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Prof. Hardi Darmawan, MD, MPH&TM.,FRSTM Department of Physiology & Biophysic ARRHYTHMIA

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  • Prof. Hardi Darmawan, MD, MPH&TM.,FRSTM

    Department of Physiology & Biophysic

    ARRHYTHMIA

  • Definition of Arrhythmia:The Origin, Rate, Rhythm, Conduct

    velocity and sequence of heart

    activation are abnormally.

    2

  • Arrhythmia

    ARRHYTHMIA VARIATION IN NORMAL RHYTHM

    DYSRHYTHMIA ABNORMAL, DISTURBED RHYTHM

    RESULTS FROM IMPULSE

    FORMATION DISTURBANCE OR

    CONDUCTION DISTURBANCE

    3

  • AXIOM

    ALL RHYTHM INTERPERTATION MUST

    BE CORRELATED WITH SIGNS &

    SYMPTOMS AND PATIENT

    CONDITION

    TREAT THE PATIENT,

    NOT THE MONITOR4

  • Impulse formation

    (site of impulse origin)

    SA Node

    AV Node

    Ventricle

    Ectopic

    Premature Beat

    Dysrhythmia

    5

  • Anatomy of the conducting system

    6

  • Normal Sinus Rhythm NORMAL SINUS RHYTHM IS PRODUCED BY

    THE SA NODE

    P WAVE FOLLOWS QRS COMPLEX IN A PREDICTABLE RELATIONSHIP

    ALL P WAVES LOOK ALIKE, ALL QRS COMPLEXES ARE NARROW

    R R INTERVAL IS REGULAR

    RATE: 60 100 bpm

    7

  • Normal Sinus Rhythm

    8

  • Normal Sinus Rhythm

    9

  • Sinus / Atrial dysrhythmia

    ORIGINATE FROM SA NODE OR ATRIA

    (ABOVE VENTRICLES)

    CONDUCTION WITH VENTRICLE IS UNDISTURBED

    USUALLY BENIGN & SYMPTOMATIC

    RHYTHM MAY BE IRREGULAR

    10

  • SINUS TACHYCARDIA SINUS BRADYCARDIAATRIAL FIBRILLATIONATRIAL FLUTTER Premature atrial contractions Paroxysmal atrial tachycardia Supraventricular Tachycardia

    Sinus / Atrial dysrhythmia

    11

  • Dysrhythmia

    Bradycardia / Tachycardia

    Flutter / Fibrillation

    Heart blocks

    12

  • 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

    13

  • Occurrence/Incidence

    80 % of patient AMI

    50 % of anesthetized patient

    25 % of digitalis patient

    14

  • 15

    Etiology Physiological

    Pathological:Valvular heart disease.Ischemic heart disease.Hypertensive heart diseases.Congenital heart disease.Cardiomyopathies.Carditis.RV dysplasia.Drug related.Pericarditis. Pulmonary diseases.Others.

  • Mechanism of Arrhythmia

    Abnormal heart pulse formation1. Sinus pulse2. Ectopic pulse3. Triggered activity

    Abnormal heart pulse conduction1. Reentry2. Conduct block

    16

  • 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 block3. Atrio-ventricular block4. Intra-ventricular block

    Abnormal heart pulse formation and conduction17

  • Classification of Arrhythmia

    18

    1. Characteristics: a. flutter very rapid but regular contractions b. tachycardia increased rate c. bradycardia decreased rate d. fibrillation disorganized contractile activity

    2. Sites involved: a. ventricular b. atrial c. sinus d. AV node e. Supraventricular (atrial myocardium or AV node)

  • 19

    Common Arrhythmias

    Atrial

    AF

    A Flutter

    Paroxs. SVT AVNRT

    AVRT (WPW)

    Multifocal atrial tachycardia

    Ventricular

    VT

    VF

    Torsades

    Bradyarrhytmia

    Medication

    AV block

    SSS

  • Ventricular fibrillation

  • Basic Rhythm Strip Interpretation

    1. Determine the rate. Does the atrial rate equal the ventricular rate.

    2. Is the rhythm regular/irregular?

    3. Find the P wave. Is there a P wave for every QRS?

    4. Determine the PRI (Normal 0.12-0.20 sec)

    5. Find the QRS (Normal

  • Diagnosis of Arrhythmia

    Medical history

    Physical examination

    Laboratory test

    25

  • Therapy Principal

    Pathogenesis therapy

    Stop the arrhythmia immediately if the hemodynamic was unstable

    Individual therapy Personalized Medicine

    26

  • Arrhythmia Assessment ECG

    24h Holter monitor

    Echocardiogram

    Stress test

    Coronary angiography

    Electrophysiology study

  • Arrhythmia Presentation Palpitation.

    Dizziness.

    Chest Pain.

    Dyspnea.

    Fainting.

    Sudden cardiac death.

  • Strategy of Antiarrhythmic Agents

    Suppression of dysrhythmias

    A. Alter automaticityi. decrease slope of Phase 4

    depolarizationii. increase the threshold potentialiii. decrease resting (maximum

    diastolic) potential

    B. Alter conduction velocityi. mainly via decrease rate of

    rise of Phase 0 upstrokeii. decrease Phase 4 slopeiii. decrease membrane restingpotential and responsiveness

    C. Alter the refractory periodi. increase Phase 2 plateau

    ii. increase Phase 3 repolarization

    iii. increase action potential duration

  • antiarrhythmic agents:

    There are five main classes in the Vaughan

    Williams classification of antiarrhythmic agents:

    1.Class I agents interfere with the sodium (Na+)

    channel.

    2.Class II agents are anti-sympathetic nervous

    system agents. Most agents in this class are beta

    blockers.

    3.Class III agents affect potassium (K+) efflux.

    4.Class IV agents affect calcium channels and the

    AV node.

    5.Class V agents work by other or unknown

    mechanisms

  • Anti-arrhythmia Agents

    Anti-tachycardia agents

    Anti-bradycardia agents

    31

  • 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, Digital

    32

  • Anti-bradycardia agents

    1. -adrenic receptor activator

    2. M-cholinergic receptor blocker

    3. Non-specific activator

    33

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