MYOCARDIAL INFARCTION Oxygen delivery and consumption and P 50 in patients with acute myocardial infarction

We investigated the relationship between oxygen delivery (DO2), oxygen consumption (V02), and influence of oxyhemoglobin dissociation (P50) on VO2 in 40 patients with complicated myocardial infarction. A decrease in V02 and an increase in P50 were observed as DO2 decreased due to pump failure. In a given range of DO2, VO2 was related to P50 in survivors (r values .472 to .647, p < .01). Each millimeter of mercury increase in P50 was associated with a 5.2 to 6.5 ml/min m2 increase in VO2 when DO2 was less than 450 ml/min m2. No similar correlation was found for nonsurvivors. Lactate was higher in nonsurvivors despite the fact that DO2 and V02 were similar in the two groups. The lack of compensatory increases in P50 may be pathologic in nonsurvivors. However, the value of V02 as an indicator of tissue oxygenation or survival in patients with acute myocardial infarction is questionable. Circulation 73, No. 6, 1183-1185, 1986. IN ADULTS with respiratory distress syndrome or in shock and in anesthesized patients, oxygen consumption (V02) has been demonstrated to be related to oxygen delivery (D02). 1' The cause of supply dependency of oxygen uptake under certain conditions and its pathophysiologic implications are uncertain.5 When DO2 is decreased, one of the compensatory mechanisms by which V02 is maintained is a decrease in oxygen affinity for hemoglobin, i.e., an increase in oxyhemoglobin dissociation (P50), to facilitate oxygen unloading and increased 02 extraction. Elevated P50 has been found in patients with anemia and low cardiac output and those living at high altitudes.6 In patients with acute myocardial infarction, elevated P is thought to improve V02 when DO2 is decreased due to low cardiac output.2 Conversely, the clinical significance of VO2 has been questioned,7 even though some investigators have observed lower VO2 in nonsurvivors than survivors of septic shock.8 The purpose of our study was to evaluate the relationship of DO2, V02, and P50 and the effect of P50 on V02 after acute myocardial infarction. From the Department of Critical Care Medicine, Mount Carmel Mercy Hospital, Detroit. Address for correspondence: Vinod K. Puri, M.D., Director, Critical Care Medicine, Mount Carmel Mercy Hospital, 6071 West Outer Dr., Detroit, MI 48235-2679. Received June 4, 1985; revision accepted March 6, 1986. This research was conducted during Dr. Yang's tenure as a research fellow in Critical Care Medicine at MCMH. His current address is: Department of Pulmonary Medicine, Loma Linda University, Loma Linda, CA. Vol. 73, No. 6, June 1986 Methods Forty consecutive patients who required hemodynamic monitoring among 147 patients with acute myocardial infarction who were admitted to our institution between January 1983 and July 1984 were evaluated. Diagnosis of acute myocardial infarction was made by history, the electrocardiogram, and measurement of the creatine kinase-MB isoenzyme level. Hemodynamic monitoring was instituted for management of cardiogenic shock in 18 patients, pulmonary edema in 12, persistent chest pain in nine, and uncontrolled arrhythmia in one. A pulmonary arterial catheter was inserted through the internal jugular or subclavian vein and an arterial catheter was inserted in the radial artery of each patient. Cardiac output was measured by the thermodilution technique in triplicate, or until three measurements varied less than 5%. Simultaneous arterial and mixed venous blood were also drawn for analysis of pH, Po2, So2, Pco2, hemoglobin, and arterial lactate. From these data, DO2 and V02 were calculated with appropriate formulas.9 P50 was calculated from the mixed venous 02 saturation with the method described by Aberman et al.'0 The mean value of 27.9 + 0.6(SEM) was obtained in 10 stable surgical patients who were electively monitored in the preoperative period. Arterial lactate was measured by an enzymatic method. The normal value for arterial lactate measured in our laboratory is 0.8 to 1.2 mmol/liter, but only values exceeding 2.4 mmol/liter are considered to indicate hypoperfusion. All of these measurements were repeated every 12 hr and whenever clinical conditions changed. Patients were managed with vasoactive agents, fluids, and supportive care according to their hemodynamic status. A total of 349 measurements were obtained in 40 patients, including 23 survivors (group 1) and 17 nonsurvivors (group 2). DO2 ranged from 94 to 552 ml/min.m2 and the values were grouped into six ranges, as listed in table 1. The value range of 50 ml/min m2 was chosen so that the relationship between P50 and V02 could be examined independent of DO2. Although use of this narrow range resulted in fewer data points in each category, more than 40 observations were available for analysis. Correlations between P50 and V02 were sought by linear regression analysis. 1183 by gest on N ovem er 7, 2017 http://ciajournals.org/ D ow nladed from