The dramatic decline in mortality related to cardiac surgery has resul
ted in over 330,000 surgeries involving cardiopulmonary bypass (CPB) b
eing performed yearly in the United States. Although few patients die
as a result of cardiac surgery, over two thirds of the patients demons
trate evidence of acute neuropsychological dysfunction postoperatively
. The potential mechanisms contributing to post-CPB neuropsychological
deficits are many, but two major inter-related etiologic factors, po
perfusion and emboli, are suggested as the probable culprits. If embol
ism is the cause of the deficits, increasing cerebral perfusion would
deliver more emboli and increase the amount and severity of injury. Co
nversely, if hypoperfusion is the cause of the injury, then decreasing
brain blood flow to minimize embolic delivery, would increase the lik
elihood of perfusion injury. By, monitoring the carotid arteries of pa
tients undergoing coronary artery bypass graft surgery, we have determ
ined the frequency and quantity of embolic signals that occur during C
PB. Although, we have not been able to determine the nature of the emb
olus, gaseous or solid, we have demonstrated a relationship between th
e overall embolic load and the probability of having NP dysfunction.