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We have described whole body oxygen (O2) extraction ratio (ER) as a reliable indicator of transfusion need in acute normovolemic anemia. In normal hearts, myocardial lactate production (-LACT), indicating anaerobic metabolism, does not occur until the ER greater than 50% and Hct less than 10%. It is not known if the ER is valid in the setting of limited coronary vascular reserve. This study assesses the effect of a critical left anterior descending (LAD) coronary stenosis on the compensation to acute blood loss anemia. Adult dogs were anesthetized, paralyzed, and mechanically ventilated. A critical LAD stenosis was created in seven animals (STEN). There were seven controls (CON). Animals underwent isovolemic exchange transfusion with 6% HES until cardiac failure (CF). Catheters were placed in the aorta, pulmonary artery, and anterior interventricular coronary vein. Cardiac failure occurred at Hct = 8.6% +/- 0.4% in the CON and 17.0% +/- 0.5% in the STEN animals. Cardiac output increased in the CON, but not in the STEN animals. Blood flow in the LAD increased in the CON but not the STEN animals. -LACT began in the CON and STEN animals at Hct less than 20% and coincided with an ER greater than 50% in both groups. We conclude that CF occurs at a higher hematocrit with a critical LAD stenosis. The whole body ER greater than 50% remains a valid indicator of myocardial metabolism in anemia in the presence of limited coronary vascular reserve. The ER may be a useful guide to transfusion therapy.

We have shown that primates adequately compensate for acute normovolemic anemia to hematocrits (HCT) of 10%. We have described a whole-body extraction ratio (O2 consumption/O2 delivery; ER) of 50% as a reliable physiologic indicator of transfusion need. There is concern that whole-body ER may not accurately reflect impaired myocardial metabolism. The onset of significant lactate production by the left ventricle is an indicator of anaerobic metabolism. Our purpose is to compare left ventricular lactate metabolism (arterial-coronary sinus lactate; delta [L]) to ER in acute normovolemic anemia. Fourteen adult baboons were anesthetized, paralyzed, and ventilated on room air. Left atrial, coronary sinus, aortic, and Swan-Ganz catheters were inserted. Experimental animals (N = 7) were hemodiluted, at constant left atrial pressure (LAP), with 5% human serum albumin (HSA) to a HCT below 4%. Control animals (N = 7) underwent similar volume exchanges, also at constant LAP, with homologous RBCs resuspended in HSA. Whole-body extraction ratio and left ventricular lactate production were measured at baseline and at hematocrits of 20, 10, 6, and 4% in the experimental group. Data were obtained at similar volume exchange points in the control group. Significant lactate production occurred only in the experimental animals (P less than 0.05) when extraction ratio exceeded 50%. Significant lactate production does not occur before the whole-body ER exceeds 50%. ER appears to be a valid indicator of myocardial metabolism in anemia, in this setting.

The two acellular oxygen carriers currently being evaluated as red cell substitutes are hemoglobin solutions and fluorocarbon emulsions. We have shown that both products can maintain normal levels of oxygen consumption, CO2 production, and circulatory dynamics in primates in the virtual absence of the red blood cell. Although each solution thus satisfies the most important criteria for a red cell substitute, development continues with both products. The clinical trials with the fluorocarbons have been discontinued due to the lack of efficacy of Fluosol-DA--20% in the setting of acute blood loss. Our current hemoglobin preparation is a polymerized, pyridoxylated product that has a normal oxygen-carrying capacity. Clinical testing must await further evaluation of the safety and efficacy of this product. Alternative uses for both of these oxygen carriers continue to be explored, and may eventually be the area of their greatest utility in the clinical setting.