Arrhythmia and ACLS Questions in CRNA Interviews: AFib, Torsades, and STEMI

How do you treat AFib with RVR when EF is low?

When a patient decompensates on telemetry, the first decision is whether the rhythm is causing the instability or compensating for something else. A heart rate of 150 in a septic, dry patient is doing a job. Slow it with a negative inotrope and the blood pressure goes with it. Panels build scenarios around that trap.

Start by asking what is driving the rate: sepsis, hypovolemia, hypoxemia, hypercapnia, pain. Treat that first. If the arrhythmia itself is causing instability (hypotension, shock, ischemia, acute heart failure), cardiovert.

If stable and you need rate control, check ejection fraction first. Preserved EF with adequate pressure tolerates diltiazem or a beta-blocker. Reduced EF, decompensated heart failure, or borderline pressure calls for amiodarone 150 mg over 10 minutes (digoxin or cautious esmolol are alternatives), because non-dihydropyridine calcium channel blockers depress contractility. Then assess stroke risk with CHA2DS2-VASc. Stable regular SVT gets vagal maneuvers, then adenosine.

Synchronized cardioversion starting energies (biphasic)

What is the sequence for pulseless VT or VF?

Tamponade and massive PE both raise neck veins and drop pressure with opposite fluid logic; the shock states guide covers both. Hyperkalemia has its own stabilize, shift, eliminate sequence.

Sequence

1. Defibrillate immediately (biphasic 120–200 J per device, escalating), with CPR between shocks.
2. Epinephrine 1 mg every 3–5 minutes, started after the second shock.
3. Amiodarone 300 mg after the third shock, then 150 mg for the next dose. Lidocaine is the alternative.

Reversible causes, the whole time

Hypoxia, hypovolemia, hydrogen ion, hypo- or hyperkalemia, hypothermia, tension pneumothorax, tamponade, toxins, and coronary or pulmonary thrombosis.

Why does torsades need magnesium and a faster heart rate?

A long QT gives cells time to fire early afterdepolarizations during repolarization. An R-on-T beat then starts polymorphic VT.

• Pulseless: defibrillate, and give magnesium 2 g IV push.
• With a pulse: magnesium 2 g IV over about 15 minutes to suppress afterdepolarizations, potassium repleted to 4.5–5.0, and every QT-prolonging drug stopped.
• Recurrent and pause-dependent: raise the heart rate with isoproterenol or overdrive pacing. A faster rate shortens the QT.

How do you treat symptomatic bradycardia?

Rule out hypoxemia, inferior ischemia, hyperkalemia, and beta-blocker or calcium channel blocker toxicity. Atropine 1 mg IV every 3–5 minutes, up to 3 mg, works at the sinus and AV node. Mobitz II and wide-complex third-degree block sit below the node, where atropine does little, so go to transcutaneous pacing or a dopamine or epinephrine infusion.

What do you say about STEMI beyond “activate the cath lab”?

Localize the vessel. Inferior changes mean you check right-sided leads for RV infarction, where preload matters and nitrates can crash the pressure. Anterior (LAD) infarcts set up cardiogenic shock and high-grade blocks.

Draw troponin, lactate, CMP, magnesium, and phosphorus. Give aspirin, support MAP with norepinephrine if hypotensive, and activate the cath lab. After PCI: dual antiplatelet therapy, a high-intensity statin, and a beta-blocker once hemodynamically stable.

How do you practice the rate-control follow-up?

A first rep sounds like this: a patient with an EF of 20% is in AFib at 155 with a pressure of 94/58, and you push diltiazem. The follow-up asks why the pressure is 60/30 three minutes later.

A repaired answer sounds like this: diltiazem is a negative inotrope, and this ventricle cannot afford one. I check whether the rate is compensating for sepsis or volume loss, use amiodarone 150 mg over 10 minutes for rate control, support perfusion with norepinephrine, and cardiovert at 200 J synchronized if the patient becomes unstable. I reassess MAP, mentation, and the rate response first.

Pick five scenarios across this series (a pressor case, an ARDS vent, hyperkalemia, AFib with low EF, torsades) and record each in the MoxPrep practice bank. Repeat any case where the follow-up stalls you until your answer reaches the first reassessment target.

Why avoid diltiazem in AFib with a low ejection fraction?

Diltiazem is a negative inotrope. In a ventricle with reduced EF it can drop stroke volume and blood pressure quickly, so amiodarone is the safer rate-control choice.

Why does atropine fail in Mobitz II or wide-complex third-degree block?

Atropine works on the sinus and AV node through vagal blockade. These blocks sit below the node, so the escape rhythm does not respond, and pacing or a chronotropic infusion is the next step.