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Dr Rob Stephens
Consultant in Anaesthesia UCLH
Hon Senior Lecturer UCL
Dr Rob Stephens
Consultant in Anaesthesia UCLH
Hon Senior Lecturer UCL
www.ucl.ac.uk/anaesthesia/people/stephens
Google UCL Stephens
talk on webpage above & supporting material
robcmstephens[at]googlemail.com
www.ucl.ac.uk/anaesthesia/people/stephens
Google UCL Stephens
Contents
Anatomy + Physiology revision
What is Anaesthesia?- triad
Anaesthesia effects
airway
respiratory depression
FRC
Hypoxaemia
after Anaesthesia
Picture of Propofol/Thio
Lethal injection drug production
ends in the US
Introduction
Why learn?- intellectually interesting
Practical understand prevent
problems
Practical find new solutions
Practical- pass exam!
Anatomy revision
Upper Airway above the vocal cords
Lower airway below the vocal cords
Conducting vs gas exchange- different
tissue types
Muscles of respiration
Airway
Airway is Lips/Nose to alveoli
Upper Airway: lips/nose to vocal Cords
Lower Airway: Vocal Cords down Pharynx
Trachea
Conducting Airways
Respiratory Airways gas exchange with
capillaries
R heart
vein
pulmonary artery
L heart
capillaries
Lower Airway
23 divisions follow down
Anatomy
Alveolus in detail pulmonary
capillary
Anatomy: Muscles of
Respiration
Physiology revision
Physiology: Spirometry
~6000ml
Inhale
At Rest
~2500ml
Exhale
0 ml
Physiology: Volumes
Tidal Volume, TV
Functional Residual Capacity, FRC
Volume in lungs at end Expiration
not a fixed volume - conditions change FRC
Residual Volume, RV
Volume at end of a forced expiration
Closing Volume, CV
Volume in expiration when alveolar closure
collapse occurs
Others
Inhale
At Rest
~2500ml
~40+ supine
~60+ standing
Exhale
0 ml
Diaghram contracts
Chest volume
Pressure
difference from
lips to alveolus
drives air into
lungs
ie air moves
down
pressure gradient
to fill lungs
Pleural pressure
-5cm H20
Alveolar
pressure falls
-2cm H20
Alveolar
pressure rises
to +1cm H20
Ratio V/Q
Perfect V/Q =1
Normal Shunt
Shunt
% Blood not going through ventilated alveoli
or blood going through unventilated alveoli
Normal- 1-2%
Pulmonary eg alveolar collapse, pus, secretions
Cardiac eg ASD/VSD hole in the heart
(but mostly left to right.
due to L pressure> R pressures)
Normal Shunt
V
Pulmonary capilary
Blood in contact
with ventilated alveolus
Sa0275%
Sa02~100%
Venous
venous admixture
Arterial
V low
Alveolus filled with pus
or collapsed..
V/Q = low
Pulmonary capilary
Blood in contact
with unventilated alveolus
Sa0275%
Sa0275%
normal
Venous
Arterial
Pulmonary Hypoxic
Vasoconstriction
A method
of
normalising the V/Q
ratio
Inflammatory exudate
eg pus or fluid
V low
V/Q =
towards normal
less
Venous
Arterial
Deadspace
That part of tidal volume that does not
come into contact with perfused alveoli
Deadspace volume ~ 200ml
Tidal volume
= anatomical
Pathological
Deadspace
V
Pulmonary capilary
Blood in contact
with ventilated alveolus
Venous
Arterial
Deadspace
Classic anatomical = trachea!
V/
Q = Hi
Blood in contact
with ventilated alveolus
Venous
Arterial
Deadspace- Anatomical
Trachea
conduction of air
Deadspace volume
gas exchange
Alveolar volume
What is Anaesthesia?
Reversable drug induced unconsciousness
Triad
Hypnosis, Analgesia, Neuromuscular Paralysis
Induction, Maintainence, Emergence, (Recovery)
Spontaneous vs Positive Pressure Ventilation
See podcast conduct of anaesthesia link from my website
Anaesthesia Timeline
Preoperative
Induction: Analgesia & IV hypnotic
Maintain: Analgesia & Volatile Hypnotic
Emergence: Analgesia Only
Recovery
Anaesthesia
Hypnosis = Unconsciousness
Gas eg Halothane, Sevoflurane
Intravenous eg Propofol, Thiopentone
Neuromuscular paralysis
Nicotinic Acetylcholine Receptor Antagonist
Anaesthetic
Machine
Picture of anaesthesia
Delivers Precise
machine
Detail of anaesthesia
machine
Hypnosis
Volatile or Inhalational
Anaesthetic Agents
Picture of Sevoflurane bottle
Eg Sevoflurane
-A halogenated ether
-with a carrier gas
-ie air/N20
Intravenous- pictures
pictures
images
Neuromuscular
Paralysis
Nicotinic AcetylCholine Channel
@ NMJ
images
Non-competitive
Suxamethonium
Competitive
All Others eg Atracurium
Different properties
Different length of action
Paralyse Respiratory muscles
Apnoea ie no breathing
Need to Ventilate
Respiratory effects of
Anaesthesia
airway
respiratory depression
Functional Residual Capacity,
FRC
Hypoxaemia
Respiratory effects of
Anaesthesia
airway
respiratory depression
Functional Residual Capacity,
FRC
Hypoxaemia
Anaesthesia Airway
Upper: loss of muscular tone eg
oropharynx
Upper: tongue falls posteriorly ie
back
images
Anaesthesia Airway
Anaesthesia
Airway
Equipment
images
Image to show how LMS sits In the airway above the vocal cords
Respiratory effects of
Anaesthesia
airway
respiratory depression
Functional Residual Capacity,
FRC
Hypoxaemia
Anaesthesia respiratory
depression
CO2 and O2 response curves of volatiles
Opioids
Respiratory depression
..is opposed by surgical stimulation
No cough good and bad
Caused by all 3 types of drug
Forced expiration: expands lungs, clears
secretions
Allows pt to tolerate airway tubeseg LMA
V
L/min
5.3
Arterial CO2
kPa
minute
V
L/min
Awake
Low concentration
High concentration
PaO2 kPa
13
Opioids
Opioids = a drug acting on Opioid
receptor
Morphine, Fentanyl
Act in CNS, PNS, GI
Reduced respiratory rate, increase
tidal volume, but still increase PaCO2
Suppress cough
Opioids
Video to show opioid induced low
respiratory rate
Respiratory effects of
Anaesthesia
airway
respiratory depression
Functional Residual Capacity,
FRC
Hypoxaemia
Anaesthesia FRC
Why important?- closing Volume and O2 store
Why would it change?
FRC is decreased by 16-20% by Anaesthesia
Falls rapidly (seconds to minutes).
FRC remains low for 1-2 days
Inhale
At Rest
~2500ml
Exhale
0 ml
Inhale
At Rest
~2500ml
Exhale
0 ml
Anaesthesia FRC
What causes these changes?
1. Cephalad (to brain) movement of the
diaphragm
2. Loss of inspiratory muscle tone
3. Reduced cross sectional rib cage area
4. Gas trapping behind closed airways
Respiratory effects of
Anaesthesia
airway
respiratory depression
FRC
Hypoxaemia
Anaesthesia Hypoxaemia
Hypoxaemia Low blood oxygen level
FRC changes- Closing Vol,
collapse/atelectasis and shunt
Position also effects eg legs/laparoscopy/head
down - Tidal volume
Hypovolaemia/vasodilation increases
deadspace,
V/low Q areas .mismatch
PHVC reduced by volatiles
increases V/Q mismatch
No cough/ yawn ?-collapse/secretions
Apnoea/Airway obstruction- no 02 in no CO2 out!
Hypoxaemia: Atelectasis
Atelectasis = the lack of gas exchange
within alveoli, due to alveolar collapse or
fluid consolidation
After Anaesthesia
Some changes persist
Summary 1
Airway conducting and respiratory
Physiology
V/Q different as you go down lung
Extreme no blood flow (Deadspace)
Extreme no ventilation (Shunt)
Anaesthesia
Hypnosis, Analgesia, Paralysis
Summary 2
Anaesthesia effects due to drugs!
Upper airway obstruction
Respiratory depression
Hypoxaemia
collapse (FRC/Closing volume) =
shunt
- pulmonary blood flow - deadspace
- PHVC drugs
Further reading
http://en.wikipedia.org/wiki/Respiratory_physiology
Articles and Podcast on my webpage
Pulmonary Physiology and Pathophysiology:
an integrated, case-based approach John
West mostly free on google books
Revision Aids
Lung volumes
Normal airway pressures / mechanics of breathing
Upper airway
Lower airway
Compliance/Resistance
V, Q and V/Q match /mis-match (?West zones)
Causes of hypoxaemia +/- hypercapnia
Muscle tone (upper airway + respiration)
Respiratory drive
CVS effects
Drug effects (Hypnosis/Analgesia/paralysis)
Other bleeding, position, age, sleep, pathology
MCQ 1
Shunt is..???
A That part of tidal volume that does
not come into contact with perfused
alveoli
B % Blood not going through
ventilated alveoli
MCQ 2
Pulmonary Embolus
(blood clot stopping blood flowing through part of the lungs)
A Is an example of a shunt
B Is an example of deadspace
C can cause hypoxia
Qn3
List as many causes of hypoxia under
anaesthesia as you can