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Chap 3 Cardiac Arrhythmia

Jiaqi Zhao
Department of Cardiology, Affiliated
Hospital of
Ji ning Medical College, Ji ning
Part 1.Overview
Cardiac Arrhythmia :abnormalities of cardiac
impulse(frequency 频率、 rhythm 节律、 the
origin 起源部位、 conduction velocity 传导速度
and order of excitement 激动次序 of cardiac
impulse )。
分类( Classification ):Disorders of
impulse formation (冲动形成异常) and/or
Abnormalities of impulse
conduction( 冲动传导异常 ) 。
一、 Disorders of impulse formation or automaticity

㈠ Cardiac arrhythmia of sinoatrial


Node( 窦房结心律失常 ) :
 1. sinus tachycardia
 2. sinus bradycardia
 3. sinus arrhythmia
 4. sinus arrest 。
 (二) Ectopic rhythm 异位心律:
 1 、 Passivity 被动性:
 ①escape beat 逸搏。
 ②escaped rhythm 逸搏心律。
 2 、 Activeness 主动性:
 ①premature contraction 期前收缩。
 ②paroxysmal tachycardia 阵发性心动过速。
 ③atrial flutter or fibrillation.
 ④ventricular flutter or fibrillation .
二、 Abnormalities of impulse
conduction

 ①sinoatrial block 窦房传导阻滞


 ②intra-atrial block 房内传导阻滞
 ③A-V block 房室传导阻滞。
 ④intraventricular block 室内传导阻滞
( LBBB and RBBB )
㈢ Accessory pathway:pre-excitation syndrome
预激综合征。
Conduction System of the Heart
Mechanisms of Arrhythmia
 Abnormal automaticity
– automatic impulse generation from unusual site or
overtakes sinus node
 Triggered activity
– secondary depolarization during or after repolarization
——after depolarization
– Dig toxicity, Torsades de Pointes
 Reentry
– 90 % of arrhythmias
Mechanisms of Arrhythmia
 Automaticity
– Enhanced automaticity
– Abnormal automaticity

Abnormal Acceleration of Phase 4


Mechanisms of Arrhythmia
 Triggered Activity
– Fluctuations in membrane
potential
– Early afterdepolarizations
 high resting potential
 slow HR
– Delayed afterdepolarizations
 Intracellular Ca++ overload
 Ischemia – reperfusion
 Digoxin toxicity
 Catecholamine excess
Mechanisms of Arrhythmia
 Reentry
– Two pathways
– Unequal refractory periods
– Slowed conduction in one
path
 Common cause of narrow

complex tachycardias
Reentry

Panel A: Most impulses conduct down Panel B: Unidirectional block, due to


both pathways. longer refractoriness in one pathway.

Panel C: Potential to have reentry back


up the previously refractory pathway Panel D: Reentry then can persist.
Diagnosis of cardiac arrhythmia
 Case history; 病史
 Physical examination 体格检查
 24 hour dynamic electrocardiographic
recording 动态心电图记录
 Stress test 运动试验
 Endocardial electrophysiologic study 心内
电生理检查
Part 2 Rhythms of the SA Node
Sinus Rhythm
Sinus Bradycardia
Sinus Tachycardia
Sinus Arrhythmia
Sinus Arrest
sick sinus syndrome , SSS
Sinus Rhythm
 Rate: 60 - 100/minute
 Regular rhythm
 P : I 、 II 、 AVF upright ; AVR
down
 PR Interval: 0.12 - .0.20 seconds
 Narrow QRS
 The relationship between P waves and
QRS complexes: 1:1 ratio

Sinus
Rate: > 100/minute
Tachycardia
 Regular rhythm
 P waves Sinus P
 PR Interval: normal to slightly shortened
 Narrow QRS
 The relationship between P waves and QRS
complexes: 1:1 ratio
Causes of Sinus tachycardia
 fever 发热(包括感染)
 emotional stress 情绪紧张)
 Anaemia 贫血
 Heartfailure 心功能不全
 hyperthyreosis 甲亢
 Drug 药物
 Shock 休克
 Hypotension 低血压
 Alcohol 饮酒
Causes of Sinus Bradycardia
 Increased vagal tone
 Drugs: beta blockers, calcium channel blockers,
amiodarone, digoxin (indirect effect)
 Myocardial ischemia/infarction
 Hypothyroidism
 “Sick sinus syndrome”
– degenerative/fibrotic atrial process
Sinus Arrhythmia
Inspirati Expiratio
on n

SA nodal accelerationSA nodal deceleration


Sinus Arrest → Asystole
P P P
Sinus
rhythm

Sinus brady. P P P P
→ Sinus arrest
→ V. escape P
rhythm

Failure of V.
escape
rhythm
→ Asystole
Tachycardia-Bradycardia
(Form of “Sick Sinus”) Syndrome

Atrial
Flutter

Atrial Sinus arrest Junctional


Flutter escape (tardy
terminates
sick sinus
syndrome , SSS
Sinus Bradycardia
Sinus Arrest
 Tachycardia-Bradycardia Syndrome
 Treatment
 Absence of symptoms NO Treatment
 Symptoms :syncope 、 dizziness 、 HF ,
 permanent pacing treatment
Part 3 Atrial Arrhythmia
Fig, 12-1. Premature atrial contractions.A, PAC after the fourth
sinus beat..B, blocking of the PAC occurs after the fourth sinus
beat. The premature P waves falls on the T wave of the
preceding beat and is not followed by a QRS complex.
Atrial Tachycardia
 Ectopic atrial focus
– Reentrant, automatic and
chaotic
 150-250 bpm
 1:1 or 2:1 AV conduction
 Paroxysmal or “warm up”
 P wave morphology variable
 COPD
Atrial Fibrillation
 The commonest arrhythmia
– 0.77% patients > 30yrs(M0.9%:F0.7%)
– 1% patients > 60yrs
– 5% patients > 70rs
– 10% patients >75yrs

 Presenting Features
– May be asymptomatic
– Vagally mediated AF
 Commoner at night; when having a large meal
– Alcohol binges
Atrial Fibrillation Epidemiology
 Affects 2 to 4% of population
 Increases to 5 to 10 % of patients over 80
 Associated with 2-fold increased risk of
death
 Risk of thromboembolism is approximately
5% per year but may be as high as 20% in
high risk groups not anticoagulated
Atrial Fibrillation
 Associated conditions
– Thyrotoxicosis
– Hypertension
– Heart failure
– Valve disease
 Drugs
– Adenosine
– Digoxin
 Miscellaneous
– Chest infection/ Surgery/ Cholecystitis etc
Mechanism of Atrial
Fibrillation
 Multiple reentrant wavelets moving between right
and left atrium
 May be initiated by rapidly firing automatic foci
found commonly in pulmonary veins, SVC, and
coronary sinus.
 Factors that shorten atrial refractoriness and slow
conduction velocity perpetuate atrial fibrillation
 Factors that lengthen atrial refractoriness
(antiarrhythmic drugs ) aid in termination
Atrial Fibrillation
 Symptoms
– Tend to be due to the ventricular response as opposed to
AF
 Exceptions
– Mitral stenosis
– Pulmonary hypertension
– Palpitations
– Increased heart rate
– Lethargy
– Dyspnoea
– Cardiac chest pain
– Features of TIA/ Stroke
Acute Management of Atrial
Fibrillation
 Focuses on Rate control
 Patient with atrial fibrillation may undergo DC
cardioversion or pharmacologic conversion if less
than 48 hours duration or following TEE on
Heparin without evidence of left atrial thrombus.
 Following cardioversion the patient should be kept
anticoagulated for 4 weeks with goal INR of 2 to 3
until atrial function normalizes. ( warfarin )
Management of Atrial Fibrillation
 Aimed at symptom relief by rate and
rhythm control
 Aimed at reducing risk of
thromboembolism by anticoagulation
 Preventing tachycardia mediated
cardiomyopathy (a progressive, reversible
rate-induced form of LV dysfunction)
Acute Management of Atrial
Fibrillation
 50% of patients with paroxysmal atrial
fibrillation will spontaneously convert within
24 hours
 Digoxin used heavily in the past for
prevention and conversion of atrial fibrillation
is ineffective at either and may be
profibrillatory as it decreases the atrial
refractory period
Acute Management of Atrial
Fibrillation
 Rate control may be attained with calcium channel
blockers or beta blockers in patients with normal
L.V. function.
 Calcium channel blockers may be used cautiously in
patients with depressed LV function but are
associated with increased mortality in the long term.
 Beta blockers should be avoided in acutely
decompensated CHF patients with atrial fibrillation
Atrial Fibrillation and
Depressed L.V. Function
 Digoxin and amiodarone may be of effective in
patients with LV dysfunction and decompensated
congestive heart failure to slow ventricular
response.
 Digoxin alone is rarely effective when the patient
is sympathetically drive
 Avoid high dose digoxin with amiodarone as
digoxin levels increase 2-fold with amiodarone
Chronic Management of Atrial
Fibrillation
 Patientswith atrial fibrillation, paroxysmal or
sustained should be anticoagulated if any of the
following risk factors for stroke are present:
– diabetes – hypertension
– valvular disease – congestive heart failure
– hyperthyroidism – age greater than 65
– Prior CVA
Chronic Management of Atrial
Fibrillation
 Rate control with  Maintenance of sinus
calcium channel is similar with class I
blockers, beta blockers and class III drugs
or combination with approaching 50%
digoxin.
recurrence at 1 year
 Digoxin may be used in
 Recurrence of atrial
bed bound patients but is
easily overcome with fibrillation 80% at 1
sympathetic stimulation. year without treatment
Chronic management of Atrial
Fibrillation
 ClassIII agents may have  Class IC agents safe in
improved efficacy absence of structural
– Amiodarone heart disease.
 pulmonary toxicity
 Few side effects
 thyroid

 liver  Need stress testing


– Dofetilide  Can lead to 1 to 1
 Torsades des Pointes
ventricular conduction
– Safe in CHF and CAD
of atrial flutter
– Limited due to side effect
profile  Use with beta blocker
Chronic Management of Atrial
Fibrillation
 Recent large trials reveal no benefit of
rhythm control over rate control.
 Trend of increased mortality in rhythm arm
likely due to proarrhythmia from drugs.
 Patients unable to tolerate atrial fibrillation
due to symptoms were not enrolled in these
studies and are increasingly undergoing
ablation , catheter and surgical procedures.
Nonpharmacologic Treatment
of Atrial Fibrillation
 Maze Procedure
– 90% freedom from atrial
fibrillation
– 2% mortality required
thoracotomy
 Catheter ablation procedure
– only moderate success
– long procedures, difficult
– selecting population
– 60% to 80% effective
– Pulmonary vein
stenosis,cva,perforation,
– esophageal fistula
Atrial Flutter
A macro re-entrant arrhythmia
– Anatomical barrier
– Zone of slow conduction

 Typical atrial flutter


– Contained within the right atrium
– Constrained anteriorly by the tricuspid valve
– Constrained posteriorly by the crista terminalis and eustachian
ridge
– Travels in a counterclockwise direction around the atrium
 Atypical atrial flutters
– Counterclockwise flutter
– ASD/ scar related flutter
– Perimitral flutter
Atrial Flutter
 Tends to occur in middle age
– Probably due to atrial dilatation
 Pulmonary embolism
– Commonly presents with a sinus tachycardia
 Associated valve disease
– Mitral or Tricuspid disease
– Atrial septal defects
– Chronic ventricular failure
 Toxic and Metabolic conditions
– Alcohol/ thyrotoxicosis/ pericarditis
 Previous ablation
Atrial Flutter
Examination
 Rarely helpful in establishing the diagnosis
 Regular pulse (150bpm- 2:1, 75bpm 4:1- can be
slower)
 May see rapid, regular flutter waves in the
JVP(jugular venous pulse)
 Heart sounds
– Constant intensity of S1 if relationship of flutter waves to
QRS is constant
 Carotid massage or adenosine
– Allows flutter waves to be seen more easily
– Ventricular rate will increase when CSM is stopped
Atrial Flutter
 Reentrant circuit localized
to the RA
 250-350 bpm
 2:1 or variable AV block
 Classic “saw-tooth” P
waves
Atrial Flutter With Variable AV
Block
Management of Atrial Flutter
 Focuses on Rate control
 Patient with atrial fibrillation may undergo
DC cardioversion or pharmacologic
conversion
 Catheter ablation procedure : achievement ratio
90%
Part 4 Atrioventricular Junctional Arrhythm

premature AV junctional beats


 AV junctional beats
produce P waves that
point upward in lead
AVR and downward in
lead II-just the opposite
of what is seen in sinus
rhythm. The P wave
may produce the QRS
complex, A, follow it,
B,or occur
simultaneously with it,
C, in the last instance
no P wave will be
visible
AV Nodal Reentrant
Tachycardia
 Recurrent palpitations
 Rapid onset and Rapid offset
 Patient may feel an ectopic beat to initiate/
terminate the arrhythmia
 Vagal maneuvres to terminate the arrhythmia
 Anxiety/ breathless/ palpitations
– Syncope (due to high rate or due to transient
asystole at termination)
AV Nodal Reentrant
TachycardiaSlow pathway
 2 pathways within or limited to
perinodal tissue
– anterograde conduction
down fast pathway blocks
with conduction down slow
pathway, with retrograde
conduction up fast pathway.
 May have very short RP interval
with retrograde P wave visible
as an R’ in lead V1 or psuedo-S
wave in inferior leads in 1/3 of
cases . No p wave seen in 2/3
Fast pathway
AV Nodal Reentrant
Tachycardia
 Responds to vagal
maneuvers in 1/3 cases
 Very responsive to AV
nodal blocking agents such
as beta blockers, CA channel
blockers, adenosine.
 Recurrences are the norm on
medical therapy
 Catheter ablation 95%
successful with 1% major
complication rate
27 y.o with palpitations
Pseudo R’ in V1 during tachycardia

NSR AVNRT
AVNRT
AVNRT
五 . 预激综合征
Wolf-Parkinson-White Syndrome
 Second electrical connection
exists between the atria and
ventricles (accessory
pathway)
– Resemble atrial tissue
– Results in
 a short PR
 Delta wave (pre-excitation)

 Some AV conducts only


retrograde (concealed)
WPW pathophysiology
 Short AV conduction The result is fusion of both normal and
accessory conduction
– early excitation of
ventricle at site of No
accessory pathway conduction
 Bizarre upstroke of QRS delay
– abnormal initial site of
depolarization
 Wide QRS
– early initiation of
ventricular depolarization AV
node Accessory
pathway
WPW pathophysiology
 Due to an accessory pathway
– Patients can have multiple pathways
 Accessory pathways may conduct
– Antegradely( 前传)
– Retrogradely (逆传)
– Combination of the two
Wolff-Parkinson-White Syndrome
WPW epidemiology
Present in 1.5% of the population
 History of structural heart disease
– Ebstein’s anomaly
 Multiple right sided accessory pathways

 Family history
– Higher prevalence in the children; especially if
multiple accessory pathways
 Examination
– Frequently normal
Clinical findings
 May be asymptomatic
 About 1.8% of the patients take place tachycardia
– 80%AVRT
– 15%-30% Atrial fibrillation
– 5% Atrial flutter
AVRT Antegradely
( Wide QRS)
Retrogradely 95%
Common cause of
narrow complex
Tachycardias
Clinical findings
 Sudden onset/ offset( 突发突止)
 Patient may feel an ectopic beat to initiate the
arrhythmia
 Vagal maneuvres (刺激迷走 N ) to terminate the
arrhythmia
 Anxiety/ breathless/ palpitations
– Syncope (due to high rate or due to transient asystole at
termination)
Sudden death /HF due to atrial fibrillation with
rapid ventricular conduction
WPW syndrome ECG
 Accelerated AV conduction PR <120 msec
 Prolonged QRS > 120 msec
 Abnormal slurred upstroke of QRS ( delta
wave)
 ST-T
 Abnormal depolarization and repolarization
may lead to pseudoinfarction pattern
 2 type : A and B
PR interval is short Rate = 100 bpm
(80 to 90 msec)

QRS is wide
(over 120 msec)

Wolf-Parkinson-White (WPW) Syndrome


(Left sided pathway type:A)
QRS is wide
Rate = 62 bpm
(over 120 msec)

PR interval is short
(80 to 90 msec)

Wolf-Parkinson-White (WPW) Syndrome


(Right sided pathway type:B)
AP conduct Antegradely
( Wide QRS)
F N
W

预激综合征合并房颤
    [ 治疗 ]
预激本身不需治疗,
并发心动过速且发作频繁伴有明显症
状者,应给予治疗。方法:药物、导
管消融术、外科手术。
若发作正向房室折返性心动过
速,可参照房室结折返性心动过速处
理。
 [治疗] 预激综合征患者发作房扑
与房颤时伴有晕厥或低血压,应立即施
行电复律。不能用西地兰、异搏定静推
经导管消融治疗预激综合征并
PSVT 应列为首选。
适应症:
1. 发作频繁者;
2. 并房颤或扑动,心室率极快者。
Part 5 Ventricular Arrhythmia
一 . 室性期前收缩( premature ventricular
beats ),是一种最常见的心律失常。
[ 病因 ] 正常人与各种心脏病患者均可发生室
性期前收缩。
心电图特点 :
①
提前出现的宽大畸形的 QRS 波,其
前无 P 波 ;
② ST 、 T 与主波方向相反 ;
③ 代偿间歇完全。
Compensatory (代偿间期)
[ 心电图检查 ]
1. 配对间期:室性期前收缩与其前面的窦性
搏动之间期。
2. 二联律是指每个窦性搏动后跟随一个室性
期前收缩;
3. 三联律是每两个正常搏动后出现一个室性
期前收缩。
4. 成对室性期前收缩:连续发生两个。
5. 连续三个或以上称室性心动过速。
[ 心电图检查 ]
6. 同一导联内,形态相同者为单形性
;不同者称多形或多源性期前收缩。
7. 间位性室早 : 室早恰巧插入两个窦
性搏动之间 , 不产生室早后停顿。
8. 室性并行心律 :
1) 配对间期不恒定 ;
2) 长短间期之间有最小公倍数 ;
3) 可产生室性融合波。
PVC Bigeminy (二联律)
PVC Couplet (成对)
Interpolated PVC( 间位)
PVC with R-on-T
PVC Triplet (室速)
[ 治疗 ]
如无明显症状,不必使用药物。
如症状明显,治疗以消除症状为目
的。药物宜选择 β 受体阻滞剂。
A 42 year old smoker presents to the ED with
palpitations. His blood pressure is 100/60. The
following rhythm strip is obtained . What is the next
appropriate step?

 A. Emergent cardioversion for polymorphic


VT.
 B. I.V. procainamide
 C. I.V. lidocaine
 D. diltiazem drip to obtain rate control.
二 . 室性心动过速
室性心动过速( ventricular tachycardia )
简称室速( VT) 。
[ 病因 ] 室速常发生于各种器质性心脏病患
者。最常见为冠心病,其次是心肌病、心衰、
心瓣膜病等,偶可发生在无器质性心脏病者。
[ 临床表现 ]
非持续性室速(短于 30s ,能自行
终止)的患者通常无症状。
持续性室速(超过 30s ,需药物
或电复律始能终止)常伴随明显血流动
力学障碍与心肌缺血。临床症状包括低
血压、少尿、晕厥、气促和心绞痛等。
Ventricular Tachycardia
 May be asymptomatic
 Heart rate is NOT a useful guide to the arrhythmia
 More likely if
– Previous MI / History of IHD
– Cardiac risk factors
 Sudden onset/ offset
 Is it recurrent?
 Do they have a pacemaker or an ICD
 Family History
– Sudden cardiac death
– Unexplained death
– HOCM/ Long QT syndrome / Brugada
Physical Examination
 Is the patient compromised?
– DC cardioversion if any doubt
 Assess the JVP
– Cannon A waves (颈静脉大炮 A 波) ?
 Assess the praecordium (胸前评估)
– Pacemaker/ ICD/ Median sternotomy scar / LV
Heave/ Double apical impulse?
 Ausculate (听诊)
– Variable S1; Ejection systolic murmer
[ 心电图检查 ] 室速的特征为;
①3 个或以上的室性期前收缩连续出现;
②QRS 波群形态畸形,时限超过 012s ; ST-T
波方向与 QRS 波群主波方向相反;
③ 室率通常为 100~250 次 / 分;心律稍不规
则;
④ 心房独立活动与 QRS 波群无固定关系形
成房室分离;
⑤ 通常发作突然;
⑥ 心室夺获与心室融合波。
ECG Findings- VT
 Regularbroad complex tachycardia (QRS >
120ms),more than 3
– Normally RBBB >140ms
– LBBB>160ms
 Evidence of A-V Dyssynchrony
 Fusion beats
 Capture beats
 Sudden onset/ offset
 If a 12 lead in sinus rhythm is available
– ?Q waves; Delta waves; RBBB and ST Elevation
Ventricular Tachycardia
Ventricular Tachycardia
Therapy for Ventricular
Tachycardia
一般遵循的原则是:
无器质性心脏病患者发生非持续性室
速,如无症状及晕厥发作,无需治疗;
持续性室速发作,无论有无器质性心
脏病,均应给予治疗;
有器质性心脏病的非持续性室速亦应
考虑治疗。
具体措施
一、终止室速发作
如无显著血流动力学障碍,首先给
予静脉注射利多卡因,索他洛尔与普罗
帕酮亦十分有效。
如患者已发生低血压、心绞痛、
休克或脑血流灌注不足等症状时,应迅
速直流电复律。洋地黄中毒者不宜电复
律。
二、预防复发
1 、应努力寻找及治疗病因与诱因

2 、应选择毒副反应较少的药物。
3 、单一药物治疗无效时,可联合应用 。
4 、抗心律失常药物亦可与埋藏式心室起搏
装置合用,治疗复发性心动过速。
三、根治 外科手术、导管消融术等亦
可成功应用于选择性病例。
Therapy for Ventricular
Tachycardia
 Clinical condition of patient
– Unstable requires DC cardioversion
– Stable may be treated with Drugs or Cardioversion
 Presence or absence of Left ventricular
dysfunction determines choice of pharmacologic
therapy
– Amiodarone 150 mg I.V. over 10 minutes may be RX
of choice maximum 1200gm/24 hours recommendation
一 . 加速性心室自主节

二、尖端扭转性室速 尖端扭转是多形性
室速的一个特殊类型。频率 200~250 次 / 分,振幅与波
峰呈周期性改变。 QT 间期通常超过 0.5s , U 波明显。
可进展为心室颤动和猝死。
本型室速的病因可为先天性、电解质紊乱、应用Ⅰ
A 或某些Ⅰ C 类药物、颅内病变及心动过缓等。
治疗:应努力寻找和去除导致 QT 间期延长的病
变和停用有关药物。首先给予静脉注射镁盐,异丙肾上
腺素或阿托品亦可应用。先天性长 QT 间期综合征应选
用 β 受体阻滞剂。
Torsades de Pointes
 Polymorphic VT associated with long QT
– increased risk if QTC 500 msec or greater QT > 600
msec.
 Frequently initiated after pause
 Usually Iatrogenic (医源性)
– Hypokalemia,Hypomagnesemia, Drugs, combination
 May be congenital (先天性)
– LQT1, LQT2,LQT3
Classic Torsades de Pointes
Polymorphic VT

“Spindle-node” pattern “Spindle”

“Node” (“point”)

“Twisting (spindle) about the Points” (node)


Treatment of Torsades de
Pointes
 Remove Offending Agent (去除诱因)
 Replete Potassium (补钾)
 Treat with Magnesium (镁剂) even if normal
 Consider increasing heart rate
– Isoproterenol (异丙肾)
– Pacing
 Treat Congenital with Beta blockers and Pacing or
ICD

Ventricular Flutter
Ventricular Fibrillation
No cardiac output
– DC Cardioversion
Normally cause is evident (病因明显)
– Myocardial ischaemia
– Cardiomyopathy- DCM/ HCM/ HOCM
– Torsade de pointes and causes of long QT syndrome
– Brugada syndrome
– Commotio Cordis
心室扑动

心室扑动呈正弦波,波幅大而规
则, 频率 150~300 次 / 分。
心室颤动

心室颤动的波形、振幅与频率均极不
规则,无法识别 QRS 波群、 ST 段与
T 波。
Ventricular Tachycardia
Flutter and Fibrillation
Needs a
Cardioverter
(essentially
a small
Requires a shock to
small shock needed Low blood pressure
CARDIOVERTER ventricles)

Needs a
Defibrillator
Requires a
(essentially
DEFIBRILLATOR
large shock needed a large
No blood pressure
shock to
ventricles)
谢谢
第六节 心脏传导阻滞
Part 6 Heart Block
 First Degree: Prolonged conduction time
 Second Degree: Intermittent non-conduction
 Third Degree: Persistent non-conduction
房室传导阻滞
房室传导阻滞( atrioventricular block ,
AVB )又称房室阻滞,是指房室交界区脱离了
生理不应期后,心房冲动传导延迟或不能传导
至心室。
[ 病因 ] 正常人或运动员可发生文氏型房
室阻滞(莫氏Ⅰ型),与迷走神经张力增高有关。
其他导致房室传导阻滞的病变有:急性心肌梗
死、冠状动脉痉挛、病毒性心肌炎、电解质紊
乱、心脏手术药物中毒等。
一 .AV Heart Block
 There are three types of AV heart block:
 1. First-degree AV block– the PR interval is uniformly prolonged
beyond 0.2 second.
 2. Second-degree AV block– there are two subtypes:
 A. wenckebach (Mobitz type 1) AV block-increasing prolongation
of the PR interval occurs until a P wave is blocked and not followed
by a QRS complex.
 B. mobitz type II AV block– a series of P waves occurs without
QRS complex; The conducted P waves have the same PR interval.
 3. Third-degree (c omplete) AV block– this shows the following:
 A. the atrial and ventricles beat independently because stimuli
cannot pass through the AV junction.
 B. the atrial rate is faster than the ventricular rate.
 C. the PR interval constantly changes
Mobitz I (Wenckebach) the PR progressively lengthens
with one P wave for every QRS until a beat is dropped.
Usually the block is above His bundle.
Mobitz II the PR is constant but with occasional dropped
beats. This is a more serious arrhythmia because the injury is
probably in fast conducting tissue below the His bundle which
is not under vagal control.
Mobitz II - 2nd degree block
Complete AV heart block. Since there is no
conduction down the AV node pathway atria and
ventricles beat regularly but at different rates.
Summary
 The (relatively) good:
Mobitz I AV block, or
Wenckebach block  The bad:
Mobitz II AV block, and...

 The ugly:
Complete heart block
[ 治疗 ]
应针对不同的病因进行治疗。
Ⅰ0AVB 与Ⅱ 0Ⅰ 型 AVB 室率不太慢者,无需接
受治疗。
Ⅱ0Ⅱ 型 AVB 与Ⅲ 0AVB 如室率显著缓慢,伴
有血流动力学障碍,甚至 Adams-Stokes 综合征发
作者,应给予治疗。
[ 治疗 ]
阿托品( 0.5~2.0mg ,静脉注射)适用于
阻滞位于房室结的患者。异丙肾上腺素
( 1~4ug/min 静脉滴注)适用于任何部位的房室
传导阻滞。以上药物使用超过数天,往往效果不
佳且易发生严重的不良反应。因此,对于症状明
显、室率缓慢者,应及早给予临时性或永久性心
脏起搏治疗。
二 . 室内传导阻滞
室内传导阻滞( intraventricular block )
又称室内阻滞,是指希氏束分叉以下部位的传
导阻滞。
右束支阻滞较为常见。左束支常发生于
充血性心力衰竭、急性心肌梗死、急性感染、
风心病、冠心病等。单支、双支阻滞通常无临
床症状。完全性三分支阻滞的临床表现与完全
性房室阻滞相同。
Right Bundle Branch Block Left Bundle Branch Block
(RBBB) (LBBB)

VAT ≥ 0.07 s
右束支阻滞( right bundle branch block )
1. QRS 时限达 0.12s 或以上 ; 2.V1 导联呈 rsR’ , R’ 波粗钝 ;
3.V5 、 V6 导联呈 qRS , S 波宽阔。 4.T 波与 QRS 波主波方向相
反。不完全右束支阻滞的图形与上述相似,但 QRS 时限小于 0.12s
Right Bundle Branch Block
(RBBB)
左束支阻滞( left bundle branch
block )
QRS 时限达 0.12s 或以上。 V5 、 V6 导联 R 波宽大
,顶部有切迹或粗钝,其前方无 q 波。 V1 、 V2 导联
呈宽阔的 QS 波或 rS 波形。 T 波与 QRS 波主波方向相
反。不完全左束支阻滞的图形与上述相似,但 QRS 时限
Left Bundle Branch Block
左前分支传导阻滞
左后分支传导阻滞
[ 治疗 ] 慢性束支阻滞患者如无症状,
无需接受治疗。双支与不完全性三分支阻滞有可
能进展为完全性房室阻滞,但是是否一定发生以
及何时发生均难以预料,不必常规施行预防性起
搏器治疗。急性前壁心肌梗死发生双分支、三分
支阻滞,或慢性双分支、三分支阻滞,伴有
Adams-Stokes 综合征发作者,则应及早考虑心
脏起搏器治疗。
第七节 抗心律失常药物的分类
I 类 延迟快速 Na+ 通道
Ia 抑制 0 相除极速度 , 减慢传导 , 延长复极作  
      用明显,延长动作电位时程 奎尼丁
Ib 轻度抑制 0 相除极速度 , 缩短动作电位时程
利多卡因
Ic 明显抑制 0 相除极速度 , 不影响动作电位时程
心律平
II 类 抑制交感神经 (β 阻断作用 ) 倍他乐克
III 类 延长复极时间 ( 复极延长作用 ) 胺碘酮
IV 类 钙拮抗剂 ( 钙拮抗作用 ) 异搏定
第八节心律失常的手术治疗

一、心脏起搏治疗
起搏器的功能及类型

起搏器命名代码
第一位 第二位 第三位 第四位 第五位
起搏心腔 感知心腔 感知后反应方式 程控功能 其他

O 无 O 无 O 无 略
A 心房 A 心房 I 抑制 R 频率调整
V 心室 V 心室 T 触发
D 心房 + 心室 D 心房 + 心室 D 双重( I+T )
S 心房或心室 S 心房或心室
起搏器的功能及类型

起搏器种

根据应用的方式分 根据电极导线植入部位分
: :
•临时心脏起搏 •单腔起搏器
•植入式心脏起搏 •双腔起搏器
•三腔起搏器
 植入永久性心脏起搏器的适应证( 1 )

•伴有临床症状的任何水平的完全或高度
房室
传导阻滞。
•伴有症状的束支 - 分支水平阻滞,间歇性

二度 Ⅱ型房室传导阻滞。
•病态窦房结综合征或房室传导阻滞,有
明显
植入永久性心脏起搏器的适应证( 2 )

• 治疗心律失常或其他疾病所必需的药物,如
引起有症状的心动过缓时,应该植入起搏器

• 反复发生的颈动脉窦性晕厥和血管迷走性晕
厥,以心脏反应为主者。
• 药物治疗效果不满意的顽固性心力衰竭(可

心脏再同步起搏治疗)。
Cardiac Resynchronization
Therapy
(心脏再同步治疗)

Right Atrial Lead


Coronary Sinus Lead

Right Ventricular Lead


第八节心律失常的介入治疗

二、心脏电复律
cardioversion
定义

  心脏电复律是在短时间内向心
脏通以高压强电流,使心肌瞬间同
时除极,消除异位性快速心律失常
,使之转复为窦性心律的方法。亦
称为心脏电除颤。
• 心室颤动和扑动:是电复律的绝对指征

• 心房颤动和扑动伴血流动力学障碍者。
• 药物及其他方法治疗无效或有严重血流
动力学障碍的阵发性室上性心动过速、
室性心动过速、预激综合征伴快速心律
失常者。
• 病史多年,心脏(尤其是左心房)明显增大
及心房内有新鲜血栓形成或近 3 个月有栓塞
史。
• 伴高度或完全性房室传导阻滞的心房颤动或
扑动。
• 伴病态窦房结综合征的异位性快速心律失常

• 有洋地黄中毒、低钾血症时,暂不宜电复律

电复律种类

 直流电非同步电除颤
用于心室颤动、心室扑

直流电同步电复律

除心室颤动以外的快速型心律失

电复律能量选择

室颤 200 ~ 360J
房颤 100 ~ 150J
室上速 100 ~
150J 室速 100 ~ 200J
房扑 50 ~ 100J
第八节心律失常的介入治疗

三、心导管射频消融

radio frequency catheter ablation , RFCA
  是治疗心律失常的一种导管治
疗技术。射频消融仪通过导管头端
的电极释放射频电能,在导管头端
与局部的心肌内膜之间电能转化为
热能,达到一定温度( 46 ~
90℃ )后,使特定的局部心肌细胞
脱水、变形、坏死,自律性和传导
性能均发生改变,从而使心律失常
得以根治。
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