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[Critical limits of hemodilution: theoretical principles]
1Institut für Physiologie und Pathophysiologie, Universität Mainz.
For daily clinical practice an isovolemic hemodilution down to an arterial O2 content of 10 ml/dl, corresponding to a hemoglobin content of 7.5 g/dl or a hematocrit value of 22.5%, is described as a tolerable value, as long as normovolemia and normoxia (no disturbances of lung function) are guaranteed and local restrictions in perfusion (coronary or cerebral sclerosis) are excluded. This value is not derived from the mixed venous O2 status but from the situation of the myocardium as the main limiting organ for anemic hypoxemia. Compensation of anemia is regulated hemodynamically: First, by an increase in stroke volume; secondary, by an increase in heart frequency and, tertiary, by an increase in venous utilization. The last may reach 100% without any restrictions from the so-called critical mixed venous pO2 as a possible limiting factor for hemodilution.
For daily clinical practice an isovolemic hemodilution down to an arterial O2 content of 10 ml/dl, corresponding to a hemoglobin content of 7.5 g/dl or a hematocrit value of 22.5%, is described as a tolerable value, as long as normovolemia and normoxia (no disturbances of lung function) are guaranteed and local restrictions in perfusion (coronary or cerebral sclerosis) are excluded. This value is not derived from the mixed venous O2 status but from the situation of the myocardium as the main limiting organ for anemic hypoxemia. Compensation of anemia is regulated hemodynamically: First, by an increase in stroke volume; secondary, by an increase in heart frequency and, tertiary, by an increase in venous utilization. The last may reach 100% without any restrictions from the so-called critical mixed venous pO2 as a possible limiting factor for hemodilution.