Suppr超能文献

感染性休克合并ST段抬高型心肌梗死

ST-Elevation Myocardial Infarction in the Presence of Septic Shock.

作者信息

Ishmael Leah, Zalocha Joseph

机构信息

HCA Healthcare/USF Morsani College of Medicine GME Programs, Northside Hospital, St. Petersburg, FL, USA.

出版信息

Case Rep Crit Care. 2020 Aug 18;2020:8879878. doi: 10.1155/2020/8879878. eCollection 2020.

Abstract

Elevated cardiac enzymes are often seen in the setting of sepsis. The mechanism involves hypoperfusion and possible compromise to myocardial tissue. Electrocardiogram (ECG) changes in the setting of septic shock are less common and can vary widely. Rarely, ST-segment elevations can occur. This case describes a 54-year-old female who presented with septic shock secondary to pyelonephritis and bacteremia. The patient was admitted to the intensive care unit on norepinephrine and required mechanical ventilation. A significant rise in troponin I (peak 19.8 ng/mL) was seen and ECG showed ST-segment elevations in leads I and aVL with reciprocal ST depressions in leads II, III, and aVF. The patient was taken urgently for left cardiac catheterization, which showed no evidence of obstructive coronary artery disease. When distinguishing between septic shock and cardiogenic shock, insertion of a pulmonary artery catheter may help with diagnosis and treatment of cardiogenic shock. Catheter hemodynamic monitoring can also confirm the diagnosis. In our patient's case, hemodynamic monitoring was initiated and was not consistent with cardiogenic shock. ST-segment elevations in the high lateral leads and elevated cardiac markers were likely due to severe transmural ischemia secondary to increased oxygen demand. The patient was continued on intravenous antibiotics for treatment of her septic shock. She was extubated and weaned off of norepinephrine within 48 hours. Repeat ECG performed after resolution of the infection showed normal sinus rhythm with no ST-segment changes. Cardiac dysfunction in the setting of septic shock is well described in medical literature; however, the mechanisms of dysfunction are not explicitly understood. Transient hypoperfusion, coronary vasospasm, and localized endothelial damage are possible components. It is important to think of varying etiologies, other than acute coronary syndrome when approaching patients in septic shock with acute ST-segment changes and elevated cardiac markers.

摘要

脓毒症时常常可见心肌酶升高。其机制包括灌注不足以及心肌组织可能受到的损害。脓毒性休克时的心电图(ECG)改变较少见,且变化范围很大。极少数情况下,可出现ST段抬高。本病例描述了一名54岁女性,因肾盂肾炎和菌血症继发脓毒性休克。患者入住重症监护病房,使用去甲肾上腺素,并需要机械通气。肌钙蛋白I显著升高(峰值19.8 ng/mL),ECG显示I导联和aVL导联ST段抬高,II、III和aVF导联出现对应性ST段压低。患者紧急接受了左心导管检查,结果显示无阻塞性冠状动脉疾病的证据。在鉴别脓毒性休克和心源性休克时,插入肺动脉导管可能有助于心源性休克的诊断和治疗。导管血流动力学监测也可确诊。在我们患者的病例中,启动了血流动力学监测,结果与心源性休克不符。高侧壁导联的ST段抬高和心肌标志物升高可能是由于氧需求增加继发的严重透壁性缺血所致。患者继续接受静脉抗生素治疗脓毒性休克。她在48小时内拔管并停用了去甲肾上腺素。感染消退后复查ECG显示窦性心律正常,无ST段改变。医学文献中对脓毒性休克时的心脏功能障碍已有充分描述;然而,其功能障碍的机制尚未完全明确。短暂性灌注不足、冠状动脉痉挛和局部内皮损伤可能是其组成部分。在处理伴有急性ST段改变和心肌标志物升高的脓毒性休克患者时,除了急性冠状动脉综合征外,考虑多种病因很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d3/7450346/33694c24739f/CRICC2020-8879878.001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验