic challenge.Fatal colitis due to C difficile develops in
upto 13% of the solid organ transplant patients warranting high index of suspicion and prompt diagnosis.
Colonoscopy findings may not be typical due to the immunosuppressant effect.
Tissue diagnosis and molecular techniques aid in confirming the diagnosis.
319
IACTACON 2016
SUCCESSFUL REVASCULARIZATION OF THE CONGENTIAL

LEFT MAIN CORONARY ARTERY ATRESIA IN AN INFANT.
Samrat. S. Madanaik, Anand Vagarali,Sharan Patil,Abhijeet Shitole.
KLES Dr. Prabhakar Kore hospital and medical research Centre, Belgaum, Karnataka, India.
ABSTRACT
Introduction
Congenital anomaly of the coronary arteries is a rare disease occurring in 1%2% of all congenital heart diseases.
Atresia of the left main coronary artery is one of its least-frequently observed variations, with very few cases presented
in the. The prognosis is unfavorable because it results in myocardial ischemia or infarction, and even sudden cardiac
death. Surgical revascularization of the left main coronary artery is recommended in most patients with atresia of
the left coronary artery because of unfavorable clinical outcome, of which only a few cases have been reported for
successful surgical revascularization .
Case Report
A 4 month old infant presented with symptoms of heart failure and echocardiography revealed dilated left atrium
and left ventricle. There was left ventricular dysfunction with hypokinesia of septal, basal and anterolateral wall.
There was no evidence of anomalous origin of the left main coronary artery. Aortogram revealed atresia of the
left main coronary artery with faint filling of hypoplastic left anterior descending artery and left circumflex artery
through collaterals. The infant underwent successful surgical revascularization using a left internal mammary graft to
left anterior descending artery. The postoperative period was uneventful and the child was discharged on the tenth
postoperative day.
Conclusion
Congenital atresia of the left main coronary artery is a rare disease. It should be considered when diagnoses of
dilated cardiomyopathy or anomalous origin of the left coronary artery from the pulmonary trunk in infants or in
adults suspected of having coronary insufficiency are made. Myocardial revascularization surgery with grafting of the
internal thoracic artery seems presently to be the method of choice; however, the possibility of surgical angioplasty
should be considered. Our case according to pubmed search is the first reported case of successful revascularization
of left main coronary artery atresia in an infant from India.
Key Words:
left main coronary artery atresia, left anterior descending artery, left internal mammary artery, successful
revascularization.
320
ABSTRACTS
ATRIAL SEPTAL DEFECT WITH HYPOPLASTIC RIGHT

VENTRICLE: THERAPEUTIC DILEMMA
Varsha A.V, Gladdy George, Raj Sahajanandan
Department of Anaesthesiology, Christian Medical College, Vellore, Tamil Nadu
ABSTRACT
Introduction:
Percutaneous transcatheter closure of ASD using atrial septal occluder device (ASO) is being increasingly used in
clinical practice. Embolisation of the ASO device into RA or LA is one of the known complications. Proper selection
of patient and device is mandatory for such procedures. The therapeutic approach in a case of ASD with hypoplastic
RV is being discussed.
Methods:
We report the case of a 29 year old man with ostium secundum ASD with a large redundant Eustachian valve and
a hypoplastic right ventricle (RV), who underwent emergency device retrieval and fenestrated patch closure of ASD
after ASO device migration into LA.
Results:
Transthoracic echocardiogram revealed an ostium secundum ASD-27mm with a deficient aortic rim, AV rim 8 mm,
superior rim 5mm and posterior rim 11mm. RA/ LA were dilated and there was a prominent Eustachian valve
diverting IVC returns to LA. CT angiography showed a small RV and main pulmonary artery (MPA) and extensive
mediastinal systemic collaterals. The ASO device migrated to the LA after placement. Emergency surgery for retrieval
of device was done. ASD was closed with a fenestrated patch in view of the hypoplastic RV and MPA and excision
of large redundant Eustachian valve was done.
Discussion:
Isolated hypoplasia of right ventricle with atrial septal defect is a rare congenital cyanotic heart disease1. Feasibility
of a complete correction of the defect and adequacy of right ventricle to receive the entire venous return must be
accurately assessed prior to and during surgery2. In this case the large redundant Eustachian valve was directing the
entire IVC returns to LA through the ASD and was probably the cause of the hypoplastic RV. After excision of the
Eustachian valve the ASD was down sized using a fenestrated patch instead of complete closure to prevent RV failure
from sudden volume overload.
References
Joy MV, Venugopalan P, Sapru A, Subramanyan R. Isolated hypoplasia of right ventricle with atrial septal defect: a
rare form of cyanotic heart disease. Indian Heart J. 1999 Jul-Aug;51(4):440-3.
Atiq M, Lai L, Lee KJ, Benson LN. Transcatheter closure of atrial septal defects in children with a hypoplastic right
ventricle. Catheter Cardiovasc Interv. 2005 Jan;64(1):112-6.
321
IACTACON 2016
TITLE INTRAOPERATIVETRANSESOPHAGEAL
ECHOCARDIOGRAPHY IN AV SEPTAL DEFECTS; WHAT
AND WHEN TO LOOK?
Dr Deepak Mathew ,Dr Srinivas Gadhinglajkar,Dr Rupa Sreedhar
Department of cardiac anesthesia,SCTIMST,Trivandrum
Introduction
Atrioventricular septal defects are a spectrum of congenital heart disease characterized by a deficiency in AV septation
resulting in common, partial or transitional type of defects. These patients present with left-to-right shunting via
atrial and ventricular septal defects leading to varying degrees of cardiac failure and pulmonary hypertension. The
anomalies consists of atrial and ventricular septal defects, morphologically different atrioventricular valves and a
narrow left ventricular outflow tract. Surgery in these patients is considered high-risk. Intraoperative transesophageal
echocardiography has a vital role before and after the cardiopulmonary bypass. We present 2 cases of AVSD
emphasizing on the role of intraoperative TEE.
Methodolgy
2 patients one with partial and another with complete AVSD underwent surgical repair. Pre CPB assessment included
the characterization of ASD and VSD, degree of shunting and its effects (PAH), morphology of AV valves, grade of
mitral regurgitation, morphology of LVOT and ventricular function. One patient underwent single patch repair. The
other was subjected to double patch repair, mitral annuloplasty and closure of mitral valve cleft. Patient with partial
AVSD required reestablishment of CPB for correction of residual MR after the primary surgery. Both patients were
weaned from CPB with minimum inotropic support and had an uneventful postoperative period.
Results
Pre-CPB TEE confirmed the echocardiographic findings on preoperative echocardiography. Patient with complete
AVSD had mild to moderate MS (Gr. 6mmHg) with trivial AVVR, which was accepted since any further attempts at
correction would have worsened the MR. Patient with partial AVSD had no MR after second run of CPB. There was
no LVOT narrowing in both the patients after the surgery.
Conclusion
Transesophageal echocardiography is a valuable tool in perioperative assessment of AVSD patients and helps in
visualizing the anomalies, guiding the surgeon in decision making, verifying the postoperative results and monitoring
the intraoperative cardiac function.
References
1. Nunn GR. Atrioventricular canal: modified single patch technique. Semin Thorac Cardiovasc Surg Pediatr Card
Surg Annu. 2007:28 31.
2. Crawford FA Jr, Stroud MR. Surgical repair of complete atrioventricular septal defect. Ann Thorac Surg.
2001;72:1621 - 1628.
3. Rastelli G, Kirklin JW, Titus JL. Anatomic observations on complete form of persistent common atrioventricular
canal with special reference to atrioventricular valves. Mayo Clin Proc 1966;41:296308.
4. Aramendi JI, Rodriguez MA, Luis T, Voces R. No patch technique for complete atrioventricular canal repair.
Interact CardioVasc Thorac Surg. doi:10.1510/icvts.2005.125799.
5. Falco S, Daliento L, Ho SY, Rigby ML, Anderson RH: Cross sectional echocardiographic assessment of the extent
of the atrial septum relative to the atrioventricular junction in atrioventricular septal defect. Heart 1999, 81:199205
322
ABSTRACTS
LOBECTOMY FOR PULMONARY ARTERIOVENOUS

MALFORMATIONS: ANAESTHESIA AND PERIOPERATIVE
CARE.
Dr Manjusha N. Pillai, Dr.Shrinivas Gadhinglajkar, Dr.Rupa Sreedhar,
Dr.UnniKrishnan.M,
Sree Chitra Thirunal Institute of Medical science and Technology, Trivandrum,India
Background:
Pulmonary arteriovenous malformations are abnormal communications between pulmonary artery and vein,
usually congenital in origin. Catheter-guided embolization is the preferred treatment for the interruption of these
abnormal arteriovenous communications. However, surgical lobectomy may be required occasionally in case of failed
embolization. Perioperative challenges during lobectomy include potential for desaturation in an already hypoxemic
patient, air embolism and massive lung bleed during resection. Lung isolation and one lung ventilation during
thoracotomy can further worsen the hypoxia. We present our experience of lobectomy in 2 patients performed for
the treatment of pulmonary arteriovenous malformations.

In the last 10 years, two patients underwent lobectomy for pulmonary arteriovenous malformations at our institute.
One patient presented with syncope, whereas the other presented with seizures. Both had cyanosis and polycythemia.
Diagnostic pulmonary angiography revealed AVMs in left upper lobe and right lower lobe respectively. Both of them
required preoperative phlebotomy to lower the hematocrit. As embolization of AVMs was not successful in reducing
the shunting, surgical lobectomy was planned. Anesthesia was induced with Propofol, Midazolam, Fentanyl and
Vecuronium and maintained with Sevoflurane. Lung isolation was achieved and one lung ventilation established with
double lumen endobronchial tube. Thoracic epidural anaesthesia was provided as adjuvant to general anesthesia. In
the patient with left upper lobe pulmonary arteriovenous malformation, left upper lobectomy was performed and he
was extubated on table. In the other patient, right lower lobectomy was done, DLT was changed over to endotracheal
tube at the end of surgery and tracheal extubation was performed within 2 hours in the ICU.
Results:
Hypoxia occurred in both patients (saturation decreased to 70%), which required early clamping of lobar pulmonary
arteries. None of them had significant blood loss. Postoperative period was uneventful in both cases. Following
resection, arterial saturation improved to 99%. Both patients were discharged on post-operative day 11 and day 8
respectively.
Conclusion:
Therapeutic lobectomy for pulmonary arteriovenous malformations carries at least the same risk as any other thoracic
procedure. Establishing one lung ventilation and clamping of pulmonary vessels early improve oxygenation during
surgery.
323
IACTACON 2016
ANAESTHETIC MANAGEMENT FOR PULMONARY

THROMBO-ENDARTERECTOMY
Dr Thushara Madathil, Dr Balasubrahmaniam, Dr.Poornima Kasthuri, Dr Abraham
Cherian,
Amrita Institute of Medical Sciences and Research Centre , Kochi, Kerala , India
ABSTRACT
Chronic pulmonary thrombo-embolic disease is an important cause of severe pulmonary hypertension and is
associated with significant morbidity and mortality. The management options can be either pulmonary thromboendarterectomy or lung transplantation based on the extent of the disease and the involvement of the peripheral
bronchial vasculature. We present the case of a 36 year old gentleman who presented with dyspnea of one month
duration. He gave history of deep vein thrombosis with pulmonary thrombo embolism diagnosed during evaluation for
left upper lobectomy for aspergilloma three years back for which he underwent thrombolysis and oral anticoagulation
therapy. Re-evaluation showed unresolved saddle shaped thrombus at the bifurcation of main pulmonary artery
extending into segmental branches of the right pulmonary artery in CT scan and severe pulmonary hypertension .
He subsequently underwent thrombo-endarterectomy under low flow cardiopulmonary bypass with total circulatory
arrest. There was a significant reduction in the pulmonary artery pressure and the patient was successfully extubated
in the postoperative period. We describe the intra operative management and post -operative care for pulmonary
thromboendarterectomy in this patient.
324
ABSTRACTS
SURGERY FOR LEFT ATRIAL MYXOMA: OUR TWELVE YEAR

EXPERIENCE OF ANAESTHESIA AND PERIOPERATIVE CARE
Dr. Saravana Babu M.S, Dr. Shrinivas Gadhinglajkar, Dr. Rupa Sreedhar, Dr. Vivek
Pillai, Dr. Vargheese T. Panicker,
Sree Chitra Tirunal Institute for Medical Sciences and Technology, India
Abstract
Introduction:
Left atrial (LA) myxomas are benign primary heart tumors, associated with preoperative complications like mitral
valve obstruction and damage, systemic embolisation, transient ischemic attacks, stroke or seizures. There remains
risk of tumor fragmentation and embolization in intraoperative period. Postoperative period may be characterized
by cardiac arrhythmias. Anesthesia and perioperative care in these high-risk patients is challenging. We present our
experience of LA myxoma surgeries over last twelve years and discuss the role of transesophageal echocardiography
(TEE) in the intraoperative period.
Materials and Methods:

43 patients operated for LA myxoma in our institute over the last twelve years (2004-2015) were analyzed retrospectively.
34 of them were operated electively and 9 on emergency basis. About 11 patients had mitral valve obstruction, 13
patients had mitral regurgitation and 16 patients had both. Anesthesia was induced and maintained with standard
institute protocol. TEE examination was performed before and after cardiopulmonary bypass (CPB). Patients were
transferred to intensive care unit and trachea extubated after adequate reversal. TEE examination was done in 35
patients.
Results:
On pre-CPB TEE examination, a right atrial clot and patent foramen ovale were detected in one and two patients
respectively. One patient turned out to be inoperable. No residual tumour or MV damage were noticed on post-CPB
TEE in any of the patients. Residual ASD was detected in 2 patients. None of the patients underwent MV repair
or replacement. Incidence of postoperative arrhythmias was 30%. 6 patients lost follow-up. None of them had
tumor recurrence. Two patients were detected to have mitral regurgitation and one had aorto-caval fistula during
postoperative follow-up.
Conclusion:
Although a high-risk surgery, LA myxoma excision can be performed under standard anesthesia care with minimum
complications. Intraoperative TEE was helpful in delineating the LA myxoma details, which guided the surgeon in
excising the tumour. It also helped them in making decisions on addressing the mitral valve pathologies. In the postCPB period, the TEE identified the presence of residual tumour and detected surgical complications, which could
be treated promptly.
325
IACTACON 2016
CARDIAC SURGERY POSTOPERATIVE ARREST AND

RESUSCITATION- A SINGLE INSTITUTION 3 YEAR
RETROSPECTIVE STUDY OF PROTOCOL AND OUTCOME
INTRODUCTION
ARREST IN CARDIAC SURGICAL PTS IS DIFFERENT BECAUSE Arrest is witnessed.
Continuous monitoring in ICU.
Intubated patient.
Venous access, invasive monitoring lines present.
Cause usually reversible, early appropriate intervention can improve outcome
HENCE RESUSCITATION CANNOT BE BASED ON CONVENTIONAL ACLS.
EACTS provides the only comprehensive post cardiac surgery cardiac arrest
guidelines
MATERIALS & METHODS

A Retrospective analysis of resuscitation methodology among post cardiac surgery patients with witnessed cardiac
arrest done at SSSIHMS, Bangalore (January 2013 December 2015).
The data was analyzed to determine the survival-to-hospital discharge rate, resternotomy rates and the trend in
these endpoints over time.
Our outcome and protocol was compared to the current guidelines.
RESULTS
5.37% patients had cardiac arrest.
74.28% patients survived to discharge.
Conventional closed chest CPR : 61.42 %
Open chest CPR : 38.58 %
Survivors among closed chest CPR : 63.46%
Survivors among opened chest CPR: 36.54%
Among the non survivors :
11 patients (30.55%) had no ROSC,
25(69.44%) had ROSC but not survived to discharge.
OUR OBSERVATION
Our survival rate to discharge is 74.28%.
Escalting doses of drugs often necessary- eg- adrenaline, calcium, inotropes.
Closed chest massage if generating adequate pressure can be continued until
recovery but this should not desist chest re-opening
326
ABSTRACTS
DISCUSSION OF OUR PROTOCOL COMPARED WITH EACTS PROTOCOL FOR POST CARDIAC
SURGERY CARDIAC ARREST
CONCLUSION
The cardiac arrest following cardiac surgery is usually preceded by a period of progressive deterioration, providing
a window of opportunity to act preemptively.
Practising protocol based management and adequate training has been shown to reduce the time to chest opening
and reduce complications in conduct of resternotomy.
Need for maintain a register of cardiac arrest cases in ICU for review and improvement in protocols
Need for development of guidelines by the Cardiac Anesthesia and Surgeons societies to address issues specific to
cardiac surgery
References
Dunning J, et al. Guideline for resuscitation in cardiac arrest after cardiac surgery. Eur J Cardiothorac Surg (2009),
doi:10.1016/j.ejcts.2009.01.033
Jan Runte et al, The new 2010 ERC resuscitation guidelines Relevance for cardiac surgery patients, Applied
Cardiopulmonary Pathophysiology 16: 113-118, 2012
Neumar RW, Otto CW, Link MS, et al. Adult cardiovascular life support: 2010 American Heart Association guidelines
for
cardiopulmonary resuscitation and emergency cardiovascular care. Circulation2010;122:S729-67.

2. I confirm that I previewed this abstract and that all information is correct. I accept that the content of the abstract
cannot be modified or corrected after final submission and I am aware that it will be published exactly as submitted.
327
IACTACON 2016
CASE REPORT; LEFT VENTRICULAR MYXOMA, A RARE

CASE
Abstract-Primary intracardiac tumours of the heart are rare. The commonest primary tumour is myxoma, found almost
exclusively in the atria, 75 persent or more occurring in the left atrium. Myxoma originating in the ventricles appears
to be extremely rare. [ 1] Multilobulated or pedunculated myxoma are often sufficiently mobile and may prolapse in
to the valve during systole. Surgical excision is recommended because of potential for embolization. The integration
of newer cardiac imaging techniques, transthoracic and intraoperative transoesophageal echocardiography proved
critical in the management of these patients. [ 2]
Introduction Intracardiac myxoma is the most common tumor of the heart with the estimated incidence of 0.5
per million populations per year. [5] Approximately 10% of myxoma are familial, as part of the autosomal dominant
Corney complex, where as the cause of sporadic cases remains unclear. [2]
We reported a case of left ventricular myxoma, surgically resected successfully and postoperative course was
uneventful. TEE is important to know the location of mass and pursue its intact position before removal of mass
and for confirmation of no residual mass in postoperative period.
Case Report- A 26-year young male patient had history of fever. During routine investigation, diagnosed to have
LV mass in 2 D echocardiography examination. Cardiac MRI was done, which showed, well defined intracavitory
mobile lesion within 70% LV cavity with irregular surface margin. Mass projects into LVOT causing nearly persent
obstruction of lumen during LV systole.LV function was normal. Patient referred to our centre for removal of LV
mass. Patient didnt have any symptoms related to embolic phenomena. Patient didnt have any co morbidity.
After inserting radial arterial line, induction was done with fentanyl 100 mcg, midazolam 2 mg, thiopentone sodium
125 mg and vecuronium 8mg.After intubation right IJV was cannulated with 7.5 F triple lumen catheter. TEE probe
was inserted which showed a large multilobular mass in LV cavity measuring 5cm by 2 cm protruding through the
LVOT during systole obstructing 70 persent of the lumen. TEE monitoring done throughout the case. TEE is
important to know the location of mass and pursue its intact position before removal of mass Surgical excision of the
myxoma was performed under extracorporeal circulation and moderate hypothermia. LV mass was removed through
transverse aortotomy. Polypoidal, papillary LV mass was noted in LV cavity extending into LVOT measuring 4.5
cm into 4.5 cm. Pedicle of the mass was attached to LV wall just close to posteromedial papillary muscle along with
chordae.
Post CPB, TEE was done. There was no residual mass and no mitral regurgitation.LV function was normal. Mass
send for histopathological examination. Pathological analysis revealed that the left ventricle mass was consistent with
myxoma. The myxoma had hyperchromatic, multinucleated myxoid cells and stellate cells along with lepidic cells
that have round to oval nuclei with indistinct eosinophilic cytoplasm. Stroma is loose and myxoid with scattered
lymphocytes.
Postoperative period was uneventful. Patient was discharged on sixth postoperative day.
DiscussionPrimary cardiac tumors are uncommon with incidence of 0.02%. Benign cardiac myxoma constitute 88% of cardiac
tumor cases. LV myxoma account for only 2.5% of cases. The clinical features of LV myxoma are mostly caused by
embolization and obstruction to LVOT. Arrhythmias, conduction disturbances, and LV dysfunction can also be seen.
Embolic phenomenon in LV myxoma are more common than LA myxoma, occur in in 64% of patient with LV
myxoma. Considering the risk of embolization, myxoma should be surgically resected as early as possible. [6]
328
ABSTRACTS
The shape, extension, site of attachment, and the functional obstruction to LV outflow tract could promptly and
easily be assessed by preoperative transthoracic and intraoperative transoesophageal echocardiography.
References:
1] Surgical Removal of an Intracavitary Left Ventricular Myxoma By Jerome Harold Kay, M.D., Robert M. Anderson,
M.D.John Meihaus, M.D., Reuben Lewis M.D., Oscar Magidson M.D.,Sol Bernstein M.D., George C. Griffith,
M.D. Circulation 1959: 20:881-886 doi;10;1161/01
2] (Circulation,2012; 125: e1003-e1005, Images in cardiovascular medicine, Multimodality Imaging in the Diagnosis
of Coexisting Left Atrial Myxoma and Aortic Valve Papillary Fibroelastoma Anshu K Buttan, BA; George
Panagiotides, MD
3] A rare case of a big left ventricular myxoma presenting with a cerebrovascular stroke Hani M. Mahmoud , Ihab
Moursi Egyptian Society of Cardiology The Egyptian Heart Journal
4] Bjessmo S, Ivert T. Cardiac myxoma: 40 years experience Ann Thorac Surg 1997; 63:697700.
5] Keeling IM, Oberwalder P, Anelli-Monti M, Schuchlenz H, Demel GP, Tilz GP, et al. Cardiac myxoma 24 years of
experience in 49 patients. Eur J Cardiothoracic Surg 2002; 22:9717.
6] Annals of cardiac anesthesia,2015, vol18, issue 1, page 95-97, Left ventricular mass: Myxoma or thrombus?
Monish S Raut, Arun Maheshwari, Sumir Dubey, Sandip Joshi
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IACTACON 2016
Ultrasound guided measurement of minimal transverse

diameter of subglottic airway (MTDSA) in determining
the endotracheal tube size in paediatric patients.
Dept. of Anaesthesia, Christian Medical College, Vellore, Tamilnadu, India.
Introduction:
Age based formulas used for choosing the ET tube in pediatric population have a reported success rate of 40-70%.
Children presenting for cardiac surgery may have failure to thrive and may not tolerate inadequate ventilation/ tube
exchange as a result of improper sizing. Recent literature search shows that MTDSA helps in predicting the size of
ETT with a success rate of 90%.
Methods:
We did a pilot study over a period of two months. A total of 17 patients* less than 8 years, undergoing cardiac surgery
were enrolled in the study. Patients with anticipated airway difficulty were excluded from the study. Tube size will be
calculated as per the formula Age/ 4+4 before induction of anaesthesia by the primary investigator. An independent
consultant with good knowledge on airway ultrasound measured MTDSA after giving relaxant (1, 2, 3). Patients were
incubated as per MTDSA measurement. If there is no leak at ventilation with Paw 30 cm H20 ETT will be changed
to one size down. If there is leak at 10 cm H2O, ETT will be replaced with one size larger tube. If there is minimal
palpable leak with 20 cm H2O Paw ETT was considered appropriate. Results: MTDSA correctly predicted ETT size
in 93.75% of children. In contrast age-related formulae, correlated with the MTDSA based ETT size only in 31.25%.
About 68.75% of children bigger ETT was used by using MTDSA when compared to that predicted by age related
formulae. The correlation of MTDSA with OD of ETT is 97.5% which is statistically significant (p < 0.0001).
Discussion: MTDSA measurement involves a learning curve, but is a useful additional tool in the cardiac anaesthetists
armamentarium to perfect the endotracheal tube selection in paediatric cardiac surgical population.
References:
1. Schramm C, Knop J, Plaschke K, Jensen K. Role of ultrasound compared to age related formulas for uncuffed
endotracheal intubation in pediatric population. paediatric anaesthesia 2012;22:781-6.
2. Shibasaki M, Nakajima Y, Ishii S, Shimizu F, Shime N, Sessler D.Prediction of pediatric endotracheal tube size by
ultrasonography. Anaesthesiology 2010;113(4):819-24.
3. Bae JY, Byon HJ, Han SS, Kim HS, Kim JT. Usefulness of ultrasound for selecting a correctly sized uncuffed
tracheal tube for paediatric patients. Anaesthesia 2011;66:994-8.
We are continuing the pilot study, hence the total number patients will exceed at the time publication/presentation.
330
ABSTRACTS
Stenting of carinal tumor in a patient with significant

CAD (coronary artery disease)
Dept. of Anaesthesia, Christian Medical College, Vellore, Tamilnadu, India.
Abstract:
Coronary heart disease associated with left ventricular dysfunction poses significant perioperative risk especially for
emergency airway surgery. Central airway obstruction (CAO) presenting as acute respiratory distress poses significant
challenge to the anaesthesiologist (1, 2) as rigid bronchoscopy and stenting involves significant haemodynamic
response with increased risk of periprocedural myocardial infarction. Loss of airway cannot be managed as per
standard guidelines and selective endobroncial intubation /ventilation may not be possible with lesions extending into
both bronchi as seen in our patient.
We describe a case of 74 year old male with carinal mass extending into both the bronchi presenting in severe
respiratory distress. He had a history of anterior and inferior wall myocardial infarction for which thrombolysis
& PTCA was done 5 years ago, recent echocardiogram showed LV dysfunction (EF-33%) with RWMA. He was
planned for emergency debulking and Y stenting. BIPAP was instituted as bridging measure till he was anesthetised.
We opted for TIVA with propofol infusion, high dose dexmedetomidine infusion, fentanyl (total dose 4mcg/kg) and
intermittent topicalization to maintain adequate depth of anesthesia and avoid the sympathetic stimulation of airway
instrumentation. We preserved spontaneous ventilation (3) with 15 l/min O2 through nasal cannula throughout.
Once rigid bronchoscope was introduced manual jet ventilation was started at 40 bpm. Ventilation was difficult with
jet ventilation but we were able to maintain spo2 and paco2 by maintaining spontaneous ventilation assisted with
jet ventilation. A brief period of hemodynamic instability was managed by noradrenaline infusion after USG and
echocardiography was done to rule out pneumothorax and acute cardiac dysfunction respectively.
We highlight the goals of managing these long cases which include preprocedural stabilization, planning with
the pulmonologist, diligent anesthetic technique directed towards maintaining adequate ventilation, permissive
hypercarbia, early diagnosis and management of potential life threatening arrhythmias, pneumothorax and acute
cardiac failure.
References:
1. Mason RA, Fiedler CP. The obstructed airway in head and neck surgery. Anaesthesia. 99954:6258.
2. Mathisen DJ, Grillo HC. Endoscopic relief of malignant airway obstruction. Ann Thorac Surg. 198948:46973.
3. Slinger P, Karsli C. Management of the patient with a large anterior mediastinal mass: recurring myths. Current
Opinions in Anesthesiology 2007; 20: 13.
331
IACTACON 2016
Bilateral Stellate ganglion block and Cardiac

denervation in case of long QT syndrome with refractory
ventricular tachycardia (Electrical storm)
Dr Dinesh Kumar DM, PDCC 1, Dr Prashant Kulkarni DM 2, Dr Shivanand Mch 3,
Dr Murugesh
Wali MD 1. Department of 1Cardiac thoracic and vascular anesthesia, 2 Cardiology, 3 Vascular surgery.
Abstract:
Long QT syndrome (LQTS) is a rare inherited or acquired condition characterized by delayed repolarization of
cardiac myocytes secondary to defects in sodium or potassium channels. Patients with long QT syndrome are prone to
develop torsades de pointes and ventricular tachycardia secondary to electrolyte disturbances like hypomagnesaemia,
hypocalcemia and hypokalemia. Various drugs like antipsychotics, anti-arrhythmics like Amiodarone, Satolol and
Cisapride may also prolong QT and increase the risk of R on T phenomenon resulting in recurrent ventricular
tachycardia. Increased adrenergic states like excitement or exercise will also increase the risk of VT. We treated the
recurrent ventricular tachycardia(electrical storm) requiring frequent DC shock in a 10 year old child with prolonged
QT syndrome initially with bilateral Stellate ganglion block followed by bilateral lower cervical and upper thoracic
Sympathectomy. Despite the correction of electrolytes, B-blockers and other drug therapy patient was requiring about
40 to 50 shocks in a day. The stokes Adam episodes secondary to ventricular tachycardia were wrongly diagnosed
as seizures by the general physician and he was on three anti-epileptics when he came to our hospital. Following the
Stellate ganglion block and cardiac denervation the episodes of ventricular tachycardia decreased to about nil to three
episodes per day. Further, he was referred to an electrophysiologist to plan for an ICD. Repeated shocks delivered
through the ICD may aggravate sympathetic stimulation, ventricular arrhythmias and initiate a series of more shocks
and electrical storm.The cardiac denervation, may complement the use of an ICD, because the denervation markedly
decreases the catecholaminergic load on the heart, which may facilitate smooth functioning of the ICD in interrupting
VF and restoring the sinus rhythm. His parents and other sibling in the family were screened and were found tohave
long QT syndrome. Ultrasound guidance enhances the success rate of the technique, reduces the quantity of local
anesthetic required to produce desired effects and prevents technical complications. Electrical Storm associated with
catecholaminergic surge may be resistant to the anti-arrhythmic drugs. Stellate ganglion block followed by surgical
cardiac denervation is an effective treatment modality to reduce the incidents of malignant ventricular arrhythmias.
The Stellate ganglion block may serve a simple bedside tool to identify the patients who are likely to respond to the
more definite but more invasive modality of Sympathectomy.
Reference:
1. Schwartz PJ, Priori SG, Cerrone M, Spazzolini C, Odero A,Napolitano C,et al. Left cardiac sympathetic denervation
in the management of high-risk patients affected by the long QT syndrome. Circulation 2004;109:1826-33
2. Proietti R, Sagone A. Electrical storm: Incidence, Prognosis and Therapy. Indian Pacing Electrophysiol J 2011;25:3442.
3. Kenyon CA, Flick R, Moir C, Ackerman MJ, Pabelick CM. Anesthesia for video scopic left cardiac sympathetic
denervation in children with congenital long QT syndrome and catecholaminergic polymorphic ventricular
tachycardia-a case series. Paediatr Anaesth 2010;20:465-70.
4. Gadhinglajkar S, Sreedhar R, Unnikrishnan M, Namboodiri N. Electrical storm: Role of stellate ganglion blockade
and anesthetic implications of left cardiac sympathetic denervation. Indian J Anaesth 2013;57:397-400
332
ABSTRACTS
PATIENT OF SV ASD WITH PAPVC AND LSVC FOR MINIMAL

ACCESS CARDIAC SURGERY
Introduction
ASD closure by minimal access route ( MACS) is gaining popularity among surgeons and patients. The commonly
preferred patients are those with OS ASD without Left SVC. Presence of LSVC and PAPVC are considered relative
contraindications for MACS (1).
We present a case of Sinus venosus ASD, PAPVC with left SVC done by MACS.
Case Report
A 33 year old lady presented with dyspnea on exertion since 6 months. Echo showed SV ASD with partial anomalous
pulmonary venous connection (PAPVC) and dilated coronary sinus. Cardiac CT done preoperatively showed right
upper pulmonary veins draining into SVC close to its junction. Distance of RUPV drainage from SVC RA junction
was 1.2 cm. Size of right and left SVC were 12 and 14 mm respectively After induction, right SVC was percutaneously
cannulated with 15 fr wire-reinforced cannula by anesthesiologist under TEE guidance. Another 15 fr cannula was
inserted through left IJV into LSVC. IVC and aorta were cannulated via femoral route under TEE guidance. On CPB,
SV ASD was closed and baffling of RUPV/ RMPV into LA and SVC augmentation done. Post operative recovery
was uneventful.
Discussion
In select patients with PAPVC repair can be done through minimally invasive route. There are 2 anatomic details that
should be considered in such patients- distance between the insertion of the anomalous veins into the SVC and the
inter-atrial communication and adequate size of SVC to allow for baffle reconstruction (2). Patients with presence of
LSVC and PAPVC draining into RSVC may have good sized bilateral SVCs. In such cases, additional cannulation of
left SVC can be considered to improve venous drainage and provide a bloodless surgical field. In cases with PAPVC
and LSVC, pre operative cardiac CT, vascular ultrasound and TEE play a pivotal role. With adequate experience and
close coordination between cardiac anesthesiologist, surgeon and perfusionist, repair of more complex ASD anatomy
via minimal access surgery can be done safely.
References
1. Jha AK, Malik V, Hote M. Minimally invasive cardiac surgery and transesophageal echocardiography. Ann Card
Anaesth 2014;17:125-32.
2. Michael W.A. Chu, K L Losenno,S A. Fox, C Adams, H Al-Habib, R Guo, A H. Menkis, B Kiaii, Can J Surg, Vol.
57, No. 3, June 2014, E 75-81
2. I confirm that I previewed this abstract and that all information is correct. I accept that the content of the abstract
cannot be modified or corrected after final submission and I am aware that it will be published exactly as submitted.
3.I declare that the submission of the abstract constitutes my consent to publication.
333
IACTACON 2016
ASD closure in postpneumonectomy patientAnaesthesia management

Dr Dhawal Wadaskar
Assistant Professor,
Department of anaesthesiology,
LTMGH & LTMMC, Sion, Mumbai
Maharashtra, India
Introduction
Fewer data is available on cardiac surgery in post-pneumonectomy patients.There is no reported case of sinus venosus
and OS-ASD (ostium secondum - atrial septal defect) surgical closure in post-pneumonectomy patient in literature.1
Cardiac surgery itself predisposes patient to postoperative pulmonary dysfunction due to intraoperative atelectasis
and CPB related complications. We report a challenging case for anaesthesiologist, where we anesthetized postpneumonectomy patient for surgical ASD closure.
Methods
10-yearold male child who had undergone left pneumonectomy 14 months back for non-functioning left lung, now
posted for ASD closure.Most probably the cause of non-functioning left lung was repeated pneumonia due to ASD.
He was having SVC type sinus venosus and OS ASD with mild pulmonary artery hypertension. Preoperative postpneumonectomy pulmonary function test(PFT) showed FVC of 1.09 L (93% of predicted), FEV1 of 0.92 L (89%
of predicted), and FEV1/FVC of 99% predicted. We used intravenous general anaesthesia with single lumen tube
avoiding elective endobronchial intubation on right. Volume control mode of ventilation used with VT 5 ml/kg along
with respiratory rate between 20-25/min. Sinus venosus ASD was closed using autologous pericardial patch and OS
ASD closed directly. Patient weaned off ventilator gradually in ICU and extubated 12 hours after surgery, Discharged
on 6th postoperative day.
Discussion
Postpneumonectomy patients undergo various anatomical and physiological changes over a period of time.2 In
left pneumonectomized patient right lung gets compensatory hyperinflation and heart deviates counterclockwise
in left side of chest. One has to be careful while doing sternotomy as it can cause trauma to hyperinflated lung.
Hyperventilation is necessary many a times to maintain normal acid-base balance. One can encounter difficulty in
Internal jugular cannulation for central venous access and fluid management.3Early ASD closure can be advisable in
postpneumonectomy patients safely.
References
1. Coronary artery bypass grafting and/orvalvular surgery in patients with previous pneumonectomy. Alexander
Fragkidis, Alexander Dimitrios, DimitriosDougenis; Journal of cardiothoracic surgery, 7:110, 2012.
2. S.E. Kopec, R.S. Irwin, C.B. Umali-Torres, J.P. Balikian, A.A. Conlan; The postpneumonectomy state Chest,
vol.114, no.4, pp 1158-1184, 1998
3. Cardiac surgery in patients with previous pneumonectomy; Sanjay V Ghotkar, VikramAerra, NeerajMediratta;
journal of cardiothoracic surgery, 2008, 3:11
334
ABSTRACTS
DIFFICULTY IN WEANING OFF CPB IN A CASE OF WILLIAMS SYNDROME WITH

SUPRAVALVULAR AORTIC STENOSIS
Introduction
Patients with congenital supravalvular aortic stenosis and associated peripheral
pulmonary artery stenoses, the majority of whom have Williams-Beuren syndrome, are
inherently at risk for development of myocardial ischemia.
The biventricular hypertrophy that accompanies these lesions increases myocardial
oxygen consumption and compromises oxygen delivery.
Several case reports have documented an increased incidence of anesthesia-related
cardiac arrest in these patients. The cause of cardiac arrest in most cases was
suspected to be myocardial ischemia caused by reduced coronary artery blood flow
Case Report
A 10 year old boy diagnosed as Williams syndrome with Supravalvular Aortic stenosis
(SVAS) came for corrective surgery. Anesthetic induction was done smoothly with
opiod-benzodiazepene combination. The patient went on CPB and Broms Aortoplasty
was done.
The patient was weaned off CPB with Dobutamine 5 mics/kg/min and Adrenaline 0.05
mics/kg/min. While attempting to come off CPB, the patient developed hypotension,
significant ST depression and TEE showed globally hypokinetic LV with EF of 25%. The
patient was put back on CPB and the heart rested for 1 hour. To improve the coronary
perfusion pressure, Adrenaline was increased to 0.2 mic/kg/min and Nor adrenaline
0.05 mic/kg/min. , The patient again developed ST depression and hypotension. After
the 2nd failed attempt at weaning from CPB, Dobutamine was replaced with Vasopressin
.0009 IU/kg/min and Adrenaline and Nor adrenaline doses were increased. The
increased systemic pressure increased coronary perfusion and the patient was slowly
weaned off CPB.
Post operatively, vasopressin was weaned off on 1st post operative day and patient had
an uneventful recovery
Discussion
The presence of LVH increases myocardial oxygen demand. Conversely, there is
impaired coronary blood flow if the CPP or SVR falls post CPB as as the coronaries are
exposed to higher perfusion pressures pre operatively due to the high prestenotic
pressure and will require a high coronary perfusion pressure post operatively as well.
335
IACTACON 2016
Vasopressors such as phenylephrine and vasopressin should be used as first-line

agents to treat hypotension and ST-T wave changes indicative of myocardial ischemia.
Drugs which reduce SVR should be avoided in patients with SVAS.
References
Thomas M. Burch, Francis X. McGowan, Jr., Barry D. Kussman, Andrew J. Powell, James A. DiNardo, Congenital
Supravalvular Aortic Stenosis and Sudden
Death Associated with Anesthesia: Whats the Mystery? Anesth Analg 2008;107:1848 54
Andrew J. Matisoff, Laura Olivieri, Jamie M. Schwartz, Nina Deutsch, Risk assessment and anesthetic management
of patients with Williams syndrome: a comprehensive review Pediatric Anesthesia Dec 2015, Volume 25, Issue 12,
120715

1. I declare that the study was conducted according to the protocol approved by the
institutional or local committee on ethics in human participation.
2. I confirm that I previewed this abstract and that all information is correct. I accept that
the content of the abstract cannot be modified or corrected after final submission and I am
aware that it will be published exactly as submitted.
Dr Sathya Swaroop Patnaik
336
ABSTRACTS
A rare case of Idiopathic Tri-saccular Left Ventricular

Outflow Tract (LVOT) pseudo aneurysm masquerading
as ruptured sinus of valsalva (RSOV) compressing
all major coronary arteries role of TransEsophageal
Echocardiography (TEE) in surgical correction
Dr.M.Karthik Babu Murugessan,
G.Kuppusamy Naidu Memmorial Hospital, Coimbatore.
Abstract
LVOT pseudo aneurysms are often a complication of Tuberculosis, aortic valve infective endocarditis, and post aortic
valve surgery or after chest trauma. Idiopathic LVOT pseudo aneurysms are exceedingly rare. We report a case of
Idiopathic trisaccular LVOT pseudo aneurysm in a 40 year old male.
Preoperative transthoracic echocardiogram revealed trisaccular aneurysm adjoining ascending aorta and left atrial
roof. He underwent CT aortogram to delineate the anatomy better, which revealed aneurysmal sac mimicking RSOV
arising from right sinus.
Coronary angiogram showed extrinsic systolic compression of left main and right coronary arteries and complete
occlusion of left circumflex artery by the aneurysmal sac.
During surgery, he had left ventricular pseudo aneurysm with two large openings, one below the Non coronary cusp
(NCC) and the other below the Left coronary cusp (LCC). All three sinus of valsalva were normal. Trileaflet aortic
valve was normal. The aneurysm opening beneath NCC was repaired with a PolyTetraFluoroEthylene patch and the
opening beneath LCC was closed directly with polypropylene.
At the end of the surgery TEE confirmed complete obliteration of the pseudoaneurysmal sacs.
Histopathology of aneurysm wall showed fibrocollagenous tissue, no hyalinization and no lining epithelium suggestive
of pseudo aneurysm. There was no significant inflammation or granuloma suggestive of Tuberculosis or other
infective pathology. He made an uneventful postoperative recovery and is on medical follow-up.
337
IACTACON 2016
SIBBLINGS WITH JERVELL AND LANGE-NIELSEN SYNDROME

FOR VIDEOSCOPIC LEFT CARDIAC SYMPATHETIC
DENERVATION
Dr.T.Vikram Kumar Naidu, Dr.Hemang Gandhi, Dr.Rajesh Thosani, Dr.Arvind Kumar

Bishnoi, Dr.Varsha Sarvaiya
U. N. Mehta Institute of Cardiology and Research Center (affiliated to BJ medical college, Ahmedabad),Ahmedabad,India.
Abstract:
Introduction:
Jervell and Lange-Nielsen syndrome (JLNS) is characterized by congenital profound bilateral sensorineural hearing loss
and long QTc, usually greater than 500 msec. Here, we report our experience in performing left cardiac sympathetic
denervation in identical twins with this setting.
Methods:
Sibblings aged 15 and 13 years presented with recurrent episodes of syncope attacks and palpitations since 2 years
and deafness since birth. Diagnosis of long QT syndrome was made on the basis of ECG which showed QT interval
of 520 msec. Initial treatment included rest, and beta blockers. As the symptoms recurred they were referred for
further management to our institute.
Results:
The twins were posted for laparoscopic left cardiac sympathetic denervation on the same day. A calm environment
was maintained and adequate premedication was given for anxiolysis. They were induced with fentanyl, propofol,
vecuronium and intubated with a 28 Fr double lumen tube and maintained in right lateral position. IV metoprolol 1mg
and magnesium sulfate 750mg was given intraoperatively. They were maintained on propofol infusion, intermittent
vecuronium, fentayl and isoflurane 1%. After an uneventful surgery they were shifted to the ICU and extubated later
without administration of reversal agents. Care was taken to avoid agents which prolonged QT interval perioperatively
and during the hospital stay. They were discharged from the hospital in a week on oral beta blockers and were
followed up later on.
Discussion:
Prolongation of the QTc interval is associated with tachyarrhythmias, including ventricular tachycardia, episodes of
torsade de pointes ventricular tachycardia, and ventricular fibrillation, which may culminate in syncope or sudden
death. Treatment strategies include -blockers, implantable cardioverter defibrillators, and left cardiac sympathetic
denervation (1).
Reference:
1. Collura CA, Johnson JN, Moir C, et al. Left cardiac sympathetic denervation for the treatment of long QT
syndrome Heart Rhythm. 2009.
338
ABSTRACTS
Anaesthetic management of a case of Gilberts

syndrome for mitral and aortic valve replacement
with tricuspid valve plasty Role of Transesophageal
echocardiography.
Dr.Sundar Subash Singh
Gilberts syndrome is an autosomal dominant, bilirubin metabolism disorder occuring in 2 to 13% population. This
condition is characterised by relative deficiency of glucuronyl transferase and poor uptake of unconjugated bilirubin
by hepatocytes. Cardiac surgery on cardiopulmonary bypass in these patients can act as a further triggering factor
for hepatic injury. Changes in hepatic blood flow during CPB can result in intra-operative hepatic injury and post
operative hepatic dysfunction. Various techniques for monitoring hepatic blood flow intraoperatively are differential
manometer, bristle flow meter, electromagnetic flow probes and implanted pulsed ultrasound flowmeters, which are
all invasive. Transesophageal echocardiography(TEE) and Doppler assessment of hepatic vein, helps in assessing
hepatic blood flow during cardiac surgery. Here we discuss, anaesthetic management and role of TEE in maintaining
hepatic blood flow perioperatively in a 24 year old male patient with Gilberts syndrome undergoing double valve
replacement with tricuspid valve plasty under CPB for severe aortic regurgitation, mitral regurgitation, tricuspid
regurgitation in atrial fibrillation with controlled ventricular rate. The anaesthetic management included avoiding
hepatotoxic agents and maintaining adequate hydration. CPB management compromised of mild hypothermia,
unobstructed hepatic hvenous drainage, higher perfusion pressure, use of ultrafiltration, restricted blood transfusion
and TEE guided hepatic blood flow monitoring and management of hepatic perfusion, which resulted in better
outcome of this patient. One year follow up of the patient showed no further deterioration in hepatic function.
339
IACTACON 2016
IMMEDIATE HYPOXIA AFTER ASD REPAIR CASE REPORT
Dr.Amol Thakre
Dept of Anesthesia Govt Medical College & Super Specialty Hospital Nagpur.
Here we are presenting a case report of 25 yr old female patient operated for atrial septal defect .
A 25 yr old female patient came with complaints of breathlessness on exertion, palpitations since 1yr . symptoms
were increasing in severity from last 3 months . on examination patient had systolic murmur with wide 2nd heart
sound fixed spiltting of P2, other system examination were normal. On investigation her Hb- 11.6gm/dl, CBC
WNL, BU-28 Sr. Creatinine- 1, Na-138 , K-4.2, INR -1.2,
On 2D echo patient was found to have atrial septal defect (ostium secundum)of 2cm . patient was posted for surgery
on next day .
Patient taken inside operation theatre, ecg leads,spo2 sensor were attached to the patient , a large bore iv line 16 g
taken , fluids started , patient sedated with iv midazolam 2mg and iv fentanyl 50 ug .
under local anesthesia , Left radial arterial line secured with 20g jelco cannula and Right sided internal jugular vein
cannulated with 7 fr triple lumen catheter .
patient induced with iv.fentanyl 200ug+ iv. Propofol 100ug+ iv vecuronium 8mg . airway secured with 7.5 number
cuffed endotracheal tube. Patient maintained on oxygen and iv sedation on closed circuit on volume controlled mode
of ventilation. defect confirmed with intropearative TEE
surgeons decided to operate by minimally invasive technique. So incision taken from 2nd intercostal space in right
side . aortic and venous cannulation done through the thoracotomy incision and patient put on cardiopulmonary
bypass . surgeons identified and repaired the atrial septal defect with pericardial patch . after Left atrial closure patient
was brought back off bypass with minimal inotropic supports ie. Iv dopamine @ 4ug/kg/min and iv Ntg @1 ug/
kg/min . all the vitals were stable (Bp 100/70 , cvp- 5mmhg, spo2- 100% ,temp-36.8 ) . after 5 min spo2 starts to
decrease and came to 90-94% . we thought it might be due to atelectasis of lung so patient was ventilated manually
for some time, PEEP was given. Saturation improved for some time , but it again starts to decrease .
ABG was done , PO2 levels were very low ie 80mmhg on 100% Fio2 . we doubt there may be right to left shunt.At
this point we decided to do a contrast ECHO to find out shunt site , so a catheter was introduced through rt. Femoral
vein into inferior vena cava.through the catheter agitated saline was injected and ECHO images were observed
simultaneously. On ECHO contrast was noted in both right and left atrium . so it was confirmed that there is right to
left sided shunt .midline sternotomy done , patient again put on bypass , cardioplegia given , on examination of repair
it was found out that at the lower end of asd repair the sutures have also included the eustatian valve of inferior vena
cava and because of that there is mixing of blood form inferior vena cava to left atrium causing hypoxemia. Atrial
septal defect was repaired again carefully ,patient again carried off bypass after spontaneous rhythm came . ABG
was done , now the PO2 levels were good ie 478 on 100% fio2 . postoperative course was uneventful and patient
discharged home after 7th postoperative day.
Discussion
Atrial septal defect is common entity having excellent prognosis after surgical repair . The common complications
were postoperative atrial arrhythmias, SA, and AV blocks necessitating pacemaker implantation, mediastinal bleeding,
and TIAs or strokes. Inadvertent diversion of the inferior vena caval flow into the LA is a very unusual cause of
morbidity following repair of ASD. Reported cases have presented primarily with cyanosis and hypoxia, which can
occur immediately postoperatively or months to years after operation. Exertional desaturation has also been reported,
as has orthodeoxia. Reported factors associated with this complication include a large secundum defect or sinus
340
ABSTRACTS
venosus defect, and anomalous pulmonary return into the RA. In most of the cases, a prominent Eustachian valve
was included in the repair of the ASD or the inferior rim of the defect was not included in the closure stitch leading to
incomplete closure of the defect. In our case patient had hypoxemia in immediate postoperative period. Hypoxemia
after cardiopulmonary bypass is usually due to atelectasis, pulmonary infection, fluid overload, pneumothorax, or
pleural effusion. All these possibilities were excluded . postoperative TEE performed but also unable to solve the
problem. A. A contrast study using agitated saline solution confirmed the shunting of inferior vena caval flow into
the LA, but not the superior vena caval flow. The turbulent flow from the IVC into the RA prevented flow from
the superior vena cava from crossing the defect, explaining the absence of contrast crossing into the LA with arm
injection of the contrast solution.
Various methods described for detecting right to left shunt includes intraoperative cardiac catheterization, dye dilution
curves , intraoperative TEE ,etc .
Out of these intraoperative TEE with agitated saline is very reliable, economical and simple test to perform . In
our case, agitated saline injected from below was necessary to diagnose this rare complication. So we propose this
technique for identification of this rare complication to prevent reoperation.
Conclusion
Atrial septal defect is a very common congenital anomaly. Operative repair have a very excellent prognosis with a low
morbidity in long run. Our patient presented with postoperative hypoxemia in immediate postoperative period . the
reason for hypoxemia was discovered by intraoperative contrast TEE by agitated saline from femoral vein. So this is
a very simple, reliable and cost effective method of diagnosing right to left shunt.
References
1) Excellent survival and low incidence of arrhythmias, stroke and heart failure long-term after surgical ASD closure
at young age,A prospective follow-up study of 2133 years,J.W Roos-Hesselink, F.J Meijboom, S.E.C Spitaels, R
van Domburg, E.H.M van Rijen, E.M.W.J Utens, A.J.J.C Bogers, M.L Simoons
2) Thompson, E., Moritz, D., Perdue, R., & Cansino, S. (2004). Diversion of the inferior vena cava following
of atrial septal defect causing hypoxemia. Echocardiography, 21(4), 329-332.
repair
3) The Assessment of Operative Results in Congenital Heart Disease by Intraoperative Indicator-Dilution Curves
By ANDREW G. MoRRow, M.D., H. NEWLAND OLDHAM, M.D., GEORGE M. CALLARD, M.D., AND
EUGENE BRAUNWALD, M.D.
4) hypoxemia following cardiopulmonary bypass, Anesthesiology 53;172-174,1980.
5) Sapin PM, Salley RK: Arterial desaturation and orthodeoxia after atrial septal defect repair: Demonstration of the
mechanism by transesophageal and contrast echocardiography. J Am Soc Echocardiogr 1997;10: 588592.
341
IACTACON 2016
RARE CAUSE OF EPICARDIAL PACING DYSFUNCTION - A

NOVEL METHOD TO DEAL WITH IT.
Dr Satwik Telkar,Dr Madhuprakash S C,Dr Srinivas Kulkarni.
Cauvery heart hospital, Mysore, Karnataka
Abstract
A middle aged lady underwent emergency redo aortic valve replacement for a severely infected bioprosthetic valve.
The aortic root abscess was cleared and 27 mechanical valve was implanted. Off bypass, in view of junctional
rhythm, two temporary epicardial pacing wires were inserted (dual chamber). In the postoperative period, it was
noticed that there was sudden loss of capture in spite of the leads being intact. Chest x-ray revealed significant
surgical emphysema which we proposed to be interfering with the unipolar leads. The external lead (the positive end)
was removed from the chest wall and inserted into the thigh, far away from the emphysematous site. It promptly
showed good sensing and capture. Air insulation due to surgical emphysema can interfere with the functioning of
unipolar pacemaker and needs to be recognized when there is unexplained loss of capture.
342
ABSTRACTS
A rare case of ruptured sinus of valsalva in the left

coronary sinus into the left atrium
Dr Sathyanarayan J, Dr Syed Mudassar A, Dr Swathi Gundlakunta, Dr Shio Priye, Dr Durga
Prasad Reddy
Department of cardiac anesthesia, Vydehi Institute of Medical Sciences and Research Centre, Whitefield, Bengaluru,
Karnataka.
Introduction:
We are reporting a rare case of ruptured sinus of Valsalva into left atrium with aortic regurgitation.
Material and methods:

A 37 year old female patient came to our hospital with complaints of chest pain palpitations and dyspnoea on exertion
since 4 months. On examination, there was a loud continuous murmur in the left upper parasternal area. Routine
blood investigations were unremarkable. Transthoracic echocardiography revealed severe aortic regurgitation (AR)
and the patient was posted for aortic valve replacement. Patient was induced with general anesthesia after invasive
cardiac monitoring. Routine intra-operative transesophageal echocardiography (TEE) revealed a ruptured aneurysm
of the left coronary sinus entering into the left atrium with severe AR. After initiating cardiopulmonary bypass, TEE
diagnosis was confirmed. The aneurysmal tissue was excised, defect was closed with synthetic patch and aortic valve
was replaced.
Discussion:
Aneurysm of sinus of Valsalva is an uncommon cardiac anomaly that can be congenital or acquired. The aneurysms
are located in the right sinus of Valsalva (76.8%), in the noncoronary sinus (20.2%) and in the left sinus (3%). (1)
Aneurysms of the sinus of Valsalva are not usually clinically apparent unless perforation occurs which simulates aortic
regurgitation. The rupture may occur into any cardiac chamber, predominantly the right ventricle, the intraventricular
septum, and the precordial space. (2)
This case report emphasizes the utility of intraoperative Transesophageal echocardiography in detecting rare cardiac
anomalies and appropriately planning the surgical correction.
References:
1. Chue SH, Hung CR, How SS, et al: Ruptured aneurysm of the sinus of Valsalva in oriental patients. J Thorac
Cardiovasc Surg 1990; 99: 288-298.
2. A Wahab, HS Khan, S Wahab. Rupture of Sinus of Valsalva Aneurysm Presenting with Left Ventricular Failure.
JIACM2008; 9(3): 209-11.
343
IACTACON 2016
PERIOPERATIVE MANAGEMENT OF CONGENITAL HEART

DISEASE WITH NEAR SYSTEMIC PULMONARY ARTERY
PRESSURE
Muthu Vijayasankar, Anuradha Mahender, Gopal Karunanidhi Jaikaran, Kasinadhan,
Arunkumar.
Institute of child health / Madras medical college, Chennai, Tamilnadu.
Introduction
Pulmonary hypertension is a known risk factor in patients with congenital heart disease. When the pulmonary artery
pressure is near systemic pressures the management becomes even more difficult.
Aims and objectives

Various pharmacological agents, surgical techniques and ventilatory managements are used perioperatively to manage
the near systemic pulmonary artery pressure patients with congenital heart disease
Methods
We treated 20 children with acyanotic CHD with near systemic pulmonary artery pressures between August 2012
to December 2015. Apart from clinical and echocardiographic evidence cardiac catheterisation was done to assess
the reversibility of PA pressures. Perioperatively PA pressure optimisation was done with PAH specific vasodilators
like oral Sildenafil, Bosentan with periodical echocardiographic assessment done done for ascertaining PA pressure
reduction. Surgical correction done with Double patch technique ( NOVICKS ) followed to prevent post operative
RV failure. Perioperative Phenoxybenzamine infusion used along with Inj. Milrinone. Elective ventilation continued
postoperatively ranging from 24 - 288 hrs. About 11 patients underwent Tracheostomy electively. All of them received
oral Sildenafil & Bosentan during the perioperative period.
Results
Though most of the cases had near systemic PA pressures about 3 cases had supra systemic PA pressures. But with
the above mentioned technique we were able to manage all the cases with mortality of 10% . ( 2 cases )
Conclusion
Given the life threatening complications associated with PA crisis proper perioperative planning can help to alleviate
cardiopulmonary complications and better outcome in this patient population.
Keywords
CHD, Near systemic pulmonary artery pressure, PAH specific vasodilators, Double patch technique, Elective
ventilation
344
ABSTRACTS
ORGANIZING COMMITTEE
Organising Chairperson
Dr.P.S.N.Raju
Organising Co-Chairperson
Dr. Shashidhar Rao
Organising Secretary
Dr. Mahesh Vakamudi
Organising Joint Secretary
Dr. N.Kanagarajan
Treasurer
Dr. Ranjith Karthekeyan
Scientific Committee Chair
DR. K.G. Suresh Rao
Scientific Committee Co-Chair
DR. Benjamin Ninan
Scientific Committee
DR. Keerthivasan
DR. Shapna varma
DR. R.Satish
DR. Ashok
DR. C.Srinivasan
R. Muralikrishna
Dr.Rajesh Kodali
Souvenior
DR.Sujatha
DR.Jyotsna
Registration
DR.N.M.Kumar
DR.Ganapathy
DR.Vijay Anandh
Hospitality
DR. Minal Vora
DR. Ajeetha
DR. Masthanamma
Transport
DR. Nedumaran
DR. Edukondalu
DR. Muthu Vijayasankar
DR. Naveen Kumar
Accomodation and Banquets
DR.A. Sitaram
DR. G.Kamalakkannan
DR. C.Kumar
DR. Gokulakrishnan
345
IACTACON 2016
346

Iactacon 2016

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19th Annual

Souvenir & Lecture Notes

Let us Learn, Advance and Excel..

Dear distinguished guest of this conference,

Dr. Suresh Rao K.G

IACTA NATIONAL EXECUTIVE COMMITTEE

Dr. Mahesh Vakamudi

Dr. Neeti Makhija

Dr. Murali Chakravarthy

IACTA CHENNAI CITY BRANCH

ADDITIONAL JOINT SECRETARY Dr. SITARAM .A.K

Dr. RANJITHA B.KARTHEKEYAN

Dr. CHARANJIT KAUR

Dr. MUTHUVIJAYA SANKAR

Dr. SUJATHA D.I

Dr. NAIDU .I.S

Dr. RAJU .P.S.N

Dr. MAHESH VAKAMUDI

Dr. BENJAMIN NINAN

Dr. SURESH RAO .K.G

International Fuculty - IACTA CHENNAI 2016

Dr. Roy Sheinbaum

Dr. Suresh Chengode

Dr. Kumar Belani

Dr. Madan Mohan Maddali

Dr. Peter Norman

Dr.Jagtar Singh Heir

Dr. Achal Dhir

Dr. Mahesh Prabhu

Dr. Douglas B Coursin

Dr.William Zev Rymer

Dr. Suresh Santhanam

Dr. Rajagopal Kailasam

Dr. Shital Shah

Dr. Sudhakar Subramani

Dr. Dilip Thaker

Dr. Rajesh Bhavsar

National Faculty - IACTA CHENNAI 2016

Dr. Suresh G Nair

Dr. Naman Shastri

9:45 - 10.10 Perioperative MI after CABG: Classification and

Dr. K.Muralidhar, Bangalore

10:15-10:40 Single ventricle physiology: A comprehensive

Dr. Chandra Ramamoorthy, USA

10:45-11:10 Myocardial protection during cardiac surgery

Dr. Suresh Nair, Kochi

Integrating 3D TEE in the OR workflow

Dr. Naman Shastri, Ahmedabad

Mediastinal mass: Anesthesiologists' Nightmare?

Pro and Con Session

Cell salvage is beneficial in all patients

Anesthesiologists should routinely be present in

Pro : Dr.Dheeraj Arora, Delhi

Pro : Dr. Abraham Cherian, Kochi

12:25-12:50 Heart Brain Cross talk: What do we need to

Dr. Gopinath, Hyderabad

12:55 - 1:20 Management of failing Fontan

Perioperative management of the congenital

Pro and Con Session

Dr. Mukul Kapoor, Delhi

Dr.Chandra Ramamoorthy, USA

Dr. Thomas Koshy, Thiruvananthapuram

12:00-12:20 Fluid management in cardiac surgery - Which

Dr. Deepak Tempe, Delhi