预激综合征P-R间期、P-J间期之相关问题

一、与预激综合征P-R间期长、短有关的因素 预激综合征的P-R间期大多在0.08～0.11s,但有短至0.06s或长达0.20s者[1].P-R间期的长短主要取决于下列因素:①房室旁道的性质,即是快旁道还是慢旁道?前者顺传不应期≤0.35s,具有全或无的传导特点,不出现传导延缓或递减性传导,因而不存在一度或二度Ⅰ型传导阻滞;而后者顺传不应期相当长,可达0.6～1.0s,甚至更长[2],大多数亦呈全或无的传导特点,少数可出现传导延缓或递减性传导,P-R间期＞0.12s,呈现一度、二度Ⅰ型传导阻滞,甚至出现交替性文氏周期、裂隙现象等少见的心电图表现.     

房室传导阻滞的定位诊断

从心房到心室的传导出现延缓或中断称为房室传导阻滞(AVB)。体表心电图上P—R间期在希氏束电图上包括:1、P—A间期:代表窦房结到房室结传导时间;2、A—H间期:代表房室结的传导时间:3、H—V间期:代表希氏束、左右束支和浦顷野氏纤维传导时间;其中BH时间代表希氏束本身传导时间。当上述间期超过正常时,示该部位发生病变,为传导阻滞的病变部位。AVB可为暂时性。间歇性或永久性。从发生机制上可为     

间歇性双束支传导阻滞1例

患者男,72岁。临床诊断:原发性高血压,冠心病。曾描记心电图为窦性心律,完全性右束支传导阻滞。入院前因情绪激动突然出现心悸、胸闷、气促及头昏,但无晕厥。当即描记心电图为三度房室传导阻滞。给予扩张冠状动脉、营养心肌及地塞米松等治疗,病情好转。在治疗期间检查心电图发现房室传导及束支传导情况多变。入院时V_1导联心电图(附图上)见P波规律出现,P-P间期0.72s,心房率83次/min,心室率40次/min,每2个P波有1个P波下传心室,P-R间期0.12s,下传的QRS呈右束支传导阻滞型。心电图诊断:莫氏Ⅱ型房室传导阻滞(2:1下传)伴完全性右束支传导阻滞。附图中见P-P规则,P-P间期0.48s,心房率125次/min;R-R间期不等,分别为1.08s、1.20s、1.40s,平均心室率49次/min,房室传导比例为2:1—3:1。QRS波群呈3种形态:第2、5个QRS形态正常,呈rS型,P-R间期0.12s;第3、6个QRS呈左束支传导阻滞型,P-R0.44s;第1、4个QRS呈右束支传导阻滞型,P-R间期0.12s。心电图诊断:高度房室传导阻滞(2:1—3:1),间歇性双束支传导阻滞。附图下见P波规律出现,心率88次/min,P-R间期0.12s,QRS波群呈rsR＇型。心电图诊断:窦性心律,完全性右束支传导阻滞。     

窦房和房室传导双重性文氏现象

窦房或房室传导阻滞Ⅱ°Ⅰ型在临床心电图上是常见,但窦房和房室传导阻滞双重性文氏现象确为少见。1 临床资料及心电图分析 患者男性,54岁,临床诊断为冠心病,急性下壁心肌梗塞。于94年5月20日描记该文心电图。 ①图A示,P—R间期有规律的逐渐延长:O.28→0.30→0.30s直至P_4后QRS脱落;R—R间期进行性缩短,并以长间歇结束一个文氏周期,各文氏周期重复出现,为Ⅱ°—Ⅰ型房室传导阻滞(wenckebach现     

隐匿性传导呈伪二度房室传导阻滞心电图分析1例

患者男性,50岁,有高血压病史,陈旧性下壁心肌梗死.心电图分析:P-R间期呈进行性延长,自0.26 s开始逐次与QRS波脱离,虽然看似房室传导阻滞文氏现象,但是不见R-R间期进行性缩短,也不见有QRS波脱落,并伴有QRS波挫折,QRS时限0.11 s.心率58次/分,绝大多数QRS与P波无关系,P-P间期、R-R间期相等.     

第70例——心房颤动伴间歇性右束支传导阻滞及超常期传导致QRS波群多形性1例

心房颤动伴频率依赖性左束支传导阻滞病例中,短于临界期的R-R间期,可通过超常期传导出现正常QRS波群,同样现象以前也曾在心房扑动伴频率依赖性右束支传导阻滞病例中见到.本文随着R-R间期短于右束支超常期的程度加重,在右束支传导阻滞基础上,电轴从显著左偏到轻度左偏、直至电轴正常.作者认为这可能与希-浦系的传导时间有关. 患者男性,72岁,因二尖瓣狭窄,心房颤动服用地高辛及速尿.心电图示心房颤动伴频率依赖性右束支传导阻滞(图1).     

Ⅳ位相传导阻滞1例

Ⅳ位相传导阻滞多见于器质性心脏病,很少单独出现,常与Ⅲ相传导阻滞相偕出现。作者报告1例完全性右束支传导阻滞(RBBB)伴阵发性高度房室传导阻滞(AVB,考虑阻滞部位可能位于左束支),最后导致Ⅲ度AVB。1临床资料患者男性,72岁,冠心病。因胸闷,一过性眼前发黑3 d来院就诊。心电图显示P-P间期0.70~0.84 s。窦性频率为71~86次/m in,P-R间期0.24 s。QRS时限为0.12 s,为窦性心律不齐,Ⅰ度AVB,完全性RBBB。心电图显示P-R间期逐渐延长,终于导致P波下传受阻,脱落一组QRS波群,形成典型的文氏现象呈4∶3房室比值传导的Ⅱ度1型AVB。入院后…     

心电向量图诊断伪装性束支传导阻滞的优势

伪装性束支传导阻滞(masquerading bundle branch block,MBBB)不同于单纯的左前分支阻滞(left anterior fascicular block,LAFB)合并右束支阻滞(right bundle branch block,RBBB),其心脏传导系统的病变程度严重且多呈进行性恶化;诊断依赖心电图但往往漏诊较多。结合临床实例,就其束支阻滞实质和心电向量图表现特征进行分析和论述。由于左束支后分支纤维传导障碍时,在心电向量图上表现为QRS环体中部泪点密集,而该图形的表达方式较心电图类本位曲折时间(或称室壁激动时间)更加直观,因此心电向量图有助于临床早期发现心电图难以诊断的伪装性束支传导阻滞。     

心电图PR间期延长面面观

1概述心电图PR间期代表心脏的房室传导,通常是在0.12～0.20s之间,在心率缓慢的状态下,PR间期也不应超过0.21s。PR间期延长说明房室传导迟缓,它可以是房室传导阻滞,也可见于其他问题,PR间期延长可以揭示多种心电现象。     

第Ⅱ度和阵发性房室传导阻滞的评价

序言 Wenckebach和Hay通过颈静脉搏动a-c间距的分析,描述有两种类型的房室传导阻滞。在采用心电图后,Mobitz分为Ⅰ型和Ⅱ型。Ⅰ型房室传导阻滞亦称为莫氏Ⅰ型或文氏现象,是指在间歇性房室传导中断之前,先有房室传导时间的进行性延长。Ⅱ型房室传导阻滞亦称莫氏Ⅱ型,其特点是间歇     

Role of the autonomic nervous system in the genesis of first and second degree atrio-ventricular nodal block

Thirty-four patients with a prolonged A-H interval (group I)and 26 with A-V nodal Wenckebach block (group II) were studiedin the basal state and after autonomic blockade (propranolol0.2mg kg^–1 and atropine 0.04 mg kg^–1 in order toassess the role of autonomic system in A-V nodal conductiondisturbances. In group I, the A-H intervals did not change significantlyafter autonomic blockade, whereas pacing cycle length for Wenckebachblock, effective and functional refractory periods of the A-Vnode decreased significantly (P<005). In the 22 patientswith organic heart disease these variables did not change significantlyafter autonomic blockade, whereas in the 12 without underlyingheart disease, they decreased in all cases (P< 0001). Inthe former, the variables of intrinsic A-V nodal conductionwere normal in only 6% of patients, whereas in the latter theywere normal in 66%. Also in group II, the intrinsic A-H intervalswere normal in only 6% of patients with cardiac disease butwere normal in 63% without underlying heart disease. These datasuggest that in the patients with first and second degree A-Vnodal block and organic heart disease, the conduction disturbanceis predominantly related to intrinsic involvement of A-V node,whereas in the subjects without underlying heart disease theA-V nodal blocks appear mainly related to autonomic alterations.     

Indications for pacemaker implantation in the Kearns-Sayre syndrome

The Kearns-Sayre syndrome is a rare condition, characterizedby progressive external ophthalmoplegia, retinal pigmentarydegeneration and progressive impairment of cardiac conduction,which mainly determines the prognosis. Two young patients (aged13 and 18 years) without symptoms of cardiac disease presentedwith an electrocardiogram showing sinus rhythm, a normal atrio-ventricularconduction time, right bundle branch block and a left anteriorfascicular block.Electrophysiologic investigation showed prolongationof His-ventricular interval at rest, which further increasedduring atrial pacing. Because of the potential progression ofthe conduction abnormalities and threatening sudden death, wedecided to implant a pacemaker in both patients. Ten monthslater one patient had become pacemaker-dependent. Prophylacticpacemaker therapy is advisable in patients suffering from theKearns-Sayre syndrome, who have bifascicular block on theprecordialelectrocardiogram.     

Indications for pacemaker therapy in ophthalmoplegia plus and Kearns-Sayre syndrome

Mitochondrial myopathies can affect the skeletal muscle, the central or peripheral nervous system, and they may be associated with chronic progressive external ophthalmoplegia (CPEO). In 7/29 patients with mitochondrial myopathies and CPEO a cardiac involvement (Kearns-Sayre syndrome) was found: incomplete right bundle branch block (n = 1), right bundle branch block (n = 1), left anterior fascicular block and right bundle branch block (n = 2), complete atrioventricular block (n = 3); congestive cardiac failure (ejection fraction 40%) (n = 2); 3/10 patients had prolonged infranodal conduction on His-bundle electrography (HV-interval 60 ms). The cardiac involvement in ophthalmoplegia plus is characterized by progressive impairment of fascicular conduction. The need for prophylactic pacemaker implantation appears to exist in patients with bifascicular block and prolonged His-ventricle conduction.     

Progressive Atrioventricular Conduction Block in a Mouse Myotonic Dystrophy Model

Introduction: Myotonic dystrophy is caused by expansion of a CTG trinucleotide repeat on human chromosome 19, and leads to progressive skeletal myopathy and atrioventricular conduction disturbances. A murine model of myotonic dystrophy has been designed by targeted disruption of the myotonic dystrophy protein kinase (DMPK) gene. The DMPK-deficient mice display abnormalities in A-V conduction characteristics, similar to the human cardiac phenotype. The purpose of this study was to determine whether age-related progression of A-V block occurs in a mouse model of DMPK-deficiency.Methods and Results: Surface ECGs and intracardiac electrophysiology (EP) studies were performed in 60 immature and 90 adult homozygous (DMPK), heterozygous (DMPK), and wild-type (WT) DMPK control mice. Complete studies were obtained on 141 of 150 mice. The RR, PR, QRS, and QT intervals were measured on ECG. Sinus node recovery time, AV refractory periods, paced AV Wenckebach and 2:1 block cycle lengths, atrial and ventricular effective refractory periods were compared between genotypes and age groups. There were no differences in ECG intervals or EP findings in the young mutant mice, but progressive PR prolongation in older mice. The A-V conduction defects are also sensitive to DMPK gene dosage. Adult DMPK mice develop 1°, 2° and 3° A-V block, whereas DMPK mice develop only 1° heart block.Conclusion: These data demonstrate that both age and DMPK dose are important factors regulating cardiac conduction in myotonic dystrophy. This mouse model of DM is remarkably similar to the human phenotype, with age-related progression in atrioventricular conduction defects.     

Progressive cardiac conduction defect is the prevailing phenotype in carriers of a Brugada syndrome SCN5A mutation

INTRODUCTION: Loss-of-function mutations in the SCN5A gene encoding the cardiac sodium channel are responsible for Brugada syndrome (BS) and also for progressive cardiac conduction disease (inherited Lenègre disease). In an attempt to clarify the frontier between these two entities, we have characterized cardiac conduction defect and its evolution with aging in a cohort of 78 patients carrying a SCN5A mutation linked to Brugada syndrome. METHODS AND RESULTS: Families were included in the study if a SCN5A mutation was identified in a BS proband and if at least two family members were mutation carriers. Sixteen families met the study criteria, representing 78 carriers. Resting ECG showed a spontaneous BS ECG pattern in 28 of 78 (36%) gene carriers. Intraventricular conduction anomalies were identified in 59 of 78 gene carriers including complete (17) or incomplete (24) right bundle branch block, right bundle branch block plus hemiblock (6), left bundle branch block (1), hemiblock (1), and parietal block (10). PR and QRS duration were longer in the gene carrier cohort in comparison with their relatives carrying no mutation. Finally, in the gene carrier cohort conduction defect progressively aggravated with aging leading in five occasions to pacemaker implantations. CONCLUSION: The present study shows that the most common phenotype of gene carriers of a BS-type SCN5A mutation is progressive cardiac conduction defects similar to the Lenègre disease phenotype. In consequence, we propose that carriers of a SCN5A mutation need a clinical and ECG follow-up because of the risk associated with severe conduction defects.     

Evolution of right bundle branch block and other intraventricular conduction abnormalities in the transplanted human heart

We performed 12-lead electrocardiography (ECG) repeatedly in 13 patients with cardiac transplants. QRS block occurred at some point in 12 patients and its course was either sporadic, progressive, persistent or fluctuating (5, 3, 3 and 1 patient (s), respectively). In the first postoperative week, complete or incomplete right bundle branch block (RBBB) occurred in 10 patients. Left anterior fascicular block also occurred in 3 of the 10 patients. However, the block(s) subsided within 1 month in the 3 and 2 more patients. Nonspecific block, isolated left anterior fascicular block and left bundle branch block also occurred occasionally. QRS block was unrelated to the occurrence of cardiac rejection, catheter injury, right ventricular pressure or volume overloading, left ventricular function, and the length of ischemic time of the donor heart. Two patients have had permanent RBBB since the immediate postoperative period despite a normal donor electrocardiogram before harvesting. The temporal courses of QRS block varied widely in 9 patients. Thus, different mechanisms may have been active in various postoperative periods. The occurrence of QRS block was unrelated to morbidity and mortality in the recipients. Therefore, longer observation will likely establish the benign nature of the QRS block in this disease.     

Acute and Long-Term Effects of Consecutive Radiofrequency Applications on Conduction Properties of the Subeustachian Isthmus in Type I Atrial Flutter

Effects of Atrial Flutter Ablation. Introduction: Bidirectional conduction block at the subeustachian isthmus predicts long-term efficacy of atrial flutter ablation. Limited data are available on the incidence and outcome of minor conduction changes such as unidirectional or incomplete block. This prospective study sought to systematically assess discrete acute and long-term alterations of bidirectional conduction prior to a complete conduction block. Methods and Results: In 41 patients with type I atrial flutter, pulse propagation through the subeustachian isthmus during low lateral and proximal coronary sinus pacing was documented and analyzed following each consecutive radiofrequency (RF) application. In cases of altered conduction properties and noninducibility of atrial flutter, patients were followed-up for 12 months. Three sets of results were found. First, following RF application. 23 patients presented a progressive conduction delay prior to a complete conduction block. Second, RF application did not always affect counterclockwise and clockwise conduction simultaneously or to the same extent. In 13 patients, an initial alteration of counterclockwise conduction was present before an alteration of clockwise conduction; in 5 patients, clockwise conduction was primarily affected. Third, the recurrence rate of typical atrial flutter was 9% (2/22) in patients with a complete bidirectional conduction block, 54% (7/13) in patients with unidirectional conduction block, and 100% (6/6) in patients with sole bidirectional conduction delay. Conclusion: In 50% of the patients, consecutive RF applications resulted primarily in a progressive conduction delay rather than a sudden conduction block. Since counterclockwise and clockwise conduction were not always affected simultaneously or to the same extent, lateral as well as septal pacing is recommended for improvement of bidirectional conduction block. Normalization of primarily altered conduction and, therefore, recurrence of atrial flutter are high in all patients without bidirectional block.     

Lyme carditis: Sequential electrocardiographic changes in response to antibiotic therapy

Lyme disease is a tick-borne spirochetal infection that may involve heart. The cardiac manifestations of Lyme disease including varying degrees of atrioventricular heart block occur within weeks to months of the infecting tick bite. This report describes a 43 year-old man with Lyme carditis who presented with complete heart block. The heart block resolved with ceftriaxone therapy. Lyme carditis should be considered in the differential diagnosis in patients who present with new onset advanced heart block.     

Complete heart block due to lyme carditis

Lyme carditis is becoming a more frequent complication of Lyme disease, primarily due to the increasing incidence of this disease in the United States. Cardiovascular manifestations of Lyme disease often occur within 21 days of exposure and include fluctuating degrees of atrioventricular (AV) block, acute myopericarditis or mild left ventricular dysfunction and rarely cardiomegaly or fatal pericarditis. AV block can vary from first-, second-, third-degree heart block, to junctional rhythm and asystolic pauses. Patients with suspected or known Lyme disease presenting with cardiac symptoms, or patients in an endemic area presenting with cardiac symptoms with no other cardiac risk factors should have a screening electrocardiogram along with Lyme titers. We present a case of third-degree AV block due to Lyme carditis, illustrating one of the cardiac complications of Lyme disease. This disease is usually self-limiting when treated appropriately with antibiotics, and does not require permanent cardiac pacing.