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 isnt 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
hypercarbiawhy?
Measuring severity of poor oxygenation
Two pulmonary playersthe 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 Burly (high V/Q) alveolus
alveolus SaO2 = 75% SaO2 = 96% 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
The burly alveolus
(shunt or V/Q mismatch)

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 cant 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

Average alveolar PACO2 =

http://focosi.altervista.org/alveolarventilation2.jpg 40 mm Hg.
Modified by Archer TL Hence, PaCO2 = 40 mm Hg
 The weakling alveolus The burly alveolus

pCO2 = 44 mm Hg
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 non-
ventilated alveoli is
SHUNT.
 V/Q mismatch

Emphasized by John West in the 1970s.

Seen in most lung diseases.
Prototypes are: asthma, COPD, ARDS.
V/Q mismatch and shunt both cause
hypoxemia despite possible
hyperventilation (burly alveoli cant
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/sectio
n4/4ch3/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

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www.lib.mcg.edu/.../section4/4ch3/s4ch3_15.htm
 ETCO2 = ETCO2 =
40 mm Hg 20 mm Hg
With no With 50%
alveolar alveolar 20
40
dead space dead space

40
20
Alveolar dead
space gas
(with no CO2)
dilutes other
alveolar gas.
0
40
40 40
0 46
46 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 Start inspiration
high lung volume at low lung
(TLC) volume (RV).

FVC
0
Inspiratory phase
Flow into
lung (-)
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 Extrathoracic
stenotic
lesions of
trachea
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 mid-
expiration 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 RV Minimal LV
distention compression

High pulmonary resistance at rest

Slight bowing of IV septum into LV
cavity.

Resistance arterioles
RV distention LV cavity compressed
and failure (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 arteriolesdecreased 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 LV dilation / hypertrophy
capillaries
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 LV failure /
capillaries ischemia
(edema)
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
hypercarbiawhy?
Measuring severity of poor oxygenation
Two pulmonary playersthe 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