Antiarrhythmics: Generic and Brand Names
- Class I Antiarrhythmics
- Class IA
- disopyramide (Norpace)
- procainamide (Pronestyl)
- quinidine (Quinaglute, Quinidex)
- Class IB
- lidocaine (Xylocaine)
- mexiletine (Mexilitil)
- Class IC
- flecainide (Tambocor)
- propafenone (Rythmol)
- Class II Antiarrhythmics
- acebutolol (Sectral)
- esmolol (Brevibloc)
- propranolol (Inderal)
- Class III Antiarrhythmics
- ibutilide (Corvert)
- sotalol (Betapace)
- Class IV Antiarrhythmics
- verapamil (Calan, Covera-HS)
- Other antiarrhythmics
- adenosine (Adenocard)
- digoxin (Lanoxin)
- dronedarone (Multaq)
Disease Spotlight: Arrhythmias
Arrhythmias (dysrhythmias) involve changes in the automaticity and conductivity of the heart cells. Two concepts drive the whole picture.
Conductivity is the property that lets heart cells transmit spontaneous impulses, starting at the sinoatrial (SA) node and activating all parts of the muscle almost simultaneously. It is the basis of cardiac contraction and relaxation. The specialized conductive system fires at set rates: SA node 60-100 impulses per minute, AV node 40-50 impulses per minute, and ventricular muscle cells 10-20 impulses per minute.
Automaticity is the property that lets heart cells depolarize spontaneously during relaxation, when potassium flows out of the cell and sodium moves in, the condition needed to produce an action potential. The action potential runs through five phases. Phase 0 is depolarization: the cell reaches its stimulation point, sodium gates open, sodium rushes in to fire the action potential, and there is no charge difference across the membrane. Phase 1 is a very short period where sodium concentration equalizes inside and outside the cell. Phase 2 is the plateau phase, where the cell starts back toward rest (repolarization): it becomes less permeable to sodium, potassium begins to leave, and calcium starts to enter. Phase 3 is rapid repolarization: the sodium gates close and potassium flows out. Phase 4 is the resting phase, where the sodium-potassium pump restores the resting membrane potential for the next action potential.
Arrhythmias fall into types by cause. Changes in rate produce tachycardia or bradycardia. Stimulation from an ectopic focus produces premature atrial contractions (PACs), premature ventricular contractions (PVCs), atrial flutter or fibrillation (AF), and ventricular fibrillation. Alterations in conduction through the muscle produce heart blocks and bundle branch block. Triggers include electrolyte disturbances, decreased oxygen supply to the cells, structural damage to the conduction system, drug effects, acidosis, and lactic acid accumulation.
Class I Antiarrhythmics
This class blocks sodium channels in the cell membrane during the action potential, and the subgroups differ by how they block those channels. They are local anesthetics and membrane-stabilizing agents because they bind quickly to sodium channels.
Therapeutic Action
Class I antiarrhythmics stabilize the cell membrane by depressing phase 0 of the action potential, binding to sodium channels and changing the duration of the action potential. Class Ia drugs depress phase 0 and prolong the duration. Class Ib drugs somewhat depress phase 0 and shorten the duration. Class Ic drugs markedly depress phase 0 and extremely slow conduction but have little effect on duration.
Indications
Primarily indicated to decrease the heart's workload and relieve HF. Digoxin is especially indicated for atrial flutter, atrial fibrillation, and paroxysmal atrial tachycardia. Antiarrhythmics are not often used in children. In adults they are usually for emergencies, with careful, regular evaluation of the regimen for effectiveness and safety; drug safety in pregnancy is not established, the drug enters breast milk with various side effects, and Antiarrhythmics I, III, and IV are strictly prohibited in lactating women. Older adults are more prone to toxicity from conditions that interfere with metabolism and excretion, so monitor renal and hepatic function.
Pharmacokinetics
| Route | Onset | Peak | Duration |
|---|---|---|---|
| IM | 5-10 min | 5-15 min | 2 h |
| IV | Immediate | Immediate | 10-20 min |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| 10 min, then 1.5-3 h | liver | urine |
Contraindications and Cautions
Allergy to Class I antiarrhythmics, to prevent severe hypersensitivity. Bradycardia and heart block, where, without an artificial pacemaker, the conduction-altering effect can cause total heart block. HF, hypotension, and shock, worsened by the drug's effect on the action potential. Electrolyte imbalance, which can alter effectiveness. Renal and hepatic dysfunction, which interfere with bioavailability and excretion. Pregnancy and lactation, for potential adverse effects on the fetus or neonate.
Adverse Effects
- CNS: dizziness, drowsiness, fatigue, twitching, mouth numbness, slurred speech, vision changes, tremors
- CV: arrhythmias, hypotension, vasodilation, potential for cardiac arrest
- Respiratory: respiratory depression
- Hema: bone marrow depression
- EENT: rash, hypersensitivity reactions, hair loss
Interactions
Digoxin and beta-blockers raise the risk of arrhythmias. Quinidine competes with digoxin at renal transport sites and can raise the risk of digoxin toxicity. Cimetidine increases Class Ia toxicity. Anticoagulants raise the risk of bleeding.
Class II Antiarrhythmics
This class blocks beta-receptors in the heart and kidneys, which blocks phase 4 of the action potential. Class II antiarrhythmics are beta-adrenergic blockers.
Therapeutic Action
They competitively inhibit beta-receptors in the heart and kidneys, decreasing heart rate, excitability, and cardiac output and slowing conduction through the AV node, while renin release drops in the kidneys. The result is lower blood pressure, a more stable heart, and a lighter workload.
Indications
Specifically indicated for supraventricular tachycardia and premature ventricular contractions (PVCs). Antiarrhythmics are not often used in children. In adults they are usually for emergencies, with careful, regular evaluation for effectiveness and safety; drug safety in pregnancy is not established, the drug enters breast milk with various side effects, and Antiarrhythmics I, III, and IV are strictly prohibited in lactating women. Older adults are more prone to toxicity from conditions that interfere with metabolism and excretion, so monitor renal and hepatic function.
Pharmacokinetics
| Route | Onset | Peak | Duration |
|---|---|---|---|
| Oral | 20-30 min | 60-90 min | 6-12 h |
| IV | Immediate | 1 min | 4-6 h |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| 3-5 h | liver | urine |
Contraindications and Cautions
Sinus bradycardia (<45 beats per minute) and heart block, worsened by the drug's effects. HF, cardiogenic shock, asthma, and respiratory depression, worsened by blocking beta-receptors. Pregnancy and lactation, for potential adverse effects on the fetus or neonate. Diabetes and thyroid dysfunction, altered by beta-receptor blockade. Renal and hepatic dysfunction, which interfere with bioavailability and excretion.
Adverse Effects
- CNS: dizziness, fatigue, dreams, insomnia
- CV: arrhythmias, hypotension, bradycardia, AV blocks, altered peripheral perfusion
- Respiratory: bronchospasm, dyspnea
- GI: anorexia, diarrhea, constipation, nausea, vomiting
- Other: loss of libido, decreased exercise tolerance, altered blood glucose
Interactions
Verapamil increases adverse drug effects. Insulin increases hypoglycemia.
Class III Antiarrhythmics
This class prolongs and slows the outward movement of potassium during phase 3 of the action potential, acting directly on the heart muscle to prolong repolarization and the refractory period. All of these drugs are proarrhythmic and can themselves induce arrhythmias.
Therapeutic Action
By prolonging the refractory period and repolarization, Class III antiarrhythmics raise the threshold for ventricular fibrillation. They treat life-threatening arrhythmias that no other drug has controlled, and they can act on peripheral tissue to decrease peripheral resistance.
Indications
Amiodarone is the first-line antiarrhythmic for shock-refractory ventricular fibrillation and pulseless ventricular tachycardia in Advanced Cardiac Life Support, given as 300 mg IV or intraosseous push, with a 150 mg repeat dose if the rhythm persists (ACLS Certification Association; StatPearls). Antiarrhythmics are not often used in children. In adults they are usually for emergencies, with careful, regular evaluation for effectiveness and safety; drug safety in pregnancy is not established, the drug enters breast milk with various side effects, and Antiarrhythmics I, III, and IV are strictly prohibited in lactating women. Older adults are more prone to toxicity from conditions that interfere with metabolism and excretion, so monitor renal and hepatic function.
Pharmacokinetics
| Route | Onset | Peak | Duration |
|---|---|---|---|
| Oral | 2-3 d | 3-7 h | 6-8 h |
| IV | Immediate | 20 min | Infusion |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| 10 d | liver | urine |
Contraindications and Cautions
AV block, which ibutilide and dofetilide worsen. Renal and hepatic dysfunction, which interfere with bioavailability and excretion. Shock, hypotension, respiratory depression, and prolonged QT interval, which depressed action potentials can worsen.
Adverse Effects
- CNS: weakness, dizziness
- CV: arrhythmias, HF
- GI: nausea, vomiting, GI distress
- Amiodarone is associated with liver toxicity, ocular abnormalities, and very serious cardiac arrhythmias.
Interactions
Digoxin and quinidine increase toxic drug effects. Antihistamines, phenothiazines, and tricyclic antidepressants raise the risk of proarrhythmias. Dofetilide with ketoconazole, verapamil, or cimetidine raises the risk of adverse effects. Sotalol with antacids, NSAIDs, and aspirin loses effectiveness.
Class IV Antiarrhythmics
This class includes two calcium-channel blockers, diltiazem and verapamil, and blocks the movement of calcium toward the cell membrane.
Therapeutic Action
Class IV antiarrhythmics depress action potential generation and slow phases 1 and 2, slowing both conduction and automaticity.
Indications
Diltiazem and verapamil are also used for hypertension and angina. Antiarrhythmics are not often used in children. In adults they are usually for emergencies, with careful, regular evaluation for effectiveness and safety; drug safety in pregnancy is not established, the drug enters breast milk with various side effects, and Antiarrhythmics I, III, and IV are strictly prohibited in lactating women. Older adults are more prone to toxicity from conditions that interfere with metabolism and excretion, so monitor renal and hepatic function.
Pharmacokinetics
| Route | Onset | Peak | Duration |
|---|---|---|---|
| Oral | 30-60 min | 2-3 h | 6-8 h |
| IV | Immediate | 2-3 min | Unknown |
| Half-life (T1/2) | Metabolism | Excretion |
|---|---|---|
| 3.5-6 h | liver | urine |
Contraindications and Cautions
Allergy to calcium-channel blockers, to prevent hypersensitivity. Heart block (sick sinus syndrome), where, without an artificial pacemaker, the drug worsens the block. HF and hypotension, worsened by the hypotensive effect. Pregnancy and lactation, for potential adverse effects on the fetus or neonate. Renal and hepatic dysfunction, which interfere with bioavailability and excretion.
Adverse Effects
- CNS: weakness, dizziness, fatigue, depression, headache
- CV: hypotension, shock, edema, HF, arrhythmia
- GI: nausea, vomiting, GI distress
Interactions
Verapamil with beta-blockers raises the risk of cardiac depression. Digoxin causes additive slowing of AV node conduction. Atracurium, pancuronium, and vecuronium increase respiratory depression. Giving the IV preparation within 48 hours of IV beta-adrenergic blockers raises the risk of cardiac depression. Diltiazem can raise the serum level of cyclosporine.
Nursing Considerations for Antiarrhythmics
Nursing Assessment
Screen for the contraindications above (renal dysfunction, heart blocks, hypersensitivity). Do a thorough baseline physical exam to gauge effectiveness and catch adverse effects. Assess neurologic status for CNS effects. Assess cardiac status closely (blood pressure, heart rate and rhythm, heart sounds) to judge whether the dose needs to change. Monitor respiratory rate, rhythm, and depth for respiratory depression and signs of developing HF. Monitor labs, including CBC and renal and liver function tests, for dose changes and toxic effects.
Nursing Diagnoses
- Decreased cardiac output related to the cardiac effects of the drug
- Ineffective tissue perfusion related to decreased blood flow
- Altered sensory perception related to CNS drug effects
- Risk for injury related to weakness and dizziness
Implementation with Rationale
Titrate to the smallest dose that controls the arrhythmia to lower toxicity risk. Monitor cardiac rhythm closely for serious adverse effects and to judge effectiveness. Provide comfort and safety measures (raised side rails, adequate lighting, noise control). Keep emergency drugs and equipment at the bedside for prompt treatment of severe toxicity. Teach the drug name, indication, and adverse effects to watch for to support adherence.
Evaluation
Monitor response through cardiac output and rhythm. Watch for adverse effects (sedation, respiratory depression, CNS effects). Confirm the patient can name the drug, its indication, and adverse effects to watch for. Track compliance.
Frequently Asked Questions
How are antiarrhythmic drugs classified? The Vaughan Williams system groups them in four classes: Class I sodium-channel blockers (subdivided IA, IB, IC), Class II beta-blockers, Class III potassium-channel blockers that prolong repolarization, and Class IV calcium-channel blockers. A few agents (adenosine, digoxin, dronedarone) fall outside the four classes.
Which antiarrhythmic is used first for shockable cardiac arrest? Amiodarone is the first-line antiarrhythmic for ventricular fibrillation or pulseless ventricular tachycardia that does not respond to defibrillation, dosed at 300 mg IV/IO with a 150 mg repeat; lidocaine is an accepted alternative (ACLS Certification Association).
Why are antiarrhythmics called proarrhythmic? Every drug that changes the action potential can also create new, sometimes lethal rhythms. Class III agents in particular can prolong the QT interval and trigger torsades de pointes, which is why continuous rhythm monitoring is required.
What should the nurse monitor during therapy? Watch the cardiac rhythm continuously, take an apical heart rate for one full minute, track blood pressure, respiratory status, and serum electrolytes, and keep emergency drugs and equipment at the bedside. Titrate to the smallest effective dose to limit toxicity.
Why does amiodarone need long-term monitoring? Amiodarone has a very long half-life (weeks) and can cause liver toxicity, thyroid dysfunction, pulmonary fibrosis, and corneal deposits. Patients need baseline and periodic liver, thyroid, eye, and lung assessment.
Can antiarrhythmics be stopped suddenly? No. Abruptly stopping these drugs, especially the beta-blocker class, can cause rebound arrhythmias, rebound hypertension, or worsening angina. Doses are tapered under provider supervision.