室上性心动过速伴室内阻滞酷似室性心动过速

患者男 ,46岁。于 2 0 0 0年 12月 7日因呼吸困难 ,尿少3ｄ而入院。患者于入院前 3ｄ食入不洁食物后 ,出现大量呕吐 ,吐物为胃内容物 ,腹泻稀水样便 ,每日 10～ 2 0次 ,伴有心悸、口干、尿少、出冷汗、胸闷。村医给予静脉滴注先锋霉素Ⅴ、西地兰等补液后 ,病情不缓解 ,且呼吸困难进行性加重 ,口渴、尿少 ,急来院就诊。继往有先天性心脏病 -法乐氏四联症(术后 ) 11年病史。查体 :体温 3 6℃ ,脉搏 170次 ｍｉｎ ,呼吸 2 5次 ｍｉｎ ,血压111 79ｍｍＨｇ。患者神志清楚、精神差、急性病容、口唇紫绀、食欲不振、小便少、嗜睡状。双肺呼吸音清…     

完全性房室阻滞室性自主性心律并反复心律伴室内差异性传导一例

临床资料　患者男性,65岁,因阵发性胸痛10年,胸闷气短3年,加重3个月,于1999年8月2日入院。10年前曾在当地医院诊断为急性心肌梗死,经治疗后好转。入院前1d服用地高辛0.25mg。查体:血压120/80mmHg(1mmHg=0.133kPa),口唇紫绀,双侧颈静脉怒张,双肺底可闻及湿音,心界向两侧扩大,心率78次/min,律不整,心音低钝,二、三尖瓣听诊区可闻及级收缩期吹风样杂音。双下肢重度可凹性水肿。彩色多普勒超声心动图示:左、右房室增大,左心室射血分数0.2,左心室短轴缩短率0.1。既往心电图示:窦性心律,陈旧性前壁心肌梗死,左前分支阻滞;临床诊断:缺血性心脏…     

房早二联律伴交替性左前分支阻滞并中隔支阻滞型室内差异性传导

患者女性,28岁,临床诊断:心肌炎.心电图(附图)示:窦性心律,房性早搏呈二联律,P-P’问期固定为0.44s,P’-R间期固定为0.14s.房早下传QRS呈2种图形交替出现:一种为正常图形,另一种在肢导联呈典型的左前分支阻滞型:Ⅰ、aVL导联呈qR型,Ⅱ、Ⅲ、aVF呈rS     

老年急性心肌硬塞并发室内阻滞与预后分析

对老年急性心肌梗塞（ＡＭＩ）并发室内阻滞（ＩＶＢ）的临床经过、严重并发症与预后进行的分析结果表明，并发ＩＶＢ者病情复杂，并发症多，其病死率高于无ＩＶＢ者，二者差异显著（Ｐ＜０．０５）。尤其并发右束支传导阻滞者（ＲＢＢＢ）及左前分枝阻滞（ＬＡＨ）并ＲＢＢＢ者的危险性更大，预后较差。提示对ＡＭＩ并发ＲＢＢＢ和ＬＡＨ＋ＲＢＢＢ患者尤其要加强监测，及时处理并发症。     

肥厚型心肌病室内3分支阻滞1例

患者女,37岁。心悸、乏力半年,头晕、阵发性心前区疼痛1月。查体：T36℃,P42次／min,R20次／min,BP90／65mmHg,神志清,颈静脉无怒张,双肺无干啰音。右肺底少许小水泡音。心浊音界不大,心率45次／min,律不齐,心音低钝,各瓣膜无明显病理性杂音。双下肢轻度水肿,彩色超声心动描记术（UCG）示：肥厚型心肌病（非对称梗阻型）,主动脉瓣、二尖瓣、三尖瓣少量返流,左室充盈不良。临床诊断：肥厚型心肌病,心律失常,心功能不全。     

非心肌梗死冠心病患者心功能变化与室性心律失常的关系

目的　了解心功能不全的恶化 ,对各种室性心律失常发生的影响。方法　选择 2 97例冠心病住院患者 ,根据心功能按纽约心脏病协会 (NYHA)标准分为四组 ,检测 2 4小时动态心电图 (Holter) ,分析有无室性心律失常及其类型 ,进行统计分析。结果　心功能 I级组中 1 8例 (4 1 .86% )发生室性心律失常 ,偶发室性早搏 1 4例 (3 2 .5 6% ) ,频发室性心律失常 4例 (9.3 0 % ) ;心功能 级组中 68例 (5 5 .74% )发生室性心律失常 ,偶发室性早搏 45例 (4 4 .2 6% ) ,频发室性心律失常 45例 (3 6.89% ) ;心功能 级组中 3 3例 (5 5 % )发生室性心律失常 ,偶发室性早搏 2 0例 (3 3 .3 3 % ) ,频发室性心律失常 1 3例 (2 1 .67% ) ;心功能 级组中 42例 (5 8.3 3 % )发生室性心律失常 ,偶发室性早搏 2 5例(3 4.72 % ) ,频发室性心律失常 1 7例 (2 3 .61 % ) ,由多格表 x2检验结果看 ,各级别心功能不全组中室性心律失常的发生率除联律和持续或非持续性室速二组外并无显著性的差异。结论　非心肌梗死患者室性心律失常发作的数量与心功能不全的程度无关 ,但联律和持续性或非持续性室性心律失常在重度心功能不全患者发生率增加。     

非特异性溃疡性结肠炎51例临床分析

炎症性肠病特别是非特异性溃疡性结肠炎（ＵＣ）,近年来在我国的发病率明显增加,但与欧美等国相比仍低得多［１］。本研究回顾分析了５１例ＵＣ患者的临床表现、肠外并发症和治疗情况,结合本组资料,对ＵＣ的研究进展进行了文献复习。材料和方法本组收集１９８８～１９...     

非特异性输尿管炎19例临床分析

非特异性输尿管炎是导致输尿管狭窄的病因之一,其临床表现多无特异性,易造成误诊、漏诊。1995-2006年,我院共收治非特异性输尿管炎性狭窄19例,现对其临床资料进行回顾性分析。     

病毒性心肌炎引起的室内3支阻滞伴房室阻滞

患者,男,20岁.发热4 d,咽痛、头晕1 d.体检:T 37.5℃,咽充血,扁桃体Ⅰ度肿大.心肺听诊无特殊.胸片:心肺无异常;血常规:白细胞5.1×109/L,中性54.4%,淋巴35.2%;病毒检测:EB病毒抗体IgG、柯萨奇病毒抗体IgG均为阳性;心肌酶谱:门冬氨酸转移酶(AST)113 IU/L,乳酸脱氢酶(LDH)265 IU/L,肌钙蛋白1.26 μg/L;血沉31 mm/h.临床诊断:上呼吸道感染;病毒性心肌炎.该患者经过利巴韦林、阿米卡星、头孢西丁、可乐必妥等药物治疗后症状迅速好转.     

尼非卡兰的临床应用研究

尼非卡兰是一种单纯的快速激活延迟整流K+通道阻滞剂,目前只有静脉制剂,常应用于急诊或急救时心律失常的治疗,如用于预防或治疗难治性心律失常,其静脉使用时间会长一些,当心律失常被控制时,再过渡至口服抗心律失常药物治疗.国内应用的历史6年余.多项临床应用表明,尼非卡兰对于心房颤动(简称房颤)的转复以及射频消融术中或术后房颤的...     

非特异性心室内传导障碍71例临床报告

目的 探讨非特异性心室内传导障碍的心电图特点及与疾病的相关性.方法 回顾性分析71例非特异性心室内传导障碍的表现形式与年龄结构、疾病的关系.结果 非特异性心室内传导障碍发生的男女比例为65∶6;在3个年龄组(10～39岁、40～ 59岁及60岁以上)的病例分别为23例(32％)、21例(30％)及27例(38％);单纯性特异性室内阻滞的发生率为35％、33％及30％;40岁以下组,无器质性心脏疾患及正常人占78％;60岁以上组,高血压、冠心病人群占59％;非特异性心室内传导障碍合并ST-T改变多见于器质性心脏病患者,占59％.结论 非特异性心室内传导障碍的发生无年龄差别,但多见于男性患者.年轻人群中,非特异性心室内传导障碍常见于无器质性心脏疾患及正常人;老年人病因以高血压、冠心病为主.非特异性心室内传导障碍合并其他心电图异常时临床意义较大.     

The linking phenomenon in tachycardia-dependent intraventricular block

Seven cases of tachycardia-dependent, or phase-3, intraventricular block have been examined. Analysis revealed a constant overlap between the range of the R-R intervals ending in normal conduction and the range of the R-R intervals where the second beat is associated with intraventricular block. The block, indeed, may occur at the end of relatively long R-R intervals, whereas R-R intervals which are shorter (up to 0.11 sec) can unexpectedly result in normal intraventricular conduction. A relatively late QRS complex, however, can reflect an intraventricular block only when the preceding complex also manifests the block. This phenomenon has been interpreted as due to the so called "linking", namely the retrograde concealed penetration of an anterogradely blocked bundle branch by the impulse traversing the controlateral bundle branch. This delays the activation of the affected bundle branch, whose refractory period is, accordingly, "shifted to the right" within the cardiac cycle. A relatively late sinus impulse, thus, can result in intraventricular block since the refractory period of the affected bundle branch ends later, with respect to the beginning of the QRS complex, than it does after a normally conducted sinus impulse.     

Mid-diastolic intraventricular functional block. A new mechanism for intermittent intraventricular blocks?

Experimental and clinical studies have demonstrated the existence of phase 3 and phase 4 functional blocks. In this report six cases are presented in which the electrophysiological study demonstrated the existence of a functional intraventricular block different from phase 3 and phase 4 blocks. In these cases the occurrence of the block was related to the presence in mid-diastole of a zone of block preceded and followed by intervals of unimpaired conduction. In two of 6 cases the functional block (infrahisian block) was not present in the basal tracing; it occurred during programmed atrial stimulation in a range of critical H1H2 coupling intervals delivered late in diastole, and did not appear after earlier stimuli. In the remaining four cases the conduction disturbance (2 RBBB, 2 infrahisian blocks) was present in the basal tracing, but disappeared both during early and late supraventricular extrastimuli, the first having short H1H2 intervals, the latter having H1H2 intervals longer than H1H1 basal cycle length. The width of the mid-diastolic zone of block varied from a few msec to hundreds of sec, and increased as heart rate increased. Two hypotheses are put forward in order to explain the electrophysiological mechanism responsible for the phenomenon: 1) a longitudinal dissociation in the conducting system, generating two different ways, one having a long refractory period, the other having a phase 4 spontaneous depolarization; they would be responsible of phase 3 and phase 4 blocks respectively. The early and late zones of conduction could be explained by an alternate conduction in one of the two ways, while the mid-diastolic zone of block could be due to a simultaneous block in both ways; 2) the existence of a diastolic oscillatory potential (late after-depolarization). In the latter case we can suppose that the mid-diastolic block was due to the stimulation of the cells of the conducting system before the restoration of the normal diastolic potential. Our electrophysiological data offer a new contribution to the understanding of intermittent intraventricular blocks. However further experimental and clinical studies are needed to confirm our electrophysiological hypotheses.