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Ann Thorac Surg 1995;60:169-170
© 1995 The Society of Thoracic Surgeons


Invited Commentary

Invited Commentary

John M. Murkin, MD

Department of Anaesthesia University Hospital University of Western Ontario London, Ontario, Canada N6A 5A5

See also page 165.

The unique circumstances of cardiopulmonary bypass allow a greater degree of control over the systemic circulation than is found in virtually any other clinical situation. Essentially all aspects of perfusion, such as selection of pulsatile or laminar flow characteristics, hypothermic or normothermic temperatures, hematocrit, high or low flow rates, and perfusion pressures that are within or below the autoregulatory range, are determined either specifically or routinely by the clinician.

Most of these clinical determinants have been adopted empirically based on more than 40 years of accumulated clinical experience. However, in an era that has seen patients who are increasingly at the extremes of age, and who are undergoing procedures of progressively greater length and complexity, the incidence of adverse neurologic events after cardiopulmonary bypass has risen substantially. To what extent hypoperfusion is contributing to this cerebral morbidity is unclear, but it is apparent that a greater understanding of the specific factors influencing cerebral physiology during cardiopulmonary bypass is essential.

In the hypothermic cardiopulmonary bypass model employed by Schwartz and associates, changes in mean arterial pressure below the apparent cerebral autoregulatory range were shown to influence cerebral blood flow directly. Conversely, profound reductions in pump flow rate produced no significant effects on cerebral blood flow. Other studies, both clinical and experimental, have suggested such effects, but generally either the variables in these studies were altered over a fairly limited range or flow rate and perfusion pressure interacted and were not kept as totally independent variables. Now that Schwartz and associates effectively have confirmed the primacy of perfusion pressure over flow rates, the clinical implications of this information, and the implications for further investigations, should be considered.

Clinically, these data suggest that when flow reductions are required during cardiopulmonary bypass, efforts must be made to maintain cerebral perfusion pressure to preserve cerebral blood flow. Similarly, even when hypotension is accompanied by high pump flow rates—such as sometimes occurs during normothermic cardiopulmonary bypass—adequacy of cerebral perfusion cannot be assumed. What specifically that perfusion pressure should be has not yet been addressed. Also, the larger question of whether the limits of cerebral autoregulation are extended during moderate hypothermic cardiopulmonary bypass, as several clinical studies have suggested, remains unclear. From the data of Schwartz and associates, cerebral autoregulation does appear to be lost at extremes of hypotension. As such, it would appear that the clinician cannot blithely accept hypotension, even during hypothermia with high flow rates, with any confidence of maintaining adequate cerebral blood flow. By default, maintaining pressures at the normal lower limit of cerebral autoregulation—50 mm Hg—appears judicious. Cerebral perfusion pressure must be maintained.


Related Article

Cerebral Blood Flow Is Determined by Arterial Pressure and Not Cardiopulmonary Bypass Flow Rate
Arthur E. Schwartz, Aqeel A. Sandhu, Richard J. Kaplon, William L. Young, Amy E. Jonassen, David C. Adams, Niloo M. Edwards, Joseph J. Sistino, Ccp, Pawel Kwiatkowski, and Robert E. Michler
Ann. Thorac. Surg. 1995 60: 165-169. [Abstract] [Full Text]




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