Hemodilution and Hematocrit: How Low Do You Go?

The advent of hypothermic cardiopulmonary bypass (CPB) has made intentional hemodilution a standard practice, as it is believed that the increase in blood viscosity without hemodilution adversely affects microcirculatory flow. In the 1980s and 1990s, the acceptable level of CPB hemodilution was lowered to hematocrit values <18% as a consequence of the heightened concern of viral transmission through blood transfusion. During the same period, a healthy canine CPB model study suggested that the hematocrit at which cerebral metabolism became delivery dependent was approximately 14% during normothermic CPB and 11% during CPB at 28C. 2 Physiologically important changes in cerebral oxygen supply were however reported in subsets of the animals at hematocrits as high as 18%. Limits to hemodilution were also suggested by other animal data 4 but, in general, the consequences of extreme hemodilution, a common clinical practice during CPB, were largely unknown. The deleterious consequences of extreme hemodilution during CPB in humans have been recently highlighted by a series of retrospective database studies. In virtually every outcome examined, an independent, direct association between the degree of hemodilution during CPB and the adverse outcome of interest was identified. For example, Karkouti et al studying 10,949 patients undergoing cardiac surgery with CPB reported a 10% increase in the odds of suffering a perioperative stroke with each percent decrease in hematocrit. (Figure 1) Potential mechanisms for this injury include increased cerebral embolic load and diminished oxygen delivery to ischemic areas of the brain. When acute renal failure was examined, these same investigators reported a 230% increase in the odds of developing acute postoperative renal failure for those with a CPB nadir hematocrit < 21% (Figure 2). Interestingly, the odds of developing renal failure