预激心房颤动合并极快型心室反应1例

患者男 ,72岁。因间歇性心悸 2年 ,加重 2ｄ就诊。体检 :呼吸 2 7次 ｍｉｎ ,血压 90 6 0ｍｍＨｇ ,脉搏测不清。面色苍白 ,焦虑 ,出冷汗。心率极为短速 ,节律相对规整 ,约 30 0次 ｍｉｎ ,两肺呼吸音粗 ,未闻及干湿性罗音。急查心电图 (图1Ａ) :Ⅱ导上未见Ｐ波及ｆ波 (ｆ波十分纤细 ) ,多数ＱＲＳ波宽大畸形 ,时间 0 10～ 0 12ｓ,其形态不一 ,间距不等 ,Ｒ -Ｒ 0 18～ 0 34ｓ(合 333～ 176次 ｍｉｎ)。ＱＲＳ波与Ｔ波相连 ,无明显界限。图中有 3次室上性ＱＲＳ波 ,时间 0 0 8ｓ,后继ＳＴ段呈下斜型压低。当时诊断 :心房颤动 (Ａｆ)…     

预激综合征合并心室颤动2例分析

例１患者男性 ,２８岁。因心悸、胸闷１０余年 ,加重３天入院。体检 :Ｐ９８次／ｍｉｎ ,ＢＰ１７／９ｋＰａ(１２８／６８ｍｍＨｇ) ,心界向左下扩大。彩色超声心动描记术示先天性心脏病 ,二尖瓣狭窄。心电图 (图１上 )示 ,电轴左偏 -１０°,ＲＶ５３．８ｍＶ ,Ｐ＿Ｐ间期均齐 ,频率９６次／ｍｉｎ ,ＱＲＳ时间０．１１ｓ ,Ｖ１～Ｖ５ 导联ＱＲＳ波群均呈Ｒ型 ,起始部可见δ波 ,ＳＴ＿Ｔ呈继发性改变。心电图诊断 :窦性心律 ,Ａ型预激综合征 ,左心室肥大。入院后心悸、气促反复发作 ,发作持续时间逐渐延长、间歇时间越来越短。心电图 (图１…     

预激综合征伴心房颤动和心室颤动

本次教学查房为患者男性，28岁。因阵发性心悸9年加重伴持续1h入院。心悸呈突发骤止，每次持续约数min～数h不等。静脉注射普罗帕酮能终止。心电图检查曾诊断预激综合征。超声心动描记术等检查未见异常。入院体检：BP120／70mmHg。心肺未见异常。     

心房颤动伴间歇性C型预激综合征1例

患者女性,64岁.临床诊断:先天性心脏病,房间隔缺损,心功能不全,心律失常.稍活动后心悸、胸闷、气急加重近1月.口服地高辛0.25mg/天,无好转.体检:神志清,呼吸较促,眼睑轻度浮肿,口唇发绀.两肺少许干啰音,心界向两侧扩大,心率87次/min,心律不齐,心音     

利用四象限散点图快速诊断心房颤动伴间歇性心室预激一例

患者女性,64岁,因胸闷、心悸入院.动态心电图检查示:心房颤动(简称房颤)伴间歇性宽Q RS波,宽Q RS波形态酷似室性早搏、室性心动过速,但其四象限散点图的第Ⅲ象限为直角扇形,故快速诊断为房颤伴间歇性心室预激.后患者行电生理检查,证实为房颤伴左侧旁道.     

1例心房颤动合并预激综合征心电图表现

心房颤动 (Ａｆ)伴宽ＱＲＳ波心动过速常见于Ａｆ伴室性心动过速 (ＶＴ)、Ａｆ伴有预激综合征 (ＷＰＷ)。由于室率快速且心室除极顺序异常 ,可明显影响血液动力学 ,鉴别二者有重要临床意义。现报告所见 1例Ａｆ合并ＷＰＷ。患者男 ,19岁 ,2 0 0 2年 3月 2日中午 12∶3 0分无明显诱因于半小时前心悸、胸闷 ,来院急诊。神清、气促 ,ＨＲ 180次 ｍｉｎ ,律不齐 ,ＢＰ 115 65ｍｍＨｇ。心电图表现见图 1。Ｐ波消失 ,Ｒ -Ｒ间期 0 16～ 0 3 2ｓ之间 ,速率约 2 2 0次 ｍｉｎ左右。ＱＲＳ波增宽时间 >0 12ｓ,ＱＲＳ形态多变 ,Ｖ1 ～Ｖ4导联基…     

预激综合征并心房颤动1例

患者男性,70岁。因心悸11h入院。既往有类风湿性关节炎。体检：BP100／50mmHg,神清,表情倦怠,大汗淋漓,心界不大,心率180次／min,律不齐,各瓣膜听诊区未闻及病理性杂音,两肺无殊。实验室检查：血钾2．3mmol／L,钠114mmol／L,氯89mmol／L。心电图检查(图略)示：各导联未见窦性P波,可见成组宽大畸形QRS,其形态在胸导联主波均向上,R-R间期极不规则,     

预激综合征改变心室除极全过程1例

1　临床资料患者 ,男性 ,2 1岁。因鼻中隔偏曲手术入院。入院前无阵发性心动过速史。查体 :体温、血压正常。心脏听诊无杂音。超声心动图示 :左房、左室大 ,各瓣膜活动正常。心室舒缩功能正常。心电图 (图 1)示 :P波规律出现 ,P , 波直立 ,Pa VR波倒置 ,P- P间隔10 4 0 ms,心率 58次 /分 ,PR间期 110 ms,QRS波初始粗钝、模糊 ,QRS间期 12 0 ms, 、a VF导联有宽深 Q波 ,V1～ V3导联预激波向上 ,与主波方向相反 ,V4 ～ V6导联预激波向上 ,与主波方向相同。 RV5=2 .8m V,RV5 SV1=5.6m V,V5的 VAT≥ 50 ms, 、 、 a VF导联 ST段…     

预激综合征并发心房颤动2例

预激综合征(WPW)并发心房颤动(Af)的发生率为11.5％-39％,当发生Af时,激动可沿房室结或旁道下传,由于旁道不应期较短,故可发生快速心室反应,导致严重的血流动力学障碍,甚至猝死。我们最近遇到2例预激综合征并发房颤的病例,报告如下。     

Sotalol prevents atrio-ventricular tachycardia but not atrial fibrillation with rapid ventricular response in a patient wiht WPW syndrome

We present a case of 23-year-old male with the Marfan syndrome multiple accessory pathways and atrio-ventricular reentry ant tachycardia (AVRT) as well as atrial fibrillation (AF). Sotalol was partially effective for AVRT, however, it did not prevent AF, RF ablation cured all arrythmias. This case shows that sotalol can attenuate AVRT recurrences, however, it does not prevent rapid conduction via accessory pathways during AF.     

Atrial fibrillation and continuous hypotension induced by sildenafil in an intermittent WPW syndrome patient

A 55-year-old Japanese man was hospitalized for palpitations and severe chest oppression one hour after he ingested about 1500 ml of beer and sildenafil (Viagra) 50 mg. At 43 years of age, he had been diagnosed with intermittent WPW syndrome following a paroxysmal supraventricular tachycardia (PSVT) attack. He took a 1 mg tablet of doxazosin daily for mild hypertension. On admission, his blood pressure was 90/54 mmHg and his heart beat was weak and irregular with a rate of about 220/min. Since atrial fibrillation (Af) was diagnosed on an electrocardiogram (minimum RR interval; 0.22 seconds), direct current shock was performed with 100 joules and 150 joules but conversion to sinus rhythm failed. Sinus rhythm returned spontaneously from Af four hours after taking sildenafil. Since blood pressure was 50/17 mmHg despite the return to sinus rhythm, blood pressure was maintained by dopamine for twelve hours after sinus rhythm returned. The patient underwent catheter ablation for curative therapy and thereafter has not had any further episodes of tachycardia.     

Atrial response during ventricular fibrillation

Electrical activity of the bundle of His and atria were recorded during sinus rhythm and electrically induced ventricular fibrillation in 23 dogs. Multiple bipolar atrial electrograms obtained from several sites within the right and left atria permitted the determination of the frequency, regularity, and sequence of atrial activation (i.e., sinus or retrograde) during ventricular fibrillation. Prior to the induction of ventricular fibrillation, the capacity to retrogradely conduct across the A-V node was tested in each animal by pacing the right ventricle at various cycle lengths. Fourteen animals demonstrated consistent 1:1 retrograde conduction at various paced cycle lengths (Group A); in four animals (Group B) retrograde conduction was intermittent and in three animals (Group C) no retrograde conduction was observed at any paced cycle length. Ventriculo-atrial conduction was also absent in two animals (Group D) with antegrade A-V block within the His-Purkinje system.The most common conduction pattern noted at the onset of ventricular fibrillation was that of rapid, irregular, retrograde activation of both the bundle of His and atria. However, the frequency of retrograde activation of the atria was less than that of the bundle of His indicating that the A-V node was a site of retrograde concealment of impulses. This conduction pattern was noted in all animals of Groups A and B. In all animals of Groups C and D, the atria continued to be activated in a sinus sequence during ventricular fibrillation. In Group C animals, the A-V node was the site of both antegrade and retrograde concealment. In the two animals with A-V block (Group D), the site of retrograde concealment was distal to the site of block.In six studies, retrograde A-V nodal Wenckebach cycles with and without re-entry were observed for varying periods of time.Less often, the irregular atrial responses during ventricular fibrillation were accounted for by short periods of sinus capture interspersed with periods of retrograde capture.During ventricular fibrillation, retrograde conduction across the A-V node could be abolished by vagal stimulation.The results of this study indicate that retrograde concealed conduction within the A-V node is the major determinant of an irregular atrial response during ventricular fibrillation just as antegrade concealed conduction is the major determinant of an irregular ventricular response during atrial fibrillation.     

Atrial fibrillation triggered by postinfarction ventricular premature beats in a patient with Wolff-Parkinson-White syndrome.

The mechanism by which atrial fibrillation is initiated in patients with accessory pathways is not fully understood. Retrograde conduction of ventricular premature beats to the atrium, causing the arrhythmia, is a very rare cause. We report a patient with Wolff-Parkinson-White syndrome (WPW), without previous tachycardias, who presented multiple episodes of paroxysmal atrial fibrillation after having a myocardial infarction. During the electrophysiological (EP) study the patient presented two spontaneous episodes of atrial fibrillation initiated by ventricular premature beats conducted to the atria through the accessory pathway. After successful catheter ablation of the accessory pathway the patient did not present arrhythmia recurrences.     

Malignant fascicular ventricular tachycardia degenerating into ventricular fibrillation in a patient with early repolarization syndrome

A 45-year-old man was hospitalized for syncope due to fascicular ventricular tachycardia degenerating into ventricular fibrillation (VF). The electrocardiogram showed an early repolarization syndrome. The arrhythmia was repetitive and disappeared after oral hydroquinidine. An implantable cardioverter-defibrillator (ICD) was implanted; subsequently, the patient was arrhythmia free at 9 months follow-up.     

Idiopathic ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome

Ventricular fibrillation in a patient with ventricular preexcitation is usually due to atrial fibrillation with an extremely rapid ventricular rate from which it degenerates. We present a case with Wolff-Parkinson-White syndrome and coexistent idiopathic ventricular fibrillation. The patient, a 23-year-old male, had had a cardiac arrest four years earlier. In electrophysiological study, the accessory pathway was located in the left posteroseptal region and successfully eliminated with radiofrequency catheter ablation. After the ablation procedure, ventricular fibrillation was induced with programmed ventricular stimulation. A dual chamber implantable cardioverter defibrillator was implanted in the patient.