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Emergency Pharmacology Flashcards

7 cards from real ACLS practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.

Read the first 7 Emergency Pharmacology flashcards as text

  1. For a stable narrow-complex tachycardia that does not respond to vagal maneuvers, what is the first drug of choice?

    Answer: Adenosine 6 mg rapid IV push

    Adenosine 6 mg rapid IV push is the first pharmacological treatment for stable regular narrow-complex SVT.

  2. Procainamide is preferred over amiodarone for stable wide-complex tachycardia in which clinical scenario?

    Answer: Pre-excitation syndrome (WPW) with AF

    Procainamide is preferred over amiodarone for WPW with AF because it does not slow AV nodal conduction preferentially.

  3. What is the primary mechanism of action of adenosine in terminating SVT?

    Answer: Temporary AV nodal blockade interrupting reentry

    Adenosine transiently blocks AV nodal conduction, interrupting the reentrant circuit responsible for most SVTs.

  4. A patient in third-degree AV block is awaiting transcutaneous pacing. Which drug can be used as a temporizing measure?

    Answer: Atropine 0.5 mg IV

    Atropine 0.5 mg IV can increase heart rate temporarily while preparing for transcutaneous pacing in symptomatic bradycardia.

  5. Dopamine infusion is used for post-resuscitation hypotension. At what dose range does it primarily act as a vasopressor?

    Answer: 10–20 mcg/kg/min

    At 10–20 mcg/kg/min, dopamine primarily stimulates alpha-1 receptors causing vasoconstriction and increased blood pressure.

  6. Which electrolyte abnormality does magnesium sulfate treat beyond Torsades de Pointes in ACLS?

    Answer: Hypomagnesemia-induced refractory VF

    Magnesium sulfate 1–2 g IV is indicated for VF/pulseless VT associated with hypomagnesemia.

  7. What is the primary reason atropine is NOT recommended for Mobitz type II second-degree AV block?

    Answer: It causes paradoxical slowing of the ventricular rate

    In Mobitz II, atropine can increase atrial rate without improving ventricular conduction, potentially worsening the block and slowing ventricular rate.