经食管左心房调搏术引发心律失常的分析及纠治

目的：探讨经食管左心房调搏术（TEAP）引发心律失常的纠治措施。方法：对我院730例行TEAP检查引发的53例心律失常进行分类。并分析其发生机制及制订纠治方案。结果：5类心律失常分别为房性过早搏动、室性过早搏动、心房颤动、心房扑动、心脏停搏。若各种类型早搏在数分钟后不能自行终止，则可应用阻断植物神经的药物；对持续时间较长的房颤、房扑，可静脉注射西地兰；在心脏停搏时间≥2.5s时，应进行保护性起搏。结论：TEAP引发的心律失常，可以得到有效的纠治。     

食管心房调搏中出现的交界性心律失常临床意义探讨

食管心房调搏(TEAP)在实施过程中,可能诱发产生多种心律失常,交界性心律失常是其中常见的一类.我们回顾分析近年来所做食管心房调搏1790例心电图记录资料,发现TEAP时诱生的交界性心律失常分为下列几种情况:单个交界性搏动;交界性逸搏心律;房室结折返性心动过速.本文对这些心律失常的产生及临床意义做初步探讨.     

氟喹诺酮类和严重心律失常危险：基于人群的研究

氟喹诺酮类药物可引起QTc延长和尖端扭转性室速，引发室颤、心脏停搏或心源性猝死。但临床数据少，尤其缺少氟喹诺酮类不同品种的资料。本课题分析氟喹诺酮类的使用以及不同品种氟喹诺酮类药物的使用与严重心律失常（室性心律失常或突发死亡）的危险度的相关性。     

迷走神经介导性停搏的心电生理分析及临床意义

心脏停搏作为一种显著性缓慢心律失常受到临床的普遍重视,通常被认为器质性心脏病而予以积极地药物治疗和起搏治疗。本研究分析了56例动态心电图（Holter）停搏患者的心脏电生理特性,旨在明确迷走神经张力增高可以引起心脏停搏,现报道如下。     

超声引导下普通电极导管临时心脏起搏应用分析

<正>紧急床边临时心脏起搏是严重心动过缓、心脏停搏及顽固性室性心律失常的抢救技术。本院自2003年2月～2007年6月对11例合并严重血流动力学障碍的缓慢型心律失常患者,采用超声监测床旁临时心脏起搏,获得良好效果。     

1例急性心肌梗死合并糖尿病患者频发阿斯综合征的急救与护理

急性心肌梗死(acute myocaydia infarction,AMI)是在冠状动脉病变的基础上发生冠状动脉血量急剧减少或中断,使相应的心肌严重而持久地急性缺血或坏死所致[1,2]。阿斯综合征(Adams-stokes)是由于心脏病变导致心排血量骤减或突然中断而引发的急性脑缺血综合征。主要表现是心脏停搏5～10 s可出现晕厥,停搏15 s以上可出现抽搐,偶有大小便失     

经食管心脏起搏在直流电复律中的应用

心脏直流电复律是临床上治疗心律失常的主要手段之一,在某些情况下任何其它治疗均无法代替.然而电复律的并发症较多,尤其是心脏停搏及导致血流动力学紊乱的心动过缓[1],容易造成患者死亡等严重事件的发生,心脏停搏最有效的治疗是人工心脏起搏.     

心律平中毒致呼吸心跳骤停1例的抢救护理

心律平,正名盐酸普罗帕酮片,为抗心律失常药,用于室性早搏、室上性心律失常等。但用量过大可产生心脏停搏及传导阻滞、低血压等。我急诊科于1997-09—04成功地抢救误服心律平50片致心跳呼吸骤停1例,抢救成功,护理体会如下。     

磷酸肌酸停搏液不同浓度下保护心肌的临床效果分析

目的探讨不同浓度的磷酸肌酸停搏液保护心肌的效果。方法选取2010年1月至2013年12月接受心脏手术治疗的患者84例,随机分为观察组和对照组各42例。观察组在冷血停搏液中灌注磷酸肌酸停搏液10mmol／L,对照组在冷血停搏液中灌注磷酸肌酸停搏液20mmol／L,观察并比较两组患者主动脉开放前及开放后2h、24h、48h肌钙蛋白I（cTnI）及肌酸激酶同工酶（CK-MB）浓度,术中复跳时间及复跳率,血管活性药物应用情况,机械通气时间,心律失常发生率。结果观察组患者主动脉开放前及开放后2h、24h、48hcTnI及CK-MB浓度均明显低于对照组（P均〈0．05）;两组患者心脏均自动复跳,复跳率均为100％。观察组患者心脏复跳时间[（57．6±31．4）s vs（87．4±36．2）s]和术后机械通气时间[（9．15±3．64）hvs（12．87±3．14）h]明显短于对照组,心律失常发生率明显低于对照组（7．14％ vs 33．33％）,术后1d、2d肾上腺素、多巴胺、米力农应用量均明显低于对照组,差异均有统计学意义（P均〈0．05）。结论作为心脏停搏液成分的磷酸肌酸停搏液可有效减少缺血／再灌注对心肌造成的损伤,其使用浓度以10mmol／L为宜,增加浓度不能更进一步改善心脏功能。     

无创体外心脏起搏抢救心脏停搏患者的临床应用及护理

目的：探讨无创性经皮体外心脏起搏（NTCP）在心脏停搏急救中的临床应用及护理。方法：回顾性分析用心脏监护除颤起搏器对70例心脏停搏患者进行NTCP。结果：40例起搏无效，起搏成功10例。临床有效13例，复苏成功7例，存活5例。结论：NTCP可作为紧急情况下抢救心脏停搏患者的一种有效手段．正确的护理配合是起搏成功的重要保证。     

Termination of Tachycardias by Transesophageal Electrical Pacing

To evaluate the therapeutic significance of noninvasive transesophageal pacing for termination of tachycardias the method of rapid atrial or ventricular transesophageal pacing was used in 233 patients with different tachycardiac arrhythmias. We were able to terminate atrial flutter in 136 of 162 patients by transesophageal rapid atrial stimulation (conversion to sinus rhythm in 75 cases, induction of atrial fibrillation in 61 cases). Atrial tachycardias were interrupted in 17 of 23 patients (sinus rhythm in 11 cases, atrial fibrillation in six cases). AV reciprocating/AV nodal supravenrricular reentry tachycardias were terminated in 62 of 63 patients (sinus rhythm in 58 cases, atrial fibrillation in four cases). By transesophageal rapid ventricular pacing ventricular tachycardias could be terminated in ten of 15 patients. The success rate of transesophageal pacing was influenced by the pacing rate, by the type of tachycardiac arrhythmia inclusive by the type of atrial flutter and by the tachycardia's cycle length. Because the success rates are comparable with invasive technique and the procedure is simpler, the noninvasive transesophageal antitachycardiac pacing should be respected as the method of the first choice in patients with supraven-tricular tachycardias.     

The effect of the atrial pacing site on the total atrial activation time

The effect of dual site pacing for prevention of atrial fibrillation may be due to synchronization of right and left atrial activation. Little is known, however, about the effect of pacing from single right atrial sites on differences in interatrial conduction. Twenty-eight patients without structural heart disease were studied following radiofrequency catheter ablation of supraventricular arrhythmias. Pacing was performed using standard multipolar catheters from the presumed insertion site of Bachmann's bundle, the coronary sinus ostium, the high lateral right atrium, and the right atrial appendage (n = 8 patients). Bipolar recording was performed from the distal coronary sinus, the high and low lateral right atrium, and the posterolateral left atrium (n = 13 patients). The longest conduction time from each pacing to each recording site was considered the total atrial activation time for the respective pacing site. During high right atrial pacing, the total atrial activation time was determined by the conduction to the distal coronary sinus (118 +/- 18 ms), during coronary sinus ostium pacing by the conduction to the high right atrium (94 +/- 18 ms), and during Bachmann's bundle pacing by the conduction to the distal coronary sinus (74 +/- 18 ms). The total atrial activation time was significantly shorter during pacing from Bachmann's bundle, as compared to pacing from other right atrial sites. Thus, in normal atria, pacing from the insertion of Bachmann's bundle causes a shorter total atrial activation time and less interatrial conduction delay, as compared to pacing from other right atrial sites. These findings may have implications for alternative pacing sites for prevention of atrial fibrillation.     

Organized incessant atrial arrhythmias in the setting of severe, isolated biatrial scarring

Introduction: Diffuse transmural fibrosis and scarring limited to the area without atrial dilation or significant structural heart or other systemic disease has not been reported. We present three cases of a syndrome characterized by refractory organized atrial arrhythmias, diffuse atrial scarring with electrical silence, and mechanical paralysis in the absence of atrial dilation or any systemic or neurodegenerative disorders.
Methods: Patients referred for electrophysiology study of atrial arrhythmias were included. Electroanatomic mapping with the Carto system (Biosense Webster, Diamond Bar, CA, USA) and magnetic resonance imaging ( MRI) with scar sequencing were performed.
Results: There was no family or personal history of cardiac, muscular, or developmental diseases. All patients had organized atrial arrhythmias. Echocardiograms showed atrial standstill with normal atrial and ventricular dimensions. No other structural abnormalities were noted. Carto mapping revealed severe biatrial diffuse scarring. The left atrial (LA) was less affected than the right atrial (RA). MRI findings confirmed biatrial scarring. During tachycardia, islands of dissociated electrical activity could be seen in the right atria. Entrainment mapping was not performed in the atria as high-output pacing could not capture the atria. Coronary sinus entrainment demonstrated the coronary sinus (CS) not to be critical to the tachycardia. Ablation was targeted toward channels of low voltage but was not successful in any cases. All required atrioventricular (AV) nodal ablation with pacing.
Conclusion: An association between biatrial cardiomyopathy and scarring with normal atrial dimensions has been described. Since severe scarring has not been reported with organized arrhythmias this may represent a new syndrome.     

室上性心动过速儿童经食管与心内电生理参数的对比研究

[目的]通过对室上性心动过速(SVT)儿童经心内电生理检查(IEPS)和食管心房调搏术(TEAP)获得的电生理数据进行对比研究,对TEAP电生理参数的可靠性进行合理的评价,为广泛开展小儿无创心脏电生理检查提供科学依据.[方法]对比研究了我院2000年8月至2008年10月住院的27例SVT儿童的TEAP和IEPS的检查结果,男12例,女15例,年龄6～15岁[平均(10.1±2.5)岁],临床均有反复多次的SVT发作史.分别通过TEAP和IEPS方法,测定窦房结恢复时间(SNRT),校正的窦房结恢复时间(CSNRT),窦房结传导时间(SACTc);以心房分级递增法S1S1测房室结的文氏型阻滞点和2∶1阻滞点;用S1S1程控早搏刺激测心房有效不应期(AERP)、房室前传有效不应期(AVERP).对所有数据采用SPSS软件进行统计学分折.[结果]27例SVT患儿中7例为房室结折返性心动过这(AVNRT),20例为房室折返性心动过速(AVRT),其中左侧旁道(LAP)6例,右侧旁道(RAP)14例;均通过射频消融(RFCA)术进行成功根治.TEAP分型诊断符合率为96.3％.通过TEAP和IEPS分别获得电生理参数,SNRT分别为(912.2±180.3)ms和(930.2±174.9)ms,CSNRT分别为(304.0±79.7)ms和(287.1±63.1)ms,SACTc分别为(84.3±21.8)ms和(94.6 ±23.2)ms,文氏点分别为(182.0±28.1)ms和(187.0 ±24.9)ms,2∶1阻滞点分别为(211.0 ±24.7)ms和(220.0±19.3)ms,AERP分别为(228.0±29.4)ms和(223.5±21.7)ms,AVERP分别为(298.5±71.8)ms和(277.7 ±57.5)ms.对两组数据进行统计学分析,P均＞0.05,差异无统计学意义.[结论]TEAP电生理参数是可靠的,值得在基层儿科临床单位进行广泛应用.     

Atrial Septal Pacing: A Method for Pacing Both Atria Simuhaneously

By pacing both atria simultaneously, one could reliably predict and optimize left-sided AV timing without concern for IACT. With synchronous depolarization of the atria, reentrant arrhythmias might be suppressed. We studied four male patients (73 ± 3 years) with paroxysmal atrial fibrillation and symptomatic bradyarrhythmias using TEE and fluoroscopy as guides; a standard active fixation screw-in lead (Medtronic model #4058) was attached to the interatrial septum and a standard tined lead was placed in the ventricle. The generators were Medtronic model 7960. The baseline ECG was compared to the paced ECG and the conduction time were measured to the high right atrium, distal coronary sinus and atrial septum in normal sinus rhytbm, atrial septal pacing, and AAT pacing. On the surface ECG, no acceleration or delay in A V conduction was noted during AAI pacing from the interatrial septum as compared with normal sinus rhythm. The mean interatrial conduction time for all 4 patients was 106 ± 2 ms; the interatrial conduction time measured during AAT pacing utilizing the atrial septal pacing lead was 97 ± 4 ms (P = NS). During atrial septal pacing, the mean conduction time to the high right atrium was 53 ± 2 ms. The mean conduction time to the lateral left atrium during atrial septal pacing, was likewise 53 ± 2 ms. We conclude that it is possible to pace both atria simultaneously from a single site using a standard active fixation lead guided by TEE and fluoroscopy. Such a pacing system allows accurate timing of the left-sided AV delay.     

Prevention of the initiation of atrial fibrillation: mechanism and efficacy of different atrial pacing modes

Several atrial pacing modes have been reported to be effective in the prevention of atrial fibrillation (AF); they included biatrial pacing, dual site right atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus pacing. However, the relative efficacy and electrophysiological mechanisms of these pacing modes in the prevention of AF are not clear. In 15 patients (age 54 +/- 14 years) with paroxysmal AF, P wave duration, effective refractory period, and atrial conduction time were determined with six different atrial drive pacings, that were right atrial appendage (RAA), BB, right posterior interatrial septum (RPS), distal coronary sinus (DCS), RAA plus RPS simultaneously (DSA), and RAA plus DCS simultaneously (BiA). All these patients consistently had AF induced with early RAA extrastimulation coupling to RAA drive pacing. No patient had AF induced with RAA extrastimulation coupled to BB, RPS, or DCS drive pacing, but seven and eight patients had AF induced with RAA extrastimulation coupled to DSA and BiA drive pacing, respectively. The P wave duration was longest during RAA pacing, and became shorter during other atrial pacing modes. Analysis of electrophysiological change showed that early RAA extrastimulation coupled to RAA drive pacing caused the longest atrial conduction delay among these atrial pacing modes; BB, RPS, and DCS drive pacing caused a greater reduction of this conduction delay than DSA and BiA drive pacing. In addition, the effective refractory periods of RAA determined with BB, RPS, and DCS drive pacing were similar and longer than that determined with DSA and BiA drive pacing. In patients with paroxysmal AF, this arrhythmia was readily induced with RAA extrastimuli coupled to RAA drive pacing. BB, RPS, and DCS pacing were similar and more effective than DSA and BiA pacing in preventing AF.     

Long-term Prevention of Vagal Atrial Arrhythmias by Atrial Pacing at 90/Minute: Experience with 6 Cases

Six patients (5 men, 1 woman) with a history ranging from 3–16 years of resistant vagal atrial arrhythmias were treated by atrial pacing at a rate of 90Jmin. These patients have been followed up for an average of 5.5 years (range 2–11 years) with favorable resutls. The arrhythmias were charactemed by daily or weekly attacks of rypical alrial flutter and atrial fibrillalion occurring mainly or exclusively at night, at rest, or in the digestive periods in otherwise normal hearts of middle-aged palients (first attack between 25 and 54, mean 40). The arrhythmias werc resistant to quinidinc, and were usually aggravated by digitalis, beta-blockers and verapamil. Amiodaroneisusually the only effective drug in this syndrome, but was not used before pacing in the 2 first cases, and was in effective in the other 4 cases. Electrophysiologic studies confirmed the absence of sick sinus syndrome, and the close relationship betwecn a relative bradycardia and the onset of the arrhythmia. Atrial pacing alone totally controiled the arrhythmia in 1 palient; amiodarone was used in conjunction with pacing in 3 palients. In 1 patient the improvement was clear but incomplete, and in 1 patient permanent alrial fibrillation occurred shortly afler pacemaker implantalion.     

Atrial Arrhythmias in Dual Chamber Pacing and Their Influence on Long-Term Mortality

A retrospective study of 252 patients who received a DDD pacemaker between October 1982 and December 1990 was performed. During a mean follow-up of 30 months, reprogramming to the VVI mode was necessary in 39 patients (15.5%). Technical problems causing downgrading occurred 15 times, of which 13 problems became permanent. A total number of 24 patients had sustained atrial arrhythmias, including 14 with atrial fibrillation and 10 with atrial flutter. In this group, conversion to sinus rhythm could be obtained in 38%. After 2 years, reliable DDD pacing was maintained in 86% of the surviving patients. The survival after 1 and 2 years was 94% and 89%, respectively, and was not influenced by arrhythmias or technical problems. We conclude that atrial arrhythmias including flutter are the most important reasons for reprogramming to the VVI mode, although in an important number of patients, predominantly those with flutter, restoration of AV synchrony can be obtained. The high number of patients with atrial flutter could imply some role for DDD devices offering the option of antitachycardia pacing. Reprogramming of the pacing mode did not influence mortality.     

Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity.

To define the role of verapamil in the treatment of ventricular tachycardia (VT), we studied 21 patients with chronic recurrent VT. Electrophysiologic studies were performed before and during intravenous infusion of verapamil (0.15 mg/kg followed by 0.005 mg/kg per min). On the basis of the mode of VT initiation and termination, we identified three groups of patients: (a) 11 patients had VT suggestive of reentry, as VT could be initiated with ventricular extrastimulation and terminated with overdrive ventricular pacing. Verapamil did not affect the inducibility and cycle length of VT. (b) 7 patients had VT suggestive of catecholamine-sensitive automaticity as VT could not be initiated with programmed electrical stimulation but could be provoked by isoproterenol infusion. Moreover, the VT could not be converted to a sustained sinus rhythm with overdrive ventricular pacing and it resolved only with discontinuing isoproterenol infusion. Verapamil exerted no effects on VT. (c) 3 patients had VT with electrophysiologic characteristics suggestive of triggered activity related to delayed afterdepolarizations. Characteristically, after attaining a range of cycle lengths, the sinus, atrial or ventricular paced rhythm could initiate VT without ventricular extrastimulation. The first beat of VT invariably occurred late in the cardiac cycle with a premature coupling interval 0-80 ms shorter than the preceding QRS cycle length; the premature coupling interval gradually decreased as the sinus, atrial or ventricular paced cycle length progressively shortened. Of note, verapamil completely suppressed VT inducibility in these three patients. These observations lead us to suggest that verapamil does not affect VT caused by reentry and catecholamine-sensitive automaticity but is effective in suppressing VT caused by triggered activity related to delayed afterdepolarizations in humans.     

Safety of Transesophageal Pacing for 24 Hours in a Canine Model

Background: Temporary epicardial pacing is often necessary following surgical correction of congenital heart disease. Epicardial pacing wires, while generally effective, can, however, become nonfunctional. Transesophageal atrial pacing (TEAP) can be a useful adjunct in this setting. The potential for esophageal damage with sustained TEAP is unknown. We assessed the safety of continuous (24 hours) TEAP by evaluating gross and histological changes to the esophagus in a canine model.
Methods: Thirteen juvenile beagle dogs were fitted with a 4-Fr multipolar catheter placed transnasally into the esophagus to a level to sustain atrial capture. Pacing was established in nine dogs for 24 hours while four control dogs had catheters but no pacing stimulus applied. Paced dogs were divided into two groups: group A (n = 5) that were euthanized immediately and group B (n = 4) that were euthanized 7 days after the pacing period. Nonpaced dogs (group C, n = 4) were treated similar to group A. Gross and histological examination of the esophageal tissue was completed.
Results: Gross and histological evidence of mild esophagitis was noted in dogs from groups A and C but not in dogs from group B. There was no evidence of esophageal stricture or fibrosis in any dog from any group.
Conclusions: TEAP did not result in permanent esophageal changes after 24 hours of stimulation. Microscopic lesions of mild erosive esophagitis, seen after 24 hours of TEAP, were absent 7 days postpacing. Mechanical irritation from the catheter cannot be ruled out as a cause of these changes.