Dysrhythmias

• Dysrhythmia


  An abnormality in the rhythm of the heartbeat (also known as arrhythmia)
• Dysrhythmia


  • Arises from impulse formation disturbances
  • Tachydysrhythmias: Supraventricular (SVT) and ventricular
  • Bradydysrhythmias
• Virtually all drugs that treat dysrhythmias can also cause dysrhythmias
• Impulse conduction


  • Pathways and timing
  • Sinoatrial (SA) node: Pacemaker of the heart
  • Atrioventricular (AV) node
  • His-Purkinje system
• Fast potentials


  • Occur in fibers of the His-Purkinje system and in atrial and ventricular muscle
  • Five distinct phases: Depolarization, (Partial) repolarization, Plateau, Repolarization, Stable potential
• Slow potentials


  • Occur in cells of the SA node and AV node
  • Phase 0: Slow depolarization mediated by calcium influx
  • Phases 1, 2, and 3: Phase 1 absent, Phases 2 and 3 not significant
  • Phase 4: Depolarization
• Electrocardiogram (ECG)


  • Provides a graphic representation of cardiac electrical activity
  • Major components: P wave, QRS complex, T wave, PR interval, QT interval, ST segment
• Generation of dysrhythmias


  • Disturbances of automaticity can occur in any part of the heart
  • Disturbances of conduction: Atrioventricular block, Reentry (recirculating activation)
• Vaughan Williams classification of antidysrhythmic drugs

  • Class I: Sodium channel blockers
  • Class II: Beta blockers
  • Class III: Potassium channel blockers
  • Class IV: Calcium channel blockers
  • Other: Adenosine, digoxin, and ibutilide
• Prodysrhythmic effects of antidysrhythmic drugs

  Prolongation of the QT interval, Torsades de pointes
• Common dysrhythmias and their treatment

  • Supraventricular: Atrial fibrillation, Atrial flutter, Sustained supraventricular tachycardia (SVT)
  • Ventricular: Sustained ventricular tachycardia, Ventricular fibrillation, Premature ventricular complexes, Digoxin-induced ventricular dysrhythmias, Torsades de pointes
• Principles of antidysrhythmic drug therapy

  • Balancing risks and benefits
  • Consider properties of dysrhythmias: Sustained versus nonsustained, Asymptomatic versus symptomatic, Supraventricular versus ventricular
  • Acute and long-term treatment phases
  • Minimizing risk
• Class IA sodium channel blockers

  • Block sodium channels, Slow impulse conduction, Delay repolarization, Block vagal input to the heart
  • Effects on ECG: Widens the QRS complex, Prolongs the QT interval
• Class IA agents


  • Quinidine
• Quinidine adverse rxns and interactions


  • Adverse effects: Diarrhea, Cinchonism, Cardiotoxicity, Arterial embolism, Alpha-adrenergic blockade resulting in hypotension, Hypersensitivity reactions
  • Drug interactions: Digoxin - double dig levels
• Class IB agents


  • Mexiletine
• Class IC agents


  • Block cardiac sodium channels, Delay ventricular repolarization, Can exacerbate existing dysrhythmias and create new ones
• Class IC agents


  • Flecainide, Propafenone
• Class II: Beta blockers approved for treating dysrhythmias


  • Propranolol, Acebutolol, Esmolol, Sotalol
• Propranolol (Class II)


  • Decreased automaticity of the SA node, Decreased velocity of conduction through the AV node, Decreased myocardial contractility
  • Therapeutic use: Dysrhythmias caused by excessive sympathetic stimulation, Supraventricular tachydysrhythmias
  • Adverse effects: Heart block, Heart failure, AV block, Sinus arrest, Hypotension, Bronchospasm (in asthma patients)
• Amiodarone (Class III) uses:


  For life-threatening atrial and ventricular dysrhythmias only,

  Recurrent ventricular fibrillation,

  Recurrent hemodynamically unstable ventricular tachycardia
• Amiodarone (Class III) ECG effects

  • Reduced automaticity in the SA node,
  • Reduced contractility,
  • Reduced conduction velocity,
  • QRS widening,
  • Prolongation of the PR and QT intervals
• Verapamil and diltiazem (Class IV)

  • 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
  • Adverse effects: Bradycardia, Hypotension, AV block, Heart failure, Peripheral edema, Constipation, Can elevate digoxin levels, Increased risk when combined with a beta blocker
• Digoxin


  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
• when conduction is through the ventricles are slowed, what happens to the QRS?

  QRS will widen
• what are the class 1C antiarrhythmic drugs?

  propafenone and flecainide
• what two class 1C doubled the mortality in preventing dysrhythmias after MI?

  encainide and flecainide
• Treatment goal for Afib

  improvement ventricular pumping and prevention of stroke
• what is the preferred method treating Afib?

  longterm: beta blocker (atenolol or meoprolol) and/or CCB (diltiazem or verapamil)

  short term: cardioversion, ablation, (amiodarone or sotalol)
• what is the treatment for Aflutter?

  cardioversion, ablation

  IV ibutilide
• what is long term treatment in preventing Aflutter?

  class 1C: flecainide or propfenone

  class 3: amiodarone, dronedarone, sotalol, dofetilide
• what is the treatment of SVT if valsalva maneuver or carotid massage doesnt work?

  IV beta blocker or CCB
• what is the treatment for Vtach?

  cardioversion

  IV amiodarone, Lidocaine, procainamide
• what are long term treatment for Vtach?

  ICD, sotalol, amiodarone
• what is the treatment of Vfib?

  Defibrillation

  IV amiodarone or lidocaine, Procainamide
• what is long term treatment of vfib?

  ICD or amiodarone
• PVCs are usually what but if the pt had an MI they may predispose pt to what?

  usually benign

  predispose to vfib

  may treat with a beta blocker
• Digoxin toxicity mimics all types of dysrhythmias but what are the most common?

  varying types of AV block
• what antidysrhythmic drugs a preferred in digoxin toxicity?

  lidocaine and phenytoin
• what class of drugs can cause a widening QT interval in torsades?

  class 1A and class 3