Transcript Slide 1

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
[email protected]
‘Lethal injection drug production
ends in the US’
Contents
• Anatomy + Physiology revision
• What is Anaesthesia?
• Anaesthesia effects…
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airway
‘respiratory depression’
FRC
Hypoxaemia
after Anaesthesia
• Tips on the essay
Introduction
• Why learn?- intellectually interesting
• Practical – understand – prevent problems
• Practical – find new solutions
Anatomy revision
• Upper Airway above the vocal cords
• Lower airway – below the vocal cords
– Conducting vs gas exchange-
• Muscles of respiration
Airway
• Airway is Lips to alveoli
• Upper Airway: lips to vocal Cords
• Lower Airway: Vocal Cords down
Pharynx
– Trachea
– Conducting Airways
– Respiratory Airways – gas exchange
– pulmonary artery – capillaries – vein – heart
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
Bronchiole
Alveolus
Anatomy: Muscles
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External Intercostals
Diaghram
Internal Intercostals
Accessory muscles
Neck
• Accessory muscles
Abdomen
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)
Lung
Elastin fibres in lung - cause recoil
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’
Air enters Alveolus
V
Pulmonary capilary
Blood in contact
with ventilated alveolus
Q
‘Shunted’ blood 1-2%
Venous
‘venous admixture’
Arterial
Increased 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
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
Conducting airways ie trachea and 1-16
• Tidal volume
Alveolar volume ~500ml
Normal
Air enters Alveolus
V
Pulmonary capilary
Blood in contact
with ventilated alveolus
Q
‘Shunted’ blood 1-2%
Venous
Arterial
Deadspace
Classic = trachea!
Air enters Alveolus
V
Pulmonary capillary low flow
eg bleeding or blocked
V/  Q
Blood in contact
with ventilated alveolus
Q
‘Shunted’ blood 1-2%
Venous
Arterial
Deadspace
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
What is Anaesthesia?
• Reversable drug induced unconsciousness
• ‘Triad’
– Hypnosis, Analgesia, Neuromuscular Paralysis
• Induction, Maintainence, Emergence, (Recovery)
• Spontaneous vs Positive Pressure Ventilation
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
Delivers Precise
Volatile Anaesthetic Agents
Carrier Gas
Other stuff
Hypnosis
Volatile or Inhalational
Anaesthetic Agents
Eg Sevoflurane
-A halogenated ether
-with a carrier gas
-ie air/N20
Intravenous
Analgesia = Pain relief
Systemic:
not limited to one
part of the body
by unknown
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
Neuromuscular
Paralysis
Nicotinic AcetylCholine Channel
@ NMJ
Drug Image
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’
FRC
Hypoxaemia
Anaesthesia Airway
• Upper: loss of muscular tone eg oropharynx
• Upper: tongue falls posteriorly ie back
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
–Into trachea = intubation
–Other devices
Laryngeal Mask Airway
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
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?
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2.
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Cephalad movement of the diaphragm
Loss of inspiratory muscle tone
Reduced cross sectional rib cage area
Gas trapping behind closed airways
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 volatiles
– increases V/Q mismatch
• No cough/ yawn?
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 missmatch
– PHVC (reduces V/Q mismatch)
• Some new changes happen
– Wound pain causing hypoventilation
– Drug overdose causing hypoventilation
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
•
Pulmonary physiology Michael G. Levitzky
• http://en.wikipedia.org/wiki/Respiratory_physiology
• Several articles 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
Underline important parts
Headline each paragraph with a statement?
• Don’t just write dense text