Out of hospital cardiac arrest is the leading cause of death in industrialized countries. Recovery of hemodynamics does not necessarily lead to recovery of cerebral perfusion. The neurological injury induced by a circulatory arrest mainly determines the prognosis of patients after cardiac arrest and rates of survival with a favourable neurological outcome are low. This review focuses on the temporal course of cerebral perfusion and changes in cerebral autoregulation after out of hospital cardiac arrest. In the early phase after cardiac arrest, patients have a low cerebral blood flow that gradually restores towards normal values during the first 72 hours after cardiac arrest. Whether modification of the cerebral blood flow after return of spontaneous circulation impacts patient outcome remains to be determined.

CrCP is high after cardiac arrest with high cerebrovascular resistance and low MFV. This suggests that cerebral perfusion pressure should be maintained at a sufficient high level to avoid secondary brain injury. Failure to normalize the cerebrovascular profile may be a parameter of poor outcome.

Cerebral blood flow is altered after cardiac arrest, with decreased spontaneous fluctuations in non-survivors. Most likely, these changes are the consequence of impaired intrinsic myogenic vascular function and autonomic dysregulation.

Experimental human endotoxemia results in a decreased CrCP due to a loss of vascular resistance of the arterial bed. Vasopressors did not prevent this decrease in CrCP. Findings in patients with sepsis are comparable to those found in subjects after LPS administration.Patients with sepsis, despite treatment with vasopressors, have a risk for low cerebral blood flow and ischemia.

This study examines the influence of a successful PCI upon preoperative patient profile, peroperative management and postoperative, including one-year follow-up, results. From January 1999 through December 2001, 1141 patients (91%) underwent coronary artery bypass grafting (CABG) as the primary intervention for myocardial revascularization (group A) and 113 patients (9%) underwent primary CABG after an initially successful PCI (group B). Patients undergoing CABG after a failed PCI were not included. Patients in group B were statistically significant younger (P=0.010), with more peripheral arterial vascular (P=0.015) and renal disease (P=0.036). Left main coronary artery stenosis was significantly lower in group B (P=0.004). The number of diseased vessels did not differ between the two groups. However, less distal anastomoses were performed in group B (P=0.001). Postoperatively there was no statistically significant differences, in the percentages of myocardial infarction, arrhythmias, reinterventions, neurological, renal and pulmonary complications, and hospital mortality. One-year follow-up did not show any statistically significant differences in cardiac related mortality (P=0.25) or recurrent ischemic events (P=0.27). Multivariate analysis did not identify a successful PCI as a risk factor for early and late adverse outcomes. Previous PCI does not seem to result in a higher postoperative mortality or morbidity after CABG.