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ReviewUsing heartlung interactions to assess fluid responsivenessduring mechanical ventilationFrdric Michard and Jean-Louis Teboul

Universit Paris XI, Kremlin Bictre, France

Abstract

According to the FrankStarling relationship, a patient is a responder to volume expansiononly if both ventricles are preload dependent. Mechanical ventilation induces cyclic changesin left ventricular (LV) stroke volume, which are mainly related to the expiratory decrease inLV preload due to the inspiratory decrease in right ventricular (RV) filling and ejection. In thepresent review, we detail the mechanisms by which mechanical ventilation should result ingreater cyclic changes in LV stroke volume when both ventricles are preload dependent.We also address recent clinical data demonstrating that respiratory changes in arterial pulse(or systolic) pressure and in Doppler aortic velocity (as surrogates of respiratory changes inLV stroke volume) can be used to detect biventricular preload dependence, and hence fluidresponsiveness in critically ill patients.

Keywords: acute circulatory failure, arterial pressure, fluid responsiveness, left ventricular stroke volume,mechanical ventilation, pleural pressure, preload, pulse pressure

Received: 21 July 2000Accepted: 24 July 2000Published: 1 September 2000

Crit Care 2000, 4:282289

Current Science Ltd (Print ISSN 1364-8535; Online ISSN 1466-609X)

LV = left ventricular; PEEP = positive end-expiratory pressure; PP = change in pulse pressure; RV = right ventricular; SPV = systolic pressure vari-ation; ZEEP = zero end-expiratory pressure.

http://ccforum.com/content/4/5/282

IntroductionVolume expansion is a frequently used therapy in criticallyill patients with acute circulatory failure. The expected

haemodynamic benefit of volume expansion is an increasein LV stroke volume, and hence in cardiac output. The rela-tionship described by Frank and Starling between preloadand stroke volume is not linear, but rather is curvilinear(Fig. 1). Thus, an increase in preload will induce a signifi-cant increase in stroke volume only if the ventricle operateson the ascending portion of the relationship (condition ofventricular preload dependence). In contrast, if the ventricleoperates on the flat portion of the curve, a similar increase

in preload will not induce any significant change in strokevolume (condition of preload independence). Therefore, apatient is a responder to volume expansion only if both

ventricles operate on the ascending portion of theFrankStarling curve (biventricular preload dependence).In contrast, if one of the ventricle or both ventricles operateon the flat portion of the curves, then the patient is a non-responder (ie his/her cardiac output will not increase sig-nificantly in response to volume expansion).

In normal physiological conditions, both ventricles operateon the ascending portion of the FrankStarling curve [1].


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This mechanism provides a functional reserve (preloadreserve) to the heart in situations of acute stress [1]. Innormal individuals, increase in preload was reported [2] toresult in a significant change in stroke volume. In contrast,analysis of the literature indicates that, in patients with

acute circulatory failure, the mean rate of responders tovolume expansion is only around 50% (Table 1). Thisfinding emphasizes the need for predictive factors ofvolume expansion efficacy in order to select patients whocould benefit from volume expansion and to avoid ineffec-tive or even deleterious fluid therapy (worsening of pul-monary oedema, haemodilution, etc) in nonresponderpatients, in whom inotropic and/or vasopressor supportshould preferentially be used.

How to predict fluid responsiveness incritically ill patients?In many patients with acute circulatory failure, a positive

response to fluid therapy can be observed despite thelack of clinical and biological indicators of hypovolaemia.Therefore, bedside indicators of RV or LV preload areusually used when deciding whether to give fluid.

A recent postal survey performed in Germany [3] showedthat central venous pressure and pulmonary artery occlu-sion pressure are used, respectively, by 93 and 58% ofintensive care unit physicians in the decision-makingprocess regarding volume expansion. However, many clini-cal studies have emphasized the poor value of right atrialpressure [47] and pulmonary artery occlusion pressure

[4,5,79] in predicting volume expansion efficacy. Indeed,in most studies, the mean baseline value of right atrialpressure and of pulmonary artery occlusion pressure wasnot significantly different between responders and non-responders to volume expansion [48,10] (Table 2). Evenwhen a significant difference was reported [9], a markedoverlap of individual baseline values was observed, so thatno threshold value could help to discriminate responderand nonresponder patients. Other bedside indicators ofpreload, such as the RV end-diastolic volume (evaluatedby thermodilution) and the LV end-diastolic area (mea-sured by echocardiography) have also been tested as pre-dictors of fluid responsiveness. Unfortunately, these

parameters were not found to be able to differentiateaccurately between responder and nonresponder patientsbefore fluid infusion was given (Table 2) [5,6,8,9,11].

All of these findings may be explained as follows. The rightatrial and pulmonary artery occlusion pressures do notalways reflect transmural pressures in patients with exter-nal or intrinsic positive end-expiratory pressure (PEEP)[12,13]. Pulmonary artery occlusion pressure is not alwaysa good indicator of LV preload, in particular in patientswith a decreased LV compliance [14]. Measurement of RVend-diastolic volume by thermodilution is influenced by tri-cuspid regurgitation [15], which is frequently encountered

in critically ill patients with pulmonary hypertension. LVend-diastolic area is not always a good indicator of the LVend-diastolic volume, and hence of the LV preload [16].RV dilatation may offset any beneficial haemodynamiceffect of volume expansion, even in case of a low LVpreload [17]. Finally, the preload-induced changes instroke volume depend also on contractility and afterload.For example, a given value of preload can be associatedwith preload dependence in normal hearts or with preloadindependence in failing hearts (Fig. 2). Therefore, assess-ment of preload is of poor value in predicting fluid respon-siveness in critically ill patients.

Table 1

Number and rate of responder (R) and nonresponder patients

(NR) to volume expansion in critically ill patients

Reference R/NR (% R) Criteria for response

[4] 20/8 (71) Increase in SV >0%

[5] 26/15 (63) Increase in CI >0%

[10] 26/29 (40) Increase in CI >20%

[11] 20/16 (56) Increase in SV >10%

[8] 21/14 (60) Increase in SV >15%

[9] 16/24 (40) Increase in SV >20%

[7] 16/24 (40) Increase in CI >15%

CI, cardiac index; SV, stroke volume.

Figure 1

Schematic representation of FrankStarling relationship betweenventricular preload and stroke volume. A given change in preloadinduces a larger change in stroke volume when the ventricle operateson the ascending portion of the relationship (A, condition of preloaddependence) than when it operates on the flat portion of the curve (B,condition of preload independence).


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Critical Care Vol 4 No 5 Michard and Teboul

Respiratory changes in right atrial pressure inspontaneously breathing patientsIn patients with significant spontaneous breathing activity,

the respiratory changes in right atrial pressure have beenproposed to differentiate patients whose hearts are func-tioning on the flat part of the cardiac function curve fromthose who still have volume reserves and are on theascending part of the curve [18,19]. Patients who had nofall in the right atrial pressure with an inspiratory effort thatwas sufficient to lower the pulmonary artery occlusionpressure by 2 mmHg were proposed to be on the flat partof their cardiac function curve [18]. Indeed, in 13 out ofthe 14 patients in whom no fall in right atrial pressure wasobserved, cardiac output did not increase with volumechallenges. In contrast, in 16 out of the 19 patients inwhom the right atrial pressure decreased by more than

1 mmHg during inspiration, cardiac output increased bymore than 250 ml/min in response to volume therapy [18].Unfortunately, many patients in the intensive care unit donot have adequate inspiratory effort, and therefore do nothave sufficient fall in pleural pressure to use this test topredict fluid responsiveness [19].

Respiratory changes in LV stroke volume inmechanically ventilated patientsIn mechanically ventilated patients, the magnitude of therespiratory changes in LV stroke volume can be used toassess fluid responsiveness. Intermittent positive-pressure

ventilation induces cyclic changes in the loading condi-tions of right and left ventricles (Fig. 3). Mechanical insuf-flation decreases preload and increases afterload of theright ventricle [20,21,22]. The RV preload reduction is dueto the decrease in the venous return pressure gradient

that is related to the inspiratory increase in pleural pres-sure [20]. The increase in RV afterload is related to theinspiratory increase in transpulmonary pressure (alveolarminus pleural pressure) [22]. The reduction in RV preloadand the increase in RV afterload both lead to a decreasein RV stroke volume, which is therefore at its minimum atthe end of the inspiratory period [23]. The inspiratoryimpairment in venous return is assumed to be the mainmechanism of the inspiratory reduction in RV ejection[24]. The inspiratory reduction in RV ejection leads to adecrease in LV filling after a phase lag of two to threeheart beats because of the long blood pulmonary transittime [25]. Thus, the LV preload reduction may induce a

decrease in LV stroke volume, which is at its minimumduring the expiratory period [23].

Two other mechanisms may also occur: mechanical insuffla-tion may induce a squeezing of blood out of alveolarvessels, and thus transiently increase LV preload [26]; andthe inspiratory increase in pleural pressure may decrease LVafterload and thus facilitate LV ejection [27,28] (Fig. 3). Thefirst mechanism in hypervolaemic conditions and thesecond mechanism in case of LV systolic dysfunction mayinduce a slight increase in LV stroke volume during theinspiratory period. However, experimental data suggest that

Table 2

Mean values of right atrial pressure (RAP), pulmonary artery

occlusion pressure (PAOP) and right ventricular end-diastolic

volume index (RVEDVI) before volume expansion in responder

and nonresponder patients to volume expansion

Reference Responder Nonresponder P

RAP (mmHg)[4] 5 1 5 2 NS[5] 9 4 8 4 NS[6] 7 2 6 3 NS[7] 9 3 9 4 NS

PAOP (mmHg)[4] 8 1 7 2 NS[5] 10 4 10 3 NS[10] 16 6 15 5 NS[8] 10 4 12 3 NS[9] 12 2 16 3


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these two mechanisms are only minor determinants of the

respiratory changes in LV stroke volume, even in the casesof hypervolaemia [29,30] and LV dysfunction [29,31].

In summary, intermittent positive-pressure ventilationinduces cyclic changes in LV stroke volume (maximumduring the inspiratory period and minimum during the expi-ratory period), which are mainly related to the expiratorydecrease in LV preload due to the inspiratory decrease inRV filling and ejection (Fig. 3).

Interestingly, the cyclic changes in RV preload induced bymechanical ventilation should result in greater cyclicchanges in RV stroke volume when the right ventricle

operates on the steep rather than on the flat portion of theFrankStarling curve [17,32]. The cyclic changes in RVstroke volume, and hence in LV preload, should also resultin greater cyclic changes in LV stroke volume when theleft ventricle operates on the ascending portion of theFrankStarling curve [17,32]. Thus, the magnitude of therespiratory changes in LV stroke volume should be an indi-cator of biventricular preload dependence [33].

Respiratory changes in systolic pressure

Because LV stroke volume is a major determinant of sys-tolic arterial pressure, analysis of respiratory changes in

systolic pressure has been proposed to assess the respi-

ratory changes in LV stroke volume during mechanicalventilation. In 1983, Coyle et al [34] proposed that therespiratory changes in systolic pressure could be analyzedby calculating the difference between the maximal and theminimal value of systolic pressure over a single respiratorycycle (Fig. 4). This difference was called systolic pressurevariation (SPV) and was divided into two components(up and down). These two components are calculatedusing a reference systolic pressure, which is the systolicpressure measured during an end-expiratory pause.

up is the difference between the maximal value of sys-tolic pressure over a single respiratory cycle and the refer-

ence systolic pressure. It reflects the inspiratory increasein systolic pressure, which results either from increase inLV stroke volume related to the increase in LV preload(squeezing of blood out of alveolar vessels) or a decreasein LV afterload, or both; or an increase in extramural aorticpressure related to the rise in pleural pressure.

down is the difference between the reference systolicpressure and the minimal value of systolic pressure over asingle respiratory cycle. It reflects the expiratory decreasein LV preload and stroke volume related to the inspiratorydecrease in RV stroke volume (see above).


Figure 3

Haemodynamic effects of mechanical insufflation. The LV stroke volume is maximum at the end of the inspiratory period and minimum two to threeheart beats later (ie during the expiratory period). The cyclic changes in LV stroke volume are mainly related to the expiratory decrease in LVpreload due to the inspiratory decrease in RV filling and output.


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In mechanically ventilated dogs, Perel and coworkers[2931,3537] demonstrated the following. First, innormo- or hypovolaemic conditions, down is the maincomponent of SPV [3537]. Second, haemorrhage

increases SPV and down [3537]. Third, the amount ofblood loss is closely correlated with SPV and down [35].Fourth, volume expansion decreases SPV and down[3537]. Finally, LV dysfunction [29,31] and hyper-volaemia [29,30] increase up, but decrease down andSPV such that, in this setting, SPV is minimal and up isthe main component of SPV.

In mechanically ventilated patients, haemorrhage has alsobeen shown to increase SPV and down [38], whereasvolume expansion has been shown to decrease SPV anddown [38,39]. More interestingly, Coriat et al [39]reported a significant relationship between down before

fluid infusion and the increase in cardiac index in responseto volume expansion in patients after aortic surgery. There-fore, down can be considered as an indicator of fluidresponsiveness, because the higher down before volumeexpansion, the greater the increase in cardiac index inresponse to fluid infusion. This finding has been recentlyconfirmed by Tavernier et al [8] in patients with sepsis-induced hypotension. In that study, a down thresholdvalue of 5 mmHg allowed prediction of volume expansionefficacy (defined as an increase in stroke volume 15%),with positive and negative predictive values of 95 and93%, respectively. Also, the baseline value of down was

significantly correlated with the volume expansion-inducedincrease in stroke volume (r= 0.76).

However, the respiratory changes in systolic pressureresult from changes in transmural pressure (mainly related

to changes in LV stroke volume) and also from changes inextramural pressure (ie from changes in pleural pressure)[40]. Therefore, respiratory changes in systolic pressuremay be observed despite no variation in LV stroke volume.In this regard, Denault et al[41] recently demonstrated, inanaesthetized cardiac surgery patients, that changes insystolic pressure may reflect changes in airway pressureand pleural pressure better than they reflect concomitantchanges in LV haemodynamics.

Respiratory changes in pulse pressure

The pulse pressure (defined as the difference between thesystolic and the diastolic pressure) is directly proportion-

nal to LV stroke volume and inversely related to arterialcompliance [42]. The pulse pressure is not directly influ-enced by the cyclic changes in pleural pressure, becausethe increase in pleural pressure induced by mechanicalinsufflation affect both diastolic and systolic pressures. Inthis regard, the respiratory changes in LV stroke volumehave been shown to be reflected by changes in peripheralpulse pressure during the respiratory cycle [23]. There-fore, it was recently proposed that fluid responsivenessmay be assessed by calculating the respiratory changes inpulse pressure (PP) as follows:

(PPmax PPmin)

PP (%) = 100 (PPmax + PPmin)/2

where PPmax and PPmin are the maximal and minimalvalues of pulse pressure over a single respiratory cycle,respectively (Fig. 5).

In 40 patients with acute circulatory failure related tosepsis, Michard et al [7] demontrated the following. First,PP accurately predicted the haemodynamic effects ofvolume expansion; a threshold value of 13% allowed dis-crimination between responder (defined as patients whoexperienced an increase in cardiac index 15% in

response to volume expansion) and nonresponder patientswith a sensitivity and a specificity of 94 and 96%, respec-tively. Second, the baseline value of PP was closely corre-lated with the percentage increase in cardiac index inresponse to volume expansion; the higher PP was beforevolume expansion, the greater the increase in cardiac index(Fig. 6). Third, PP was a more reliable indicator of fluidresponsiveness than were the respiratory changes in sys-tolic pressure. Finally, the decrease in PP induced byvolume expansion was correlated with the increase incardiac index, such that changes in PP could be used toassess the haemodynamic effects of volume expansion.


Figure 4

Respiratory changes in systolic pressure in a mechanically ventilatedpatient. The difference between the maximal and minimal value ofsystolic pressure over a single respiratory cycle is called SPV (forSystolic Pressure Variation). The reference systolic pressure ismeasured during an end-expiratory pause (line of reference) and SPVis divided in two components: up and down. up is the differencebetween the maximal and the reference systolic pressure. down is thedifference between the reference and the minimal systolic pressure.Adapted with permission [33].


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In summary, calculation of PP may be of particular help inthe decision-making process regarding whether to institutevolume expansion. Indeed, if PP is low (13%), then a significant increase in cardiacindex in response to fluid infusion is very likely. However, thedecision regarding whether to institute volume expansionmust take into account the risk of fluid therapy (worsening ingas exchange), and a decrease in the mean airway pressure(ie a decrease in tidal volume or in PEEP) is an alternativetherapeutic approach in this instance.

Interestingly, the assessment of cardiac preload depen-dence is not only useful in predicting volume expansionefficacy, but also in predicting the haemodynamic effects

of any therapy that induces changes in cardiac preloadconditions. In this regard, PP has been shown to beuseful in monitoring the haemodynamic effects of PEEP inmechanically ventilated patients with acute lung injury.Indeed, the decrease in mean cardiac output induced byPEEP and the decrease in RV stroke volume induced bymechanical insufflation share the same mechanisms (iethe negative effects of increased pleural pressure on RVfilling and of increased transpulmonary pressure on RVafterload). Thus, the magnitude of the expiratory decreasein LV stroke volume would correlate with the PEEP-induced decrease in mean cardiac output.

In 14 mechanically ventilated patients with acute lunginjury [43] the following was demonstrated. First, PP onzero end-expiratory pressure (ZEEP) was closely corre-lated with the PEEP-induced decrease in cardiac index;the higher PP was on ZEEP, the greater the decrease incardiac index when PEEP was applied (Fig. 7). Also, the

increase in PP induced by PEEP was correlated with thedecrease in cardiac index, such that changes in PP fromZEEP to PEEP could be used to assess the haemody-namic effects of PEEP without the need for a pulmonaryartery catheter. Finally, when cardiac index decreased withPEEP, volume expansion induced an increase in cardiacindex that was proportional to PP before fluid infusion.

It is likely that analysis of the respiratory changes in LVstroke volume could also be useful to monitor the haemo-dynamic effects of ultrafiltration during dialysis or of anychange in ventilatory parameters.

LimitationsAnalysis of the respiratory changes in arterial pressure isnot possible in patients with cardiac arrythmias. Moreover,these parameters have been validated in sedated andmechanically ventilated patients. Therefore, whether therespiratory changes in LV stroke volume predict fluidresponsiveness in nonsedated and in spontaneouslybreathing patients remains to be evaluated.

As mentioned above, the respiratory changes in LV strokevolume might also result from a decrease in LV afterloadcaused by the inspiratory increase in pleural pressure


Figure 5

Respiratory changes in airway and arterial pressures in a mechanicallyventilated patient. The pulse pressure (systolic minus diastolicpressure) is maximal (PPmax) at the end of the inspiratory period andminimal (PPmin) three heart beats later (ie during the expiratoryperiod). The respiratory changes in pulse pressure (PP) arecalculated as the difference between PPmax and PPmin, divided bythe mean of the two values, and expressed as a percentage (see textfor details). Adapted with permission [33].

Figure 6

Relationship between the respiratory changes in pulse pressure beforevolume expansion (Baseline PP) and the volume expansion-inducedchanges in cardiac index (y-axis) in 40 septic patients with acutecirculatory failure. The higher PP is before volume expansion, themore marked the increase in cardiac index induced by volumeexpansion. Adapted with permission [7].


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[21,28]. Thus, the respiratory changes in LV stroke volumecould theoretically be an indicator of afterload dependence,rather than of preload dependence, for example in patientswith congestive heart failure. In fact, it is unlikely that theinspiratory increase in LV stroke volume can be responsiblefor large variations in LV stroke volume and hence in arterialpressure, even in the case of LV dysfunction [29,31]. In

animals, induction of an experimental cardiac dysfunctionwas showed to result in a decrease rather than an increasein systolic pressure variation [29,31].

Because the pulse pressure depends not only on strokevolume, but also on arterial compliance, large changes inpulse pressure could theoretically be observed despitesmall changes in LV stroke volume if arterial compliance islow (elderly patients with peripheral vascular disease). Sim-ilarly, small changes in pulse pressure could be observeddespite large changes in LV stroke volume if arterial com-pliance is high (young patients without any vasculardisease). In fact, a close relationship between baseline

PP and the changes in cardiac index induced by volumeexpansion was observed in a series of patients with a largerange of ages and comorbidities [7], suggesting that thearterial compliance poorly affected the relationshipbetween respiratory changes in LV stroke volume and PP.

Noninvasive assessment of respiratory changes in LV

stroke volume

Although less invasive than pulmonary artery catherization,femoral or radial arterial catheterization remains an inva-sive procedure. Infrared photoplethysmography coupledwith the volume clamp technique [44] allows a non-

invasive and continuous measurement of finger bloodpressure, which has been shown to track changes inblood pressure accurately [45]. In mechanically ventilatedpatients, we recently found a close correlation and a goodagreement between PP measured from intra-arterial

recordings and PP measured noninvasively using thecontinuous measurement of finger blood pressure [46].

The respiratory changes in LV stroke volume can also beassessed noninvasively by Doppler echocardiography.Indeed, by assuming that aortic annulus diameter is con-stant over the respiratory cycle, the changes in aorticblood flow should reflect changes in LV stroke volume.Therefore, the respiratory changes in aortic blood velocityhave also been proposed to assess fluid responsivenessin mechanically ventilated patients [47].

Whether other methods, such as beat-to-beat measure-

ments of aortic blood flow by oesophageal Doppler or ofstroke volume from the pulse contour analysis, may beused to assess the respiratory changes in LV strokevolume and hence cardiac preload dependence remainsto be determined.

ConclusionRight atrial and pulmonary artery occlusion pressures arestill extensively used to decide whether to employ fluidtherapy [3], although many clinical studies have empha-sized the poor value of cardiac filling pressures in predict-ing volume expansion efficacy. In sedated andmechanically ventilated patients, analysis of the respiratory

changes in LV stroke volume allows an accurate evalua-tion of cardiac preload dependence, and thus of fluidresponsiveness. In the future, the assessment of respira-tory changes in arterial pressure should be automated anddisplayed on a monitor, which may facilitate and possiblyimprove the cardiorespiratory management of mechani-cally ventilated patients.

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Authors affiliation: Service de ranimation mdicale, CHU deBictre, Universit Paris XI, Kremlin Bictre, France

Correspondence: Frdric Michard, Service de RanimationMdicale, CHU de Bictre, Universit Paris XI, 78, rue du GnralLeclerc, 94275 Kremlin Bictre Cedex. E-mail: [email protected]

Respuesta a Liquidos en UCI

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