心房复极波增大诱发异位心房激动3例

<正>心房复极波(Ta波)增大引起PR段及ST段下移常见于心动过速及P波高大时,Ta波增大诱发异位心房激动尚未见报道,本文报道3例。例1患者女、88岁。临床诊断:重型颅脑外伤,低钾血症。因     

普遍PR段下移伴普遍ST段抬高——急性心包炎早期心电图的特征性改变

目的 探讨急性心包炎心电图PR段的改变并对相关因素分析。方法 对78例急性心包炎患者不同时间记录的心电图进行分析,测量各导联PR段和ST段改变的方向和幅度,测量心率,并探讨PR段改变与ST段改变以及与心率的关系。以78例早期复极综合征为对照。结果 78例急性心包炎患者中,55例（75．1％）在Ⅰ、Ⅱ、Ⅲ、aVF、V3-V6导联普遍出现PR段下移,aNF导联出现PR段抬高,aVL导联仅3例有PR段改变。上述导联PR段下移幅度为0．05－0．15mV。第1次记录中69例（87．2％）出现Ⅰ、Ⅱ、Ⅲ、aVF、V3-V6导联ST段抬高。普遍导联PR段下移伴随ST段抬高的检出率在发病第1d记录的心电图中最高,随后记录的心电图中逐渐降低。PR段的下移与心率无关。在早期复极综合征中仅2．6％记录到PR段下移。结论 普遍导联PR段下移伴随ST段招高是急性心包炎早期心电图的特征性改变。     

房性早搏前PR段和ST段压低患者的临床和心电图分析

目的观察房性早搏(PAC)前PR段和ST段压低患者的临床和心电图(ECG)特征。方法分析PAC前PR段和ST段压低332例(观察组)的临床和ECG表现,并与558例PAC前无PR段和ST段压低(对照组)进行比较。结果①PR段和ST段压低导联分布广,以Ⅰ、Ⅱ、Ⅲ、aVF、V2～V6导联常见,V3、V4导联出现率最高,且PR段和ST段压低最显著。②观察组的PAC有如下特点:联律间期(CI)短且固定、提前指数(PI)小、多数呈PonT现象,PAC的P(P′)波时限长、P′波多呈高尖或切迹,绝大多数PAC的PR段和ST段也压低;PAC成对及连续发生或阵发心房扑动和心房颤动均较多;PAC发生前心动周期多不稳定;观察组年龄较大,窦性P波电压较高及时限较大,房内阻滞较多。以上指标与对照组比较差异均有显著性意义。结论 PR段和ST段压低是心房电不稳定的表现,具有这一特征的PAC属高危PAC,常常伴有其他更为严重的房性心律失常。     

PR段偏移的特点及临床意义

目的探讨PR段偏移的特点及临床意义。方法收集不同时期首次心电图记录有PR段偏移者68例,测量各导联PR段及ST段的偏移情况,观察其各项临床资料特点。结果①PR段改变的方向与同导联ST段改变的方向相反,下移的幅度在0.05-0.15mV,抬高的幅度在0.05-0.10 mV;②68例PR段偏移者中急性心包炎59例（其中肿瘤性13例、结核性10例、尿毒症性8例、心脏手术性7例、化脓性7例、病毒性5例、自身免疫性5例、外伤性4例）,在Ⅰ、Ⅱ、Ⅲ、aVL、aVF、V3-V6导联出现普遍PR段下移而ST段抬高,aVR导联则表现为PR段抬高而ST段下移;③急性心肌梗死或合并有心房梗死9例,在面向梗死区的导联PR段下移而ST段抬高,对应导联PR段抬高而ST段下移。结论心电图PR段偏移强烈提示为急性心包炎或心房梗死。     

心房复极波增大诱发房早与阵发房颤的关系

目的 探讨心房复极波增大诱发的房性早搏与阵发性心房颤动的关系.方法 对频发房早患者进行随访,行心电图和动态心电图检查,房早前有心房复极波增大的为观察组,反之为对照组.观察两组阵发房颤的发生率、持续时间、发作时的临床诊断和并发症.结果 与对照组比较,观察组阵发房颤的发病率较高、发作阵次较多、持续时间较长,分别为31.13...     

心电图PR段改变对急性心包炎的临床诊断价值

目的探讨体表心电图PR段改变对急性心包炎的临床诊断价值。方法对60例急性心包炎病人不同时间记录的首次心电图进行分析,测量各导联PR段的方向和幅度。以60例心肌梗死和60例早期复极综合征为对照。结果60例急性心包炎病人中,44例(73.3%)在I、Ⅱ、Ⅲ、aVF、V3~V6导联普遍出现PR段下移,aVR导联出现PR段抬高。普遍导联PR段改变的检出率在发病第l天,第2天记录的心电图中最高,达88.6%,随后记录的心电图中逐渐降低。在心肌梗死中有1.7%记录到普遍PR段下移,在早期复极综合征中普遍PR段下移的检出率也为1.7%。结论普遍导联PR段下移是急性心包炎早期心电图的特征性改变。     

用心电图标准判别运动试验假阳性:心房复极波是可能的因素

已知与运动试验假阳性有关的因素是:电解质紊乱,药物与静臭状态下复极异常。然而,通常并无上述因素存在,此时无心肌缺血而运动可诱发ST段压低的原因仍不明。心房复极波与P波方向相反,振幅100～200μv,可能一直延伸至ST和T波中。本研究目的是验证一个假设:即运动中增大的心房复极波可能酷似心肌缺血的ST段压低,用心电图(ECG)标准可加以判别。方法运动试验阳性标准:至少一个导联,ST段J点后80ms水平型或下斜型压低≥100uV或轻度上斜型压低≥150uV。所有病人运动前ECG均正常。25例假阳性者,其中5例     

阵发性房颤心房易颤期时限的探讨

对32例阵发性短阵性房颤动态心电图的观察,发现房颤发生前均有房性早搏出现,而且呈进行性增多,甚至呈联律;诱发房颤的房早多出现在前一心动周期的收缩中期,且诱发房颤的房早 P 波落在 ST 段上及 T 波升肢时限内占87.6%。提出心房易颤期可能不在 R 波降肢至 S 波时限内,而是位于 ST 段至 T 波升肢时限内。     

Brugada波与特发性J波

一、Brugada波Brugada波的典型心电图表现是 ,右胸前V1～V3 导联的ST段抬高和右束支阻滞共同称为Bru gada波。因此 ,正确识别Brugada波对诊断Brugada综合征是十分重要的。1.Brugada波的典型心电图特点⑴右胸前导联的ST段抬高 :右心室肌的期前复极和 或传导延迟引起的右胸前导联V1～V3 的ST段抬高 ,呈穹隆型或马鞍型及下斜型两种表现 ,偶尔有电轴左偏 ,并伴有T波倒置 ,某些病例可在其他导联 (V4)上出现ST段的抬高 ,而且绝大多数Brugada波并无对应导联的ST段下移改变 ,QT间期并不延长。ST段抬高的诊断标准是 ,V1～V3 导联上J点至…     

起源于上腔静脉的房性心律失常体表心电图心房波特征

分析起源于上腔静脉的房性心律失常的体表心电图心房波变化特征,以了解心房波形态对判断房性心律失常起源部位的价值。测量8例上腔静脉起源的房性心律失常患者窦性心律(简称窦律)及阵发性房性心律失常时心电图12导联的心房波时限、振幅及极性,并比较二种节律各导联房波的变化特点。结果:房性心律失常时各导联异位心房波的时限与窦律时相比无明显变化;其Ⅱ、Ⅲ、aVF导联心房波振幅明显高于窦律时;I导联P波由窦律时的明显正向变为低平,基本处于等电位线,aVL导联的P波由窦律下的低平变为负向,振幅仍很低;胸前导联心房波无明显变化。房性心律失常时Ⅱ导联心房激动振幅高于Ⅲ、aVF。结论:上腔静脉起源的房性心律失常其典型心电图特征为,Ⅱ、Ⅲ、aVF导联心房波直立高大,在I导联为正向低平波,aVL导联为负向低幅波。     

ST segment elevation in the right precordial leads induced with class IC antiarrhythmic drugs: insight into the mechanism of Brugada syndrome

We evaluated two patients without previous episodes of syncope who showed characteristic ECG changes similar to Brugada syndrome following administration of Class IC drugs, flecainide and pilsicainide, but not following Class IA drugs. Patient 1 had frequent episodes of paroxysmal atrial fibrillation resistant to Class IA drugs. After treatment with flecainide, the ECG showed a marked ST elevation in leads V2 and V3, and the coved-type configuration of ST segment in lead V2. A signal-averaged ECG showed late potentials that became more prominent after flecainide. Pilsicainide, a Class IC drug, induced the same ST segment elevation as flecainide, but procainamide did not. Patient 2 also had frequent episodes of paroxysmal atrial fibrillation. Pilsicainide changed atrial fibrillation to atrial flutter with 2:1 ventricular response, and the ECG showed right bundle branch block and a marked coved-type ST elevation in leads V1 and V2. After termination of atrial flutter, ST segment elevation in leads V1 and V2 continued. In this patient, procainamide and quinidine did not induce this type of ECG change. In conclusion, strong Na channel blocking drugs induce ST segment elevation similar to Brugada syndrome even in patients without any history of syncope or ventricular fibrillation.     

Electrocardiographic differentiation of atrial flutter from atrial fibrillation by physicians

The purpose of this study was to determine the ability of physicians to differentiate atrial flutter from atrial fibrillation on a surface electrocardiogram (ECG). A questionnaire containing three 12-lead ECGs was mailed to 689 physicians, with multiple-choice questions asking whether the rhythm on each ECG was atrial flutter or atrial fibrillation. ECG 1 showed atrial fibrillation with prominent atrial activity (>0.2 mV) in lead V1; ECG 2 displayed atrial fibrillation with prominent atrial activity (>0.2 mV) in leads III and V1; and ECG 3 displayed atrial flutter. Overall, ECG1 was correctly identified as atrial fibrillation by 79% of physicians, ECG 2 was correctly identified as atrial fibrillation by 31%, and ECG 3 was correctly identified as atrial flutter by 90%. Cardiology fellows and cardiologists correctly identified ECG 1 more often than house officers and internists (95% vs 63%; P < or = .01). ECG 2 was correctly identified by 26% of cardiology fellows and cardiologists and by 37% of house officers and internists (P = .10). ECG 3 was correctly identified by 91% of cardiology fellows and cardiologists and by 82% of house officers and internists (P = .06). In conclusion, atrial fibrillation is frequently misdiagnosed as atrial flutter. Misdiagnosis of atrial fibrillation occurs more often when atrial activity is prominent on an ECG in more than one lead.     

Identification of false positive exercise tests with use of electrocardiographic criteria: a possible role for atrial repolarization waves

Atrial repolarization waves are opposite in direction to P waves, may have a magnitude of 100 to 200 mu V and may extend into the ST segment and T wave. It was postulated that exaggerated atrial repolarization waves during exercise could produce ST segment depression mimicking myocardial ischemia. The P waves, PR segments and ST segments were studied in leads II, III, aVF and V4 to V6 in 69 patients whose exercise electrocardiogram (ECG) suggested ischemia (100 mu V horizontal or 150 mu V upsloping ST depression 80 ms after the J point). All had a normal ECG at rest. The exercise test in 25 patients (52% male, mean age 53 years) was deemed false positive because of normal coronary arteriograms and left ventricular function (5 patients) or normal stress single photon emission computed tomographic thallium or gated blood pool scans (16 patients), or both (4 patients). Forty-four patients with a similar age and gender distribution, anginal chest pain and at least one coronary stenosis greater than or equal to 80% served as a true positive control group. The false positive group was characterized by 1) markedly downsloping PR segments at peak exercise, 2) longer exercise time and more rapid peak exercise heart rate than those of the true positive group, and 3) absence of exercise-induced chest pain. The false positive group also displayed significantly greater absolute P wave amplitudes at peak exercise and greater augmentation of P wave amplitude by exercise in all six ECG leads than were observed in the true positive group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Induction of nonsustained atrial flutter by programmed atrial stimulation in children: Incidence,mechanisms, and clinical implications

Nonsustained atrial flutter was induced by programmed atrial extrastimulation in 6 (4%) of 137 children with preoperative congenital heart defects, who underwent electrophysiologic evaluation as part of cardiac catheterization. None of these patients had ECG or clinical evidence of arrhythmias. Atrial reentry was induced by programmed atrial extrastimulation in these six patients at coupling intervals slightly longer than the coupling interval at which flutter was induced. The flutter cycle length was similar to the atrial refractory periods. The duration ranged between 0.4 second and 60 seconds. The PA interval and the duration of the P wave were normal in all of the patients. Five of the six had normal PR intervals. It is concluded that nonsustained atrial flutter may be induced by programmed atrial extrastimulation in dysrhythmia-free children. The cycle length is determined by atrial refractoriness and, contrary to adults with clinical atrial flutter, prolonged PA and P wave duration are not predisposing factors.     

Atypical atrial flutters.

Typical atrial flutter is due to a counterclockwise macro-re-entry circuit localized in the right atrium with a surface ECG pattern showing predominantly negative F waves in the inferior leads and positive F waves in V1. Recently it has been proposed to classify atrial flutter on the basis of its cavo-tricuspid isthmus dependence rather than on the ECG pattern. Therefore some atrial flutters are considered typical even if the ECG does not exhibit a typical pattern. This is the case for reverse typical atrial flutter, lower loop re-entry and partial-isthmus-dependent short circuit flutter. The term atypical flutter refers to a non-isthmus dependent flutter. Usually these patients have had previous cardiac surgery with a right or left atriotomy. Flutter involving a spontaneous right atrial scar is not uncommon.     

A peculiar form of focal atrial tachycardia mimicking atypical atrial flutter

A 55-year-old man was referred because of congestive heart failure and atrial flutter. A 12-lead electrocardiogram (ECG) showed positive P waves in leads II, III, and aVF with a continuously undulating pattern that lacked an isoelectric baseline. Tachycardia was diagnosed as atypical atrial flutter based on classical criteria. An electrophysiological study and catheter ablation using an electroanatomical system revealed the mechanism of the tachycardia to be focal atrial tachycardia originating from the left atrial roof. This case indicates that focal atrial tachycardia may present as atypical atrial flutter on the surface ECG.     

Variable electrocardiographic characteristics of isthmus-dependent atrial flutter

OBJECTIVES: The purpose of this study was to characterize variations in flutter-wave (F-wave) morphology among patients with clockwise isthmus-dependent (CWID) and counterclockwise isthmus-dependent (CCWID) right atrial flutter (AFL) and to attempt to correlate F-wave morphology with echocardiographic data and clinical patient characteristics. BACKGROUND: Variations in F-wave morphology on surface electrocardiogram (ECG) during CCWID and CWID flutter have been reported but never systematically characterized. METHODS: Over a four-year period, 139 patients with AFL on ECG underwent electrophysiologic study and echocardiography at our institution. Electrocardiographic data, intracardiac recordings, echocardiographic data, and patient characteristics were reviewed retrospectively. RESULTS: Of 156 AFLs evaluated, 130 were CCWID, 26 were CWID. Three types of CCWID flutter were observed: type 1 had purely negative F-waves inferiorly, types 2 and 3 had F-waves inferiorly with small (type 2) or broad (type 3) positive terminal deflections; CCWID flutter types 2 and 3 were associated with higher incidence of left atrial (LA) enlargement, heart disease, and atrial fibrillation (Afib) than type 1. Two types of CWID flutter were observed: type 1 had notched positive F-waves with a distinct isoelectric segment inferiorly. Type 2 had broader F-waves inferiorly with positive and negative components and a short isoelectric segment. CONCLUSIONS: Variable ECG patterns for CCWID and CWID AFL exist. A positive component of the F-wave in the inferior leads during CCWID flutter is associated with an increased likelihood of heart disease, Afib, and LA enlargement.     

Abnormalities of the S-T segment—Part I

The usual normal S-T segment of the surface electrocardiogram (ECG) contributes little to the diagnostic procedure. When the S-T segment is too long or too short, or when it is displaced upward or downward, it is commonly abnormal. Under such circumstances, an S-T segment abnormality usually contributes considerable diagnostic information. When the Grant method of ECG interpretation is used, it is possible to perceive abnormalities of the S-T segment that may otherwise be ignored or misinterpreted. This paper describes the method of identification and the significance of primary and secondary S-T segment abnormalities. When a mean vector constructed for the S-T segment displacement seen in 12 ECG leads is relatively parallel with a mean vector representing the T wave, it is, with a few exceptions, part of the repolarization process and is therefore part of the T wave. This may be called a secondary S-T segment abnormality. When a mean vector constructed for the S-T segment displacement seen in 12 ECG leads is not relatively parallel with a mean vector representing the T wave, it is, with a few exceptions, not part of the repolarization process and is therefore not part of the T wave. This may be called a primary S-T segment abnormality.     

Simultaneous occurrence of atrial fibrillation and atrial flutter

INTRODUCTION: Early reports suggested that some patients with "atrial fibrillation/flutter" might have atrial fibrillation in one atrium and atrial flutter in the other. However, more recent conceptions of atrial fibrillation/flutter postulate that the pattern is due to a relatively organized (type I) form of atrial fibrillation. We report the occurrence and ECG manifestations of simultaneous atrial fibrillation and flutter in patients undergoing attempted catheter ablation of atrial flutter. METHODS AND RESULTS: In patients undergoing radiofrequency ablation for atrial flutter, an attempt was made to entrain atrial flutter by pacing in the right atrium. The arrhythmias observed occurred following attempts at entrainment, or spontaneously in one case. Twelve transient episodes of simultaneous atrial fibrillation and flutter were observed in five patients. The atrial fibrillation was localized to all or a portion of one atrium, during which the other atrium maintained atrial flutter. In each case, the surface 12-lead ECG reflected the right atrial activation pattern. No patients had interatrial or intra-atrial conduction block during sinus rhythm, suggesting functional intra-atrial block as a mechanism for simultaneous atrial fibrillation/flutter. CONCLUSION: In certain patients, the occurrence of transient, simultaneous atrial fibrillation and flutter is possible. In contrast to prior studies in which it was suggested that left atrial or septal activation determines P wave morphology, the results of the present study show that P wave morphology is determined by right atrial activation. Functional interatrial block appears to be a likely mechanism for this phenomenon.