Anaesthesia & Respiratory

System

Dr Rob Stephens
Consultant in Anaesthesia UCLH Thanks to Dr Roger Cordery

Hon Senior Lecturer UCL

Positive Pressure Ventilation

Dr Rob Stephens
Consultant in Anaesthesia UCLH Thanks to Dr Roger Cordery

Hon Senior Lecturer UCL

 Anaesthesia & Respiratory
System

Dr Rob Stephens
Consultant in Anaesthesia UCLH Thanks to Dr Roger Cordery

Hon Senior Lecturer UCL

 Anaesthesia & Respiratory
System

Dr Rob Stephens
Consultant in Anaesthesia UCLH Thanks to Dr Roger Cordery
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
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 pulmonary artery capillaries
vein L heart
 Lower Airway

23 divisions follow down 1-16 conduction of air

from L +R main bronchus

bronchi through to terminal bronchi
bronchioles
17-23 gas exchange
respiratory bronchioles
alveolar ducts
alveolar sacs or alveoli
 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

Diaghram contracts
-2cm H20

Chest volume

Pleural pressure
Pressure
difference from
lips to alveolus -5cm H20
drives air into
lungs
Alveolar
ie air moves pressure falls
down -2cm H20
pressure gradient
to fill lungs
 Physiology: Normal Spontaneous breat
Normal breath expiration animation, awake

-5cm H20
Diaghram relaxes

Pleural /
Chest volume

Pleural pressure
rises
+1cm H20 Alveolar
pressure rises
to +1cm H20
Air moves down
pressure gradient
out of lungs
 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 Ratio V/Q
Blood flow, Q Perfect V/Q =1
V/Q mismatching

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 Sa02~100%
Q
with ventilated alveolus
Sa0275%

Shunted blood 1-2%

Venous Arterial
venous admixture
 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% Q normal

Shunted blood 1-2%

Venous Arterial
 Pulmonary Hypoxic
Vasoconstriction
A method of
normalising the V/Q
ratio Less air enters V low
Inflammatory exudate
eg pus or fluid V/Q =
towards normal

Q 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
Conducting airways ie trachea
and 1-16= Anatomical
Tidal volume deadspace
= anatomical Alveolar volume ~400ml

Pathological
 Deadspace

V
Air enters Alveolus

Pulmonary capilary
Blood in contact
Q
with ventilated alveolus

Shunted blood 1-2%

Venous Arterial
 Deadspace
Classic anatomical = trachea!

V
Air enters Alveolus

Pulmonary capillary low

flow V/ Q = Hi
eg bleeding or blocked

Blood in contact
Q
with ventilated alveolus

Shunted blood 1-2%

Venous Arterial
 Deadspace- Anatomical
conduction of air
Deadspace volume
Trachea
from L +R main bronchus
bronchi through to terminal bronchi
bronchioles
respiratory bronchioles gas exchange
Alveolar volume
alveolar ducts
alveolar sacs or alveoli
 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

Eg Sevoflurane
Picture of Sevoflurane bottle
-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

Non-competitive
images
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 images
Equipment
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 7 9
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

5 8 13
PaO2 kPa
 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