Ebook Practical cardiovascular hemodynamics: Part 2

(BQ) Part 2 book Practical cardiovascular hemodynamics has contents: Assessment of mixed valvular disorders, pulmonary hypertension, hemodynamics in shock and fluid responsiveness, hemodynamics of left ventricular support devices and left ventricular pressure volume loop in various cardiac conditions,... and other contents.

XIII

Tamponade

In tamponade, intrapericardial pressure usually increases to ~10 to 25 mmHgand compresses the cardiac chambers until the pressure inside these chambersequalizes with the intrapericardial pressure (Figure XIII.1).1-5 This leads toequalization of diastolic pressures of the 4 cardiac chambers Because the right-sided chambers have thin walls, they tend to collapse when intrapericardialpressure is equal to or larger than their intracavitary pressure

Pressure-volume curve of the pericardium showing the intrapericardial pressure in rapidly and slowly developing effusions

or cardiac dilatation In acute conditions, the pericardium cannot

stretch, and its pressure rises markedly with small volume changes.

This explains how tamponade may develop with small acute effusion and how the pericardium may be stretched in case of acute

RV dilatation leading to a “functional” CP Once the pericardial

pressure exceeds a stretch limit (bar), it increases exponentially

with any change in volume Even when intrapericardial pressure is lower than right-sided pressure, the RV or RA transmural pressure (RA pressure or RV pressure minus intrapericardial pressure) is reduced, which impairs RV outward expansion and filling; in addition, at this point, pericardial pressure is at a steep slope, and there is at least a threatened tamponade Although fluid

administration may initially increase RV pressure and RV transmural pressure, intracardiac volume can stretch the pericardium and further increase intrapericardial pressure even if intrapericardial volume is unchanged; this explains how fluid administration in euvolemic or hypervolemic patients may be harmful.

This graph also shows that patients with high intrapericardial pressure resulting from CP or severe RV dilatation stretching the pericardium may have LVEDP >20 mmHg, yet the transmural LV pressure is almost nil and the LV volume cannot expand These patients have low LV volume yet increased pulmonary capillary pressure The amount of fluid in the pulmonary veins is modest, and thus, the lungs are almost always clear despite sometimes severe

dyspnea Modified from Spodick DH Acute cardiac tamponade N

Engl J Med 2003; 349: 684–690.

The equalization of diastolic pressures is similar to what is observed in CP

As opposed to CP however, the respiratory changes of intrathoracic pressure aretransmitted to the cardiac chambers.1,2 This explains why RA pressure decreasesduring inspiration and thus venous flow from the SVC to the RA increasesduring inspiration (absence of the Kussmaul’s sign) Left-sided flow does notincrease because pulmonary veins and LV are both exposed to the negative

and explains the reduction of systolic arterial pressure by more than 10 mmHg

During inspiration, the negative pressure is transmitted to PV and SVC and to the intracardiac chambers (this is different from constriction) This increases flow between both IVC and SVC on the one hand and the RA then RV on the other hand, which pushes the septum to the left and reduces LV filling from LA and PV X descent is deep especially during inspiration, but Y descent is flat because of impeded RA-to-RV flow throughout all diastole,

including early diastole.

E: mitral inflow Doppler wave; PV: pulmonary vein; S:

systolic flow wave of IVC, SVC, and PV on Doppler, corresponds

to X descent; D: diastolic flow wave of IVC, SVC, and PV on Doppler, corresponds to Y descent.

Although ventricular interdependence is present in both CP andtamponade, a different mechanism is incriminated in each case: duringinspiration, RV pushes LV in tamponade, whereas RV is sucked by LV in CP

As opposed to CP, LV flow is reduced in tamponade because of RVcompression, not because of a lack of transmission of the negative intrathoracicpressure to LV In addition, because of the uniform pericardial fluid, theconstraint is more uniform across both LV and RV in case of tamponade As aresult of this different mechanism, ventricular interdependence is moreprominent in tamponade and leads to pulsus paradoxus, which is only present inone third of cases of CP

Furthermore, as opposed to CP where the heart briefly expands in earlydiastole before getting constrained, the heart is compressed throughout alldiastole in tamponade, including early diastole Thus, RA-to-RV flow isimpeded throughout all diastole, including early diastole, and there is no deep Y

on the RA tracing and no diastolic dip on the RV tracing There is a deep X inearly systole as RV annulus moves down and stretches out the compressed RA

Cardiac tamponade is defined as a pericardial effusion compressing the cardiacchambers and leading to hemodynamic compromise This compromise manifestsclinically as any or all of the following: elevated JVP, systemic blood pressurealteration with pulsus paradoxus early on, tachycardia, andtachypnea/dyspnea/orthopnea with clear lungs (PCWP is increased, but theintracardiac and pulmonary venous volume is low, hence the lack of pulmonaryedema)

On invasive hemodynamics, the following 3 findings are characteristic oftamponade:

1-On RA and SVC tracings: elevated mean pressure with a deep X descent(mainly during inspiration) and a flat Y descent (Figure XIII.3)

2-Elevation and equalization of diastolic pressures of the 4 cardiac chambers andequalization of PA diastolic pressure with RV end-diastolic pressure(RVEDP), similarly to CP:

CVP = mean RA pressure = RVEDP = PA diastolic pressure = mean PCWP

= LVEDP

(normally, RVEDP < PA diastolic pressure = PCWP = LVEDP)

Note the deep X and the blunted Y descents in a patient with tamponade.

3-Although the systolic aortic pressure is initially normal or even elevated as a

as well However, an increase in systolic pressure up to 150 to 210 mmHg anddiastolic blood pressure up to 100 to 130 mmHg is frequent in tamponade andoccured in up to one third of tamponade cases in one report, particularly inpatients with a history of hypertension who are sensitive to the catecholaminesurge.6,7 Hypertension does not mean preserved cardiac output; in fact, cardiacoutput is as low as in cases of normal arterial pressure, but increased peripheralvascular resistance preserves blood pressure (pressure = flow × resistance).Patients with tamponade and hypertension had a reduction in blood pressure,reduction in SVR, and increase in cardiac output following pericardiocentesis.

Typical arterial pressure in tamponade Tachycardia at 120 bpm.

The arterial pressure is reduced, the tracing is narrow based, and the pulse pressure is reduced The systolic pressure and the pulse

pressure decline with inspiration (blue arrow), and the tracing almost collapses at end inspiration (vertical arrow).

Note: Besides respiratory variation of arterial pressure, pulsus paradoxusmanifests as exaggerated respiratory variation of RV and LV systolic pressures

In patients who are hypovolemic, compression of intracardiac chambers (ie,tamponade), particularly right-sided chambers, may occur at a lowerintrapericardial pressure of 6 to 12 mmHg In this case, there will be equalization

of intrapericardial pressure and RA pressure at 6 to 12 mmHg.3 Thus, tamponadewith pulsus paradoxus or hypotension occurs with a high-normal or mildlyincreased right-sided filling pressure and jugular venous pressure If it was notfor hypovolemia and the low right-sided filling pressure, this pericardial effusionwould not be hemodynamically significant Fluid administration may correct thepulsus paradoxus; however, excessive fluid administration may increase right-sided volume, which further stretches the already distended pericardium andelevates its pressure, leading to a full-blown tamponade picture.8-10 That is whyfluids are helpful in hypovolemic patients with tamponade but may harmeuvolemic or hypervolemic patients Thus, in order to increase the transmuralpressures of the cardiac chambers (ie, intracavitary pressure minus pericardialpressure) and allow the expansion of these cavities in patients with tamponade, it

is important to maintain a higher level of right- and left-sided pressure withoutexcessive volume resuscitation Ultimately, patients with low-pressuretamponade require pericardiocentesis because even at 6 to 12 mmHg, theintrapericardial pressure is prone to rising with any change in pericardial volume(Figure XIII.1)

OF ABSENT PULSUS PARADOXUS

While it is easy to induce tamponade in case of hypovolemia, it is harder toinduce tamponade physiology in patients with severely increased right-sided orleft-sided pressure.3 In fact, it is harder for the pericardial pressure to compressboth ventricles, and tamponade develops when pericardial pressure equilibrateswith the lower pressure ventricle Moreover, the respiratory variation in venousreturn does not significantly change the cardiac output and the systolic pressure

of the failing ventricle (flat portion of the Frank-Starling curve) The latter 2conditions, that is, the lack of biventricular compression and interdependenceand the lack of respiratory variation in ventricular output explain the lack ofpulsus paradoxus This situation may be seen in patients with end-stage renaldisease who develop tamponade and who have an underlying left heart failure

In addition, pulsus paradoxus may not be seen in cases of (1) ASD, as theincrease in right-sided flow during inspiration is balanced by an increase inright-to-left shunt or reduction in left-to-right shunt, leading to less ventricularinterdependence; (2) local tamponade (eg, compression of LA or RA by a clotafter cardiac surgery, leading to a localized increase in pressure); (3) AI, wherethe diastolic regurgitant flow damps down respiratory fluctuations of flow Inaddition, pulsus paradoxus is difficult to detect in case of an irregular rhythmsuch as atrial fibrillation

This occurs when only one cardiac chamber, a pulmonary vein, or the SVC orIVC is compressed by a loculated effusion Because there is no uniformcompression of the 4 chambers, there is no equalization of diastolic pressuresand no ventricular interdependence/pulsus paradoxus There is increasedpressure of the compressed chamber, for example, increased RA pressure orPCWP, and hypotension, which in the right context suggest tamponade (eg, aftercardiac surgery) However, loculation can also produce classic tamponade,presumably by tightening the uninvolved pericardium

Some patients have pericardial effusion with the hemodynamics of tamponade,that is, pulsus paradoxus and elevated and equalized right- and left-sided fillingpressure However, upon drainage of the pericardial fluid, the hemodynamiccompromise does not fully resolve, RV and LV diastolic pressures remainequalized, and RA pressure remains elevated (RA pressure declines by less than50%) A flat RA Y descent (tamponade) may become deep (constriction) afterdrainage of the pericardial fluid Thus, effusive-constrictive pericarditis is aneffusion that occurs on a background of CP In patients with noncompliantpericardium, tamponade can occur with relatively little accumulation of fluid.Effusive-constrictive pericarditis may be seen with CP of any origin, particularlythe idiopathic or radiation-induced CP, and is usually seen early in the diseasecourse In fact, up to 24% of constrictive pericarditis cases and 7% of tamponadecases have an effusive-constrictive pathophysiology.11,12 When idiopathic,effusive-constrictive pericarditis is often an inflammatory CP that is transient in50% of the cases and resolves with anti-inflammatory therapy; this is not thecase of radiation-induced effusive-constrictive pericarditis.11

XIII.7 COPD AND OTHER CAUSES OF PULSUS PARADOXUS AND RV-LV RESPIRATORY DISCORDANCE

Because of large intrathoracic pressure swings, COPD, asthma, obesity, orpositive pressure ventilation may lead to discordance in RV and LV filling andpulsus paradoxus (see Sections XII.5-7)13

1 LeWinter MM Pericardial diseases In: Libby P, Bonow RO, Mann DL, Zipes DP, eds.

Braunwald’s Heart Disease 8th ed 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:

XIV

Pulmonary hypertension

Pulmonary hypertension (PH) is defined as a mean PA pressure ≥25 mmHg atrest.1,2 An increase in mean PA pressure to >30 mmHg with exercise used to beincluded in the definition but is less specific, particularly in patients older than

50 years of age who may normally have an increase in mean PA pressure to 45mmHg with exercise The classification of PH severity is shown in Table XIV.1

up to 5 mmHg higher than PCWP

-PVR is <3 Wood units (the normal PVR being <2 Wood units), and thetranspulmonary gradient, that is, mean PA pressure minus PCWP, is <12mmHg (some investigators use a cutoff of 20 mmHg).1

-Left heart failure is the most common cause of PH Heart failure may beobvious in some patients but may be occult in others, especially whenisolated LV diastolic dysfunction is present.4 Furthermore, with chronicvenous PH, pulmonary arteries may undergo reactive changes, and PHmay become a mixed venous and arterial PH, in which case PCWP iselevated but diastolic PA pressure is >5 mmHg higher than PCWP andPVR is >3 Wood units.5,6 Pulmonary hypertension with a precapillarycomponent is seen in 20% to 35% of patients with advanced left HF.6-8This situation may also be seen in patients with mixed disorders, such asleft HF and COPD The active PH component fully resolves aftertreatment of HF but may take weeks to months to resolve.3

-Resting PCWP may be normal despite LV failure, especially in patientsappropriately treated with diuretics Exercise testing, volume loading, andpulmonary vasodilator challenge are appropriate strategies that increasePCWP in case of occult LV dysfunction and thus unveil the diagnosis ofpostcapillary PH Patients with PH and normal LVEF who are suspected

of having diastolic left heart disease–associated PH or mixedpostcapillary PH and precapillary PH are approached as in Figure XIV.1

normal EF; 83% of patients in this study had PH, the median PA systolicpressure being 48 mmHg.10 Interestingly, PA pressure was out ofproportion to what would be expected from the rise in PCWP For thesame PCWP, patients with heart failure with normal EF had a muchhigher PA pressure than patients with hypertension and no heart failure.Thus, in addition to the postcapillary component, a precapillarypulmonary arterial hypertension frequently coexists or develops duringthe course of heart failure with normal EF.

2-Precapillary PH

Precapillary PH is characterized by PCWP ≤15 mmHg (except in mixed PH),PVR ≥3 Wood units, and a transpulmonary gradient >12 mmHg.1,2,11However, in cases of precapillary PH associated with severe RV failure,pericardial distension and functional pericardial constriction may occurleading to ventricular interdependence and equalization of RV and LVend-diastolic pressures, with a subsequent increase in LV end-diastolicpressure and PCWP to 15 to 20 mmHg.12 This case may be confused withpost-capillary PH associated with a secondary precapillary component Asopposed to postcapillary PH, the increase in PCWP in this case is the resultrather than the cause of PH The presence of signs of LV diastolicdysfunction on echocardiography supports the diagnosis of left heartdisease–associated PH, whereas a significant increase in PVR >7 Woodunits and severe RV dilatation support the diagnosis of precapillary PH

Diagnostic approach to distinguish between PAH and PH related to diastolic left heart disease *PVR <3 correlates with a

transpulmonary gradient (mean PA pressure − PCWP) <20 mmHg and a diastolic PA pressure within 5 mmHg of PCWP Wood unit is

because it reduces afterload and may actually reduce PCWP DHF, diastolic heart failure; LAE, LA enlargement Adapted with

In congenital heart disease with a large left-to-right shunt (eg, VSD, PDA,

or less often ASD), PA pressure initially increases as a result of theincrease in right-sided flow, PVR being low at this stage (pressure ~ flow

× resistance, an increase in flow leads to an increase in pressure); this

“dynamic” PH resolves with shunt closure Over time, the increasedpulmonary flow induces progressive pulmonary vascular disease andsevere increase in PVR to a point that PVR approaches SVR, PA pressureapproaches systemic pressure, and the shunt reverses and becomesbidirectional or right to left This is Eisenmenger syndrome and, except inASD, is usually established in infancy

Pulmonary veno-occlusive disease is characterized by primary venularabnormalities similar to the arteriolar abnormalities seen in idiopathic PAHand may be idiopathic or associated with scleroderma Similar to PAH,true wedging is difficult in this disease, and if successful, it creates acolumn of stagnant blood between the catheter and the LA; thus, the trulywedged PCWP approximates LA pressure, albeit damped through thevenular obstruction, and is normal in value The pulmonary capillarypressure is increased, but not the wedged PA pressure

2 Pulmonary hypertension secondary to thromboembolic disease

3 Pulmonary hypertension secondary to lung disease: mild PH is common inpatients with COPD, but severe PH is very unusual In fact, moderate andsevere 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 lungdisease that obliterates the pulmonary capillaries, sarcoidosis, or obesity-hypoventilation syndrome

HYPERTENSION

1 In case of chronic severe PH, the PA pressure number may start declining intothe mild range because of the development of severe RV failure that is unable

to generate high PA pressure Pulmonary vascular resistance, on the otherhand, remains severely elevated

2 In case of acute PH (eg, pulmonary embolism), the RV is not able to generate

a systolic PA pressure higher than 45 to 50 mmHg A systolic PA pressurehigher than 40 mmHg implies significant PH in case of acute pulmonaryembolism.11 A systolic PA pressure higher than 50 mmHg hints to a subacute

or chronic process

In both cases, the PA pressure number underestimates the true severity ofthe pulmonary vascular abnormality The presence of severe RV dysfunction, aseverely elevated RA pressure, or a severely elevated PVR >6 to 7 Wood units isdiagnostic of severe PH In addition, a pulsus alternans on RV or PA tracing(similar to the aortic pulsus alternans) or a narrow PA pulse pressure (eg, 30/23)

is diagnostic of severe RV failure In fact, in patients with severe PH that isevidenced by elevated PVR and RV failure, a high systolic PA pressure predictsrecovery of RV function with PH therapies or left heart treatment and betteroutcomes than patients with lower systolic PA pressure; a higher systolic PApressure corresponds to a better RV function.15,16

PULMONARY HYPERTENSION

Pulmonary hypertension is often initially diagnosed by echocardiography.Echocardiography estimates PA pressure and suggests a left-sided etiology Inaddition to valvular function and LV systolic function, echocardiographyassesses LV filling pressures, LV diastolic function, and LA size.Catheterization is needed to confirm the diagnosis and the etiology of PHparticularly in cases of moderate-to-severe PH without a clear left heart orthromboembolic cause The goals of catheterization are the following:

1 Confirm the diagnosis of PH The spectral Doppler profile of TR is too weak

or insufficient to measure the PA pressure in approximately 25% to 55% ofpatients referred for PA pressure evaluation.17 The echocardiographicdiagnosis of PH is falsely positive in up to 50% of patients, and the PApressure value differs by >10 mmHg with the catheterization value in 50% ofpatients Echocardiography may under- or overestimate PA pressure invarious causes of PH.17,18

2 Assess PCWP to determine if PH is secondary to left HF The assessment ofPCWP may be difficult in patients with severe PH.19,20 A hybrid PCWP-PApressure tracing may be obtained and lead to overestimation of the true PCWP(Figure XIV.2) On the other hand, the true PCWP may be flattened withoutdistinct waves, as the retrograde transmission of LA pressure through thepulmonary vasculature is damped Moreover, wedging a PA catheter in apatient with PH is associated with increased risk of PA rupture

to wedging issues, damping of the pressure transmission from LA to the wedged

PA, the use of the digitally derived mean PCWP rather than the expiratoryPCWP, but also to the fact that LVEDP is larger than PCWP in patients withcompensated LV dysfunction.21

Patients with normal LVEDP may still have occult HF If suspectedclinically, give a volume load or perform exercise testing and see if PCWP orLVEDP increases, unveiling HF as the cause of PH

3 Assess for left-to-right shunt (oximetry screen of SVC and PA)

4 Perform acute vasoreactivity testing if PAH is suspected Vasodilatorchallenge should not be performed in case of left HF, as it may increasepulmonary blood flow and thus PCWP leading to pulmonary edema It shouldnot be performed in case of PH secondary to lung disease, as vasodilatorsworsen V/Q mismatch and hypoxemia Only 10% of patients with PAH have

a positive response The rationale for vasodilator testing is threefold: (1)positive responders to vasodilator testing may respond to chronic oral calciumchannel blocker therapy;22 (2) positive responders have a better long-termprognosis; (3) assess the hemodynamic tolerance to vasodilator therapy, that

is, ensure that PCWP does not increase and CO and systemic pressure do notdecrease with vasodilators Nonresponders still respond well to the chronicadministration of potent pulmonary vasodilators (prostacyclin, bosentan, andsildenafil)

An acute response to vasodilator testing is defined by the ACC andpulmonary societies as a drop of mean PA pressure by ≥10 mmHg to a value

<40 mmHg without a decrease in cardiac output Other investigators havedefined a positive response as a decrease in PA pressure and PVR by ≥20%.19Some patients have a decrease in PVR and an increase in CO, in a way that PApressure (~CO × PVR) remains unchanged Thus, the sole reliance on PApressure to assess vasoreactivity has a limited sensitivity, yet it more specificallypredicts a response to oral vasodilators During testing, it is also important toassess (1) CO (CO generally increases with vasodilator therapy, except in severe

RV failure with no contractile reserve), (2) PCWP (an increase in PCWP unveils

an overlooked left heart failure), (3) O2 saturation (may drop in case of lungdisease), (4) RA pressure (may increase in case of severe RV failure that getsoverwhelmed as vasodilators increase venous return), and (5) systemic bloodpressure

Additional note: Vasoreactivity testing is useful in 2 more situations.Patients with left-to-right shunt (ASD, VSD, and PDA) who have PH with a PApressure >2/3 systemic pressure or PVR >2/3 SVR or >6 Wood units need tohave vasoreactivity testing before correction of the shunt to ensure that PH isreversible, otherwise closing the shunt may be harmful Patients with advancedleft HF who are considered for cardiac transplantation and who have PH withhigh PVR require vasoreactivity testing to assess the reversibility of PH and theiroperability In this case, however, the use of prostanoids may increase PCWPand is poorly tolerated Nitroprusside may be the vasodilator of choice, as itreduces PVR in case of reactive PH and reduces LV afterload, which preventsthe increase in PCWP Milrinone may also be used Nitroprusside will have this

hypertension with nitroprusside is useful in defining a high risk group J Am Coll

Cardiol 1992;19:48–54.

9 Moraes DL, Colucci WS, Givertz MM Secondary pulmonary hypertension in chronic heart failure: the role of the endothelium in pathophysiology and management.

Circulation 2000;102:1718–1723.

10 Lam CS, Roger VL, Rodeheffer RJ, Borlaug BA, Enders FT, Redfield MM Pulmonary hypertension in heart failure with preserved ejection fraction: a community-based study.

pulmonary hypertension in patients with advanced lung disease Am J Resp Crit Care

XV

Hemodynamics in shock and fluid responsiveness

Shock is defined as hypotension along with evidence of low tissue perfusion

(oliguria, cold extremities) Hypotension is usually defined as a mean systemicpressure <60 to 65 mmHg or a systolic pressure <90 mmHg However, systemicpressure may be higher in shock patients with chronic hypertension; a decline insystolic pressure of >40 mmHg is commonly used to define hypotension in thepreviously hypertensive patients There are 4 mechanisms of shock: (1)hypovolemia; (2) low cardiac output as in left or right cardiogenic shock;(3) low SVR shock or distributive shock (septic shock, anaphylactic shock,excessive amount of sedatives and vasodilators); and (4) obstructive shock,where LV filling is prevented by a right-sided obstruction, such as pulmonaryembolism or tamponade or isolated RV shock

Right heart catheterization establishes the mechanism of the shock byassessing the 3 determinants of shock (Table XV.1):

Some shock states may be mixed In septic shock, one may have ahypovolemic component and a cardiogenic component with reduced myocardialcontractility and, at some point, elevated PCWP, the so-called septiccardiomyopathy Furthermore, in septic shock, cardiac output needs to be highenough to match the increase in tissue demands and to compensate for themaldistribution of flow A cardiac output that is “normal” in absolute values may

be inappropriate in the context of septic shock; this is suggested when the tissueperfusion and SvO2 are low (SvO2 <65%) despite normalization of the systemicpressure or when cardiac filling pressures are elevated Both an adequate mean

arterial pressure and an adequate cardiac output are required for end-organ

perfusion

In the SHOCK trial of cardiogenic shock secondary to acute MI, 20% ofpatients had reduced CO and elevated PCWP but relatively low SVR (800-1100); this was related to a concomitant infection or to a systemic inflammatoryresponse associated with nitric oxide release in cardiogenic shock.1 Incardiogenic shock, SVR increases to maintain systemic pressure; SVR that is

“normal” in value in the absence of vasodilator therapy may be relatively low inthe context of cardiogenic shock and implies a mixed shock

A shock state with a wide pulse pressure is characteristic of septic shock,

AI, or any vasodilatory condition (cirrhosis, vasodilatory drug excess)

Fluid responsiveness addresses the improvement of CO with fluidadministration As shown under Sections I.4 and V, PCWP >12 to 15 mmHg orCVP >8 to 12 mmHg in chronic systolic HF predicts the lack of fluidresponsiveness; in diastolic HF or acute systolic HF, PCWP >18 to 20 mmHgpredicts the lack of fluid responsiveness In fact, CO improves with diuresis inthese cases However, although CVP and PCWP are helpful in establishing themechanism of a shock, they only weakly predict fluid responsiveness,particularly when they are not severely reduced or severely elevated (eg, CVPbetween 5 and 12 mmHg), or when the patient does not have an underlyingmyocardial systolic dysfunction (Figure XV.1) In fact, a high CVP does not ruleout volume responsiveness in a critically ill patient who has no prior history ofchronic systolic heart failure (eg, sepsis, trauma), especially if atrial, venous orventricular compliance is impaired, as is seen sometimes with hypoxia (normalsystolic function curve in Figure XV.1) Thus, some patients with normal or highCVP are fluid responsive, whereas others are not Note also the limitations ofPCWP in critically ill patients, discussed on pages 17-19 Fluid responsiveness is

better assessed using the dynamic response of stroke volume and systemic

arterial waveform to positive pressure ventilation in mechanically ventilated

patients or to passive leg raising in both mechanically ventilated or

spontaneously breathing patients

Relationship between stroke volume (SV) and CVP The true

Frank-Starling curve is the relationship between stroke volume and the preload measured as volume rather than pressure Preload

volume and CVP do not linearly correlate, and their relationship

mmHg (A to B), as the ventricle is already on a flat portion of the Frank-Starling curve In patients with normal systolic function, stroke volume continues to increase even when CVP rises from 10

to 15 and 20 mmHg, as the ventricle has a steeper Frank-Starling curve (A’ to B’ to C’ to D’); this is more marked if ventricular or atrial compliance is impaired.

In patients who are mechanically ventilated, the positive intrathoracicpressure reduces cardiac output in patients who are fluid-responsive, andanalysis of the respiratory change in stroke volume or analysis of systemicarterial waveform from an arterial line is very helpful in addressing fluidresponsiveness.2 If the ventricles are on the steep portion of the Frank-Starlingcurve, an increase in venous return increases stroke volume; thus, the respiratorychanges in venous return lead to respiratory fluctuations of the stroke volume Ifthe stroke volume varies by >20% with respiration or if the systolic pressure orthe pulse pressure decreases by >13% between an end-expiratory hold and thepositive ventilation, the RV and the LV are sensitive to volume changes and aretherefore volume responsive LVOT or aortic valve velocity (VTI) onechocardiography may be used as surrogate of stroke volume;3,4 in fact, strokevolume = (LVOT VTI × LVOT area) or (aortic VTI × AVA)

Although the respiratory fluctuation in stroke volume and systolic arterialand pulse pressure may reflect hypovolemia (pulsus paradoxus), this is notsensitive or specific enough in patients who are spontaneously breathing.5,6 Inthe latter patients, rely on the clinical evidence of hypervolemia (peripheraledema), assess the change in cardiac output after passive leg raising or after asmall volume load (500 mL) Passive leg raising–induced change in strokevolume, cardiac output, or pulse pressure reliably predicts volumeresponsiveness, whatever the breathing conditions.7-9 An increase in CO orstroke volume of >10% or a change in pulse pressure of ≥9% with passive legraising suggests volume responsiveness; if a Swan catheter is not in place, thechange in stroke volume or CO may be assessed using echocardiography Adecrease in CVP during inspiration may also predict fluid responsiveness inpatients who are breathing spontaneously but not deeply (in severe RV failure,CVP increases with inspiration or remains unchanged rather than decreases).10,11

As described in the prior paragraphs, echocardiography may be used toassess volume responsiveness An increase in CO >10% with passive leg raisingbut also an IVC diameter <1.2 cm predict volume responsiveness in

spontaneously breathing or mechanically ventilated patients.9,12 Furthermore,IVC collapsibility >12% or a change in CO or aortic valve VTI >12% betweeninspiration and expiration predicts volume responsiveness in mechanicallyventilated patients.3,13,14 Patients who are mechanically ventilated tend to have alarger IVC diameter and reduced IVC collapsibility because of the positiveintrathoracic pressure that impedes venous return; that’s why 12% collapsibility,

as opposed to 50% in spontaneously breathing patients, is considered a sign ofvolume responsiveness.13 In any patient, whether spontaneously breathing ormechanically ventilated, a hyperdynamic LV with systolic cavity collapse or ahyperdynamic LV with intracavitary LV pressure gradient and possibly SAM ofthe mitral valve implies severe hypovolemia, particularly hypovolemiaassociated with excessive use of inotropes

In mechanically ventilated patients who do not have an arterial line, thepulse oximetry tracing may be used to predict volume responsiveness Theplethysmographic waveform of pulse oximeters is a qualitative indicator ofblood volume changes in the fingertip One study suggested a correlationbetween pulse waveform variation provided by pulse oximeters and systolicpressure variation; thus, pulse waveform variation predicts volumeresponsiveness in mechanically ventilated patients.21 Similarly to thefluctuations of arterial pressure, the respiratory fluctuations of the pulsewaveform are less useful in patients breathing spontaneously In addition, theyare not useful in hypotensive patients whose finger perfusion is reduced

11 Heenen S, De Backer D, Vincent JL How can the response to volume expansion in

patients with spontaneous respiratory movements be predicted? Crit Care.

2006;10(4):R102.

12 Jue J, Chung W, Schiller NB, et al Does inferior vena cava size predict right atrial

pressure in patients receiving mechanical ventilation? J Am Soc Echocardiogr.

1992;5:613–618.

13 Barbier C, Loubieres Y, Schmit C, et al Respiratory changes in inferior vena cava

diameter are helpful in predicting fluid responsiveness in ventilated septic patients.

XVI