Cardiac Microemboli During Cardiopulmonary Bypass: Structural Sources, Hemodynamics, and Neurologic Sequelae

Cardiopulmonary bypass (CPB) has been linked with the introduction of particulate matter and gaseous microemboli, which are believed to contribute to neurologic dysfunction after cardiac surgery. During CPB, microemboli can originate in the aorta from manipulation, valve decalcification, cardiotomy suction, cavitation, and air entrainment into the extracorporeal circuit. Perfusion factors including pump flow, perfusion pressure, venous drainage, cannulation site turbulence, and temperature may also alter embolic load. Anesthetic manipulation can modulate cerebral autoregulation, vascular tone, and neuroinflammation and may also play a role in determining brain vulnerability to injury. Despite relatively low risk for clinically evident stroke after CPB, diffusion‐weighted MRI reveals silent cerebral infarcts in up to 50% of patients, which have been linked with cognitive dysfunction and delayed postoperative neurocognitive recovery. This review will focus on the relationship between embolic sources, perfusion factors, and physiologic effects of anesthesia that influence cerebral embolic injury during CPB, as well as practical methods to minimize microembolic load.