室上性心律失常英文版PPT课件
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Factors associated with Sinus Tachycardia Pathologic factors
Fever,Hyperthyroidism发热甲亢 Hemorrhage,Shock 出血休克 Anemia,Infection贫血,感染 Congestive heart failure 心衰 Myocarditis心肌炎 Hypoxia缺氧
病窦起搏治疗 Pacemaker therapy of SSS • 提高心率(单腔、双腔起搏) • 预防房颤(双房起搏) • 便于应用抗心律失常药物
45
房性早搏 atrial premature beats
• 见于正常人及各种器质性心脏病、甲亢
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房性早搏atrial premature beats
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Sinus Bradycardia
• Drug Digitalis洋地黄 Morphine吗啡 Quinidine奎尼丁 Propranolol普奈洛尔
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窦性心动过缓--病因
• 生理状态:运动员、睡眠 • 原发病:病窦、缺血、高颅压、甲减、
低温 • 药物:β受体阻滞、钙拮抗剂、
抗心律失常药物
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Common causes of sinus bradycardia
Physiologic bradycardia 迷走神经activation of vagus nerve
• Laborers and trained athletes • Carotid sinus pressure • eyeball pressure • Sleep
Abnormal conduction传导异常 ----physiological block: ----pathological block: S-AB; A-VB; LBBB; RBBB ----accessory pathway: pre-excitation syndrome
Factors associated with Sinus Tachycardia Pathologic factors
Fever,Hyperthyroidism发热甲亢 Hemorrhage,Shock 出血休克 Anemia,Infection贫血,感染 Congestive heart failure 心衰 Myocarditis心肌炎 Hypoxia缺氧
病窦起搏治疗 Pacemaker therapy of SSS • 提高心率(单腔、双腔起搏) • 预防房颤(双房起搏) • 便于应用抗心律失常药物
45
房性早搏 atrial premature beats
• 见于正常人及各种器质性心脏病、甲亢
46
房性早搏atrial premature beats
26
Sinus Bradycardia
• Drug Digitalis洋地黄 Morphine吗啡 Quinidine奎尼丁 Propranolol普奈洛尔
27
窦性心动过缓--病因
• 生理状态:运动员、睡眠 • 原发病:病窦、缺血、高颅压、甲减、
低温 • 药物:β受体阻滞、钙拮抗剂、
抗心律失常药物
24
Common causes of sinus bradycardia
Physiologic bradycardia 迷走神经activation of vagus nerve
• Laborers and trained athletes • Carotid sinus pressure • eyeball pressure • Sleep
Abnormal conduction传导异常 ----physiological block: ----pathological block: S-AB; A-VB; LBBB; RBBB ----accessory pathway: pre-excitation syndrome
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病态窦房结综合征
Sick Sinus Syndrome (SSS)
由于窦房结功能减退导致以长期心 动过缓为主,可合并多种房性快速 型心律失常的综合表现。
37
病态窦房结综合征-病因 causes of SSS
• 退行性改变degenerative disease • 慢性缺血chronic ischemia • 炎症后遗症lingering effects of inflamation
6
心律失常分类classification
• 冲动形成abnormal impulse generating – 窦性心律失常sinus arrythmia – 异位心律ectopic rhythm • 慢速型--逸搏escape • 快速型--早搏premature beat • 正速型--加速性自主心律accelerated
8
快速性心律失常的机制 mechanisms of tachyarrhythmias
• 折返Reentry:解剖学上有折返环(4个条件) 突发突止、程序刺激诱发及终止 • 自律性增高Abnormal Automaticity:洋地 黄中毒、电解质紊乱、炎症、缺血等诱发,心 率逐渐升高和降低,程序刺激不能诱发及终止 • 触发活动:Triggered Activity洋地黄中毒、 电解质紊乱等诱发
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食管心电图及食道调搏
Transesophageal Electrocardiography
• 心动过速机制初步判断 • 窦房结、房室结功能测定 – SNRT、SACT、房室结文氏点 • 程序刺激诱发室上速 • 超速抑制
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心腔内电生理检查作用invasive cardiac electrophysiological testing
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Isopotential map and Virtual electrograms
at RVOT ablation target
•22
靶Hale Waihona Puke 图出口处提前31ms•23
使用球囊标明激动起始处
•24
室早消融指征
频发室早>1万/24hHolter 有明显自觉症状/药物无效或不愿服药 希望根治 消融无症状性室早以预防或治疗心动过速性心肌 病( IIb ) 非频发的室早、无症状者不属适应征
•20
Ensite Aray标测系统
多电极网篮状导管 64 对电极组成 电极网具有记录和起搏功 能 根据同步记录的局部电活 动迅速判断最早激动部位
•21
RVOT Tachycardias-Problems Targeting the PVC!
ENSITE Array in RVOT
非接触式标测系统 ENSITE3000 ●在一个心跳周期内完成 标测,适用于多源性,非持续 早搏和心跳过速及血液动 力学不稳定者
洛尔)
Zipes DP, et al. Am J Cardiol. 1979; 4•41:61 Belhassen B, et al. Br Heart J. 1981;46: 679
源于左后分支 ILVT(常见)
例1
例2
例3
RBBB+ 电轴左偏
•17
ILVT
RBBB +
起
源 于 左 前 分
电
( 少
临床特点:多见于年轻人男性,发生与运动无关, 有无休止发作倾向。 ECG:QRS波一般比较窄,多为100~140 ms,RBBB+ 电轴左或右偏 EPS : 心室或心房分级递增刺激或程序刺激可诱发VT 发生机制:主要是局灶性折返(触发活动和自律性增加) 有效药物:急: 维拉帕米 ;长期:维拉帕米或硫氮卓酮,胺碘酮或素他
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临床表现 ▪ 心动过速发作常突然发作、突然终止 持续时间长短不一
概述
▪ 病症:可表现为心悸、焦虑不安、眩晕、晕厥、心绞 痛、心力衰竭与休克,病症轻重取决于发作时心室率 的快慢、持续时间及原心脏病的严重程度等。
▪ 听诊:S1强度不变、心律绝对规那么。
房室结折返性心动过速 •〔AVNRT )
房室结折返性心动过速
• 旁路的本质:胚胎期心脏发育过程中,房室 之间纤维分隔不完全,致使有残存的心肌束 通过纤维隔。
• 旁路与其它的心肌组织一样,具有兴奋性和 传导性
• 由房性期前收缩触发室上速
房室折返性心动过速
• 房室折返性心动过速是由旁道参与的折返性心动过速,又称为预激综合征 • 折返环路包括: 心房、房室结、心室及旁道四局部 ,缺一不可
• 大局部为折返机制引起,折返可发生于窦房结 、心房、房室结及房室之间分别引起。
概述
• PSVT的起源部位及电生理分类
折返机制
房室旁路前传性心动过速
房室旁路逆传性心动过速 房室交界性慢旁路折返性心动过速 房室结折返性心动过速 房内折返性心动过速 窦房结区域折返性心动过速
触发机制
洋地黄中毒性房性及房室交界性心 动过速
力学障碍
房性心动过速
➢ ECG诊断: ➢ 心房率150-200bpm ➢ P波形态与窦性不同 ➢ P波之间有等电位线 ➢ 刺激迷走神经不能终止 ➢ 常合并房室阻滞 ➢ 有加温〔warm up)现象
房性心动过速
自律性房速
房性心动过速
➢ 治疗; ① 洋地黄中毒引起,按洋地黄中毒处理 ② 非洋地黄中毒:β受体阻滞剂、洋地黄、 胺碘酮、异 搏定、ⅠA、ⅠC类 ③ 导管射频消融,成功率可超过90%,复发率5%
•ST-T 变 化 明 显 , 除 AVR 外 各 导 联 ST-T 下 移 明 显 ,在AVRT时易出现,本例EP检查证实为AVRT
概述
▪ 病症:可表现为心悸、焦虑不安、眩晕、晕厥、心绞 痛、心力衰竭与休克,病症轻重取决于发作时心室率 的快慢、持续时间及原心脏病的严重程度等。
▪ 听诊:S1强度不变、心律绝对规那么。
房室结折返性心动过速 •〔AVNRT )
房室结折返性心动过速
• 旁路的本质:胚胎期心脏发育过程中,房室 之间纤维分隔不完全,致使有残存的心肌束 通过纤维隔。
• 旁路与其它的心肌组织一样,具有兴奋性和 传导性
• 由房性期前收缩触发室上速
房室折返性心动过速
• 房室折返性心动过速是由旁道参与的折返性心动过速,又称为预激综合征 • 折返环路包括: 心房、房室结、心室及旁道四局部 ,缺一不可
• 大局部为折返机制引起,折返可发生于窦房结 、心房、房室结及房室之间分别引起。
概述
• PSVT的起源部位及电生理分类
折返机制
房室旁路前传性心动过速
房室旁路逆传性心动过速 房室交界性慢旁路折返性心动过速 房室结折返性心动过速 房内折返性心动过速 窦房结区域折返性心动过速
触发机制
洋地黄中毒性房性及房室交界性心 动过速
力学障碍
房性心动过速
➢ ECG诊断: ➢ 心房率150-200bpm ➢ P波形态与窦性不同 ➢ P波之间有等电位线 ➢ 刺激迷走神经不能终止 ➢ 常合并房室阻滞 ➢ 有加温〔warm up)现象
房性心动过速
自律性房速
房性心动过速
➢ 治疗; ① 洋地黄中毒引起,按洋地黄中毒处理 ② 非洋地黄中毒:β受体阻滞剂、洋地黄、 胺碘酮、异 搏定、ⅠA、ⅠC类 ③ 导管射频消融,成功率可超过90%,复发率5%
•ST-T 变 化 明 显 , 除 AVR 外 各 导 联 ST-T 下 移 明 显 ,在AVRT时易出现,本例EP检查证实为AVRT
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An ICD is a small device that is implemented in the chest to monitor heart rhythm and deliver electrical shocks to correct arrhythmias
Surgical treatment
Antichromic therapy
Antichromic therapy involves using blood thinners to prevent clots from forming in the heart and causing arrhythmias
Implantable cardioverter defibrillator (ICD)
risk of coronary artery disease and heart failure
Pathological factors
01
Cardiovascular disease
Armenia is a common complication of cardiovascular disease,
01
What is arrhythmia?
Definition of arrhythmia
Rhythmia refers to any deviation from the normal rhythm of the heartbeat, which may be caused by various factors such as disease, bugs, and stress
Types of arrhythmia
Bradycardia
A slow heartbeat that may cause dizziness, fatigue, and shortness of breath
Surgical treatment
Antichromic therapy
Antichromic therapy involves using blood thinners to prevent clots from forming in the heart and causing arrhythmias
Implantable cardioverter defibrillator (ICD)
risk of coronary artery disease and heart failure
Pathological factors
01
Cardiovascular disease
Armenia is a common complication of cardiovascular disease,
01
What is arrhythmia?
Definition of arrhythmia
Rhythmia refers to any deviation from the normal rhythm of the heartbeat, which may be caused by various factors such as disease, bugs, and stress
Types of arrhythmia
Bradycardia
A slow heartbeat that may cause dizziness, fatigue, and shortness of breath
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2.临床意义 :窦房结发放冲动障碍 ⑴生理性:迷走神经张力增高 ⑵病理性:窦房结病变、AMI、 脑血管意外、应用 某些药物等
3.治疗: ⑴ 无症状,可暂时观察。 ⑵ 去除诱因,可用阿托品, 如出现晕厥、黑蒙或阿斯 综合症,可行起搏治疗。
(四)病态窦房结综合征(sick sinus syndromeSSS) 1.定义:由于窦房结病变导致功能减退,产生多种
产生折返激动基本条件是: 心脏有两个以上传 导通道,相互连结形成一个闭合环; 其中一通 道发生单向传导阻滞; 另一条通道传导缓慢, 使原先发生阻滞的通道有足够时间恢复兴奋性:
原先阻滞的通道再次激动,从而完成一次折返 激动。
(2)房室间传导途径异常:预激综合征
(3)传导障碍
由于生理性不应期所引起,可行成 生理性阻滞或干扰现象。
(3)触发激动异常(后除极): 心房、心室与希氏束—浦肯野组织 受到异常因素作用,可在动作电位 后产生后除极。若后除极达到一定 阈值,便可引起异常激动。
2.冲动传导异常:
(1)折返激动:当激动从某处循一条径路传 出后,又从另一条径路返回原处,使该处 再次发生激动的现象称为折返激动,为快 速性心律失常最常见的发生机制。
第二节:窦性心律失常
窦性心律(sinus rhythm)心电图特点:P波在Ι Ⅱ、aVF导联直立,aVR导联倒置,称为窦性P波; P-R间期固定于0.12~0.20s;P-P间期互差 <0.12~0.16s④P波频率60~100次/分。
第二节:窦性心律失常
(一)窦性心动过速(sinus tachycardia) 1.心电图诊断:窦性心率大于100次/分 2.临床意义 : 生理性:饮茶、饮酒、体力活动、情绪激动 病理性:继发性多见(如发热、甲亢、贫 血、心衰等)。 治疗原发病,去除诱因,可用ß-受体阻制剂。
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2020/9/21
15
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Premature Beat Impulse
Repolarizing Tissue (long refractory period)
Cardiac Conduction
Tissue
Fast Conduction Path Slow Recovery
Cardiac Conduction
Tissue
Slow Conduction Path Fast Recovery
3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore 2020/9/2t1ravels retrogradely (backwards) up the fast pathway 17Biblioteka 2020/9/2118
Re-entry Circuits as Ectopic Foci and Arrhythmia Generators
Atrial Re-entry
• atrial tachycardia • atrial fibrillation • atrial flutter
Atrio-Ventricular Nodal Re-entry
1. 2 distinct pathways that come together at beginning and end to form a loop.
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msec) • Retrograde P wave within QRS with distortion of
terminal portion of the QRS • Atrium, His bundle and ventricle not required , vagal
maneuvers slow and then terminate SVT
• AV nodal blocking agents (diagnosis/treatment)
– Adenosine – BB/CCB – Digoxin
JACC 2009; 53:2353-58
EKG
• AV node dependent (Y/N) • Re-entrant circuit (Y/N)
– Circuit (Macro/Micro) – Anatomic (e.g. previous ASD repair, CVTI) – Accessory pathway ( WPW, Mahaim, etc. )
• Ends with a P wave: suggests an AV nodal dependent arrhythmia because the generation of the P wave without a QRS suggests block in the AV node… this is more likely to be AVNRT or AVRT
Supraventricular arrhythmias
Jerry John July 29, 2009
Objectives
• Supraventricular Arrhythmias • How do supraventricular arrhythmias manifest? • What are the common supraventricular arrhythmias? • What is the mechanism of atrioventricular arrhythmias? • Which drugs are used in the management of supraventricular
terminal portion of the QRS • Atrium, His bundle and ventricle not required , vagal
maneuvers slow and then terminate SVT
• AV nodal blocking agents (diagnosis/treatment)
– Adenosine – BB/CCB – Digoxin
JACC 2009; 53:2353-58
EKG
• AV node dependent (Y/N) • Re-entrant circuit (Y/N)
– Circuit (Macro/Micro) – Anatomic (e.g. previous ASD repair, CVTI) – Accessory pathway ( WPW, Mahaim, etc. )
• Ends with a P wave: suggests an AV nodal dependent arrhythmia because the generation of the P wave without a QRS suggests block in the AV node… this is more likely to be AVNRT or AVRT
Supraventricular arrhythmias
Jerry John July 29, 2009
Objectives
• Supraventricular Arrhythmias • How do supraventricular arrhythmias manifest? • What are the common supraventricular arrhythmias? • What is the mechanism of atrioventricular arrhythmias? • Which drugs are used in the management of supraventricular
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并发症预防与处理策略
心律失常性心肌病预防
早期识别和治疗
对室上性心动过速患者进行早期诊断 和有效治疗,以降低心律失常持续时 间和严重程度,从而预防心肌病的发 生。
控制心室率
生活方式干预
建议患者改善生活方式,如戒烟、限 酒、避免过度劳累等,以降低心律失 常的发作风险。
通过药物或非药物治疗手段,将心室 率控制在合适范围内,减轻心脏负担 ,防止心肌病的发生。
01
导管消融术
通过导管将射频电流引入心脏内特定部位,破坏引起室上速的异常传导
通路,达到根治目的。该方法具有成功率高、并发症少等优点。
02 03
外科手术
对于合并其他心脏疾病或导管消融术失败的患者,可考虑外科手术治疗 ,如心内膜切除术、冠状动脉旁路移植术等。但外科手术风险较高,应 谨慎选择。
新兴技术
随着医学技术的不断发展,一些新兴技术如基因治疗、细胞治疗等正在 研究阶段,未来可能为室上速患者提供更多根治性治疗选择。
80%
药物治疗
长期口服抗心律失常药物,如β 受体阻滞剂、钙通道阻滞剂等, 以减少复发和改善预后。
100%
导管消融术
对于反复发作且症状明显的患者 ,导管消融术是首选治疗方法, 可有效根治室上速并减少复发。
80%
生活方式调整
避免诱发因素如过度劳累、情绪 激动等,保持规律作息和健康生 活方式。
根治性治疗方法探讨
血栓形成风险评估及干预措施
血栓形成风险评估
根据患者的病史、症状、体征及实验室检查结果,综合评 估血栓形成的风险。
抗凝治疗
对高风险患者给予抗凝治疗,如华法林、新型口服抗凝药 物等,以降低血栓形成的风险。
生活方式干预
【医学课件】室性心律失常:成功与失败ppt课件
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10
ICD Therapy
Primary Prevention ICM
11
MADIT
• Multicenter Automatic Defibrillator Implantation Trial
• Hypothesis: ICD will reduce mortality (allcause) in high-risk CAD patients.
2
Management
• Management of PVCs differs in patients with and without structural heart disease.
• To define structural heart disease, consider:
– Echocardiography. – ETT. – Left heart catheterization.
Buxton AE. N Engl J Med. 1999;341:1882-90.
EP-Guided Rx ACE I & ßB
N=351
21
MUSTT Conclusions
For CAD patients with EF < .40, asymptomatic NSVT and inducible VT:
Evaluate and Treat Ischemia
EPS N=2202
No Sustained VT Induced N=1435 (65%)
Inducible Sustained VT
N=767 (35%)
Registry
Buxton AE. N Engl J Med. 1999;341:1882-90.
ICD Therapy
Primary Prevention ICM
11
MADIT
• Multicenter Automatic Defibrillator Implantation Trial
• Hypothesis: ICD will reduce mortality (allcause) in high-risk CAD patients.
2
Management
• Management of PVCs differs in patients with and without structural heart disease.
• To define structural heart disease, consider:
– Echocardiography. – ETT. – Left heart catheterization.
Buxton AE. N Engl J Med. 1999;341:1882-90.
EP-Guided Rx ACE I & ßB
N=351
21
MUSTT Conclusions
For CAD patients with EF < .40, asymptomatic NSVT and inducible VT:
Evaluate and Treat Ischemia
EPS N=2202
No Sustained VT Induced N=1435 (65%)
Inducible Sustained VT
N=767 (35%)
Registry
Buxton AE. N Engl J Med. 1999;341:1882-90.
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AVNRT
• Most common cause of a regular narrow complex tachycardia
• Involves a slow and a fast pathway in the region of the AV node
• Turn around point appears above the bundle of His
arrhythmias? • Which patients should be offered catheter ablation? • Atrial Fibrillation and Atrial Flutter • What are the incidence and prevalence of atrial fibrillation? • What are the major sequelae of atrial fibrillation? • What are the risk factors for stroke in atrial fibrillation? • What are the treatment options for patients with atrial
RP relationship
• Short “RP” Tachycardias: Typical AVNRT AVRT
• Long “RP” Tachycardias: Atrial Tachycardia Atypical AVNRT AVRT with long retrograde conduction PJRT
vagal , maneuvers slow and then terminate SVT, always in the retrograde slow pathway
AVNRT Treatment
• Low threshold for catheter ablation given long term success rate > 90% and low risk of complications
2) (-) or biphasic in V1
• Left atrial focus:
1) (-) or isoelectric in aVL 2) (+) V1 suggests back to front
Tachycardia onset
• Most SVTs triggered by a PAC • If the PAC conducts with a long PR, dual AV
Supraventricular arrhythmias
Jerry John July 29, 2009
Objectives
• Supraventricular Arrhythmias • How do supraventricular arrhythmias manifest? • What are the common supraventricular arrhythmias? • What is the mechanism of atrioventricular arrhythmias? • Which drugs are used in the management of supraventricular
• AVNRT p waves however can be buried in the QRS if VA conduction is very short
• Ends with a QRS : almost always atrial tachycardia (some rare AV node dependent tachycardias can terminate in this manner)
wave absence help distinguish AVNRT from AVRT and atrial tachycardia
AVNRT
• Initiation and termination by APDs, VPDs or atrial pacing during AVW
• Dual AVN physiology • Initiation depends on critical A-H delay • Concentric retrograde atrial activation(V-A -42 to 70
nodal physiology is suggested with the conduction being through the slow pathway • If a PVC initiates SVT, it is likely to be AV node dependent
Tachycardia termination
(short/long)
P waves
• (-) Inferior leads atrial activation from low to high: AVNRT, atypical AVNRT; AVRT
• Right atrial focus:
1) (-/+) in aVL right atrium activated first and then left atrium)
(caffeine); and potentiated by dipyridamole
P waves
• Rate • Morphology (Sinus/Retrograde/abnormal) • Conduction (2:1; 3:1, etc.) • Response to AV Block • VA conduction (i.e. R-P relationship):
• P wave
– Rate – Morphology (Sinus/Retrograde/abnormal): look at the T waves and
the psuedo R (V1) and psedo S (inferior leads) – Conduction (2:1; 3:1, etc.) – Response to AV Block – VA conduction (i.e. R-P relationship): (short/long)
JACC 2009; 53:2353-58
EKG
• AV node dependent (Y/N) • Re-entrant circuit (Y/N)
– Circuit (Macro/Micro) – Anatomic (e.g. previous ASD repair, CVTI) – Accessory pathway ( WPW, Mahaim, etc. )
Where’s the P wave
• Valsalva • Carotid sinus massage
– Slows SA nodal; and/or AV nodal conduction
• Adenosine
– Slows sinus rate – Increases AV nodal conduction delay – T ½ 5 seconds – 6 or 12 mg bolus – Effect blocked by theophylline, methylxanthines
• Ends with a P wave: suggests an AV nodal dependent arrhythmia because the generation of the P wave without a QRS suggests block in the AV node… this is more likely to be AVNRT or AVRT
AV Node Depdendence (Y/N)
AV nodal dependent arrhythmias • AVNRT (micro-reentrant circuit) • AVRT (macro-reentrant circuit): anti/orthodromic • JET (junctional ectopic tachycardia) - childhood and
• AV nodal blocking agents (diagnosis/treatment)
– Adenosine – BB/CCB – Digoxin
Atypical AVNRT
• Initiation and termination by APDs, VPDs, or ventricular pacing during retrograde AVW
• Dual retrograde AVN physiology • Initiation dependent on critical H-A delay • Earliest retrograde activation at CS os • Retrograde P wave with long R-P interval • Atrium, His bundle, and ventricle not required,
• 160-190 bpm but may exceed 200 bpm • Slow-fast form accounts for 90% of AVNRT • Fast-slow or slow-slow AVNRT accounts for 10% • Pseudo r’ in V1, pseudo S wave in 2,3,avf, and p
msec) • Retrograde P wave within QRS with distortion of
terminal portion of the QRS • Atrium, His bundle and ventricle not required , vagal