Effects of Vasopressor Agents and Epoprostenol on Systemic Hemodynamics and Oxygen Transport in Fulminant Hepatic Failure

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Abstract
Hypotension is a serious complication in patients with fulminant hepatic failure, because it is associated with tissue hypoxia and a further compromise to end–organ function. In this study we investigated the effects of epinephrine and norepinephrine on hemodynamics and oxygen transport variables in 30 patients with fulminant hepatic failure. All had a mean arterial pressure of less than 60 mm Hg, despite adequate intravascular filling pressures. Both epinephrine (n = 15) and norepinephrine (n = 15) improved mean arterial pressure (p < 0.001 epinephrine and norepinephrine), although this was not associated with a rise in oxygen delivery. Oxygen consumption fell (p<0.05 epinephrine, p<0.001 norepinephrine) because of a lower oxygen extraction ratio (p<0.01 epinephrine and norepinephrine). The addition of epoprostenol, a microcirculatory vasodilator, in 10 patients from each group led to an increase in oxygen consumption (p<0.001 epinephrine and norepinephrine) because of a rise in oxygen delivery (p<0.05 epinephrine, p<0.01 norepinephrine) and oxygen extraction ratio (p<0.01 epinephrine, p<0.001 norepinephrine), without a fall in mean arterial pressure. The fall in oxygen consumption after the institution of vasopressor therapy could exacerbate tissue hypoxia and thus contribute to further organ damage in an already susceptible patient. In patients with fulminant hepatic failure who are given vasopressor support, the addition of epoprostenol may prevent the development of tissue hypoxia. (Hepatology 1992;15:1067–1071).