¹Bristol Heart Institute and Department of Anaesthesia, Faculty of Medicine and Dentistry, University of Bristol, Bristol, UK

Correspondence: Professor M-S Suleiman, Bristol Heart Institute and Department of Anaesthesia, Faculty of Medicine and Dentistry, Bristol Royal Infirmary, University of Bristol, Level 7, Bristol BS2 8HW, UK. E-mail: m.s.suleiman@bristol.ac.uk

Received 5 June 2007; Revised 6 September 2007; Accepted 2 October 2007; Published online 22 October 2007.

Abstract

Open-heart surgery triggers an inflammatory response that is largely the result of surgical trauma, cardiopulmonary bypass, and organ reperfusion injury (e.g. heart). The heart sustains injury triggered by ischaemia and reperfusion and also as a result of the effects of systemic inflammatory mediators. In addition, the heart itself is a source of inflammatory mediators and reactive oxygen species that are likely to contribute to the impairment of cardiac pump function. Formulating strategies to protect the heart during open heart surgery by attenuating reperfusion injury and systemic inflammatory response is essential to reduce morbidity. Although many anaesthetic drugs have cardioprotective actions, the diversity of the proposed mechanisms for protection (e.g. attenuating Ca²⁺ overload, anti-inflammatory and antioxidant effects, pre- and post-conditioning-like protection) may have contributed to the slow adoption of anaesthetics as cardioprotective agents during open heart surgery. Clinical trials have suggested at least some cardioprotective effects of volatile anaesthetics. Whether these benefits are relevant in terms of morbidity and mortality is unclear and needs further investigation. This review describes the main mediators of myocardial injury during open heart surgery, explores available evidence of anaesthetics induced cardioprotection and addresses the efforts made to translate bench work into clinical practice.