Ventilationperfusioninhealth& disease

Arjun Srinivasan

Wherewasthebeginning?

Distributionofventilation
Spatial&anatomicalvariation

Rateofalveolarfilling

Rateofalveolaremptying

Ventilationdistribution RCt
f a s t s l o w 100 volume (% % of final) ) 75 50 25 0

R=1 C=.5 t=.5

R=2 C 1 C=1 t=2 R=1 C 1 C=1 t=1

1 2 sekundy seconds

Clinicalrelevance
Perfusionispoor&pulsatile atapex Pa &Pv proportionatelyincreasesfromtopto bottom PA changes h minimally i i ll with i hgravity i Pressuresaremaxatbottom
Pulm edemastartsatbottom Redistributionofbloodflowtoapex antlers horn

Itsnotjustgravity!

Lungperfusioninzerogravitysituationsismoreuniformbutbynomeans equallydistributed
NunnsAppliedrespiratoryphysiology,6th edition

UnderstandingV/Qrelationships
Consider C id lung l assingle i l unit it
Relationships l h between b PA O2,PA CO2,alveolar l l ventilation&pulmonarybloodflow Alveolargasequation

ConsiderlungasmultipleunitsofvaryingV/Q
Clinicalconsequencesinhealth&disease

AlveolarPO2 andPCO2
D Determined i db bythe h ratio i between b ventilation il i and d bloodflow:V/Q PO2 andPCO2 areinverselyrelatedthroughalveolar ventilation il i IncreasingV/QproduceshigherPAO2 andlowerPACO2 DecreasingV/QproduceslowerPAO2 andhigher PACO2

GasCompositionintheAlveolarSpace
PiO2=(barometricpressureH2Ovaporpressure)xFiO2 =(760 ( 47) )x0.21=150mmHg

AlveolarGasEquation
PAO2 =(PiO2) (PaCO2/R) PaCO2 approximatesPACO2 duetotherapiddiffusionof CO2 R=RespiratoryQuotient(VCO2/V02)=0.8 Inanormalindividualbreathingroomair: PAO2 =150 40/0.8 / =100mmHg g

Ventilation/perfusion il i / f i ratio i ( (V/Q) / )

V/Qdistributioninhealth

WestJB,RespiratoryPhysiology, TheEssentials,6th ed.2000,Lippincott,p.54.

V/Qratioindisease
obstruction alveolus vessel

50 40 PCO2 ( (mmHg) ) 20 10 0 0 40 30

ideal V/Q V/Q shunt/ venous admixture V/Q dead space

embolus

80 120 PO2 (mmHg)

160

LowV/QEffectonOxygenation
Onelungunithas normalventilationand perfusion,whilethe hasinadequateventilation

Normal

Low L V/Q

PCO2 PO2

PO2 50 PO2 100 PO2?

Oxyhemoglobin DissociationCurve
CO2=(1.3 ( xHGBxSat) )+( (.003xPO2) )
100

80

16

60

12

40

20

4 0 0 20 40 60 80 100

PO mmHg 2

Oxy ygen C Content t (ml/10 00 ml)

20

%Hemog globinSaturatio on

LowV/QEffectonOxygenation

Normal

Low L V/Q

PO250mmHg Sat80% O2content16ml/dl

PO2 50
PO2 100mmHg g Sat100% O2content20ml/dl

PO2 100

PO2 =60 Sat90% O2content18ml/dl

HIGHV/QEffectonOxygenation

Normal

HIGH V/Q

PO2130mmHg Sat100% O2content20ml/dl

PO2 130
PO2 100mmHg g Sat100% O2content20ml/dl

PO2 100

PO2 =100 Sat100% O2content20ml/dl

High+lowV/Q=?

HIGHV/Q

Low L V/Q

PO250mmHg Sat80% O2content16ml/dl

PO2 50
PO2 130mmHg g Sat100% O2content20ml/dl

PO2 130

PO2 =60 Sat90% O2content18ml/dl

Local V/Qabove~1hasminimal effecton[O2]

160 PaO2 (mmHg) 120 23 O2 content 21 (ml/100 ( / ml) ) 22 20 80 19 18 40 17 16 0 0.001 0.01 0.1 1 V/Q Thus V/Q in one part of lung cant compensate for elsewhere 10 15 100

PCO2 inV/QMismatch
CO2 CONTENT T (ml/100 m ml)

Increasedventilation cancompensatefor lowV/Qunits

ShapeofCO2curve

80

60

40

Totalventilation( (VE) ) mustincreaseforthis compensation

20

20

40

60

80

P CO (mmHg) 2

Infinity fi i

V/Q Deadspace

Zero

V/Q Shunt Venousadmixture

VentilationtoPerfusionMismatch
Pure Shunt
Perfusionwith No Ventilation ShuntLike Units
shunt

Pure DeadSpace
DeadSpace LikeUnits Ventilationwith No Perfusion

Deadspace

3 compartmentmodel

Deadspace
Definedaswastedventilation Classification
Anatomical(1ml/poundofidealbodywt) Alveolar Physiological
Anatomical+alveolar

PhysiologicalDeadSpacebyBohrs Method(forCO2)
VT XFE =VAXFA VT =VA +VD VA =VT VD VT XFE =(VT VD)XFA VD =FA FE VT FA VD =PACO2 PECO2 (BohrEquation),so VT PACO2 VD =PaCO aCO2 PECO2 CO VT PaCO2

PhysiologicDeadSpace& V/QMismatch
Hyperinflation
AirwayObstruction DynamicHyperinflation TidalVolume PEEP

LowPerfusion
LowCardiacOutput PulmonaryVascular Injury Extravascular Compression

NoPerfusion
PulmonaryEmbolus VascularObliteration Emphysema

Shuntequation
Qtx CaO2 =[(Qt Qs)x CcO2]+[QsxCvO2]

Qs Cc ' O2 CaO 2 = Qt Cc ' O2 CvO 2

CausesofShunt
Physiologicshunts
Bronchialveins, , p pleuralveins

Pathologic P th l i shunts h t
Intracardiac Intrapulmonary
Vascularmalformations Unventilatedorcollapsedalveoli

Normalshuntfraction
~5% Dueto
Physiologicalshunt Gravity yrelatedV/Qmismatch

ContributestoAaDO2
10 15mmhg

Aa DO2
PAO2(alveolar ( l l gasequation) ti ) arterial t i lPaO2 P O2 I Inat totally t ll efficient ffi i tl lungunit itwith ithmatched t h dV/Q V/Q, alveolarandcapillaryPO2wouldbeequal AdmixtureofvenousbloodorV/Qscatterfromlow V/Qlungunitswill increaseAa DO2 Increases~3mmhgeverydecadeafter30yrsofage

ShuntVS. VS V/Qscatter
Calculated C l l dshunt h fraction f i orAa DO O2
Doesnotdifferentiate

ResponseofpaO2toincreasingFi O2 V/Qscatter
PaO2 increasewithsmallincreaseinFiO2(.21.35)

Pureshunt
Notmuchresponse p

MIGET

50parallelgasexchangeunits characterizedbyVAQratio. FitpredictedPE &Pa to experimentaldata. Output:Ventilationand perfusiondistributions.

CompensationofV/Qinequality?
V/Q localhypocapnia pH local bronchoconstriction (V/Q) V/Q CO2 ventilation improvesCO2 >O2 (dissociationcurves) V/Q hypoxicpulmonaryvasoconstriction

Pointstoremember
VentilationandPerfusionmustbematchedatthealveolarcapillary level Mostimportantcauseofhypoxemiainmostrespiratorydiseases V/Qratioscloseto1.0resultinalveolarPO2closeto100mmHg andPCO2closeto40mmHg V/Qgreaterthan1.0increasePO2andDecreasePCO2.V/Qless than1 1.0 0decreasePO2andIncreasePCO2 ShuntandDeadSpaceareExtremesofV/Qmismatching. AaGradientof1015ResultsfromgravitationaleffectsonV/Qand PhysiologicShunt