Transcript Ventilation talk

Anaesthesia & Respiratory System
Dr Rob Stephens
Consultant in Anaesthesia UCLH
Hon Senior Lecturer UCL
Thanks to Dr Roger Cordery
the centre for
Anaesthesia
UCL
Positive Pressure Ventilation
Dr Rob Stephens
Consultant in Anaesthesia UCLH
Hon Senior Lecturer UCL
Thanks to Dr Roger Cordery
the centre for
Anaesthesia
UCL
Anaesthesia & Respiratory System
Dr Rob Stephens
Consultant in Anaesthesia UCLH
Hon Senior Lecturer UCL
Thanks to Dr Roger Cordery
the centre for
Anaesthesia
UCL
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…
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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
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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
L heart
capillaries
vein
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
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Upper airway muscles
External Intercostals
Diaghram
Internal Intercostals
Accessory muscles
Neck
• Accessory muscles
Abdomen
upper airway tone
Inspiration
Inspiration
Forced Expiration
Forced Inspiration
Forced Expiration
Physiology revision
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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 breath
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 breath
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 Δ for a given pressure Δ
A measure of ease of expansion
ΔV / ΔP
Normally ~ 200ml / 1 cm H2O for the chest
2 types: static & dynamic
Elastance = the pressure Δ for a given volume Δ
= the opposite of compliance
The tendency to recoil to its original dimensions
A measure of difficulty of expansion
ΔP / ΔV
eg blowing a very tight balloon
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
eg lung fibrosis, chest wall joint disease
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’
Air enters Alveolus
V
Pulmonary capilary
Blood in contact
with ventilated alveolus
Q
Sa02~100%
Sa0275%
‘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%
Q 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
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
• Tidal volume
= anatomical
• Pathological
Conducting airways ie trachea and 116= Anatomical deadspace
Alveolar volume ~400ml
Deadspace
Air enters Alveolus
V
Pulmonary capilary
Blood in contact
with ventilated alveolus
Q
‘Shunted’ blood 1-2%
Venous
Arterial
Deadspace
Classic anatomical = trachea!
Air enters Alveolus
Pulmonary capillary low flow
eg bleeding or blocked
V
V/  Q = Hi
Blood in contact
with ventilated alveolus
Q
‘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
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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
machine
Delivers Precise
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
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airway
‘respiratory depression’
Functional Residual Capacity, FRC
Hypoxaemia
Respiratory effects of Anaesthesia
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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
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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
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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 tubes…eg LMA
Anaesthesia ‘respiratory depression’
Volatiles  response to CO2
Awake
Increasing concentration of volatile
V
L/min
5.3
7
Arterial CO2
kPa
9
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
PaO2 kPa
13
Opioids
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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
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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 aren’t 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.
2.
3.
4.
Cephalad (to brain) movement of the diaphragm
Loss of inspiratory muscle tone
Reduced cross sectional rib cage area
Gas trapping behind closed airways
Respiratory effects of Anaesthesia
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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
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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
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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
• Don’t just write dense text
Revision Aids
• When answering question on Anaesthesia or IPPV
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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