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The effects of high shear stress on platelet function as a result of pulsatile cardiopulmonary bypass / Justin D. Krueger, B.S.

by Krueger, Justin D.

Extracorporeal Circulation

Cardiopulmonary bypass -- Adverse effects

Blood -- Circulation, Artificial -- Complications.

Blood Coagulation.

61 leaves : ill. ; 29 cm.

Advisor: Dr. Ronald Gerrits.

Committee members: Dr. Larry Fennigkoh, Dr. Charles Tritt.

Background -- Hypothesis -- Methods and materials -- Results -- Discussion -- References -- Appendix A) Derivation of wall shear stress equation under turbulent flows and data for Reynolds number and shear stress calculation B) Two-way ANOVA SigmaStat report for percent platelet aggregation C) SigmaStat multiple linear regression report for percent platelet aggregation D) One-way ANOVA SigmaStat report for baseline platelet counts E) One-way ANOVA SigmaStat report for baseline HCTs F) Two-way ANOVA SigmaStat report for change in blood temperature G) Raw data.

Pulsatile cardiopulmonary bypass has been associated with better patient outcomes in respect to postoperative organ function and hemodynamics. In theory, this is because pulsatile flow better imitates the flow characteristics of the native heart, which can be described as having a "pulse pressure" in the arterial pressure waveform. When utilizing a pulsatile pump, an increase in the pulse pressure can be obtained by decreasing the "base flow percent" parameter of the pulse cycle as long as there is a concomitant increase in the high flow rate phase of the pulse cycle. This is necessary to maintain the same average flow rate. However, the higher peak flow rates and increased turbulence that occurs with the high flow rate results in increased shear stresses being applied to the blood and its components. These shear stresses are in the ranges that have been shown to cause shear-induced platelet activation/aggregation (SIPA). It is known that many factors of cardiopulmonary bypass lead to platelet dysfunction; which, consequently result in an increased tendency of uncontrolled bleeding in the post-CPB patient. Therefore, with the use of pulsatile CPB it is possible that the increased shear stresses produced may cause increased platelet dysfunction in comparison to non-pulsatile CPB.

The goal of this study was to determine the effect of increased shear stress as a result of pulsatile cardiopulmonary bypass on platelet function, as assessed by the platelets' ability to aggregate in the presence of a platelet agonist. To perform this study, a total of 16 experimental trials were conducted in which bovine blood was perfused through extracorporeal circuits and exposed to increased levels of shear stress produced by varying the base flow percentage setting of the pulsatile cycle. Each trial length was 90 minutes at a base flow percentage of 100% (non-pulsatile), 70%, 50%, or 30%, with all trials utilizing an average flow rate of 5 L/min. The Platelet Works platelet function analysis system (which utilized ADP as the agonist) was used to determine platelet function at the initial, 45 minute, and 90 minute intervals. All statistical analyses performed were considered significant at a p<0.05.

No significant differences were found to exist between base flow percentage group (shear stress), time, and percent platelet aggregation. Platelet counts were unexpectedly found not to have decreased as time progressed. Additionally, no significant differences were found between base flow percentage groups and change in blood temperature. However, there was a significant change in blood temperature found to exist in all groups between the initial time point and 45 minutes.

The results of this study were in agreement with those that had determined that pulsatile flow does not lead to increased post-surgical blood loss. However, these results differ from those that have found increased platelet dysfunction and increased SIPA with increased shear stress and increased time of exposure to shear stress. There were multiple factors that could have possibly influenced the results of this study.

This appears to be the first study to attempt to determine what effect pulsatile CPB has on the ability of platelets to aggregate in the presence of an agonist. Based on the results of this study it is suggested that further research be performed using larger sample sizes and a direct thrombin inhibitor as an anticoagulant. Additionally, clinical patient studies would be beneficial to determine if the platelet dysfunction resulting from the shear stress produced by pulsatile CPB is significantly small in comparison to the global dysfunction that occurs upon exposure to the extracorporeal circuit and heparin.

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