Dysfonction myocardique post-arrêt cardiaque

Hemodynamic instability following successful treatment of cardiac arrest is frequent, independently of its etiology. In the absence of multiple organ failure leading to death, this postresuscitation syndrome may increase initial brain damages and constitutes a major therapeutic target of hospital management. This shock is characterized by the occurrence of an early myocardial failure, including both ventricular systolic and diastolic dysfunction, usually reversible within 48 to 72 hours. Its severity seems to be linked with the resuscitation characteristics and with the necessary delay for the restoration of a spontaneous circulatory activity. The evoked pathophysiological mechanisms are multiple and complex, involving mainly ischemia-reperfusion injury leading to a decreased responsiveness of contractile filaments to calcium. This myocardial stunning is secondarily associated with superimposed vasodilatation, as a consequence of the systemic inflammatory response introduced by the reperfusion. Early inotropic treatment allows to partially reverse the myocardial dysfunction, suggesting the existence of a contractile reserve. The correction of a potential volemic deficit, even the use of vasoactive drugs in case of strong vasoplegia, are also key points of the treatment. Echocardiography allows the diagnosis and the adapted treatment of each component of the postresuscitation shock, necessary for the improvement of the outcome.