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SVTagents SVTagents Presentation Transcript

  • Antiarrhythmic Agents in SVT: MOA & ADEs Don Wiest, Pharm.D.
  • Drugs in Acute Management of SVT
  • Vaughn-Williams Classification
    • Based on cellular properties of normal His-Purkinje cells
    • Classified on drug’s ability to block ionic currents (i.e. Na + , K + , Ca ++ ) and β -adrenergic receptors
    • Advantages:
      • Physiologically based
      • Highlights beneficial/deleterious effects
    • Disadvantages
      • All cells not normal
      • All cells not His-Purkinje in origin
  •  
  • Antiarrhythmic Agents Vaughn-Williams Classification
    • Class I - Na + - channel blockers
      • Direct membrane action
      • Slows conduction velocity
        • IA- Moderately slow: A, V
          • Quinidine, Procainamide , Disopyramide
        • IB- Minimally slow: V
          • Lidocaine, Mexiletine, Phenytoin, Tocainide
        • IC- Markedly slow: A, V
          • Flecainide, Propafenone, Moricizine
    A: atrium; V: ventricle
  • Antiarrhythmic Agents Vaughn-Williams Classification
    • Class II – Blocks Beta receptors
      • Slows sinus rate, AVN conduction, & depress LVF
        • Propranolol, atenolol, metoprolol, etc.
    • Class III - Blocks K + channels
      • Prolongs repolarization ( refractory period)
        • Amiodarone, Sotalol, NAPA, Ibutilide, Azimilide
    • Class IV- Ca ++ channel blockers
      • Affects primarily SA and AV nodes
        • Verapamil , Diltiazem, Bepridil
    • Purinergic agonists: Adenosine
    • Digitalis glycosides
    AVN: atrioventricular node LVF: left ventricle function;
  • Purinergic Agonists Adenosine
    • Mode of action
      • Endogenous nucleoside
      • A1 receptor agonist
      • Depresses slow inward Ca ++ current
      • Increases K + conductance (hyperpolarizes)
    • Kinetics
      • Metabolized by RBCs and vascular endothelial cells
      • t 1/2 = 5-10 secs
    • ECG/EP changes
      • Slows sinus rate
      • Slows AV node conduction
  • Purinergic Agonists Adenosine
    • Drug interactions
      • Methylxanthines (caffeine/theophylline):
        • Decreased effect by blocking receptors
      • Dipyridamole:
        • Prolonged effects by inhibiting adenosine uptake
    • Side effects (10-20%; transient: 2-3 min)
      • Flushing/headache/nausea/dyspnea = most common
      • A. Fib/ V. tach/ sinus arrest/ sinus bradycardia, bronchospasms = rare
    • Caution: heart transplant patients, asthmatics
    • Contraindications: wide QRS tachycardia
  • Class IA - Na+ Channel Blockers Procainamide
    • Mode of action
      • Slows conduction and prolong refractoriness
        • Atrial, His-Purkinje, ventricular tissue
      • Peripheral alpha block
      • Vagolytic
      • Minimal negative inotropic effect
    • Active metabolite: NAPA (Class III activity)
    • ECG changes
      • Increase PR, QRS
      • Toxicity: QTc increases by 30% or QT > 0.5 sec
  • Class IA - Na+ Channel Blockers Procainamide
    • Side effects:
      • Arteriolar vasodilation with IV
        • Slow infusion rate
      • Negative inotrope (esp. with levels > 12 mcg/ml)
      • Pro-arrhythmia: 2-3%
    • Drug interactions
      • Decrease metabolism of amiodarone
  • Class III- K + channel Amiodarone
    • Mainly class III- Blocks K + channels
      • Has characteristics of all 4 classes
    • Acute actions very different from chronic
    • Acute Therapy (intravenous)
      • Prolongs AV node refractory period
      • Lesser effect on the refractory period of the atrium, ventricle or His-Purkinje system
      • Minimal effect on contractility
  • Amiodarone: Acute Therapy
    • Side Effects:
      • Acute Treatment (IV)
        • Transient hypotension, bradycardia
        • Proarrhythmia <2% (e.g., torsade de pointes)
        • Hepatocellular necrosis (Polysorbate 80?; rare)
        • Benzyl Alcohol (monitor)
      • Chronic (PO)
        • hyper and hypothyroidism
        • Photosensitivity
        • Pulmonary fibrosis
        • Corneal deposits
        • Peripheral neuropathy
    • Drug Interactions
      • Many
      • Digoxin: reduce dose by 50%; monitor Cp
  • Class IV- Ca ++ channel blocker Verapamil
    • Mode of Action
      • Slows conduction velocity of SA and AV nodes
      • Lengthens antegrade & retrograde refractory periods of AV node
      • Slows sinus rate and increases PR interval on ECG
    • Side Effects
      • Negative inotrope, hypotension, dizziness, fatigue
    • Do not use with other negative inotropes (e.g., beta blocker)
  • Verapamil
    • Contraindications
      • Infants < 1 year of age (apnea, hypotension, bradycardia, CV collapse)
      • Heart failure
      • Suspected or known WPW
      • Wide QRS tachycardia
      • Sick Sinus Sydrome
  • Proarrhythmia
    • Anitarrhythmic drug facilitates emergence of new arrhythmia (e.g., torsade de pointes)
    • Increased risk
      • Children with structural heart disease
      • Class IA: Procainamide 2-3%
      • Class IC agents (e.g., Flecainide up to 7.5%)
      • Class III: Amiodarone <1%, Sotalol 1-5%
  • Conclusion
    • Antiarrhythmic drugs act by altering the conduction velocity and refractory periods changing the substrate for reentry.
    • Must be used with caution due to proarrhythmic effects