Cardiovascular and neurohumoral responses following burn injury
R. L. Crum, W. Dominic, J. F. Hansbrough, S. R. Shackford and M. R. Brown
Department of Surgery, University of California, San Diego.
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.