Changes in Redox Status of Cerebral Cytochrome Oxidase during Periods of Hypoperfusion in Patients Undergoing Cardiopulmonary Bypass

Abstract

Cognitive impairment is a well-recognised complication following cardiac surgery. Even though major advances in anaesthetic, perfusion and surgical techniques have significantly reduced morbidity and mortality rates¹, recent studies have found cognitive impairment was prevalent in as many as 53% patients at discharge following coronary artery bypass grafting (CABG)². The aetiology of cognitive impairment is complex, with many contributory factors. The primary cause of neurological injury is the occurrence of global or focal cerebral ischaemia. Numerous studies have been undertaken to minimise incidence of cerebral ischaemia, the majority of which have been in animal models. Cooling has long been used for protection of the brain and heart during cardiopulmonary bypass (CPB)³. Decreasing the metabolic rate by cooling to hypothermia reduces the metabolic demand, and therefore reduces the likelihood of a mismatch between oxygen supply and demand. Recent studies have suggested that increasing the period of cooling on CPB before instituting deep hypothermic circulatory arrest (DHCA), cooling the head with ice packs and introducing short periods of intermittent reperfusion during DHCA could reduce cerebral injury⁴. However, recent concerns have been raised about the potential harmful effects of re-warming on neurological outcome following hypothermia. An increase in brain temperature of 0.5–2.0 °C at the time, or immediately after an ischaemic insult can significantly affect neurological outcome⁵.