Global end-diastolic volume increases to maintain fluid responsiveness in sepsis-induced systolic dysfunction

Ronald J Trof,Ibrahim Danad,Ab Johan Groeneveld

doi:10.1186/1471-2253-13-12

Abstract

BackgroundSepsis-induced cardiac dysfunction may limit fluid responsiveness and the mechanism thereof remains unclear. Since cardiac function may affect the relative value of cardiac filling pressures, such as the recommended central venous pressure (CVP), versus filling volumes in guiding fluid loading, we studied these parameters as determinants of fluid responsiveness, according to cardiac function.MethodsA delta CVP-guided, 90 min colloid fluid loading protocol was performed in 16 mechanically ventilated patients with sepsis-induced hypotension and three 30 min consecutive fluid loading steps of about 450 mL per patient were evaluated. Global end-diastolic volume index (GEDVI), cardiac index (CI) and global ejection fraction (GEF) were assessed from transpulmonary dilution. Baseline and changes in CVP and GEDVI were compared among responding (CI increase ≥10% and ≥15%) and non-responding fluid loading steps, in patient with low (<20%, n = 9) and near-normal (≥20%) GEF (n = 7) at baseline.ResultsA low GEF was in line with other indices of impaired cardiac (left ventricular) function, prior to and after fluid loading. Of 48 fluid loading steps, 9 (of 27) were responding when GEF <20% and 6 (of 21) when GEF ≥20. Prior to fluid loading, CVP did not differ between responding and non-responding steps and levels attained were 23 higher in the latter, regardless of GEF (P = 0.004). Prior to fluid loading, GEDVI (and CI) was higher in responding (1007 ± 306 mL/m2) than non-responding steps (870 ± 236 mL/m2) when GEF was low (P = 0.002), but did not differ when GEF was near-normal. Increases in GEDVI were associated with increases in CI and fluid responsiveness, regardless of GEF (P < 0.001).ConclusionsAs estimated from transpulmonary dilution, about half of patients with sepsis-induced hypotension have systolic cardiac dysfunction. During dysfunction, cardiac dilation with a relatively high baseline GEDVI maintains fluid responsiveness by further dilatation (increase in GEDVI rather than of CVP) as in patients without dysfunction. Absence of fluid responsiveness during systolic cardiac dysfunction may be caused by diastolic dysfunction and/or right ventricular dysfunction.

Highlights

Sepsis-induced cardiac dysfunction may limit fluid responsiveness and the mechanism thereof remains unclear
In the low global ejection fraction (GEF) group, other function indices pointed to systolic cardiac dysfunction, prior to and after fluid loading, even though the cardiac index (CI) attained with fluid loading did not differ among the groups
The number of fluid loading responses did not differ according to GEF, but the increase in CI decreased with increasing fluid loading steps only when

Summary

Introduction

Sepsis-induced cardiac dysfunction may limit fluid responsiveness and the mechanism thereof remains unclear. Patients with severe sepsis or septic shock commonly develop cardiac dysfunction, even in the absence of cardiac ischemia [1,2,3] These abnormalities may include depression of left and/or right ventricular systolic function and/or diastolic dysfunction and may be accompanied by ventricular dilatation, as estimated from echocardiography or radionuclide cineangiography [4,5]. Filling pressures, like CVP, have been used to guide fluid loading in sepsis-induced hypotension [17,18,19,20], even though its predictive value for fluid responsiveness during mechanical ventilation and altered cardiac function is doubtful [21,22,23]. The GEDVI represents the volumes of the right and left heart at the end of diastole and often reflects left ventricular end-diastolic volume estimated by echocardiography provided that right ventricular dilatation is absent [25]

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