交接区逸搏揭示房室结双径路1例

患者女 ,5 5岁。因咳嗽、气喘、胸闷 2 0年 ,加重伴心悸3ｄ ,于 2 0 0 2年 3月 2日就诊。体检、神志清楚、双肺哮鸣音 ,心率 10 6次 ｍｉｎ ,心律不齐 ,Ｐ2 >Ａ2 ,未闻及病理性心脏杂音 ,腹部无异常。心电图 (图 1)上行Ⅱ导联示窦性Ｐ波匀齐 ,ＰＰ间距 0 5 6ｓ,心率 10 6次 ｍｉｎ ,前 9个Ｐ -Ｒ间期 0 2 0ｓ基本一致 ,第 10个Ｐ -Ｒ间期 0 40ｓ ,提示房室交接区有双径路传导 ,Ｐ1 1 未下传心室 ,其后的 1个Ｐ -Ｒ间期稍短 0 18ｓ。下行ａＶＦ导联窦性Ｐ波匀齐 ,Ｒ1、4、7的Ｐ -Ｒ间期小于 0 12ｓ ,且Ｒ3～ 4与Ｒ6～ 7间距相等 ,ＱＲ…     

房室结双径路1：2传导致非折返性室上性心动过速1例

室上性心动过速是临床最常见的心律失常之一，常见原因有多种。房室结双径路传导现象，为一常见的电生理现象，是房室结内存在着功能性纵行分离的两条不同性能的传导径路，即快径路和慢径路。而房室结双径路1：2传导是由一次窦性激动经房室结双径路同步下传两次激动心室，这种情况连续发生就会导致两倍于心房率的心室率，表现为非折返性室上性心动过速。     

房室结双径路参与的房室折返性心动过速

患者男性,38岁。有阵发性室上性心动过速(室上速)史10余年,近2年发作频繁,室上速发作时各种抗心律失常药物均不能直接终止,每次均需食管调搏超速或亚速刺激方可终止。此次因心悸5ｈ就诊。查体:神志清晰,血压12080ｍｍＨｇ(1ｍｍＨｇ=0133ｋＰａ),心率190次ｍｉｎ,律齐,各瓣膜听诊区未闻杂音。心动过速发作时心电图如图1所示。ＱＲＳ波形为室上性,在Ｖ1导联呈ＱＳ型,时限008ｓ,频率190次ｍｉｎ。ＲＲ间期长短交替,分别为320ｍｓ和270ｍｓ。食管导联可见Ｐ′波在ＱＲＳ波群之后,ＲＰ′间期固定,为012ｓ,Ｐ′波形态一致。Ｐ′Ｒ间期则长短交替,…     

逆向型房室结内双径路传导

随着大量的心脏电生理研究证明 ,多径路传导现象可以发生于心脏传导系统的任何部位 ,但多见于房室结。房室结内可以存在 2条或更多条传导性能不同、不应期不一致的传导径路 ,以房室结双径路最为多见 ;而逆向性房室结内双径路检出率为 3 5 % [1] ,临床较为少见。本文就此例与同行做一讨论。患者男 ,6 3岁 ,农民。因活动后胸闷、乏力来院就诊。临床诊断 :冠心病。心电图表现如图所示 :为V1导联连续记录 ,QRS时间 <0 12s,呈室上性 ,R R间距均齐 ,频率为 5 8次 /min。每个QRS波之后均有形态一致的P′波。R P′间期长短交替 :R1、3、5的R …     

房室结双径路特殊心电图表现1例

患者男性,33岁。因反复头昏、心悸就诊。既往体健，查体：BP 115／80mmHg，心界不大，各瓣膜听诊区未闻及病理性杂音。临床诊断：心悸待查。心电图示：窦性心律，P-P间距规则，频率平均75次／分，图1是Ⅱ导联连续记录，前半     

房室结折返性心动过速与房室结双径路的相关性研究

目的　探讨房室结折返性心动过速 (AVNRT)与房室结双径路 (DAVNP)的相关性。方法　回顾性分析成功射频导管消融的单一类型 AVNRT的心内电生理和食管心房调搏 (GEAP)资料。结果　10 7例单一类型的 AVNRT,存在 DAVNP者 10 1例 ,其中慢 -快型 AVNRT99例 ,慢 -慢型 AVNRT2例 ;DAVNP阴性者 6例 ,其中慢 -快型 AVNRT1例 ,慢 -慢型 AVNRT3例 ,快 -慢型 AVNRT2例 ;慢 -快型 AVNRT DAVNP阳性检出率明显高于慢 -慢型和快 -慢型 AVNRT(P<0 .0 1)。 10 0例慢 -快型AVNRT中 ,5 8例女性较 42例男性年轻 (4 2 .0± 12 .9比 49.6± 11.8,P<0 .0 1) ,分别有 11例和 10例心内电生理检查时 DAVNP阴性 ,而 TEAP存在 DAVNP。结论　 DAVNP是慢 -快型 AVNRT的发生基础 ,而慢 -慢型和快 -慢型 AVNRT与 DAVNP的相关性较差。     

隐匿性交接性早搏致假性房室结双径路

患者男性，25岁。上呼吸道感染1W，自觉胸闷、心悸。临床体查、心肌酶学、X线胸片、血电解质等均属正常。常规心电图(图1)：窦性心律。心率约65次／min。ST-T未见异常。QT间期正常。在aVR导联和aVF、导联可见两种P-R间期。即在P—R间期0．19s基础上。突然出现一种单个P-R间期0．40s的搏动，P—P间隔基本相等。长短P-R间期间差0．21s。每次长P—R间期下传的QRS之后均可见逆行P波，     

房室结双径路前向传导的食管心房调搏电生理特征

以食管心房调搏检查有心悸及各种心律失常病史的700例患者,发现房室结双径路前向传导101例,占14.4％。依房室传导曲线特点分上坡型19例、平坦型51例、下坡型31例,诱发阵发性室上性心动过速(SVT)29例。同时发现双径路传导与文氏现象之间有密切联系。并就双径路的心电图诊断等进行讨论。     

房室结双径路和左侧旁路参与的室上性心动过速体表心电图分析

患者 ,男 ,65岁。因阵发性心悸 5 0年 ,加重 3个月入院。患者从 1 5岁起间断出现阵发性心悸 ,呈突发突止状 ,因无明显不适 ,未予治疗。近 6年发作次数增加 ,每年 2～ 3次 ,需用异搏定等药物终止。近 3个月每天发作 3～ 4次 ,持续数分 ,数小时不等 ,伴烦躁不适。但无意识障碍及呼吸困难。为行射频消融治疗收入我院。入院时血压 1 2 0 /80 mm Hg( 1mm Hg=0 .1 33k Pa) ,一般状态好 ,心肺无阳性体征 ,X线胸片、心脏彩超均正常。入院诊断 :心律失常 ,阵发性室上性心动过速 (室上速 )。结果见图 1 ,图 2。在行食管调搏检查时 ,给予适当程控刺激…     

加速性房性逸搏心律伴房室结内折返性心动过速1例

患者女性,30岁。因心悸、咳嗽2天入院。查：HP95次／分,BP100／65mmHg、R18次／分、双肺呼吸音清,未闻及哕音,心界不大,无杂音,心率95次／分,律不齐,腹软,肝脾未触及,双下肢无水肿。入院时心电图考虑为：①窦性心律;②室上性心动过速;③加速性逸搏心律。经食管心电图标测见图1（室上速段SVT起始pr-R间期延长,R-P’100ms,P1为窦P,P2～7为房性P’（P’-R〉0．12s）,其中P’7-R较前P＇-R延长,     

经房室结双径路1:2传导引起的一种新型室上性心动过速

目的 报告一种新型的室上性心动过速；方法 总结该心动过速的电生理特点及射频消融治疗方法；结果 该型室上速的发生机制是窦性激动连续经房室结1：2下传激动心室，导致心室率经常是心房率的两倍，心动过速呈无休止性发作，并引起心动过速性心肌病。结论 这种心动过速可以经心内电生理检查确诊并通过射频消融改良房室结而根治。     

房室结双径路合并房室旁路的折返性心动过速及射频消融治疗

目的本研究旨在探讨房室结双径路（ＤＡＶＮＰ）合并房室旁路（ＡＰ）的电生理特征和射频消融要求。方法对２１８例阵发性室上性心动过速（ＰＳＶＴ）进行电生理检查，观察ＰＳＶＴ的前传和逆传途径，然后对ＡＰ或房室结慢径（ＳＰ）进行消融治疗。结果２１８例ＰＳＶＴ中检出ＤＡＶＮＰ＋ＡＰ１０例，检出率为４．６％。其中ＳＰ前传、ＡＰ逆传（ＳＰ－ＡＰ折返）４例，快径（ＦＰ）前传、ＡＰ逆传（ＦＰ－ＡＰ折返）１例，ＳＰ－ＡＰ折返并ＦＰ－ＡＰ折返或ＳＰ／ＦＰ交替前传折返４例，ＳＰ前传、ＦＰ逆传（ＡＰ旁观）１例。１０例患者均作ＡＰ消融，诱发房室结折返性心动过速（ＡＶＮＲＴ）的３例加作ＳＰ消融，术后随访均无复发。结论ＤＡＶＮＰ合并ＡＰ者ＡＰ均作为逆传途径，阻断ＡＰ是消融关键；ＡＰ旁观者也应作ＡＰ消融；仅有ＡＨ跳跃延长者不必接受房室结改良；ＡＰ消融者应作ＤＡＶＮＰ电生理检查。     

Demonstration of dual atrioventricular nodal pathways utilizing a ventricular extrastimulus in patients with atrioventricular nodal re-entrant paroxysmal supraventricular tachycardia.

In patients with atrioventricular (A-V) nodal re-entrant paroxysmal supraventricular tachycardia (PSVT), atrial extrastimulus technique frequently reveals discontinuous A1-A2, H1-H2 curves suggestive of dual A-V nodal pathways. To further test the hypothesis that these curves in fact reflect dual A-V nodal pathways, a ventricular extrastimulus (VS) was coupled either to A2 at a fixed A1-A2 interval which reliably produced an A-V nodal re-entrant atrial echo (E) with a constant A2-E interval in two patients, or to QRS complex (V) during sustained PSVT with a constant E-E interval in one patient. Three response zones were defined: at longer A2-VS or V-VS coupling interval, VS manifested no effect on the timing of E (Zone 1). At closer A2-VS or V-VS coupling interval, VS conducted to the atrium, shortening the apparent A2-E or E-E interval (Zone 2). At shortest A2-VS or V-VS coupling interval, VS was blocked retrogradely, and no E was induced (Zone 3). The ability of VS to preempt control of the atria (Zone 2 response) strongly suggests the presence of dual A-V nodal pathways in these PSVT patients. If only a single pathway were present, VS would of necessity collide with the antegrade impulse and could not reach the atria. The Zone 3 response occurs because of retrograde refractoriness of the fast pathway. Failure of the echo during Zone 3 probably reflects concealed conduction to the fast pathway, or possibly interference in the slow pathway.     

Surface electrocardiographic recognition of dual atrioventricular nodal pathways during sinus rhythm

Atrioventricular nodal reentry is the most common mechanism of paroxysmal supraventricular tachycardia. Electrocardiograms obtained during sinus rhythm rarely serve to identify the mechanism of paroxysmal supraventricular tachycardia. We report two cases of dual atrioventricular nodal reentry in which electrocardiograms recorded during sinus rhythm disclosed two separate PR intervals that suggested dual atrioventricular nodal pathways.     

室性早搏致房室结双径路间交替蝉联现象

患者男性，46岁，因阵发性心悸1个月就诊，高血压病史三年余。体格检查：血压170／105mmHg（1mmHg：0．133kPa）心律不齐，闻及频发早搏，心前区未闻及病理性杂音。超声心动图及胸部X线检查均未见明显异常，常规12导联心电图示完全性右束支阻滞。临床诊断为，高血压病。动态心电图示窦性PP间期在0．90～1．12S之间，PR间期表现有长、短二种，长者为0.36～0.40S。短者为0．16～0．18S，二者相差大于60ms达0．20S，且长、短PR间期与PP间期长短无关，可以排除3相或4相阻滞，提示为房室结双径路（dual atrio—ventricular nodal pathways，DAVNP）传导。窦性P波下传的QRS波呈Rs形，S波粗钝，其间夹有宽大畸形的室性早搏（室早），RR问期亦表现有长短两种，     

Determinants of tachycardia induction using ventricular stimulation in dual pathway atrioventricular nodal reentrant tachycardia

Factors determining tachycardia induction using ventricular stimulation in atrioventricular (AV) nodal reentrant tachycardia utilizing the slow pathway for anterograde and the fast pathway for retrograde conduction were analyzed in 53 patients. Sixteen patients had tachycardia induced by ventricular stimulation. In 15, tachycardia was inducible with incremental ventricular pacing. In 4 of these 15 patients, the tachycardia was also induced with V1V2 testing, while in 11 patients, the tachycardia was not induced with V1V2 testing. In 9 of the latter 11 patients, tachycardia could be induced with V1V2V3 testing, suggesting that the retrograde effective refractory period (ERP) of the right bundle (RB) or the relative refractory period of the His-Purkinje system (HPS) was the limiting factor for tachycardia induction during V1V2 testing. In the remaining one patient, tachycardia was induced with V1V2V3 testing, which provoked a premature ventricular beat, leading to tachycardia induction. Tachycardia was not induced by ventricular stimulation in 37 patients. Factors deterring tachycardia induction in these patients may be related to the retrograde ERP or functional refractory period (FRP) of the HPS, the retrograde ERP of the fast pathway, and an insufficient conduction delay of the circuit (retrograde fast and anterograde slow pathway) to allow anterograde conduction of the slow pathway. In conclusion, AV nodal reentrant tachycardia can be induced by ventricular stimulation in approximately 30% of patients with incremental ventricular pacing and/or ventricular extrastimulus testing. Induction of tachycardia with ventricular stimulation, nevertheless, is frequently limited by the retrograde FRP or ERP of the HPS, the retrograde ERP of the fast pathway, and possibly by an insufficient conduction delay of the circuit.     

Nonreentrant atrioventricular nodal tachycardia due to triple nodal pathways manifested by radiofrequency ablation at coronary sinus ostium

We report a case of complex supraventricular tachycardia manifested by radiofrequency delivery. Initially, the patient presented with orthodromic atrioventricular reentrant tachycardia via a left-sided accessory pathway that was successfully eliminated. Atrial tachycardia originating from coronary sinus ostium was also induced. Radiofrequency delivery at the coronary sinus ostium induced a narrow QRS tachycardia with irregular R-R intervals. A detailed analysis explained that the tachycardia could be a nonreentrant mechanism due to triple atrioventricular nodal pathways: an atrial excitation evokes double ventricular response due to simultaneous activation of the fast and slow pathways, and the next one activates ventricle through the intermediate pathway.