Pulmonary and systemic hemodynamics are associated with myocardial injury in the acute respiratory distress syndrome

急性呼吸窘迫综合征中,肺部和全身血流动力学与心肌损伤相关。

阅读:1

Abstract

BACKGROUND: Whether right and left heart hemodynamics are associated with myocardial injury in the acute respiratory distress syndrome (ARDS) is not known. METHODS: We performed a retrospective cohort study of subjects who had right heart catheterization within the ALVEOLI trial and Fluid and Catheter Treatment Trial. Myocardial injury was assessed using a highly sensitive troponin assay (hsTn; Abbot ARCHITECT). Hemodynamic variables included right atrial pressure, pulmonary artery wedge pressure, cardiac index and stroke volume, pulmonary vascular resistance, pulmonary arterial compliance, and pulmonary effective arterial elastance. We performed linear, logistic, and Cox regression to determine the association of hemodynamic variables with myocardial injury and to determine if hemodynamics mediated the association between myocardial injury and death. RESULTS: Among 252 ARDS patients, median day 0 troponin was 65.4 (13.8-397.8) ng/L. Lower cardiac index (β -0.23 SE 0.10; P < 0.001) and stroke volume (β -0.26 SE 0.005; P < 0.001), higher pulmonary vascular resistance (β 0.22 SE 0.11; P < 0.001), lower pulmonary arterial compliance (β -0.24 SE 0.06; P < 0.001), and higher arterial elastance (β 0.27 SE 0.43; P < 0.001) were associated with greater myocardial injury in univariable and adjusted models. Changes in stroke volume, cardiac index, pulmonary arterial compliance, pulmonary vascular resistance, and arterial elastance were all associated with progressive myocardial injury over three days. hsTn levels were associated with mortality; however, the association was attenuated after adjustment for each of stroke volume, pulmonary vascular resistance, pulmonary arterial compliance, and arterial elastance. CONCLUSION: Pulmonary vascular hemodynamics are associated with myocardial injury in ARDS, while filling pressures are not. Pulmonary vascular disease may represent a treatable contributor to myocardial injury in ARDS.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。