A 60-year-old man comes to the office for follow-up due to persistent atrial fibrillation. He reports occasional palpitations and poor exercise tolerance. For the past year, the patient's atrial fibrillation has been managed with a rate-control strategy using metoprolol. Three months ago, his metoprolol dosage was increased for improved rate control, but today in the office, he reports that he was unable to tolerate the new dosage due to dizziness. Blood pressure is 110/70 mm Hg and pulse is 105/min and irregular. Examination shows no abnormalities. Echocardiography reveals left atrial enlargement, an ejection fraction of 59%, and no significant valvular disease. The patient is advised to remain on his previously tolerated metoprolol dose, and digoxin is added to the medication regimen. Four weeks later, he reports symptom improvement. Resting pulse is 84/min and irregular. Which of the following best explains digoxin's effect on heart rate in this patient?

Question

A 60-year-old man comes to the office for follow-up due to persistent atrial fibrillation.  He reports occasional palpitations and poor exercise tolerance.  For the past year, the patient's atrial fibrillation has been managed with a rate-control strategy using metoprolol.  Three months ago, his metoprolol dosage was increased for improved rate control, but today in the office, he reports that he was unable to tolerate the new dosage due to dizziness.  Blood pressure is 110/70 mm Hg and pulse is 105/min and irregular.  Examination shows no abnormalities.  Echocardiography reveals left atrial enlargement, an ejection fraction of 59%, and no significant valvular disease.  The patient is advised to remain on his previously tolerated metoprolol dose, and digoxin is added to the medication regimen.  Four weeks later, he reports symptom improvement.  Resting pulse is 84/min and irregular.  Which of the following best explains digoxin's effect on heart rate in this patient?

Quizplus · Accepted Answer

11ec160b_3b86_4835_9249_2ffd1eb24621_MD0001_00 Adequate rate control (eg, resting heart rate <85/min) is important in atrial fibrillation because it minimizes symptoms and helps decrease the risk of tachycardia-induced cardiomyopathy. Beta blockers (eg, metoprolol) slow conduction through the atrioventricular (AV) node via inhibition of sympathetic stimulation and are typically first-line therapy for rate control in patients with atrial fibrillation. This patient was unable to tolerate the dose of metoprolol needed to maintain an appropriate resting heart rate; therefore, digoxin was added for increased rate control. Digoxin slows conduction through the AV node via increased parasympathetic (vagal) tone. Several mechanisms may explain the parasympathetic effects of digoxin. Inhibition of the sodium-potassium ATPase pump in vagal afferent fibers sensitizes arterial baroreceptors (eg, carotid, aortic) and cardiac volume receptors, augmenting afferent input from the cardiovascular system to the brain. In addition, digoxin enhances efferent parasympathetic ganglionic transmission, leading to increased vagal output. This mechanism of increased parasympathetic tone is effective in controlling heart rate at rest but is limited in controlling heart rate during exercise, when sympathetic tone is high. Therefore, digoxin is rarely used as monotherapy for rate control and is more typically combined with a beta blocker or nondihydropyridine calcium channel blocker (eg, verapamil, diltiazem). (Choices A and B) Decreased atrial refractoriness and decreased cardiomyocyte action potential duration both occur with digoxin, increasing the automaticity of the atrial myocardium and encouraging the development of atrial fibrillation and other atrial arrhythmias. However, these effects are typically problematic only at toxic digoxin levels and at therapeutic levels are outweighed by the beneficial effect of increased parasympathetic tone. (Choice C) Digoxin increases (rather than decreases) Purkinje fiber automaticity, encouraging the development of ventricular arrhythmias (eg, ventricular tachycardia). Like the proarrhythmic effects on the atrial myocardium, this effect is typically problematic only at toxic digoxin levels. (Choice E) Digoxin increases ventricular contractility (positive inotropy) by inhibiting the sodium-potassium ATPase pump to increase intracellular sodium and consequently increase intracellular calcium. This effect can improve cardiac output and symptoms (eg, dyspnea, orthopnea) in patients with left ventricular systolic dysfunction, but it does not contribute to improved rate control. Educational objective: Digoxin can be used to improve ventricular rate control in patients with atrial fibrillation, as it decreases atrioventricular node conduction by increasing parasympathetic (vagal) tone. Digoxin also has a positive inotropic effect that can be useful in patients with left ventricular systolic dysfunction. __________ References: Digoxin in the management of cardiovascular disorders. (http://www.ncbi.nlm.nih.gov/pubmed/15210613)

A 60-Year-Old Man Comes to the Office for Follow-Up Due