ARRHYTHMIA

dr Putra hendra SpPD UNIBA

Normal Impulse Conduction

Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers

Impulse Conduction & the ECG

Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers

Sifat sifat otot Jantung

Inherent 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.

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 with an intrinsic rate of 20 - 45 bpm.

Sinus rhythm
Sinoatrial node is cardiac pacemaker Normal sinus rhythm 60100 beats/min Depolarisation triggers depolarisation of atrial myocardium (forest fire) Conducts more slowly through AV node Conducts rapidly through His bundles and Purkinje fibres

 Definition of Arrhythmia: The Origin, Rate, Rhythm, Conduct velocity and sequence of heart activation are abnormally.

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

Classification of Arrhythmia
Abnormal heart pulse formation
1. 2. 3. 4. 1. 2. 3. 4. Sinus arrhythmia Atrial arrhythmia Atrioventricular junctional arrhythmia Ventricular arrhythmia Sinus-atrial block Intra-atrial block Atrio-ventricular block Intra-ventricular block

Abnormal heart pulse conduction

Abnormal heart pulse formation and conduction

Diagnosis of Arrhythmia
Medical history Physical examination Laboratory test

Management of arrhythmias
Acute Acute management (clinical assessment of patient and diagnosis) Prophylaxis Chronic Non-pharmacological Pharmacological (some antiarrhythmics are also proarrhythmic)

Non-pharmacological treatment
Acute
Vagal manoeuvres DC cardioversion

Prophylaxis
Radiofrequency ablation Implantable defibrillator

Pacing (external, temporary, permanent)

Phases of action potential of cardiac cells

Phase 0 rapid depolarisation (inflow of Na+) Phase 1 Phase 1 partial repolarisation (inward Na+ current deactivated, 0 mV outflow of K+) Phase 2 plateau (slow inward Phase 0 calcium current) I Phase 3 repolarisation (calcium current inactivates, K+ outflow) Phase 4 pacemaker potential (Slow-80mV Phase 4 II Na+ inflow, slowing of K+ outflow) autorhythmicity Refractory period (phases 1-3)

IV
Phase 2

III
Phase 3

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 potential and prolong refractory period (suppress re-entrant rhythms) (amiodarone, sotalol) Class IV: Calcium channel antagonists. Impair impulse propagation in nodal and damaged areas (verapamil)
Phase 1

IV
0 mV Phase 0 Phase 2

III
Phase 3

-80mV

Phase 4

II

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

Anti-arrhythmia Agents
Anti-tachycardia agents Anti-bradycardia agents

Anti-tachycardia agents
1. 2. 3. 4. 5. 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, Digitalis

Anti-bradycardia agents
Isoprenaline Epinephrine Atropine Aminophylline

Sinus Arrhythmia
Sinus tachycardia Sinus Bradycardia Sinus Arrest Sinu atrial exit block (SAB Sick sinus syndrome (SSS)

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, myocarditis 3. Some drugs: Atropine, Isoprenaline Neednt therapy

Sinus Bradycardia
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.

Atrial arrhythmia
Atrial premature contractions (APCs) Atrial tachycardia Atrial flutter Atrial fibrillation

SVT

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 angina and CHF.

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

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

Paroxysmal tachycardia
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.

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 and underlying disease

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, and stimulate the vagal nerve. 2. Drug: propafenone, sotalol, amiodarone RFCA

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

WPW syndrome
Therapy: 1. Pharmacologic therapy: orthodrome AVRT 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 Afi produce agina, syncope and hypotension 4. RFCA

Ventricular arrhythmia
Ventricular Premature Contractions (VPCs) Ventricular tachycardia Ventricular flutter and fibrillation Intraventricular Block

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

VPCs
1. 2. 3. 4. Manifestation: palpitation dizziness syncope loss of the second heart sound

PVCs
1. 2. 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): 1. Treat the underlying diseas 2. -blocker, amiodarone 3. Class I especially class Ic agents should be avoided because of proarrhytmia and lack of benefit of prophylaxis

Ventricular tachycardia

1. 2. 3. 4. 5. 6.

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

Ventricular Tachycardia

Ventricular tachycardia

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

Ventricular flutter and fibrillation

Manifestation: Unconsciousness, twitch, no blood pressure and pulse, going to die Therapy: 1. Cardio-Pulmonary Resuscitate (CPR) 2. ICD

Ventricular Fibrillation

Cardiac arrest

Asystole

Ventricular fibrillation

Rhythms Produced by Conduction Block

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)

st 1

Degree AV 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

nd 2

Degree AV Block
Type 1 (Wenckebach) 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:

Type 2

EKG Characteristics:

Constant PR interval with intermittent failure to conduct

3rd Degree (Complete) AV Block

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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

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

AV Block
Treatment: 1. I or II degree AV block neednt antibradycardia agent therapy 2. II degree II type and III degree AV block need antibradycardia agent therapy 3. Implant Pace Maker

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 is asymptom; tri-fascicular block may have dizziness; palpitation, syncope and Adamsstokes syndrome

Intraventricular Block
1. 2. 3. 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