Vous êtes sur la page 1sur 85

Anaesthesia & Respiratory

System
Dr Rob Stephens
Consultant in Anaesthesia UCLH
Hon Senior Lecturer UCL

Thanks to Dr Roger Cordery

Positive Pressure Ventilation

Dr Rob Stephens
Consultant in Anaesthesia UCLH
Hon Senior Lecturer UCL

Thanks to Dr Roger Cordery

Anaesthesia & Respiratory


System
Dr Rob Stephens
Consultant in Anaesthesia UCLH
Hon Senior Lecturer UCL

Thanks to Dr Roger Cordery

Anaesthesia & Respiratory


System
Dr Rob Stephens
Consultant in Anaesthesia UCLH
Hon Senior Lecturer UCL

Thanks to Dr Roger Cordery

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

Tips on the essay


Break then Lecture 2: Positive Pressure Ventilation

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

1-16 conduction of air

from L +R main bronchus


bronchi through to terminal bronchi
bronchioles
respiratory bronchioles
alveolar ducts
alveolar sacs or alveoli

17-23 gas exchange

Anatomy
Alveolus in detail pulmonary
capillary

Image to show alveolus and bronchiole

Section to show the upper airway

CXR carina, lungs, heart

Anatomy: Muscles of
Respiration

Upper airway muscles upper airway tone


External IntercostalsInspiration
Diaghram Inspiration
Internal Intercostals Forced Expiration
Accessory muscles Forced Inspiration
Neck
Accessory muscles Forced Expiration
Abdomen

Physiology revision

Spirometry- basic volumes


How we breathe spontaneously
Compliance / elastance
Deadspace and shunt
V / Q ratios

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

Physiology: Closing Capacity


~6000ml

Inhale

At Rest

~2500ml

~40+ supine
~60+ standing
Exhale

0 ml

Physiology: Normal Spontaneous breat


Normal breath inspiration animation, awake
Lung @ FRC= balance
-2cm H20

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

Physiology: Normal Spontaneous breat


Normal breath expiration animation, awake
-5cm H20
Diaghram relaxes
Pleural /
Chest volume
Pleural pressure
rises
+1cm H20

Air moves down


pressure gradient
out of lungs

Alveolar
pressure rises
to +1cm H20

Physiology: Compliance & Elastance


Compliance = the volume for a given
pressure
A measure of ease of expansion
V / P
Normally ~ 200ml / 1 cm H2O for the
chest
2 types: static & dynamic
Elastance = the pressure for a given
volume
= the opposite of compliance
The tendency to recoil to its original

Physiology: Compliance & Elastance


Chest, Lung, Thorax (= both together)
Lung
Elastin fibres in lung - cause recoil =
collapse
Alveolar surface tension - cause recoil
Alveolar surface tension reduced by
surfactant
For the chest as a whole, it depends on
Lungs and Chest Wall
Diseases affect separately

Physiology: Deadspace and shunt


Each part of the lung has
Gas flow, V
Blood flow, Q
V/Q mismatching

Ratio V/Q
Perfect V/Q =1

Deadspace = Ratio: V Normal/ Low Q


That part of tidal volume that does not come
into contact with perfused alveoli
Shunt =
Ratio: V low/ Normal Q
That % of cardiac output bypasses ventilated
alveoli
Normally = 1-2%

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

Air enters Alveolus

Pulmonary capilary
Blood in contact
with ventilated alveolus

Sa0275%

Sa02~100%

Shunted blood 1-2%

Venous

venous admixture

Arterial

Increased Pulmonary Shunt


Not much air enters Alveolus

V low
Alveolus filled with pus
or collapsed..

V/Q = low
Pulmonary capilary
Blood in contact
with unventilated alveolus

Sa0275%

Sa0275%

normal

Shunted blood 1-2%

Venous

Arterial

Pulmonary Hypoxic
Vasoconstriction
A method
of
normalising the V/Q
ratio

Less air enters

Inflammatory exudate
eg pus or fluid

V low
V/Q =
towards normal

less

Blood diverted away


from hypoxic alveoli

Venous

Arterial

Deadspace
That part of tidal volume that does not
come into contact with perfused alveoli
Deadspace volume ~ 200ml

Tidal volume
= anatomical
Pathological

Conducting airways ie trachea


and 1-16= Anatomical
deadspace
Alveolar volume ~400ml

Deadspace
V

Air enters Alveolus

Pulmonary capilary
Blood in contact
with ventilated alveolus

Shunted blood 1-2%

Venous

Arterial

Deadspace
Classic anatomical = trachea!

Air enters Alveolus

Pulmonary capillary low


flow
eg bleeding or blocked

V/

Q = Hi

Blood in contact
with ventilated alveolus

Shunted blood 1-2%

Venous

Arterial

Deadspace- Anatomical
Trachea

conduction of air
Deadspace volume

from L +R main bronchus


bronchi through to terminal bronchi
bronchioles
respiratory bronchioles
alveolar ducts
alveolar sacs or alveoli

gas exchange
Alveolar volume

Physiology: V/Q in lung


Both V and Q increase down lung

Q increases more than V


down lung

V/Q ratios change down lung


If patient supine (on back)
V/Q changes front to back
Another way to think about
Q/V is west zones

Physiology: V/Q in lung

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

Patient can be paralysed vs not=


Needs ventilation vs spontaneously
breathing

Anaesthesia
Hypnosis = Unconsciousness
Gas eg Halothane, Sevoflurane
Intravenous eg Propofol, Thiopentone

Analgesia = Pain Relief


Different types: ladder, systemic vs other

Neuromuscular paralysis
Nicotinic Acetylcholine Receptor Antagonist

Anaesthetic
Machine
Picture of anaesthesia
Delivers Precise
machine

Volatile Anaesthetic Agents


Carrier Gas
Other stuff

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

Analgesia = Pain relief


Systemic:
not limited to one
part of the body

pictures

Analgesia = Pain relief


Systemic: not limited to one part of the body
Simple
eg Paracetamol
Non Steroidal Anti-Inflammatory Drugs
eg Ibuprofen
Opiods
weak eg Codeine
strong eg Morphine, Fentanyl
Others
Ketamine, N2O, gabapentin..

Analgesia = Pain relief


Regional: limited to one part of the body

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

Upper: loss of muscular tone eg oropharynx


Upper: tongue falls posteriorly ie back
Need to keep it open to allow airflow!
Airway obstruction = no airflow
Keep Airway open:
Airway manoeuvres (chin lift etc)
Airway devices- above vs blow cords
Above eg , gudel, LMA
Below - Into trachea = intubation, paralysis

Anaesthesia
Airway
Equipment

images

Laryngeal Mask Airway

Video of LMA insertion

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

Anaesthesia respiratory depression


Volatiles response to CO2
Awake

Increasing concentration of volatile

V
L/min

5.3

Arterial CO2
kPa

Anaesthesia respiratory depression


Volatiles reduce minute ventilation
Unstimulated volatiles
Reduce Vtidal and therefore V

minute

Make you less responsive to the effects of


CO2
ie slope is more flat
= the normal increase in ventilation that

occurs when CO2 rises is reduced

Anaesthesia respiratory depression


Volatiles response to hypoxaemia

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

Weak but significant correlation with age


Less FRC reduction if patient is in the
sitting position
but most operations arent done sitting!

Physiology: Closing Volume


~6000ml

Inhale

At Rest

~2500ml

Exhale

0 ml

Physiology: Closing Volume


~6000ml

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

CT scan of Diaphragm during


awake spontaneous breathing

CT scan of Diaphragm during


anaesthesia: Atelectasis

After Anaesthesia
Some changes persist

Collapse/Atelectasis abnormal 1-2 days


FRC abnormal 1-2 days
CO2 and O2 responses normal in hours
V/Q mis-smatch
PHVC (reduces V/Q mismatch)

Some new changes happen


Wound pain causing hypoventilation
Drug overdose causing hypoventilation
Pneumonia, cough supression, PE, LVF etc

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

Writing the essay

Break the answer down into parts


Lots of space
Graphs and diagrams, labelled- colour?
Underline important parts
Headline each paragraph with a
statement?
GA causes V/Q mismatch

Dont just write dense text

Revision Aids

When answering question on Anaesthesia or


IPPV

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

Vous aimerez peut-être aussi