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ARRHYTHMIA
dr Putra hendra SpPD
UNIBA
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Normal Impulse Conduction
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
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Impulse Conduction & the ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
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Sifatsifat otot JantungI nherent rhythmycity( chronotropic ) kesanggupan jantung dengan
cara otomatis dan secara periodik merangsang dirinya sendiri.
Conductivity( dromotropic )
kesanggupan jantung untuk menghantar rangsang, baik dari jaringan
kusus penghantar rangsang maupun dari ototnya.
Exitability( bathmotropic )
kemampuan jantung untuk dapat dirangsang.
Contractility( inotropic)
kemampuan jantung untuk berkontraksi.
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Pacemakers of the Heart
SA Node- Dominant pacemaker with an
intrinsic rate of 60 - 100 beats/minute.
AV Node- Back-up pacemaker with an
intrinsic rate of 40 - 60 beats/minute.
Ventricular cells- Back-up pacemaker withan intrinsic rate of 20 - 45 bpm.
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Sinus rhythm Sinoatrial node is cardiac
pacemaker
Normal sinus rhythm 60-100 beats/min
Depolarisation triggersdepolarisation of atrialmyocardium (forest fire)
Conducts more slowlythrough AV node
Conducts rapidly throughHis bundles and Purkinjefibres
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Definition of Arrhythmia:
The Origin, Rate, Rhythm, Conduct
velocity and sequenceof heart activation
are abnormally.
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Pathogenesis and Inducement
of Arrhythmia Some physical condition
Pathological heart disease
Other system disease
Electrolyte disturbance and acid-base
imbalance
Physical and chemical factors or
toxicosis
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Classification of Arrhythmia
Abnormal heart pulse formation1. Sinus arrhythmia2. Atrial arrhythmia3. Atrioventricular junctional arrhythmia4. Ventricular arrhythmia
Abnormal heart pulse conduction1. Sinus-atrial block2. Intra-atrial block
3. Atrio-ventricular block4. Intra-ventricular block
Abnormal heart pulse formation andconduction
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Diagnosis of Arrhythmia
Medical history
Physical examination
Laboratory test
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Management of arrhythmias
Acute
Acute management (clinical assessment of
patient and diagnosis)
Prophylaxis
Chronic
Non-pharmacological
Pharmacological (some antiarrhythmics are
also proarrhythmic)
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Non-pharmacological treatment
Acute
Vagal manoeuvres
DC cardioversion Prophylaxis
Radiofrequency ablation
Implantable defibrillator Pacing(external, temporary, permanent)
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Phases of action potential of
cardiac cells Phase 0rapid depolarisation
(inflow of Na+)
Phase 1partial repolarisation
(inward Na+current deactivated,
outflow of K+)
Phase 2plateau (slow inward
calcium current)
Phase 3repolarisation (calcium
current inactivates, K+outflow)
Phase 4pacemaker potential (SlowNa+inflow, slowing of K+outflow)
autorhythmicity
Refractory per iod(phases 1-3)
Phase 4
Phase 0
Phase 1
Phase 2
Phase 3
0 mV
-80mV
II
IIII
IV
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Vaughan Williams classification of
antiarrhythmic drugs Class I:block sodium channels
Ia (quinidine, procainamide,disopyramide) AP
Ib (lignocaine) AP
Ic (flecainide) AP Class II: -adrenoceptor
antagonists (atenolol, sotalol)
Class III:prolong action potentialand prolong refractory period(suppress re-entrant rhythms)
(amiodarone, sotalol) Class IV:Calcium channel
antagonists. Impair impulsepropagation in nodal and damagedareas (verapamil)
Phase 4
Phase 0
Phase 1
Phase 2
Phase 3
0 mV
-80mV
II
IIII
IV
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Antiarrhythmic Agents
Vaughn-Williams Classification Class I Na+ - channel blockers (direct membrane action)
A: Procainamide, Quinidine, diisopyramide
B: Lidocain. Mexilletine, Phenytoin C: Flecainide
Class II - Sympatholytic agents : Beta blocker
Class III - Prolong repolarization: Amiodarone Class IV- Ca++ - channel blockers : verapamil
Purinergic agonists : Adenosine
Digitalis glycosides: digoxin
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Anti-arrhythmia Agents
Anti-tachycardia agents
Anti-bradycardia agents
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Anti-tachycardia agents
Modified Vaugham Williams classification
1. I class: Natrium channel blocker
2. II class: -receptor blocker
3. III class: Potassium channel blocker
4. IV class: Calcium channel blocker
5. Others: Adenosine, Digitalis
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Anti-bradycardia agents
Isoprenaline
Epinephrine
Atropine
Aminophylline
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Sinus Arrhythmia
Sinus tachycardia
Sinus Bradycardia Sinus Arrest
Sinu atrial exit block (SAB
Sick sinus syndrome (SSS)
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Sinus tachycardia
Sinus rate > 100 beats/min (100-180)
Causes:
1. Some physical condition: exercise,anxiety, exciting, alcohol, coffee
2. Some disease: fever, hyperthyroidism,
anemia, myocarditis3. Some drugs: Atropine, Isoprenaline
Neednt therapy
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SinusBradycardia
Sinus rate < 60 beats/min
Normal variant in many normal and older people
Causes: Trained athletes, during sleep, drugs (-
blocker) , Hypothyriodism, CAD or SSS Symptoms:
1. Most patients have no symptoms.
2. 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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Atrial arrhythmia
Atrial premature contractions (APCs)
Atrial tachycardia
Atrial flutter
Atrial fibrillation
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SVT
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Atrial flutter
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 anginaand CHF.
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Atrial flutter
Therapy:
1. Treat the underlying disease
2. To restore sinus rhythm: Cardioversion,Esophageal Pulsation Modulation,RFCA, Drug (III, Ia, Ic class).
3. Control the ventricular rate: digitalis.CCB, -block
4. Anticoagulation
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Atrial fibrillation
Therapy:
1. Treat the underlying disease
2. Restore sinus rhythm: Drug,Cardioversion, RFCA, Maze surgery
3. Rate control:digitalis. CCB, -block
4. Antithrombotic therapy: Aspirine,
Warfarin
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Paroxysmal tachycardia
Most PSVT (paroxysmal supraventriculartachycardia) is due to reentrant mechanism.
The incidence of PSVT is higher in AVNRT
(atrioventricular node reentry tachycardia) andAVRT (atioventricular reentry tachycardia), the
most common is AVNRT (90%)
Occur in any age individuals, usually nostructure heart disease.
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Paroxysmal tachycardia
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 andunderlying disease
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Paroxysmal tachycardia Therapy:
AVNRT & orthodromic AVRT
1. Increase vagal tone: carotid sinus massage,Valsalva maneuver.if no successful,
2. Drug: verapamil, adrenosine, propafenone
3. DC shock
Antidromic AVRT:
1. Should not use verapamil, digitalis, andstimulate the vagal nerve.
2. Drug: propafenone, sotalol, amiodarone
RFCA
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WPW syndrome
Manifestation:
Palpitation, syncope, dizziness
Arrhythmia: 80% tachycardia isAVRT, 15-30% is AFi, 5% is AF,
May induce ventricular fibrillation
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WPW syndrome Therapy:
1. Pharmacologic therapy: orthodromeAVRT or associated AF, AFi, may use Ic
and III class agents.2. Antidromic AVRT cant use digoxin and
verapamil.
3. DC shock: WPW with SVT, AF or Afiproduce agina, syncope and hypotension
4. RFCA
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Ventricular arrhythmia
Ventricular Premature Contractions (VPCs)
Ventricular tachycardia
Ventricular flutter and fibrillation
Intraventricular Block
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Ventricular Premature Contractions
(VPCs)
Etiology:
1. Occur in normal person
2. Myocarditis, CAD, valve heart disease,
hyperthyroidism, Drug toxicity (digoxin,
quinidine and anti-anxiety drug)
3. electrolyte disturbance, anxiety,
drinking,coffee
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VPCs
Manifestation:
1. palpitation
2. dizziness
3. syncope
4. loss of the second heart sound
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PVCs Therapy:treat underlying disease, antiarrhythmia
No structure heart disease:
1. Asymptom: no therapy
2. Symptom caused by PVCs: antianxiety agents, -
blocker and mexiletine to relief the symptom.
With structure heart disease (CAD, HBP):
1. Treat the underlying diseas
2. -blocker, amiodarone3. Class I especially class Ic agents should be avoided
because of proarrhytmia and lack of benefit of
prophylaxis
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Ventricular tachycardia
Torsades de points (Tdp):A special type ofpolymorphic VT,
Etiology:
1. congenital (Long QT),2. electrolyte disturbance,
3. antiarrhythmia drug proarrhythmia (IA or IC),
4. antianxiety drug,
5. brain disease,
6. bradycardia
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Ventricular Tachycardia
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Ventricular tachycardia
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Treatment of VT
1. Treat underlying disease
2. Cardioversion: Hemodynamic unstable
VT (hypotension, shock, angina, CHF)
or hemodynamic stable but drug was no
effect
3. Pharmacological therapy: -blockers,
lidocain or amiodarone
4. RFCA, ICD or surgical therapy
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Ventricular flutter and fibrillation
Manifestation:
Unconsciousness, twitch, no blood
pressure and pulse, going to die
Therapy:
1. Cardio-Pulmonary Resuscitate(CPR)
2. ICD
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Ventricular Fibrillation
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Cardiac arrest
Asystole Ventricular
fibrillation
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Rhythms Produced by Conduction Block
AV Block (relatively common)
1stdegree AV block
Type 1 2nddegree AV blockType 2 2nddegree AV block
3rddegree AV block
SA Block (relatively rare)
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1stDegree AV Block
EKG Characteristics: Prolongation of the PR interval, which is constant
All P waves are conducted
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/
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2ndDegree AV BlockType 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
EKG Characteristics: Constant PR interval with intermittent failure to conduct
Type 2
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3rdDegree (Complete) AV Block
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
www.uptodate.com
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AV Block
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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AV Block
Treatment:
1. I or II degree AV block neednt
antibradycardia agent therapy2. II degree II type and III degree AV
block need antibradycardia agent
therapy3. Implant Pace Maker
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Intraventricular Block
Etiology: Myocarditis, valve disease, cardiomyopathy,
CAD, hypertension, pulmonary heart
disease, drug toxicity, Lenegre disease,Levs disease et al.
Manifestation:
Single fascicular or bifascicular block isasymptom; tri-fascicular block may havedizziness; palpitation, syncope and Adams-stokes syndrome
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Intraventricular Block
Therapy:
1. Treat underlying disease
2. If the patient is asymptom; no treat,
3. bifascicular block and incomplete
trifascicular block may progress to
complete block, may need implant pace
maker if the patient with syncope
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