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Upon completion of the chapter, the reader will be able to:

  1. Describe the phases of the cardiac action potential, compare and contrast the cellular ionic changes corresponding to each phase, and explain the relationship between the cardiac action potential and the electrocardiogram (ECG).

  2. Describe the modified Vaughan Williams classification of antiarrhythmic drugs, and compare and contrast the effects of available antiarrhythmic drugs on ventricular conduction velocity, refractory period, automaticity, and inhibition of ion flux through specific myocardial ion channels.

  3. Compare and contrast the risk factors for and the features, mechanisms, etiologies, symptoms, and goals of therapy of (a) sinus bradycardia, (b) atrioventricular (AV) nodal blockade, (c) atrial fibrillation (AF), (d) paroxysmal supraventricular tachycardia (PSVT), (e) ventricular premature depolarizations (VPDs), (f) ventricular tachycardia (VT, including torsades de pointes), and (g) ventricular fibrillation (VF).

  4. Compare and contrast appropriate nonpharmacologic and pharmacologic treatment options for sinus bradycardia and AV nodal blockade.

  5. Compare and contrast the mechanisms of action of drugs used for ventricular rate control, conversion to sinus rhythm and maintenance of sinus rhythm in patients with AF, and explain the importance of anticoagulation for patients with AF.

  6. Discuss nonpharmacologic methods for termination of PSVT, and compare and contrast the mechanisms of action of drugs used for acute termination of PSVT.

  7. Compare and contrast the role of drug therapy versus nonpharmacologic therapy for long-term prevention of recurrence of PSVT.

  8. Describe the role of drug therapy for management of asymptomatic and symptomatic VPDs.

  9. Compare and contrast the mechanisms of action of drugs used for the treatment of acute episodes of VT (including torsades de pointes), and describe options and indications for nonpharmacologic treatment of VT and VF.

  10. Design individualized drug therapy treatment plans for patients with (a) sinus bradycardia, (b) AV nodal blockade, (c) AF, (d) PSVT, (e) VPDs, (f) VT (including torsades de pointes), and (g) VF.




  • Image not available. Cardiac arrhythmias may be caused by abnormal impulse formation (automaticity), abnormal impulse conduction (reentry), or both.

  • Image not available. Numerous drugs (β-blockers, diltiazem, verapamil, digoxin, dronedarone, and amiodarone) can cause bradyarrhythmias (sinus bradycardia and/or atrioventricular [AV] nodal blockade).

  • Image not available. Individualized goals of treatment for atrial fibrillation (AF) include (a) ventricular rate control with drugs that inhibit AV nodal conduction, (b) restoration of sinus rhythm with direct current cardioversion or antiarrhythmic drugs (commonly referred to as "cardioversion" or "conversion to sinus rhythm"), (c) maintenance of sinus rhythm/reduction in the frequency of episodes, and (d) prevention of stroke.

  • Image not available. Antiarrhythmic drug therapy for maintenance of sinus rhythm/reduction in frequency of episodes of AF should be initiated only in patients in whom symptoms persist despite maximal tolerated doses of appropriate drugs for ventricular rate control.

  • Image not available. Most patients with AF require therapy with dabigatran or warfarin for stroke prevention; in some patients with no additional risk factors for stroke, anticoagulation may not be necessary.

  • Image not available. Adenosine is the drug of choice for termination of paroxysmal supraventricular tachycardia.

  • Image not available. Asymptomatic ventricular premature depolarizations (VPDs) should not ...

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