Respiratory physiology
Tom Archer, MD, MBA
UCSD Anesthesia
www.argentou
r.com/tangoi.ht
ml
The dance of pulmonary physiology—
Blood and oxygen coming together.
But sometimes the match between blood and
oxygen isn’t perfect!
http://www.bookmakersltd.com/art/edwards_art/3PrincessFrog.jpg
Outline (1)
• Failures of gas exchange
• In anesthesia– think mechanical first!
• Hypoxemia is easier to produce than
hypercarbia—why?
• Measuring severity of poor oxygenation
• Two pulmonary players—the burly and weakling
alveoli (V/Q mismatch)
• Shunt
• He3 MR imaging in V/Q mismatch
• Diffusion barrier
Outline (2)
Dead Space (anatomical + alveolar = physiologic)
Capnography and ETCO2
Airway flow problems and flow volume loops
Large airway-- Intra and extra thoracic
Small airway (Intrathoracic, e.g. asthma, COPD)
Pulmonary hypertension
Exactly how does it kill patients?
Interventricular septum bowing
Common hemodynamic management of all stenotic
cardiopulmonary lesions.
Failures of gas exchange
Shunt
Low V/Q
Alveolar dead space
Diffusion barrier
High V/Q
For gas exchange problems:
• Always think of mechanical problems first:
– Mainstem intubation
– Partially plugged (blood, mucus) or kinked ETT.
– Disconnect or other hypoventilation
– Low FIO2
– Pneumothorax
For gas exchange problems:
– Hand ventilate and feel the bag!
– Examine the patient!
– Look for JVD.
– Do not Rx R mainstem intubation with albuterol!
– Do not Rx narrowed ETT lumen with furosemide!
– Consider FOB and / or suctioning ETT with NS.
– THINK OF MECHANICAL PROBLEMS FIRST!
In life / medicine / gas exchange
problems:
– Beware of tunnel vision. Get used to asking
yourself, “What am I not thinking of?”
– “Asthma” = tracheal stenosis / tumor?
– “Bronchospasm” = dried secretions in ETT?
– Hypotension despite distended peripheral veins =
pneumothorax?
– “Coagulopathy” = chest tube in liver?
All That
Wheezes Is Not
Asthma:
Diagnosing the
Mimics
www.mdchoice.com/emed/main.
asp?template=0&pag...
Failures of gas exchange
causing hypoxemia
• External compression of lung causing atelectasis.
– Obesity, ascites, surgical packs, pleural effusion
• Parenchymal disease (V/Q mismatch and shunt)
– Asthma, COPD, pulmonary edema, ARDS, pneumonia,
– Tumor, fibrosis, cirrhosis
• (Intra-cardiac shunts)
Measuring severity
of oxygenation problem:
• A-a gradient (from alveolar gas equation).
– Calculates “PAO2”
– Needs FIO2, PB, PaCO2, PaO2
• Shunt fraction equation
– Needs PAO2, CcO2, CvO2, CaO2
• PaO2 / FIO2 (< 200 in ARDS)
• None of these give us etiology or physiology
(shunt vs. V/Q mismatch).
Hypoxia occurs more easily
than hypercarbia.
Why?
Two pulmonary players:
• The burly alveolus (high V/Q).
Two pulmonary players:
• The weakling alveolus (low V/Q).
A fundamental question:
• In terms of arterial O2 and CO2 tensions, can
the burly alveolus compensate for the weakling
alveolus?
• No, for PaO2.
• Yes, for PaCO2.
• This basic fact explains a lot. Know it cold.
Shunt, or “weakling” (low V/Q)
Normal alveolus
alveolus SaO2 = 75%
SaO2 = 96%
“Burly” (high V/Q) alveolus
SaO2 = 99%
Equal admixture of “weakling”
and “burly” alveolar blood has
SaO2 = (75 + 99)/ 2 = 87%.
http://www.biotech.um.edu.mt/home_pages/chris/Respiration/oxygen4.htm
Modified by Archer TL 2007
The weakling alveolus
(shunt or V/Q mismatch)
The burly alveolus
pO2 = 50 mm Hg
pO2 = 130 mm Hg
SaO2 = 80%
SaO2 = 75%
SaO2 = 98%
SaO2 = 75%
pO2 = 50 mm Hg
pO2 = 40 mm Hg
pO2 = 130 mm Hg
pO2 = 40 mm Hg
Can the burly alveolus compensate for the weakling alveolus?
Not for oxygen! The burly alveolus can’t saturate hemoglobin more than 100%.
SaO2 of equal admixture of burly and weakling alveolar blood = 89%
Low V/Q alveoli cause widened A-a gradient, just like shunt
Normal
Weakling
Burly
http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch5/s4ch5_11.htm
For CO2, burly alveolus CAN compensate for the weakling alveolus.
Weakling
alveolus
Normal alveolus
Burly alveolus
Admixture of burly and
weakling alveolar blood
http://focosi.altervista.org/alveolarventilation2.jpg
Average alveolar PACO2 =
40 mm Hg.
Modified by Archer TL
Hence, PaCO2 = 40 mm Hg
The weakling alveolus
pCO2 = 44 mm Hg
The burly alveolus
pCO2 = 36 mm Hg
pCO2 = 44 mm Hg
pCO2 = 46 mm Hg
pCO2 = 36 mm Hg
pCO2 = 46 mm Hg
Can the burly alveolus compensate for the weakling alveolus?
Yes, for CO2! The burly alveolus, if it tries real hard, can blow off extra CO2.
Pulmonary venous blood pCO2 and PaCO2 = 40 mm Hg
Shunt etiologies
• Normal
– Bronchial circulation
– Thebesian veins
• Intracardiac
– Tetralogy of Fallot, VSD, etc.
• Intrapulmonary
–
–
–
–
Bronchial intubation
Obesity
Cirrhosis
Osler-Weber-Rendu
Hypoxemia due to shunt
• Increased FIO2 helps at low shunt percentages
by dissolving more O2 in oxygenated blood.
• At high shunt percentages, increased FIO2
does not help appreciably.
• HPV decreases perfusion of hypoxic alveoli.
http://advan.physiology.org/cgi/content/full/25/3/159
Normal shunt– bronchial circulation and Thebesian veins
aorta
Pulmonary
veins
http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch5/s4ch5_10.htm
Modified by Archer TL 2007
Intrapulmonary
shunt in obesity:
When FRC is below
closing capacity,
perfusion of nonventilated alveoli is
SHUNT.
V/Q mismatch
•
•
•
•
Emphasized by John West in the 1970’s.
Seen in most lung diseases.
Prototypes are: asthma, COPD, ARDS.
V/Q mismatch and shunt both cause
hypoxemia despite possible
hyperventilation (burly alveoli can’t
compensate for weakling alveoli).
He3 MR
showing
ventilation
defects in a
normal subject
and in
increasingly
severe
asthmatics.
Author Samee, S ; Altes T ; Powers P ; de Lange EE ; Knight-Scott J ; Rakes G
Title Imaging the lungs in asthmatic patients by using hyperpolarized helium-3 magnetic resonance: assessment of response to methacholine and exercise challenge
Journal Title Journal of Allergy & Clinical Immunology
Volume 111 Issue 6 Date 2003 Pages: 1205-11
Baseline
Methacholine
Albuterol
He3 MR scans – ventilation defects in
asthmatics
Modified by Archer TL 2007
Diffusion barrier (DB) to O2 and CO2
and DLCO
•
•
•
•
Conceptually difficult
Thickened alveolar capillary membrane.
Exercise induced hypoxemia d/t dec transit time
DLCO related to many factors:
–
–
–
–
Membrane barrier thickness
Perfused alveolar surface area (COPD, lung resection)
Cardiac output
Hemoglobin concentration
• DB not usually a significant clinical problem for us.
DLCO related to many factors:
Membrane barrier thickness
Perfused alveolar surface area (COPD, lung resection)
Cardiac output
Hemoglobin concentration
http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch3/s4ch3_25.htm
Diffusion in alveolar
capillaries normally
complete in 0.25
seconds.
Thickened alveolar
membrane may
require more time
for equilibration,
which may not be
available at higher
cardiac outputs.
Result:
desaturation with
exercise.
http://www.lib.mcg.edu/edu
/eshuphysio/program/secti
on4/4ch3/s4ch3_27.htm
Dead space (DS)
• Volume of expired gas which has not participated in gas
exchange.
• Physiological DS = Anatomical DS + Alveolar DS
• VT (minute vent) = VA (alv vent) + VD (DS vent).
• PaCO2 is inversely proportional to alveolar ventilation.
• Know these facts cold.
PaCO2 is inversely proportional to alveolar
ventilation.
http://focosi.altervista.org/alveolarventilation2.jpg
Modified by Archer TL
The same minute
ventilation can
cause markedly
different amounts
of alveolar
ventilation,
depending on tidal
volume.
http://www.lib.mcg.edu/edu/e
shuphysio/program/section4/
4ch3/s4ch3_22.htm
Anatomic and alveolar dead space
• Anatomic dead space gas comes out
BEFORE alveolar CO2.
• Alveolar dead space gas comes out at the
same time as CO2 from perfused alveoli.
• Alveolar dead space gas DILUTES CO2
from perfused alveoli. This is why
ETCO2 < PaCO2.
Capnographs– two types
• CO2 vs. time (commonest, what we have).
• CO2 vs. expired volume (more useful)
Anatomical
dead space
Single breath
oxygen
technique
http://images.google.com/imgres?imgurl=http://www.li
b.mcg.edu/edu/eshuphysio/program/section4/4ch3/4c
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www.lib.mcg.edu/.../section4/4ch3/s4ch3_15.htm
40
ETCO2 =
40 mm Hg
ETCO2 =
20 mm Hg
With no
alveolar
dead space
With 50%
alveolar
dead space
20
40
20
Alveolar dead
space gas
(with no CO2)
dilutes other
alveolar gas.
40
46
40
46
0
0
40
46
Capnography
• Obvious: picks up changes in ventilation (such as
disconnection).
• Not so obvious: picks up changes in pulmonary
perfusion.
• Commonest cause of abrupt fall in ETCO2 is
hypotension (+ fall in PA pressure) with acute increase
in alveolar dead space.
• Also think air / clot embolus
Capnography
• Upsloping alveolar plateau as sign of V/Q
mismatch and / or delayed expiration.
http://www.caep.ca/CMS/images/cjem/v53-169-f1.png
Diagnosing airway flow problems
with flow volume loops.
Clinically used and useful? Not!
On the test? Probably!
Interesting? Maybe.
www.lib.mcg.edu/.../section4/4ch8/s4ch8_22.htm
Why are flow volume loops so confusing?
Flow rate L/s
Flow out of
lung (+)
Expiratory phase
Peak inspiration at
high lung volume
(TLC)
0
FVC
Inspiratory phase
Flow into
lung (-)
Start inspiration
at low lung
volume (RV).
Obstructive
lesions of
large airways
www.nature.com/.../pt1/fig_tab/gimo73_F6.html
Intrathoracic obstruction is most severe during expiration and is relieved during inspiration.
Extrathoracic obstruction is increased during inspiration because of the effect of atmospheric
pressure to compress the trachea below the site of obstruction.
Flow-volume loop mnemonic
(Jensen)
• “Ex – In, In – Ex”
• Expiratory obstruction = Intrathoracic
variable obstruction
• Inspiratory obstruction = Extrathoracic
variable obstruction
“In-Ex”
Variable Extrathoracic Obstruction
Typically the expiratory part of the F/V-loop is normal: the obstruction is pushed
outwards by the force of the expiration.
During inspiration the obstruction is sucked into the trachea with partial obstruction
and flattening of the inspiratory part of the flow-volume loop.
This is seen in cases of vocal cord paralysis, extrathoracic goiter and laryngeal
“Ex-In”
Variable Intrathoracic Obstruction
This is the opposite situation of the extrathoracic obstruction. A tumour located
near the intrathoracic part of the trachea is sucked outwards during inspiration
with a normal morphology of the inspiratory part of F/V-loop.
During expiration the tumour is pushed into the trachea with partial obstruction
and flattening of the expiratory part of the F/V loop.
Fixed
stenotic
lesions of
trachea
Extrathoracic
Intrathoracic
Typical flattening of flow-volume loop in fixed airway
obstruction
Fixed Large Airway Obstruction
This can be both intrathoracic as extrathoracic.
The flow-volume loop is typically flattened during inspiration and expiration.
Examples are tracheal stenosis caused by intubation and a circular tracheal
tumour.
Obstructive
lesions of small
airways show
up in midexpiration as
“bowing”
of expiratory
tracing
Obstructive Lung Disease
In patients with obstructive lung disease, the small airways are partially obstructed
by a pathological condition. The most common forms are asthma and COPD.
A patient with obstructive lung disease typically has a concave F/V loop.
Pulmonary hypertension—
What causes it?
Exactly how does it kill patients?
What is the flow-limiting resistance
in the entire circulation?
• Normally it is NOT the pulmonary
circulation or any of the heart valves.
• Normally it is the systemic resistance
arterioles (<0.4 mm in diameter)
Pulmonary vascular resistance
in normal lung
• Normally, increased CO causes decreased
Pulmonary Vascular Resistance via
recruitment and distention of pulmonary
capillaries.
• Normally, PA pressure stays the same despite
increased CO.
Passive Influences on PVR:
Capillary Recruitment and Distension
http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch4/s4ch4_19.htm
Pulmonary
vasculature
Tricuspid
Aortic
Pulmonic
Mitral
Normal circulation at rest.
Cardiac output is limited by SVR.
Heart gives body tissues what they “ask
for”.
Resistance arterioles
Pulmonary vascular
resistance falls
Tricuspid
Aortic
Pulmonic
Mitral
Normal circulation during
exercise / arteriolar dilation:
SVR falls, CO increases.
Pulmonary resistance falls.
Resistance arterioles– decreased SVR
http://www.pathguy.com/lectures/hipbp.gif
Pulmonary hypertension
• Acute pulmonary thromboembolism
Pulmonary hypertension
• Chronic pulmonary thromboembolism
Pulmonary hypertension develops
when pulmonary arteries develop
abnormal resistance
• When pulmonary vessels become high
resistance (fibrosis, muscular hypertrophy)
they can NOT dilate or recruit and PA pressure
rises with increased CO.
Minimal LV
compression
Minimal RV
distention
High pulmonary resistance at rest
Slight bowing of IV septum into LV
cavity.
Resistance arterioles
RV distention
and failure
LV cavity compressed
(diastole)
Fixed or increased pulmonary
resistance and / or increased CO
RV distention and failure
Intraventricular septal bulging poor LV filling fall
in CO / BP death.
Resistance arterioles—decreased SVR
Marcus JT
Dong SJ. Smith ER. Tyberg JV. Changes in the radius of curvature of the ventricular septum at end diastole during pulmonary
arterial and aortic constrictions in the dog. [Journal Article] Circulation. 86(4):1280-90, 1992 Oct.
How does pulmonary hypertension
kill patients?
• By causing the interventricular septum to
bow into the LV cavity, diminishing its
capacity.
• Cardiac output falls, BP falls, patient dies.
How do we keep PH from killing
patients?
• Keep Pulmonary Vascular Resistance down.
• Keep Systemic Vascular Resistance up.
• Prevent increases in CO.
• This same logic applies to any stenotic cardiac
lesion, such as AS!
Pulmonary
capillaries
LV dilation / hypertrophy
Tricuspid
Aortic
stenosis
Pulmonic
Mitral
Aortic stenosis at rest
Cardiac output not sufficient to cause
critically high LV intracavitary pressure /
LV failure.
Resistance arterioles
Pulmonary
capillaries
(edema)
LV failure /
ischemia
Tricuspid
Aortic
Stenosis
Pulmonic
Mitral
Aortic stenosis with
increased cardiac output /
arteriolar vasodilation:
Decreased SVR Fall in systemic BP and
/ or increase in LV intracavitary pressure
ischemia or LV failure.
Resistance arterioles– decreased SVR
Hemodynamic management of all
stenotic cardio-pulmonary lesions:
• Keep systemic vascular resistance up and CO
down.
• Avoid anemia, vasodilating anesthetic
techniques.
• In PH, keep PVR as low as possible (avoid
hypoxia, acidosis, hypothermia, consider
pulmonary vasodilators)
Outline (1)
• Failures of gas exchange– 5 generic types.
• In anesthesia– think mechanical first!
• Hypoxemia is easier to produce than
hypercarbia—why?
• Measuring severity of poor oxygenation
• Two pulmonary players—the burly and weakling
alveoli (V/Q mismatch)
• Shunt
• He3 MR imaging in V/Q mismatch
• Diffusion barrier
Outline (2)
Dead Space (anatomical + alveolar = physiologic)
Capnography and ETCO2
Airway flow problems and flow volume loops
Large airway-- Intra and extra thoracic
Small airway (Intrathoracic, e.g. asthma, COPD)
Pulmonary hypertension
Exactly how does it kill patients?
Interventricular septum bowing
Common hemodynamic management of all stenotic
cardiopulmonary lesions.
Outstanding resources for
pulmonary physiology
• Medical College of Georgia:
http://www.lib.mcg.edu/edu/eshuphysio/pr
ogram/section4/4outline.htm
• Capnography.com
The End