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Definition of Arrhythmia:

The Origin, Rate, Rhythm, Conduct


velocity and sequence of heart
activation are abnormally.

Anatomy of the conducting system

Some physical condition


Pathological heart disease
Other system disease
Electrolyte disturbance and acidbase imbalance
Physical and chemical factors or
toxicosis


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Abnormal heart pulse


formation
Sinus pulse
Ectopic pulse
Triggered activity
Abnormal heart pulse
conduction
Reentry
Conduct block


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Abnormal heart pulse formation


Sinus arrhythmia
Atrial arrhythmia
Atrioventricular junctional
arrhythmia
Ventricular arrhythmia
Abnormal heart pulse conduction
Sinus-atrial block
Intra-atrial block
Atrio-ventricular block
Intra-ventricular block
Abnormal heart pulse formation
and conduction

Medical history
Physical examination
Laboratory test

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Sinus rate > 100 beats/min (100180)


Causes:
Some physical condition: exercise,
anxiety, exciting, alcohol, coffee
Some disease: fever,
hyperthyroidism, anemia,
myocarditis
Some drugs: Atropine, Isoprenaline

Neednt therapy

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Sinus tachycardia

Ectopic atrial tachycardia


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Junctional tachycardia

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Sinus rate < 60 beats/min


Normal variant in many normal and older
people
Causes: Trained athletes, during sleep,
drugs (-blocker) , Hypothyriodism, CAD
Symptoms:
Most patients have no symptoms.
Severe bradycardia may cause dizziness,
fatigue, palpitation, even syncope.
Neednt specific therapy, If the patient has
severe symptoms, planted an pacemaker
may be needed.

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Sinus Bradycardia

The term premature contractions


are used to describe non sinus
beats.
Common arrhythmia
The morbidity rate is 3-5%

APCs arising from somewhere in either


the left or the right atrium.
Causes: rheumatic heart disease, CAD,
hypertension, hyperthyroidism,
hypokalemia
Symptoms: many patients have no
symptom, some have palpitation, chest
incomfortable.
Therapy: Neednt therapy in the
patients without heart disease. Can be
treated with -blocker, propafenone,
moricizine or verapamil.

Classify by automatic atrial tachycardia


(AAT); intra-atrial reentrant atrial
tachycardia (IART); chaotic atrial
tachycardia (CAT).
Etiology: atrial enlargement, MI;
chronic obstructive pulmonary disease;
drinking; metabolic disturbance;
digitalis toxicity; electrolytic
disturbance.

May occur transient; intermittent; or


persistent.
Symptoms: palpitation; chest
uncomfortable, tachycardia may
induce myopathy.
Auscultation: the first heart sound is
variable


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ECG characters:
Atrial rate is around 130-150bpm;
P wave is different from sinus P wave;
P-R interval 0.12
Often appear type I or type II, 2:1 AV
block;
EP study: atrial program pacing can
induce and terminate tachycardia


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ECG characters:
Atrial rate is around 100-200bpm;
Warmup phenomena
P wave is different from sinus P
wave;
P-R interval 0.12
Often appear type I or type II, 2:1 AV
block;
EP study: Atrial program pacing cant
induce or terminate the tachycardia

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Also termed Multifocal atrial


tachycardia.
Always occurs in COPD or CHF,
Have a high in-hospital mortality ( 2556%). Death is caused by the severity of
the underlying disease.
ECG characters:
Atrial rate is around 100-130bpm;
The morphologies P wave are more than
3 types.
P-P, P-R and R-R interval are different.
Will progress to af in half the cases
EP study: Atrial program pacing cant
induce or terminate the tachycardia

IRAT: Esophageal Pulsation


Modulation, RFCA, Ic and IV class
anti-tachycardia agents
AAT: Digoxin, IV, II, Ia and III class
anti-tachycardia agents; RFCA
CAT: treat the underlying disease,
verapamil or amiodarone.
Associated with SSS: Implant pacemaker.


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Etiology:
It can occur in patients with
normal atrial or with abnormal
atrial.
It is seen in rheumatic heart
disease (mitral or tricuspid valve
disease), CAD, hypertension,
hyperthyroidism, congenital heart
disease, COPD.
Related to enlargement of the
atria
Most AF have a reentry loop in
right atrial

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Most cases of atrial flutter are caused by a large reentrant circuit in the wall of the
right atrium

EKG Characteristics:

Biphasic sawtooth flutter waves at a rate of ~ 300 bpm


Flutter waves have constant amplitude, duration, and
morphology through the cardiac cycle
There is usually either a 2:1 or 4:1 block at the AV node,
resulting in ventricular rates of either 150 or 75
bpm

Symptoms: depend on underlying


disease, ventricular rate, the patient
is at rest or is exerting
With rapid ventricular rate:
palpitation, dizziness, shortness of
breath, weakness, faintness,
syncope, may develop angina and
CHF.


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Therapy:
Treat the underlying disease
To restore sinus rhythm:
Cardioversion, Esophageal Pulsation
Modulation, RFCA, Drug (III, Ia, Ic
class).
Control the ventricular rate:
digitalis. CCB, -block
Anticoagulation

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Subdivided into three types:


paroxysmal, persistent, permanent.
Etiology:
Morbidity rate increase in older
patients
Etiology just like atrial flutter
Idiopathic
Mechanism:
Multiple wavelet re-entry;
Rapid firing focus in pulmonary vein,
vena cava or coronary sinus.

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Atrial fibrillation is caused by numerous wavelets of depolarization spreading


throughout the atria simultaneously, leading to an absence of coordinated
atrial contraction.

Atrial fibrillation is important because it can lead to:


Hemodynamic compromise
Systemic embolization
Symptoms

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EKG Characteristics:

Absent P waves
Presence of fine fibrillatory waves which vary in
amplitude and morphology
Irregularly irregular ventricular response

Manifestation:
Affected by underlying diseases,
ventricular rate and heart function.
May develop embolism in left atrial.
Have high incidence of stroke.
The heart rate, S1 and rhythm is
irregularly irregular
If the heart rhythm is regular, should
consider about (1) restore sinus rhythm;
(2) AF with constant the ratio of AV
conduction; (3) junctional or ventricular
tachycardia; (4) slower ventricular rate
may have complete AV block.


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Therapy:
Treat the underlying disease
Restore sinus rhythm: Drug,
Cardioversion, RFCA, Maze surgery
Rate control: digitalis. CCB, -block
Antithrombotic therapy: Aspirine,
Warfarin

Etiology and manifestation is like


APCs
Therapy the underlying disease
Neednt anti-arrhythmia therapy.

Mechanism: relate to hyperautomaticity or trigger activity of


AV junctional tissue
Etiology: digitalis toxicity; inferior
MI; myocarditis; acute rheumatic
fever and postoperation of valve
disease
ECG: the heart rate ranges 70-150
bpm or more, regular, normal QRS
complex, may occur AV dissociation
and wenckebach AV block

Therapy:
Treat underlying disease;
stopping digoxin, administer
potassium, lidocaine, phenytoin
or propranolol.
Not for DC shock
It can disappear spontaneously.
If had good tolerance, not
require therapy.

Most PSVT (paroxysmal supraventricular


tachycardia) is due to reentrant
mechanism.
The incidence of PSVT is higher in AVNRT
(atrioventricular node reentry tachycardia)
and AVRT (atioventricular reentry
tachycardia), the most common is AVNRT
(90%)
Occur in any age individuals, usually no
structure heart disease.

Manifestation:

Occur and terminal abruptly.

Palpitation, dizziness,
syncope, angina, heart
failure and shock.
The sever degree of the
symptom is related to
ventricular rate, persistent
duration and underlying
disease


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ECG characteristic of AVNRT


Heart rate is 150-250 bpm, regular
QRS complex is often normal,
wide QRS complex is with aberrant
conduction
Negative P wave in II III aVF,
buried into or following by the QRS
complex.
AVN jump phenomena


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ECG characteristic of AVRT


Heart rate is 150-250 bpm, regular
In orthodromic AVRT, the QRS
complex is often normal, wide QRS
complex is with antidromic AVRT
Retrograde P wave, R-P>110ms.

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Therapy:
AVNRT & orthodromic AVRT
Increase vagal tone: carotid sinus
massage, Valsalva maneuver.if no
successful,
Drug: verapamil, adrenosine,
propafenone
DC shock
Antidromic AVRT:
Should not use verapamil, digitalis,
and stimulate the vagal nerve.
Drug: propafenone, sotalol,
amiodarone
RFCA

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There are several type of accessory


pathway
Kent: adjacent atrial and ventricular
James: adjacent atrial and his
bundle
Mahaim: adjacent lower part of the
AVN and ventricular
Usually no structure heart disease,
occur in any age individual

Manifestation:
Palpitation, syncope, dizziness
Arrhythmia: 80% tachycardia is
AVRT, 15-30% is AFi, 5% is AF,
May induce ventricular
fibrillation


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Therapy:
Pharmacologic therapy: orthodrome
AVRT or associated AF, AFi, may use
Ic and III class agents.
Antidromic AVRT cant use digoxin
and verapamil.
DC shock: WPW with SVT, AF or Afi
produce agina, syncope and
hypotension
RFCA


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Etiology:
Occur in normal person
Myocarditis, CAD, valve heart
disease, hyperthyroidism, Drug
toxicity (digoxin, quinidine and antianxiety drug)
electrolyte disturbance, anxiety,
drinking, coffee


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Manifestation:
palpitation
dizziness
syncope
loss of the second heart sound

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Therapy: treat underlying disease,


antiarrhythmia
No structure heart disease:
Asymptom: no therapy
Symptom caused by PVCs: antianxiety
agents, -blocker and mexiletine to
relief the symptom.
With structure heart disease (CAD, HBP):
Treat the underlying diseas
-blocker, amiodarone
Class I especially class Ic agents should
be avoided because of proarrhytmia and
lack of benefit of prophylaxis

Etiology: often in organic heart


disease
CAD, MI, DCM, HCM, HF,
long QT syndrome
Brugada syndrome
Sustained VT (>30s), Nonsustained
VT
Monomorphic VT, Polymorphic VT

Ventricular tachycardia
Ventricular tachycardia is usually caused by reentry, and most
commonly seen in patients following myocardial infarction.

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Torsades de points (Tdp): A special


type of polymorphic VT,
Etiology:
congenital (Long QT),
electrolyte disturbance,
antiarrhythmia drug proarrhythmia
(IA or IC),
antianxiety drug,
brain disease,
bradycardia


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Accelerated idioventricular rhythm:


Related to increase automatic tone
Etiology: Often occur in organic
heart disease, especially AMI
reperfusion periods, heart
operation, myocarditis, digitalis
toxicity


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Manifestation:
Nonsustained VT with no symptom
Sustained VT : with symptom and
unstable hemodynamic, patient
may feel palpitation, short of
breathness, presyncope, syncope,
angina, hypotension and shock.


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ECG characteristics:
Monomorphic VT: 100-250 bpm, occur
and terminate abruptly,regular
Accelerated idioventricular rhythm: a
runs of 3-10 ventricular beats, rate of
60-110 bpm, tachycardia is a capable of
warm up and close down, often seen AV
dissociation, fusion or capture beats
Tdp: rotation of the QRS axis around the
baseline, the rate from 160-280 bpm, QT
interval prolonged > 0.5s, marked U
wave

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Treat underlying disease


Cardioversion: Hemodynamic
unstable VT (hypotension, shock,
angina, CHF) or hemodynamic
stable but drug was no effect
Pharmacological therapy: blockers, lidocain or amiodarone
RFCA, ICD or surgical therapy

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Accelerated idioventricular rhythm:


usually no symptom, neednt
therapy.
Atropine increased sinus rhythm
Tdp:
Treat underlying disease,
Magnesium iv, atropine or
isoprenaline, -block or pacemaker
for long QT patient
temporary pacemaker

Often occur in severe organic heart


disease: AMI, ischemia heart disease
Proarrhythmia (especially produce
long QT and Tdp), electrolyte
disturbance
Anaesthesia, lightning strike, electric
shock, heart operation
Its a fatal arrhythmia

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Manifestation:
Unconsciousness, twitch, no blood
pressure and pulse, going to die
Therapy:
Cardio-Pulmonary Resuscitate (CPR)
ICD

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Block position:
Sinoatrial; intra-atrial;
atrioventricular; intra-ventricular
Block degree
Type I: prolong the conductive time
Type II: partial block
Type III: complete block

AV block is a delay or failure in


transmission of the cardiac impulse
from atrium to ventricle.
Etiology:
Atherosclerotic heart disease;
myocarditis; rheumatic fever;
cardiomyopathy; drug toxicity;
electrolyte disturbance, collagen
disease, levs disease.

AV Block (relatively common)


1st degree AV block
Type 1 2nd degree AV block
Type 2 2nd degree AV block
3rd degree AV block

SA Block (relatively rare)

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AV block is divided into three


categories:
First-degree AV block
Second-degree AV block: further
subdivided into type I and type II
Third-degree AV block: complete
block

The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/

EKG Characteristics:

Prolongation of the PR interval, which is constant


All P waves are conducted

Type 1 (Wenckebach)

EKG Characteristics:

Progressive prolongation of the PR interval until a P


wave is not conducted.
As the PR interval prolongs, the RR interval actually
shortens

Type 2

EKG Characteristics:

Constant PR interval with intermittent failure to conduct

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EKG Characteristics:

No relationship between P waves and QRS complexes


Relatively constant PP intervals and RR intervals
Greater number of P waves than QRS complexes

Manifestations:
First-degree AV block: almost no
symptoms;
Second degree AV block: palpitation,
fatigue
Third degree AV block: Dizziness, agina,
heart failure, lightheadedness, and
syncope may cause by slow heart rate,
Adams-Stokes Syndrome may occurs in
sever case.
First heart sound varies in intensity, will
appear booming first sound


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Treatment:
I or II degree AV block neednt
antibradycardia agent therapy
II degree II type and III degree AV
block need antibradycardia agent
therapy
Implant Pace Maker


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Intraventricular conduction system:


Right bundle branch
Left bundle branch
Left anterior fascicular
Left posterior fascicular

Etiology:
Myocarditis, valve disease,
cardiomyopathy, CAD, hypertension,
pulmonary heart disease, drug
toxicity, Lenegre disease, Levs
disease et al.
Manifestation:
Single fascicular or bifascicular block
is asymptom; tri-fascicular block may
have dizziness; palpitation, syncope
and Adams-stokes syndrome


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Therapy:
Treat underlying disease
If the patient is asymptom; no treat,
bifascicular block and incomplete
trifascicular block may progress to
complete block, may need implant
pace maker if the patient with
syncope

Pathogenesis therapy
Stop the arrhythmia immediately if
the hemodynamic was unstable
Individual therapy

Anti-tachycardia agents
Anti-bradycardia agents

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Modified Vaugham Williams


classification
I class: Natrium channel blocker
II class: -receptor blocker
III class: Potassium channel blocker
IV class: Calcium channel blocker
Others: Adenosine, Digital

Cardioversion: For tachycardia


especially hemodynamic unstable
patient
Radiofrequency catheter ablation
(RFCA): For those tachycardia
patients (SVT, VT, AF, AFL)
Artificial cardiac pacing: For
bradycardia, heart failure and
malignant ventricular arrhythmia
patients.

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-adrenic receptor activator


M-cholinergic receptor blocker
Non-specific activator

Anti-tachycardia agents:

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Ia class: Less use in clinic


Guinidine
Procainamide
Disopyramide: Side effect: like Mcholinergic receptor blocker

Anti-tachycardia agents:
Ib class: Perfect to
ventricular tachyarrhythmia
1. Lidocaine
2. Mexiletine

Anti-tachycardia agents:
Ic class: Can be used in ventricular
and/or supra-ventricular tachycardia
and extrasystole.
1. Moricizine
2. Propafenone


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II class: -receptor blocker


Propranolol: Non-selective
Metoprolol: Selective 1-receptor
blocker, Perfect to hypertension
and coronary artery disease
patients associated with
tachyarrhythmia.

III class: Potassium channel blocker,


extend-spectrum anti-arrhythmia
agent.
Amioarone: Perfect to coronary
artery disease and heart failure
patients
Sotalol: Has -blocker effect
Bretylium

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IV class: be used in supraventricular


tachycardia
Verapamil
Diltiazem
Others:
Adenosine: be used in
supraventricular tachycardia

Isoprenaline
Epinephrine
Atropine
Aminophylline

Ia, Ic class: Prolong QT interval, will


cause VT or VF in coronary artery
disease and heart failure patients
III class: Like Ia, Ic class agents
II, IV class: Bradycardia

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