A Look at Antiarrhythmics
Almost half a million Americans die each year from cardiac arrhythmias; countless others suffer symptoms or lifestyle limitations. Along with other treatments, antiarrhythmic drugs can help alleviate symptoms and improve quality of life. It is important to keep in mind that all of these drugs have potential adverse effects, possibly life-threatening in nature, and must be prescribed with caution and the patients carefully monitored.
Antiarrhythmic drugs affect the movement of ions across the cell membrane and alter the electrophysiology of the cardiac cell. They’re classified according to their effect on the cell’s electrical activity (action potential) and their mechanism of action. (See Antiarrhythmics and the action potential)
Drugs in the same class are similar in action and adverse effects. When you know where a particular drug fits in the classification system, you’ll be better able to remember its actions and adverse effects.
Classifying Antiarrhythmics
The classification system divides antiarrhythmic drugs into four major classes. Let’s take a look at each one.
Class I Blocks Sodium
Class I drugs block the influx of sodium into the cell during phase 0 (rapid depolarization) of the action potential, which minimizes the chance of sodium reaching its threshold potential and causing cells to depolarize. Because phase 0 is also referred to as the sodium channel or fast channel, these drugs may also be called sodium channel blockers or fast channel blockers. Drugs in this class are potentially proarrhythmic, meaning they can cause or worsen arrhythmias.
Antiarrhythmic drugs in this class are further categorized as:
- Class Ia, which prolong conduction and repolarization
- Class Ib, which slow phase 0 depolarization, don’t affect conduction, and shorten phase 3 repolarization
- Class Ic, which markedly slow phase 0 depolarization and prolong conduction, with little effect on repolarization.
Class II Blocks Beta Receptors
Class II drugs block sympathetic nervous system beta-adrenergic receptors and thereby decrease heart rate. Phase 4 depolarization is diminished, resulting in depressed sinoatrial (SA) node automaticity and increased atrial and atrioventricular (AV) nodal refractoriness, or resistance to stimulation.
Class III Blocks Potassium
Class III drugs are called potassium channel blockers because they block the movement of potassium during phase 3 of the action potential and prolong repolarization and the refractory period.
Class IV Blocks Calcium
Class IV drugs block the movement of calcium during phase 2 of the action potential. Because phase 2 is also called the calcium channel or the slow channel, drugs that affect phase 2 are also known as calcium channel blockers or slow channel blockers. They prolong conductivity and increase the refractory period at the AV node.
Some Drugs Don’t Fit
Not all drugs fit neatly into these classifications. For example, sotalol possesses characteristics of both class II and class III drugs. Some drugs used to treat arrhythmias don’t fit into the classification system at all, including adenosine (Adenocard), atropine, digoxin (Lanoxin), epinephrine, and magnesium sulfate. Despite these limitations, the classification system helps nurses understand how antiarrhythmic drugs prevent and treat arrhythmias.
Drug Distribution and Clearance
Many patients receive antiarrhythmic drugs by IV bolus or infusion to improve bioavailability over the oral route of administration. The cardiovascular system then distributes the drugs throughout the body, specifically to the site of action.
Most drugs are changed, or biotransformed, into active or inactive metabolites in the liver. The kidneys are the primary sites for the excretion of those metabolites. When administering these drugs, remember that patients with impaired heart, liver, or kidney function may suffer from inadequate drug effect or toxicity. (See Drug metabolism and elimination across the life span.)
Antiarrhythmics by Class
Broken down by classes, the following section describes commonly used antiarrhythmic drugs. It highlights their dosages, adverse effects, and recommendations for patient care.
Class Ia antiarrhythmic drugs are called sodium channel blockers. They include quinidine (the prototype drug), procainamide, and disopyramide. These drugs reduce the excitability of the cardiac cell, have an anticholinergic effect, and decrease cardiac contractility. Because these drugs prolong the QT interval, the patient is prone to polymorphic ventricular tachycardia (VT). (See Effects of class Ia antiarrhythmics.)
Quinidine
Quinidine is effective against supraventricular and ventricular arrhythmias. It is no longer commonly prescribed, but was used to treat atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia (PSVT), AV node reentrant tachycardia (AVNRT), and Wolff–Parkinson–White (WPW) syndrome.
Quinidine has more recently been studied in patients with life-threatening ventricular arrhythmias, such as idiopathic ventricular fibrillation (VF) and Brugada syndrome, and has been found to be effective.
The drug comes in several forms, including quinidine sulfate and quinidine gluconate.
How to Give It
Here’s how to administer quinidine:
- To convert atrial flutter or fibrillation—Give 200 mg of quinidine sulfate orally every 2 to 3 hours for five to eight doses, with subsequent daily increases until sinus rhythm is restored or toxic effects develop. NOTE: It is critical to control AV node conduction before administering quinidine, as the drug can slow the atrial rate and increase conduction over the AV node, causing rapid 1:1 conduction of atrial arrhythmias. Class II or class IV medications are used for this purpose.
- Initial dosage for PSVT—Give 400 to 600 mg of quinidine sulfate orally every 6 hours.
- Initial dosage for premature atrial and ventricular contractions, paroxysmal AV junctional rhythm, paroxysmal atrial tachycardia (PAT), paroxysmal VT, or maintenance after cardioversion of atrial fibrillation or flutter—Give 200 mg of quinidine sulfate orally, then 200 to 300 mg orally every 4 to 6 hours, or 300 to 600 mg of extended-release quinidine every 8 to 12 hours. IV quinidine is no longer commercially available.
- Daily dosage for patients with life-threatening VT/VF, such as idiopathic VF or Brugada syndrome, is approximately 900 mg QD, in divided doses.
What Can Happen
Adverse cardiovascular effects of quinidine include hypotension, cardiotoxicity, VT, ECG changes (widening of the QRS complex, widened QT and PR intervals), torsades de pointes, AV block, and exacerbation of heart failure. (See Noncardiac adverse effects of quinidine)
How You Intervene
Keep the following points in mind when caring for a patient taking quinidine:
- Monitor the patient’s ECG, heart rate, and blood pressure closely. Don’t give more than 4 g/day. Adjust dosages in patients with heart failure and liver disease.
- Obtain a baseline QT interval measurement before the patient begins therapy. Watch for and notify the practitioner if the patient develops prolongation of the QT interval, a sign that the patient is predisposed to developing polymorphic VT. Also notify the practitioner if the QRS complex widens by 25% or more.
- Remember that quinidine should be avoided in patients with second- or third-degree AV block who don’t have pacemakers. It should also be avoided in patients with profound hypotension, myasthenia gravis, intraventricular conduction defects, or hypersensitivity to the drug. Use it cautiously in elderly patients and in those with renal disease, hepatic disease, or asthma.
- Avoid rapidly conducted atrial fibrillation or atrial flutter by administering AV nodal blocking agents, such as beta blockers or calcium channel blockers, before giving quinidine.
- Closely monitor patients receiving quinidine and digoxin for signs and symptoms of digoxin toxicity, such as nausea, vision changes, or arrhythmias. Digoxin levels will be increased.
- Monitor serum drug levels. The therapeutic level for arrhythmia control is 2 to 5 mcg/mL.
- Ask the patient about herb use. Concomitant use with jimsonweed may adversely affect cardiovascular function. Licorice combined with quinidine use may prolong the patient’s QT interval.
Procainamide
Procainamide is indicated for supraventricular and ventricular arrhythmias. It is used intravenously to acutely convert atrial fibrillation, atrial flutter, or VT. It is the drug of choice for atrial fibrillation with conduction over an accessory pathway. It is also used for AVNRT.
How to Give It
Here’s how to administer procainamide:
- Orally—Initial dosage is 50 mg/kg/day of conventional formulation in divided doses every 3 hours until a therapeutic level is reached. For maintenance, an extended-release form is substituted to deliver the total daily dose divided every 6 hours. An extended-release form may be used to deliver the dose divided every 12 hours.
- IM—Initial daily dosage is 50 mg/kg divided into equal doses every 3 to 6 hours.
- IV—Slow injection of 100 mg is given with the patient in a supine position, no faster than 25 to 50 mg/min until the arrhythmia is suppressed, adverse effects develop, or 500 mg has been given. The usual loading dose is 500 to 600 mg.
- IV infusion—Infuse at 1 to 6 mg/min for a maintenance dosage.
What Can Happen
Adverse cardiovascular effects of procainamide include bradycardia, hypotension, worsening heart failure, AV block, VF, and asystole. (See Noncardiac adverse effects of procainamide.)
How You Intervene
Keep the following points in mind when caring for a patient taking procainamide:
- Monitor the patient’s heart rate, blood pressure, and ECG. Notify the practitioner if the patient has hypotension or if you notice widening of the QRS complex by 50% or more. Also report a prolonged QT interval if it’s more than one-half of the R-R interval—a sign that the patient is predisposed to developing polymorphic VT.
- Warn the patient taking procainamide orally not to chew it, which causes rapid absorption and intensified drug effect.
- Monitor serum drug levels. (See Monitoring procainamide.)
- Remember that procainamide should be avoided in patients with second- or third-degree AV block who don’t have pacemakers and in patients with blood dyscrasias, myasthenia gravis, profound hypotension, or known hypersensitivity to the drug. Procainamide may also aggravate digoxin toxicity.
Disopyramide
Disopyramide (Norpace) is effective in digitalis-induced arrhythmias, atrial arrhythmias, AVNRT, supraventricular tachycardia (SVT) because of accessory pathways, and ventricular tachyarrhythmias. The negative inotropic action of disopyramide can be useful in neurocardiogenic (vasodepressor) syncope and hypertrophic cardiomyopathy.
How to Give It
Here’s how to give disopyramide:
- Orally, 100 mg to 150 mg every 6 hours or 200 mg to 300 mg every 12 hours (controlled release formula)
What Can Happen
Adverse cardiovascular effects include sinus bradycardia in patients with sick sinus syndrome (SSS), QRS and QT prolongation by 10% to 15%, variable AV conduction changes, and proarrhythmia including VF and torsades de pointes.
How You Intervene
Keep the following points in mind when caring for a patient taking disopyramide:
- Monitor ECG and HR closely.
- Obtain 12-lead ECG for baseline and periodically for accurate interval measurements.
- Give AVN blocking agents prior to disopyramide, when treating atrial fibrillation or atrial flutter.
- Reduce dose in renal and hepatic dysfunction.
- Do not use in patients with systolic congestive heart failure (CHF).
- Check K+ and magnesium levels before initiating Norpace and replete if necessary.
- Avoid use of erythromycin with Norpace as it can increase levels and lead to torsades de pointes.
Class Ib antiarrhythmics in use include such drugs as lidocaine and mexiletine. Because of their actions on ventricular muscle and Purkinje fibers, these drugs are effective in suppressing ventricular ectopy but do not affect atrial muscle. (See Effects of class Ib antiarrhythmics.) These drugs slow phase 0 depolarization and shorten phase 3 repolarization and the action potential. Sinus node automaticity and AV node automaticity and conductivity are not affected by lidocaine.
Lidocaine
Lidocaine was once the drug of choice for suppressing ventricular arrhythmias; however, amiodarone is now favored. When lidocaine is used, a patient is generally first given a loading dose and then an infusion.
How to Give It
Here’s how to administer lidocaine:
- IV bolus injection—Administer 1 to 1.5 mg/kg (usually 50 to 100 mg) at 25 to 50 mg/min and repeat every 3 to 5 minutes to a maximum of 300 mg total bolus during a 1-hour period.
- IV infusion immediately following the bolus dose—Infuse at 1 to 4 mg/min.
What Can Happen
Cardiovascular adverse effects of lidocaine include hypotension, bradycardia, and cardiac arrest. (See Noncardiac adverse effects of lidocaine)
How You Intervene
Keep the following points in mind when caring for a patient receiving lidocaine:
- Monitor the patient’s heart rate, blood pressure, and ECG.
- Watch for signs and symptoms of drug toxicity. Seizures may be the first sign of toxicity. The potential for toxicity is increased if the patient has liver disease, is elderly, is taking cimetidine (Tagamet) or propranolol (Inderal), or receives an infusion of the drug for longer than 24 hours.
- Avoid use of the drug in patients known to be hypersensitive to it or in severe sinus node disease, AV block or intraventricular block in the absence of an artificial pacemaker.
- Administer cautiously with other antiarrhythmics.
Mexiletine
Mexiletine is an oral congener of lidocaine, used in the treatment of ventricular arrhythmias. It has no activity against atrial arrhythmias.
How to Give It
- 150 to 200 mg every 8 hours to a maximum dose of 400 mg every 8 hours. Decrease dose in hepatic disease. No adjustment required in renal disease or with CHF.
What Can Happen
- Proarrhythmia is very rare, about 1.3%.
- Very little effect on HR, blood pressure, or cardiac output.
- Exacerbation of CHF is rare, about 2%.
- Monitor for GI side effects including nausea and CNS effects of tremor, blurred vision, dysarthria, ataxia, and confusion.
How You Intervene
- Monitor ECG for efficacy in controlling ventricular arrhythmias.
- Give medication with food to avoid GI effects.
Class Ic antiarrhythmic drugs include flecainide (Tambocor) and propafenone (Rythmol). These drugs decrease intracardiac conduction in all parts of the heart. (See Effects of class Ic antiarrhythmics.) These drugs are primarily used for supraventricular arrhythmias. Because of their proarrhythmic potential, they are avoided in patients with structural heart disease such as coronary artery disease, cardiomyopathy, and CHF.
Flecainide
Flecainide is used to treat paroxysmal atrial fibrillation or flutter in patients without structural heart disease. It is also used to prevent PSVT.
How to Give It
The dosage for flecainide is 50 to 200 mg orally every 12 hours, to a maximum of 400 mg/day.
What Can Happen
Adverse cardiovascular effects of flecainide include bradycardia (in the presence of sinus node disease), chest pain, palpitations, heart failure, new or worsened arrhythmias, and cardiac arrest.
Flecainide can decrease the atrial rate in atrial fibrillation or atrial flutter, facilitating AV node conduction and faster ventricular rate. Class II or IV antiarrhythmic medication is given to slow AV conduction and prevent rapid ventricular response when using flecainide for atrial arrhythmias. (See Noncardiac adverse effects of flecainide.)
How You Intervene
Keep the following points in mind when caring for a patient taking flecainide:
- Monitor the patient’s heart rate, blood pressure, and ECG. Report widening of the QRS complex by 25% or more and watch closely for signs of heart failure.
- Use flecainide cautiously in SSS or in patients with heart, kidney, or liver failure. Avoid its use entirely in second- or third-degree AV block and use caution in bifascicular block.
- Administer flecainide cautiously in patients receiving cimetidine, digoxin, or propranolol.
- Correct electrolyte imbalances before starting flecainide therapy.
- Administer AV node blocking agents (Class II or IV medications) with flecainide, to avoid rapid ventricular conduction of atrial flutter or atrial fibrillation.
Propafenone
Propafenone slows conduction in all cardiac tissues. The drug is used for the treatment of SVT, including atrial fibrillation, atrial flutter, AVNRT, and arrhythmias because of accessory pathways.
How to Give It
The usual dosage of propafenone is 150 to 300 mg orally every 8 hours, to a maximum dosage of 900 mg/day.
What Can Happen
Propafenone’s adverse effects on the cardiovascular system include exacerbation of heart failure, AV block, and proarrhythmia (VT, VF, and premature ventricular contraction [PVCs]). However, proarrhythmia is rare in patients treated for SVT, with a structurally normal heart. (See Noncardiac adverse effects of propafenone.)
How You Intervene
Keep the following points in mind when caring for a patient taking propafenone:
- Monitor the patient’s heart rate, blood pressure, and ECG. Report widening of the QRS complex greater than 25%. If widening occurs, the dosage may need to be reduced. Monitor the patient closely for exacerbation of heart failure.
- Correct electrolyte imbalances before starting propafenone therapy.
- Remember that propafenone should be avoided in patients with a structurally abnormal heart (low ejection fraction, previous myocardial infarction [MI], cardiomyopathy or significant left ventricular hypertrophy), bronchospastic disorders, hypotension, or sinus node disease, AV, block, or bifascicular blocks.
- Propafenone is contraindicated in the presence of CHF and cardiogenic shock, as well as in SA, AV, and intraventricular conduction disorders in the absence of an artificial pacemaker.
- Administer propafenone cautiously in patients also receiving cimetidine, propranolol, or metoprolol.
- Be aware that patients receiving digoxin along with propafenone may have increased plasma concentration of digoxin, leading to digoxin toxicity.
- Use cautiously in patients also taking warfarin (Coumadin); propafenone can increase the plasma concentration of the anticoagulant.
Class II antiarrhythmic drugs are used to treat supraventricular and ventricular arrhythmias, especially those caused by excess catecholamines. The drugs are called beta-adrenergic blockers because they block beta-adrenergic receptors in the sympathetic nervous system. (See Effects of class II antiarrhythmics)
Two types of beta-adrenergic receptors exist: beta1 and beta2. Beta1-adrenergic receptors increase heart rate, contractility, and conductivity. Blocking those receptors decreases the actions listed above.
Beta2-adrenergic receptors relax smooth muscle in the bronchi and blood vessels. Keep in mind that blocking these receptors may result in vasoconstriction and bronchospasm.
Beta-adrenergic blockers that block only beta1-adrenergic receptors are referred to as cardioselective. Those that block both beta1-adrenergic and beta2-adrenergic receptors are referred to as noncardioselective. Cardioselective formulations are preferred in patients with asthma.
Beta blockers depress the slope of phase 4 depolarization, suppress automaticity, and prolong AV node conduction. These drugs are used to control ventricular rate in atrial fibrillation and atrial flutter, reduce the risk of sudden cardiac death (SCD) in patients with nonsustained VT and structural heart disease, reduce SCD in patients post-MI, prevent SCD in long QT interval syndrome, prevent recurrence of SVT, and to slow HR in PAT.
Beta-Adrenergic Blockers
The following beta-adrenergic blockers are approved by the US Food and Drug Administration for use as antiarrhythmics:
- Acebutolol (Sectral), which is classified as cardioselective and decreases contractility, heart rate, and blood pressure
- Propranolol (Inderal), which is classified as noncardioselective; decreases heart rate, contractility, and blood pressure; and reduces the incidence of SCD after MI
- Esmolol (Brevibloc), which is a short-acting, cardioselective drug administered by IV titration that decreases heart rate, contractility, and blood pressure
- Sotalol (Betapace), which is a noncardioselective drug that also has class III characteristics, decreases heart rate, slows AV conduction, decreases cardiac output, and has proarrhythmic effects and increases the QT interval. It has little effect on blood pressure. It is used primarily to maintain SR with atrial fibrillation or atrial flutter.
Other beta blockers often used to treat arrhythmias include metoprolol, atenolol, nadolol, bisoprolol, and nebivolol. These agents are briefly described:
- Metoprolol (cardioselective) is available in short-acting (metoprolol tartrate) or extended-release (metoprolol succinate) oral formulations, as well as in IV form. This is the most commonly used medication to slow AV node conduction and to treat atrial and ventricular ectopy.
- Atenolol (cardioselective) is desirable for its once-daily dosing. It has become less preferred to other drugs in this class, but is still used.
- Nadolol (noncardioselective) is the preferred beta-blocker in treating potentially life-threatening ventricular arrhythmias in patients with some forms of long QT syndrome (LQTS).
- Bisoprolol (cardioselective) is sometimes used when other beta-blocking medications cause significant adverse reactions, as this formulation is often associated with improved tolerance.
- Nebivolol (cardoselective, at low doses), like bisoprolol, is often better tolerated than other agents in this class.
How to Give It
These four beta-adrenergic blockers should be administered as follows:
- Acebutolol—The normal dosage is 200 mg orally twice daily, increased as needed to a usual dosage of 600 to 1,200 mg daily.
- Propranolol—It may be given orally or IV. The oral dosage is 10 to 30 mg three or four times daily. The IV dose is 0.5 to 3.0 mg, at a rate not to exceed 1 mg/min. If necessary, a second IV dose may be administered after 2 minutes; subsequent doses may be given no sooner than every 4 hours.
- Esmolol—The loading dose is 500 mcg/kg over 1 minute, then 50 mcg/kg/min for 4 minutes. If an adequate response doesn’t occur within 5 minutes, repeat the loading dose and infuse 100 mcg/kg/min for 4 minutes. If needed, increase infusion to a maximum of 200 mcg/kg/min.
- Sotalol—The initial dosage is 80 mg orally twice daily. Most patients respond to a daily dose of 160 to 320 mg.
What Can Happen
The adverse effects of beta-adrenergic blockers on the cardiovascular system may vary, but they include bradycardia, hypotension, and AV block. (See Noncardiac adverse effects of class II beta-adrenergic blockers)
How You Intervene
Keep the following points in mind when caring for a patient taking a beta-adrenergic blocker:
- Monitor the patient’s heart rate, blood pressure, and ECG.
- Remember that beta-adrenergic blockers should be avoided in patients with symptomatic bradycardia, second- or third-degree AV block without a pacemaker, and shock. Use them cautiously in patients with diabetes mellitus (they mask the signs of hypoglycemia), heart failure, kidney disease, liver disease, myasthenia gravis, peripheral vascular disease, and hypotension.
- Keep in mind that noncardioselective beta-adrenergic blockers are contraindicated in patients with asthma or other bronchospastic disease.
- Correct electrolyte imbalances before starting therapy with a beta-adrenergic blocker.
- Remember that beta-adrenergic blockers diminish the patient’s ability to withstand exercise because the heart rate can’t increase. These drugs also block sympathetic response to shock.
Class III antiarrhythmics are called potassium channel blockers. (See Effects of class III antiarrhythmics.) They include amiodarone hydrochloride (Cordarone), ibutilide (Corvert), and dofetilide (Tikosyn). Sotalol has qualities of both class II and class III antiarrhythmics. All class III antiarrhythmics have proarrhythmic potential.
Amiodarone
Amiodarone is used to treat supraventricular arrhythmias, including atrial fibrillation and atrial flutter, as well as ventricular arrhythmias.
How to Give It
Here’s how to administer amiodarone:
- Orally—Give 800 to 1,600 mg daily in divided doses for 1 to 3 weeks, followed by 400 to 800 mg/day for 4 weeks, followed by 200 to 400 mg/day as a maintenance dosage.
- IV infusion—Infuse 150 mg over 10 minutes (15 mg/min); then infuse 360 mg over the next 6 hours (1 mg/min), followed by 540 mg infused over 18 hours (0.5 mg/min). After the first 24 hours, a maintenance IV infusion of 720 mg per 24 hours (0.5 mg/min) should be continued.
What Can Happen
Adverse cardiovascular effects of amiodarone given by IV infusion include bradycardia, hypotension, AV block, heart failure, asystole, and pulseless electrical activity.
Long-term oral therapy can be associated with bradycardia, pulmonary fibrosis, thyroid dysfunction, elevated liver function tests, and corneal deposits, not usually leading to visual disturbances. (See Noncardiac adverse effects of amiodarone)
How You Intervene
Keep the following points in mind when caring for a patient taking amiodarone:
- Monitor the patient’s vital signs, ECG, and respiratory status.
- Monitor laboratory test results, such as electrolyte levels, liver function studies, thyroid function studies, pulmonary function studies, and chest X-rays.
- Check for signs of digoxin toxicity or increased prothrombin time. Amiodarone can increase the serum levels of digoxin and warfarin.
- Remember that amiodarone should be avoided in patients with hypersensitivity to the drug, cardiogenic shock, marked sinus bradycardia, and second- or third-degree AV block without a pacemaker. Use the drug cautiously in patients with cardiomegaly, preexisting bradycardia or sinus node disease, conduction disturbances, or depressed ventricular function.
- Be aware that the drug has a long half-life (56 days, with a range from 13 to 103 days) and therefore takes weeks to reach therapeutic levels and possibly up to 3 months to be cleared by the body.
- Know that amiodarone may increase theophylline levels in patients taking theophylline. Monitor the patient for signs of theophylline toxicity.
- Be aware that amiodarone may increase phenytoin (Dilantin) levels. Monitor phenytoin levels closely.
- Instruct the patient to wear sunscreen and protective clothing to avoid photosensitivity reactions. A blue-gray discoloration of exposed skin may occur.
- Recommend that the patient have yearly ophthalmic examinations. Within 1 to 4 months after beginning amiodarone therapy, most patients show corneal microdeposits upon slit-lamp ophthalmic examination. Instillation of methylcellulose ophthalmic solution minimizes corneal microdeposits.
- Administer the IV drug through a central venous access device to avoid phlebitis.
- The lowest possible effective maintenance dose should be used to avoid toxicity.
Ibutilide
Ibutilide is used for the rapid conversion of recent-onset atrial fibrillation or flutter to sinus rhythm. The drug increases atrial and ventricular refractoriness.
How to Give It
If your adult patient weighs greater than 132 lb (60 kg) or more, he or she will receive 1 mg of ibutilide IV over 10 minutes. If they weigh less than 132 lb, the dose is 0.01 mg/kg.
If the arrhythmia is still present 10 minutes after the infusion is complete, the dose may be repeated.
What Can Happen
Adverse cardiovascular effects of ibutilide include PVCs, nonsustained VT, sustained polymorphic VT, hypotension, bundle branch block, AV block, hypertension, bradycardia, tachycardia, palpitations, heart failure, and lengthening of the QT interval. Noncardiac adverse effects include headache, nausea, and renal failure.
How You Intervene
Keep these points in mind when giving ibutilide:
- Correct electrolyte abnormalities before administering ibutilide.
- Monitor the patient’s vital signs and ECG continuously during the infusion and for at least 4 hours afterward. The infusion will be stopped if the arrhythmia terminates or if the patient develops VT or marked prolongation of the QT interval, which signals the risk of polymorphic VT.
- Have emergency equipment and medication nearby for the treatment of sustained VT.
- Don’t give ibutilide to patients with a history of polymorphic VT.
- Give the drug cautiously in patients receiving digoxin (Lanoxin) because it can mask signs and symptoms of cardiotoxicity associated with excessive digoxin levels.
- Don’t administer ibutilide at the same time or within 4 hours of class Ia or other class III antiarrhythmics.
- Don’t give ibutilide with other drugs that prolong the QT interval, such as phenothiazines and tricyclic or tetracyclic antidepressants.
- Be aware that patients with atrial fibrillation that has lasted longer than 24 to 48 hours must receive anticoagulants for at least 3 weeks before the initiation of ibutilide therapy, unless atrial thrombosis is confirmed negative by transesophageal echocardiogram.
Dofetilide (Tikosyn)
Dofetilide is used to maintain normal sinus rhythm in patients with symptomatic atrial fibrillation or atrial flutter. It is also used to convert atrial fibrillation and atrial flutter to normal sinus rhythm.
How to Give It
Dosage is based on creatinine clearance and QTc interval, which must be determined before the first dose (QT interval should be used if the heart rate is less than 60 beats/min). The usual recommended dosage is 500 mcg orally twice per day for patients with a creatinine clearance greater than 60 mL/min. The dose is 250 mcg twice daily if the creatinine clearance is 40 to 60 mL/min and 125 mcg twice daily if the creatinine clearance is 20 to 40 mL/min. QTc should be <440 ms before administration of the first dose of dofetilide.
Dofetilide is initiated in the hospital setting, with continuous cardiac monitoring, for 72 hours. The possibility of life-threatening ventricular arrhythmias is greatest during this time. Twelve-lead ECG tracings are obtained frequently to assess medication effect on the QTc interval, and dose adjustment made as indicated.
What Can Happen
Adverse cardiovascular effects of dofetilide include VF, VT, torsades de pointes, AV block, bundle branch block, heart block, bradycardia, chest pain, edema, cardiac arrest, and MI. (See Noncardiac adverse effects of dofetilide.)
How You Intervene
Remember these facts when giving dofetilide:
- Use cautiously in patients with severe hepatic impairment.
- Provide continuous ECG monitoring for at least 3 days.
- Avoid discharging the patient within 12 hours of conversion to normal sinus rhythm.
- Monitor the patient for prolonged diarrhea, sweating, and vomiting. Report these signs to the practitioner because electrolyte imbalance may increase the potential for arrhythmia development.
- Assess for hypokalemia and hypomagnesemia if the patient is receiving potassium-depleting diuretics, which increase the risk of torsades de pointes. Potassium level should be within normal range before giving dofetilide and kept in normal range. Use of hydrochlorothiazide should be avoided in patients treated with dofetilide.
- Stop antiarrhythmic therapy under careful monitoring for a minimum of three plasma half-lives before starting dofetilide.
- Don’t give dofetilide after amiodarone therapy until the amiodarone level is below 0.3 mcg/mL or until amiodarone has been stopped for at least 3 months.
- Provide a washout period of at least 2 days before starting other drug therapy if dofetilide is stopped to allow treatment with other drugs (such as those that interact with dofetilide).
- Don’t give dofetilide with grapefruit juice; it may decrease hepatic metabolism and increase the drug level.
- Don’t give with drugs that prolong the QT interval, such as phenothiazines, tricyclic or tetracyclic antidepressants, and erythromycin.
- Avoid using with cimetidine (Tagamet), ketoconazole (Nizoral), co-trimoxazole (Bactrim), verapamil (Calan), and inhibitors of CYP3A4, such as amiodarone (Cordarone), diltiazem (Cardizem), norfloxacin (Noroxin), and selective serotonin reuptake inhibitors.
- Avoid using with inhibitors of renal cationic secretion, such as megestrol (Megace), amiloride (Midamor), metformin (Glucophage), and triamterene (Dyrenium).
Class IV antiarrhythmic drugs are called calcium channel blockers. They include verapamil and diltiazem. These drugs prolong conduction time and the refractory period in the AV node. (See Effects of class IV antiarrhythmics)
Other calcium channel blockers, including nifedipine (Procardia) and amlodipine (Norvasc), don’t cause electrophysiologic changes and aren’t used as antiarrhythmics. They’re used primarily to treat hypertension.
Verapamil
Verapamil is used for PSVT because of its effect on the AV node. It also slows the ventricular response in atrial fibrillation and flutter.
How to Give It
Here’s how to administer verapamil:
- Orally for chronic atrial fibrillation—Give 80 to 120 mg three or four times per day to a maximum of 480 mg/day.
- IV injection for supraventricular arrhythmias—Give 0.075 to 0.15 mg/kg (usually 5 to 10 mg) over 2 minutes; you can repeat in 30 minutes if no response occurs.
What Can Happen
Cardiovascular adverse effects of verapamil include bradycardia, AV block, hypotension, heart failure, edema, and VF. (See Noncardiac adverse effects of verapamil.)
How You Intervene
Keep the following points in mind when caring for a patient taking verapamil:
- Monitor the patient’s heart rate, blood pressure, and ECG. Also monitor liver function studies.
- Note that calcium may be given before verapamil to prevent hypotension.
- Advise the patient to change position slowly to avoid orthostatic hypotension.
- Remember that verapamil should be avoided in SSS or second- or third-degree AV block without a pacemaker and in atrial fibrillation or flutter in a patient with WPW syndrome. It also should be avoided in patients with hypersensitivity to the drug, advanced heart failure, cardiogenic shock, profound hypotension, acute MI, or pulmonary edema.
- Give the drug cautiously to patients receiving digoxin or oral beta-adrenergic blockers, elderly patients, and patients with heart failure, hypotension, liver disease, or kidney disease. Don’t give verapamil to patients receiving IV beta-adrenergic blockers.
Diltiazem
Diltiazem is administered IV to treat PSVT and for ventricular rate control with atrial fibrillation or flutter.
How to Give It
Here’s how to give diltiazem:
- IV injection—Give 0.25 mg/kg (usually 20 mg) over 2 minutes; you can repeat in 15 minutes at 0.35 mg/kg (usually 25 mg) over 2 minutes.
- IV infusion—Infuse at a rate of 5 to 15 mg/hr; increase dose by 5 mg/hr increments. Continuous infusion should generally be used for ≤24 hours, because of drug accumulation.
- Oral dosing—start immediate-release oral formulation 1 hour before stopping the IV infusion. Immediate-release doses are given four times daily. Usual effective total daily dose is 360 mg, in divided doses. Once stable daily dose is reached, extended-release dosing can be given once or twice daily, depending on formulation.
What Can Happen
Adverse cardiovascular effects of diltiazem include edema, flushing, bradycardia, hypotension, heart failure, arrhythmias, conduction abnormalities, sinus node dysfunction, and AV block. (See Noncardiac adverse effects of diltiazem)
How You Intervene
Keep the following points in mind when caring for a patient receiving diltiazem:
- Monitor the patient’s heart rate, blood pressure, and ECG.
- Diltiazem should be avoided in patients with SSS or second- or third-degree AV block without a pacemaker, atrial fibrillation or flutter with WPW syndrome, advanced heart failure, cardiogenic shock, profound hypotension, acute MI, pulmonary edema, or sensitivity to the drug.
- Use cautiously in elderly patients; in patients with heart failure, hypotension, or liver or kidney disease; and in those receiving digoxin or beta-adrenergic blockers. (See Prolonged effects in elderly patients)
- Give cautiously to patients receiving IV beta-adrenergic blockers. IV diltiazem and IV beta-adrenergic blocker shouldn’t be given within a few hours of each other.
- Advise the patient to change position slowly to avoid orthostatic hypotension.
Unclassified Antiarrhythmics
Some antiarrhythmic drugs defy categorization. Let’s look at some of those drugs, which are called unclassified or miscellaneous antiarrhythmic drugs.
Adenosine
Adenosine is a naturally occurring nucleoside used to treat PSVT. It acts on the AV node to slow conduction and inhibit reentry pathways. It’s also useful in treating PSVT associated with WPW syndrome.
Although adenosine isn’t effective for atrial fibrillation or atrial flutter, it does slow conduction through the AV node enough to determine the atrial rhythm and to allow for appropriate treatment of the arrhythmia.
How to Give It
Administer 6 mg of adenosine IV over 1 to 2 seconds, immediately followed by a rapid flush with 20 mL normal saline solution. Because the drug’s half-life is less than 10 seconds, it needs to reach the circulation quickly. The intravenous line should be placed at the antecubital space, rather than more distal to the heart. Repeat with an IV injection of 12 mg of adenosine if the rhythm doesn’t convert within 1 to 2 minutes.
What Can Happen
Adverse cardiovascular effects of adenosine include transient arrhythmias such as a short asystolic pause at the time of conversion. Other adverse effects include hypotension (if large doses are used), facial flushing, diaphoresis, chest pressure, and recurrence of the arrhythmia. (See Noncardiac adverse effects of adenosine.)
How You Intervene
Keep the following points in mind when caring for a patient receiving adenosine:
- Monitor the patient’s heart rate, blood pressure, ECG, ventilatory rate and depth, and breath sounds for wheezes.
- Remember that adenosine should be avoided in patients with hypersensitivity to the drug, second- or third-degree AV block, or SSS without a pacemaker. Use cautiously in older adults and in patients with asthma or those receiving dipyridamole (Persantine) or carbamazepine (Tegretol).
- Store adenosine at room temperature.
- Be aware that the patient may require a higher dose or may not respond to therapy at all if he or she is also taking aminophylline or another xanthine derivative.
Atropine
Atropine is an anticholinergic drug that blocks vagal effects on the SA and AV nodes. This enhances conduction through the AV node and speeds the heart rate. Atropine is used to treat symptomatic bradycardia and asystole. However, atropine is ineffective in patients following dissection of the vagus nerve during heart transplant surgery. Isoproterenol (Isuprel) can be used to treat symptomatic bradycardia in these patients.
How to Give It
Administer atropine by a 0.5- to 1-mg IV injection repeated as needed at 3- to 5-minute intervals, to a maximum dose of 2 mg. The initial dose for asystole is 1 mg. The maximum dose is 3 mg.
What Can Happen
Adverse cardiovascular effects of atropine include tachycardia (with high doses), palpitations, bradycardia if given slowly or in a dose of less than 0.5 mg, hypotension, and chest pain and increased myocardial oxygen consumption in patients with coronary artery disease. (See Noncardiac adverse effects of atropine.)
How You Intervene
Keep the following points in mind when caring for a patient receiving atropine:
- Monitor the patient’s heart rate, blood pressure, ECG, urine output, and bowel sounds.
- Remember that atropine should be avoided in patients with hypersensitivity to belladonna, acute angle closure glaucoma, GI obstruction, obstructive uropathy, myasthenia gravis, and tachyarrhythmias.
- Use atropine cautiously in patients with renal disease, heart failure, hyperthyroidism, hepatic disease, hypertension, and acute MI. Don’t give atropine for bradycardia unless the patient is symptomatic.
Digoxin
Digoxin (Lanoxin) was historically used to treat PSVT, atrial fibrillation, and atrial flutter for the purpose of decreasing heart rate. It provides antiarrhythmic effects by enhancing vagal tone and slowing conduction through the SA and AV nodes. Class II and IV drugs are now the preferred medications for controlling heart rate. Digoxin has visible effects on the patient’s ECG. (See Effects of digoxin.)
How to Give It
To administer digoxin rapidly and orally or IV, give a digitalizing dose of 0.5 to 1 mg divided into two or more doses every 6 to 8 hours. The usual maintenance dosage is 0.125 to 0.5 mg daily. The dose is reduced, or the medication avoided, in the patient with renal insufficiency or renal failure.
What Can Happen
Too much digoxin in the body causes toxicity. Toxic cardiac effects include SA and AV blocks and junctional and ventricular arrhythmias. Digoxin toxicity is treated by discontinuing digoxin; correcting oxygenation and electrolyte imbalances; treating arrhythmias with phenytoin, lidocaine, atropine, or a pacemaker; giving digoxin immune fab (Digibind) to reverse life-threatening arrhythmias or blocks (reversal occurs within 30 to 60 minutes of administration); and correcting the potassium level before giving digoxin immune fab. (See Noncardiac adverse effects of digoxin.)
How You Intervene
Keep the following points in mind when caring for a patient receiving digoxin:
- Check for signs of digoxin toxicity, especially in patients with hypokalemia, hypocalcemia, hypercalcemia, or hypomagnesemia. Monitor serum electrolyte levels as ordered.
- Monitor the patient’s apical heart rate and ECG. A heart rate below 60 beats/min or a change in rhythm can signal digoxin toxicity. If this occurs, notify the practitioner.
- Remember that digoxin should be avoided in patients with known hypersensitivity to the drug; SSS, SA, or AV block (without an implanted cardiac pacemaker); VT; hypertrophic cardiomyopathy; or WPW syndrome. Use cautiously in older adults and in patients with acute MI, liver or kidney disease, or hypothyroidism.
- Withhold digoxin for 1 to 2 days before performing electrical cardioversion.
- Be sure to question the patient about herbal preparation use because digoxin reacts with many preparations. Fumitory, lily of the valley, goldenseal, motherwort, shepherd’s purse, and rue may enhance the cardiac effects of digoxin. Licorice, oleand er, Siberian ginseng, foxglove, and squill may increase the risk of digoxin toxicity.
Epinephrine
Epinephrine is a naturally occurring catecholamine. It acts directly on alpha-adrenergic and beta-adrenergic receptor sites of the sympathetic nervous system, and it’s used to help restore cardiac rhythm in cardiac arrest and to treat symptomatic bradycardia. Its actions include increasing the systolic blood pressure, slightly decreasing diastolic blood pressure, and increasing heart rate and cardiac output.
How to Give It
To restore sinus rhythm in cardiac arrest in adults, administer epinephrine by IV injection as a 1 mg dose (10 mL of 1:10,000 solution). Each dose given by peripheral IV injection should be followed by a 20 mL flush of IV fluid to ensure quick delivery of the drug. Doses may be repeated every 3 to 5 minutes as needed. (Some practitioners advocate doses of up to 5 mg, especially for patients who don’t respond to the usual IV dose.) After initial IV administration, an infusion may be given at 1 to 4 mcg/min.
What Can Happen
Adverse cardiovascular effects include palpitations, hypertension, tachycardia, VF, anginal pain, shock, and ECG changes, including a decreased T-wave amplitude. (See Noncardiac adverse effects of epinephrine.)
How You Intervene
Keep these points in mind when administering epinephrine:
- Be sure to document the concentration of the epinephrine solution used. (Remember that 1 mg equals 1 mL of 1:1,000 or 10 mL of 1:10,000 concentration.)
- When administering IV epinephrine, monitor the patient’s heart rate, ECG rhythm, and blood pressure throughout therapy.
- Don’t mix the drug with alkaline solutions. Use D5W, lactated Ringer’s solution, or normal saline solution or a combination of dextrose and saline solution.
- Remember that some epinephrine products contain sulfites. Use of those products usually should be avoided in patients with sulfite allergies. The only exception is when epinephrine is being used in an emergency.
- Know that the use of epinephrine with digoxin (Lanoxin) or such general anesthetics as cyclopropane or a halogenated hydrocarbon like halothane (Fluothane) may increase the risk of ventricular arrhythmias.
- Avoid giving epinephrine with other drugs that exert a similar effect. Doing so can cause severe adverse cardiovascular effects.
Magnesium Sulfate
Magnesium sulfate is used to treat ventricular arrhythmias, especially polymorphic VT and PAT. Magnesium sulfate acts similarly to class III antiarrhythmic drugs because it decreases myocardial cell excitability and conduction. It slows conduction through the AV node and prolongs the refractory period in the atria and ventricles.
How to Give It
For life-threatening arrhythmias, administer 1 to 2 g magnesium sulfate over 5 to 60 minutes. Follow with an infusion of 0.5 to 1 g/hr. The dosage and duration of therapy depend on the patient’s response and serum magnesium levels. The optimum dosage is still under study.
What Can Happen
Adverse cardiovascular effects of magnesium sulfate include diaphoresis, flushing, depressed cardiac function, bradycardia, hypotension, and circulatory collapse. (See Noncardiac adverse effects of magnesium sulfate)
How You Intervene
Keep the following points in mind when caring for a patient receiving magnesium sulfate:
- Monitor the patient’s heart rate, blood pressure, ventilatory rate, ECG, urine output, deep tendon reflexes, and mental status.
- Remember that magnesium sulfate should be avoided in patients with renal disease. Use it cautiously in patients with renal insufficiency and in those taking digoxin.
- Monitor closely for signs and symptoms of hypermagnesemia, such as hypotension, AV block, CNS depression, depressed or absent deep tendon reflexes, muscle weakness or paralysis, and respiratory arrest.
- Have IV calcium available to counteract the effects of hypermagnesemia.
- Have intubation equipment and a mechanical ventilator available.
- Magnesium sulfate is contraindicated in heart block.
Teaching About Antiarrhythmics
Here are some important points to emphasize when teaching your patient about antiarrhythmic drugs:
- Take the drug exactly as prescribed. Don’t stop taking the drug without consulting your practitioner.
- Call the practitioner if you experience chest pain, shortness of breath, cough, palpitations, dizziness, fatigue, a weight gain of more than 2 lb (0.9 kg) per day, a very fast or slow heart rate, or a change in the regularity of the heartbeat or if you notice persistent changes you feel might be related to drug therapy.
- See your practitioner for regular checkups, as scheduled. Periodic physical examinations, ECGs, chest X-rays, and laboratory studies will help evaluate the effectiveness of therapy.
- Use herbal preparations with care. Some preparations can cause life-threatening interactions. Notify your provider of any herbal or over-the-counter medications you are taking.
