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Blockade of beta-adrenergic receptors
0%
0/210
Calcium channel blockade
1%
2/210
Blockade of Na-K-ATPase on cardiac myocytes
58%
121/210
Vagal stimulation
37%
78/210
Increased ventricular contractility
3%
6/210
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This patient presents with symptoms of atrial fibrillation and is treated with digoxin, which slows his heart rate. Digoxin slows heart rate by inducing vagal stimulation. Digoxin is a second-line treatment for atrial fibrillation with rapid ventricular response. Digoxin induces vagal stimulation, which leads to a decrease in AV nodal conduction by increasing parasympathetic tone; atria will continue to fibrillate but the rate of ventricular contraction will slow. Digoxin does also block the Na-K-ATPase (Answer 3), which leads to increased intracellular calcium and therefore increased contractility, but this is not responsible for the AV nodal blockade. Gutierrez reviews atrial fibrillation. Decreasing the ventricular response rate is a key goal of atrial fibrillation treatment. Digoxin slows the ventricular response rate by enhancing vagal tone, but is most often used concomitantly with beta blockers or calcium channel blockers. It is not a first-line agent for atrial fibrillation because studies have shown that it has little effect during exercise. Nagai et al. compared the use of digoxin and the beta blocker landiolol in 200 patients presenting with left ventricular dysfunction and atrial fibrillation. Landiolol successfully controlled heart rate in 48% of patients, while digoxin successfully controlled heart rate in 13.9% of patients. Illustration A shows the mechanism of action of digoxin. Incorrect answers: Answer 1: Beta blockers control heart rate by blocking beta adrenergic receptors. Answer 2: Calcium channel blockers exert their negative chronotropic effect through calcium channel blockade. Answer 3: Digoxin does also block the Na-K-ATPase, which leads to increased intracellular calcium and therefore increased contractility, but this is not responsible for AV nodal block. Answer 5: Digoxin and other cardiac glycosides do increase contractility, but this is not responsible for AV nodal block.
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