房室传导文氏现象的多种不典型心电图表现形式探讨

不典型的文氏周期比典型的文氏周期更为常见，这是因为绝大多数情况下，PP间期并非绝对整齐、PR／RP的关系并不恒定，以及患者自主神经张力有着变化，这些因素都能影响房室结的传导，都能使典型的文氏周期发生改变。本文分析30例不典型Ⅱ度Ⅰ型房室传导阻滞的心电图片段，旨在探讨其可能出现的表现形式。     

心电图诊断心脏传导延迟在健康查体中的应用与分析

心脏传导阻滞以部位分为窦房传导阻滞、房内传导阻滞、房室传导阻滞、室内传导阻滞4类。心脏各类传导阻滞程度分为三度传导阻滞,即Ⅰ度、Ⅱ度和Ⅲ度传导阻滞,其中Ⅲ度传导阻滞为完全性传导阻滞,Ⅰ、Ⅱ度传导阻滞又称不完全性传导阻滞,且Ⅰ度传导阻滞又称传导延迟。各类传导延迟常不被临床注意,尤其是传统心电图检查分析更易漏诊,随着心电图自动分析数字化12导同步心电图机及技术应用,提高了心脏传导延迟的诊断率。现国内文献报道较少,为此作者分析了1 226例健康体检者的心电图检查结果,旨在对心脏各类传导延迟进行探讨。     

二度Ⅰ型伴一度、间歇性高度、间歇性三度房室传导阻滞1例

[目的]揭示不同类型房室传导阻滞发生病因及阻滞部位,根据阻滞图形,实施应采取的措施。[方法]通过病史,冠状动脉造影,5年前后心电图、动态心电图的检查及图形的衍变,分析其病情及发展变化。[结果]病人二度Ⅰ型伴一度、少见高度房室传导阻滞发展为二度Ⅰ型伴一度、间歇性高度、间歇性三度房室传导阻滞。[结论]通过图形得出阻滞部位为房室结,无分支及双束支阻滞,且病人交界区逸搏的频率过缓,应考虑安装永久性起搏器。     

病理性Ⅰ度房室阻滞误诊38例分析

心电图Ⅰ度房室阻滞（Ⅰ°AVB）又称房室传导延迟，临床常见且多为功能性Ⅲ。少数病理性Ⅰ°AVB容易误诊。本文就所收集的38例分析如下。     

房室传导分层阻滞误诊为Ⅲ度房室传导阻滞心电图分析

正分层阻滞是因为心脏传导系统的不同层次存在不同不应期和传导性,所以有不同程度和不同方式的传导障碍,心脏传导系统横向或水平分离,出现分层阻滞现象。这种现象经常发生在房室交界区,房室传导分层阻滞现象在心电图上十分少见,易与Ⅲ度或高度房室传导阻滞相混淆。我院近期诊治房室传导分层阻滞1例,心电图误诊为Ⅲ度房室传导阻滞,现分析报告如下。1病例资料男,85岁。因劳力性心悸、气促5年,加重1周     

1例Ⅲ度房室传导阻滞置入起搏器后再通的观察及护理

Ⅲ度房室传导阻滞是指所有来自心房的激动都不能传至心室[1],患者可出现心悸、头晕、晕厥,甚至阿—斯综合征、心室纤颤、心房停搏、甚致猝死。反复发作,药物治疗无效,一般需置入永久性起搏器,患者终身携带。我院于2004年4月8-29日,收治1例Ⅲ度房室传导阻滞患者,在置入永久性起搏器后,心律转为右束支阻滞,临床症状消失,无需携带起搏器。取出起搏器后,心电图显示右束支阻滞,无临床症状,现报道如下。病例介绍患者,男,49岁,农民,初中文化程度。于2年前无明显诱因出现发作性头晕、心悸,持续数秒钟后消失。无血压增高,胸闷、心前区疼痛,呼吸困难等…     

1例Ⅲ度房室传导阻滞并阿-斯综合征护理体会

房室传导阻滞即指当房室结未处于不应期时心房激动向心室传导延迟或完全不能传至心室。依其严重性可分为Ⅰ度，Ⅱ度和Ⅲ度。其中Ⅲ度房室传导阻滞是最严重的类型。Ⅲ度房室传导阻滞又称完全性房室传导阻滞。当完全性房室传导阻滞时心房活动不能传至心室，心房与心室被不同的起搏点控制，造成完全性房室分离，心室率慢于心房率。临床表现不一，最严重的表现为阿-斯综合征发作即急性心脑缺氧综合征。因Ⅲ度房室传导阻滞时心室收缩减慢，心输出量明显减少，造成心脏及其他组织发生严重缺血缺氧，导致突然晕厥，肢体抽搐，患者意识丧失甚至死亡，故应高度重视。     

永久性心脏起搏器安置术患者的全程健康教育

我院2004年6月-2006年6月对收治的96例永久性心脏起搏器安置术患者实施全程健康教育,取得满意的效果,现报道如下. 临床资料 1.一般资料.我院2004-2006年96例永久性心脏起搏器安置术患者,其中男67例,女29例,年龄22～83岁.病窦综合征28例,Ⅱ度Ⅱ型房室传导阻滞24例,Ⅲ度房室传导阻滞42例,心房纤颤伴房室传导阻滞2例.全部患者有胸闷、心悸、头晕等症状,其中37例次伴晕厥或阿斯综合征发作史.     

双腔起搏器治疗严重缓慢性心律失常

目的 :评价双腔起搏器治疗严重缓慢性心律失常的临床疗效及价值。方法 :5 2例双腔起搏器 ,其中 41例DDD起搏器 ,11例DDDR起搏器。病态窦房结综合征 (sicksinussyndrome,SSS) 39例 ,房室传导障碍 13例 ,其中包括Ⅲ度房室传导阻滞 (thirddegreeAVblock ,Ⅲ°AVB) 3例 ,高度房室传导阻滞 (highdegreeAVblock ,HDAVB) ,Ⅱ度Ⅱ型房室传导阻滞 (typeⅡseconddegreeAVblock ,Ⅱ°Ⅱ型AVB) ,三分支传导阻滞 (threefascicularblock ,TFB)病人 ,以上病人均伴有昏厥、黑朦或严重头晕。电极植入途径为锁骨下静脉或头静脉。结果 :5 2例术后随访 1 78个月 ,临床疗效显著 ,不仅防止心博骤停发生 ,脑缺血症状消失 ,而且生活质量明显提高。 3例SSS者阵发房颤 (atrialfibrillation ,Af)术后消失 ,10例SSS者结合药物治疗Af发作次数减少。 1例扩张性心肌病死于左心衰竭。并发症 :心房感知过度 2例 ,心房感知不足 1例 ,心室电极阈值升高 1例 ,囊袋感染 1例 ,血肿 1例。结论 :双腔起搏器为较理想的生理性起搏 ,本研究证实能有效地治疗严重SSS和房室传导障碍的病人     

低钾性房室结双径路伴双文氏现象

患者男 ,19岁 ,因四肢无力 1天来我院就诊。体检 :呼吸、血压平稳 ,心率 92次 /min ,心律不齐 ,血钾 2 .4mmol/L。心电图 :Ⅱ度Ⅰ型房室传导阻滞 ,伴房室结双径路。临床诊断 :低钾性麻痹。予静脉补钾 ,6小时后复查心电图 ,Ⅱ度Ⅰ型房室传导阻滞消失 ,PR间期为 0 .16秒。　　讨论　低钾可以引起房室传导阻滞既往已有报道 ,但本例患者的Ⅱ度Ⅰ型房室传导阻滞有其特殊性 ,主要表现为PR间期突然成倍地延长。P1～P7下传时PR间期为 0 .16～ 0 .2 0秒 ,当P8下传时PR间期突然延长至 0 .4 0秒 ,其后的P波下传时PR间期在此基础上再发生延长 ,直…     

室间隔缺损介入治疗术后Ⅲ度房室传导阻滞的特点及防治

目的探讨经导管介入治疗先天性心脏病室间隔缺损（ventricular septal defect,VSD）发生Ⅲ度房室传导阻滞的特点及防治。方法观察本院先天性心脏病诊疗中心VSD患者763例,男352例,女411例,年龄1．6～18岁,平均（8．2±6．0）岁。分析所有患者封堵术前后心电图的变化、经胸心脏彩色超声多普勒的VSD病变特点及植入的封堵器的情况。结果术后3～5天发生Ⅲ度房室传导阻滞5例,其中1例术中出现Ⅲ度房室传导阻滞,药物治疗后恢复窦性心律;3侧术前心电图即存在右束支传导阻滞;1例封堵器型号偏大。4例经激素治疗、营养心肌治疗在发生Ⅲ度房室传导阻滞7～10天内心电图恢复正常;1例经临时心脏起搏7天后心电图恢复正常,该患者在术后3个月再次间断出现Ⅲ度房室传导阻滞,内科治疗无效,于15个月后安装永久起搏器。结论术前有柬支传导阻滞、术中出现一过性柬支传导阻滞或房室传导阻滞的膜周部VSD是术后发生Ⅲ度房室传导阻滞的高危因素。对于这类患者,在介入操作中要动作轻柔,切忌粗暴牵拉,谨慎选择封堵器,术后强化激素治疗。     

急性下壁心肌梗死出现房室传导阻滞的时间与临床的关系

目的　探讨急性下壁心肌梗死时发生房室传导阻滞的时间与病情发展的关系。方法　对１６２ 例下壁心梗患者的临床心电图资料和３２ 例冠脉造影资料进行分析。根据心电图表现将其分成超急性期、演变期和恢复期组。结果　有５９ 例患者在不同时期发生不同程度的房室传导阻滞,其中超急性期发生３０ 例（５０８ ％ ） ,其房室传导阻滞的程度和临床严重并发症发生数均高于演变期和恢复期组, Ｐ＜ ００５ 。后二期多表现为Ⅰ度房室传导阻滞, Ｐ＜ ００５ 。结论　下壁心梗早期发生房室传导阻滞多标志病情严重,阻滞程度较高,心梗面积较大。     

胎儿期Ⅰ°房室传导阻滞的诊断性研究分析

目的：选择较理想的指标及临界值点用于筛查胎儿Ⅰ°房室传导阻滞。方法：对62例晚孕孕妇（均大于38周）,进行组织多普勒成像（TDI）检测,记录Aa-IV（心房收缩期起点至等容收缩期起点的时间间隔）及Aa-Sa（心房收缩期起点至心室收缩射血期起点的时间间隔）,作为胎儿房室传导时间的评价指标。出生后一周内行新生儿心电图检查,测量PR间期。应用直线回归分析,比较Aa-IV、Aa-Sa与PR测值的相关性。绘制受试者工作特征曲线（ROC曲线）,分析比较Aa-IV、Aa-Sa的诊断准确性。结果：Aa-IV与PR的相关性更好。ROC曲线显示Aa-IV具有中等诊断意义;Aa-Sa诊断价值较低。根据敏感度及特异度分析,认为Aa-IV≥93.7 ms可作为筛查胎儿Ⅰ°房室传导阻滞的最佳临界值。结论：Aa-IV更适用于胎儿Ⅰ°房室传导阻滞的诊断,筛查胎儿Ⅰ°房室传导阻滞的最佳临界值为Aa-IV≥93.7 ms。     

Relationship between polymorphism of non-coding regions of human mitochondrial genome and primary cardiac conduction disorders

AIM: Analysis of associations between idiopathic disturbances of cardiac conduction (DCC) and polymorphism of mitochondrial genome. MATERIAL AND METHODS: A family examination was performed in 431 probands with various DCC and 1347 relatives of the first, second and third degree of kinship (the study group). All the examinees were divided into four subgroups. These included 158 probands with atrioventricular block (AVB) of various degree and their 518 relatives (subgroup 1); 50 probands with a complete right bundle-branch block (BBB) and their 161 relatives (subgroup 2); 108 probands with a complete left BBB and left anterior branch of the His bundle and their 152 relatives (subgroup 3); 115 probands with sick sinus syndrome (SSS) and their 327 relatives (subgroup 4). The control group consisted of 104 probands without clinical ECG manifestations of cardiac diseases and their 321 relatives. All the examinees have undergone ECG, atropin test, echocardioscopy, electrophysiological examination of the heart and mitochondrial DNA (mDNA). RESULTS: Comparison of the incidence of mDNA D-loop restriction sites in the group of patients with idiopathic DCC and controls has found higher frequency of the Hae III 16517 site in the group of the patients (p = 0.0480). By location of the blocks (atrioventricular and intraventricular), the site occurred more frequently in patients with AVB (86.36%). The variant "+" by the site of Hae III 16517 mDNA was found to associate with disturbances of cardiac conduction, more closely in AVB. CONCLUSION: Variability of mDNA may be an etiological factor of idiopathic DCC pathogenesis.     

New data on etiology of heart conduction disturbances

AIM: To make a clinicogenealogical analysis of different types of heart conduction disturbances in families of Krasnoyarsk city. MATERIALS AND METHODS: 104 probands with ECG-verified idiopathic forms of atrioventricular and intraventricular blocks of different severity and 331 their close relatives (kinship degree I and II) were examined using standard clinical investigations, ECG, echocardioscopy, electrophysical investigations in some cases and coronarography. RESULTS: All the observed 104 families were divided into 3 groups according to the type of heart conduction in proband. Group 1 consisted of 24 probands with atrioventricular block and 80 their relatives. The sick relatives had for the most part atrioventricular blocks (31.2%). 26 probands of group 2 had complete right bundle branch blocks. Of their 81 relatives, the sick ones had primarily conduction disturbances in right bundle branch (incomplete block--44.7%, a complete block--5.2%). Group 3 consisted of 54 probands with left bundle branch block and 170 relatives. The left bundle branch block was present in 27.4% of the relatives. CONCLUSION: A definite family aggregation of heart conduction disturbances was found. This proves genetic determination of this pathology.     

急性下壁心肌梗死合并高度房室传导阻滞患者临床特征及预后

目的观察急性下壁心肌梗死合并高度房室传导阻滞(AVB)患者的临床特点及预后。方法选取急性下壁心肌梗死合并高度AVB患者36例和不合并高度AVB患者116例,比较两组间一般临床特点(年龄、性别、高血压、高脂血症、糖尿病、吸烟)、CK峰值以及主要不良事件(包括右室心肌梗死、心力衰竭、低血压休克、恶性心律失常发生率,胸前导联ST段压低出现率及住院死亡率)的差异性。结果相比较于不合并AVB组,急性下壁心肌梗死合并高度AVB组患者年龄、CK峰值显著增加(P0.05),胸前导联ST段压低、右室梗死、心力衰竭及低血压休克发生率明显升高,住院死亡率亦明显增加,组间差异均有统计学意义(P0.05)。结论高度AVB是急性下壁心肌梗死的常见并发症,能够显著增加近期住院死亡率及不良事件的发生。     

Atrioventricular block during upright tilt table test

Patients with a cardioinhibitory response (asystole or atrioventricular block [AVB]) during upright tilt table test (UTT) constitute a therapeutic challenge. Our present knowledge is partial and in those who experience AVB is absent. Furthermore, we ignore if there is any difference between both groups, particularly pacemaker indication. We aimed to study patients with a cardioinhibitory response during UTT and incidence of AVB during UTT, compared to asystole; plus the outcome during prolonged follow-up. Of 867 patients who underwent UTT, 172 were positive for a neurally mediated response, all with normal neurocardiovascular evaluation. Of the 172 patients, 6 (3.4%) developed AV block (group A), and 26 (15.1%) experienced asystole (group B). Group A included 6 women (100%), mean age 21 +/- 12 years. All patients in group A had sinus rate deceleration during AVB. Group B included 10 women (38%), mean age 28 +/- 17 years, and a mean pause of 15 +/- 9 seconds. We contacted 30 of 32 patients, mean follow-up of 45 +/- 38 months. Seven patients in group B had syncopal recurrences; five had 2 or more episodes. One patient from group B received a DDD pacemaker. In group A, one had one recurrence. No deaths were observed. AVB during UTT is rare, occurs in young women, and is always associated with sinus rate deceleration. Medium- to long-term prognosis is good, and equivalent to patients with asystole. There is no evidence that patients with AVB during UTT require a pacemaker implant.     

85例伴长RR间期患者的动态心电图分析

[目的]探讨动态心电图分析长RR间期的临床价值.[方法]对85例动态心电图检查结果出现长RR间期(RR≥2 000 ms)者结合其日常生活日志进行回顾性分析.[结果]85例患者出现长RR的状况如下:①长RR间期可出现在房颤伴长RR 33例,窦性停搏15例,窦房传导阻滞12例,房室传导阻滞(包括Ⅰ度、Ⅱ度、Ⅲ度及高度房室传导阻滞)26例,早搏后长代偿8例;②最长RR可达8.68 s;③长RR间期多见于夜间睡眠期(0:00~5:00)及白天休息期(12:00~14:00),活动及清醒期比较少见;④长RR＞3 000 ms时患者会出现黑曚、晕厥甚至抽搐.[结论]动态心电图长RR分析对于减少临床上心源性猝死是简单有效的预测方法.     

高龄老年人安置永久心脏起搏器临床分析

目的分析高龄老年人安置心脏永久起搏器的临床特点及并发症治疗。方法12例高龄老年患者,年龄80~96岁。心律失常类型分别为快-慢综合征6例,Ⅱ度Ⅱ型以上房室传导阻滞4例,窦性停搏2例。安置起搏器类型:DDDR 1例,DDD 5例,VVIR 4例,VVI 2例。结果(1)高龄老年患者心内膜阻抗增高。12例高龄老年患者心内膜阻抗870~1 460Ω。(2)3例85岁以上高龄老年患者术后1周后活动上肢导致起搏器囊袋内出血皮下血肿,发现后局部压迫和上肢制动,均自行吸收痊愈。(3)4例发生术中恶性心律失常。结论高龄老年人由于生理性衰老变化,在安置心脏永久起搏器的过程中及术后易发生手术并发症,临床治疗中应加以重视。     

小剂量胺碘酮联合倍他乐克在肥厚型心肌病伴恶性室性心律失常治疗中的应用研究

目的探讨和分析小剂量胺碘酮联合倍他乐克治疗肥厚型心肌病伴恶性室性心律失常治疗中的临床效果。方法将94例肥厚型心肌病伴恶性室性心律失常患者按照住院时间先后顺序分组为对照组和观察组;对照组:采用倍他乐克治疗;观察组:采用小剂量胺碘酮联合倍他乐克治疗。对两组患者进行为期6~12个月随访。结果观察组和对照组的治疗有效率分别为95.7%(45/47)、80.9%(38/47)。除QT间期最大值以外,两组心电图指标和LVEF治疗后均较治疗前显著改善(P0.05),观察组治疗后心率和QT间期最小值以及QT散度、LVEF、再住院率、猝死率等方面均优于对照组(P0.05)。治疗和随访期间均没有发现明显性不良反应。结论采用小剂量胺碘酮联合倍他乐克治疗肥厚型心肌病伴恶性室性心律失常,可有效地改善患者的临床症状,效果明确。