恶性快速性室性心律失常的发作方式及其临床意义

探讨恶性快速性室性心律失常的发作方式及其临床意义,分析64例在入院后至少发生≥1次由室性早搏(简称室早)诱发的恶性快速性室性心律失常患者发作时与发作前后的常规12导联心电图或持续心电监护心电图。结果:根据诱发恶性快速性室性心律失常的室早的联律间期及其前间歇的长短,64例的发作方式大致可分为以下几种类型:①单纯室早诱发;②长间歇依赖性室早诱发,此型根据基础心律QT(U)间期的长短又可分为:a.QT间期正常;b.长QT(U)间期两种形式。不同发作方式之干预措施亦异。结论:恶性快速性室性心律失常是由不同形式的室早所诱发的,他们具有不同的临床、心电学特征及干预措施。     

快速性恶性室性心律失常的发作方式及其临床干预

目的探讨快速性恶性室性心律失常的发作方式及其临床干预。方法对我院收治的快速性恶性室性心律失常56例(入院后至少发生1次以上),根据基础Q-T间期是否延长分为Q-T间期正常和长Q-T(U)间期,并按不同的发作方式临床干预治疗。结果基础心律Q-T间期正常(0.38±0.03s)33例,以室性心动过速或多形性室性心动过速多见,多数可用直流电复律。而Q-T间期延长(0.51±0.04s)23例,以尖端扭转型室性心动过速多见,多数经大剂量补钾、镁+异丙肾上腺素或阿托品静脉治疗。结论快速性恶性室性心律失常由不同形式的室性期前收缩诱发,应针对不同的临床、心电学特征,采取临床干预措施。     

扭转型室性心动过速11例报告

11例扭转型室性心动过速（TDP）,其中间歇依赖性长 QT 综合征与 TDP10例,肾上腺依赖性长 QT 综合征与 TDP1例。心电图11例均有“长短”系列特征,5例 TDP 发作前U 波显著增高。8例 TDP 发作前呈二联室性早搏。对两型长 QT 综合征及 TDP 的病因、临床、心电图特点及治疗作了探讨。     

长Q-T间期T波电交替致室性心律失常1例

患者女性,37岁。因反复晕厥3年,加重3个月就诊。其母有类似发作史。心电图示：窦性P-P间距匀齐,频率80次／分,P-R间期0．13s,QRS为室上性。各导联均可见呈同向、一高一低的直立T波。图1为Ⅱ导联。P及QRS波形态时间正常,T波呈一高一低的1：1交替,低T波的QT间期0．57s,高大T波的QT间期显著大于0．57s。描记至V5导联时可见频发室性期前收缩并短阵室性心动过速（VT）。图1V5为连续记录,V5中可见3阵短阵VT,第1阵呈尖端扭转型VT。心电图诊断：①窦性心律;②长Q-T间期综合征（LQTS）;③T波电交替;④频发室性期前收缩伴频发短阵性VT,部分呈尖端扭转型。     

冠心病患者Tp-e间期与复杂性室性心律失常关系的研究

目的观察不同方法（Tmax法、T均法和TV3法）测得的冠心病患者Tp—e间期差异以及其与复杂性室性心律失常的关系。方法315例患者的12导联心电图通过计算机图像软件处理获得Tp—e间期资料,同时行动态心电图检查并按检查结果分组：A组,冠心病单纯室性期前收缩频发组（室性期前收缩≥30次／h）;B组,冠心病复杂性室性期前收缩组（多形性、多源性、R在T上、连发室性期前收缩,可合并室性逸搏）;C组,冠心病室性心动过速、心室扑动及颤动组;D组．冠心病对照组（无明显快速性室性心律失常,室性期前收缩〈30次／h,且无其他室性心律失常）;E组．正常对照组。评价上述3种不同方法测得的Tp-e间期对室性心律失常的预测能力并将Tp—e间期与Q—T间期离散度（Q—Td）进行比较。结果B、C组的Tp-e问期不仅显著大于正常对照组,也显著大于冠心病对照组（P〈0．05）。而A组Tp—e间期大于对照组,但差异无统计学意义（P〉0.05）。结论Tp—e间期对复杂性室性心律失常有预测价值。且优于Q-Td。     

QT间期>PP间期引发尖端扭转性室性心动过速一例

长QT综合征 (LQTS)中有时可呈现QT间期 >PP间期现象。此时因复极明显延迟 ,可导致尖端扭转性室性心动过速 (TdP)。患者女性 ,6 2岁。因头晕反复发作 8年 ,烦渴消瘦 4年 ,加重伴偶有晕厥发作 1个月而入院。近期内未应用可影响QT间期之药物。入院后生化检验除血糖增高 (12 6mmol/L)外 ,血钾、血钠和血钙均在正常范围内。临床诊断为 (1)原发性高血压病 ,心律失常 ,三度房室阻滞 ,频发室性早搏 (室早 ) ;(2 )Ⅱ型糖尿病 ;(3)腔隙性脑梗死。入院时心电图示窦性心律 ,心率 10 0次 /min左右 ,轻度室相性窦性心律不齐 ,逸搏QRS时限正常 ,34…     

由旁道逸搏产生的特殊室性融合波群

患者男,28岁,体检时心脏听诊偶闻期前收缩。以往健康。常规心电图(附图上)示P-R间期0.08s,QRS时间0.13s,各导联QRS起始均可见预激波,胸导联预激波及QRS主波向上,是一典型的A型预激综合征。附图中、下行Ⅱ导联不连续记录均有室性期前收缩,偶联间期及形态均一致,代偿间歇不完全。中行开始处仅记录到一上升线段及等电位线,但其后无T波,从回归周期分析,可确定是一室性期前收缩的代偿间歇。下行两个室性期前收缩后的第1个QRS较其它QRS窄小,考虑是长间歇后房室结传导速度较快,使心室预激程度较轻所致。值得注意的是中行R_1及R_5,其前后均无P波,预激波形态与上图Ⅱ导联一致,考虑是起源于旁道的逸搏。R_1较宽,是预激面积较大之故,R_5较窄,其预激面积相对较小。R_1及R_5的T波低平,U波增高,可能与旁道逸搏使心室复极顺序改变有关。室性期前收缩的QRS与ST段交界处有一逆行P~-波,是室性期前收缩心房夺获,此P~-波侵入窦房结,使室性期前收缩代偿间歇不完全。心电图诊断:窦性心律,A型预激综合征,室性期前收缩,旁道逸搏自身心室内融合。     

尖端扭转型室性心动过速与多形性室性心动过速的鉴别及处理

多形性室性心动过速是临床常见的快速性室性心律失常之一,一般为恶性,常导致严重血流动力学异常,可伴有意识丧失或转化为心室颤动而危及患者的生命。根据发作前后心电图特点,可分为长QT依赖的尖端扭转型室性心动过速和非长QT依赖的多形性室性心动过速,两者在病因、电生理机制、发作前后心电图表现和治疗方法等方面均存在显著不同,是临床需要鉴别的重要问题。该文总结两者的特点,以期帮助临床医生进行更准确地诊断和干预。     

偶联间期相等的室性并行心律1例

患者男性，69岁。因胸闷、心悸3天急诊入院。有冠心病史14年。心电图V1导联(图1A)可见一种提早的QRS波群宽大畸形，呈完全性右束支传导阻滞型，时间0.14s，其前无P波，为室性期前收缩。另一种矮小，时间0．08s，频率相近；其前有一P波，P—R间期不固定，P波未能下传心室，为房室交接区性搏动。两种波形交替出现，偶联间期相等为0．66s，频率相近，相同形态的R—R间期为1．60s，室性期前收缩与前一P波距离为0．70—0．74s。随后心电图(图1B)V1导联可见矮小的QRS波群，其前已无明显P波，QRS形态稍有改变，室性期前收缩的ST段上隐约可见逆行P波重叠在R波下降支末，R—P间期恒等，均为0．14s。相同形态的R—R间期仍为1.60s，两种QRS波群的偶联间期与图1A相同，为0．66s。心电图诊断：房室交接区性逸搏—室性期前收缩二联律，房室干扰。经吸氧及静脉注射利多卡因50mg，10min后再次长II导联(图2)示主导心律为窦性及形态与图1完全相同的频发室性期前收缩，且联律间期不等，长间歇为短间歇的倍数，符合室性并行心律的诊断。同时发现，当室性期前收缩出现较早时，后面接着就出现交接区性逸搏；当室性期前收缩出现较晚时，后面就出现窦性心律；且交接区性逸搏联律间期无明显差异，不符合并行心律的诊断标准。心电图最后诊断：窦性心律，频发房室交接区性逸搏，逆配对现象造成的配对间期相等的室性并行心律(图1)。     

低钾血症致多形性室性心动过速1例

患者男性,45岁。高血压史7年,双下肢无力10个月,加重20天入院。查体：血压160／110mmHg,心律齐,心率58次／分,心前区可闻及Ⅲ／Ⅵ级吹风样收缩期杂音。查CT示：左侧肾上腺囊肿。血钾1．5mmol／L。查心电图示：窦性心律,P—R间期0．15s,QRS波时限0．08s,Q—T间期0．32s,V2、V3导联U波高于T波,Q—u间期0．48s。图1示窦性T波后可见高大U波,在室性期前收缩代偿间歇之后的第1个窦性心律中U波振幅增大更明显,之后出现一阵多形性室性心动过速,心室率200次／分。心电图诊断：①窦性心律;②U波增大;③室性期前收缩;④短阵多形性室性心动过速。     

冠心病室性心律失常患者的QT间期变异性与室性心律失常的相关分析

目的 现已明确冠心病患者发生猝死与恶性室性心律失常密切相关，本文旨在探讨冠心病患者Q-T间期变异性与发生室性心律失常的相关性。方法 采用动态心电图分析54例冠心病室性心律失常患者24hQ-T间期变异性。结果 冠心病室性心律失常患者24hQ-T间期变异性明显减低。结论 冠心病室性心律失常患者24h Q-T间期变异性较正常人明显减低，其发生心律失常的可能性将明显增加。     

Effect of ventricular filling volume on the R-amplitude in the ECG

Among others as cause of the sigma R-amplitude in the ECG changes of the ventricular filling and the stroke volume, respectively, the sympathetic tone and the coronary blood supply are discussed. Patients with absolute arrhythmia in atrial fibrillation as well as patients with extrasystoles represent model examples, in whom of the three factors mentioned above only the stroke volume is changed. Measurements of the sigma R-amplitude as well as of the Einthoven/Goldberger leads as well as of the Wilson leads on the same patient showed higher sigma R-values for the heart beats which were preceded by a short diastolic filling phase (rapid phase of the absolute arrhythmia, interpolated extrasystoles) than in the heart beats with previous long diastolic filling time (slow form of the absolute arrhythmia, extrasystole with compensatory interval). The findings considerably change in their size from patient to patient, however, they are statistically to be ascertained in their tendency. In the practical valuation deviations of the sigma R-amplitude values which do not correspond to this relation should be referred to other determinants of the R-amplitude.     

Polymorphous ventricular tachycardia associated with normal and long Q-T intervals

Polymorphous ventricular tachycardia may occur in the setting of either a normal or a prolonged Q-T interval. Torsade de pointes is a form of polymorphous ventricular tachycardia in which the polarity of the QRS complex exhibits phasic alterations in both axis and rate. Traditionally, torsade de pointes has been described in association with a variety of congenital and acquired (including drug and metabolic) causes of Q-T prolongation. The distinction between torsade de pointes and those polymorphous ventricular tachycardias occurring in patients with a normal Q-T interval has important therapeutic implications. The former requires strict avoidance of all drugs that may potentially further delay repolarization, including class I antiarrhythmic agents; immediately, the initiation of cardiac pacing is often necessary for control of arrhythmia, and on a long-term basis, sympathetic nervous blockade is often efficacious. In contrast, the polymorphous ventricular tachycardias with a normal Q-T interval usually respond to conventional therapy, including administration of class I antiarrhythmic agents. Thus, the management of polymorphous ventricular tachycardia should be based on the presence or absence of associated repolarization alterations rather than on the morphologic features of the tachycardia. Unfortunately, recent advances in basic and clinical electrophysiology have not yet elucidated the pathophysiologic basis for these arrhythmias, although this is an area of active investigative interest.     

肥厚型心肌病患者发生室性心律失常的相关危险因素分析

目的探讨肥厚型心肌病（hypertrophic cardiomyopathy,HCM）患者室性心律失常发生的相关性因素及特点。方法回顾性分析95例经临床及超声心动图检查确诊的HCM患者的临床资料,并与80例无心脏病对照组进行比较。结果室性心动过速（室速）组与非室速组的晕厥发生率（61．74％vs11．76％,P〈0．05）、家族史（38．9％vs11．7％,P〈0．05）、Q-Tc间期[（448．83±28．22）msvs．（427．38±25．55）ms,P〈0．05]、T波峰-末（T—peak—end,Tp．e）间期[（108．33±6．85msvs（100．00±11．32）ms,P〈0．051、经心率校正后T波峰-末（Tp—ec）间期[（126．33±12．13）msvs（95．95±12．15）ms,P〈0．05]、射血分数（53．03％±14．31％眠71．00％±8．63％,P〈0．05）比较,差异有统计学意义。Logistic回归分析结果显示,Tp—e间期、Tp—ec间期、Q—T间期延长、左心室流出道梗vs与HCM恶性室性心律失常的发生相关。结论HCM患者的心肌结构排列紊乱和心电紊乱严重,易发生快速性心律失常。Tp—e间期、Tp—ec间期、Q—T间期延长、左心室流出道梗vs与恶性室性心律失常的发生关系密切。Tp—e间期、Tp—ec间期可能具有预测室性心律失常发生的价值。     

Prolongation of the Q-T interval caused by sotalol-Possible association with ventricular tachyarhythmias

The case history of a patient is reported who had two episodesof unconsciousness while on anti-hypertensive therapy consistingof hydrochloroihiazide, hydralazine, and sotalol (480-640 mgas a single daily dose). Ventricular fibrillation which wassuccessfully reverted to sinus rhythm was verified as the causeof the second episode. A ventricular arrhythmia might also havebeen the cause of the first attack. Marked prolongation of theQ- Tc interval (up to 0'68 s), which returned to normal afterdiscontinuation of sotalol was observed in connection with theepisodes. Except for sotalol, no other factors known to causeprolongation of the Q-T interval were found. Later, administrationof a single dose of 640 mg of sotalol in the coronary care unitcaused a reversible prolongation of the Q-T interval parallelingthe course of sotalol concentration in the serum. Atenolol ina dose of 100 mg was associated with a reduction in the responseof the pulse to tilting and nitroglycerin administration similarto that observed after sotalol administration, but prolongationof the Q-T interval did not occur after atenolol. Thus, theeffect on the Q- T interval was not related to the beta-blockingeffect of sotalol. These observations suggest that high therapeuticdoses of sotalol can cause a marked prolongation of the Q-Tinterval which may be associated with ventricular arrhythmias     

Delayed repolarization syndrome

The electrocardiograms of 18 patients with atypical ventricular tachycardia manifested as torsade de pointes, ventricular fibrilloflutter, polymorphous ventricular tachycardia, and uniform ventricular tachycardia were analyzed. The patients were divided into two groups: The first group included 10 patients with prolonged Q-T intervals or abnormal U waves (delayed repolarization) and the second group included eight patients with normal ventricular repolarization. All of the electrocardiographic manifestations of atypical ventricular tachycardia were seen in both groups, regardless of the duration of the Q-T interval or the presence of an abnormal U wave. It is suggested that QRS morphology during the tachycardia is not sufficient to distinguish between delayed repolarization and other causes of atypical ventricular tachycardia. Finally, because the electrocardiogram may vary among different patients and from one episode to the next in a single patient due to abnormal repolarization, it is recommended that the term delayed repolarization syndrome be used to identify the arrhythmia.     

低血钾患者的Q—T离散度与室性心律失常关系的探讨

为探讨低血钾时Q-T离散度(Q-Td)与室性心律失常的关系,测量37例低血钾患者补钾前后的Q-Td并与30例血钾正常者作对照。结果显示低血钾组Q-Td显著高于补钾后和对照组(P〈0.001),心律失常发生率明显大于补钾后和对照组(P〈0.01)。说明Q-Td是低血钾患者的心律失常监测的重要指标。     

心脏病室性心律失常患者Tp-e间期、Tp-e/Q-T比值的研究

目的探讨器质性心脏病患者Tp-e间期、Tp-e/Q-T比值与室性心律失常的关系。方法选择器质性心脏病患者85例,分为两组,器质性心脏病室性心律失常组(A组)43例,并进一步按LOWN分级分为两个亚组,A1组(LOWN2-3级)20例,A2组(LOWN3级以上)23例;器质性心脏病无室性心律失常组(B组)42例。另选择健康体检者40例为正常对照组(C组)。采用常规12导联同步心电图及24小时动态心电图分析比较各组的Q-T间期、Q-Tc间期、Tp-e间期、Tp-ec间期和Tp-e/Q-T测值。结果 A组Q-T间期、Q-Tc间期、Tp-e间期、Tp-ec间期、Tp-e/Q-T测值比C组显著升高,差异有统计学意义(P<0.05),而Q-Tc间期、Tp-e间期、Tp-ec间期、Tp-e/Q-T比B组显著升高,差异有统计学意义(P<0.05)。上述各测值A2组比A1组显著升高,差异有统计学意义(P<0.05或P<0.01)。结论 Tp-e间期、Tp-e/Q-T等心电学指标与室性心律失常的发生有关,对室性心律失常的发生具有预测意义。     

Congenital complete heart block and long Q-T syndrome requiring ventricular pacing for control of refractory ventricular tachycardia and fibrillation.

A three-year-old girl with congenital complete heart block presented with repeated bouts of ventricular tachycardia and ventricular fibrillation. The ECG was remarkable for both complete heart block and a long Q-T interval, when corrected for rate. The Q-T interval was longer than the Q-T interval of children with congenital complete heart block and of children without heart disease. Overdrive ventricular pacing was necessary to control the arrhythmias. A prolonged Q-T interval in patients with complete heart block, even in the presence of a normal QRS duration, may predispose the patient to sudden death. Permanent pacing can suppress these arrhythmias by overdriving.