Dialysis hypotension: A hemodynamic analysis

Abstract

An analysis of the normal compensatory responses to hypovolemia reveals that central redistribution of the blood volume (due to changes in TPR and possibly also to venoconstriction) may be an important means of maintaining cardiac output. Chronotropic and inotropic cardiac changes during hypovolemia appear to play a relatively minor role in supporting blood pressure. Increased TPR is important in that it supports overall proximal blood pressure and also helps augment venous return. Cardiopulmonary and pressoreceptor reflexes are primarily responsible for increasing TPR during volume depletion by increasing sympathetic nerve activity to resistance vessels. Cutaneous resistance and capacity are affected by body temperature as well, and splanchnic resistance and capacity are modulated by both body temperature and by ingestion of food. In uremic patients, the most easily demonstrable evidence of baroreflex impairment, alteration of heart rate responses, may be hemodynamically the least relevant. Further studies of cardiopulmonary and pressoreceptor function as reflected by their effects on vascular resistance are needed. There are several treatment-associated causes of dialysis hypotension: With low sodium dialysis solution the primary cause of hypotension is probably a reduced plasma refilling rate, although studies of TPR and cardiac output have been done in dogs only. Acetate lowers the TPR, may impair plasma refilling, and may also induce pooling of blood in splanchnic and other capacitance beds, causing diminished cardiac filling and a relatively decreased cardiac output. Dialysis-associated heat stress may lower TPR and may also cause blood pooling in the cutaneous vasculature. The hemodynamic mechanism of post-prandial hypotension in dialysis patients needs to be studied, but probably revolves around reduced splanchnic (and total peripheral) vascular resistance, and splanchnic blood pooling. Several other potential treatment-related causes of dialysis hypotension warrant further study. The most important candidates include the role played by changes in the plasma potassium level and the potential effects of monokines (IL-1 and tumor necrosis factor) which may be released during dialysis. Also, whether adenosine [163, 164], cGRP, and other vasoactive peptides participate in the causation of 'sympathetic failure' during dialysis hypotension warrants further investigation.