Transcript Bronchiole Alveolus

Anaesthesia & Respiratory System
Dr Rob Stephens
Thanks to Dr Roger Cordery
Consultant in Anaesthesia UCLH
Hon. Senior Lecturer UCL
www.ucl.ac.uk/anaesthesia/people/stephens
talk on page above and ‘Anaesthesia basics’
[email protected]
Contents
• Anatomy + Physiology revision
• What is Anaesthesia?
• Anaesthesia effects…
– airway
– ‘respiratory depression’
– FRC
– Hypoxaemia
– after Anaesthesia
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
•
•
•
•
External Intercostals
Diaghram
Internal Intercostals
Accessory muscles
Neck
• Accessory muscles
Abdomen
Inspiration
Inspiration
Forced Expiration
Forced Inspiration
Forced Expiration
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 Volume
~6000ml
Inhale
At Rest
~2500ml
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 change for a given pressure
change
A measure of ease of expansion
ΔV / ΔP
Normally ~ 200ml / 1 cm H2O for the chest
Elastance = the pressure change for a given volume
change
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
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
• 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
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
Analgesia = Pain relief
Regional: limited to one part of the body
Neuromuscular
Paralysis
Nicotinic AcetylCholine Channel
Non competitive
Suxamethonium
Competitive
Others eg Atracurium
Different properties
Different length of action
Paralyse Respiratory muscles
Apnoea – ie no breathing
Need to ‘Ventilate’
Effects of Anaesthesia
•
•
•
•
airway
‘respiratory depression’
FRC
Hypoxaemia
Anaesthesia Airway
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•
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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
Airway manoeuvres to open
Airway devices – to keep it open
• Into trachea = intubation
• Other devices
Laryngeal Mask Airway
Anaesthesia ‘respiratory depression’
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•
•
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CO2 and O2 response curves of volatiles
Opioids
Resp. depression opposed by surgical stimulation
No cough – good and bad
– Caused by all 3 types of drug
– Forced expiration: expands lungs, clears secretions,
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
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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•
•
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Opioids = a drug acting on Opioid receptor
Morphine, Fentanyl
Act in CNS
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!
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 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 is defined as 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
– 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
• http://books.google.co.uk/books?id=bhxNUxOaYHkC&printse
c=frontcover&dq=respiratory+physiology&hl=en&ei=jWtITYy
wI9yShAfNiIX6BA&sa=X&oi=book_result&ct=result&resnum=
10&ved=0CF4Q6AEwCTgU#v=onepage&q=respiratory%20phy
siology&f=false
• Pulmonary Physiology and Pathophysiology: an integrated,
case-based approach John West mostly free on google books