The three syndromes described all represent situations in which there is an imbalance between cardiac output and the peripheral needs for blood flow. As opposed to shock, in which the imbalance is more fulminant and progressive, hepatocirculatory failure is characterized by an imbalance which appears to be in large part assuaged by chronic reduction in the kidney's share of cardiac output. Individual patients certainly do not always fall neatly into one of the classifications described. Nonhemodynamic factors also may play a role in the genesis of the oliguria, but these have been disregarded in this discussion in an attempt to develop a thesis which can explain the syndrome as the natural progression of a disturbed circulatory state. The renal aspect of this syndrome has traditionally been stressed because it is so clinically apparent. Thus, hypoperfusion of the kidneys results in a dramatic reduction of the urine output, which can easily be measured and a rise in blood urea nitrogen and creatinine. In contrast, severe restriction of flow to other vascular beds may not be as easily detected. Reduction in hepatic blood flow may lead to progression of hepatic failure which may not be easy to detect by routine chemistries and, if it were detected, might be interpreted as part of the natural history of the liver disease. Cerebral hypoperfusion may lead to alteration in the state of consciousness, but these changes are more often attributed in such patients to the development of hepatic encephalopathy. Circulatory factors may therefore be of more importance than generally recognized in progressive hepatic failure. An understanding of the mechanism of hepatocirculatory failure has not yet resulted in significant improvement in therapy. Perhaps it is because our knowledge about pathophysiology is still incomplete, or because our therapeutic tools are inadequate or are being applied too late. As we gain a better understanding of the long natural history of the various forms of hepatocirculatory failure, it may eventually be possible to intervene effectively and rationally at an earlier stage of the disease.
Bibliographical noteFunding Information:
'Professor of Medicine and Head. Cardiovascular Division, University of Minnesota School of Medicine, Minneapolis Supported in part by Public Health Service Grants HLl1533 and HL18020 from the National Heart and Lung Institute.