Perioperative
hyperoxia has been claimed to have a number of therapeutic advantages. However, in the setting of cardiac surgery and
cardiopulmonary bypass (CPB), enthusiasm for its use has been tempered by concerns regarding the effect of high partial pressures of
oxygen on cardiac, vascular, and respiratory function and the potential for exacerbation of
ischemia-reperfusion injury. There is encouraging evidence from animal studies that
hyperoxia is effective in myocardial preconditioning, at least in nondiseased hearts. There is also evidence that
hyperoxia reduces gas microemboli production and longevity during CPB, although it is unclear whether this translates into a clinical benefit in terms of a reduction in postoperative neurological morbidity.
Hyperoxia leads to changes in cardiovascular function. However, the effects of these changes remain unclear. At a tissue level, there is evidence that
hyperoxia does not lead to improvement in partial pressure of
oxygen. Indeed, the opposite may be the case with reductions in capillary density leading to areas of reduced tissue oxygenation. The risks of
hyperoxia in association with CPB include
lung injury, increased systemic
reactive oxygen species generation, and exacerbation of
reactive oxygen species-mediated myocardial injury at the time of reperfusion. Again, it is difficult to know whether the changes demonstrated are temporary or if they translate into a worsening of clinical outcomes. In conclusion, perhaps the key to the use of
hyperoxia is in the timing. In the period pre-CPB,
hyperoxia may precondition the myocardium and, paradoxically, confer a degree of protection against
reactive oxygen species-induced injury at the time of reperfusion.
Hyperoxia during CPB is probably harmful and should be avoided unless the risk from gas microemboli is thought to be significant, in which case the risks and benefits to the individual patient must be weighed.