For stable monomorphic VT with no hemodynamic compromise, what is the first-line pharmacologic therapy?

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Multiple Choice

For stable monomorphic VT with no hemodynamic compromise, what is the first-line pharmacologic therapy?

Explanation:
For stable monomorphic VT without hemodynamic compromise, the first-line pharmacologic therapy is IV amiodarone given as a bolus. Amiodarone works across multiple ion channels and receptors, so it effectively interrupts reentrant VT circuits and suppresses automaticity without causing large drops in blood pressure. It has a broad antiarrhythmic effect that is useful in various VT etiologies, including scar-related and ischemic hearts, and it tends to have a favorable safety profile with a lower risk of proarrhythmia compared to some other antiarrhythmics. Dosing typically starts with a 150 mg IV bolus, followed by a continuous infusion to maintain effect, which helps prevent recurrence while the rhythm converts or stabilizes. Lidocaine is more targeted for ischemia-related VT or VT in the setting of acute MI and is generally not as reliably effective as a first-line option for stable, wide-complex VT. Procainamide and sotalol can terminate VT but carry higher risks in this scenario—procainamide can cause hypotension and QRS widening, while sotalol can prolong the QT interval and provoke torsades de pointes.

For stable monomorphic VT without hemodynamic compromise, the first-line pharmacologic therapy is IV amiodarone given as a bolus. Amiodarone works across multiple ion channels and receptors, so it effectively interrupts reentrant VT circuits and suppresses automaticity without causing large drops in blood pressure. It has a broad antiarrhythmic effect that is useful in various VT etiologies, including scar-related and ischemic hearts, and it tends to have a favorable safety profile with a lower risk of proarrhythmia compared to some other antiarrhythmics. Dosing typically starts with a 150 mg IV bolus, followed by a continuous infusion to maintain effect, which helps prevent recurrence while the rhythm converts or stabilizes.

Lidocaine is more targeted for ischemia-related VT or VT in the setting of acute MI and is generally not as reliably effective as a first-line option for stable, wide-complex VT. Procainamide and sotalol can terminate VT but carry higher risks in this scenario—procainamide can cause hypotension and QRS widening, while sotalol can prolong the QT interval and provoke torsades de pointes.

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