Sumimoto, Tsutomu, Takayama, Yasuo, Iwasaka, Toshiji, Sugiura, Tetsuro, Takeuchi, Masaharu, Tarumi, Noritaka, Takashima, Hirofumi, and Inada, Mitsuo
The interrelations of oxygen delivery ([DO.sub.2]), oxygen consumption ([VO.sub.2]) and hemoglobin-oxygen affinity assessed by [P.sub.50] were investigated in 43 patients with acute myocardial infarction. As [DO.sub.2] declined due to low cardiac output, a significant decrease in [VO.sub.2] (r = 0.75, p [is less than]0.001) and a significant increase in [P.sub.50] (r = -0.74, p [is less than]0.001) were observed. In the [DO.sub.2] range between 300 and 450 ml/min/[m.sup.2], in which the [DO.sub.2] of 32 survivors and 11 nonsurvivors overlapped, the [P.sub.50] of nonsurvivors was significantly higher than that of survivors (31.5 [+ or -] 1.6 vs 27.9 [+ or -] 1.5 torr, p [is less than]0.001), but there were no significant differences in any other oxygen transport variable. As a result of differences in [P.sub.50], [VO.sub.2] in this range was significantly higher in nonsurvivors compared to survivors (169 [+ or -] 17 vs 148 [+ or -] 13 ml/min/[m.sup.2], p [is less than]0.001). These data suggest that a normal or increased [VO.sub.2] alone does not ensure survival in patients with acute myocardial infarction, and increased [P.sub.50] leads to an increase in [VO.sub.2]. Nevertheless, the interpretation of an increased [P.sub.50] in patients with acute myocardial infarction must be made with caution, even with adequate [DO.sub.2] and [VO.sub.2], because it may imply a precarious oxygen transport/requirement balance in peripheral tissue and, hence, a fatal outcome. (Am J Cardiol 1989;64:975-979), Oxygen is necessary for the body's tissues and measurement of the amount of oxygen consumed by the heart (oxygen consumption, VO2) after a heart attack, or myocardial infarction (MI), is important for assessing the extent of damage. Under normal conditions the heart can adjust its metabolic rate to compensate for decreased supply if delivery of oxygen (DO2) to it is reduced. After certain acute illnesses, such as septic shock, however, it appears that VO2 remains dependent on DO2 as normal compensatory mechanisms fail. One mechanism that then comes into play is a decrease in hemoglobin-oxygen affinity, the measure of how tightly bound oxygen in the blood is to its carrier molecule, hemoglobin. If the hemoglobin-oxygen affinity decreases, oxygen detaches from its hemoglobin and is more readily available for use by oxygen-starved tissues. However, medical treatment aimed primarily at increasing both VO2 and DO2 - delivery of oxygen to the organ as a whole - may fail to take into account possible damage to the heart cells' metabolic machinery, which is no longer able to effectively use the excess oxygen it receives. To measure compensatory changes in hemoglobin-oxygen affinity (P50, which increases when affinity decreases) after an MI, 43 patients who had received treatment within 24 hours after the onset of chest pains were assessed by means of a catheter inserted into the pulmonary artery, which carries blood to the lungs after it has circulated through the body. Oxygen tension (a measure of the amount of oxygen in the blood relative to other gases in the blood), carbon dioxide tension, oxygen saturation (the amount of oxygen bound to hemoglobin) and hemoglobin concentration were measured and used to compute P50, the overall measure of hemoglobin-oxygen affinity. Results showed that increased oxygen extraction had a significant correlation with an increase in P50; so, too, did an increase in VO2 and DO2. When survivors (32) were compared with nonsurvivors (11), they had a higher DO2; but when the records from both groups for patients with approximately equal DO2 were compared, the P50 of nonsurvivors was higher, with no differences in other measures. This suggests that increased P50 may itself be a predictor of death after MI for patients whose DO2 and VO2 values lie in the middle range (extreme values of DO2 and VO2 are still good predictors of mortality). If the compensatory increase in P50 during impaired DO2 is not enough to meet tissue needs, an oxygen debt may be incurred that can lead to irreversible tissue damage even with increased VO2. This debt may increase in patients with more serious myocardial infarctions. (Consumer Summary produced by RMI, Inc.)