Antiarrhythmics
High-yield High-alert Verified · Oct 2026Prototype: amiodarone
Antiarrhythmics are a class of medications used for atrial fibrillation / flutter.
Medical view → mechanisms, drug comparisons and Step 1 pharmacology
Agents that modify cardiac conduction, grouped by the Vaughan-Williams classification (I–IV).
How it works in the body
The system involved, what goes wrong, and how the drug and body interact.
01 The heartbeat is electrical — the cardiac action potential
Every heartbeat starts as an electrical impulse. In each cardiac cell, ions flow across the membrane in a set sequence that makes up the action potential: sodium (Na⁺) rushes in to fire the impulse (depolarization), calcium (Ca²⁺) sustains it and drives contraction, and potassium (K⁺) flows out to reset the cell (repolarization). The pacemaker (SA node) sets the rate; the AV node gates how fast impulses pass to the ventricles.
An arrhythmia is this orderly sequence going wrong — the heart beating too fast, too slow, or chaotically (as in atrial fibrillation), often from an abnormal focus firing or an impulse looping back on itself (re-entry). Antiarrhythmics work by adjusting the very ion channels that shape the action potential.
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02 The four Vaughan-Williams classes
Antiarrhythmics are grouped by which ion channel they block — the Vaughan-Williams classification. Class I blocks sodium channels, slowing the initial upstroke (phase 0), in three subgroups: Ia (quinidine, procainamide, disopyramide) blocks moderately and lengthens the action potential and the QT interval; Ib (lidocaine, mexiletine) blocks weakly, shortens the action potential, and is used for ventricular arrhythmias; Ic (flecainide, propafenone) blocks most strongly while leaving action-potential duration unchanged. Class II are the beta-blockers, which slow the SA/AV nodes via the sympathetic system. Class III blocks potassium channels, prolonging repolarization (e.g. sotalol, amiodarone, and dofetilide, which blocks only the rapid delayed-rectifier current IKr); ibutilide reaches the same longer repolarization by activating a slow inward, mainly sodium, current instead. Class IV are the non-dihydropyridine calcium channel blockers (diltiazem, verapamil), slowing AV conduction.
Amiodarone is the exception that proves the rule: it shows properties of all four classes at once. That broad action makes it highly effective — and, as the side effects show, uniquely toxic. Dronedarone, a non-iodinated amiodarone derivative, also has properties of all four classes; it is better tolerated but less effective, and it is harmful in permanent atrial fibrillation or decompensated heart failure. Adenosine sits outside the classification: it briefly blocks the AV node to stop a re-entrant SVT.
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03 The paradox — and the price of amiodarone
Antiarrhythmics carry a built-in paradox: a drug that alters the heart’s electrical timing to fix one arrhythmia can create another. This is proarrhythmia. Class III agents (and others) prolong the QT interval, which can trigger a dangerous rhythm called torsades de pointes — so the QT is watched closely.
Amiodarone’s all-class potency comes at a cost seen nowhere else: because it is fat-soluble and stored in tissues with an extremely long half-life (weeks to months), it accumulates in the lungs (fibrosis), liver, thyroid (it is iodine-rich → hypo- or hyperthyroidism), eyes, and skin (blue-gray discoloration, photosensitivity). These slow, cumulative toxicities are the reason for its boxed warning and its intensive monitoring schedule.
Drug names
Generic Brand
amiodarone Pacerone
procainamide —
quinidine —
disopyramide Norpace
lidocaine —
mexiletine —
flecainide —
propafenone —
sotalol Betapace
dofetilide Tikosyn
ibutilide Corvert
dronedarone Multaq
adenosine —
Indications
- 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
Mechanism of action
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.
In plain terms
They steady the heart’s electrical signals to restore or keep a normal rhythm.
Therapeutic effects — what you'll see working
The goal is a stable rhythm at a safe rate — confirmed on the ECG/telemetry monitor, not by how the patient feels. Because these drugs can also cause arrhythmias, "success" means watching the rhythm — continuously when therapy starts or the dose changes.
Rhythm control Rate control Terminates SVT (adenosine)
- Rhythm control
- Restoring and maintaining normal sinus rhythm by damping abnormal foci or interrupting re-entry circuits — the aim in atrial fibrillation or ventricular tachycardia.
- Rate control
- Slowing AV-node conduction (class II and IV) to bring a rapid ventricular rate down to a safe range, even if the underlying rhythm remains abnormal.
- Terminates SVT (adenosine)
- A rapid IV push of adenosine briefly blocks the AV node — breaking the re-entrant loop of a paroxysmal SVT and often converting it back to sinus rhythm in seconds.
Adverse effects
Two themes run through the whole class: proarrhythmia (a rhythm drug can cause new rhythms, especially via QT prolongation) and, for amiodarone, cumulative multi-organ toxicity from tissue storage.
Caution: Common
Bradycardia, hypotension, dizziness, GI upset. Amiodarone: photosensitivity, blue-gray skin discoloration, corneal deposits.
Slowing conduction naturally tends toward bradycardia and hypotension. Amiodarone’s skin, corneal, and photosensitivity changes come from the drug depositing in tissues over time — corneal deposits reverse with dose reduction or stopping, but blue-gray skin may only partly fade, and these changes are a visible clue the patient is accumulating drug.
Warning: Serious Report immediately
Proarrhythmia; QT prolongation → torsades de pointes (sotalol, dofetilide, ibutilide — class III); amiodarone thyroid dysfunction.
Proarrhythmia is the central danger — prolonging the QT interval can trigger torsades de pointes, a life-threatening ventricular rhythm, so a lengthening QT means reassess the drug. Sotalol carries a boxed warning for this: it is started (or restarted) only where continuous ECG monitoring and resuscitation are available; if the QT reaches 500 ms or more, the dose is reduced, the interval lengthened, or the drug stopped, and the dose is set from the calculated creatinine clearance. Flecainide carries a boxed warning from the CAST trial: after a recent myocardial infarction, flecainide-treated patients had more deaths or non-fatal cardiac arrests than placebo (5.1% vs 2.3%), so class IC agents are generally unacceptable in patients without life-threatening ventricular arrhythmias, and flecainide is not recommended in chronic atrial fibrillation. Because amiodarone is iodine-rich, it disrupts the thyroid, causing either hypo- or hyperthyroidism.
Black-box warning — most severe: ■ Boxed warning · procainamide Report immediately
Positive ANA with or without a lupus-like syndrome; increased mortality in non-life-threatening arrhythmias (CAST); potentially fatal blood dyscrasias such as agranulocytosis.
Prolonged procainamide often produces a positive ANA, with or without a lupus-like syndrome (arthralgia, pleuritic or abdominal pain, fever) — perhaps more often in slow acetylators; a positive titer prompts a benefit–risk review. Because of proarrhythmia and the CAST results, it is reserved for life-threatening ventricular arrhythmias. Agranulocytosis, bone-marrow depression, neutropenia, hypoplastic anemia and thrombocytopenia occur in about 0.5% (agranulocytosis has been fatal), mostly in the first 12 weeks: the label calls for a CBC with differential and platelets weekly for the first 3 months, then periodically, and promptly for fever, chills, sore throat, mouth sores, bruising or bleeding — and procainamide is stopped if a blood disorder is found.
Black-box warning — most severe: ■ Boxed warning · disopyramide, mexiletine, propafenone, quinidine (mortality) Report immediately
Increased mortality with antiarrhythmic therapy for non-life-threatening arrhythmias — reserve for life-threatening ventricular arrhythmias; propafenone carries proarrhythmic risk in structural heart disease.
In CAST, patients after a myocardial infarction with asymptomatic, non-life-threatening ventricular arrhythmias had more deaths or non-fatal cardiac arrests on encainide or flecainide than on placebo (7.7% vs 3.0%). The disopyramide and mexiletine boxes therefore reserve these drugs for life-threatening ventricular arrhythmias; the propafenone box treats any class IC drug as carrying significant proarrhythmic risk in structural heart disease and advises avoiding antiarrhythmics for non-life-threatening ventricular arrhythmias. The quinidine label reports mortality more than three times that of placebo when it was used to prevent atrial fibrillation/flutter recurrence. The mexiletine box also warns of liver injury: abnormal liver tests have been reported after marketing, some in the first few weeks of therapy.
Caution: Class I · common, drug-specific
Quinidine: diarrhea, nausea. Disopyramide: dry mouth, urinary hesitancy, constipation, blurred vision. Mexiletine: upper GI distress, tremor, lightheadedness, poor coordination. Propafenone: unusual taste, dizziness, nausea, constipation.
Diarrhea and other GI effects are the most frequently reported quinidine reactions. Disopyramide’s common effects are anticholinergic and dose-dependent (dry mouth 32%, urinary hesitancy 14%, constipation 11%). Mexiletine’s GI distress (41% in controlled trials), tremor and lightheadedness are dose-related and ease when it is taken with food or an antacid. Propafenone’s most common effects include an unusual taste, dizziness, nausea or vomiting and constipation, plus first-degree AV block and intraventricular conduction delay on the ECG.
Warning: Quinidine · immune thrombocytopenia, cinchonism Hold & notify
Immune thrombocytopenia (can cause fatal hemorrhage); cinchonism — tinnitus, hearing loss, vertigo, blurred vision, headache, confusion; QT prolongation and torsades; rare hepatotoxicity.
Quinidine-induced thrombocytopenia is immune-mediated and usually appears after about a week of therapy (or after intermittent use) as petechiae or bruising; quinidine is stopped at the first sign, and a patient with quinidine-dependent antibodies must not be re-exposed. Cinchonism — tinnitus, high-frequency hearing loss, vertigo, blurred or double vision, photophobia, headache, confusion — usually signals chronic toxicity, and vomiting or diarrhea may be its first sign. Like all class Ia drugs, quinidine prolongs the QTc and can cause torsades de pointes.
Warning: Disopyramide · urinary retention, heart failure, hypoglycemia Hold & notify
Urinary retention (especially with prostatic hypertrophy), glaucoma risk, worsening heart failure or severe hypotension, hypoglycemia, QRS/QT prolongation and torsades.
Urinary retention is the most serious anticholinergic effect, and men with benign prostatic hypertrophy are at particular risk; it should not be used in glaucoma, myasthenia gravis or urinary retention without overriding measures. Its negative inotropy can cause or worsen heart failure or produce severe hypotension — the most serious reactions. Significant hypoglycemia has been reported, especially with heart failure, malnutrition, liver or kidney disease, or β-blockers or alcohol. QRS widening of more than 25% means stopping the drug, and it has been associated with torsades de pointes.
Warning: Lidocaine (IV) · CNS toxicity, conduction depression Hold & notify
Drowsiness, dizziness, paresthesia, tinnitus, twitching or tremor progressing to convulsions and respiratory depression; bradycardia, hypotension, worsening conduction.
Lidocaine’s toxicity is mainly neurologic — drowsiness, light-headedness, numbness or paresthesia, tinnitus, blurred vision, tremor and twitching, then convulsions, unconsciousness and respiratory arrest — with bradycardia and hypotension that can progress to cardiac arrest. PR prolongation, QRS widening or new arrhythmias mean prompt cessation of the infusion. Renal or hepatic insufficiency raises the risk, and resuscitation equipment and drugs must be immediately available.
Warning: Propafenone · Brugada unmasking, heart failure, agranulocytosis Hold & notify
New or worsened arrhythmias; may unmask Brugada syndrome; heart failure (negative inotropy plus β-blockade); conduction block; agranulocytosis; altered pacemaker thresholds.
Propafenone can unmask Brugada syndrome, so an ECG is done after it is started and it is stopped for Brugada-type changes. It has negative inotropic and β-blocking effects that may provoke heart failure, and it slows AV conduction with dose-related PR and QRS prolongation. Agranulocytosis usually appears in the first 2 months; unexplained fever or a falling white count prompts evaluation. It can change the pacing and sensing thresholds of pacemakers and defibrillators.
Warning: Procainamide (IV) · hypotension, QRS widening Hold & notify
Hypotension with rapid IV administration; QRS widening, PR and QT prolongation, heart block; accumulation in renal insufficiency.
Transient high levels during IV administration can cause hypotension, so it is given slowly with the patient supine, and administration is paused if systolic pressure falls 15 mm Hg or more. ECG monitoring watches for QRS widening, PR prolongation and heart block: QRS widening over 25% raises concern for overdosage, and the infusion is interrupted at a 50% increase. Renal insufficiency lets procainamide accumulate to overdose levels.
Black-box warning — most severe: ■ Boxed warning · amiodarone Report immediately
Potentially fatal pulmonary toxicity, hepatotoxicity, and proarrhythmia — reserve for life-threatening arrhythmias.
Amiodarone accumulates in the lungs and can cause pulmonary fibrosis / pneumonitis — a potentially fatal, sometimes irreversible scarring — along with hepatotoxicity and proarrhythmia. Because of this, it is reserved for life-threatening arrhythmias when safer agents have failed, and it requires scheduled lung, liver, thyroid, and eye monitoring. Because it can also worsen arrhythmias, the box says to start it where continuous ECG monitoring and cardiac resuscitation are available.
Black-box warning — most severe: ■ Boxed warning · dofetilide Report immediately
Start (or restart) only in a facility for at least 3 days, with creatinine clearance calculation, continuous ECG monitoring and cardiac resuscitation.
Dofetilide can cause torsades de pointes, and the QT lengthens in direct proportion to its plasma concentration. Reduced creatinine clearance and certain interacting drugs raise that concentration. The dose is therefore set from the calculated creatinine clearance and the QTc, under continuous ECG monitoring for at least 3 days. Most torsades episodes in trials occurred within those first 3 days.
Black-box warning — most severe: ■ Boxed warning · ibutilide Report immediately
Can cause potentially fatal arrhythmias — give only with continuous ECG monitoring and staff trained to treat polymorphic VT.
Ibutilide can cause sustained polymorphic ventricular tachycardia, usually with QT prolongation (torsades de pointes) but sometimes without it. In registration studies 1.7% of patients needed cardioversion for it, during or within hours of the infusion, and the arrhythmia can be reversed if treated promptly. Patients whose atrial fibrillation has lasted more than 2–3 days must be adequately anticoagulated, generally for at least 2 weeks, before conversion.
Black-box warning — most severe: ■ Boxed warning · dronedarone Report immediately
Doubles the risk of death in recently decompensated or NYHA class IV heart failure, and of death, stroke and heart-failure hospitalization in permanent atrial fibrillation.
Dronedarone is contraindicated in symptomatic heart failure with recent decompensation requiring hospitalization or NYHA class IV symptoms, and in atrial fibrillation that will not or cannot be cardioverted to sinus rhythm (permanent AF). It offers no benefit in permanent AF. Rhythm is checked at least every 3 months, and if AF is found the patient is cardioverted or the drug is stopped.
Warning: Dronedarone · liver, lung, heart failure, kidney Hold & notify
Diarrhea, nausea, abdominal pain, bradycardia and rash are most common; hepatocellular liver injury, interstitial lung disease and new or worse heart failure are labeled warnings.
Severe hepatocellular liver injury, including acute liver failure needing transplant, has been reported, typically within the first months. Report anorexia, nausea, fever, fatigue, right-upper-quadrant pain, jaundice, dark urine or itching, and stop the drug if liver injury is suspected. Interstitial lung disease (pneumonitis, pulmonary fibrosis) can present as dyspnea or a dry cough. New or worsening heart failure shows as weight gain, dependent edema or increasing breathlessness. Serum creatinine rises slightly (about 0.1 mg/dL) because tubular secretion of creatinine is inhibited, but true renal failure has also occurred, often with heart failure or hypovolemia. Dronedarone can cause fetal harm, so effective contraception is needed during treatment and for 5 days afterward.
Interactions
Digoxin drug
Amiodarone raises serum digoxin — reduce the digoxin dose and monitor levels. Quinidine slows digoxin elimination (levels may as much as double), and propafenone can also raise digoxin levels.
Warfarin drug
Amiodarone raises warfarin levels → the INR rises — reduce the warfarin dose. Quinidine potentiates warfarin, and propafenone can raise warfarin levels.
CYP2D6 and CYP3A4 inhibitors together (propafenone) drug
Combined inhibition raises propafenone levels and the risk of proarrhythmia — avoid using both kinds of inhibitor at once.
CYP3A4 inhibitors such as clarithromycin or erythromycin (disopyramide) drug
Life-threatening interactions have been reported; also, disopyramide is not given within 48 hours before or 24 hours after verapamil.
β-blockers, CYP1A2 or CYP3A4 inhibitors (lidocaine) drug
Reduced hepatic blood flow or metabolism raises lidocaine levels — monitor for toxicity.
Theophylline (mexiletine) drug
Mexiletine raises theophylline levels — monitor theophylline levels.
Other QT-prolonging drugs drug
Additive QT prolongation → torsades de pointes risk.
Dofetilide + drugs that block its renal secretion or metabolism drug
Cimetidine, trimethoprim, ketoconazole, verapamil and hydrochlorothiazide are contraindicated. Drugs secreted by the same renal route (triamterene, metformin, amiloride) and CYP3A4 inhibitors are used with care, because a higher dofetilide level means a longer QT. For an acid-suppressant, omeprazole, ranitidine or antacids can be used instead of cimetidine.
Ibutilide + class Ia or other class III antiarrhythmics drug
Do not give them together or within 4 hours after the infusion, because refractoriness is prolonged further.
Dronedarone + digoxin drug
Dronedarone raises digoxin exposure (P-glycoprotein inhibition), and digoxin adds to its AV-node slowing. Consider stopping digoxin; if it is continued, halve the dose and monitor levels.
Dronedarone + CYP3A drugs (inhibitors, inducers, grapefruit juice), statins, warfarin, β-blockers or calcium channel blockers drug
Strong CYP3A inhibitors are contraindicated; avoid inducers (rifampin, St. John’s wort) and grapefruit juice. Dronedarone raises simvastatin exposure, and INR can rise in patients on warfarin. β-blockers and non-dihydropyridine calcium channel blockers add bradycardia, so they are started low and increased after ECG checks.
Contraindications
Contraindications are largely class-specific, but the shared theme is a heart that is already too slow or too blocked, or an ECG that is already primed for torsades.
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.
Labs & levels
Test Therapeutic / normal Toxic / critical
TSH (thyroid function) Baseline & periodically — amiodarone is iodine-rich (hypo- or hyperthyroidism) Normal range 0.4–4.5 mU/L —
LFTs (hepatic function) Baseline & periodically — hepatotoxicity (boxed warning): reduce the dose or stop if transaminases exceed 3× normal (or double from an elevated baseline); stop for signs of clinical liver injury Normal range Typical ALT 4–36 · AST 5–30 IU/L (lab-specific) —
Pulmonary — chest x-ray / PFTs Baseline chest x-ray and PFTs (including diffusion capacity), then history, exam, and chest x-ray every 3–6 months (boxed warning) — watch for pulmonary fibrosis / pneumonitis Normal range Clear CXR; normal DLCO at baseline —
QT interval / ECG Intermittent or continuous ECG during initial therapy and dose changes; continuous ECG when sotalol, dofetilide or IV ibutilide is started — a lengthening QT warns of torsades Normal range QTc ≤ 440 ms (M) / ≤ 460 ms (F) > 500 ms → torsades de pointes risk
Nursing considerations
The RN-specific layer — each action paired with the reason it matters.
Monitoring
Monitor the ECG — continuously when sotalol, dofetilide or IV ibutilide is started, and intermittently or continuously during initial therapy and dose changes with the others; watch the QT interval, heart rate, and BP.
Why: These drugs can cause the very arrhythmias they treat; a lengthening QT is the early warning for torsades and prompts reassessment.
Amiodarone: obtain baseline and periodic pulmonary (PFTs / chest x-ray), liver (LFTs), thyroid (TSH), and eye exams.
Why: Amiodarone’s tissue accumulation causes slow, cumulative organ toxicity (the boxed warning) — scheduled monitoring catches it before it becomes irreversible.
Adenosine: give as a rapid IV push immediately followed by a saline flush; expect a brief pause/asystole.
Why: Adenosine’s half-life is only seconds, so it must reach the heart fast; the short pause is how it breaks the SVT and is expected.
Class I agents (procainamide, quinidine, disopyramide, lidocaine, mexiletine, propafenone)
Start procainamide, disopyramide, mexiletine (and propafenone for ventricular arrhythmias) in the hospital, with ECG monitoring; watch the QRS, PR and QT intervals.
Why: They are reserved for life-threatening arrhythmias and can themselves provoke arrhythmias; QRS widening or a lengthening QT is the warning sign, and none has been shown to improve survival in ventricular arrhythmias.
Procainamide IV: give slowly with the patient supine, check BP often and pause if systolic pressure falls 15 mm Hg or more; get a CBC weekly for the first 3 months and promptly for fever, sore throat, mouth sores, bruising or bleeding.
Why: Rapid IV administration causes hypotension, and blood dyscrasias (sometimes fatal agranulocytosis) cluster in the first 12 weeks; the injection also contains a sulfite.
Lidocaine IV: run on a calibrated infusion device with constant ECG monitoring and resuscitation equipment at hand; stop and report drowsiness, numbness or tingling, tinnitus, twitching, or PR/QRS widening.
Why: CNS toxicity precedes seizures and respiratory depression, and clearance falls during prolonged infusions and in hepatic or renal insufficiency.
Quinidine: teach the patient to report bruising, petechiae or bleeding at once, and ringing in the ears, hearing or vision changes; avoid grapefruit juice and keep dietary salt steady.
Why: Immune thrombocytopenia can cause fatal hemorrhage unless quinidine is stopped; tinnitus and visual change signal cinchonism; grapefruit juice inhibits quinidine’s metabolism, and a drop in salt intake can raise its levels.
Disopyramide: check for urinary retention (especially in men with an enlarged prostate), ask about glaucoma, and follow blood glucose in patients at risk of hypoglycemia.
Why: Its anticholinergic effects can cause retention and precipitate glaucoma, and significant hypoglycemia has been reported with heart failure, malnutrition, liver or kidney disease, or β-blockers.
Mexiletine: take it with food or an antacid; report tremor, unsteadiness, signs of liver injury, or a rash with fever.
Why: Food or antacid eases its common GI and nervous-system effects; liver injury and DRESS have been reported.
Propafenone: report fever, sore throat or chills promptly, and diarrhea, sweating or vomiting; do not double a missed dose; have pacemakers or defibrillators checked.
Why: Agranulocytosis can occur early in therapy, marked electrolyte imbalance is a contraindication, and propafenone alters device thresholds.
Patient teaching
Amiodarone: use sun protection, and report a new cough or shortness of breath promptly.
Why: Photosensitivity causes severe sunburn; new respiratory symptoms may be early pulmonary toxicity, which must be caught quickly.
Understand amiodarone’s effects persist for weeks to months after stopping; attend all follow-up labs and ECGs and never adjust the dose independently.
Why: Its very long half-life means both benefit and toxicity linger, so monitoring continues even after discontinuation and dose changes must be supervised.
Dofetilide
Before the first dose, check the QTc and the calculated creatinine clearance; keep the patient on continuous ECG for at least 3 days, and check the QTc 2–3 hours after each in-hospital dose.
Why: The QT lengthens in proportion to the dofetilide level, which depends on kidney function. The label stops dofetilide if the QTc exceeds 500 ms (550 ms with a ventricular conduction abnormality).
Keep potassium and magnesium in the normal range, and report diarrhea, vomiting, heavy sweating, loss of appetite or thirst.
Why: Hypokalemia and hypomagnesemia raise torsades risk, and these symptoms can signal an electrolyte imbalance.
Teach: never double a missed dose, and check with the prescriber or pharmacist before any new prescription, OTC or herbal product (for example, cimetidine).
Why: Several drugs raise dofetilide levels or add QT prolongation, and QTc and renal function are rechecked about every 3 months.
Ibutilide
Correct hypokalemia and hypomagnesemia first, and have a defibrillator, pacing and drugs for polymorphic VT at the bedside.
Why: Proarrhythmia must be anticipated. Low potassium and magnesium raise the risk of torsades.
Stop the infusion as soon as the arrhythmia converts, or for any ventricular tachycardia or marked QT prolongation. Keep continuous ECG monitoring for at least 4 hours afterward, or until the QTc returns to baseline.
Why: Most polymorphic VT began within 40 minutes of starting the infusion, often after it was stopped, but recurrences occurred about 3 hours later.
Dronedarone
Confirm the patient is in sinus rhythm on appropriate antithrombotic therapy, and check the rhythm at least every 3 months.
Why: In permanent AF dronedarone doubles the risk of death, stroke and heart-failure hospitalization, so AF found on follow-up means cardioversion or stopping the drug.
Teach: take it with meals, avoid grapefruit juice, and report weight gain, swelling or breathlessness and any liver symptoms (dark urine, jaundice, right-upper-quadrant pain).
Why: Food increases absorption and grapefruit raises exposure. Heart failure and hepatocellular liver injury are labeled warnings that require stopping the drug.
Keep potassium and magnesium normal, watch for bradycardia, and check renal function periodically; confirm a negative pregnancy test and contraception in females of reproductive potential.
Why: Electrolyte depletion raises torsades risk, and dronedarone slows the heart and can impair renal function. It may cause fetal harm.
Common questions
What are Antiarrhythmics used for?
Antiarrhythmics are used for atrial fibrillation / flutter, ventricular tachycardia / fibrillation, documented life-threatening ventricular arrhythmias, and termination of paroxysmal SVT. 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. 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.
How do Antiarrhythmics work?
They steady the heart’s electrical signals to restore or keep a normal rhythm.
What are the serious side effects of Antiarrhythmics?
Watch for proarrhythmia; QT prolongation → torsades de pointes (sotalol, dofetilide, ibutilide — class III); amiodarone thyroid dysfunction; (with procainamide) positive ANA with or without a lupus-like syndrome; increased mortality in non-life-threatening arrhythmias (CAST); potentially fatal blood dyscrasias such as agranulocytosis; increased mortality with antiarrhythmic therapy for non-life-threatening arrhythmias — reserve for life-threatening ventricular arrhythmias; propafenone carries proarrhythmic risk in structural heart disease.
What labs should be monitored with Antiarrhythmics?
Monitor TSH (thyroid function), LFTs (hepatic function), pulmonary — chest x-ray / PFTs, and QT interval / ECG.
Why are Antiarrhythmics considered high-alert?
Within Antiarrhythmics, the ISMP list of high-alert medications includes ibutilide: an error in dosing or administration carries a heightened risk of serious patient harm, so extra safeguards are required.
Conditions treated
Amyotrophic Lateral Sclerosis
Patho · Nervous Mexiletine for cramps — "a sodium channel-blocking antiarrhythmic drug"; it "can cause gastrointestinal upset and arrhythmias." Quinine: "Caution is advised with the use of quinine sulfate as it has been associated with QT prolongation, arrhythmias, and bradycardia."
Cardiomyopathies
Patho · Cardiovascular Disopyramide is a negative-inotrope option in symptomatic obstructive HCM; its anticholinergic effects can cause urinary retention and worsen glaucoma or myasthenia gravis.
Dysrhythmias
Patho · Cardiovascular The rhythm-specific toolbox. Adenosine is the first-line drug for stable SVT — 6 mg rapid IV push through a large vein with a 20-mL flush, then 12 mg — because its half-life is seconds; warn the patient first about flushing, chest pressure, and a brief “impending doom”/transient asystole. Stable VT with structural disease: IV procainamide, amiodarone, or sotalol. Refractory VF: amiodarone after at least 3 defibrillation attempts. Torsades: magnesium 2 g IV first. In acute afib, rhythm control (e.g., amiodarone) is not first-line — rate control is.
See also
Beta-Blockers
Cardiovascular Slow heart rate & lower BP by blocking β-adrenergic receptors. Watch for bradycardia.
ACE Inhibitors
Cardiovascular Lower BP by blocking angiotensin conversion. Classic dry cough & angioedema risk.
Statins
Cardiovascular Lower LDL cholesterol via HMG-CoA reductase inhibition. Monitor for myopathy.
PCSK9 Inhibitors
Cardiovascular Injectable antibodies that protect the liver’s LDL receptors, cutting LDL cholesterol by about half and lowering cardiovascular events. Given subcutaneously every 2–4 weeks.
Fibrates
Cardiovascular PPAR-α agonists that mainly lower triglycerides — used with diet for severe hypertriglyceridemia — with muscle, gallbladder, liver and kidney risks, highest for gemfibrozil combined with a statin.
Bile Acid Sequestrants
Cardiovascular Non-absorbed resins that trap bile acids in the gut, forcing the liver to use cholesterol and pull LDL from the blood. Constipation, drug binding and rising triglycerides are the issues to manage.
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)
Reviewed by Hae Suk Lee, RN
Educational summary for nursing students. Always verify against current prescribing information and your institution's protocols before administering. Not medical advice.