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DOI: 10.1055/s-2007-1007251
© 1996 by Thieme Medical Publishers, Inc.
Circulatory, Respiratory, Cerebral, and Renal Derangements in Acute Liver Failure: Pathophysiology and Management
Publication History
Publication Date:
17 March 2008 (online)
ABSTRACT
Many of the hemodynamic abnormalities seen in acute liver failure (ALF) have now been characterized. A lowered systemic vascular resistance with a raised cardiac output are prominent features, which in part are modulated by nitric oxide (NO). At a cellular level, oxygen supply and utilization are impaired by changes in vascular tone, plugging of nutritive vessels, and pathological shunting. The use of N-acetylcysteine (NAC) and prostacy-clin, a vasodilator, have been shown to increase oxygen utilization in the microcirculation. NAC may act by enhancing the effect of NO on guanylate cyclase, increasing the formation of cyclic 3′,5′-guanosine monophosphate (cGMP), and thereby resulting in vasodilatation. This suggests that despite overproduction of NO in ALF, there is a shortage! failure of utilization at a cellular level. Appropriate management of these patients should be based on a good knowledge of the underlying pathophysiology, and thus on monitoring, during the course of the disease.
KEY WORDS
liver failure - hemodynamics - cerebral edema - renal