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ST-Segment Changes After Loss of Consciousness.
Circulation ( IF 37.8 ) Pub Date : 2019-12-30 , DOI: 10.1161/circulationaha.119.044403
Arianne Clare Agdamag 1 , Darshan Krishnappa 1 , David G Benditt 1
Affiliation  

An 85-year-old woman with history of hypertension, atrial fibrillation, and right subdural and bilateral subarachnoid hemorrhage 1 month ago after an accidental fall, presented to the emergency department with altered mental status. There was a history of multiple falls 2 days before this presentation. She had a CHADS2VaSc score of 4 and was initially on Coumadin, which was discontinued after the intracranial bleed.


ECG at baseline is shown in Figure 1. On admission, a computerized tomography scan of the head showed hydrocephalus with no change in size of the subdural hematoma and an external ventricular drain was placed. Urine cultures grew Klebsiella pneumonia, and she was treated with levofloxacin. A lower limb compression device was used to prevent deep venous thrombosis. Transthoracic echocardiogram obtained at admission showed normal left ventricular function and wall motion; there were no valvular abnormalities and no thrombi. Subsequently, her neurologic status improved, external ventricular drain was removed and she was ambulatory and was planned for discharge when she had sudden onset of hypotension and loss of consciousness. An ECG obtained in association with this collapse event is shown in Figure 2.


Figure 1. Baseline 12-lead ECG.


Figure 2. ECG obtained during sudden onset hypotension and loss of consciousness.


Please turn the page to read the diagnosis.


The baseline 12-lead ECG shows atrial fibrillation with left ventricular hypertrophy and secondary ST-segment depression. ECG obtained in conjunction with the hypotensive event (Figure 2) showed atrial fibrillation with new right bundle branch block morphology and a prominent ST elevation in leads II, III, aVF, and V1–V3, and ST depression in I, aVL, and V5–V6. The coved ST segments in V1–V3 were deemed consistent with a Brugada pattern.


The new ECG changes combined with the sudden onset of hypotension and loss of consciousness was concerning for an acute coronary syndrome. However, a coronary angiogram showed only nonobstructive coronary artery disease. Thereafter, she continued to exhibit persistent hypotension and an intra-aortic balloon pump was placed. A repeat transthoracic echocardiogram (Figure 3) showed massive dilatation of the right ventricle (RV) with significant reduction in RV function raising concern for pulmonary embolism. Unfortunately, her clinical condition worsened with recurrent episodes of ventricular fibrillation and cardiac arrest. Ultimately, she could not be resuscitated.


Figure 3. Apical 4-chamber view on transthoracic echocardiography showing new onset massive RA and RV dilatation.


The ST elevation in V1–V3 are suggestive of a Type I Class B Brugada phenocopy (BrP). Brugada phenocopies are Brugada-like ECG patterns from reversible conditions such as metabolic imbalances, ischemia, and pulmonary embolism.1 Criteria used for a diagnosis of Class A BrP include: a typical Type I or Type 2 Brugada pattern on ECG in a patient with a low probability of Brugada syndrome based on age, family history of sudden death, and absence of symptoms such as unexplained syncope or palpitations with a negative provocation test with ajmaline, flecainide, or procainamide and resolution of BrP with resolution of underlying cause.1 A diagnosis of Class B BrP is made in the absence of provocative testing.


Pulmonary embolism has been recognized as one of the causes of BrP.2 Massive pulmonary embolism results in an increase in RV afterload, leading to increased RV metabolic demands and RV ischemia. This ischemia may lead to an RV strain pattern on the ECG, or if very severe may result in a current of injury leading to ST-segment elevation in V1–V3 or aVR and inferior leads giving rise to a BrP pattern.3


Our patient had several risk factors for pulmonary embolism: a high CHADS2VaSc score, discontinuation of therapeutic anticoagulation, and prolonged immobilization, which likely led to the development of deep venous thrombosis with subsequent massive pulmonary embolism leading to RV strain and RV ischemia. Although a CT scan was not done to prove the presence of pulmonary embolism, it was the most likely cause in the setting of the clinical findings mentioned above. The main learning point of this case is that pulmonary embolism may present with Brugada pattern ECG changes in the right precordial leads as was the case in which there was a >2-mm ST-segment elevation followed by a down-sloping concave ST-segment with a negative T wave.


Dr Benditt is a recipient of a grant from the Dr Earl E. Bakken family in support of Heart-Brain research.


None.


https://www.ahajournals.org/journal/circ




中文翻译:

失去意识后,ST段会发生变化。

一名意外摔倒后1个月前有高血压,房颤,右硬脑膜和双侧蛛网膜下腔出血病史的85岁女性因精神状况改变而转诊至急诊科。在此演示文稿的前两天有多次跌倒的历史。她的CHADS 2 VaSc得分为4,最初接受香豆素治疗,颅内出血后停药。


基线时的心电图如图1所示。入院时,头部的计算机X线断层扫描显示脑积水,硬膜下血肿的大小无变化,并放置了外部心室引流管。尿培养中会出现肺炎克雷伯菌,她接受了左氧氟沙星治疗。下肢压迫装置用于预防深静脉血栓形成。入院时经胸超声心动图显示正常的左心室功能和壁运动。没有瓣膜异常和血栓形成。随后,她的神经系统状况得到改善,外脑室引流得到了消除,可以动态行走并且计划在突然出现低血压和意识丧失的情况下出院。与此崩溃事件相关联的心电图如图2所示。


图1. 基线12导联心电图。


图2. 突然发作的低血压和意识丧失期间获得的心电图。


请翻页阅读诊断。


基线12导联心电图显示房颤伴左心室肥大和继发性ST段压低。伴有降压事件的心电图(图2)显示房颤,伴有新的右束支传导阻滞形态,II,III,aVF和V1-V3导联明显ST升高,I,aVL和V5导联ST凹陷–V6。V1-V3中的弧形ST段被认为与Brugada模式一致。


新的ECG改变与突然出现的低血压和意识丧失有关,这与急性冠状动脉综合征有关。但是,冠状动脉造影仅显示非阻塞性冠状动脉疾病。此后,她继续表现出持续性低血压,并置入了主动脉内球囊泵。再次经胸超声心动图(图3)显示右心室(RV)大量扩张,RV功能显着降低,引起了肺栓塞的担忧。不幸的是,她的临床状况因反复出现心室纤颤和心脏骤停而恶化。最终,她无法复活。


图3. 经胸超声心动图的心尖四腔视图显示新发的大量RA和RV扩张。


V1-V3的ST升高提示I型B级Brugada表型(BrP)。Brugada表型是可逆条件下的Brugada样ECG模式,例如代谢失衡,局部缺血和肺栓塞。1用于诊断A类BrP的标准包括:基于年龄,猝死家族史和缺乏症状(如无法解释的症状)的患有Brugada综合征的可能性低的患者的典型I型或2型Brugada心电图模式晕厥或心pit,用阿玛琳,氟卡尼或普鲁卡因胺进行否定激发试验,BrP消退并潜在原因消退。1在没有进行刺激性试验的情况下,诊断为BB BrP。


肺栓塞已被认为是BrP的病因之一。2大量肺栓塞导致RV后负荷增加,导致RV代谢需求增加和RV缺血。这种缺血可能导致ECG出现RV应变模式,或者如果非常严重,可能导致受伤电流,导致V1-V3或aVR中ST段抬高,而劣等的导线则导致BrP模式。3


我们的患者患有肺栓塞的几个危险因素:CHAD S 2VaSc评分高,治疗性抗凝药物的中止治疗和固定时间延长,可能导致深静脉血栓形成,随后发生大量肺栓塞,导致RV株和RV缺血。尽管没有进行CT扫描来证明肺栓塞的存在,但这是上述临床发现最有可能的原因。这种情况的主要学习点是,右前胸导联可能伴有Brugada模式的ECG改变而出现肺栓塞,如ST段抬高> 2 mm,然后凹ST段向下倾斜负T波


本迪特博士获得了伯爵(Earl E. Bakken)家族的一笔赠款,以支持心脏脑部研究。


没有。


https://www.ahajournals.org/journal/circ


更新日期:2019-12-31
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