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素材来源： JOSEPHSON AND WELLENS ECG LESSONS Heart Rhythm 2018;15(5):790–791 Let's enjoy the English learning in the EP world！ 病 例 简 介 Brief introduction 患者男性，62岁，因“胸痛20小时”入院。图1为入院时的心电图。 A 62-year-old man was admitted to hospital 20 hours after the onset of chest pain. The ECG recorded at that time is shown in Figure 1.
Figure 1: ECG recorded on admission shows sinus rhythm with an extensive subacute anteroseptal myocardial infarction with sub-AV nodal conduction abnormalities. Two types of QRS configuration are seen: type A during 1:1 AV conduction and type B after a pause. The PR interval before B is 60 ms longer than the PR before A (see text for discussion). 提 问 Questions 1、潜在的心血管疾病是什么？ 1、What is the underlying cardiac disease? 2、这是何种房室传导紊乱？ 2、What kind of AV conduction disturbance is present? 3、你能解释图1中标记A和标记B的QRS波形态吗？ 3、Can you explain the QRS configuration in the beats labeled A and B in Figure 1? 4、接下来你会如何治疗？ 4、What will be your treatment? 讨 论 Discussions 1. 心电图（图1）示窦性心律伴广泛前壁心肌梗死。V1和Ⅲ导联呈右束支阻滞伴QR形提示围绕左室心尖的前降支近端出现闭塞。多导联呈QR形且同时伴有显著的ST段抬高提示心肌梗死处于亚急性期。上述情况与胸痛发病到记录心电图的时间间期相吻合。 1. The ECG (Figure 1) shows sinus rhythm with a large anterior wall myocardial infarction. The presence of right bundle branch block (RBBB) with QR complexes in leads V1 and III indicates a proximal occlusion in the left anterior descending (LAD) coronary artery, which wraps around the apex of the left ventricle. The QR complexes,together with the presence of marked ST-segment deviations in many leads, suggest a subacute phase of infarction, which is in agreement with the time interval between the onset of chest pain and the ECG recording. 2. 窦性心律伴第2、第8、第15个P波发生房室阻滞，而其余P波均为1：1房室传导。除了P波阻滞后的PR间期，1：1房室传导的PR间期均固定为230ms。而P波阻滞后的PR间期测值为290ms。这种房室阻滞的模式是一种莫氏2型房室阻滞的少见变异。 2. Sinus rhythm is present with AV block of the 2nd, 8th, and 15th P waves. There is 1:1 AV conduction of the other P waves. Other than the PR interval after the blocked P wave, the PR interval during 1:1 AV conduction stays fixed at 230 ms. However, the PR interval after the blocked P wave measures 290 ms. This mode of AV block is an unusual variant of Mobitz 2 sub-AV nodal block. 3. 不仅是停搏之前或之后的PR间期不同，同时QRS波形态也存在变化。这里存在两种类型的房室传导紊乱，标记为A和B（如图1所示，解释见图2）。A的QRS波表现为完全性右束支阻滞伴额面中间电轴；B的QRS波也显示完全性右束支阻滞，但伴-30°的额面电轴偏转。如2所示，除了额面电轴变化，停搏后的PR间期较停搏前的PR间期延长了60ms。针对PR间期和QRS形态变化的最佳解释（如图2所示）为：发生了停搏依赖的4相左前分支阻滞，而激动只能通过左后分支延迟传导至心室。 3.Not only is thePRinterval different before and after the pause but also the QRS configuration. As shown in Figure 1 and explained in Figure 2, there are 2 types of sub-AV nodal conduction disturbances, labeled A and B. QRS A shows complete RBBB and an intermediate frontal QRS axis. QRS B also shows complete RBBB but with a frontal QRS axis of –30. As indicated under 2, other than the frontal axis change there is also PR interval prolongation of 60 ms after compared to before the pause. The best explanation for these PR and QRS changes as shown in Figure 2 is the occurrence of pause-dependent phase 4 block in the left anterior fascicle and delayed conduction to the ventricle over the left posterior fascicle.
Figure 2: A: Portion of Figure 1 showing QRS A before and QRS B after the pause. As indicated, QRS A with a PR interval of 230 ms is the result of complete right bundle branch block (RBBB) with ventricular activation over the left anterior fascicle (LAF). After the pause caused by a blocked sinus P wave, the PR interval prolongs to 290 ms, and QRS B shows complete RBBB with block in the LAF, resulting in ventricular activation over the slowly conducting left posterior fascicle. Pause-dependent phase 4 block in the LAF seems to be the best explanation for QRS B. 4.上述表现清楚提示广泛前壁心肌梗死伴房室结以下双束支传导异常。Q波提示已存在心肌组织坏死。心电图是在胸痛发作20小时后记录的，那么又存在一个问题“还有尝试冠脉再灌注治疗的指征吗?”多导联ST段抬高提示缺血仍存在。我们期望前降支的再灌注可以改善房室传导。结果不出意外，冠状动脉造影提示前降支于第一间隔支和第一对角支近端水平发生阻塞。该血管被开通并在右室心尖部植入临时起搏器。 4.It is clear that a large anterior wall myocardial infarction is present with conduction disturbances below the AV node in both bundle branches. The Q waves indicate that there is already loss of myocardial tissue. The ECG was recorded 20 hours after the onset of chest pain, and the question arises: “Is a coronary reperfusion attempt still indicated?” The ST-segment deviation in many leads suggests that ischemia is still ongoing. One can hope that reperfusion of the LAD will improve sub-AV nodal conduction. Not surprisingly, coronary angiography showed an LAD occlusion proximal to the first septal and first diagonal branch. The vessel was reopened, and a temporary pacing wire was placed in the apex of the right ventricle. 该患者仍有3点需要强调： In this patient, 3 points have to be addressed： A. 心衰的风险 A. The risk of heart failure B.是否需要植入起搏器 B. Whether a pacemaker should be implanted C.室速/室颤的风险 C. The risk of ventricular tachycardia/ventricular fibrillation A 前壁和室间隔存在广泛心肌组织损伤使患者很可能发生心衰，因此需要加强药物治疗，包括β阻滞剂、血管紧张素转化酶抑制剂、抗栓剂、利尿剂和他汀治疗。 The extensive tissue damage in the anterior wall and interventricular septum makes heart failure development likely, requiring careful pharmacologic management, including beta–blocker, angiotensin-converting enzyme inhibitor, anticoagulant, diuretic, and statin therapy. B 前降支闭塞后出现严重的双束支传导异常提示预后不佳。房室传导恢复正常的几率依赖于前降支闭塞到再灌注的时间间隔。这突显了所有涉及急性胸痛患者管理的医务人员须存尽快尝试再灌注的重要性。是否需要植入起搏器取决于房室传导是否可恢复正常。可以通过入院后1周测量带有His束电位的房室传导功能来帮助制定是否行起搏器植入。 Severe conduction abnormalities in both bundle branches after a proximal LAD occlusion carry a poor prognosis.The chance that normal sub-AV nodal conduction will return depends on the time interval between LAD occlusion and reperfusion. This stresses the importance of awareness by all practitioners involved in the management of acute chest pain that in such patients, reperfusion should be attempted as soon as possible. The decision to implant a pacemaker depends on whether normalization of sub-AV nodal conduction occurs. The decision can be assisted by measuring AV conduction with a His-bundle recording 1 week after admission. C 既往研究显示广泛前壁心肌梗死伴房室传导异常的患者在随后的6周存在高室速/室颤的风险，可能是因为左室很大一部分的心室重构和疤痕形成促使了折返性室性心动过速。目前，一种“LifeVest”的穿戴式心脏除颤背心可用于这个时期患者的除颤需求。该病例发生于“LifeVest”问世之前。因为存在持续的房室传导异常和35%的左室射血分数，故该患者在植入起搏器和除颤器后出院。 In the past it was shown that patients with persistence of sub-AV nodal conduction disturbances in the setting of a large anterior wall infarction had a high incidence of ventricular tachycardia / ventricular fibrillation in the subsequent 6 weeks, probably because of remodeling and scar formation in a large part of the left ventricle facilitating reentrant ventricular arrhythmias.2 Currently, a LifeVest wearable cardioverter–defibrillator can be used to cover that period. Our patient was seen before the introduction of the LifeVest. Because of persistence of sub-AV nodal conduction abnormalities and a left ventricular ejection fraction of 35%, the patient was discharged after a pacemaker and a defibrillator were implanted . ONE 审 校：杜先锋 编 译：傅国华 编 辑：方任远  书心剑律｜心律最前沿  |
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