Studies in Clinical Shock and Hypotension. II. Hemodynamic Effects of Norepinephrine and Angiotensin*

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Abstract
The hemodynamic effects of norepinephrine and angiotensin were studied in 31 patients with nonhemorrhagic shock or hypotension. The rise in blood pressure with norepinephrine was accompanied by a slight increase in heart rate and an increase in cardiac output in most subjects, although the increase was attenuated in those patients with a reduced total blood volume. Peripheral vascular resistance was increased by the drug, but usually not to so great an extent as the cardiac output, and in several patients calculated resistance was not significantly increased. Central blood volume was increased in most patients, but care in preventing excessive blood pressure rises may have been responsible for the absence of episodes of pulmonary congestion in these patients. Blood pressure was adequately controlled by angiotensin in all but 3 of the patients. Cardiac output was increased during 14 of the infusions and fell during 7, 5 of which were in patients with congestive heart failure. An increase in left ventricular stroke work was accompanied by evidence of increased cardiac filling pressure in most patients, but improved myocardial function during angiotensin infusion was demonstrated in some subjects. The increase in central blood volume usually was asymptomatic, but 3 patients with heart disease developed acute left ventricular failure requiring discontinuation of the drug. Direct comparison between the hemodynamic effects of equipressor doses of the 2 drugs in 16 patients revealed that norepinephrine produced a slightly higher cardiac output than angiotensin. Norepinephrine was considerably more effective in patients with heart failure but not in those with reduced blood volumes. The data indicate that these pressor drugs usually increase the cardiac output in hypo-tensive patients. The need for correction of occult volume depletion before administering norepinephrine and for caution in the use of angiotensin in patients with left ventricular failure is stressed. Since cardiac output was increased to normal in only 6 patients, it is suggested that these drugs seldom correct the hemodynamic abnormality and should be viewed primarily as emergency supportive therapy.