questions 3

Antiarrhythmics

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Topic updated on 06/12/17 11:43pm

Overview

Class I - Na+ Channel Blockers
  • General principles
    • slow or block Na+ conduction preferentially in depolarized cells
      • selective for abnormal cardiac tissue that is frequently depolarized
      • use and state dependence
    • phase 4 depolarization in SA node (automaticity current) is dependent on Na+ channel opening
      • blockage results in ↓ slope of phase 4 depolarization and ↓ SA node rate
    • hyperkalemia causes ↑ toxicity for all class I drugs
Class IA
  • iaExamples
    • quinidine, procainamide, disopyramide
      • remember: quin + the amides
  • Effects
    • acts on atrial and ventricular arrhythmias
      • especially reentrant and ectopic supraventricular and ventricular tachycardia
    • ↓ rate of phase 0 depolarizating resulting in
      • ↑ QT interval
      • ↑ AP duration 
      • ↑ effective refractory period (ERP)
  • Toxicity
    • quinidine
      • cinchonism
        • headache, tinnitus, vertigo
      • thrombocytopenia
      • ↑ QT interval
        • can result in torsades de pointes
      • can enchance digoxin toxicity
    • procainamide
      • reversible SLE-like syndrome
        • remember: procAiNAmide (antinuclear antibody in SLE)
Class IB
  • ibExamples
    • lidocaine, mexiletine, tocainide
      • phenytoin can also fall into class IB
  • Effects
    • acts on ischemic or depolarized Purkinje and ventricular tissue
      • does not act on healthy or atrial tissue
      • effective in treating structurally abnormal tissue (especially post-MI)
      • useful in acute ventricular arrhythmias and in digitalis-induced arrhythmias
    • ↓ rate of phase 3 repolarization resulting in
      • ↓ AP duration
  • Toxicity
    • local anesthetic
    • CNS stimulation/depression
Class IC
  • icExamples
    • flecainide, encainide, propafenone
  • Effects
    • acts on His-Purkinje system in cardiac tissue WITHOUT structural abnormalities
      • useful in V-tachs progressing to VF and refractory SVT
      • drugs of last resort
    • no effect on AP duration
  • Toxicity
    • proarrhythmic
    • contraindicted with structural abnormalities
      • e.g., post-MI
    • significantly prolongs refractory period in AV node
Use Dependence
  • Higer rates of depolarization = increased Na+ channel blockade due to channels spending less time in the resting state
    • type 1C antiarrythmics
      • bind Na+ channels the strongest
      • have the highest likelihood of use dependence
    • type 1B antiarrythmics
      • bind the least avidly to Na+ channels
      • minimal cumulative effect over multiple cardiac cycles
      • more selective for ischemic myocardium
      • lowest likelihood of use dependence
  • Na+ channel binding strength:
    • 1C > 1A > 1B
Class II - β-blockers
  • Examples
    • propranolol, esmolol, metoprolol, atenolol, timolol
      • esmolol very short acting
  • Mechanism
    • ↓ slope of phase 4 resulting in ↓ automaticity
      • due to ↓ cAMP, ↓ Ca2+ currents
      • results in ↑ PR interval, ↓ conduction in AV node
  • Clinical use
    • ventricular tachycardia, SVT
    • slowing ventricular rate during atrial fibrillation and atrial flutter
    • post-MI arrhythmia prophylaxis (cardioprotective)
  • Toxicity
    • cardiovascular effects
      • bradycardia, AV block, CHF
    • CNS effects
      • sedation, sleep alterations, depression
    • may mask the signs of hypoglycemia
    • impotence
    • exacerbation of asthma
      • only for non-selective (non-beta1 specific)
    • metoprolol can cause dyslipidemia
    • treat overdose with glucagon 
      • ↑ cAMP via a mechanism independent of beta receptors
Class III - K+ Channel Blockers
  • iiiExamples 
    • sotalol, ibutilide, bretylium, dofetilide, amiodarone
  • Mechanism 
    • ↑ phase 3
      • due to ↓ K+ current
      • results in ↑ AP duration, ↑ ERP, ↑ QT interval
    • effective for antrial and ventricular arrhythmias
    • antiarrhythmics of last resort
    • amiodarone has class I, II, III, and IV effects
      • due to alterations lipid membrane
  • Toxicity
    • torsades de pointes due to ↑ QT interval
      • amiodarone is the only example of a drug that lengthens QT but does not have risk of torsades de pointes
    • sinus bradycardia
    • sotalol
      • excessive β blockade 
    • bretylium
      • new arrhythmias
      • ↓ BP
    • amiodarone
      • pulmonary fibrosis
      • hepatotoxicity
      • hypothyroidism/hyperthyroidism
        • amiodarone is 40% iodine by weight (amIODarone)
        • must watch LFTs, TFTs, PFTs
      • corneal deposits
      • photosensitivity
      • skin color changes (blue/gray)
      • neurologic effects
      • constipation
      • cardiovascular effects
        • bradycardia, heart block, CHF
Class IV - Ca2+ Channel Blockers
  • Examples
    • verapamil, diltiazem
      • note: other Ca2+ channel blockers (nifedipine, amlodipine) have little action on the heart
  • Mechanism
    • ↓ L-type Ca2+ channels current primarily in AV nodal cells
      • L-type Ca2+ channels responsible for the plateau phase
    • results in ↓ conduction velocity, ↑ ERP, ↑ PR interval
    • used in prevention of nodal arrhythmias, AV nodal reentry
  • Toxicity
    • antimuscarinic effects
      • constipation, diziness, flushing
    • edema
    • CV effects
      • negative ionotropy, AV block, sinus node depression 


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(M2.CV.49) A 21-year-old college female presents after her swim practice with persistent palpitations. The palpitations began 3 hours ago during a rigorous swim and are not accompanied by chest pain, shortness of breath, nausea or vomiting. The patient has a documented history of Wolff-Parkinson-White (WPW). She denies recent alcohol or drug use. On physical exam, the patient's blood pressure is 115/70. EKG shows atrial fibrillation with a rate of 170/min. What is the most appropriate next step in management? Topic Review Topic

1. Procainamide
2. Adenosine
3. Atenolol
4. Diltiazem
5. Digoxin

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