A B S T R A C T The effect of intra-aortic counterpulsation (IACP, 22-94 hr) on hemodynamics and cardiac energetics was evaluated in 10 patients in shock after acute myocardial infarction. The data clearly indicate that IACP improves myocardial oxygenation, enhances peripheral perfusion, and probably improves myocardial contractility in the severely diseased heart.Before treatment, decreases in cardiac index (mean value, 1.22 liter/min per m'), systolic ejection rate (67 ml/sec), and time-tension index per minute (1280 mm Hg -sec/min) were observed. Systemic vascular resistance varied widely. Low coronary blood flow (68 ml/min per 100 g) was associated with increased myocardial oxygen extraction (79%), low coronary sinus oxygen tension (20 mm Hg), and abnormal myocardial lactate-pyruvate metabolism.During 4-6 hr of IACP, systolic pressure and left ventricular outflow resistance decreased by 18% and 24%, respectively, while cardiac index improved by 38%. Diastolic arterial pressure rose 98%. Increase in coronary blood flow from an average of 68 to 91 ml/100 g per min (P < 0.001) was significantly correlated with rise in mean arterial pressure (r = 0.685). This correlation was best expressed in a third-order curve, which intercepts the point of no flow at a mean aortic pressure of 30 mm Hg. The flow-pressure curve is relatively flat above 65-70 mm Hg, but becomes steeper as mean aortic pressure falls below this point. Myocardial oxygen consumption remained essentially unchanged during early IACP and tended to rise during the later stages.However, the relationship of cardiac work performed to oxygen availability was markedly improved. Myocardial

SUMMARYThe effects of isoproterenol, l-norepinephrine, and intraaortic counterpulsation on hemodynamics and myocardial metabolism were evaluated in shock due to acute myocardial infarction. Before treatment, the cardiac index was markedly reduced, averaging 1.35 liters/min/m2. Mean aortic pressures ranged from 40 to 65 mm Hg.Decreases in coronary blood flow (mean, 68 ml/100 g/min) and in myocardial oxygen consumption (mean, 8.11 ml/100 g/min) were associated with abnormally high myocardial oxygen extractions (mean, 78%) and with lactate production (mean, 9%). Isoproterenol increased cardiac index 63% and heart rate 26%. Coronary blood flow rose an average of 12 ml/100 g/min in the face of decreased diastolic aortic pressure.Rate of myocardial lactate production increased. 1-Norepinephrine increased mean aortic pressure and coronary blood flow an average of 21 mm Hg and 27 ml/ 100 g/min. Mean myocardial oxygen consumption rose 2.24 ml/ 100 g/min. While myocardial lactate production shifted to extraction (mean, 12%), myocardial oxygen extraction remained abnolmally high (mean, 73%). Cardiac index did not change. Intraaortic counterpulsation increased mean aortic pressure and coronary blood flow an average of 15 mm Hg and 23 ml/100 g/min. Myocardial oxygen consumption remained essentially unchanged. Both myocardial lactate and oxygen extraction improved toward normal values (15 and 61%). Cardiac index increased an average of 0.45 liters/min/m2. Hemodynamics and myocardial metabolism then were markedly abnormal in shock due to acute myocardial infarction. Isoproterenol improved cardiac performance but myocardial oxygenation deteriorated. Therefore isoproterenol does not seem to be helpful in coronary shock. 1-Norepinephiine improved myocardial perfusion and oxygenation, but did not change cardiac output. It appears to be the vasoactive agent of choice in the initial treatment of coronary shock. Intraaortic counterpulsation changed myocardial metabolism toward normal and improved systemic perfusion. Mortality remained unchanged however during the three different therapeutic interventions emphasizing the importance of early recognition of the shock state and of further aggressive diagnostic and therapeutic management.

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