Respiratory physiology

Tom Archer, MD, MBAUCSD Anesthesia

The dance of pulmonary physiology—

Blood and oxygen coming together.

www.argentour.com/tangoi.html

http://www.bookmakersltd.com/art/edwards_art/3PrincessFrog.jpg

But sometimes the match between blood and oxygen isn’t perfect!

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 hypertensionExactly how does it kill patients?Interventricular septum bowing

Common hemodynamic management of all stenotic cardiopulmonary lesions.

Alveolar dead space

High V/Q

Shunt

Low V/Q

Diffusion barrier

Failures of gas exchange

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 exchangecausing 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.

http://www.biotech.um.edu.mt/home_pages/chris/Respiration/oxygen4.htm

Modified by Archer TL 2007

Shunt, or “weakling” (low V/Q)

alveolus SaO2 = 75%

“Burly” (high V/Q) alveolus

SaO2 = 99%

Normal alveolus

SaO2 = 96%

Equal admixture of “weakling” and “burly” alveolar blood has SaO2 = (75 + 99)/ 2 = 87%.

The weakling alveolus (shunt or V/Q mismatch) The burly alveolus

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%

pO2 = 50 mm Hg

SaO2 = 75%

pO2 = 50 mm Hg

SaO2 = 80%

SaO2 = 75%SaO2 = 98%

pO2 = 130 mm Hg

pO2 = 40 mm Hg pO2 = 130 mm Hg pO2 = 40 mm Hg

http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch5/s4ch5_11.htm

Low V/Q alveoli cause widened A-a gradient, just like shunt

Normal Burly

Weakling

http://focosi.altervista.org/alveolarventilation2.jpg

Modified by Archer TL

Weakling alveolus

Burly alveolus

Average alveolar PACO2 = 40 mm Hg.

Hence, PaCO2 = 40 mm Hg

Normal alveolus

Admixture of burly and weakling alveolar blood

For CO2, burly alveolus CAN compensate for the weakling alveolus.

The weakling alveolus The burly alveolus

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

pCO2 = 44 mm Hg

pCO2 = 44 mm Hg

pCO2 = 36 mm Hg

pCO2 = 46 mm Hg pCO2 = 36 mm Hg pCO2 = 46 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

http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch5/s4ch5_10.htm

Modified by Archer TL 2007

Normal shunt– bronchial circulation and Thebesian veins

aortaPulmonary veins

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 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).

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 challengeJournal Title Journal of Allergy & Clinical ImmunologyVolume 111   Issue 6   Date 2003   Pages: 1205-11

He3 MR showing ventilation defects in a normal subject and in increasingly severe asthmatics.

Baseline Methacholine Albuterol

Modified by Archer TL 2007

He3 MR scans – ventilation defects in asthmatics

Diffusion barrier (DB) to O2 and CO2and 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.

http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch3/s4ch3_25.htm

DLCO related to many factors:Membrane barrier thicknessPerfused alveolar surface area (COPD, lung resection)Cardiac outputHemoglobin concentration

http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch3/s4ch3_27.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.

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.

http://focosi.altervista.org/alveolarventilation2.jpg

Modified by Archer TL

PaCO2 is inversely proportional to alveolar ventilation.

http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch3/s4ch3_22.htm

The same minute ventilation can cause markedly different amounts of alveolar ventilation, depending on tidal volume.

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 whyETCO2 < PaCO2.

Capnographs– two types

• CO2 vs. time (commonest, what we have).

• CO2 vs. expired volume (more useful)

http://images.google.com/imgres?imgurl=http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch3/4ch3img/page15b.jpg&imgrefurl=http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch3/s4ch3_15.htm&h=379&w=271&sz=57&hl=en&start=33&tbnid=9bhXZpatrf-ajM:&tbnh=123&tbnw=88&prev=/images%3Fq%3Dalveolar%2Bventilation%2B%26start%3D20%26ndsp%3D20%26svnum%3D10%26hl%3Den%26lr%3D%26sa%3DN

Anatomical dead space

Single breath oxygen technique

http://images.google.com/imgres?imgurl=http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch3/4ch3img/page15b.jpg&imgrefurl=http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch3/s4ch3_15.htm&h=379&w=271&sz=57&hl=en&start=33&tbnid=9bhXZpatrf-ajM:&tbnh=123&tbnw=88&prev=/images%3Fq%3Dalveolar%2Bventilation%2B%26start%3D20%26ndsp%3D20%26svnum%3D10%26hl%3Den%26lr%3D%26sa%3DN

www.lib.mcg.edu/.../section4/4ch3/s4ch3_15.htm

46046

4640

40

4040

40

ETCO2 = 40 mm Hg

With no alveolar dead space

0

20

20

ETCO2 = 20 mm Hg

With 50% alveolar dead space

Alveolar dead space gas (with no CO2) dilutes other alveolar gas.

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?

Start inspiration at low lung volume (RV).

Peak inspiration at high lung volume (TLC)

Flow rate L/s

0

Flow into lung (-)

Flow out of lung (+)

Expiratory phase

Inspiratory phase

FVC

www.nature.com/.../pt1/fig_tab/gimo73_F6.htmlIntrathoracic 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.

Obstructive lesions of large airways

Flow-volume loop mnemonic (Jensen)

• “Ex – In, In – Ex”

• Expiratory obstruction = Intrathoracic variable obstruction

• Inspiratory obstruction = Extrathoracic variable obstruction

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 tumours.

“In-Ex”

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.

“Ex-In”

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.

Typical flattening of flow-volume loop in fixed airway obstruction

Fixed stenotic lesions of trachea

Extrathoracic

Intrathoracic

Obstructive Lung DiseaseIn 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.

Obstructive lesions of small airways show up in mid-expiration as “bowing”

of expiratory tracing

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 resistancein 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

Tricuspid

Pulmonic

Pulmonary vasculature

Mitral

Aortic

Resistance arterioles

Normal circulation at rest.Cardiac output is limited by SVR.

Heart gives body tissues what they “ask for”.

Tricuspid

Pulmonic

Pulmonary vascular resistance falls

Mitral

Aortic

Resistance arterioles– decreased SVR

Normal circulation during exercise / arteriolar dilation:SVR falls, CO increases.

Pulmonary resistance falls.

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.

High pulmonary resistance at rest

Slight bowing of IV septum into LV cavity.

Minimal RV distention

Minimal LV compression

Resistance arterioles

Fixed or increased pulmonary resistance and / or increased CO RV distention and failure

Intraventricular septal bulging poor LV filling fall in CO / BP death.

RV distention and failure

LV cavity compressed (diastole)

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!

Tricuspid

Pulmonic

Pulmonary capillaries

Mitral

Aortic stenosis

Resistance arterioles

Aortic stenosis at rest Cardiac output not sufficient to cause critically high LV intracavitary pressure / LV failure.

LV dilation / hypertrophy

Tricuspid

Pulmonic

Pulmonary capillaries (edema)

Mitral

Aortic

Stenosis

Resistance arterioles– decreased SVR

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.

LV failure / ischemia

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 hypertensionExactly 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/program/section4/4outline.htm

• Capnography.com

The End