Background
Patients undergoing cardiac surgery have a substantial incidence of neurologic complications related to cerebral embolization during cardiopulmonary bypass. The purpose of this study was to determine if adjustments in the arterial carbon dioxide (PaCO2) level can reduce cerebral and ocular embolization.
Methods
Twenty pigs underwent cardiopulmonary bypass at 38 degrees C. At either hypercarbia (PaCO2 = 50-55 mmHg, group H, n = 10) or hypocarbia (PaCO2 = 25-30 mmHg, group L, n = 10), an embolic load of 1.2 x 10(50 67-microm orange fluorescent microspheres was injected into the aortic cannula. Before and after embolization, cerebral and ocular blood flows were determined at normocapnia using 15-microm fluorescent microspheres. After cardiopulmonary bypass was completed, the eyes were enucleated and brain tissue samples were collected. Microspheres were isolated and the fluorescence was measured.
Results
In groups H and L, the mean PaCO2 values at embolization were 52+/-3 mmHg and 27+/-2 mmHg, respectively (P < 0.0001). Total and regional embolization were significantly less in hypocapnia than in hypercapnic animals: 142% more emboli were detected in the brain in group H than in group L (P < 0.0001). Cerebral blood flow after embolization was unchanged in both groups. Similarly, fewer ocular emboli occurred in hypocapnic animals than in hypercapnic animals (P = 0.044), but in contrast to the brain, ocular blood flow decreased significantly in both groups after embolization.
Conclusions
Cerebral embolization is determined by the PaCO2 at the time of embolization. In cardiopulmonary bypass practice, reductions in PaCO2 during periods of embolic risk may reduce the risk for brain injury.
Lipopolysaccharide decreases cochlear blood flow dose dependently in a guinea pig animal model via TNF signaling
