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Shark Fin Electrocardiogram in the Intensive Care Unit
Circulation ( IF 37.8 ) Pub Date : 2022-10-03 , DOI: 10.1161/circulationaha.122.062034
Bin Zhang 1 , Zhao-Wei Yin 2 , Wenbiao Chen 3
Affiliation  

A 54-year-old woman was admitted to the intensive care unit with septic shock induced by intraabdominal infection. An initial physical examination revealed a body temperature of 38.6°C, a blood pressure of 82/56 mm Hg, a pulse rate of 109 beats per minute, and a respiratory rate of 26 breaths/minute. At admission, a 12-lead ECG was performed (Figure 1). Serum troponin I level was 2.02 ng/mL (normal value <0.10 ng/mL) and NT-proBNP (N-terminal pro–B-type natriuretic peptide) level was 5300 pg/mL (normal value <450 pg/mL). What are the important findings on the ECG? What is the most likely diagnosis? How would you manage the patient?


Figure 1. Initial ECG at admission.


Please turn the page to read the diagnosis.


The initial ECG showed diffuse ST-segment elevations in leads I, II, III, aVF, and V3 through V6 (Figure 1), which suggested a diagnosis of anterior and inferior wall ST-segment–elevation myocardial infarction. However, ST-segment depressions in leads aVR and V1 were inconsistent with that diagnosis. The prominent ST-segment depression in aVR might reflect a ST-segment elevation in lead aVR, which faces the apical and inferolateral regions. Diffuse ST-segment elevations (most prominent in leads II and aVR) might reflect extensively distributed wall motion abnormalities centered around the apex, which extended beyond the perfusion territory of any single coronary artery. The ST-segment depression in lead V1 indicated that wall motion abnormalities did not involve the right ventricular anterior region and the right paraseptal region faced by lead V1.1,2 The V3 through V6 leads showed giant R waves (amplitude ≥1 mV) that merged with markedly elevated ST segments, which formed a triangular morphology known as the same configuration called shark-fin sign and lambda-wave pattern (Figure 1). This electrocardiographic presentation is characteristic of ST-segment–elevation myocardial infarction, where the QRS complex, the ST segment, and the T wave are fused in a unique complex. Although acute coronary ischemia is traditionally associated with a shark-fin sign, this unusual tracing is also occasionally found in takotsubo cardiomyopathy (TTC), associated with hemodynamic instability and shock.3 In addition, the rise in serum troponin I level was disproportionately lower than expected for the degree of left ventricular contractile impairment and the NT-proBNP level was much higher than typically observed in a myocardial infarction, which suggested a high degree of acute left ventricular dilation and myocardial stretch. The ECG and cardiac biomarkers provided a clue that this patient might have TTC. Confirmation of TTC diagnosis requires coronary angiography and left ventriculography. In this patient, coronary angiography revealed normal coronary arteries (Figure 2A and 2B) and left ventriculography showed systolic apical ballooning in the left ventricle (Figure 2C and 2D) with a low left ventricular ejection fraction of 38%, consistent with a diagnosis of TTC. TTC was the final diagnosis in this patient.


Figure 2. Emergent coronary angiography and left ventriculography. A and B, Emergent coronary angiography showed no evidence of obstructive or spastic coronary disease. C and D, Left ventriculography revealed systolic apical ballooning in the apical region of the left ventricle.


The patient was treated in an intensive care unit with a trachea cannula and mechanical ventilation. She was given empiric broad-spectrum antibiotics, intravenous fluids, and vasopressor support. The empiric antimicrobial therapy was replaced once the underlying pathogen was recognized and antimicrobial sensitivities were established. Systolic apical ballooning in the left ventricle was treated with levosimendan, a noncatecholamine inotrope that does not increase myocyte cyclic adenosine monophosphate or oxygen consumption. Six days later, the disease had abated and the ECG (Figure 3) showed resolution of ST-segment elevations in leads I, II, III, aVF, and V2 through V6; T-wave flatness in leads I, II, III, aVR, aVL, aVF, V5, and V6; T-wave inversion in leads V1 through V4; and mild QT prolongation. A repeat ultrasonic cardiogram 5 weeks after discharge showed resolution of left ventricular systolic function (left ventricular ejection fraction, 59%).


Figure 3. ECG after resolution.


TTC is characterized by systolic dysfunction typically localized in the apical aspect (81.7%) and less frequently localized in the midventricular aspect (14.6%), basal aspect (2.2%), or focal aspect (1.5%) of the left ventricle. The most accepted hypothesis to explain how TTC arises is an elevation in circulating catecholamines and stress hormones, typically related to physical or emotional stress. Sepsis, a state of severe physical stress, can raise catecholamine levels, which activates the central autonomic nervous system and causes calcium overload in cardiac myocytes, leading to stunning of the myocardium and precipitation of cardiomyopathy. The rather specific ECG changes in TTC are T-wave inversion, often deep and widespread, and substantial QT prolongation, usually developing 24 to 48 hours after the onset of symptoms or the precipitating stressful trigger. ST-segment elevation involving precordial leads is seen in ≈40% of cases. In our case, cardiac involvement was associated with sepsis caused by an intraabdominal infection. The shark-fin sign, described in high-level stressors like critical illness, is an uncommon electrocardiographic finding that typically results from the fusion of the QRS complex, ST segment, and T wave. A proposed mechanism of ST-segment elevation in TTC is a mismatch between endo-epicardial wall tension and stretch-activated channel activation, which eventually leads to a transmural repolarization gradient and hence a coved-type ST modification that mimics the ischemic shark-fin sign. Mounting evidence has associated this feature with increased risk of ventricular fibrillation and cardiogenic shock.3


In a critically ill patient with shark-fin sign on ECG and septic shock, TTC needs to be considered, and TTC should be included in the differential diagnosis for patients with sepsis and ST elevation that mimics acute anterior ST-segment–elevation myocardial infarction.


None.


Disclosures None.


*B. Zhang and Z.-W. Yin contributed equally.


Circulation is available at www.ahajournals.org/journal/circ


For Sources of Funding and Disclosures, see page 1101–1102.




中文翻译:

重症监护室的鲨鱼鳍心电图

一名 54 岁女性因腹腔感染引起的感染性休克住进重症监护室。初步体格检查显示体温 38.6°C,血压 82/56 mm Hg,脉搏 109 次 / 分钟,呼吸频率 26 次 / 分钟。入院时进行了 12 导联心电图检查(图 1)。血清肌钙蛋白 I 水平为 2.02 ng/mL(正常值 <0.10 ng/mL),NT-proBNP(N-末端 pro-B 型利钠肽)水平为 5300 pg/mL(正常值 <450 pg/mL)。心电图的重要发现是什么?什么是最可能的诊断?你会如何管理病人?


图 1. 入院时的初始心电图。


请翻页阅读诊断。


最初的心电图显示 I、II、III、aVF 和 V 3至 V 6导联的弥漫性 ST 段抬高(图 1),这表明前壁和下壁 ST 段抬高型心肌梗死的诊断。然而,aVR 和 V 1导联的 ST 段压低与该诊断不一致。aVR 中显着的 ST 段压低可能反映导联 aVR 中的 ST 段抬高,该导联面向心尖和下外侧区域。弥漫性 ST 段抬高(在 II 和 aVR 导联中最为突出)可能反映以心尖部为中心的广泛分布的室壁运动异常,其超出任何单个冠状动脉的灌注区域。V 1导联ST段压低表明室壁运动异常不涉及导联 V 1所面临的右心室前区和右室间隔区。1,2 V 3至 V 6导联显示巨大的 R 波(幅度≥1 mV)与明显升高的 ST 段合并,形成三角形形态,称为相同的配置,称为鲨鱼鳍征和 λ 波模式(图 1)。这种心电图表现是 ST 段抬高型心肌梗死的特征,其中 QRS 复合波、ST 段和 T 波融合成一个独特的复合波。尽管传统上急性冠状动脉缺血与鱼翅征相关,但这种不寻常的追踪也偶尔在 takotsubo 心肌病 (TTC) 中发现,与血流动力学不稳定和休克有关。3此外,血清肌钙蛋白 I 水平的升高不成比例地低于左心室收缩功能障碍程度的预期,并且 NT-proBNP 水平远高于心肌梗塞中通常观察到的水平,这表明高度急性左心室扩张和心肌牵张。心电图和心脏生物标志物提供了该患者可能患有 TTC 的线索。TTC 诊断的确认需要冠状动脉造影和左心室造影。在该患者中,冠状动脉造影显示冠状动脉正常(图 2A 和 2B),左心室造影显示左心室收缩期心尖气球样变(图 2C 和 2D),左心室射血分数低 38%,与 TTC 诊断一致. TTC 是该患者的最终诊断。


图 2. 急诊冠状动脉造影和左心室造影。AB,急诊冠状动脉造影未显示阻塞性或痉挛性冠状动脉疾病的证据。CD,左心室造影显示左心室心尖区收缩期心尖气球样变。


患者在重症监护病房接受气管插管和机械通气治疗。她接受了经验性广谱抗生素、静脉输液和血管加压药支持。一旦识别出潜在的病原体并确定了抗菌药物敏感性,就更换了经验性抗菌治疗。左心室收缩期心尖球囊肿用左西孟旦治疗,左西孟旦是一种非儿茶酚胺正性肌力药,不会增加肌细胞环磷酸腺苷或耗氧量。6 天后,疾病减轻,心电图(图 3)显示 I、II、III、aVF 和 V 2至 V 6导联 ST 段抬高消退;I、II、III、aVR、aVL、aVF、V 5和 V 6导联的 T 波平坦度; V 1至 V 4导联 T 波倒置;和轻度 QT 延长。出院后 5 周重复超声心电图显示左心室收缩功能消退(左心室射血分数,59%)。


图 3. 解决后的心电图。


TTC 的特征是收缩功能障碍,通常局限于心尖部 (81.7%),而较少见于左心室中部 (14.6%)、基底方面 (2.2%) 或局灶方面 (1.​​5%)。解释 TTC 如何产生的最被接受的假设是循环儿茶酚胺和压力荷尔蒙的升高,通常与身体或情绪压力有关。脓毒症是一种严重的身体压力状态,可提高儿茶酚胺水平,从而激活中枢自主神经系统,导致心肌细胞钙超载,导致心肌昏迷和心肌病沉淀。TTC 中相当具体的心电图变化是 T 波倒置,通常深而广泛,QT 显着延长,通常在症状出现或诱发压力触发后 24 至 48 小时出现。约 40% 的病例可见 ST 段抬高涉及胸前导联。在我们的案例中,心脏受累与腹腔感染引起的败血症有关。在危重病等高水平压力源中描述的鲨鱼鳍征是一种罕见的心电图表现,通常由 QRS 复合波、ST 段和 T 波融合引起。TTC 中 ST 段抬高的一个建议机制是心外膜内壁张力和拉伸激活通道激活之间的不匹配,最终导致透壁复极梯度,从而导致模拟缺血性鲨鱼鳍征的凹型 ST 修改.3


对于心电图有鲨鱼鳍征和感染性休克的危重患者,需要考虑 TTC,对于类似急性前 ST 段抬高型心肌梗死的脓毒症和 ST 段抬高患者的鉴别诊断应包括 TTC。


没有任何。


披露无。


*B。张和 Z.-W。尹同样贡献。


流通可在 www.ahajournals.org/journal/circ


有关资金来源和披露信息,请参见第 1101-1102 页。


更新日期:2022-10-04
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