Abstract

IntroductionWe found that pulse pressure variation (PPV) did not predict volume responsiveness in patients with increased pulmonary artery pressure. This study tests the hypothesis that PPV does not predict fluid responsiveness during an endotoxin-induced acute increase in pulmonary artery pressure and right ventricular loading.MethodsPigs were subjected to endotoxemia (0.4 μg/kg/hour lipopolysaccharide), followed by volume expansion, subsequent hemorrhage (20% of estimated blood volume), retransfusion, and additional stepwise volume loading until cardiac output did not increase further (n = 5). A separate control group (n = 7) was subjected to bleeding, retransfusion, and volume expansion without endotoxemia. Systemic hemodynamics were measured at baseline and after each intervention, and PPV was calculated offline. Prediction of fluid-challenge-induced stroke volume increase by PPV was analyzed using receiver operating characteristic (ROC) curves.ResultsSixty-eight volume challenges were performed in endotoxemic animals (22 before and 46 after hemorrhage), and 51 volume challenges in the controls. Endotoxin infusion resulted in an acute increase in pulmonary artery and central venous pressure and a decrease in stroke volume (all P < 0.05). In endotoxemia, 68% of volume challenges before hemorrhage increased the stroke volume by > 10%, but PPV did not predict fluid responsiveness (area under the ROC curve = 0.604, P = 0.461). After hemorrhage in endotoxemia, stroke volume increased in 48% and the predictive value of PPV improved (area under the ROC curve for PPV = 0.699, P = 0.021). In controls after hemorrhage, stroke volume increased in 67% of volume challenges and PPV was a predictor of fluid responsiveness (area under the ROC curve = 0.790, P = 0.001).ConclusionsFluid responsiveness cannot be predicted with PPV during acute pulmonary hypertension in porcine endotoxemia. Even following severe hemorrhage during endotoxemia, the predictive value of PPV is marginal.

Highlights

  • We found that pulse pressure variation (PPV) did not predict volume responsiveness in patients with increased pulmonary artery pressure

  • We have shown that PPV does not predict fluid responsiveness in critically ill patients with increased pulmonary arterial pressure [13]

  • Endotoxin infusion resulted in tachycardia, increased pulmonary artery and central venous pressures, and decreased stroke volume, but no change in PPV (Table 1)

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Summary

Introduction

We found that pulse pressure variation (PPV) did not predict volume responsiveness in patients with increased pulmonary artery pressure. This study tests the hypothesis that PPV does not predict fluid responsiveness during an endotoxin-induced acute increase in pulmonary artery pressure and right ventricular loading. Once the flat part of the cardiac function curve has been reached, the patients are no longer volume responsive [1] In such cases, further fluid administration can be detrimental due to unnecessary loading of the heart, increased tissue edema, and consequent risk of impaired tissue perfusion. The preload reduction induced by positive inspiratory pressure should enhance stroke volume variation and PPV This hypothesis has been demonstrated in experimental studies [5] and in patients [2,3,6,7,8], and has been widely adopted in clinical practice to guide fluid therapy

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