Cardiovascular and Neurohumoral Responses Following Burn Injury

Abstract

Cardiovascular and endocrine responses were evaluated in 12 adult patients over a 5-day period following 30% to 66% burn injury. Heart rate, mean arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac output, systemic vascular resistance, and stroke volume were measured. Plasma concentrations of angiotensin II, atrial natriuretic peptide, vasopressin, neuropeptide Y, norepinephrine, and epinephrine were measured. On the day of burn injury, systemic vascular resistance was markedly elevated, and stroke volume and cardiac output were low, but all normalized by day 3, and cardiac output and stroke volume increased by day 5 without significant changes of central venous pressure or pulmonary capillary wedge pressure. Mean arterial pressure and heart rate did not change significantly over the 5-day period. Vasopressin, angiotensin II, neuropeptide Y, norepinephrine, and epinephrine concentrations in plasma were elevated on admission. Vasopressin concentrations were elevated 50 times normal on admission and returned to normal levels by days 4 to 5. Plasma atrial natriuretic peptide concentrations were normal on admission and increased significantly on days 3 to 5. The reciprocal relationship between systemic vascular resistance and cardiac output and between vasopressin and atrial natriuretic peptide correlate with each other and the observed physiologic events that occurred following burn injury and resuscitation. All of these changes in cardiac performance occurred without significant alterations in preload or afterload as measured by central venous pressure, pulmonary capillary wedge pressure, and mean arterial pressure. Increases in plasma levels of atrial natriuretic peptide correlated with the increased stroke volume and cardiac output observed in these patients. The results of this study are consistent with the conclusion that the extreme elevations of plasma vasopressin levels contribute to the vascular complications of increased systemic vascular resistance and decreased cardiac output and contractility seen following burn injury.