BCCCP Cardiology Prep: High-Yield Topics on Arrhythmias and Heart Failure for the Specialist Board Exam

Arrhythmias and heart failure show up again and again on specialist board exams. They are common in the ICU. Their treatments are nuanced. Small mistakes can harm patients. This guide focuses on high-yield points you can recall under pressure. It explains the “why,” so the right choice feels obvious when you see it on test day. The emphasis is practical: recognition, drug selection, dosing, contraindications, and monitoring.

How to read the rhythm strip fast (and why it matters)

Every arrhythmia question starts with the strip. Classify before you treat. Drugs that help one rhythm can worsen another.

Rate: Tachy (>100) or brady (<60)? Fast tells you “tachy algorithm;” slow tells you “brady algorithm.”
Regularity: Regular suggests SVT or monomorphic VT; irregular suggests AF or polymorphic VT.
P-waves: Present and related to QRS? If no, think AF or AV dissociation (VT).
QRS width: Narrow (<120 ms) means supraventricular. Wide (≥120 ms) means ventricular or SVT with aberrancy.

Why it matters: AV nodal blockers (adenosine, diltiazem, beta-blockers, digoxin) are great for narrow-complex reentry tachycardias but dangerous in pre-excited AF. Wide-complex tachycardia is VT until proven otherwise; give antiarrhythmics that work in the ventricle.

SVT and atrial flutter: quick control, clear logic

Stable, regular narrow-complex tachycardia (likely AVNRT/AVRT)

Vagal maneuvers first. Breaks reentry.
Adenosine 6 mg rapid IV push, then 12 mg if needed (may repeat 12 mg). Use a large bore IV near the heart. Follow with flush. Avoid in severe asthma (bronchospasm risk) and in WPW with AF (can accelerate conduction down the accessory pathway).
If adenosine fails or is contraindicated: diltiazem 0.25 mg/kg IV bolus, then 0.35 mg/kg; infusion 5–15 mg/h. Or metoprolol tartrate 5 mg IV q5 min up to 15 mg. Avoid non-dihydropyridine calcium channel blockers in decompensated HFrEF (negative inotropy).

Atrial flutter

Often 2:1 conduction with ventricular rate ~150. It responds to rate control similar to AF.
Synchronized cardioversion is very effective (50–100 J biphasic).
Anticoagulation follows AF rules. Stroke risk is similar to AF.

Why: These rhythms rely on reentry through the AV node (SVT) or the atrial macroreentry circuit (flutter). Adenosine or AV nodal blockade interrupts the circuit. Cardioversion is definitive for flutter.

Atrial fibrillation: rate versus rhythm and anticoagulation

When to cardiovert now: Hemodynamic instability (hypotension, ischemia, pulmonary edema, altered mental status). Give immediate synchronized cardioversion (120–200 J biphasic for AF), and start anticoagulation as soon as possible.

Anticoagulation (nonvalvular AF)

Use CHA2DS2-VASc. Oral anticoagulation is recommended for score ≥2 in men, ≥3 in women. Consider for 1 in men or 2 in women based on risk/benefit.
Apixaban 5 mg BID. Reduce to 2.5 mg BID if patient has 2 of: age ≥80, weight ≤60 kg, or SCr ≥1.5 mg/dL.
Rivaroxaban 20 mg nightly with food (15 mg if CrCl 15–50 mL/min).
Dabigatran 150 mg BID (75 mg BID if CrCl 15–30 mL/min). Avoid in mechanical valves.
Edoxaban 60 mg daily (30 mg if CrCl 15–50 mL/min, weight ≤60 kg, or with certain P-gp inhibitors). Avoid if CrCl >95 mL/min due to reduced efficacy.

Cardioversion and anticoagulation timing

AF <48 hours: cardiovert and start anticoagulation; continue for at least 4 weeks.
AF ≥48 hours or unknown: anticoagulate ≥3 weeks before cardioversion, or use TEE-guided strategy with immediate anticoagulation and continue ≥4 weeks.

Rate control (stable patients)

Diltiazem if no HFrEF: 0.25 mg/kg IV bolus (repeat 0.35 mg/kg), infusion 5–15 mg/h. Fast onset, strong AV nodal block.
Metoprolol tartrate 5 mg IV q5 min up to 15 mg. Or esmolol 500 mcg/kg bolus, then 50–200 mcg/kg/min infusion. Esmolol is useful in tenuous hemodynamics due to short half-life.
Amiodarone 150 mg IV over 10 min, then 1 mg/min for 6 h, then 0.5 mg/min if HFrEF or hypotension limits other agents. It offers both rate and rhythm effect but is slower for rate.
Digoxin (0.25 mg IV q6h to total 0.75–1 mg, then 0.125–0.25 mg daily) is helpful in HFrEF and at rest. It is slower and less effective during exertion or high sympathetic tone. Aim level 0.5–0.9 ng/mL. Adjust for renal function.

Rhythm control (selected patients: symptomatic despite rate control, new AF with HF, younger patients)

Amiodarone is the safest in HFrEF. Watch interactions: reduce warfarin 30–50% and digoxin 50%; monitor TSH, LFTs, chest imaging, and eyes.
Dofetilide for HFrEF if rhythm control is needed. Initiate in hospital with QT monitoring. Dosing by CrCl: >60 mL/min 500 mcg BID; 40–60 mL/min 250 mcg BID; 20–39 mL/min 125 mcg BID; <20 mL/min contraindicated.
Sotalol for patients with preserved EF; monitor QT and renal function. Avoid in severe renal impairment and prolonged QT.
Flecainide or propafenone for patients without structural heart disease. Must pair with an AV nodal blocker to prevent 1:1 atrial flutter conduction.
Dronedarone is contraindicated in decompensated HF or permanent AF due to increased mortality.

Why: In AF, fast rates reduce cardiac output and worsen HF. AV nodal blockers slow the ventricular response. HFrEF limits CCB use due to negative inotropy. Rhythm strategies need drugs that do not increase mortality in structural heart disease; that is why amiodarone and dofetilide are preferred in HFrEF.

AF with pre-excitation (WPW): the “do not” list

Clue: Very fast, irregular wide-complex rhythm with variable QRS morphologies in a young patient. That is AF with an accessory pathway.

Do not use AV nodal blockers (adenosine, diltiazem, verapamil, beta-blockers, digoxin). They can accelerate conduction down the accessory pathway and trigger VF.
Treat with procainamide (20–50 mg/min IV until arrhythmia terminates, hypotension, QRS widens >50%, or maximum 17 mg/kg; then 1–4 mg/min infusion). Or perform synchronized cardioversion if unstable.

Why: In pre-excitation, the AV node is not the only gate. Blocking it hands the pathway full control. You need a drug that slows conduction in the atria and accessory pathway.

Ventricular tachycardia, torsades, and arrest pearls

Monomorphic VT (stable)

Procainamide IV (as above) is effective and often first choice if BP allows.
Amiodarone 150 mg IV over 10 min, then 1 mg/min for 6 h, then 0.5 mg/min. Repeat bolus for recurrence.
Sotalol 1.5 mg/kg IV over 5 min if QT normal and BP stable.
Choose based on BP, QT, and LV function.

Polymorphic VT / torsades de pointes

Magnesium sulfate 2 g IV. Give as a push in arrest; over 5–15 min if perfusing. Then consider infusion.
Correct K to >4.5 mEq/L and stop QT-prolonging drugs.
Overdrive pacing or isoproterenol for pause-dependent torsades when bradycardic.

Cardiac arrest (VF/pulseless VT)

High-quality CPR, early defibrillation.
Epinephrine 1 mg IV/IO every 3–5 min.
Amiodarone 300 mg IV/IO bolus, then 150 mg if needed. Lidocaine 1–1.5 mg/kg as an alternative, then 0.5–0.75 mg/kg; max 3 mg/kg; infusion 1–4 mg/min.

Why: Ventricular arrhythmias often reflect scar, ischemia, or QT issues. The drugs above target reentry or triggered activity and stabilize myocardium. Torsades is about repolarization; magnesium and pace rate fix the substrate.

Antiarrhythmic classes you must know

Class I (Na+ blockers): flecainide, propafenone, lidocaine. Use flecainide/propafenone only in patients without structural heart disease. Lidocaine is for VT/ischemia.
Class II (beta-blockers): metoprolol, esmolol. Great for rate control and ischemia-driven arrhythmias.
Class III (K+ blockers): amiodarone, dofetilide, sotalol. Watch QT and renal dosing (dofetilide, sotalol).
Class IV (non-DHP CCBs): diltiazem, verapamil. Avoid in decompensated HFrEF.
Other: adenosine (transient AV block), digoxin (vagal effect), magnesium (torsades).

Key interactions: Amiodarone increases warfarin and digoxin levels. Diltiazem/verapamil raise serum levels of drugs cleared by CYP3A4/P-gp. Dofetilide has many contraindicated co-meds (e.g., cimetidine, HCTZ) due to QT risk.

Bradycardia and AV block: stabilize first

Symptomatic bradycardia (hypotension, shock, chest pain, altered mental status)

Atropine 1 mg IV every 3–5 min to 3 mg.
If ineffective: transcutaneous pacing and/or dopamine 5–20 mcg/kg/min or epinephrine 2–10 mcg/min.

Drugs that worsen AV block: beta-blockers, diltiazem/verapamil, digoxin, amiodarone. Hold or reverse if drug-induced.

Why: In bradycardia, perfusion is the goal. Atropine blocks vagal tone. Pacing and catecholamines buy time while you fix the cause (ischemia, drugs, hyperkalemia).

Drug-induced QT prolongation and proarrhythmia

QTc >500 ms or an increase >60 ms from baseline predicts torsades. Risk rises with hypokalemia, hypomagnesemia, bradycardia, female sex, structural heart disease, and polypharmacy.

High-risk drugs: class Ia (procainamide), class III (dofetilide, sotalol), certain antibiotics, antifungals, antipsychotics, methadone.
Maintain K ≥4.5 mEq/L and Mg ≥2.0 mg/dL in high-risk patients.
Stop the offending drug and correct electrolytes at the first sign of QTc ≥500 ms or new ventricular ectopy.

Why: Early after-depolarizations occur during prolonged repolarization. Electrolyte correction and drug removal shorten QT and prevent torsades.

Heart failure foundations: HFrEF vs HFpEF

HFrEF: LVEF ≤40%. Systolic dysfunction. Benefits from neurohormonal blockade. Mortality benefit drugs exist.

HFpEF: LVEF ≥50%. Diastolic dysfunction. Few mortality-proven drugs. Focus on blood pressure, diuresis, and comorbidities.

Common precipitants: ischemia, arrhythmias (AF with RVR), infection, uncontrolled hypertension, dietary indiscretion, medication nonadherence, drugs that cause fluid retention (NSAIDs, thiazolidinediones), and negative inotropes.

Acute decompensated heart failure in the ICU

Classify perfusion (warm vs cold) and congestion (wet vs dry). Treatment follows the profile.

Wet and warm (most common): IV loop diuretics first. Give a dose equal to 1–2.5 times the total daily oral loop dose as IV bolus (e.g., home furosemide 40 mg BID → 80–100 mg IV). Reassess urine output at 2 hours. Target net negative 1–2 liters/day if tolerated.
Hypertensive pulmonary edema: Add vasodilators early. Nitroglycerin infusion (start 40–80 mcg/min; titrate quickly). Consider nitroprusside if severe afterload and BP allows. Noninvasive ventilation reduces preload and work of breathing.
Cold and wet (cardiogenic shock): Support BP with norepinephrine as first-line vasopressor. Add inotrope (dobutamine 2–20 mcg/kg/min or milrinone 0.125–0.375 mcg/kg/min) if hypoperfusion persists. Choose dobutamine if hypotensive or renal failure; choose milrinone if on high-dose beta-blockers and BP can tolerate it.
Diuretic resistance: Continuous loop infusion (furosemide 10–40 mg/h) or add thiazide-type agent: metolazone 2.5–5 mg PO 30 min before loop, or chlorothiazide 500–1000 mg IV. Consider acetazolamide 500 mg IV daily (especially if metabolic alkalosis). Monitor Na, K, Mg, bicarbonate closely.
Ultrafiltration if severe congestion with diuretic failure and adequate BP/vascular access.

Why: Decongestion improves symptoms and renal perfusion. Vasodilators reduce preload/afterload fast. Pressors and inotropes are bridges; they improve perfusion but can raise arrhythmia risk.

Chronic HFrEF therapy that improves survival

Use the “quadruple therapy” unless contraindicated. Start low and titrate every 1–2 weeks as tolerated.

ARNI (sacubitril/valsartan): Preferred over ACEi/ARB if possible. Start 24/26 mg, 49/51 mg, or 97/103 mg BID depending on BP and prior RAAS dose. Requires a 36-hour washout after an ACEi to avoid angioedema.
Evidence beta-blocker: carvedilol, metoprolol succinate, or bisoprolol. Start low (e.g., carvedilol 3.125 mg BID; metoprolol succinate 12.5–25 mg daily). Titrate to target (carvedilol 25–50 mg BID; metoprolol succinate 200 mg daily) as BP and HR allow.
MRA: spironolactone 12.5–25 mg daily or eplerenone 25–50 mg daily if eGFR ≥30 and K ≤5.0 mEq/L. Monitor K and creatinine at 3 and 7 days after start or dose change, then monthly.
SGLT2 inhibitor: dapagliflozin 10 mg daily or empagliflozin 10 mg daily, regardless of diabetes status. Watch for volume depletion and mycotic infections.

Additional options

Hydralazine/isosorbide dinitrate 20/37.5 mg TID (up-titrate) for Black patients with HFrEF on standard therapy or those who cannot take RAAS blockers.
Ivabradine for sinus rhythm HR ≥70 on max beta-blocker; reduces HF hospitalization.
Iron deficiency (ferritin <100 ng/mL or 100–299 with TSAT <20%): IV iron can improve symptoms and exercise capacity.
Potassium binders (patiromer, sodium zirconium cyclosilicate) to maintain RAAS inhibitors if hyperkalemia limits therapy.

Drugs to avoid or use with caution: NSAIDs, most antiarrhythmics (except amiodarone and dofetilide), non-dihydropyridine CCBs, thiazolidinediones. These worsen fluid retention or mortality.

Why: Neurohormonal blockers reverse maladaptive RAAS and sympathetic activation, lowering mortality and hospitalizations. SGLT2 inhibitors improve hemodynamics and renal handling of sodium and glucose, reducing events.

HFpEF: what actually helps

Diuretics for congestion. The only consistent symptomatic benefit.
SGLT2 inhibitors reduce HF hospitalization.
Blood pressure control with ACEi/ARB/ARNI as tolerated; target guideline BP goals to lower afterload and LV stiffness.
MRA may reduce hospitalization in selected patients with elevated natriuretic peptides and adequate renal function.
Manage comorbidities: obesity, diabetes, sleep apnea, AF (often rhythm control improves symptoms), and ischemia.

Why: HFpEF is about stiff ventricles and comorbid burden. Decongestion and blood pressure control target the true drivers of symptoms and hospitalizations.

Putting decongestion into practice

Loop equivalence: furosemide 40 mg ≈ torsemide 10 mg ≈ bumetanide 1 mg (IV:PO conversion for furosemide ~1:2, others ~1:1). If on oral loop at home, a reasonable initial IV dose is 1–2.5 times the total daily oral amount.

Assess response at 2 and 6 hours: urine output, net fluid balance, weight, dyspnea, and spot urinary sodium if available (low suggests resistance). Increase dose or add synergy if poor response. Aim to maintain K 4.0–5.0 and Mg ≥2.0.

Why: Early and adequate diuresis prevents spiral into worsening renal function and longer stays. The two-hour check keeps therapy on track.

Inotropes and vasopressors: choose by physiology

Norepinephrine is the preferred vasopressor in cardiogenic shock. It raises MAP with less tachyarrhythmia than dopamine.
Dobutamine increases contractility via beta-1 stimulation. Useful when BP is borderline and the patient is not on high-dose beta-blockers.
Milrinone is an inodilator (PDE3 inhibitor). It can work despite beta-blockade but may cause hypotension and arrhythmias; reduce dose in renal impairment.
Vasopressin is an add-on to reduce catecholamine dose and support SVR.

Why: Pressors stabilize perfusion; inotropes improve forward flow. Matching drug to the hemodynamic profile improves outcomes and avoids adverse effects.

Devices and advanced therapies

ICD for primary prevention if LVEF ≤35% after at least 3 months of optimized therapy (or 40 days post-MI) with expected survival >1 year.
CRT if LVEF ≤35%, sinus rhythm, LBBB with QRS ≥150 ms, and NYHA II–III despite GDMT.
Mechanical support (IABP, Impella, VA-ECMO) for refractory cardiogenic shock as a bridge to recovery or advanced therapy.

Why: When drugs cannot fix conduction delay or severe pump failure, devices restore coordination or provide temporary support.

High-yield pitfalls you can avoid

Giving AV nodal blockers in AF with WPW. Use procainamide or cardioversion instead.
Using diltiazem or verapamil in decompensated HFrEF. They worsen output.
Starting dronedarone in persistent decompensated HF. It increases mortality.
Skipping anticoagulation after cardioversion. Continue for at least 4 weeks even if sinus rhythm is restored.
Ignoring renal dosing and QT with dofetilide or sotalol. Hospitalize for initiation and monitor QT.
Under-dosing diuretics in acute HF. Start with 1–2.5× home oral dose IV and reassess early.
Choosing dopamine over norepinephrine in cardiogenic shock. Higher arrhythmia risk with dopamine.
Missing drug interactions with amiodarone. Reduce warfarin and digoxin doses; monitor levels and organ toxicity.
Not correcting electrolytes in arrhythmias. Maintain K ≥4.0–4.5 and Mg ≥2.0, especially with QT-prolonging drugs.
Using flecainide/propafenone in structural heart disease. Risk of proarrhythmia; choose amiodarone or dofetilide instead.

Rapid case drills

Case 1: 28-year-old with palpitations, narrow-complex regular tachycardia at 190. Vagal maneuvers fail. You give adenosine 6 mg, then 12 mg. Rhythm converts. Why adenosine? AV nodal reentry needs the node; brief block terminates the loop.
Case 2: 72-year-old with HFrEF (EF 25%), AF with RVR at 140, BP 92/58. You avoid diltiazem. Start amiodarone infusion for rate, and begin heparin. Why amiodarone? Negative inotropes worsen shock; amiodarone gives rate and rhythm support with less hemodynamic hit.
Case 3: 60-year-old with irregular wide-complex tachycardia at 220, variable QRS. You withhold adenosine and diltiazem. Start procainamide. Why? Likely AF with WPW; AV nodal blockers can trigger VF.
Case 4: 68-year-old with “wet and warm” HFrEF, home furosemide 40 mg BID. You give 100 mg IV furosemide. At 2 hours, urine output is minimal. You add 2.5 mg metolazone and repeat furosemide. Why? Early intensification prevents resistance and renal injury.
Case 5: 75-year-old post-MI with stable monomorphic VT at 160, BP 110/70, normal QT. You choose procainamide. Why? It has high efficacy in VT with acceptable hemodynamic profile when BP is stable.

Exam-day checklist

Identify rhythm by rate, regularity, P-waves, QRS width.
For narrow regular tachycardia: vagal → adenosine → AV nodal blocker.
AF with instability: synchronized cardioversion and anticoagulate.
HFrEF + AF: prefer beta-blocker or amiodarone; avoid diltiazem/verapamil.
AF ≥48 hours or unknown: anticoagulate 3 weeks before or TEE-guided; continue 4 weeks after cardioversion.
VT is VT until proven otherwise; use procainamide or amiodarone.
Torsades: magnesium first; fix K and stop QT-prolongers.
Atropine 1 mg q3–5 min to 3 mg for bradycardia; then pace or infusions.
Acute HF: adequate loop dose, early reassessment, add thiazide or acetazolamide if needed.
Chronic HFrEF: ARNI/ACEi/ARB + beta-blocker + MRA + SGLT2i unless contraindicated. Titrate.

Master the logic, not just the lists. If you know why a drug helps or harms a specific rhythm or HF profile, the right answer is hard to miss. That is the key to both safe practice and a strong exam performance.

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

Mail- Sachin@pharmacyfreak.com