Myocardial Infarction with Shock

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Abstract
The hemodynamic effects of acute myocardial infarction were measured in 23 patients, the effects of pressor amines studied in 13, and the effects of low viscosity dextran studied in 2. Aortic and superior vena cava pressures were measured through polyethylene catheters. Myocardial infarction without shock-11 patients. The average cardiac output (CO) by indicator dilution was 3.8 [plus or minus] 1.5 (S.D.) 1/min., mean arterial pressure (MAP) 92 [plus or minus] 23 mm Hg and systemic vascular resistance (SVR) was 26 [plus or minus] 9 mm Hg/1/min. Two of these patients were given norepinephrine, and both showed a rise in mean arterial pressure with a fall in CO. Myocardial infarction with shock -12 patients. Control studies showed an average CO of 2.2 [plus or minus] 0.9 1/min., MAP of 50 [plus or minus] 12 mm Hg and SVR of 27.4 [plus or minus] 23.5 mm Hg/l/min. Seven patients received methoxamine and 11 received norepinephrine. The patients in shock with SVR above 20 mm Hg/l/min. during the control period responded to norepinephrine with an increase in cardiac output and could be brought to normotensive levels. Only 1 could be taken off vasopressors, and he had the highest output and lowest resistance. The 6 patients in shock with SVR below 20 mm Hg/ 1/min. during the control period were considered to have an inappropriately small rise in vascular resistance. Two did not respond the methoxamine or norepinephrine, and both died within 8 hr. of the onset of shock. They are considered to have vasomotor unresponsiveness due to the products of tissue anoxia. The 4 other patients in this group responded to methoxamine (2 patients) with a rise in resistance sufficient to produce normotension and to norepinephrine (all 4 patients) with a rise in cardiac output and systemic resistance. Three of these patients recovered from shock and vasopressors could be discontinued. They are considered to represent reflex inhibition of peripheral vaso-constrictlon. Two patients with low central venous pressure after vasopressors were given low viscosity dextran and had a 14% and 54% rise in cardiac output.