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Pharmacotherapy of arrhythmia
The document covers the topic of cardiac arrhythmias, providing definitions, mechanisms, clinical presentations, and treatment options, particularly pharmacotherapy. It emphasizes that arrhythmias can range from asymptomatic to life-threatening and highlights the importance of non-pharmacological treatment alongside drug therapy. The document also categorizes antiarrhythmic agents and discusses the drugs used for managing various types of arrhythmias.
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Pharmacotherapy of arrhythmia
- 1. Pharmacotherapy: Cardiac Arrhythmias Dr. PravinPrasad MBBS, MD Clinical Pharmacology Assistant Professor, Department of Clinical Pharmacology Maharajgunj Medical Campus, Kathmandu 15 June 2020 (1 Asar 2077), Monday
- 2. By the endof this class, B. Pharm 2nd year students will be able to: Define the term arrhythmia Explain the basic mechanism of arrhythmias List the clinical presentation of arrhythmias Outline the therapeutic objective and treatment options of arrhythmias Explain the pharmacotherapy of arrhythmia List the drugs used for treatment of different arrhythmias
- 3. Introduction Arrhythmia isloss of cardiac rhythm, especially irregularity of heartbeat Can be physiological as well as pathological Arrhythmias may require treatment if: Rhythms that are too rapid, too slow, or asynchronous leading to reduced cardiac output Has potential to precipitate more serious or even lethal rhythm disturbances Asymptomatic or minimally symptomatic arrhythmias should not be treated with drugs Anti-arrhythmic drugs can precipitate lethal arrhythmias
- 4. The normal conductionpathway
- 5.
- 6. Arrhythmias: Mechanism Basicmechanism: Disturbances in impulse formation Disturbances in impulse conduction Precipitating factors: Ischemia, hypoxia Acidosis or alkalosis, electrolyte abnormalities Excessive catecholamine exposure, autonomic influences Drug toxicity (eg, digitalis or antiarrhythmic drugs) Overstretching of cardiac fibers Presence of scarred or otherwise diseased tissue
- 7. Arrhythmias: abnormal impulse formation Enhanced/ectopic pacemaker activity From the automatic fibres of heart Damaged tissue of heart
- 8. Arrhythmias: abnormal impulse formation After-depolarizations Secondary depolarizations accompanying a normal or premature action potential Early after-depolarization (EAD) Large impulse is generated during repolarization that gets propagated
- 9. Arrhythmias: abnormal impulse formation After-depolarizations Secondary depolarizations accompanying a normal or premature action potential Delayed after-depolarization (DAD): Secondary deflection after reaching RMP Generally results from Ca2+ overload (digitalis toxicity, ischaemia- reperfusion).
- 10. Arrhythmias: Abnormal impulse transmission Reentry Primarily due to abnormality of conduction Impulse recirculate and cause repetitive activation Are called reentrant arrhythmias Of several types: Circus movement entry Functional re-entry Fractionation of impulse
- 11. Clinical Presentation Supraventriculartachycardias: No symptoms to minor palpitations or irregular pulse to severe and even life-threatening symptoms Dizziness or acute syncopal episodes, symptoms of HF, anginal chest pain, or a choking or pressure sensation during the tachycardia episode AF or atrial flutter: Similar to SVTs, but syncope is uncommon Embolic stroke
- 12. Clinical Presentation PrematureVentricular Contractions: Mild palpitations Ventricular tachycardia: Totally asymptomatic to pulseless hemodynamic collapse Ventricular proarrhythmia: No symptoms to worsening of symptoms to sudden death Ventricular Fibrillation: Hemodynamic collapse, syncope, and cardiac arrest
- 13. Clinical Presentation Brady-arrhythmias Symptomssuggestive of hypotension: dizziness, syncope, fatigue, and confusion Associated with LV dysfunction: worsening HF symptoms.
- 14. Treatment Objectives Donot treat asymptomatic arrhythmias Aim of therapy: Reduce ectopic pacemaker activity Blockade of Na+ or Ca2+ channels, beta receptor blockade Modify conduction or refractoriness in reentry circuits to disable circus movement Additional objectives: Prevent future episodes of arrhythmias Avoid complications (embolism)
- 15. Treatment options ofArrhythmia General Information Non-pharmacological treatment Pharmacological treatment Referral All arrhythmias need not be treated Physiological arrhythmias subsides by itself
- 16. Treatment options ofArrhythmia General Information Non-pharmacological treatment Pharmacological treatment Referral • Surgical Procedures: • Radiofrequency catheter ablation • Cryoablation • Permanent pacemaker implantation • Implantable cardio-defibrillator • Carotid sinus massage
- 17. Treatment options ofArrhythmia General Information Non-pharmacological treatment Pharmacological treatment Referral • Drugs to terminate an episode of arrhythmia • Drugs to prevent future episodes of arrhythmia • Drug to prevent development of complications • Heart failure • Haemodynamic collapse • Anti-thrombotic
- 18.
- 19. Other Anti-dysrhythmic drugs Drugsnot classified by Williams Drugs Use Atropine Sinus bradycardia Adrenaline Cardiac Arrest Isoprenaline Heart block Digoxin Rapid atrial fibrillation Adenosine Supraventricular tachycardia Calcium chloride Ventricular tachycardia due to hyperkalemia Magnesium chloride Ventricular fibrillation, digoxin toxicity 19
- 20. Clinical Classification: Anti- dysrhythmicdrugs Supraventricular arrhythmias only Supraventricular and ventricular arrhythmias Ventricular arrhythmias only • Adenosine • Verapamil, Diltiazem • Dronedarone • Digoxin • Amiodarone • β – blockers • Sotalol • Propranolol • Esmolol • Procainamide • Disopyramide • Quinidine • Flecainide • Propafenone • Lidocaine • Mexiletine 20
- 21. Arrhythmias and Choiceof treatment
- 22. Arrhythmias and Choiceof treatment
- 23. Conclusion Arrhythmia isloss of cardiac rhythm, especially irregularity of heartbeat Occurs due to improper impulse formation and/or conduction Can present asymptomatically to life threatening condition Non-pharmacological treatment is most effective in arrhythmia Drugs act by inhibiting either of Na+, K+, Ca2+ ions or blocking beta receptors Amiodarone is used for multiple arrhythmias
Editor's Notes
- #4 Arrhythmias may require treatment because rhythms that are too rapid, too slow, or asynchronous can reduce cardiac output Some arrhythmias can precipitate more serious or even lethal rhythm disturbances; for example, early premature ventricular depolarizations can precipitate ventricular fibrillation. In such patients, antiarrhythmic drugs may be lifesaving. On the other hand, the hazards of antiarrhythmic drugs—and in particular the fact that they can precipitate lethal arrhythmias in some patients—have led to a reevaluation of their relative risks and benefits. In general, treatment of asymptomatic or minimally symptomatic arrhythmias should be avoided for this reason.
- #8 Enhanced/ectopic pacemaker activity The slope of phase-4 depolarization may be increased pathologically in the automatic fibres or such activity may appear in ordinary fibres. Ectopic impulse may also result from current of injury. Myocardial cells damaged by ischaemia become partially depolarized: a current may flow between these and normally polarized fibres (injury current) and initiate an impulse.
- #9 After-depolarizations These are secondary depolarizations accompanying a normal or premature action potential (AP), Fig. 38.1. Early after-depolarization (EAD): Repolarization during phase-3 is interrupted and membrane potential oscillates. If the amplitude of oscillations is sufficiently large, neighbouring tissue is activated and a series of impulses are propagated. EADs are frequently associated with long Q-T interval due to slow repolarization and markedly prolonged APs. They result from depression of delayed rectifier K+ current.
- #10 After-depolarizations These are secondary depolarizations accompanying a normal or premature action potential (AP), Fig. 38.1. Delayed after-depolarization (DAD): After attaining resting membrane potential (RMP) a secondary deflection occurs which may reach threshold potential and initiate a single premature AP. This generally results from Ca2+ overload (digitalis toxicity, ischaemia-reperfusion).
- #11 Circus movement entry: often responsible for PSVT, atrial flutter and atrioventricular reciprocal rhythm in WPW.
- #12 Supraventricular tachycardias may cause clinical manifestations ranging from no symptoms to minor palpitations or irregular pulse to severe and even life-threatening symptoms. Patients may experience dizziness or acute syncopal episodes, symptoms of HF, anginal chest pain, or, more often, a choking or pressure sensation during the tachycardia episode. AF or atrial flutter may be manifested by the entire range of symptoms associated with other supraventricular tachycardias, but syncope is uncommon. Arterial embolization from atrial stasis and poorly adherent mural thrombi may result in embolic stroke.
- #13 PVCs often cause no symptoms or only mild palpitations. The presentation of VT may vary from totally asymptomatic to pulseless hemodynamic collapse. Consequences of proarrhythmia range from no symptoms to worsening of symptoms to sudden death. VF results in hemodynamic collapse, syncope, and cardiac arrest.
- #15 Modify conduction or refractoriness in reentry circuits to disable circus movement Decrease the number of available Na+ channels decreased current Increased time to reach to resting state (prolonged refractory period)