Ebook Practical cardiovascular hemodynamics: Part 2

XIII


Tamponade


XIII.1.OVERVIEWOFTHEHEMODYNAMICSOFTAMPONADE
In tamponade, intrapericardial pressure usually increases to ~10 to 25 mmHg
and compresses the cardiac chambers until the pressure inside these chambers
equalizes with the intrapericardial pressure (Figure XIII.1).1-5 This leads to
equalizationofdiastolicpressuresofthe4cardiacchambers.Becausetherightsided chambers have thin walls, they tend to collapse when intrapericardial
pressureisequaltoorlargerthantheirintracavitarypressure.


FIGUREXIII.1

Pressure-volumecurveofthepericardiumshowingthe
intrapericardialpressureinrapidlyandslowlydevelopingeffusions
orcardiacdilatation.Inacuteconditions,thepericardiumcannot
stretch,anditspressurerisesmarkedlywithsmallvolumechanges.
Thisexplainshowtamponademaydevelopwithsmallacute
effusionandhowthepericardiummaybestretchedincaseofacute
RVdilatationleadingtoa“functional”CP.Oncethepericardial
pressureexceedsastretchlimit(bar),itincreasesexponentially
withanychangeinvolume.Evenwhenintrapericardialpressureis
lowerthanright-sidedpressure,theRVorRAtransmuralpressure
(RApressureorRVpressureminusintrapericardialpressure)is
reduced,whichimpairsRVoutwardexpansionandfilling;in
addition,atthispoint,pericardialpressureisatasteepslope,and
thereisatleastathreatenedtamponade.Althoughfluid
administrationmayinitiallyincreaseRVpressureandRV

transmuralpressure,intracardiacvolumecanstretchthepericardium
andfurtherincreaseintrapericardialpressureevenifintrapericardial
volumeisunchanged;thisexplainshowfluidadministrationin
euvolemicorhypervolemicpatientsmaybeharmful.
Thisgraphalsoshowsthatpatientswithhighintrapericardial
pressureresultingfromCPorsevereRVdilatationstretchingthe
pericardiummayhaveLVEDP>20mmHg,yetthetransmuralLV
pressureisalmostnilandtheLVvolumecannotexpand.These
patientshavelowLVvolumeyetincreasedpulmonarycapillary
pressure.Theamountoffluidinthepulmonaryveinsismodest,and
thus,thelungsarealmostalwayscleardespitesometimessevere
dyspnea.ModifiedfromSpodickDH.Acutecardiactamponade.N
EnglJMed.2003;349:684–690.

TheequalizationofdiastolicpressuresissimilartowhatisobservedinCP.
AsopposedtoCPhowever,therespiratorychangesofintrathoracicpressureare
transmittedtothecardiacchambers.1,2ThisexplainswhyRApressuredecreases
during inspiration and thus venous flow from the SVC to the RA increases
during inspiration (absence of the Kussmaul’s sign). Left-sided flow does not
increase because pulmonary veins and LV are both exposed to the negative
intrathoracic pressure; actually, the pulmonary veins are more affected by this
negativepressure.TheincreasedvenousflowtotherightcavitiesmakestheRV
pushagainsttheLVindiastole,ratherthanpushagainstthepericardiumsince
thehighpericardialpressurepreventsthat.ThisreducesLVfillingininspiration


andexplainsthereductionofsystolicarterialpressurebymorethan10mmHg
withnormalinspiration(pulsusparadoxus)(FigureXIII.2).

FIGUREXIII.2

Sequenceofeventsduringinspirationintamponade.(−)sign
adjacenttoastructuresignifiesthereistramsmissionofthenegative
intrathoracicpressuretothisstructure,whereas(0)correspondsto
thelackoftransmissionoftheintrathoracicpressuretothis
structure.Grayarrowssignifyincreasedflowbetween2chambers,
whereasthebluearrowssignifyreducedflowbetween2chambers.


Duringinspiration,thenegativepressureistransmittedtoPV
andSVCandtotheintracardiacchambers(thisisdifferentfrom
constriction).ThisincreasesflowbetweenbothIVCandSVCon
theonehandandtheRAthenRVontheotherhand,whichpushes
theseptumtotheleftandreducesLVfillingfromLAandPV.X
descentisdeepespeciallyduringinspiration,butYdescentisflat
becauseofimpededRA-to-RVflowthroughoutalldiastole,
includingearlydiastole.
E:mitralinflowDopplerwave;PV:pulmonaryvein;S:
systolicflowwaveofIVC,SVC,andPVonDoppler,corresponds
toXdescent;D:diastolicflowwaveofIVC,SVC,andPVon
Doppler,correspondstoYdescent.

Although ventricular interdependence is present in both CP and
tamponade, a different mechanism is incriminated in each case: during
inspiration,RVpushesLVintamponade,whereasRVissuckedbyLVinCP.
As opposed to CP, LV flow is reduced in tamponade because of RV
compression,notbecauseofalackoftransmissionofthenegativeintrathoracic
pressure to LV. In addition, because of the uniform pericardial fluid, the
constraintismoreuniformacrossbothLVandRVincaseoftamponade.Asa
result of this different mechanism, ventricular interdependence is more

prominentintamponadeandleadstopulsusparadoxus,whichisonlypresentin
onethirdofcasesofCP.
Furthermore, as opposed to CP where the heart briefly expands in early
diastole before getting constrained, the heart is compressed throughout all
diastole in tamponade, including early diastole. Thus, RA-to-RV flow is
impededthroughoutalldiastole,includingearlydiastole,andthereisnodeepY
ontheRAtracingandnodiastolicdipontheRVtracing.ThereisadeepXin
earlysystoleasRVannulusmovesdownandstretchesoutthecompressedRA.


XIII.2.SUMMARYOFHEMODYNAMICFINDINGSINTAMPONADE
Cardiactamponadeisdefinedasapericardialeffusioncompressingthecardiac
chambersandleadingtohemodynamiccompromise.Thiscompromisemanifests
clinicallyasanyorallofthefollowing:elevatedJVP,systemicbloodpressure
alteration with pulsus paradoxus early on, tachycardia, and
tachypnea/dyspnea/orthopnea with clear lungs (PCWP is increased, but the
intracardiacandpulmonaryvenousvolumeislow,hencethelackofpulmonary
edema).
Oninvasivehemodynamics,thefollowing3findingsarecharacteristicof
tamponade:
1-On RA and SVC tracings: elevated mean pressure with a deep X descent
(mainlyduringinspiration)andaflatYdescent(FigureXIII.3)
2-Elevationandequalizationofdiastolicpressuresofthe4cardiacchambersand
equalization of PA diastolic pressure with RV end-diastolic pressure
(RVEDP),similarlytoCP:
CVP=meanRApressure=RVEDP=PAdiastolicpressure=meanPCWP
=LVEDP
(normally,RVEDP

FIGUREXIII.3

NotethedeepXandthebluntedYdescentsinapatientwith
tamponade.

3-Althoughthesystolicaorticpressureisinitiallynormalorevenelevatedasa
result of adrenergic release, pulsus paradoxus is present and pulse pressure is
abnormalearlyon.Onanyarterialoraortictracing,pulsusparadoxusmeansthat
systolicpressuredecreases>10mmHgwithnormalinspiration.Inaddition,the
aortic waveform is narrow, and the pulse pressure is reduced (aortic tracing is
“short”andnarrow)(FigureXIII.4).Ultimately,thesystolicpressure decreases


aswell.However,anincreaseinsystolicpressureupto150to210mmHgand
diastolicbloodpressureupto100to130mmHgisfrequentintamponadeand
occured in up to one third of tamponade cases in one report, particularly in
patients with a history of hypertension who are sensitive to the catecholamine
surge.6,7Hypertensiondoesnotmeanpreservedcardiacoutput;infact,cardiac
outputisaslowasincasesofnormalarterialpressure,butincreasedperipheral
vascular resistance preserves blood pressure (pressure = flow × resistance).
Patients with tamponade and hypertension had a reduction in blood pressure,
reductioninSVR,andincreaseincardiacoutputfollowingpericardiocentesis.


FIGUREXIII.4

Typicalarterialpressureintamponade.Tachycardiaat120bpm.
Thearterialpressureisreduced,thetracingisnarrowbased,andthe
pulsepressureisreduced.Thesystolicpressureandthepulse
pressuredeclinewithinspiration(bluearrow),andthetracing

almostcollapsesatendinspiration(verticalarrow).

Note: Besides respiratory variation of arterial pressure, pulsus paradoxus
manifestsasexaggeratedrespiratoryvariationofRVandLVsystolicpressures.


XIII.3.LOW-PRESSURETAMPONADE
In patients who are hypovolemic, compression of intracardiac chambers (ie,
tamponade), particularly right-sided chambers, may occur at a lower
intrapericardialpressureof6to12mmHg.Inthiscase,therewillbeequalization
ofintrapericardialpressureandRApressureat6to12mmHg.3Thus,tamponade
with pulsus paradoxus or hypotension occurs with a high-normal or mildly
increased right-sided filling pressure and jugular venous pressure. If it was not
forhypovolemiaandthelowright-sidedfillingpressure,thispericardialeffusion
wouldnotbehemodynamicallysignificant.Fluidadministrationmaycorrectthe
pulsus paradoxus; however, excessive fluid administration may increase rightsided volume, which further stretches the already distended pericardium and
elevatesitspressure,leadingtoafull-blowntamponadepicture.8-10Thatiswhy
fluids are helpful in hypovolemic patients with tamponade but may harm
euvolemic or hypervolemic patients. Thus, in order to increase the transmural
pressures of the cardiac chambers (ie, intracavitary pressure minus pericardial
pressure)andallowtheexpansionofthesecavitiesinpatientswithtamponade,it
isimportanttomaintainahigherlevelofright-andleft-sidedpressurewithout
excessive volume resuscitation. Ultimately, patients with low-pressure
tamponade require pericardiocentesis because even at 6 to 12 mmHg, the
intrapericardialpressureispronetorisingwithanychangeinpericardialvolume
(FigureXIII.1).


XIII.4.CASESOFUNDERLYINGRVORLVFAILUREANDCAUSES
OFABSENTPULSUSPARADOXUS

While it is easy to induce tamponade in case of hypovolemia, it is harder to
inducetamponadephysiologyinpatientswithseverelyincreasedright-sidedor
left-sidedpressure.3Infact,itisharderforthepericardialpressuretocompress
bothventricles,andtamponadedevelopswhenpericardialpressureequilibrates
withthelowerpressureventricle.Moreover,therespiratoryvariationinvenous
returndoesnotsignificantlychangethecardiacoutputandthesystolicpressure
of the failing ventricle (flat portion of the Frank-Starling curve). The latter 2
conditions, that is, the lack of biventricular compression and interdependence
and the lack of respiratory variation in ventricular output explain the lack of
pulsus paradoxus. This situation may be seen in patients with end-stage renal
diseasewhodeveloptamponadeandwhohaveanunderlyingleftheartfailure.
Inaddition,pulsusparadoxusmaynotbeseenincasesof(1)ASD,asthe
increase in right-sided flow during inspiration is balanced by an increase in
right-to-left shunt or reduction in left-to-right shunt, leading to less ventricular
interdependence; (2) local tamponade (eg, compression of LA or RA by a clot
aftercardiacsurgery,leadingtoalocalizedincreaseinpressure);(3)AI,where
the diastolic regurgitant flow damps down respiratory fluctuations of flow. In
addition, pulsus paradoxus is difficult to detect in case of an irregular rhythm
suchasatrialfibrillation.


XIII.5.REGIONALTAMPONADE
Thisoccurswhenonlyonecardiacchamber,apulmonaryvein,ortheSVCor
IVC is compressed by a loculated effusion. Because there is no uniform
compression of the 4 chambers, there is no equalization of diastolic pressures
and no ventricular interdependence/pulsus paradoxus. There is increased
pressure of the compressed chamber, for example, increased RA pressure or
PCWP,andhypotension,whichintherightcontextsuggesttamponade(eg,after
cardiac surgery). However, loculation can also produce classic tamponade,
presumablybytighteningtheuninvolvedpericardium.

XIII.6.EFFUSIVE-CONSTRICTIVEPERICARDITIS
Somepatientshavepericardialeffusionwiththehemodynamicsoftamponade,
thatis,pulsusparadoxusandelevatedandequalizedright-andleft-sidedfilling
pressure. However, upon drainage of the pericardial fluid, the hemodynamic
compromise does not fully resolve, RV and LV diastolic pressures remain
equalized,andRApressureremainselevated(RApressuredeclinesbylessthan
50%). A flat RA Y descent (tamponade) may become deep (constriction) after
drainage of the pericardial fluid. Thus, effusive-constrictive pericarditis is an
effusion that occurs on a background of CP. In patients with noncompliant
pericardium, tamponade can occur with relatively little accumulation of fluid.
Effusive-constrictivepericarditismaybeseenwithCPofanyorigin,particularly
the idiopathic or radiation-induced CP, and is usually seen early in the disease
course.Infact,upto24%ofconstrictivepericarditiscasesand7%oftamponade
cases have an effusive-constrictive pathophysiology.11,12 When idiopathic,
effusive-constrictivepericarditisisoftenaninflammatoryCPthatistransientin
50% of the cases and resolves with anti-inflammatory therapy; this is not the
caseofradiation-inducedeffusive-constrictivepericarditis.11


XIII.7.COPDANDOTHERCAUSESOFPULSUSPARADOXUSAND
RV-LVRESPIRATORYDISCORDANCE
Because of large intrathoracic pressure swings, COPD, asthma, obesity, or
positivepressureventilationmayleadtodiscordanceinRVandLVfillingand
pulsusparadoxus(seeSectionsXII.5-7)13


REFERENCES

1. LeWinterMM.Pericardialdiseases.In:LibbyP,BonowRO,MannDL,ZipesDP,eds.
Braunwald’sHeartDisease.8thed.Philadelphia,PA:Saunders,Elsevier;2008:1829–
1854.
2. Robb JF, Laham RJ. Profiles in pericardial disease. In: Baim DS, ed. Grossman’s
Cardiac Catheterization, Angiography, and Intervention. 7th ed. Philadelphia, PA:
LippincottWilliamsandWilkins;2006:725–743.
3. SpodickDH.Acutecardiactamponade.NEnglJMed.2003;349:684–6906.
4. Reddy PS, Curtis EI, O’Toole JD, Shaver JA. Cardiac tamponade. Hemodynamic
observationsinmen.Circulation.1978;58:265.
5. HolmesDRJr,NishimuraR,FountainR,ZoltanG.Iatrogenicpericardialeffusionand
tamponade in the percutaneous intracardiac intervention era. J Am Coll Cardiol Intv.
2009;2:705–717.
6. Ramsaran EK, Benotti JR, Spodick DH. Exacerbated tamponade: deterioration of
cardiac function by lowering excessive arterial pressure in hypertensive cardiac
tamponade.Cardiology.1995;86:77–79.
7. Brown J, MacKinnon D, King A, Vanderbush E. Elevated arterial blood pressure in
cardiactamponade.NEnglJMed.1992;327:463–466.
8. Spodick DH. Threshold of pericardial constraint: the pericardial reserve volume and
auxiliarypericardialfunctions.JAmCollCardiol.1985;6:296–297.
9. Hashim R, Frankel H, Tandon M, Rabinovici R. Fluid resuscitation-induced cardiac
tamponade.Trauma.2002;53:1183–1184.
10. Cogswell TL, Bernath GA, Keelan MH, Wann LS, Klopfenstein HS. The shift in the
relationship between intrapericardial fluid pressure and volume induced by acute left
ventricularpressureoverloadduringcardiactamponade.Circulation.1986;74:173–180.
11. Sagrista-SauledaJ,AngelJ,SanchezA,etal.Effusive-constrictivepericarditis.NEngl
JMed2004;350:469.
12. Cameron J, Oesterle SN, Baldwin JC, Hancock EW. The etiologic spectrum of
constrictivepericarditis.AmHeartJ1987;113:354–360
13. KhasnisA,LokhandwalaY.Clinicalsignsinmedicine:pulsusparadoxus.JPostGrad
Med.2002;48:46–49.

XIV


Pulmonaryhypertension


XIV.1.DEFINITION
Pulmonary hypertension (PH) is defined as a mean PA pressure ≥25 mmHg at
rest.1,2AnincreaseinmeanPApressureto>30mmHgwithexerciseusedtobe
includedinthedefinitionbutislessspecific,particularlyinpatientsolderthan
50yearsofagewhomaynormallyhaveanincreaseinmeanPApressureto45
mmHgwithexercise.TheclassificationofPHseverityisshowninTableXIV.1.
TABLEXIV.1

ClassificationofseverityofPH
SYSTOLICPAPRESSURE

MEANPAPRESSURE

MildPH

35-50mmHg

25-35mmHg

ModeratePH

50-70mmHg

35-45mmHg

SeverePH

>70mmHg

>45mmHg
orPVR>6-7Woodunits


XIV.2.CATEGORIESOFPULMONARYHYPERTENSION
Thereare2majorcategoriesofPH.
1-PH secondary to left heart failure (also called pulmonary venous
hypertensionorpost-capillaryPH)
-Left-sided ventricular or valvular diseases may produce an increase in LA
pressure with passive backward transmission of pressure to the
pulmonarycirculationleadingtoincreasedPApressure.Inthiscase:3
-PCWPiselevated(>15mmHg).
-DiastolicPApressureispassivelyincreasedandisequaltoPCWPoris
upto5mmHghigherthanPCWP.
-PVRis<3Woodunits(thenormalPVRbeing<2Woodunits),andthe
transpulmonarygradient,thatis,meanPApressureminusPCWP,is<12
mmHg(someinvestigatorsuseacutoffof20mmHg).1
-Left heart failure is the most common cause of PH. Heart failure may be
obvious in some patients but may be occult in others, especially when
isolatedLVdiastolicdysfunctionispresent.4 Furthermore, with chronic
venous PH, pulmonary arteries may undergo reactive changes, and PH
may become a mixed venous and arterial PH, in which case PCWP is
elevated but diastolic PA pressure is >5 mmHg higher than PCWP and

PVR is >3 Wood units.5,6 Pulmonary hypertension with a precapillary
componentisseenin20%to35%ofpatientswithadvancedleftHF.6-8
Thissituationmayalsobeseeninpatientswithmixeddisorders,suchas
left HF and COPD. The active PH component fully resolves after
treatmentofHFbutmaytakeweekstomonthstoresolve.3
-Resting PCWP may be normal despite LV failure, especially in patients
appropriatelytreatedwithdiuretics.Exercisetesting,volumeloading,and
pulmonary vasodilator challenge are appropriate strategies that increase
PCWPincaseofoccultLVdysfunctionandthusunveilthediagnosisof
postcapillaryPH.PatientswithPHandnormalLVEFwhoaresuspected
of having diastolic left heart disease–associated PH or mixed
postcapillaryPHandprecapillaryPHareapproachedasinFigureXIV.1.
-Upto70%ofpatientswithsystolicLVdysfunctionorisolatedLVdiastolic
dysfunctionmaydevelopPH,andthepresenceofPHisassociatedwitha
poor prognosis in these patient populations.2,9,10 A recent study
documented a high prevalence of PH in patients with heart failure and


normalEF;83%ofpatientsinthisstudyhadPH,themedianPAsystolic
pressure being 48 mmHg.10 Interestingly, PA pressure was out of
proportion to what would be expected from the rise in PCWP. For the
same PCWP, patients with heart failure with normal EF had a much
higherPApressurethanpatientswithhypertensionandnoheartfailure.
Thus, in addition to the postcapillary component, a precapillary
pulmonary arterial hypertension frequently coexists or develops during
thecourseofheartfailurewithnormalEF.
2-PrecapillaryPH
PrecapillaryPHischaracterizedbyPCWP≤15mmHg(exceptinmixedPH),
PVR ≥3 Wood units, and a transpulmonary gradient >12 mmHg.1,2,11
However, in cases of precapillary PH associated with severe RV failure,

pericardial distension and functional pericardial constriction may occur
leading to ventricular interdependence and equalization of RV and LV
end-diastolic pressures, with a subsequent increase in LV end-diastolic
pressureandPCWPto15to20mmHg.12Thiscasemaybeconfusedwith
post-capillaryPHassociatedwithasecondaryprecapillarycomponent.As
opposedtopostcapillaryPH,theincreaseinPCWPinthiscaseistheresult
rather than the cause of PH. The presence of signs of LV diastolic
dysfunction on echocardiography supports the diagnosis of left heart
disease–associated PH, whereas a significant increase in PVR >7 Wood
unitsandsevereRVdilatationsupportthediagnosisofprecapillaryPH.


FIGUREXIV.1

DiagnosticapproachtodistinguishbetweenPAHandPHrelatedto
diastolicleftheartdisease.*PVR<3correlateswitha
transpulmonarygradient(meanPApressure−PCWP)<20mmHg
andadiastolicPApressurewithin5mmHgofPCWP.Woodunitis
thePVRunitusedinthisFigure.**HTN,age>65years,diabetes,
LVH,LAE,atrialfibrillation,lowE’,E/E’>15.***Avoid
vasodilatorchallengewithadenosineorepoprostenolincaseofleft
heartfailurebecausethismayfurtherincreaseLVpreloadand
PCWP.Theuseofniprideasapulmonaryvasodilatorispreferred


becauseitreducesafterloadandmayactuallyreducePCWP.DHF,
diastolicheartfailure;LAE,LAenlargement.Adaptedwith
permissionfromHoeperMM,etal.JAmCollCardiol.
2009;54:S85-S96.

Thereare3majorcategoriesofprecapillaryPH:
1. Pulmonary arterial hypertension, which is related to a pulmonary vascular
disease affecting the pulmonary arterioles. Pulmonary arterial hypertension
may be idiopathic or may be related to connective tissue disease, cirrhosis
(porto-pulmonary hypertension), human immunodeficiency virus, or
Eisenmengersyndrome.
Incongenitalheartdiseasewithalargeleft-to-rightshunt(eg,VSD,PDA,
or less often ASD), PA pressure initially increases as a result of the
increaseinright-sidedflow,PVRbeinglowatthisstage(pressure~flow
× resistance, an increase in flow leads to an increase in pressure); this
“dynamic” PH resolves with shunt closure. Over time, the increased
pulmonary flow induces progressive pulmonary vascular disease and
severeincreaseinPVRtoapointthatPVRapproachesSVR,PApressure
approaches systemic pressure, and the shunt reverses and becomes
bidirectionalorrighttoleft.ThisisEisenmengersyndromeand,exceptin
ASD,isusuallyestablishedininfancy.
Pulmonary veno-occlusive disease is characterized by primary venular
abnormalitiessimilartothearteriolarabnormalitiesseeninidiopathicPAH
and may be idiopathic or associated with scleroderma. Similar to PAH,
true wedging is difficult in this disease, and if successful, it creates a
columnofstagnantbloodbetweenthecatheterandtheLA;thus,thetruly
wedged PCWP approximates LA pressure, albeit damped through the
venular obstruction, and is normal in value. The pulmonary capillary
pressureisincreased,butnotthewedgedPApressure.
2. Pulmonaryhypertensionsecondarytothromboembolicdisease.
3. Pulmonary hypertension secondary to lung disease: mild PH is common in
patients with COPD, but severe PH is very unusual. In fact, moderate and
severe PH are only seen in 5% to 10% and 2% of severe COPD cases,
respectively.13,14 Severe PH may be seen with advanced stage fibrotic lung
disease that obliterates the pulmonary capillaries, sarcoidosis, or obesityhypoventilationsyndrome.

XIV.3.TWOTIPSONTHEEVALUATIONOFPULMONARY
HYPERTENSION
1. IncaseofchronicseverePH,thePApressurenumbermaystartdeclininginto
themildrangebecauseofthedevelopmentofsevereRVfailurethatisunable
to generate high PA pressure. Pulmonary vascular resistance, on the other
hand,remainsseverelyelevated.
2. IncaseofacutePH(eg,pulmonaryembolism),theRVisnotabletogenerate
a systolic PA pressure higher than 45 to 50 mmHg. A systolic PA pressure
higher than 40 mmHg implies significant PH in case of acute pulmonary
embolism.11AsystolicPApressurehigherthan50mmHghintstoasubacute
orchronicprocess.
Inbothcases,thePApressurenumberunderestimatesthetrueseverityof
thepulmonaryvascularabnormality.ThepresenceofsevereRVdysfunction,a
severelyelevatedRApressure,oraseverelyelevatedPVR>6to7Woodunitsis
diagnostic of severe PH. In addition, a pulsus alternans on RV or PA tracing
(similartotheaorticpulsusalternans)oranarrowPApulsepressure(eg,30/23)
is diagnostic of severe RV failure. In fact, in patients with severe PH that is
evidencedbyelevatedPVRandRVfailure,ahighsystolicPApressurepredicts
recovery of RV function with PH therapies or left heart treatment and better
outcomes than patients with lower systolic PA pressure; a higher systolic PA
pressurecorrespondstoabetterRVfunction.15,16


XIV.4.RIGHTANDLEFTHEARTCATHETERIZATIONFOR
PULMONARYHYPERTENSION
Pulmonary hypertension is often initially diagnosed by echocardiography.
Echocardiography estimates PA pressure and suggests a left-sided etiology. In
addition to valvular function and LV systolic function, echocardiography

assesses LV filling pressures, LV diastolic function, and LA size.
Catheterization is needed to confirm the diagnosis and the etiology of PH
particularly in cases of moderate-to-severe PH without a clear left heart or
thromboemboliccause.Thegoalsofcatheterizationarethefollowing:
1. ConfirmthediagnosisofPH.ThespectralDopplerprofileofTRistooweak
orinsufficientto measure the PA pressure in approximately 25% to 55% of
patients referred for PA pressure evaluation.17 The echocardiographic
diagnosis of PH is falsely positive in up to 50% of patients, and the PA
pressurevaluediffersby>10mmHgwiththecatheterizationvaluein50%of
patients. Echocardiography may under- or overestimate PA pressure in
variouscausesofPH.17,18
2. AssessPCWPtodetermineifPHissecondarytoleftHF.Theassessmentof
PCWPmaybedifficultinpatientswithseverePH.19,20AhybridPCWP-PA
pressuretracingmaybeobtainedandleadtooverestimationofthetruePCWP
(FigureXIV.2).Ontheotherhand,thetruePCWPmaybeflattenedwithout
distinct waves, as the retrograde transmission of LA pressure through the
pulmonary vasculature is damped. Moreover, wedging a PA catheter in a
patientwithPHisassociatedwithincreasedriskofPArupture.