The role of oxygen-carrying capacity in myocardial ischemia.
Myocardial ischemia results when myocardial oxygen demand exceeds oxygen supply. The oxygen content of blood is only one of several interdependent variables influencing myocardial oxygen supply. The impetus for assessing the contribution of the oxygen content of blood to myocardial ischemia, and thus the need to treat anemia, stems from current concern about the risks associated with blood transfusion and the recognition that hemodilution has protean effects on the oxygen-carrying capacity of blood. The rheological changes that accompany hemodilution favorably influence the delivery of oxygen to the tissues and have the capacity to at least partially compensate for the decrease in blood oxygen content during hemodilution. However, nonrheological compensatory mechanisms (e.g., cardiac effects) also influence oxygen delivery and may profoundly influence the adequacy of tissue oxygenation. Furthermore, occlusive vascular lesions that restrict blood flow to the tissues also profoundly influence tissue oxygenation. The evidence in the myocardium and in systemic tissues indicates that considerable degrees of normovolemic hemodilution are well tolerated in physiological settings. In contrast, coexisting disease such as coronary artery stenosis may limit the patient population that benefits from normovolemic hemodilution. Unfortunately, well-controlled prospective studies of normovolemic hemodilution in patients with severe vascular or cardiac disease have not yet been conducted. As we progress to that point, it will be especially important to critically examine studies that use anesthetized or revascularized preparations. Results obtained under controlled conditions of hemodilution may not apply to postoperative anemia in awake patients with coronary artery disease who are experiencing the stress of surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
Nyhan
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Schulthesis
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D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology*; D006438:Hemodilution; D006801:Humans; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption / Q000502:physiology*
D010100:Oxygen