Principle defects which account for shock following acute myocardial infarction in man: implications for treatment.

Abstract

Shock following acute myocardial infarction is closely related to the volume of damaged myocardium. For this reason, the main therapeutic effort should be directed towards improvement of myocardial oxygenation rather than improvement of cardiac performance. Hemodynamics and cardiac energetics were studied in 25 patients in myocardial infarction shock. Hemodynamic abnormalities associated with shock were emphasized when compared to data from 40 patients with acute myocardial infarction but not in shock. Isoproterenol increased cardiac index an average of 0.87 1/min/M2 and heart rate by 20 beats/min; coronary blood flow rose an average of 12 ml/100g/min in face of decreased diastolic aortic (coronary perfusion) pressure; rate of myocardial lactate production increased. L-norepinephrine increased mean aortic pressure and coronary blood flow an average of 21 mm Hg and 27 ml/100g/min; mean myocardial oxygen consumption rose 2.24 ml/100g/min; myocardial lactate production shifted to extraction (mean, 12%); myocardial oxygen extraction remained abnormally high (mean, 73%); cardiac index did not change. Intra-aortic counterpulsation in-creased mean aortic pressure and coronary blood flow an average of 14 mm Hg and 23 ml/100g/ min; myocardial oxygen consumption remained essentially unchanged; both myocardial lactate and oxygen extraction improved toward normal values (15% and 61%); cardiac index in-creased an average of 0.48 1/min/M2. Isoproterenol appears to be harmful in myocardial infarction shock in that it increased myocardial oxygen demand more than oxygen supply. L-norepinephrine seems to be the vasoactive agent of choice in the initial treatment of shock because it improved myocardial perfusion and metabolism but not cardiac index. Intra-aortic counterpulsation improved both coronary and peripheral circulation and the myocardial metabolism changed towards normal. Mortality remained unchanged during the three different therapeutic interventions; emphasizing the importance of early recognition of the pre-shock state and of further aggressive diagnositc and therapeutic measures.