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Experimental evidence has indicated that inhalational anesthetics have protective effects against the consequences of cardiac ischemia-reperfusion injury. These protective properties have been related to pharmacologic pre- and postconditioning effects but also to a modulation of the inflammatory response. Although quite a number of underlying pathways have been identified, the exact mechanisms still remain to be fully elucidated. It is beyond the scope of this chapter to discuss this point, and the interested reader is referred to a number of review articles that have been published on the topic over the past years.
Cardiovascular complications still represent a significant health risk to the surgical population. Therefore any measure that may help reduce these adverse events should be part of the perioperative treatment of patients, especially those patients who are at increased risk for perioperative myocardial ischemia.
Prevention of myocardial ischemia is traditionally focused on maintaining the delicate balance between myocardial oxygen supply and demand. Inhalational anesthetics decrease myocardial loading conditions and contractility. Even the newer compounds such as desflurane and sevoflurane demonstrate a similar dose-dependent depression of myocardial function. These depressant effects decrease myocardial oxygen demand and may therefore have a beneficial role on the myocardial oxygen balance. In addition to these indirect protective effects, inhalational anesthetics also have—as discussed earlier—direct protective properties against the consequences of ischemia-reperfusion injury. These direct and indirect effects may therefore provide an additional tool in the prevention and treatment of perioperative ischemic cardiac dysfunction.
On the basis of these theoretical considerations and the vast amount of experimental evidence, several study groups have hypothesized that the implementation of the cardioprotective properties of inhalational anesthetics in clinical practice might be associated with less myocardial damage and dysfunction after ischemia-reperfusion injury, ultimately resulting in a better postoperative outcome with less morbidity and mortality.
To translate the available experimental evidence into the clinical setting, the experimental protocol would necessitate myocardial ischemia to be instituted in a standardized and reproducible way. This situation is normally not present in clinical practice, where all efforts are directed toward the prevention of myocardial ischemia. The clinical situation that most closely resembles the sequence of standardized myocardial ischemia and reperfusion is in the setting of coronary artery surgery. This type of surgery therefore allows us to transpose the experimental setting of preconditioning and postconditioning protocols into a clinical protocol sequence.
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