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Ann Thorac Surg 1995;59:1624-1626
© 1995 The Society of Thoracic Surgeons
Department of Thoracic and Cardiovascular Surgery, Sahlgrenska University Hospital, University of Gothenburg, S-413 45 Gothenburg, Sweden
To the Editor:
We read with interest the letter to the editor by Dr Ranucci [1]. The letter suggested that shear stress during cardiopulmonary bypass (CPB) induces postoperative leukocytosis. Hematocrit during CPB was positively correlated with postoperative white blood cell count in his ongoing study. Hematocrit was used to represent blood viscosity and shear stress level.
To confirm the effect of intraoperative hematocrit or blood viscosity on postoperative leukocytosis, we looked at our unpublished data from 40 patients undergoing coronary artery bypass grafting. Whole blood viscosity, hematocrit, and white blood cell count were analyzed before the operation, six times during the operation, and twice after the operation. Whole blood viscosity was measured by a capillary viscometer at a shear rate of 20, 30, 40, 60, and 80 per second and expressed as ratio to the viscosity of normal saline solution. Hematocrit and white blood cell count were done by a semiautomatic flow cytometer. No correlations were found between the postoperative white blood cell count and any intraoperative hematocrit or viscosity estimation. Correlations of white blood cell count at 24 hours after the operation with whole blood viscosity (shear rate = 20 per second) and hematocrit at 5 minutes after the start of CPB are shown in Figures 1 and 2
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Reference
Centro Cardiovascolare ``E. Malan'', Ospedale Clinicizzato S. Donato, Via Morandi 30, 20097 San Donato Milanese, Milan, Italy
Reply To the Editor:
In their interesting letter Drs Liu and Roberts comment on my previous letter to the editor [1] in which I presented data concerning postoperative leukocytosis and hematocrit during cardiopulmonary bypass (CPB). Doctors Liu and Roberts present a series of patients in whom they measured blood viscosity and hematocrit after 5 minutes of CPB. They did not find any correlation between both these parameters and leukocyte count 24 hours after the end of the operation. They conclude that the hypothesis that shear stress during CPB induces leukocyte increase should be sustained by means of further data basically investigating leukocyte activation (release of leukotriene and other mediators).
I absolutely agree that more sophisticated data are required to determine the correlation between blood viscosity, shear stress, and blood cell activation. Anyway, I do believe that the positive correlation between hematocrit during CPB and postoperative leukocytosis is a reliable phenomenon, and that in Drs Liu and Roberts' data there is an important factor hiding this relationship.
In their series of patients, only 4 demonstrated a hematocrit value greater than 30% (after 5 minutes of CPB, but they failed to say if it was before or after cardioplegia administration; maybe this value subsequently decreased). They did not specify the temperature during CPB; I hypothesize a moderate hypothermia (considering the coronary artery bypass grafting operation) at 28° to 30°C. In these conditions, hypothermia induces an increase in blood viscosity of about 35% (5% per each degree below 37°C). At a hematocrit level of 30%, there is a decrease in blood viscosity of about 30%, and more for lower hematocrit values. Therefore, the experimental conditions of Liu and Roberts almost always provide a normal or reduced blood viscosity, as confirmed by their own measurements.
I think that the viscosity-related postoperative leukocytosis probably is much more evident at supraphysiologic levels of blood viscosity, as happens at 28°C when the hematocrit is greater than 30%. This was the situation of more than 50% of the patients reported in my letter [1]. To confirm this observation, I took a look at another series of 164 consecutive patients undergoing coronary artery bypass grafting during the last 2 months in my institution. Data in Figure 1
confirm the existence of a positive correlation between hematocrit during CPB (it is the mean of the values measured throughout perfusion) and postoperative leukocytosis (at arrival in the intensive care unit) (r = 0.382; p < 0.001). Nevertheless, considering only patients with a mean hematocrit during CPB of 28% or less, there is no more correlation, and my data become very similar to those reported by Liu and Roberts.
Let me add a further consideration. The reason for my high hematocrit values during CPB is that I am convinced that limiting the degree of hemodilution during CPB improves postoperative course. My colleagues and I [2] demonstrated that the rate of renal dysfunction after coronary artery bypass grafting operations is higher in grossly hemodiluted patients.
We have reduced our priming volume to no more than 800 mL of colloid solution, and our cardioplegia delivery rarely exceeds 500 mL of crystalloid solution. Following this method, our mean drop in hematocrit from baseline to CPB is about 8%.
Anyway, we must consider that this approach requires careful control of the rheologic conditions during CPB. We use a nomogram to control pre-CPB hematocrit whenever it is too high [3], but sometimes the hematocrit values exceed 35%.
We believe that this condition probably could be associated with unknown blood cell reaction due to the high viscosity and shear stress during CPB. Doctors Liu and Roberts' suggestions will help us in studying these reactions.
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28%; open circles = hematocrit > 28%.)