Mechanisms of sepsis-induced cardiac dysfunction

作者：Alain Rudiger, Mervyn Singer · 发表于：Critical Care Medicine · 年份：2007 · DOI：10.1097/01.ccm.0000266683.64081.02 · 被引用次数：703 · 研究领域：Sepsis Diagnosis and Treatment、Intensive Care Unit Cognitive Disorders、Takotsubo Cardiomyopathy and Associated Phenomena

OBJECTIVES: To review mechanisms underlying sepsis-induced cardiac dysfunction in general and intrinsic myocardial depression in particular. DATA SOURCE: MEDLINE database. DATA SYNTHESIS: Myocardial depression is a well-recognized manifestation of organ dysfunction in sepsis. Due to the lack of a generally accepted definition and the absence of large epidemiologic studies, its frequency is uncertain. Echocardiographic studies suggest that 40% to 50% of patients with prolonged septic shock develop myocardial depression, as defined by a reduced ejection fraction. Sepsis-related changes in circulating volume and vessel tone inevitably affect cardiac performance. Although the coronary circulation during sepsis is maintained or even increased, alterations in the microcirculation are likely. Mitochondrial dysfunction, another feature of sepsis-induced organ dysfunction, will also place the cardiomyocytes at risk of adenosine triphosphate depletion. However, clinical studies have demonstrated that myocardial cell death is rare and that cardiac function is fully reversible in survivors. Hence, functional rather than structural changes seem to be responsible for intrinsic myocardial depression during sepsis. The underlying mechanisms include down-regulation of beta-adrenergic receptors, depressed postreceptor signaling pathways, impaired calcium liberation from the sarcoplasmic reticulum, and impaired electromechanical coupling at the myofibrillar level. Most, if not all, of these cha...