High-volume hemofiltration improves hemodynamics of endotoxin-induced shock in the pig

Abstract

This study was designed to assess the influence of high-volume continuous hemofiltration on the hemodynamics of endotoxin-induced shock in pigs. Eighteen anesthetized and ventilated pigs were studied for 240 minutes following the start of a 30-minute infusion of 0.5 mg/kg endotoxin. They were randomly divided into three groups: group 1 served as a control group, receiving endotoxin only; group 2 received zero balance, high-volume, venovenous hemofiltration with the removal of 6,000 mL ultrafiltrate/hr; and group 3 was used to evaluate the hemodynamic effect of the extracorporeal circuit itself. The decline in mean arterial pressure for group 2 was less than for group 1 (24 ± 7.8 mm Hg [mean ± SEM] versus 60 ± 3.4 mm Hg; P < .001) as was the drop in cardiac output (0.35 ± 0.24 L/min versus 1.53 ± 0.59 L/min; P < .01). The decline in cardiac output was more pronounced in group 3 than in group 1 (3.98 ± 0.21 L/min versus 1.53 ± 0.59 L/min; P < .01). Left ventricular stroke work decreased by 61 ± 6.8 g in group 1 versus 14 ± 2.0 g in group 2 ( P < .01), while left ventricular stroke work in group 3 was lower than that in group 1 ( P < .02). Right ventricular stroke work increased further in group 2 than in group 1 (16 ± 2.1 g v 3 ± 0.8 g; P < .01). The pulmonary vascular resistance, systemic vascular resistance, right atrial pressure, and pulmonary artery wedge pressure in groups 2 and 3 did not differ from those in group 1. We conclude that in this model, high-volume venovenous hemofiltration significantly improves cardiac function but does not affect pulmonary vascular resistance or systemic vascular resistance, while the use of the extracorporeal circuit adversely affects cardiac function. The effect of hemofiltration was more pronounced in this study than in others, probably because of the higher ultrafiltrate volume.