Medical Pharmacology: Chapter 8: Antiarrhythmic Drugs -- Module 3: Class II Beta-Blockers in Arrhythmia Management

Chapter 8: Antiarrhythmic Drugs — Module 3: Class II Beta-Blockers in Arrhythmia Management
Tier: 1 — Foundational Recall (16 questions)

1. A 19-year-old man with catecholaminergic polymorphic ventricular tachycardia (CPVT) confirmed by RyR2 mutation analysis has been on metoprolol succinate 100 mg daily for two years. His electrophysiologist notes breakthrough bidirectional VT on a recent exercise stress test and considers switching agents. What is the primary pharmacologic rationale for preferring nadolol over metoprolol in CPVT?

A) Nadolol's hepatic metabolism generates an active metabolite that directly stabilizes the RyR2 channel
B) Nadolol's non-selective β1+β2 blockade and 14–24-hour half-life provide more complete and consistent suppression of catecholamine-driven RyR2 phosphorylation than β1-selective metoprolol
C) Nadolol has stronger membrane-stabilizing activity than metoprolol, directly reducing SR Ca2+ leak independent of adrenergic tone
D) Nadolol's CNS penetration suppresses central sympathetic outflow more effectively than the hydrophilic metoprolol
E) Nadolol selectively blocks β2 receptors in the SR membrane, preventing PKA-mediated phospholamban phosphorylation

ANSWER: B

Rationale:

CPVT arrhythmias are driven by both β1- and β2-adrenergic stimulation of RyR2, producing pathologic SR Ca2+ leak and delayed afterdepolarizations (DADs). β1-selective agents such as metoprolol leave β2-mediated RyR2 phosphorylation intact, providing incomplete suppression. Nadolol's non-selective blockade of both receptor subtypes eliminates this gap. Its 14–24-hour half-life and renal elimination without hepatic metabolism produce consistent plasma levels without the troughs associated with shorter-acting agents, minimizing windows for breakthrough adrenergic arrhythmias. Beta-blockers should never be abruptly discontinued in CPVT — withdrawal can precipitate ventricular fibrillation.

2. A 71-year-old man develops AF with rapid ventricular response (rate 148 bpm) on postoperative day 1 following elective colectomy. He is hemodynamically stable (BP 118/74 mmHg) but has no prior cardiac history and was not on beta-blockers preoperatively. Which agent is most appropriate for acute rate control in this setting?

A) IV digoxin — vagotonic mechanism provides reliable rate control in the postoperative sympathetic state
B) IV amiodarone — broad antiarrhythmic coverage ensures rate control and possible rhythm conversion
C) Oral metoprolol succinate 25 mg — appropriate for new-onset postoperative AF without hemodynamic compromise
D) IV esmolol — β1-selective blockade with 9-minute half-life allows precise titration and rapid reversal if hemodynamic instability develops
E) IV propranolol — non-selective blockade provides faster and more complete AV nodal slowing than β1-selective agents

ANSWER: D

Rationale:

Postoperative AF in a beta-blocker-naive patient requires careful hemodynamic monitoring. IV esmolol is the preferred agent because its ultra-short half-life (approximately 9 minutes, from red blood cell esterase hydrolysis) allows precise titration — if hypotension or excessive bradycardia develops, the drug's effects dissipate within 20–30 minutes of discontinuation. This reversibility is critical in the postoperative setting where hemodynamic tolerance is uncertain. IV digoxin is inadequate for rate control in the high-sympathetic-tone postoperative state. Oral metoprolol succinate is appropriate for non-urgent rate control but lacks the rapid titratability needed here. Propranolol's non-selectivity offers no advantage and increases bronchospasm risk.

3. A 28-year-old man is brought to the emergency department with agitation, diaphoresis, BP 192/110 mmHg, and heart rate 136 bpm. Urine toxicology is positive for cocaine. A medical student suggests IV metoprolol for rate and blood pressure control. What is the correct response?

A) IV metoprolol is contraindicated — beta-blockade leaves α-adrenergic vasoconstriction unopposed, paradoxically worsening hypertension and coronary vasospasm; benzodiazepines are the appropriate first-line treatment
B) IV metoprolol is appropriate because β1-selectivity avoids β2-mediated vasodilation and focuses blockade on the cardiac rate
C) IV metoprolol is appropriate at half the standard dose given the cocaine-induced catecholamine excess
D) IV metoprolol is contraindicated only if the patient has structural heart disease; in a young patient with normal cardiac function it is safe
E) IV metoprolol is contraindicated, but IV propranolol is safe because its non-selective blockade counterbalances both α and β stimulation simultaneously

ANSWER: A

Rationale:

Cocaine inhibits neuronal norepinephrine reuptake, producing simultaneous intense α- and β-adrenergic stimulation. β2-adrenergic activation normally provides a partial counterbalance to α1-mediated vasoconstriction. Beta-blockade — including β1-selective agents — eliminates this β2-vasodilatory counterbalance while leaving α1-mediated coronary and peripheral vasoconstriction unopposed, paradoxically worsening hypertension and precipitating coronary vasospasm. This contraindication applies to all beta-blockers without exception. First-line management is benzodiazepines (reducing central sympathetic outflow), with phentolamine (α-blockade) added if hypertension persists. Propranolol is not a safe alternative — non-selective blockade still removes β2-vasodilation while leaving α1 unopposed.

4. A 54-year-old woman with AF on metoprolol tartrate 50 mg twice daily (well-controlled at heart rate 68 bpm) is started on fluoxetine for major depressive disorder. Two weeks later she presents with symptomatic bradycardia (heart rate 38 bpm) and lightheadedness. Her metoprolol dose has not changed. What is the mechanism of this interaction?

A) Fluoxetine directly blocks cardiac β1-adrenergic receptors, additive with metoprolol's blockade
B) Fluoxetine increases renal clearance of metoprolol, paradoxically causing accumulation through a compensatory mechanism
C) Fluoxetine is a potent CYP2D6 inhibitor that substantially reduces metoprolol hepatic metabolism, causing 3–5-fold elevation in plasma metoprolol concentrations and exaggerated β1-blockade
D) Fluoxetine displaces metoprolol from plasma protein binding sites, acutely increasing free drug concentration
E) Fluoxetine inhibits the P-glycoprotein transporter responsible for metoprolol efflux from cardiac myocytes

ANSWER: C

Rationale:

Metoprolol is a CYP2D6 substrate with a narrow pharmacodynamic window — small increases in plasma concentration produce clinically significant bradycardia and AV block. Fluoxetine (and paroxetine) are potent CYP2D6 inhibitors that effectively convert an extensive metabolizer into a functional poor metabolizer phenotype, raising plasma metoprolol concentrations 3–5-fold at unchanged doses. The clinical consequence is exaggerated β1-blockade. Management options include reducing the metoprolol dose, switching to a beta-blocker not dependent on CYP2D6 (atenolol or nadolol, both renally eliminated), or selecting an antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram).

5. A 61-year-old man with heart failure with reduced ejection fraction (HFrEF; EF 32%) is admitted for an elective procedure and found to be on atenolol 50 mg daily, prescribed by his primary care physician for hypertension years before his heart failure diagnosis. He is currently euvolemic and asymptomatic. Which action regarding his beta-blocker is most appropriate?

A) Continue atenolol — all beta-blockers are equivalent in HFrEF and atenolol is appropriate
B) Discontinue all beta-blockers — the negative inotropy of beta-blockade is harmful in HFrEF with EF below 35%
C) Switch to propranolol — its non-selective blockade provides broader neurohormonal suppression in HFrEF
D) Reduce atenolol to 25 mg daily — lower doses of any beta-blocker are safe in HFrEF
E) Switch to carvedilol, metoprolol succinate, or bisoprolol — only these three agents have demonstrated mortality benefit in HFrEF; atenolol does not carry this evidence

ANSWER: E

Rationale:

The mortality benefit of beta-blockers in HFrEF is not a class effect — it is agent-specific, established only for carvedilol (COPERNICUS, CAPRICORN), metoprolol succinate (MERIT-HF), and bisoprolol (CIBIS-II). Atenolol, propranolol, metoprolol tartrate, and other agents have not demonstrated survival benefit in HFrEF and should not be used for this indication. When a patient on any non-evidence-based beta-blocker is identified with HFrEF, conversion to one of the three proven agents at the lowest starting dose is standard quality care. The transition should occur while the patient is euvolemic and clinically stable, with uptitration over weeks to months.

6. A 16-year-old girl with long QT syndrome type 1 (LQT1) — caused by a KCNQ1 loss-of-function mutation reducing IKs (the slow delayed rectifier K+ current that provides rate-adaptive repolarization reserve during sympathetic activation) — experiences a syncopal episode while swimming competitively. Which pharmacologic strategy is most appropriate for long-term arrhythmia prevention?

A) Mexiletine — blocks the persistent late INa current that is elevated in LQT1
B) Nadolol or atenolol — non-selective or long-acting β1-selective beta-blocker to prevent sympathetic activation from triggering torsades de pointes via adrenergic worsening of IKs-dependent repolarization failure
C) Flecainide — Class Ic sodium channel blockade suppresses triggered activity in LQT1
D) Verapamil — ICaL blockade reduces Ca2+ entry and shortens the action potential in LQT1
E) Amiodarone — multi-channel blockade provides the broadest QT stabilization in LQT1

ANSWER: B

Rationale:

In LQT1, IKs is the primary repolarization reserve recruited during sympathetic activation to shorten the action potential duration at faster heart rates. With IKs reduced by the KCNQ1 mutation, sympathetic activation paradoxically worsens QT prolongation, precipitating torsades de pointes — characteristically triggered by exercise or sudden auditory/emotional stimuli. Beta-blockers prevent this by attenuating the adrenergic signal that would otherwise worsen QT prolongation. They reduce event rates by approximately 50–70% in symptomatic LQT1 patients. Nadolol and atenolol are preferred for their consistent half-lives and predictable plasma levels. Mexiletine targets INaL — the mechanism relevant to LQT3, not LQT1. Amiodarone prolongs the QT interval and would be counterproductive.

7. A 68-year-old man with a history of MI three years ago and an EF of 38% is admitted for elective knee replacement. The anesthesiologist orders his home metoprolol succinate 100 mg daily to be held perioperatively due to concern about intraoperative hypotension. On postoperative day 2 he develops sinus tachycardia at 118 bpm followed by a run of non-sustained ventricular tachycardia. What is the most likely explanation and what should have been done differently?

A) The patient developed electrolyte disturbance from surgical blood loss — metoprolol would not have prevented this
B) The patient's tachycardia reflects normal postoperative sympathetic response — no intervention was necessary
C) The patient has underlying CPVT that was unmasked by surgery — ICD implantation is indicated
D) Abrupt beta-blocker discontinuation caused β-receptor upregulation; the supersensitive receptor population, exposed to postoperative catecholamine surge without drug coverage, precipitated rebound tachycardia and ventricular arrhythmia — metoprolol should have been continued perioperatively
E) The anesthesiologist's decision was correct — continuing beta-blockers in post-MI patients perioperatively increases stroke risk per the POISE trial

ANSWER: D

Rationale:

Long-term beta-blocker therapy causes compensatory upregulation of β-adrenergic receptor density. Abrupt discontinuation exposes this supersensitive receptor population to the substantial catecholamine surge that accompanies surgery and the postoperative period, producing rebound tachycardia, hypertension, and — in patients with CAD or reduced EF — ventricular arrhythmias. Continuing established beta-blockers perioperatively is unambiguous standard of care and is specifically recommended by ACC/AHA perioperative guidelines. The POISE trial warning applies to initiating high-dose beta-blockers in naive patients on the day of surgery — not to continuing chronic therapy. If IV administration is required perioperatively, IV metoprolol or esmolol can bridge oral therapy.

8. A 74-year-old woman with HFrEF (EF 28%) and persistent AF presents with a ventricular rate of 122 bpm at rest, dyspnea on minimal exertion, and bilateral ankle edema. She is euvolemic after diuresis. Which agent is most appropriate for long-term ventricular rate control in this patient?

A) Oral metoprolol succinate — β1-selective blockade is the preferred rate control strategy in AF with HFrEF; non-DHP calcium channel blockers (verapamil, diltiazem) are avoided due to negative inotropy
B) Oral verapamil — non-dihydropyridine calcium channel blocker (non-DHP CCB) providing effective AV nodal slowing without the negative chronotropy of beta-blockers
C) Oral diltiazem — preferred non-DHP CCB for rate control in AF with reduced EF
D) Oral digoxin monotherapy — vagotonic mechanism provides adequate rate control in HFrEF without negative inotropy
E) Oral amiodarone — rhythm control is preferred over rate control in HFrEF and amiodarone is the safest antiarrhythmic in reduced EF

ANSWER: A

Rationale:

In AF with HFrEF, beta-blockers are the preferred agents for ventricular rate control. Non-DHP CCBs (verapamil and diltiazem) are contraindicated in HFrEF due to their significant negative inotropic properties, which can precipitate acute decompensation in patients with already-impaired systolic function. Metoprolol succinate provides effective AV nodal slowing through β1-blockade and carries proven mortality benefit in HFrEF (MERIT-HF). Digoxin can be added as adjunct rate control but is inadequate as monotherapy in patients with exercise-related rate acceleration. The 2023 ACC/AHA/ACCP/HRS AF guideline targets a resting rate below 110 bpm as initial rate control, with tighter targets for symptomatic patients.

9. A 38-year-old woman with known Graves' disease presents with fever (39.4°C), agitation, AF at 158 bpm, and tremor. Thyroid storm is diagnosed. Which beta-blocker is preferred and why?

A) Esmolol — its short half-life allows rapid titration as the thyroid storm is treated and the catecholamine excess resolves
B) Nadolol — its long half-life ensures consistent adrenergic blockade throughout the multi-day course of thyroid storm management
C) Propranolol — non-selective β1+β2 blockade controls the tachycardia and additionally blocks peripheral conversion of T4 to the more biologically active T3 via β2-mediated deiodinase inhibition, reducing the hormonal burden
D) Atenolol — β1-selectivity provides cardiac rate control with minimal effect on peripheral thyroid hormone metabolism
E) Carvedilol — combined α1 and β-blockade reduces both the tachycardia and the hypertension characteristically seen in thyroid storm

ANSWER: C

Rationale:

Propranolol is the preferred beta-blocker in thyroid storm for two distinct pharmacologic reasons. First, its non-selective β1+β2 blockade rapidly controls the tachycardia, hypertension, tremor, and agitation driven by catecholamine hypersensitivity. Second, propranolol blocks peripheral conversion of thyroxine (T4) to the more biologically active triiodothyronine (T3) by inhibiting the peripheral deiodinase enzyme — an effect mediated through β2 receptor blockade. This reduces the acute hormonal burden independently of sympathetic blockade and is a mechanism unique to propranolol among beta-blockers. IV propranolol (0.5–1 mg IV over 10 minutes, titrated) is used acutely; oral propranolol 60–80 mg every 4–6 hours for sustained management. If propranolol is contraindicated (severe reactive airway disease), high-dose esmolol provides titratable rate control without the T4→T3 conversion benefit.

10. A 70-year-old man with moderate COPD (FEV1 58% predicted) and paroxysmal AF requires long-term rate control therapy. He is hemodynamically stable with a resting heart rate of 92 bpm. Which approach is most appropriate?

A) Oral propranolol 40 mg twice daily — non-selective blockade provides superior AV nodal slowing in AF
B) Oral nadolol 40 mg daily — its renal elimination avoids pulmonary side effects from hepatically cleared agents
C) Avoid all beta-blockers; prescribe oral diltiazem as sole rate control agent given the COPD diagnosis
D) Oral carvedilol 6.25 mg twice daily — combined α1/β-blockade reduces bronchospasm risk by lowering airway smooth muscle tone
E) Oral metoprolol succinate 25 mg daily — β1-selective agent at lowest effective dose with monitoring for bronchospasm; COPD is not an absolute contraindication to cardioselective beta-blockers

ANSWER: E

Rationale:

COPD is not an absolute contraindication to β1-selective beta-blockers. Bronchospasm in COPD is mediated by β2-blockade; β1-selective agents (metoprolol, atenolol, bisoprolol) have substantially reduced β2 activity at therapeutic doses and are generally well tolerated in COPD, particularly at low doses. Starting at the lowest dose with close monitoring for bronchospasm is appropriate. Non-selective agents (propranolol, nadolol, carvedilol) block β2 receptors and should be avoided in reactive airway disease — the bronchospasm risk is related to receptor selectivity, not route of elimination. If bronchospasm develops despite β1-selectivity, a non-DHP CCB (diltiazem or verapamil) is an appropriate alternative, provided EF is preserved.

11. A 66-year-old man with stage 4 chronic kidney disease (CKD; creatinine clearance 22 mL/min) and Child-Pugh class B cirrhosis develops AF with rapid ventricular response (rate 138 bpm) in the ICU. He requires acute IV rate control. Which beta-blocker is most appropriate given his organ impairment?

A) IV metoprolol — hepatic metabolism via CYP2D6 is unaffected by cirrhosis at standard doses
B) IV esmolol — eliminated by red blood cell esterases independent of hepatic or renal function, making it safe in combined organ impairment with rapid reversibility if hemodynamically unstable
C) IV metoprolol at 25% of the standard dose — dose reduction compensates for the CYP2D6 impairment caused by cirrhosis
D) IV propranolol — extensive hepatic first-pass metabolism is actually reduced in cirrhosis, increasing bioavailability and lowering required doses
E) IV carvedilol — combined α1/β-blockade reduces portal hypertension as an added benefit in cirrhosis

ANSWER: B

Rationale:

Esmolol's elimination by red blood cell esterases is entirely independent of hepatic metabolism and renal clearance. This makes it uniquely suitable for patients with significant hepatic or renal impairment who require precise, titratable, rapidly reversible IV beta-blockade. In ICU patients with hemodynamic uncertainty, esmolol's 9-minute half-life and the fact that effects dissipate within 20–30 minutes of discontinuation make it the safest choice for acute rate control. Metoprolol and carvedilol require hepatic metabolism and accumulate in cirrhosis. Nadolol requires dose reduction in CKD and is not available in IV formulation. IV propranolol, while reduced in first-pass in cirrhosis, has unpredictable kinetics in severe hepatic disease.

12. A 58-year-old man is admitted with an anterior STEMI and undergoes successful primary PCI. His post-procedure EF is 34%. He is currently euvolemic and hemodynamically stable on day 3 of admission. Which beta-blocker regimen is most appropriate at this stage?

A) Initiate IV esmolol infusion — continuous IV beta-blockade is superior to oral therapy in the early post-MI period
B) Defer all beta-blockers until EF improves above 40% — negative inotropy is too risky in LV dysfunction
C) Initiate high-dose metoprolol succinate 200 mg daily immediately — early high-dose therapy maximizes mortality benefit per the BHAT trial
D) Initiate carvedilol at the lowest dose (3.125 mg twice daily) and uptitrate over weeks to months — CAPRICORN demonstrated mortality benefit with carvedilol in post-MI patients with LV dysfunction when started in the stabilized, euvolemic state
E) Initiate atenolol 50 mg daily — proven post-MI agent with the longest evidence base for arrhythmia prophylaxis

ANSWER: D

Rationale:

CAPRICORN (2001) randomized 1,959 post-MI patients with LV dysfunction (EF 40% or less) to carvedilol or placebo on background ACE inhibitor therapy, demonstrating a 23% reduction in all-cause mortality (hazard ratio 0.77). Carvedilol's combined β+α1-blockade and proven trial data make it guideline-preferred in post-MI LV dysfunction. The critical initiation rule is that the patient must be clinically stable and euvolemic — not in pulmonary edema or cardiogenic shock. Starting at the lowest available dose (3.125 mg twice daily) with uptitration over weeks to months to the maximum tolerated dose is the correct approach. Atenolol does not carry proven HFrEF or post-MI LV dysfunction mortality data. Deferring beta-blockers until EF recovers is incorrect — the neurohormonal benefit begins immediately in the stabilized patient.

13. A 72-year-old man on chronic metoprolol succinate 50 mg daily for hypertension is scheduled for elective hip replacement. His pre-anesthesia assessment recommends continuing his metoprolol perioperatively. A junior resident questions this, citing the POISE trial which showed increased mortality with metoprolol. What is the correct interpretation of the POISE trial for this patient?

A) The POISE trial found excess mortality from high-dose metoprolol initiation immediately before surgery in beta-blocker-naive patients — it does not apply to patients already on chronic beta-blocker therapy, who should always have their medication continued perioperatively
B) The POISE trial demonstrated that all beta-blockers increase perioperative mortality and should be discontinued 48 hours before elective surgery
C) The POISE trial applies to this patient because he is on metoprolol succinate, the same agent studied — his dose should be halved preoperatively
D) The POISE trial finding means oral metoprolol should be switched to IV esmolol perioperatively to avoid the stroke risk associated with oral dosing
E) The POISE trial results mandate cardiology consultation before continuing any beta-blocker perioperatively in patients over 65

ANSWER: A

Rationale:

The POISE trial randomized beta-blocker-naive patients to high-dose metoprolol succinate (100 mg starting 2–4 hours before surgery, then 200 mg postoperatively) or placebo and found increased 30-day mortality attributable to hypotension and stroke in the high-dose initiation arm. This finding does not apply to patients already on chronic beta-blocker therapy. Abruptly discontinuing established beta-blockers perioperatively causes β-receptor upregulation and rebound tachyarrhythmia — a well-documented, preventable harm. ACC/AHA perioperative guidelines are unambiguous: continue beta-blockers in patients already taking them. The POISE lesson is specifically that high-dose initiation on the day of surgery in naive patients is harmful — not that perioperative beta-blockade is generally contraindicated.

14. A 31-year-old man with long QT syndrome type 3 (LQT3) caused by a gain-of-function SCN5A mutation producing persistent late INa (INaL — an abnormal persistent inward sodium current during phases 2–3 of the action potential that prolongs QT independent of adrenergic tone) has been on nadolol with suboptimal QT control (QTc 532 ms). His cardiologist considers adding a second agent. Which pharmacologic adjunct is most appropriate and why?

A) Flecainide — Class Ic sodium channel blockade eliminates the SCN5A gain-of-function current at the channel level
B) Amiodarone — multi-channel blockade including IKr reduction provides additive QT stabilization in LQT3
C) Mexiletine — a Class Ib sodium channel blocker (lidocaine analog) that preferentially blocks INaL at therapeutic concentrations, directly targeting the LQT3 pathophysiologic mechanism
D) Verapamil — ICaL reduction shortens phase 2, compensating for the QT prolongation caused by excess INaL
E) Ivabradine — heart rate reduction lowers the rate-dependent component of QT prolongation in LQT3

ANSWER: C

Rationale:

In LQT3, the pathophysiologic current is INaL — a gain-of-function persistent late sodium current that prolongs action potential duration independent of adrenergic tone. Beta-blockers do not meaningfully reduce INaL and have limited antiarrhythmic efficacy in LQT3. Mexiletine is a Class Ib agent (lidocaine analog) that preferentially inhibits INaL at low concentrations while minimally affecting peak INa — directly targeting the pathophysiologic current. Case series and small trials demonstrate QTc shortening of 20–40 ms and arrhythmia reduction with mexiletine in LQT3. Flecainide (Class Ic) powerfully blocks peak INa but is contraindicated in structural heart disease and does not preferentially target INaL. Amiodarone further prolongs the QT interval through IKr blockade — counterproductive in an already prolonged-QT state.

15. A 67-year-old woman with HFrEF (EF 30%) on carvedilol 25 mg twice daily presents with acute decompensated heart failure with pulmonary edema and bilateral crackles. She remains on her home medications. What is the correct management of her carvedilol in this setting?

A) Continue carvedilol at the current dose — beta-blockers protect against arrhythmia during decompensation and should never be altered
B) Increase carvedilol to 50 mg twice daily — higher doses of beta-blockade provide more complete neurohormonal suppression during decompensation
C) Abruptly discontinue carvedilol immediately — negative inotropy is contraindicated in acute decompensated HFrEF and the drug must be stopped
D) Switch carvedilol to IV esmolol to maintain beta-blockade while allowing more precise hemodynamic titration during the acute phase
E) Halve the carvedilol dose to 12.5 mg twice daily — do not abruptly discontinue, as sudden withdrawal causes β-receptor upregulation and rebound adrenergic arrhythmia, but reduce the dose to minimize negative inotropic burden during the acute decompensation

ANSWER: E

Rationale:

Patients with HFrEF on chronic beta-blocker therapy who decompensate should have their dose halved — not stopped entirely. Abrupt discontinuation causes β-receptor upregulation (a compensatory response to chronic blockade) that exposes the patient to rebound adrenergic tachycardia and ventricular arrhythmia when suddenly withdrawn. This is especially dangerous in patients with reduced EF and established coronary artery disease. The reduced dose maintains partial neurohormonal protection while lowering the negative inotropic burden during the acute decompensation. Once the patient is re-stabilized and euvolemic, the beta-blocker dose is uptitrated back toward the previous therapeutic target.

16. A 34-year-old woman with no structural heart disease presents with palpitations and a narrow-complex regular tachycardia at 182 bpm consistent with AV nodal re-entrant tachycardia (AVNRT). She has had three prior episodes in the past year, each self-terminating. She declines catheter ablation. Which statement best describes the role of beta-blockers in her management?

A) IV metoprolol is the first-line acute treatment for AVNRT and should be administered immediately
B) Adenosine is first-line for acute termination of AVNRT; oral metoprolol or atenolol are first-line for long-term prophylaxis in patients declining ablation
C) Beta-blockers are contraindicated in AVNRT because AV nodal slowing can paradoxically accelerate the re-entrant circuit
D) Oral propranolol is preferred over metoprolol for AVNRT prophylaxis due to its membrane-stabilizing activity
E) IV esmolol is first-line for acute AVNRT because its short half-life allows termination of the arrhythmia without sustained AV nodal suppression

ANSWER: B

Rationale:

For acute termination of AVNRT, adenosine (6 mg IV rapid push, repeat 12 mg if needed) is first-line — it transiently blocks AV nodal conduction, interrupting the re-entrant circuit. IV beta-blockers (metoprolol or esmolol) can terminate AV nodal-dependent re-entrant tachycardias by blocking the slow pathway or retrograde limb, but they are considered second-line to adenosine for acute termination. For long-term prophylaxis in patients declining or not eligible for ablation, oral metoprolol or atenolol are first-line agents, reducing the frequency of episodes by suppressing sympathetically triggered re-entry. Beta-blockers are preferred over CCBs for chronic prophylaxis when CCBs are contraindicated or poorly tolerated, and when rate control rather than immediate rhythm restoration is the goal.