Antiarrhythmics | Bone Wizardry

01 · The Framework

Vaughan-Williams Overview

Four classes, each attacking a different ion channel or receptor. One concept: interrupt the abnormal electrical circuit.

The core principle: arrhythmias arise from abnormal automaticity, triggered activity, or reentry circuits. Antiarrhythmics interrupt these by slowing conduction, prolonging refractoriness, or blocking the ion channels that sustain the circuit.

Class I · Sodium Channel Blockers

Block Fast Na+ Channels

Mechanism: Block fast inward Na+ channels, slowing phase 0 depolarization and conduction velocity. Mostly affect non-nodal (His-Purkinje, ventricular, atrial) tissue.

Three subtypes defined by how quickly they dissociate from the Na+ channel:
• Ia: intermediate unbinding. Moderate slow phase 0. Also block K+ channels.
• Ib: fast unbinding. Use-dependent; preferentially bind depolarized (ischemic) tissue. Shorten action potential duration.
• Ic: slowest unbinding. Strongest Na+ block. Markedly slow conduction.

Slows phase 0 Widens QRS Non-nodal tissue

Class II · Beta-Blockers

Block Beta-1 Receptors

Mechanism: Beta-1 blockade lowers cAMP, which decreases I_f (funny current) and I_Ca. Result: slows spontaneous SA node depolarization and slows AV node conduction.

ECG effect: Prolongs PR interval (slows AV conduction). Slows heart rate.

Uses: Rate control in AF/AFL, SVT termination, post-MI arrhythmia prevention, AVNRT.

Examples: Metoprolol, esmolol, propranolol, atenolol.

Slows SA node Slows AV conduction Prolongs PR Negative inotrope

Class III · Potassium Channel Blockers

Block K+ Repolarization

Mechanism: Block outward K+ channels, prolonging phase 3 repolarization. This extends action potential duration and the effective refractory period (ERP). The circuit cannot reenter because it is still refractory.

ECG effect: Prolongs QT interval. The dark side: prolonged QT predisposes to torsades de pointes, especially in bradycardia (reverse use-dependence).

Examples: Amiodarone (multi-channel), sotalol (K+ + beta), ibutilide, dofetilide.

Prolongs QT Torsades risk Prolongs ERP

Class IV · Calcium Channel Blockers

Block L-type Ca2+ Channels

Mechanism: Block L-type Ca2+ channels in nodal tissue. SA and AV node depolarization depends on Ca2+ (not fast Na+ like non-nodal tissue). Blocking Ca2+ slows automaticity and AV conduction.

ECG effect: Prolongs PR interval (AV block). Slows ventricular rate in AF/AFL.

Non-DHP only: Verapamil and diltiazem. Dihydropyridines (nifedipine, amlodipine) work on vascular smooth muscle, not the heart's electrical system.

Critical contraindication: WPW syndrome. Blocking AV node forces conduction through the accessory pathway, which can precipitate VF.

Nodal tissue only Prolongs PR WPW contraindicated Rate control AF/AFL

Other · Adenosine

Adenosine

Activates K+ channels (G-protein coupled) in AV node, causing brief but profound AV block. Half-life of about 10 seconds. IV push into a large vein.

Use: Terminate AVNRT and AVRT (AV-node-dependent SVTs). Does NOT terminate AF, AFL, or VT (those don't depend on the AV node).

Side effects: Flushing, chest tightness, bronchospasm (brief). Warn the patient.

SVT termination 10-sec half-life Asthma caution

Other · Digoxin

Digoxin

Inhibits Na/K-ATPase, raising intracellular Na+, which secondarily raises intracellular Ca2+. Also increases vagal tone on the AV node, slowing conduction.

Use: Rate control in AF (not first-line), heart failure with reduced EF.

Toxicity: Narrow therapeutic window. Hypokalemia, hypomagnesemia, and hypercalcemia potentiate toxicity. Presents as nausea, xanthopsia (yellow-green vision), and any arrhythmia.

Narrow window Xanthopsia Vagal + Na/K ATPase

Other · Magnesium

Magnesium

IV magnesium is the first-line treatment for torsades de pointes, regardless of the serum magnesium level. Mechanism: stabilizes the cardiac membrane, inhibits early afterdepolarizations that trigger torsades.

Torsades Tx First-line IV Mg2+

02 · Sodium Channel Blockers

Class I Deep Dive

Same channel, three very different drugs. Unbinding speed determines the clinical profile.

The kinetics key: all three subtypes block the same Na+ channel, but Ia dissociates at intermediate speed, Ib fastest, Ic slowest. Slower unbinding means the drug "stays" in the channel longer, producing stronger conduction slowing at all heart rates. Ib is use-dependent and only clinically relevant when the heart is firing fast (ischemia, VT).

Class Ia · Intermediate Unbinding Slow and Steady Quinidine · Procainamide · Disopyramide

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Mechanism: Moderate Na+ channel block (slows phase 0, widens QRS) PLUS K+ channel block (prolongs phase 3, prolongs QT). Double-channel effect is what makes them both effective and dangerous.

Uses: AF/AFL, VT conversion and maintenance. Now largely replaced by safer agents, but still high-yield for boards.

Toxicities:

Quinidine: Cinchonism (tinnitus, headache, visual changes at toxic doses). Torsades de pointes (K+ block widens QT). Thrombocytopenia.
Procainamide: Drug-induced lupus (anti-histone antibodies positive). Agranulocytosis with long-term use. Active metabolite NAPA also blocks K+ channels.
Disopyramide: Strong anticholinergic effects: urinary retention, dry mouth, constipation, blurry vision. Contraindicated in BPH and glaucoma.

Mnemonic Quinidine Quivers (torsades), Procainamide Pretends to have Lupus, Disopyramide Dries you out.

Prolongs QRS + QT Torsades (quinidine) Drug-induced lupus (procainamide) Anticholinergic (disopyramide)

Class Ib · Fast Unbinding Fast In, Fast Out Lidocaine · Mexiletine · Phenytoin

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Mechanism: Fast unbinding creates use-dependence: the drug binds much more avidly to channels that fire rapidly. Ischemic and depolarized tissue fires faster, so Ib drugs preferentially suppress ischemic ventricular tissue without much effect on healthy atrial tissue. They also slightly shorten action potential duration (unlike Ia/Ic).

Uses: Ventricular arrhythmias only: post-MI VT/VF, digitalis-induced arrhythmias. NOT effective for atrial arrhythmias (atrial tissue unbinding is too fast for much binding). Lidocaine is IV only. Mexiletine is the oral equivalent.

Toxicities:

Lidocaine: CNS toxicity dominates: seizures, tinnitus, perioral numbness, slurred speech (dose-dependent). Minimal cardiac toxicity at therapeutic doses.
Mexiletine: GI side effects: nausea, vomiting. Used for chronic oral ventricular arrhythmia suppression.
Phenytoin: Historically used for digoxin-induced arrhythmias. Now rarely used for arrhythmias alone.

Mnemonic "Lidocaine Likes Ischemia" = use-dependent, works where the tissue is sick. CNS before cardiac toxicity.

Post-MI VT/VF Use-dependent CNS toxicity (lidocaine) NOT for atrial arrhythmias

Class Ic · Slowest Unbinding The Strong Brake Flecainide · Propafenone

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Mechanism: Strongest Na+ channel block of all Class I agents. Markedly slows conduction at all heart rates (not just rapid ischemic rates). Minimal effect on repolarization (no QT prolongation). Primarily widens QRS.

Uses: AF, AFL, and SVT in patients with structurally normal hearts only. Highly effective for rhythm control in otherwise healthy hearts.

Critical contraindication: Post-MI, structural heart disease, reduced EF. The CAST trial showed flecainide and encainide increased mortality in post-MI patients despite suppressing ectopy. Proarrhythmic: the slowed conduction creates conditions for dangerous reentrant circuits in scarred myocardium.

Propafenone also has mild beta-blocking properties (avoid in asthma/COPD).

Mnemonic "Ic = I see structural disease, I'm contraindicated." CAST trial = Class Ic killed post-MI patients.

Structurally normal hearts ONLY Post-MI contraindicated CAST trial: increased mortality Widens QRS, no QT change

03 · Classes III, IV & Specials

Classes III & IV + Special Agents

The heavy hitters. Amiodarone works on every channel. Adenosine lasts 10 seconds.

Amiodarone rule: it is technically Class III, but it blocks Na+, K+, Ca2+ channels AND has beta-blocking activity. It is the most effective antiarrhythmic for almost every arrhythmia type, but its long-term toxicity profile means it is not used first-line for stable patients.

Class III · Multi-channel

Amiodarone

Blocks Na+, K+, Ca2+ channels + beta receptors. Prolongs action potential duration and QT. Long half-life (weeks to months). Highly effective for VF/VT (ACLS), AF (rate + rhythm control).

Toxicities (multi-organ):
Pulmonary fibrosis (most serious, CXR annually), thyroid dysfunction (hypo- and hyperthyroidism, TFTs every 6 months), hepatotoxicity (LFTs annually), corneal microdeposits (benign, slit-lamp annually), photosensitivity, blue-gray skin discoloration, peripheral neuropathy.

Monitoring: TFTs, LFTs, PFTs, eye exam, CXR annually.

Pulmonary fibrosis Thyroid (hypo + hyper) Hepatotoxicity Corneal deposits Blue-gray skin

Class III · K+ + Beta

Sotalol

K+ channel block + non-selective beta-block. Prolongs QT and has negative chronotropic/inotropic effects. Used for AF/AFL and VT maintenance.

Key toxicity: Torsades de pointes (prolonged QT). Risk increased with bradycardia, hypokalemia, hypomagnesemia. Avoid combining with other QT-prolonging agents.

Requires QTc monitoring at initiation, usually done in-hospital.

Torsades de pointes Prolongs QT K+ + beta block

Class III · Pure K+

Ibutilide & Dofetilide

Pure potassium channel blockers. Prolongs repolarization (QT) without Na+ or beta effects.

Ibutilide: IV, used for acute chemical cardioversion of AF/AFL. Highly effective within minutes.

Dofetilide: Oral, used for AF/AFL maintenance. Requires in-hospital initiation with continuous QTc monitoring (3 days).

Both: Torsades risk proportional to QT prolongation. Renal dosing required (dofetilide cleared renally).

Torsades risk Chemical cardioversion (ibutilide) In-hospital QTc monitoring

Class IV · Non-DHP CCBs

Verapamil & Diltiazem

Block L-type Ca2+ channels in SA and AV node. Slow automaticity and AV conduction. Used for rate control in AF/AFL and termination of AVNRT.

Critical contraindication: WPW with AF. Blocking the AV node forces all atrial impulses through the accessory pathway (bundle of Kent), which can conduct very rapidly and degenerate into VF. NEVER give verapamil or diltiazem in WPW.

Other contraindications: AV block (2nd/3rd degree), severe bradycardia, acute decompensated heart failure (negative inotrope).

Verapamil has more cardiac effect; diltiazem has mixed cardiac/vascular.

WPW contraindicated Rate control AF/AFL AV node block Negative inotrope

Other · Purinergic Agonist

Adenosine

Activates A1 receptors in AV node, opening K+ channels and hyperpolarizing the node. Causes 3 to 6 seconds of complete AV block, interrupting reentrant circuits that depend on the AV node (AVNRT, AVRT).

IV push technique matters: push fast into an antecubital or larger vein, followed immediately by a 20 mL saline flush. Too slow = degraded before reaching the heart.

Does NOT terminate: AF, AFL, VT (these are not AV-node-dependent).

Side effects: Flushing, chest tightness, dyspnea, bronchospasm. Brief (10-second half-life).

Contraindicated: 2nd/3rd degree AV block, sick sinus syndrome, WPW (can precipitate VF by unmasking accessory pathway).

AVNRT termination 10-sec half-life Asthma caution WPW risk

WPW + rapid AF = electrical emergency. The accessory pathway conducts without the AV node's rate-limiting effect. Avoid all AV-node blockers: adenosine, verapamil, diltiazem, beta-blockers, and digoxin. Treatment: IV procainamide or electrical cardioversion.

04 · High-Yield Reference

Toxicity Danger Chart

The boards love toxicity. Know the drug, the effect, and the ECG trigger.

Drug	Class	Key Toxicity	Boards Trigger
Quinidine	Ia	Torsades de pointes, cinchonism	Prolonged QT + tinnitus / visual changes
Procainamide	Ia	Drug-induced lupus, agranulocytosis	Anti-histone Ab positive + arthralgia + pleurisy
Disopyramide	Ia	Anticholinergic effects	Urinary retention, dry mouth, constipation
Lidocaine	Ib	CNS toxicity	Seizures, tinnitus, perioral numbness (dose-dependent)
Flecainide / Propafenone	Ic	Proarrhythmic in structural heart disease	Post-MI contraindicated (CAST trial: increased mortality)
Amiodarone	III	Pulmonary fibrosis, thyroid, hepatotoxicity, skin	Multi-organ toxicity; bilateral infiltrates on CXR + thyroid abnormality
Sotalol	III	Torsades de pointes	Prolonged QT + beta-blocker effects
Ibutilide / Dofetilide	III	Torsades de pointes	In-hospital QTc monitoring required at initiation
Verapamil / Diltiazem	IV	AV block, negative inotrope	WPW contraindicated; can precipitate VF
Adenosine	Other	Flushing, bronchospasm, chest tightness	Asthma caution; brief (10-sec half-life)
Digoxin	Other	Any arrhythmia, xanthopsia, nausea	Hypokalemia potentiates toxicity; narrow therapeutic window

Torsades de pointes pattern: prolonged QT + polymorphic VT that twists around the isoelectric baseline. Caused by Class Ia (quinidine), Class III (sotalol, ibutilide, dofetilide). Precipitants: bradycardia, hypokalemia, hypomagnesemia, QT-prolonging drugs. Treatment: IV magnesium (first-line) regardless of serum Mg2+ level. Definitive: correct the cause, increase heart rate (pacing or isoproterenol).

Amiodarone monitoring checklist (annual): TFTs (thyroid), LFTs (liver), PFTs + CXR (pulmonary), slit-lamp exam (corneal deposits), skin inspection (photosensitivity, blue-gray discoloration). The boards will give you ONE of these findings and ask which drug.

05 · Clinical Reasoning

Elimination Game

Use the clues to eliminate. One drug survives.

A 50-year-old man with a structurally normal heart and paroxysmal AF is started on an antiarrhythmic for rhythm control. Six months later he presents with bilateral patchy infiltrates on CXR and new fatigue and weight gain. Thyroid labs show TSH 48 mIU/L (high), free T4 low. Which drug was most likely prescribed?

Flecainide Class Ic

Amiodarone Class III

Sotalol Class III

Digoxin Other

Clue 1: Bilateral pulmonary infiltrates plus thyroid dysfunction (hypothyroidism here, but can also cause hyperthyroidism) are classic side effects of a Class III antiarrhythmic. Flecainide (Class Ic) does not cause pulmonary or thyroid toxicity. Digoxin does not either.

Clue 2: The surviving Class III agents are amiodarone and sotalol. Sotalol is a pure K+ channel blocker + beta-blocker. It does NOT cause pulmonary fibrosis or thyroid dysfunction. Amiodarone has ~37% iodine by weight and blocks Na+, K+, Ca2+ channels AND beta receptors. Its iodine load saturates the thyroid, causing both hypo- and hyperthyroidism.

Amiodarone. Bilateral infiltrates = amiodarone pulmonary toxicity. Hypothyroidism = iodine overload suppressing the thyroid (Wolff-Chaikoff effect). No other antiarrhythmic causes this multi-organ picture. Annual monitoring: TFTs, LFTs, PFTs, CXR, eye exam.

06 · Board Practice

Quiz

Four questions. Boards-style. No clues.

0/4

Complete all questions to see your score.

Question 1 of 4

A 34-year-old woman with Wolff-Parkinson-White syndrome presents to the ED with rapid AF at 210 bpm. The ECG shows a wide, irregular rhythm with delta waves. Her blood pressure is 88/60 mmHg. Before electrical cardioversion can be performed, a resident gives IV verapamil. What is the immediate danger?

A Severe bradycardia from AV block in normal conduction tissue

B Verapamil blocks the AV node, forcing all conduction through the accessory pathway, which can trigger ventricular fibrillation

C Verapamil prolongs the QT interval and causes torsades de pointes

D Verapamil accelerates conduction through the AV node, increasing the ventricular rate further

B is correct. In WPW with rapid AF, the AV node acts as a partial brake on ventricular rate. Verapamil (and other AV-node blockers: diltiazem, beta-blockers, adenosine, digoxin) removes that brake. The unblocked accessory pathway conducts the rapid, disorganized atrial impulses directly to the ventricles at full speed. The ventricles cannot handle rates above 250 bpm and can degenerate into VF. Correct treatment: electrical cardioversion (unstable) or IV procainamide (stable, slows accessory pathway directly).

A (Severe bradycardia from AV block): Good instinct: verapamil does block the AV node, and AV block causing bradycardia is a real verapamil risk in normal rhythms. The problem here is the accessory pathway. Blocking the AV node in WPW does not cause bradycardia. It removes the only speed limiter on the bypass tract, flooding the ventricles with 200+ atrial impulses per minute. Think of a highway with two lanes: closing the main lane normally slows traffic, but in WPW it just forces everything through the unregulated side street with no speed limit. Break it down: Verapamil in WPW-AF danger = VF from unbraked accessory pathway conduction, not bradycardia; the AV block removes the speed limiter on the bypass tract.

C (QT prolongation and torsades): Tempting if you associate calcium channel blockers with cardiac toxicity. But verapamil actually shortens the QT interval (blocking inward Ca2+ current reduces the action potential plateau). QT-prolonging drugs are Class Ia (quinidine), Class III (amiodarone, sotalol, dofetilide), and certain antihistamines and antibiotics. Think of verapamil as braking the plateau phase of the action potential: shortening the plateau shortens QT. Break it down: Verapamil shortens QT (Ca2+ block reduces plateau); QT prolongation and torsades come from Class Ia and Class III agents; verapamil danger in WPW is VF from accessory pathway, not torsades.

D (Verapamil accelerates AV node): Tempting if you confuse "slows conduction through the AV node" with the outcome in WPW. Verapamil BLOCKS the AV node (slows conduction). But in WPW, slowing the AV node makes things worse: it redirects impulses to the unbraked accessory pathway. Think of the AV node as a bouncer at the main entrance: slowing the bouncer does not calm the crowd, it just forces everyone through the unguarded side door at full speed. The danger is too much speed through the bypass tract, not acceleration through the AV node. Break it down: Verapamil slows AV nodal conduction; in WPW-AF this redirects impulses to the unbraked accessory pathway; ventricular rates can exceed 250 bpm and degenerate to VF.

Question 2 of 4

A 58-year-old man is brought in post-resuscitation from cardiac arrest due to ventricular fibrillation. He is now in sinus rhythm and hemodynamically stable. His ECG shows Q waves in leads II, III, and aVF consistent with an inferior MI two hours ago. Which antiarrhythmic is most appropriate for sustained VT prophylaxis in this setting?

A Flecainide, because it has the strongest Na+ channel block and will prevent VT recurrence

B Quinidine, because Class Ia agents treat both atrial and ventricular arrhythmias

C Lidocaine (IV), because Class Ib agents preferentially suppress ischemic, depolarized ventricular tissue

D Verapamil, because it slows conduction and will terminate the reentrant circuit

C is correct. Class Ib agents (lidocaine, mexiletine) have fast unbinding that creates use-dependence: they bind preferentially to channels firing at high rates in depolarized (ischemic) tissue. In the post-MI setting, ischemic ventricular tissue is the arrhythmia substrate, and Ib drugs suppress it without much effect on healthy tissue.

A (Flecainide): Tempting because flecainide (Class Ic) has the strongest sodium channel block and does suppress VT effectively in structurally normal hearts. But flecainide is absolutely contraindicated post-MI. The CAST trial showed that flecainide increased mortality in post-MI patients with asymptomatic VT, despite suppressing the arrhythmia. Think of it like using powerful weed killer that also kills the grass: you eliminated the symptom (VT) but made the underlying injured heart more prone to fatal arrhythmia. Strong sodium block in a structurally diseased heart is dangerous. Break it down: Flecainide (Ic) = contraindicated post-MI (CAST trial showed increased mortality despite arrhythmia suppression); use lidocaine (Ib) for post-MI VT.

B (Quinidine): Good instinct: quinidine (Class Ia) does treat both atrial and ventricular arrhythmias and is the right drug class in concept. But quinidine prolongs the QT interval and risks torsades, especially dangerous in a recently ischemic heart that is already electrically unstable. Think of giving an unstable vehicle a speed boost: you might move it, but the instability makes a crash more likely. Break it down: Quinidine (Ia) prolongs QT and risks torsades; post-MI ischemic hearts are already arrhythmia-prone; QT-prolonging agents add arrhythmia risk on top; choose lidocaine (Ib) instead.

D (Verapamil): Tempting because verapamil slows conduction and could seem to interrupt a reentrant circuit. But verapamil targets nodal tissue (the AV node), not ventricular ectopy. Post-MI VT originates from ischemic ventricular muscle, not the AV node. Think of verapamil as a traffic cop stationed at an intersection when the accident is on the highway: it is not at the right location. Break it down: Verapamil targets AV nodal tissue; post-MI VT arises from ischemic ventricular muscle; verapamil has no effect on the arrhythmia substrate and can cause hemodynamic compromise in a damaged heart.

Question 3 of 4

A 45-year-old woman on a cardiac medication develops arthritis in multiple joints, pleuritis, and a facial rash. Labs show ANA positive, anti-histone antibody positive, anti-dsDNA negative, complement levels normal. Which two drugs are the most common causes of this syndrome, and what makes her serologic pattern different from true SLE?

A Amiodarone and sotalol; anti-dsDNA is positive in drug-induced lupus but negative in true SLE

B Procainamide and hydralazine; anti-histone antibodies are positive in drug-induced lupus, while anti-dsDNA (specific to true SLE) is negative

C Quinidine and disopyramide; drug-induced lupus spares the kidneys and brain but anti-dsDNA is positive

D Flecainide and propafenone; anti-histone Ab distinguishes drug-induced lupus from true SLE only when complement is low

B is correct. Procainamide (Class Ia) is the most common antiarrhythmic cause of drug-induced lupus (DIL). Hydralazine (a vasodilator) is the other classic culprit. The serologic fingerprint of DIL: ANA positive, anti-histone antibodies positive, anti-dsDNA NEGATIVE. In true SLE, anti-dsDNA is positive and highly specific. DIL classically spares the kidneys and CNS.

A (Amiodarone and sotalol): Tempting because both are common antiarrhythmics and amiodarone especially has a long list of toxicities. But neither causes drug-induced lupus. Amiodarone's signature toxicities are pulmonary fibrosis, thyroid dysfunction, hepatotoxicity, corneal deposits, and blue-gray skin discoloration. Sotalol prolongs QT and risks torsades. Think of amiodarone's side effect list as a full toolbox with dozens of items, but lupus is simply not in that box. Break it down: Amiodarone toxicities = pulmonary, thyroid, hepatic, corneal, skin; sotalol = torsades risk; neither causes DIL; the DIL pair is procainamide and hydralazine.

C (Quinidine and disopyramide): Good instinct on quinidine: it is Class Ia like procainamide and is occasionally associated with DIL as a rare side effect. But the question asks for the most common causes, which are procainamide and hydralazine by a wide margin. Quinidine's primary toxicities are cinchonism and torsades. Think of drug side effect profiles as specialty menus: procainamide's headliner is DIL, quinidine's headliner is cinchonism. You cannot order the headliner dish from the wrong menu. Disopyramide is notable for strong anticholinergic effects (urinary retention, dry mouth), not DIL. Break it down: The high-yield DIL pair = procainamide plus hydralazine; quinidine is a rare third option but is not the primary answer; disopyramide = anticholinergic side effects, not DIL.

D (Flecainide and propafenone): Both are Class Ic agents with strong sodium channel block. Neither causes drug-induced lupus. Flecainide is notable for CAST trial contraindication post-MI. Propafenone has additional beta-blocking activity. Think of Class Ic agents as occupying a completely different shelf in the side effect store: their risks are arrhythmia in structurally diseased hearts, not autoimmunity. Break it down: Class Ic agents (flecainide, propafenone) do not cause DIL; flecainide = contraindicated post-MI; the DIL pair is procainamide and hydralazine, not any Class Ic drug.

Question 4 of 4

A 62-year-old woman with AF is started on dofetilide. On day 2 of in-hospital initiation, telemetry shows a polymorphic VT with a sinusoidal, twisting pattern around the isoelectric baseline. Her QTc was 520 ms before the event. Her potassium is 3.0 mEq/L. What is the immediate pharmacologic treatment?

A Amiodarone IV, because it is the most effective antiarrhythmic and will terminate the polymorphic VT

B Lidocaine IV, because Class Ib agents shorten action potential duration and suppress ventricular ectopy

C IV magnesium sulfate, regardless of serum magnesium level, to stabilize the myocardial membrane and suppress early afterdepolarizations

D Adenosine IV push, because torsades is an AV-node-dependent arrhythmia

C is correct. This is torsades de pointes: polymorphic VT with twisting around the baseline, triggered by prolonged QT (dofetilide, a Class III agent) plus hypokalemia (K+ 3.0 mEq/L), which independently prolongs QT. IV magnesium is the immediate pharmacologic treatment regardless of serum magnesium levels. Mechanism: Mg2+ blocks early afterdepolarizations (the trigger for torsades) by inhibiting L-type Ca2+ channels and stabilizing the membrane. After Mg2+, correct the electrolyte abnormality, discontinue the offending drug, and consider overdrive pacing or isoproterenol (torsades is worse at slow rates).

A (Amiodarone IV): Tempting because amiodarone is the most versatile antiarrhythmic and terminates many types of VT. But amiodarone is a Class III agent that significantly prolongs the QT interval. Giving amiodarone to a patient who already has a QTc of 520 ms from dofetilide would be pouring fuel on the fire that started the torsades. Think of the QT interval as a fuse length: dofetilide already made the fuse dangerously long, amiodarone would lengthen it further. Break it down: Amiodarone prolongs QT; torsades in a QT-prolonged patient requires QT-shortening or membrane stabilization (magnesium), not more QT prolongation; amiodarone is contraindicated in torsades.

B (Lidocaine IV): Good instinct: lidocaine (Class Ib) shortens action potential duration and suppresses ventricular ectopy, which sounds like exactly what you want. But torsades is driven by early afterdepolarizations (EADs) generated by prolonged QT, not by the ischemic reentrant substrate that lidocaine targets. Magnesium specifically suppresses EADs by blocking the L-type calcium channel that generates them. Think of lidocaine as a fire extinguisher designed for electrical fires being used on a chemical fire: wrong agent for the specific mechanism. Break it down: Torsades = EADs from prolonged QT; treatment = IV magnesium (blocks EAD-generating Ca2+ current); lidocaine targets reentrant arrhythmias in ischemic tissue, not EAD-driven torsades.

D (Adenosine IV): Tempting if you think of adenosine as a universal rhythm-terminator for rapid VT. Adenosine terminates AV-node-dependent arrhythmias: AVNRT and AVRT. Torsades de pointes is NOT AV-node dependent. It arises from abnormal ventricular automaticity (EADs) in a patient with critically prolonged QT. Think of adenosine as a remote control for the AV node: it has no signal to change on a ventricular arrhythmia that does not involve the AV node. Break it down: Adenosine terminates AV-node-dependent SVT (AVNRT, AVRT); torsades de pointes is a ventricular arrhythmia driven by EADs, not AV nodal reentry; adenosine has no role in torsades.

07 · Board-Style Walkthrough

25-Question Walkthrough

Original board-style vignettes. Shuffled, never-repeat, full Chicago explanations.