Abstract

At the level of the heart, oxygen extraction is already nearly maximal under resting conditions. 3 Therefore, maintenance of myocardial oxygen delivery during isovolemic hemodilution depends essentially on the increase in coronary blood flow. This is achieved by a reduction in coronary vascular resistance related to the decreased blood viscosity but also to specific coronary vasodilation as demonstrated by analysis of vascular hindrance (vascular resistance/blood viscosity). 3 In addition, isovolemic hemodilution is associated with an increased cardiac work resulting in an augmentation of myocardial oxygen demand. Indeed, heart rate, 4 but also possibly myocardial contractility, 5 has been shown to increase during isovolemic hemodilution. When the hematocrit is reduced to 10 to 12%, myocardial oxygen consumption more than doubles. 6 In these conditions, coronary vasodilatation is near maximal. Below a hematocrit of 10%, coronary blood flow can no longer match the increased myocardial oxygen demand and ischemia develops, ultimately resulting in cardiac failure. This is in accordance with experimental data showing a decrease in systemic oxygen uptake at hematocrit values close to 10%. 7 As maximal coronary blood flow is not influenced by hemodilution, the coronary reserve (the ratio between maximal coronary blood flow and resting coronary blood flow) is significantly reduced during isovolemic anemia. Geha 8 demonstrated in intact dogs a 50% reduction in the coronary flow reserve when hematocrit is decreased from 43 to 20%. This indicates the vulnerability of the heart during anemia, especially if coronary artery disease (decreased maximal coronary blood flow) or higher work demands on the myocardium should co-exist. The lowest tolerable hematocrit in coronary artery disease patients is not known but experimental data in animals with extrinsically applied coronary stenosis have demonstrated a significant increase in the value of the hematocrit associated with the development of cardiac failure. 9 Based on a theoretical analysis, Kettler 10 estimated that coronary artery disease patients may tolerate some degree of hemodilution intraoperatively but will require a higher hematocrit in the early postoperative period to meet the increased tissue, and especially cardiac, oxygen demand. This has been confirmed by the study of Nelson et al., 11 showing that a postoperative hematocrit below 28% was associated with increased myocardial ischemic episodes and morbid cardiac events. Cardiovascular disease patients with a lower preoperative hematocrit have an increased risk of death when compared to non-cardiovascular disease patients with the same preoperative hematocrit. 12

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