Anti-Dysrhythmic Drugs PDF

Dysrhythmias Cardiovascular Medications Part II  Dysrhythmia Dysrhythmia – An abnormality in the rhythm of the heartbeat (also known as arrhythmias) – Arises from impulse formation disturbances Tachydysrhythmias: SVT and ventricular Bradydysrhythm...

Dysrhythmias Cardiovascular Medications Part II  Dysrhythmia Dysrhythmia – An abnormality in the rhythm of the heartbeat (also known as arrhythmias) – Arises from impulse formation disturbances Tachydysrhythmias: SVT and ventricular Bradydysrhythmias Virtually all drugs that treat dysrhythmias can also cause dysrhythmias  Electrical Properties of the Heart Impulse conduction: pathways and timing – Sinoatrial (SA) node: pacemaker of heart – Atrioventricular (AV) node – His-Purkinje system Fig. 49–1. Cardiac conduction pathways.  The Electrocardiogram Provides a graphic representation of cardiac electrical activity Major components of an ECG – P wave Depolarization in the atria – QRS complex Depolarization of the ventricles – T wave Repolarization of the ventricles Three other components – PR interval – QT interval – ST segment Fig. 49–3. The electrocardiogram.  Generation of Dysrhythmias Two fundamental causes Disturbances of automaticity Disturbances of conduction – Atrioventricular block – Reentry (recirculating activation)  Classification of Antidysrhythmic Drugs Vaughan Williams classification – Class I: sodium channel blockers – Class II: beta blockers – Class III: potassium channel blockers – Class IV: calcium channel blockers – Other: adenosine, digoxin, and ibutilide  Common Dysrhythmias and Their Treatment Supraventricular – Impulse arises above the ventricle – Atrial fibrillation – Atrial flutter – Sustained supraventricular tachycardia (SVT) Ventricular – Sustained ventricular tachycardia – Ventricular fibrillation – Ventricular premature beats – Digoxin-induced ventricular dysrhythmias – Torsades de pointes Atrial Flutter Atrial Fib Ventricular Fib Ventricular Tachycardia  Principles of Antidysrhythmic Drug Therapy Balancing risks and benefits – Consider properties of dysrhythmias Sustained vs. nonsustained Asymptomatic vs. symptomatic Supraventricular vs. ventricular Acute and long-term treatment phases Minimizing risk  Class I: Sodium Channel Blockers Class IA agents Class IB agents Class IC agents  Class IA Agents Quinidine Quinidine (cont’d) – Effects on the heart – Adverse effects Blocks sodium channels Diarrhea Slows impulse conduction Cinchonism: Quinidine Delays repolarization overdose Blocks vagal input to the Cardiotoxicity heart Arterial embolism – Effects on ECG Alpha-adrenergic Widens the QRS complex blockade, resulting in Prolongs the QT interval hypotension – Therapeutic uses Hypersensitivity reactions Used against – Drug interactions supraventricular and Digoxin ventricular dysrhythmias  Class IB Agents Lidocaine (Xylocaine) – Effects on the heart and ECG Blocks cardiac sodium channels – Slows conduction in the atria, ventricles, and His-Purkinje system Reduces automaticity in the ventricles and His- Purkinje system Accelerates repolarization – Adverse effects CNS effects Drowsiness Confusion Paresthesias  Class IC Agents Block cardiac sodium channels Delay ventricular repolarization All class IC agents can exacerbate existing dysrhythmias and create new ones Two class IC agents – Flecainide – Propafenone  Class II: Beta Blockers Beta-adrenergic blocking agents – Only four approved for treating dysrhythmias 1. Propranolol 2. Acebutolol 3. Esmolol 4. Sotalol  Class II: Beta Blockers Propranolol (Inderal): Propranolol (Inderal) nonselective beta- (cont’d) adrenergic antagonist – Adverse effects – Effects on the heart and ECG Heart block Decreased automaticity of the Heart failure SA node AV block Decreased velocity of Sinus arrest conduction through the AV Hypotension node Bronchospasm (in asthma Decreased myocardial patients) contractility Other class II: beta blockers – Therapeutic use – Acebutolol (Sectral) Dysrhythmias caused by – Esmolol (Brevibloc) excessive sympathetic stimulation Supraventricular tachydysrhythmias – Suppression of excessive discharge – Slowing of ventricular rate  Class III: Potassium Channel Blockers Amiodarone (Cordarone, Pacerone) – Therapeutic use Recurrent ventricular fibrillation Recurrent hemodynamically unstable ventricular tachycardia  Class III: Potassium Channel Blockers Amiodarone Amiodarone (Cordarone, Pacerone) (Cordarone, Pacerone) (cont’d) (cont’d) – Effects on the heart and – Drug interactions ECG (increases levels) QRS widening Quinidine Prolongation of the PR Cyclosporine and QT intervals Digoxin Reduced automaticity in Procainamide the SA node Diltiazem Reduced contractility Phenytoin Reduced conduction Warfarin velocity Lovastatin, simvastatin, atorvastatin  Class III: Potassium Channel Blockers Amiodarone (Cordarone, Pacerone) (cont’d) – Adverse effects Protracted half-life Pulmonary toxicity Cardiotoxicity Toxicity in pregnancy and breast-feeding Corneal microdeposits Optic neuropathy  Class III: Potassium Channel Blockers The risk of severe dysrhythmias is increased by diuretics (because they can reduce levels of potassium and magnesium) and by drugs that prolong the QT interval, of which there are many (see Chapter 7) Combining amiodarone with a beta blocker, verapamil, or diltiazem can lead to excessive slowing of heart rate  Class IV: Calcium Channel Blockers Verapamil (Calan, Isoptin, Verelan) and diltiazem (Cardizem) – Reduce SA nodal automaticity – Delay AV nodal conduction – Reduce myocardial contractility – Therapeutic uses Slow ventricular rate (atrial fibrillation or atrial flutter) Terminate SVT caused by an AV nodal reentrant circuit  Class IV: Calcium Channel Blockers Verapamil (Calan, Isoptin, Verelan) and diltiazem (Cardizem) (cont’d) – Adverse effects Bradycardia Hypotension AV block Heart failure Peripheral edema Constipation Can elevate digoxin levels Increased risk when combined with a beta blocker  Other Antidysrhythmic Drugs Digoxin (Lanoxin) – Primary indication is heart failure – Also used to treat supraventricular dysrhythmias (inactive against ventricular dysrhythmias) Suppresses dysrhythmias by decreasing conduction through AV node and automaticity in the SA node QT interval may be shortened – Adverse effect: cardiotoxicity Risk increased by hypokalemia