1. MECHANISMS OF CARDIAC ARRHYTHMIAS. DR AMNA TAHIR PHYSIOLOGY DEPARTMENT. KEMU.

2. 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.

4. TERMINOLOGIES Brady 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

5. 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.

6. MECHNISMS OF CARDIAC ARRHYTHMIAS 1-Increased automaticity in any part of cardiac tissue 2-Triggered automaticity 3-Re-entry or Circus movement.

7. 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 afterdepolarization 2.Abnormal impulse conduction (more common mechanism) a. AV block – ventricle free to start own pacemaker rhythm b. 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

8. 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.

9. ANS AND SINUS NODE FUNCTION

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

11. MECHANISM OF TRIGGERED ARRHYTHMIAS

13. 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.

14. REENTRY ARRHYTHMIAS

15. TYPICAL ATRIOVENTRICULAR NODAL REENTRY TACHYCARDIA ( AVNRT)

16. SINO-ATRIAL NODE Sinus arrhythmias Sinus tachycardia

18. SINUS TACHYCARDIA.

20. 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.

22. ATRIAL ARRHYTHMIAS. Atrial tachycardia increased automaticity by sympathetic stimulation Atrial flutter re-entry F waves Atrial fibrillation multiple ectopic foci f waves

24. ATRIAL FLUTTER.

25. 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.

26. AV NODAL OR JUNCTIONAL BRADY CARDIAS Heart blocks.

27. 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.

29. 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

30. CARDIAC BRADYARRHYTHMIA-RX Treatment 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

31. CARDIAC TACHYARRHYTHMIA - RX STRATEGIES Long term treatment RF ablation Medication Anticoagulation Devices (pacemaker, AICD) Surgery Short term treatment Electrical Therapy in unstable patients Cardioversion, Defibrillation Control ventricular rate Ventricular rate control Rhythm control: Medical / Electrical Identify and treat reversible causes Considering factors Type of tachyarrhythmia Mechanism of tachyarrhythmia Underlying Cardiovascular pathology Local expertise Patient factors

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