Antiarrhythmics
High-yield Verified · Oct 2026Map each class to a phase: Na⁺ (class I) shapes phase 0 and the QRS, K⁺ (class III) shapes phase 3 and the QT, and Ca²⁺ (class IV) drives the nodal upstroke — so every class has a predictable ECG signature and a predictable way to cause arrhythmias.
Nursing view → administration, monitoring and patient teaching
Compare: Antiarrhythmics by Vaughan-Williams class →
Drugs
Mechanism
Alter cardiac ion channels and conduction per the Vaughan-Williams classes: I = sodium-channel blockers (Ia, Ib, Ic), II = beta-blockers, III = potassium-channel blockers (prolong repolarization; ibutilide does so by activating a slow inward sodium current), IV = non-dihydropyridine calcium channel blockers. Amiodarone — and its non-iodinated derivative dronedarone — show properties of all four classes.
Two action potentials: working myocyte and pacemaker
The ventricular myocyte action potential has five phases. Phase 4 is the resting potential (about −90 mV), held there by passively open K⁺ channels. In phase 0, voltage-gated Na⁺ channels open at about −70 mV and depolarize the cell to about +50 mV, then close quickly. Phase 1 is a small repolarization through outward K⁺ channels; phase 2, the plateau, balances outward K⁺ against inward Ca²⁺ through voltage-gated calcium channels; in phase 3 the calcium channels close and outward K⁺ current repolarizes the cell.
Pacemaker cells work differently. Their phase 4 is not flat: a passive inflow of Na⁺ (the “funny” current) drifts the membrane from about −60 mV up to the threshold of −40 mV, where voltage-gated Ca²⁺ channels open and carry the phase 0 upstroke; outward K⁺ then repolarizes (phase 3). The slope of phase 4 sets the heart rate, and the calcium-driven upstroke is why the SA and AV nodes respond to calcium channel blockers.
The classes map onto these currents: class I blocks the fast Na⁺ channels of phase 0; class II (β-blockers) reduces cAMP and slows SA-node pacing; class III blocks K⁺ channels and prolongs phase 3; class IV blocks slow Ca²⁺ channels, reducing the slope of phases 0 and 4 in nodal tissue. Ivabradine (sometimes called class 0) blocks the funny current and slows phase 4.
Class I: sodium-channel block and use dependence
All class I drugs block the fast Na⁺ channels responsible for phase 0, flattening the upstroke and slowing conduction — seen as a wider QRS. The subgroups differ in strength and in what they do to the action potential: the block is marked in Ic, moderate in Ia and weak in Ib. Ia (quinidine, procainamide, disopyramide) lengthens the action potential and prolongs the QT; Ib (lidocaine, mexiletine) shortens the action potential and has the least effect on it — mexiletine leaves the QRS and QT unchanged; Ic (flecainide, propafenone) leaves action-potential duration unchanged, with minimal effect on the QT.
Most class I drugs show use dependence: they bind sodium channels that are open or inactivated, so the faster the heart beats, the more channels are blocked. Mexiletine unbinds rapidly once the cell repolarizes, whereas flecainide dissociates slowly, so its block persists across heart rates and markedly lowers the maximal upstroke velocity. The flip side of use dependence is that toxicity and adverse effects rise during tachycardia.
Lidocaine and mexiletine are indicated only for ventricular arrhythmias (lidocaine IV, for example during acute myocardial infarction); Ia drugs are the most proarrhythmic sodium blockers because they prolong the QT.
Class III, the QT interval and torsades de pointes
Class III drugs block K⁺ channels, prolonging atrial, Purkinje and ventricular action-potential recovery and the effective refractory period — which makes re-entry less likely — at the cost of a reduced repolarization reserve and a longer QT. Dofetilide and sotalol target the rapid delayed-rectifier current (IKr); amiodarone blocks several K⁺ channels and also has sympatholytic, sodium- and calcium-blocking actions.
Torsades de pointes follows from the same physics. Inhibiting the delayed rectifier K⁺ current prolongs repolarization; an ectopic beat landing in that long repolarization (R-on-T) can start the twisting polymorphic rhythm, which may self-terminate or degenerate into ventricular fibrillation. Virtually all drugs that cause long QT block the outward IKr current encoded by KCNH2. Risk rises with hypokalemia, hypomagnesemia, hypocalcemia, bradycardia, structural heart disease, diuretic use, female sex and age over 65.
Sotalol shows reverse use dependence: its K⁺-blocking effect is greatest when the heart rate is slow, which is when QT prolongation and torsades are most likely. That is also why speeding the heart with isoproterenol helps refractory torsades, after IV magnesium, the first-line drug.
Classes II and IV, adenosine, and the channelopathy models
Class II (β-blockers) inhibit β-adrenergic activation of adenylate cyclase, lowering cAMP and slowing SA-node pacing and triggered activity. Class IV (verapamil, diltiazem) block the L-type Ca²⁺ current, inhibiting SA pacing and AV-node conduction and lengthening the PR interval — the basis for rate control in atrial fibrillation. (The β-blocker and calcium channel blocker pages teach these mechanisms in detail.)
Adenosine acts on receptors in the AV node and slows conduction through it, interrupting re-entry pathways that run through the node — which is how it restores sinus rhythm in paroxysmal SVT. Methylxanthines such as caffeine and theophylline antagonize it competitively, and dipyridamole potentiates it. Digoxin activates muscarinic M2 receptors and inhibits the Na⁺/K⁺-ATPase, slowing AV-node conduction.
Inherited channel diseases mirror the drugs. Brugada syndrome is most often a loss-of-function mutation in SCN5A, the cardiac sodium channel; potent sodium blockers (procainamide, flecainide, ajmaline) can unmask its ECG pattern, and quinidine is used for electrical storm. In long QT syndrome, type 1 (the most common) involves KCNQ1; mexiletine, by inhibiting the increased late sodium current, is effective in type 3, and it shortens the QTc in potassium-channel type 2.
Comparing the drugs
Vaughan-Williams classes by current and phase
| Drug | Main target | Effect on the action potential | ECG signature | Examples on this page |
|---|---|---|---|---|
| Class Ia | Fast Na⁺ channels (moderate) | Slower phase 0; longer action potential | Wider QRS, longer QTc | Quinidine, procainamide, disopyramide |
| Class Ib | Fast Na⁺ channels (weakest) | Shorter action potential | Little QRS or QT change | Lidocaine, mexiletine |
| Class Ic | Fast Na⁺ channels (strongest) | Much slower phase 0; duration unchanged | Wider QRS; little QT change | Flecainide, propafenone |
| Class II | β-adrenergic receptors (↓ cAMP) | Slower SA-node pacing | Slower rate | β-blockers; sotalol has class II and III actions |
| Class III | K⁺ channels | Longer phase 3 and refractory period | Longer QT | Amiodarone, sotalol (dofetilide: IKr) |
| Class IV | L-type Ca²⁺ channels | Lower slope of nodal phases 0 and 4 | Longer PR | Verapamil, diltiazem (CCB page) |
| Adenosine | Adenosine receptors in the AV node | Slower AV-node conduction | Interrupts AV-node re-entry | Adenosine |
Amiodarone shows properties of all four classes. Sodium-channel block: marked (Ic), moderate (Ia), weak (Ib).
The class I drugs at a glance
| Drug | Subgroup and route | Distinguishing toxicity | Clearance | Boxed warning |
|---|---|---|---|---|
| Procainamide | Ia · IV | Positive ANA / lupus-like syndrome; agranulocytosis; IV hypotension | Acetylated to NAPA; renal — accumulates in renal insufficiency | ANA/lupus, mortality, blood dyscrasias |
| Quinidine | Ia · oral | Immune thrombocytopenia; cinchonism; diarrhea | Hepatic CYP3A4 (3-hydroxyquinidine active); inhibits CYP2D6 | Mortality (coded on some labels) |
| Disopyramide | Ia · oral | Anticholinergic (urinary retention); heart failure; hypoglycemia | Over 50% renal, unchanged | Mortality (CAST) |
| Lidocaine | Ib · IV | CNS toxicity → seizures | Hepatic; clearance falls in long infusions | None |
| Mexiletine | Ib · oral (structurally like lidocaine) | GI distress, tremor; liver injury | Hepatic CYP2D6, CYP1A2 | Mortality (CAST) + liver injury |
| Flecainide | Ic · oral | Proarrhythmia; AF → 1:1 atrial flutter | Renal: about 30% unchanged, most of the rest as urinary metabolites | Mortality (CAST) |
| Propafenone | Ic · oral | β-blockade, unusual taste; Brugada unmasking; agranulocytosis | CYP2D6 (polymorphic), CYP3A4, CYP1A2 | Mortality (CAST) |
Pharmacokinetics
- Procainamide: acetylation to NAPA and renal clearance — procainamide
- Procainamide is acetylated in the liver to N-acetylprocainamide (NAPA); its half-life is 2.5–5 hours. Procainamide is cleared mainly by the kidney, so renal insufficiency or older age lets procainamide and NAPA accumulate toward overdose levels. Transient high plasma levels during IV administration — before the drug distributes to its volume of distribution, about 50 times the plasma volume — cause hypotension.
- Quinidine: CYP3A4 substrate, CYP2D6 inhibitor — quinidine
- Quinidine is 70–80% bioavailable, has an elimination half-life of 6–8 hours in adults, and is cleared mostly by hepatic CYP3A4; its metabolite 3-hydroxyquinidine has at least half the parent’s antiarrhythmic activity. It is not metabolized by CYP2D6 but inhibits it, turning extensive metabolizers into poor metabolizers. It slows digoxin elimination — digoxin levels may double.
- Disopyramide: renal, and anticholinergic — disopyramide
- More than half of a dose is excreted unchanged in the urine, so the dose is reduced in renal impairment; hepatic impairment also prolongs its half-life. CYP3A4 inhibitors such as clarithromycin and erythromycin have caused life-threatening interactions.
- Lidocaine IV and its oral relative mexiletine — lidocaine, mexiletine
- Lidocaine is given intravenously for acute management of ventricular arrhythmias; it is metabolized mainly in the liver and excreted by the kidneys, and its clearance falls during prolonged infusion and with β-blockers (lower hepatic blood flow) or CYP1A2/CYP3A4 inhibitors. Mexiletine is structurally similar to lidocaine but orally active, and is metabolized by CYP2D6 and CYP1A2.
- Propafenone: a genetic split in metabolism — propafenone
- In over 90% of patients propafenone is rapidly metabolized (half-life 2–10 hours) to two active metabolites: 5-hydroxypropafenone (by CYP2D6) and norpropafenone (by CYP3A4 and CYP1A2). In fewer than 10% the 5-hydroxy metabolite is barely formed, and the half-life is 10–32 hours. Severe liver dysfunction raises bioavailability to about 70% from 3–40%.
- Liver versus kidney across the class
- Hepatic impairment slows the elimination of lidocaine, propafenone and verapamil, among others. Disopyramide, sotalol and procainamide are cleared mainly by the kidney, so renal function matters more for them than liver disease.
Pharmacogenomics
Uses & drug choice
- Atrial fibrillation / flutter (rate and rhythm control)
- Ventricular tachycardia / fibrillation (amiodarone, lidocaine)
- Documented life-threatening ventricular arrhythmias (procainamide, quinidine, disopyramide, mexiletine, propafenone)
- Propafenone for delaying recurrence of paroxysmal atrial fibrillation/flutter or PSVT without structural heart disease
- Quinidine for converting AF/flutter and reducing relapse when rate control is inadequate
- Termination of paroxysmal SVT (adenosine)
- Ibutilide IV for rapid conversion of recent-onset atrial fibrillation/flutter to sinus rhythm
- Dofetilide for converting atrial fibrillation/flutter and keeping sinus rhythm afterward
- Dronedarone to lower AF hospitalization in patients in sinus rhythm with paroxysmal or persistent AF
Adverse effects
- Proarrhythmia: QT prolongation and torsades de pointes (class Ia and III)
- Blocking the delayed-rectifier K⁺ current prolongs repolarization; an ectopic beat during that period (R-on-T) triggers torsades. Bradycardia, low K⁺, Mg²⁺ or Ca²⁺, structural heart disease and interacting drugs add to the risk.
- QRS widening, ventricular tachycardia and the CAST mortality signal (class I, especially Ic)
- Strong use-dependent Na⁺ block slows conduction and widens the QRS. In CAST, post-MI patients on encainide or flecainide had more deaths or cardiac arrests than on placebo, so class Ic drugs are avoided in structural heart disease.
- Faster ventricular rate in atrial flutter (1:1 conduction)
- Class Ic and Ia drugs can slow the atrial rate enough that the AV node conducts every beat; flecainide can convert atrial fibrillation to flutter with 1:1 conduction, so a β-blocker or calcium channel blocker is given with it (the flecainide label advises against verapamil unless the benefits outweigh the risks).
- Bradycardia, AV block, hypotension, dizziness
- Slowing nodal pacing and AV conduction (class II, IV and adenosine) and conduction block from class I and III lowers rate; negative inotropy (disopyramide, propafenone) and vasodilation from high IV procainamide levels lower blood pressure.
- GI upset
- Diarrhea and nausea are the most frequent quinidine reactions and can be the first sign of cinchonism; mexiletine’s upper GI distress eases with food or an antacid.
- Procainamide lupus-like syndrome
- Prolonged use often produces a positive ANA, with arthralgia, pleuritis, fever or pericarditis in some patients — perhaps more often in slow acetylators — and symptoms usually resolve when the drug is stopped.
- Quinidine thrombocytopenia and cinchonism
- A quinidine-dependent antibody binds platelet membrane glycoproteins only when the drug is present, destroying platelets. Cinchonism (tinnitus, hearing loss, vertigo, blurred vision, confusion) reflects quinidine’s relationship to quinine and signals chronic toxicity.
- Disopyramide urinary retention and dry mouth
- Its anticholinergic activity causes dry mouth, urinary hesitancy or retention (worst with prostatic hypertrophy), constipation and blurred vision, and can precipitate glaucoma.
- Lidocaine seizures
- Rising levels act on the CNS — drowsiness, paresthesia, tinnitus, twitching — before convulsions and respiratory arrest; CNS reactions are associated with venous levels above 6 µg/mL of free base.
- Amiodarone thyroid, eye and lung toxicity
- Amiodarone is highly lipophilic and accumulates in tissue with a half-life of weeks; its iodine content can cause thyrotoxicosis in susceptible patients, though hypothyroidism is about twice as common. Corneal microdeposits (in at least 90%) form as the drug is secreted by the lacrimal gland and taken up by the corneal epithelium; pulmonary toxicity usually appears in the first year.
Toxicity & antidote
Class I overdose slows conduction: QRS widening, PR and QT prolongation, AV block, ventricular tachycardia, hypotension and, with flecainide, seizures and cardiac arrest. Hypertonic sodium bicarbonate is the antidote strategy for class Ia and Ic sodium-channel toxicity — it is given first-line when the QRS is wide in flecainide poisoning, alongside fluids and IV magnesium. Lidocaine overdose is mainly neurologic (seizures, respiratory depression) with cardiovascular collapse; there is no specific antidote, and the infusion is stopped.
For drug-induced torsades de pointes, stop QT-prolonging drugs and correct potassium, magnesium and calcium. Unstable torsades with a pulse needs synchronized cardioversion, and pulseless torsades defibrillation. IV magnesium is the first-line drug; for recurrent runs despite magnesium, raising the heart rate with isoproterenol shortens the QT and lowers the chance of an R-on-T beat.
Interactions
Contraindications
- 2nd/3rd-degree AV block or sick sinus syndrome (without a pacemaker) — Most antiarrhythmics further slow conduction — several can themselves cause heart block — amiodarone, and second- or third-degree block with flecainide, adenosine, sotalol and dronedarone — so an existing 2nd/3rd-degree block without a pacemaker is a labeled contraindication for many of them. Among the class I drugs, the labels name complete heart block (procainamide), complete AV block or a junctional/idioventricular rhythm without a pacemaker (quinidine), 2nd/3rd-degree AV block without a pacemaker (disopyramide, mexiletine), severe sinoatrial, AV or intraventricular block and Stokes-Adams syndrome (lidocaine), and conduction disorders without a pacemaker, including sick sinus syndrome (propafenone). Dronedarone is also contraindicated with a heart rate below 50/min or a PR interval above 280 ms.
- Baseline QT prolongation or long QT syndrome (sotalol; congenital QT prolongation — disopyramide; torsades — procainamide and other class Ia drugs; dofetilide if QTc > 440 ms, or > 500 ms with a ventricular conduction abnormality; dronedarone if QTc > 500 ms; amiodarone also lengthens QT) — These agents lengthen the QT further, sharply raising the risk of torsades de pointes.
- Cardiogenic shock or severe bradycardia — Negative effects on rate, conduction, and contractility would worsen an already-compromised circulation.
- Procainamide: systemic lupus erythematosus — Procainamide itself can cause a lupus-like syndrome, and in established lupus aggravation of symptoms is highly likely.
- Quinidine: prior quinidine- or quinine-induced thrombocytopenia; myasthenia gravis — The thrombocytopenia is immune-mediated and recurs, often faster, on re-exposure; quinidine’s anticholinergic action can worsen myasthenia gravis.
- Lidocaine: amide local anesthetic hypersensitivity; Wolff-Parkinson-White syndrome — Lidocaine is an amide-type local anesthetic; the label contraindicates it in Wolff-Parkinson-White syndrome.
- Propafenone: heart failure, Brugada syndrome, bronchospastic disease or severe COPD, marked hypotension or electrolyte imbalance — Its negative inotropy and β-blocking effects can provoke heart failure, and it can unmask Brugada syndrome; bronchospastic disease, marked hypotension and marked electrolyte imbalance are also labeled contraindications.
- Disopyramide: glaucoma, urinary retention, myasthenia gravis (anticholinergic) use caution — Its anticholinergic activity can precipitate glaucoma, urinary retention or myasthenic weakness, so it is not used unless overriding measures are in place.
- Dofetilide: creatinine clearance < 20 mL/min, or taking verapamil, hydrochlorothiazide or a renal cation-transport inhibitor (cimetidine, trimethoprim, ketoconazole, dolutegravir, prochlorperazine, megestrol) — Dofetilide is cleared mainly by the kidneys through glomerular filtration and cation-transport secretion; these states and drugs raise its level (or, with hydrochlorothiazide, also lower potassium), and torsades risk rises with the level.
- Dronedarone: permanent AF, decompensated or NYHA class IV heart failure, strong CYP3A inhibitors, other QT-prolonging drugs, previous amiodarone liver or lung toxicity, or severe hepatic impairment — Labeled contraindications: the boxed death, stroke and heart-failure risks; dronedarone exposure rises sharply with strong CYP3A inhibitors; and added QT prolongation raises torsades risk.
- Amiodarone: iodine hypersensitivity (thyroid disease needs caution and monitoring) use caution — Amiodarone is iodine-based and directly disrupts thyroid function, so pre-existing thyroid disease needs caution and monitoring.
High-yield
- Na⁺ block (class I) slows phase 0 → wider QRS
- K⁺ block (class III) prolongs phase 3 → longer QT → torsades (class Ia lengthens the QT too)
- Ca²⁺ block (class IV) slows the nodal upstroke → longer PR
Class Ib shortens the action potential with little QRS or QT change; class Ic widens the QRS with minimal QT effect.
- Lupus — procainamide: positive ANA and lupus-like syndrome (plus agranulocytosis)
- Ears — quinidine: cinchonism with tinnitus and hearing loss (plus thrombocytopenia)
- Bladder — disopyramide: anticholinergic urinary retention
All three prolong the QT, so torsades is the shared Ia risk.
Practice questions
Q1A 58-year-old man is treated with procainamide for ventricular tachycardia. Months later he develops arthralgias, pleuritic chest pain and fever. His antinuclear antibody test is positive.
Which factor most likely increased his risk of this reaction?
- A.CYP2D6 poor metabolizer status
- B.Hypokalemia
- C.Concomitant digoxin
- D.Slow acetylator phenotype
- E.High dietary salt intake
Show answer
D. Slow acetylator phenotype — Procainamide is acetylated to NAPA, and its lupus-like syndrome — positive ANA with arthralgia, pleuritis, fever — is fairly common with prolonged use and perhaps more frequent in slow acetylators. It usually resolves when the drug is stopped. CYP2D6 status matters for propafenone, and dietary salt alters quinidine levels, not procainamide toxicity.
Q2A 66-year-old woman taking quinidine for recurrent atrial fibrillation presents with petechiae and gum bleeding after 10 days of therapy. Her platelet count is 18,000/µL.
What is the mechanism of her thrombocytopenia?
- A.A drug-dependent antibody that binds platelet glycoproteins only in the presence of quinidine
- B.Dose-related bone-marrow suppression
- C.Splenic sequestration from quinidine-induced portal hypertension
- D.Folate deficiency from impaired absorption
- E.Platelet consumption by disseminated intravascular coagulation
Show answer
A. A drug-dependent antibody that binds platelet glycoproteins only in the presence of quinidine — Quinidine-induced thrombocytopenia is immune-mediated: a drug-dependent antibody, nonreactive by itself, binds tightly to platelet membrane glycoproteins when quinidine is present and destroys platelets. It typically appears after about a week of therapy as petechiae or bruising. Quinidine is stopped at once — the count usually recovers within a week — and the patient must not be re-exposed.
Q3A 34-year-old woman with paroxysmal atrial fibrillation and a structurally normal heart starts flecainide. Two weeks later she presents with palpitations; the ECG shows atrial flutter with a ventricular rate of 250/min and a wide QRS.
Which measure would most likely have prevented this?
- A.Adding a second class Ic drug
- B.Taking flecainide with food
- C.Adding a β-blocker
- D.Switching to a higher flecainide dose
- E.Adding a loop diuretic
Show answer
C. Adding a β-blocker — Flecainide can convert atrial fibrillation to atrial flutter with 1:1 conduction, so a β-blocker or calcium channel blocker is given with it to slow AV-node conduction. The flecainide label names digoxin or β-blockers for this, and advises that verapamil, a negative inotrope, not be given with flecainide unless the benefits outweigh the risks; there is too little experience with diltiazem to recommend it. Its strong, slowly dissociating sodium block also widens the QRS, especially at fast rates (use dependence). Class Ic drugs are reasonable only in hearts without structural or ischemic disease. A second class Ic drug or a higher dose would only add sodium-channel block — flecainide’s PR, QRS and QT increases are dose-related, and serious adverse events become more frequent at higher trough levels; food does not affect its absorption; and diuretic use and hypokalemia are risk factors for torsades, which is why hypokalemia is corrected before flecainide is given.
Q4A 72-year-old woman on sotalol and furosemide is found to have a QTc of 580 ms. On telemetry she has runs of a polymorphic ventricular tachycardia whose QRS axis twists around the baseline. Her blood pressure is stable. Potassium is 3.1 mEq/L.
Which is the best first drug?
- A.IV procainamide
- B.IV lidocaine
- C.IV amiodarone
- D.IV adenosine
- E.IV magnesium
Show answer
E. IV magnesium — This is torsades de pointes from potassium-channel block: sotalol prolongs repolarization, and its reverse use dependence makes it worse at slow rates; hypokalemia and diuretic use add risk. IV magnesium is the first-line drug, with stopping QT-prolonging drugs and correcting potassium. Procainamide (Ia) and amiodarone (III) prolong the QT further; adenosine restores sinus rhythm in PSVT, not torsades. Isoproterenol is used for runs that persist despite magnesium. Lidocaine is not the first-line drug for torsades — magnesium is.
Q5A 40-year-old man with recurrent syncope has a baseline ECG suggestive of, but not diagnostic for, Brugada syndrome. A cardiologist plans a drug challenge.
Which drug would be used, and why?
- A.Lidocaine, because it shortens the QT interval
- B.Procainamide, because potent sodium-channel block can unmask the Brugada pattern
- C.Adenosine, because it hyperpolarizes the SA node
- D.Sotalol, because it blocks the rapid delayed-rectifier current
- E.Verapamil, because it blocks L-type calcium channels
Show answer
B. Procainamide, because potent sodium-channel block can unmask the Brugada pattern — Brugada syndrome is most often a loss-of-function mutation in SCN5A, the cardiac sodium channel. Potent sodium blockers — procainamide, flecainide, ajmaline — can convert a non-diagnostic pattern to the diagnostic type 1 pattern. Quinidine, by contrast, is used to treat Brugada electrical storm. Lidocaine is a weak (Ib) sodium blocker; adenosine, sotalol and verapamil act on other targets.
Sources
- Antiarrhythmic Medications — Vaughan-Williams classes, amiodarone boxed warnings — StatPearls (NCBI)
- Pacerone (amiodarone) — FDA label: boxed pulmonary/hepatic/cardiac toxicity, monitoring, interactions — FDA / DailyMed
- Betapace / Betapace AF (sotalol) — FDA label: boxed proarrhythmia, QT thresholds, contraindications — FDA / DailyMed
- Flecainide acetate tablets — FDA label — FDA / DailyMed
- Adenosine injection — FDA label (rapid bolus; PSVT; half-life under 10 seconds) — FDA / DailyMed
- Open RN Nursing Pharmacology — Ch. 6 (antiarrhythmics: classes I–IV, sotalol, amiodarone, adenosine) — Open RN (NCBI Bookshelf)
- QT Prolonging Drugs — normal QTc and torsades de pointes — StatPearls (NCBI)
- Physiology, Thyroid Stimulating Hormone — TSH reference range — StatPearls (NCBI)
- Amiodarone — distribution, half-life, thyroid, skin, interactions — StatPearls (NCBI)
- Adenosine — rapid IV push with saline flush, very short half-life — StatPearls (NCBI)
- Liver Function Tests — typical ALT/AST reference ranges — StatPearls (NCBI)
- The use of stems in the selection of International Nonproprietary Names (-alol) — World Health Organization
- Flecainide acetate tablets (Unichem) — FDA label: boxed CAST mortality warning — FDA / DailyMed
- Procainamide hydrochloride injection (Hospira) — FDA label: boxed ANA/lupus, mortality and blood-dyscrasia warnings; IV hypotension; QRS monitoring — FDA / DailyMed
- Quinidine gluconate extended-release tablets — FDA label: mortality warning, thrombocytopenia, cinchonism, digoxin interaction — FDA / DailyMed
- Norpace / Norpace CR (disopyramide) — FDA label: boxed mortality warning, anticholinergic effects, heart failure, hypoglycemia — FDA / DailyMed
- Lidocaine hydrochloride and 5% dextrose injection (Baxter) — FDA label: ventricular arrhythmias, ECG monitoring, CNS toxicity — FDA / DailyMed
- Mexiletine hydrochloride capsules (ANI) — FDA label: boxed mortality and liver-injury warning, take with food — FDA / DailyMed
- Propafenone hydrochloride tablets (ANI) — FDA label: boxed mortality warning, Brugada, agranulocytosis, CYP2D6/3A4 — FDA / DailyMed
- Procainamide — class IA mechanism, lupus-like syndrome, blood dyscrasias, QRS monitoring — StatPearls (NCBI)
- Mexiletine — class IB antiarrhythmic — StatPearls (NCBI)
- Tikosyn (dofetilide) — FDA label: boxed in-hospital initiation, IKr block, creatinine-clearance and QTc dosing, interactions — FDA / DailyMed
- Dofetilide — class III agent, torsades risk factors, monitoring — StatPearls (NCBI)
- Corvert (ibutilide) — FDA label: boxed life-threatening arrhythmias, mechanism, post-infusion monitoring — FDA / DailyMed
- Ibutilide — conversion of recent-onset atrial flutter and fibrillation — StatPearls (NCBI)
- Multaq (dronedarone) — FDA label: boxed heart-failure and permanent-AF risk, contraindications, liver and lung injury, interactions — FDA / DailyMed
- Dronedarone — non-iodinated amiodarone derivative; hepatotoxicity — LiverTox (NCBI)
- Physiology, Cardiac — myocyte and pacemaker action potentials — StatPearls (NCBI)
- Torsade de Pointes — mechanism, risk factors, magnesium, isoproterenol — StatPearls (NCBI)
- Long QT Syndrome — KCNQ1, IKr (KCNH2) block by drugs — StatPearls (NCBI)
- Brugada Syndrome — SCN5A, sodium-blocker challenge, quinidine — StatPearls (NCBI)
- Flecainide — use-dependent block, 1:1 flutter, toxicity and sodium bicarbonate — StatPearls (NCBI)
- Sotalol — reverse use dependence — StatPearls (NCBI)
- Table of Pharmacogenomic Biomarkers in Drug Labeling — U.S. FDA
By LearnDrugs
Educational summary for medical students. Always verify against current prescribing information and guidelines. Not medical advice.