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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