Effect of Isoproterenol, l -Norepinephrine, and Intraaortic Counterpulsation on Hemodynamics and Myocardial Metabolism in Shock following Acute Myocardial Infarction

Abstract

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.

Intraaortic balloon counterpulsation with and without reperfusion for myocardial infarction shock.

“…Our results with intraaortic counterpulsation alone are comparable to those of other reported series8 9, [16][17][18][19] and the outcome, in some respects, is more favorable.…”

“…Of the five long-term survivors, two had previous infarc- The major determinant of a favorable result in group 2 (table 4) appeared to be the time from the onset of infarction to the institution of treatment with bypass grafting and counterpulsation. The subset of patients treated more than 18 hours after the onset of infarction had a 71.4% (five of seven) in-hospital mortality, while the patients treated within 16 hours had a 25% (three of 12) mortality rate. No patient was treated between 16 and 18 hours from the onset of infarction.…”

“…The bulk of previous clinical experience8 16 shock reported only slight improvement in the longterm mortality of patients treated with this modality alone. However, recent reports suggest that the longterm prognosis for patients with coronary shock treated with counterpulsation alone may be comparable to that for patients undergoing surgery and mechanical assistance.…”

“…Shock was defined as 1) central systolic arterial blood pressure less than 85 mm Hg (mean blood pressure less than 70 mm Hg), 2) functional volume expansion characterized by elevation of left ventricular filling pressure . [16][17][18]3) clouded sensorium, 4) evidence of peripheral hypoperfusion on clinical exam (i.e., cold extremities with prolonged capillary filling time), 5) depressed urine flow, and 6) continued need for vasopressor support despite volume expansion. All criteria were necessary for inclusion.…”

Management of Shock in Acute Myocardial Infarction: Changing Concepts; Past, Present and Future

“…Studies with pure va soconstrictors such as methoxamine showed that arterial pressure and peripheral resis tance could be increased in cardiogenic shock but that cardiac output was simulta neously decreased [10], Isoproterenol in creased cardiac output, but at the expense of increased heart rate and decreased coro nary perfusion pressure, while norepineph rine, which has both alpha-and beta-agonistic properties, increased both arterial pressure and cardiac output [11,12]. Thus, norepinephrine emerged as the agent of choice for the initial treatment of shock complicating myocardial infarction.…”