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.jpgBut sometimes the match between blood and oxygen isnt perfect!

Outline (1)Failures of gas exchangeIn anesthesia think mechanical first!Hypoxemia is easier to produce than hypercarbiawhy?Measuring severity of poor oxygenationTwo pulmonary playersthe burly and weakling alveoli (V/Q mismatch)ShuntHe3 MR imaging in V/Q mismatchDiffusion 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 spaceHigh V/QShuntLow V/QDiffusion barrierFailures of gas exchange

For gas exchange problems:Always think of mechanical problems first:

Mainstem intubationPartially plugged (blood, mucus) or kinked ETT.Disconnect or other hypoventilationLow FIO2Pneumothorax

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 PAO2Needs 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.htmModified by Archer TL 2007Shunt, or weakling (low V/Q) alveolus SaO2 = 75%Burly (high V/Q) alveolus SaO2 = 99%Normal alveolusSaO2 = 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 alveolusCan 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%pO2 = 50 mm Hg SaO2 = 75%pO2 = 50 mm HgSaO2 = 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.htmLow V/Q alveoli cause widened A-a gradient, just like shuntNormal Burly Weakling

http://focosi.altervista.org/alveolarventilation2.jpgModified by Archer TLWeakling alveolusBurly alveolusAverage alveolar PACO2 = 40 mm Hg.Hence, PaCO2 = 40 mm HgNormal alveolusAdmixture of burly and weakling alveolar bloodFor CO2, burly alveolus CAN compensate for the weakling alveolus.

The weakling alveolusThe burly alveolusCan 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 HgpCO2 = 44 mm Hg pCO2 = 44 mm HgpCO2 = 36 mm Hg pCO2 = 46 mm Hg pCO2 = 36 mm Hg pCO2 = 46 mm Hg

Shunt etiologiesNormalBronchial circulation Thebesian veins

IntracardiacTetralogy of Fallot, VSD, etc.

IntrapulmonaryBronchial intubationObesityCirrhosisOsler-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.htmModified by Archer TL 2007

Normal shunt bronchial circulation and Thebesian veinsaortaPulmonary 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 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).

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

BaselineMethacholineAlbuterolModified by Archer TL 2007He3 MR scans ventilation defects in asthmatics

Diffusion barrier (DB) to O2 and CO2and DLCOConceptually difficultThickened alveolar capillary membrane.Exercise induced hypoxemia d/t dec transit timeDLCO related to many factors:Membrane barrier thicknessPerfused alveolar surface area (COPD, lung resection)Cardiac outputHemoglobin concentrationDB not usually a significant clinical problem for us.

http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch3/s4ch3_25.htmDLCO 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.htmDiffusion 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.jpgModified by Archer TLPaCO2 is inversely proportional to alveolar ventilation.

http://www.lib.mcg.edu/edu/eshuphysio/program/section4/4ch3/s4ch3_22.htmThe same minute ventilation can cause markedly different amounts of alveolar ventilation, depending on tidal volume.

Anatomic and alveolar dead spaceAnatomic 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%3DNAnatomical dead spaceSingle 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%3DNwww.lib.mcg.edu/.../section4/4ch3/s4ch3_15.htm

46046464040404040ETCO2 = 40 mm HgWith no alveolar dead space02020ETCO2 = 20 mm HgWith 50% alveolar dead spaceAlveolar dead space gas (with no CO2) dilutes other alveolar gas.

CapnographyObvious: 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

CapnographyUpsloping 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/s0Flow into lung (-)Flow out of lung (+)Expiratory phaseInspiratory phaseFVC

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 obstructionInspiratory 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 tracheaExtrathoracicIntrathoracic

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 bowingof 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 (

Pulmonary vascular resistancein normal lungNormally, 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

TricuspidPulmonicPulmonary vasculatureMitralAorticResistance arteriolesNormal circulation at rest.Cardiac output is limited by SVR.Heart gives body tissues what they ask for.

TricuspidPulmonicPulmonary vascular resistance fallsMitralAorticResistance arterioles decreased SVRNormal circulation during exercise / arteriolar dilation:SVR falls, CO increases.Pulmonary resistance falls.

http://www.pathguy.com/lectures/hipbp.gif

Pulmonary hypertensionAcute pulmonary thromboembolism

Pulmonary hypertensionChronic 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 restSlight bowing of IV septum into LV cavity.Minimal RV distentionMinimal LV compressionResistance arterioles

Fixed or increased pulmonary resistance and / or increased CO RV distention and failureIntraventricular septal bulging poor LV filling fall in CO / BP death.RV distention and failureLV cavity compressed (diastole)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!

TricuspidPulmonicPulmonary capillariesMitralAortic stenosisResistance arteriolesAortic stenosis at rest Cardiac output not sufficient to cause critically high LV intracavitary pressure / LV failure.LV dilation / hypertrophy

TricuspidPulmonicPulmonary capillaries (edema)MitralAortic StenosisResistance arterioles decreased SVRAortic 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 hypercarbiawhy?Measuring severity of poor oxygenationTwo pulmonary playersthe burly and weakling alveoli (V/Q mismatch)ShuntHe3 MR imaging in V/Q mismatchDiffusion 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