Pathophysiology of the cerebral circulation during cardiac surgery

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Although mortality rate after cardiac surgery has been drastically reduced, neurological complications remain a significant problem. Several etiologic factors have been proposed, including previous unrecognized neurological abnormality, embolic events, hypoxic insult, low cardiac output, systemic inflammatory response, and altered cerebral blood flow (CBF) and metabolism. Cerebral ischemia can occur when cerebral oxygen is insufficient to meet the global or regional cerebral oxygen consumption. Cerebral circulation is normally regulated by several complex mechanisms, such as metabolic stimuli, chemical stimuli, perfusion pressure, and neural stimuli [1].

During and after cardiac surgery, CBF and metabolism can also be affected by other factors including arterial PCO₂, temperature, anesthesia depth, and perfusion flow rate during cardiopulmonary bypass. As a consequence of the effects of anesthetic agents and hypothermia, CBF is generally reduced during cardiac surgery. Cerebral metabolic regulation refers to the mechanism describing the adaptation of CBF to the metabolic demands of the brain. Although CBF-metabolism coupling is fairly well maintained during cardiopulmonary bypass, cerebral metabolic rate for oxygen (CMRO₂) decreases significantly more than CBF [3]. The increase in CBF to CO₂ is preserved during hypothermic cardiopulmonary bypass, but the response can be diminished when using pH-stat management of blood gases due to the powerful vasodilator effect of CO₂ on the cerebral vasculature [4]. Moderate changes in arterial PO₂do not significantly alter CBF, but CBF increases once PaO₂ drops below 50mmHg so that cerebral oxygen delivery remains constant.

Pressure autoregulation refers to the ability of the brain to maintain total and regional CBF nearly constant despite large changes in systemic arterial blood pressure, independently of flow-metabolism coupling [5]. Pressure autoregulation is generally preserved during hypothermic cardiopulmonary bypass. Impaired autoregulation has been reported mainly in pH-stat conditions due to increasing PaCO₂. Interestingly, CBF and metabolismseem to be unaffected during pulsatile flow as compared with nonpulsatile flow during cardiopulmonary bypass [6]. Different data found by other investigators may be easily explained by changes in perfusion variables, such as temperature or PaCO₂. Variation in the systemic flow rate from the pump oxygenator per se hardly influences CBF or CMRO₂during hypothermic CPB [7]. Conflicting results reported by others are difficult to interpret because of confounding effects of differences in the management of CO₂, and anesthetic and vasoactive drugs during hypothermic cardiopulmonary bypass. Since blood viscosity represents a major determinant of vascular resistance, CBF is inversely related to hematocrit. Nevertheless, a continuing controversy pertains to whether CBF is purely rheologic or a function of changes in oxygen delivery to the tissue.

In conclusion, CBF and CMRO₂ drop during cardiac surgery due to combined effects of both anesthesia and hypothermia. Regulatory mechanisms of CBF are little affected by hypothermic cardiopulmonary bypass, but can be influenced by other determinants of cerebral perfusion.