Send to

Choose Destination
See comment in PubMed Commons below
Semin Thorac Cardiovasc Surg. 2001 Apr;13(2):170-5.

Importance of blood pressure regulation in maintaining adequate tissue perfusion during cardiopulmonary bypass.

Author information

Department of Cardiovascular and Thoracic Surgery, The Albert Einstein College of Medicine-Montefiore Medical Center, Bronx, NY, USA.


Patients undergoing surgery with the aid of cardiopulmonary bypass (CPB) have an incidence of end-organ dysfunction, caused by embolization, regional hypoperfusion, or some combination of the two. In this article, we attempt to define the effect of mean arterial pressure (MAP) during CPB on postoperative end-organ function. Although early studies reported that cerebral perfusion during hypothermic CPB is independent of MAP, recent laboratory and clinical reports have shown a positive slope in the MAP versus cerebral blood flow relationship. In clinical studies, patients who had higher MAPs during CPB had a lower incidence of cardiac and neurologic complications, as well as late neurocognitive abnormalities compared with patients with lower MAPs. Improving collateral flow in the setting of cerebral embolization has been postulated as the main mechanism for the improved neurologic outcomes in the high MAP groups. Higher perfusion pressure during CPB affects regional blood flow to the kidneys and visceral organs. However, the lower autoregulatory limits of perfusion to abdominal organs differ from the limits to the brain. Enhanced visceral perfusion during CPB is best achieved by increasing perfusion pressure via increases in perfusion flow rates rather than by using peripheral vasoconstriction alone. In conclusion, it is clear that maintenance of a high MAP during CPB may have a significant impact in protecting the brain and abdominal organs, particularly in the subset of patients at high risk for embolization and end-organ dysfunction.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center