TACHYARRHYTHMIAS pathophysiology and management.pptx

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1. TACHYARRHYTHMIAS DR. PATIENCE MUSELEPETE [Dr S. N. Kanyimba

2. Physiology of a normal heart SA node generates action potential and delivers it to the atria and the AV node The AV node delivers the impulse to Purkinje fibers Purkinje fibres conduct the impulse to the ventricles The passage of ions across the myocyte cell membrane is regulated through specific ion channels that produce cyclical depolarisation and repolarisation of the cell, call an action potential The electrophysiological events can be divided into 5 phases: 0, 1, 2, 3 and 4 Electrophysiology of cardiac cells Phase 0 – Upstroke (Rapid Depolarisation ) Rapid depolarisation of the cell membrane in response to fast inflow of sodium ions Speed of Phase 0 depolarisation determines the velocity of impulse conduction

3. Phase 1 – Partial Repolarisation Short period of repolarisation due to rapid flow of potassium ions Phase 2 - Plateau Slow entry of calcium (a depolarising event) balances the flow of potassium (a repolarising event) resulting in a plateau phase of the action potential Calcium entering the cell is responsible for myocyte contraction Phase 3 - Repolarisation Calcium entry stops and potassium flow increases Potassium flow results in rapid repolarisation Phase 4 – Resting membrane potential (diastole) Fully repolarised state with a trans-membrane potential of -90mv 3

4. Cells that possess automaticity depolarise (due to sodium and calcium entry) till threshold potential (-50mv) when they depolarise rapidly & generate an impulse (Phase 0) Refractory period While depolarized, the cell is resistant (refractory) to a subsequent depolarization event Absolute (effective) refractory period: period of time during which a new action potential cannot be initiated once an action potential is initiated (i.e. period during which a subsequent depolarization is not possible when an action potential has been initiated) Relative refractory period: after partial (but incomplete repolarization), a subsequent depolarization is possible but occurs slowly 4

5. Pacemaker activity Normally the SA node has the most rapid rate of spontaneous diastolic depolarization so its cells produce spontaneous action potentials at a higher frequency than other tissues Thus the SA node is the dominant automatic (pacemaker) tissue in the normal heart If the SA node does not produce impulses, tissue with the next highest automaticity rate (typically the AV node) functions as the pacemaker Sympathetic stimulation increases the discharge frequency of pacemaker tissue and parasympathetic stimulation decreases

6. Non-pacemaker action potential Phase 0: fast upstroke Due to Na + influx Phase 3: repolarization Due to K + efflux Phase 4: resting membrane potential Phase 2: plateu Due to Ca ++ influx Phase 1: partial repolarization Due to rapid efflux of K + N.B. The slope of phase 0 = conduction velocity Also the peak of phase 0 = V max 6

7. Arrhythmia (dysrhythmia) Definition: Abnormality in the site of origin of impulse, rate or conduction Causes of arrhythmias: congenital structural abnormalities, rheumatic heart disease, hypoxia, hypercapnia, electrolyte imbalances, hormonal imbalances, drugs, toxins, arteriosclerosis, coronary artery spasm, myocardial ischaemia If the arrhythmia arises from atria, SA node, or AV node it is called supraventricular arrhythmia If the arrhythmia arises from the ventricles it is called ventricular arrhythmia

8. Pathophysiology of arrhythmias: (1) Abnormal impulse generation (2) Abnormal conduction 9 Delayed afterdepolarization Early afterdepolarization ↑ AP from SA node AP arises from sites other than SA node

9. This is when the impulse is not conducted from the atria to the ventricles 1-This pathway is blocked 2-The impulse from this pathway travels in a retrograde fashion ( backward ) 3-So the cells here will be re-excited (first by the original pathway and the other from the retrograde) 10

10. Clinical classification of arrhythmias Site of origin of the abnormality Atrial Junctional Ventricular Whether rate is increased or decreased Tachyarrhythmias Bradyarrhythmias

11. Supraventricular arrhythmias Sinus tachycardia : high sinus rate of 100-180 beats/min, occurs during exercise or other conditions that lead to increased SA nodal firing rate Atrial tachycardia : a series of 3 or more consecutive atrial premature beats occurring at a frequency >100/min Paroxysmal atrial tachycardia (PAT) : tachycardia which begins and ends in acute manner Atrial flutter : sinus rate of 250-350 beats/min Atrial fibrillation (AF) : uncoordinated atrial depolarizations AV blocks : A conduction block within the AV node , occasionally in the bundle of His, that impairs impulse conduction from the atria to the ventricles

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14. Management of atrial fibrillation (AF) Initial goal: rate control & anti-coagulation Rate control: beta-blockers, calcium channel blockers, digoxin Anti-coagulation: IV heparin, warfarin (target INR 2 - 3) - reduces risk of stroke x3 Eventual goal: restoration & maintenance of sinus rhythm To i mprove cardiac hemodynamics & quality of life & reduce the risk of thromboembolic complications Restoration of sinus rhythm: DC cardioversion Maintenance of sinus rhythm: quinidine, flecainide, propafenone, sotalol and amiodarone 

15. Ventricular arrhythmias Ventricular premature beats (VPBs): caused by ectopic ventricular foci; characterized by widened QRS Ventricular tachycardia (VT): high ventricular rate caused by abnormal ventricular automaticity or by intra-ventricular reentry; can be sustained or non-sustained (paroxysmal); characterized by widened QRS; rates of 100 to 200 beats/min; life-threatening Ventricular flutter : ventricular depolarizations >200/min Ventricular fibrillation (VF) : uncoordinated ventricular depolarizations Torsade de pointes : a polymorphic ventricular tachycardia with a characteristic illusion of a twisting of the QRS complex around the isoelectric baseline. Torsades de pointes can degenerate into ventricular fibrillation which will lead to sudden death in the absence of medical intervention.

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17. Pharmacologic rationale & goals in treatment of arrhythmias The ultimate goal of anti-arrhythmic drug therapy: Restore normal sinus rhythm and conduction Prevent more serious and possibly lethal arrhythmias from occurring Antiarrhythmic drugs are used to: Decrease or increase conduction velocity in tachyarrhythmias and bradyarrhythmias respectively Change the duration of the effective refractory period Suppress abnormal automaticity

18. Anti-arrhythmic drugs 19 Class Mechanism Action Notes I Na + channel blocker (membrane stabilising agents) Reduce maximum rate of depolarisation therefore reduce conduction velocity Can abolish tachyarrhythmia caused by reentry circuit II β blocker ↓ heart rate and conduction velocity Can indirectly alter K and Ca conductance III K + channel blocker ↑ action potential duration (APD) or effective refractory period (ERP) Delay repolarization Inhibit reentry tachycardia IV Ca ++ channel blocker Suppress automatic activity of pacemaker cells ↓ conduction velocity in SA and AV node Most anti-arrhythmic drugs are pro-arrhythmic (promote arrhythmia) They are classified according to Vaughan William into four classes according to their effects on the cardiac action potential

19. Class 1B drugs – Na + channel blockers Shorten action potential and therefore decrease the effective refractory period Examples: lignocaine , mexiletine , phenytoin Class II – Beta adrenergic blockers Examples: propranolol, metoprolol, esmolol Esmolol is a very short-acting β 1 blocker that is used by intravenous route in acute arrhythmias occurring during surgery or emergencies. Class III – K + channel blockers Block potassium channels Delay repolarization (prolong action potential) thereby prolonging effective refractory period Examples: amiodarone, sotalol, ibutilide , dofetilide and bretylium Can all cause Torsade de pointes 20

20. Digitalis: digoxin & digitoxin Enhances vagal activity (stimulates central vagal nuclei) Through this action, digitalis: Decreases automaticity of SA node Slows AV conduction Increases refractoriness of the AV node Shortens refractory period of atrial muscle cells Decreases myocardial excitability Uses Ventricular rate control in atrial fibrillation Contra-indication Supraventricular arrhythmias associated with accessory conducting pathways (e.g. Wolf-Parkinson-White syndrome) 21

21. Digitalis: adverse effects Cardiac: ectopic dysrhythmias (ventricular ectopic beats), ventricular tachydysrhythmias , paroxysmal supraventricular tachycardia, bradycardia & heart block, and ventricular fibrillation CNS: confusion, restlessness, agitation, nightmares, acute psychosis GIT: anorexia, nausea, vomiting, diarrhoea Visual: disturbances of colour vision, photophobia, blurring Others: gynaecomastia 22

22. Proposed anti-arrhythmic drugs of choice for long term treatment of AF Selection is based on underlying heart disease: Structurally normal heart and young age - propafenone, flecainide, sotalol Coronary artery disease - sotalol, amiodarone Congestive heart failure - amiodarone Left ventricular hypertrophy – sotalol Atrial flutter Treatment of symptomatic atrial flutter: Ventricular rate control - drugs that block the AV node: IV calcium channel blockers or beta-blockers can be used, followed by initiation of oral agents Termination of sustained episodes - (1) Electrical cardioversion: 50 - 100 J (2) Pharmacological cardioversion: procainamide, flecainide, propafenone, amiodarone (3) Atrial overdrive pacing (4) Combination therapy of above 23

23. References: Medscape Dr N.S Kanyimba PPT Cadiovascular physiology 9 th edition LANGE 24