Continuous venovenous hemofiltration improves cardiac performance by mechanisms other than tumor necrosis factor-alpha attenuation during endotoxic shock
P. Rogiers et al., Continuous venovenous hemofiltration improves cardiac performance by mechanisms other than tumor necrosis factor-alpha attenuation during endotoxic shock, CRIT CARE M, 27(9), 1999, pp. 1848-1855
Objective: To assess the effects of continuous venovenous hemofiltration (C
VVH) on global and regional hemodynamics, plasma lactate, and tumor necrosi
s factor-alpha (TNF-alpha) levels during endotoxic shock in dogs.
Methods: Thirty pentobarbital-anesthetized and mechanically ventilated dogs
were divided into six groups of five dogs each. Group 1 served as a contro
l, undergoing CVVH at 3 L/hr without endotoxin. Group 2 served as the endot
oxin-alone time-matching group. Group 3 received CVVH 1 hr after endotoxin
at 3 L/hr for 270 mins. Group 4 received CVVH 1 hr after endotoxin at 3 L/h
r for 150 mins and at 6 L/hr for an additional 120 mins. Group 5 and group
6 received the ultrafiltrate from group 1 and group 3, respectively.
Measurements and Main Results: Three hours after endotoxin challenge, dogs
treated with CVVH at 3 L/hr had a higher cardiac output (4.9 +/- 0.6 vs. 2.
9 +/- 0.6 L/min; p < .05) and stroke volume (35 +/- 7 vs. 20 +/- 4 mt; p <
.05) and a lower pulmonary vascular resistance (116 +/- 26 vs. 331 +/- 126
dyne sec/cm(5); p < .05) than the endotoxin-alone group. Five hours after e
ndotoxin, dogs treated with CVVH at 6 L/hr also had higher hepatic (464 +/-
164 vs. 126 +/- 75 mL/min; p < .05) and femoral (95 +/- 46 vs. 30 +/- 34 m
L/min; p < .05) blood flow. Moreover, dogs treated with CVVH at 6 L/hr had
higher mean arterial blood pressure (84 +/- 24 vs. 40 +/- 15 mm tig; p < .0
5) and left ventricular stroke work index (1.1 +/- 0.6 vs. 0.2 +/- 0.2 g/kg
; p < .05) than the endotoxin-alone group, Plasma lactate levels were lower
in the CVVH group at 6 L/hr (2.7 +/- 1.1 mmol/L) than in the endotoxin-alo
ne group (4.4 +/- 0.6 mmol/L; p < .05), Plasma TNF-alpha levels were unaffe
cted, and only minor amounts of TNF-alpha were found in the ultrafiltrate.
Conclusion: In this acute endotoxic shock model, CVVH at 3 L/hr improved ca
rdiac performance and decreased pulmonary vasoconstriction. Moreover, CVVH
at 6 L/hr also increased arterial blood pressure and left ventricular strok
e work, increased hepatic and femoral arterial blood flow, and decreased bl
ood lactate levels. These effects were not attributable to TNF-alpha remova
l.