Septic cardiomyopathy.
Septic cardiomyopathy.
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DOI：
10.1097/aia.0b013e3182603ec1
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发表时间：
2012
影响因子：
0.6
通讯作者：
Kaynar AM
中科院分区：
文献类型：
--
作者：
Phillips DP;Kaynar AM
脓毒症患者无结构改变的心肌抑制称为“脓毒症心肌病”。1-6 Calvin等人在1981年证实了容量复苏的脓毒症患者存在心肌功能障碍，患者射血分数降低，舒张期容积指数升高。随后，Parker等人使用肺动脉导管（PAC）进行一系列放射性核素成像，8进一步证实了这些观察结果，得出两个主要发现：(a)感染性休克幸存者舒张末期容积指数升高，射血分数降低，而非幸存者通常保持正常的心脏容积；(b)舒张末期容积指数和射血分数的急性变化虽然持续数天，但是可逆的。最近，超声心动图研究表明，在脓毒症患者左心室收缩和舒张功能受损。9,10总的来说，脓毒性心肌病的特点是尽管儿茶酚胺水平升高，心输出量却突然下降；(2)输液后血压反应降低；(3)喷射分数可逆降低；(4)双室扩张。11-16尽管左室舒张末期容量正常，但患者的脑卒中容量和左室射血分数也可能显著降低，低于30%。14,17,18脓毒性心肌病被认为发生在脓毒症连续体的晚期；然而，它也在疾病的早期被证实并损害两个心室。4,14,19临床前和临床数据表明，心肌抑制发生在促炎细胞因子水平升高的情况下。20、21
Myocardial depression without structural changes in patients with sepsis is termed “septic cardiomyopathy.” 1–6 Calvin et al 7 in 1981 demonstrated myocardial dysfunction in volume-resuscitated septic patients, who had decreased ejection fraction and increased enddiastolic volume index. Subsequently, using pulmonary artery catheters (PAC) with serial radionuclide imaging, Parker et al 8 furthered these observations with the 2 major findings that (a) survivors of septic shock had increased end-diastolic volume index and decreased ejection fraction, whereas nonsurvivors typically maintained normal cardiac volumes; and (b) these acute changes in end-diastolic volume index and ejection fraction, although sustained for several days, were reversible. More recently, echocardiographic studies have demonstrated impaired left ventricular systolic and diastolic function in septic patients. 9, 10 Overall, septic cardiomyopathy can be characterized by sudden (1) depression of cardiac output despite elevated levels of catecholamines;(2) decreased blood pressure response to fluid boluses;(3) reversible reduction in ejection fraction; and (4) biventricular dilation. 11–16 Patients may also have profoundly reduced stroke volumes and left ventricular ejection fractions of< 30% despite exhibiting normal left ventricular end-diastolic volumes. 14, 17, 18 Septic cardiomyopathy was believed to occur late in the sepsis continuum; however, it has been also demonstrated early in the disease state and impairs both ventricles. 4, 14, 19 Preclinical and clinical data suggest that myocardial depression occurs in the presence of elevated levels of proinflammatory cytokines. 20, 21