MECHANISMS OF CARDIAC ARRHYTHMIAS.

DR AMNA TAHIR

PHYSIOLOGY DEPARTMENT.

KEMU.

CRITERIA FOR NORMAL CARDIAC RHYTHM

Heart Rate between 60-100 beats per minute

Every heart beat originate from SA node

All cardiac impulses should pass through normal conduction pathway.

It should pass through normal pathway with normal velocity.

TERMINOLOGIESBrady arrhythmias

Tachy arrhythmias---100-150 simple tachyarrhythmia

If 150-250 HR --paroxysmal tachy arrhythmia

If HR 250-350---flutters atrial or ventricular

If HR above350---fibrillation atrial or ventricular(medical emergency)

If HR 40-60mild brady

If HR 20-40moderate

If HR <20severe

CLASSIFICATION ACCORDING TO SITE OF ORIGIN OF ABNORMAL RHYTHM.

From SA node—Sinus arrhythmias

From atrial muscle—atrial arrhythmias

From AV node—junctional or nodal arrhythmias

From ventricles---ventricular arrhythmias

First three are known as SVT or supraventricular tachy arrhythmias.

MECHNISMS OF CARDIAC ARRHYTHMIAS

1-Increased automaticity in any part of cardiac tissue

2-Triggered automaticity

3-Re-entry or Circus movement.

MECHANISMS OF ARRHYTHMIAS

1. Abnormal impulse generation (abnormal automaticity)a. increased automaticity of normally automatic cells (SA, AV, His)b. generation of impulses in normally non-automatic cells

- development of phase 4 depolarization in normally non-automatic cells- ‘triggered activity’ due to afterdepolarizations

- early afterdepolarization2.Abnormal impulse conduction (more common

mechanism)a. AV block – ventricle free to start own pacemaker rhythmb. Re-entry: re-excitation around a conducting loop, which produces tachycardia

- unidirectional conduction block- establishment of new loop of excitation- conduction time that outlasts refractory period

INCREASED AUTOMATICITY.

SA node under goes depolarization spontaneously. Why? Under effect of sympathetic stimulation and sinus tachycardia.

Early after depolarization or late after depolarization---triggered automaticity.injury or catecholamines—produce cationic load leading to triggering.

ANS AND SINUS NODE FUNCTION

Early after depolarization or late after depolarization---triggered automaticity. Injury to myocardium or catecholamine's or caffeine —produce cationic load leading to triggering.

MECHANISM OF TRIGGERED ARRHYTHMIAS

MECHANISM OF TRIGGERED ARRHYTHMIAS

RE-ENTRY.

If cardiac impulse moves around an electrically dead area and on one side of this area impulse is blocked.The other side impulse reaches the previously blocked area and finds it excitable and enters into it .then it starts moving in circles increasing the heart rate.

REENTRY ARRHYTHMIAS

TYPICAL ATRIOVENTRICULAR NODAL REENTRY TACHYCARDIA ( AVNRT)

SINO-ATRIAL NODE

Sinus arrhythmias

Sinus tachycardia

SINUS TACHYCARDIA.

SINUS BRADYCARDIA.

Athletes have increased vagal tone

Hypothyroidism

Hypothermia

Cholestasis jaundice –bile salts accumulate and slow down SA node.

Sick sinus syndrome—is tachy- brady syndrome due to variations in SA node firing.

ATRIAL ARRHYTHMIAS.

Atrial tachycardia increased automaticity by sympathetic stimulation

Atrial flutter re-entry F waves

Atrial fibrillation multiple ectopic foci f waves

ATRIAL FLUTTER.

AV NODE OR JUNCTIONAL ARRHYTHMIAS.

Av node specialized electrical connection between atria and ventricles.

AV node is specialized in slow conduction.AV-nodal delay.

Juntional tachy and brady arrhythmias.

RMP is -60 mv.fast Na channels are closed.

If something slow down AV node PR segment prolonged.

Caffine increases AN node conduction and shortening of PR segment.

AV NODAL OR JUNCTIONAL BRADY CARDIAS

Heart blocks.

WPW SYNDROME.

Re-entrent tachy cardia through bundle of Kent

Avoid coffee, smoking ,stress,anxiety.this can produce an ectopic and start re-entry through the bundle of Kent.

The slurring of QRS and short PR-interval.PJ interval is normal however.

VENTRICULAR ARRHYTHMIAS.Irritable foci –extra systole.

Ischemia or injury—less oxygen supply—less ATP produced –decreased Na-K pumping—cationic load in side vent muscle cell—RMP fluctuate and when touches threshold level it fires—giving rise to VPCs and V-Tach

Caffiene –inhibit phosphodiesterase and increase cAMP—protein kinse A—phosphorylation of Ca Channels—cationic load—Fluctuating RMP—late after depolarizations.

Ventricular Tachycardia.

Ventricular flutter

Ventricular fibrillation

CARDIAC BRADYARRHYTHMIA-RXTreatment strategy

Short term Rx

Treat reversible / underlying causes

Medication to increase heart rate

Temporary pacemaker

Long term Rx

Permanent pacemaker

Factors

Type of bradyarrhythmia

Severity of symptoms

Severity of underlying cardiac pathology

Severity of co-morbid diseases

CARDIAC TACHYARRHYTHMIA - RX STRATEGIES

Long term treatmentRF ablationMedicationAnticoagulationDevices (pacemaker, AICD)Surgery

Short term treatmentElectrical Therapy in unstable patients

Cardioversion, Defibrillation Control ventricular rate

Ventricular rate controlRhythm control: Medical / Electrical

Identify and treat reversible causes

Considering factorsType of tachyarrhythmiaMechanism of tachyarrhythmiaUnderlying Cardiovascular pathologyLocal expertisePatient factors

THANK YOU FOR YOUR ATTENTION