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Home , Esmolol, Ibutilide, Procainamide, Sotalol

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Keeping up with the pace of antiarrhythmic drugs ANNMARIE PALATNIK, APN,BC, MSN Coordinator of Continuing Education • Virtua Health • Marlton, N.J.

HAVE YOU NOTICED how challenging it is to Conducting impulses keep pace with the The conduction system of the , shown below, begins with the heart’s natural pacemaker, the changing beat of phar- sinoatrial (SA) node. When an impulse leaves the SA node, it travels through the atria along macology? Just as you Bachmann’s bundle and the internodal pathways on its way to the atrioventricular (AV) node. After learn the latest drugs the impulse passes through the AV node, it travels to the ventricles, first down the bundle of His, and classifications, new then along the bundle branches and, finally, down the Purkinje fibers. classes are developed and new drugs added to Bachmann’s bundle classes. Even drugs that have been on the mar- ket a long time can have dosing and indica- SA node tion changes. Antiarrhythmic Internodal tracts drugs, which restore Posterior (Thorel’s) normal rhythm and Middle (Wenckebach’s) conduction to the heart, Anterior are no exception. In this AV node article, I’ll bring you up-to-date on the Bundle of His antiarrhythmics now Right bundle branch available. Left bundle branch

Class assignments Most antiarrhythmic drugs used to slow a rapid heart rate are classified according to the Vaughn Williams classification system Purkinje fibers (see Classifying Anti- arrhythmics the Vaughn Williams way). These drugs fall Class I into four general groups in this classification system blockers stop the flow of sodium into with each group having several subgroups. Drugs are as- the cell during the initial phase of the . signed to classes I through IV according to their effects The blocking action slows the exchange of ions through on the heart’s action potential; each class acts on a dif- the sodium- channel, resulting in conduction ferent phase. For details on cardiac conduction, see Con- and repolarization delays. ducting impulses. Drugs in Class I are further broken down into three Of course, it’s not completely straightforward: The subcategories: classes can be quite confusing because they include some • Class IA drugs, which moderately block the effect of types of drugs that have properties of more than one the sodium channels, reducing conductivity and pro- class; others don’t fit into any class at all. Let’s break it longing repolarization and the action potential down, class by class, and review some examples. • Class IB drugs, which cause a minimal blocking effect

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Classifying antiarrhythmics the Vaughn with an accessory pathway. Because this drug has nega- Williams way tive inotropic effects, it shouldn’t be used in patients Here are examples of the four classes: with impaired left ventricular function. is another Class IC drug that’s ap- Class I: sodium channel Class III: potassium proved for oral use only in the United States. It’s indi- blockers channel blockers cated to treat ventricular and supraventricular dys- Class IA • (Cordarone) rhythmias. • • (Corvert) Don’t give propafenone to patients who’ve had an MI • (Pronestyl) • (Tikosyn) or who have CAD because it’s been found to increase the • (Norpace) • (Betapace) risk of death in patients who’ve had an MI. Be sure to fre- Class IB quently check levels and the international nor- • Class IV: calcium • (Dilantin) channel blockers malized ratio when propafenone is taken with digoxin or • (Mexitil) • (Cardizem) warfarin, because it can increase digoxin and warfarin lev- Class IC • (Isoptin, Calan) els. Propafenone also has significant negative inotropic • flecainide (Tambocor) effects, so it won’t be ordered if left ventricular function • propafenone (Rythmol) Other agents is impaired. • Class II: beta- • digoxin (Lanoxin) Class II blockers • (Adenocard) Beta-receptor blockers decrease sinoatrial (SA) nodal • (Inderal) • automaticity, increase AV nodal refractoriness, and • (Sectral) decrease AV nodal conduction velocity. These drugs • (Brevibloc) are used to control ventricular response and to con- vert the rhythm in PSVT, AF, and atrial flutter. The and shorten repolarization cardiac conduction effects of beta-blockers are similar • Class IC drugs, which have marked sodium channel to those of the blockers diltiazem and blocking effects and significantly reduce conductivity. verapamil. Procainamide, a Class IA drug, is used to convert atrial Beta-blockers are divided into three categories: fibrillation (AF) or flutter to normal sinus rhythm and to • nonselective beta- receptor blockers, including control the rate if ventricular function is preserved. propranolol. These drugs decrease heart rate and con- Procainamide can also be used for paroxysmal supraven- tractility but also block beta-receptors in the lungs. tricular (PSVT) that’s uncontrolled by vagal • cardiac selective beta- blockers, which maneuvers and adenosine, or for stable wide-complex include , , and esmolol. They block tachycardia of unknown origin, as long as cardiac func- beta-receptors in the heart only. tion is preserved. • combination alpha-beta receptor blockers, such as , Because procainamide may cause dysrhythmias, use it which block alpha-receptors in the peripheral blood ves- cautiously, especially if the patient has had an acute sels, resulting in vasodilation, and beta-receptors in the (MI), if he’s hypokalemic or hypo- heart. magnesemic, or if he’s receiving other drugs that prolong the QT interval, such as amiodarone or sotalol. Reduce Class III the dosage if he has renal impairment. blockers inhibit the movement of Lidocaine, a Class IB drug, may be used to treat hemo- potassium during the third phase of the action potential dynamically stable (VT) or car- (cell membrane recovery), prolonging repolarization and diac arrest from VT or ventricular fibrillation (VF). the refractory period. Lidocaine isn’t recommended in acute MI to prevent Ibutilide is used to convert recent-onset AF and atrial ventricular dysrhythmias. flutter. Ibutilide prolongs the action potential and , a Class IC drug, is approved in oral form increases atrial and ventricular refractoriness. only in the United States. It’s indicated to treat ventricu- Be alert for potential adverse reactions when adminis- lar dysrhythmias and supraventricular tachycardia (SVT) tering ibutilide. Ventricular , such as torsade in patients without coronary artery disease (CAD). It’s de pointes, occur in about 3% of patients who receive also been found to stop AF, atrial flutter, SVT, and atri- ibutilide. Patients with significantly impaired left ventric- oventricular (AV) nodal reentry tachycardia associated ular function are at greatest risk for these dysrhythmias.

48 LPN2008 l Volume 4, Number 3 Monitor the patient’s cardiac rhythm during the infusion In addition, because of reduced , the and for 4 to 6 hours postinfusion. drug may accumulate to toxic levels. Amiodarone is an example of a Class III drug that has Atropine can be administered through an endotracheal properties of all four Vaughn Williams classes. Patients tube in an emergency when I.V. or intraosseous routes may develop from this drug, so monitor aren’t possible. blood pressure frequently. Also watch for compatibility If the patient doesn’t respond to atropine, an epineph- with other drugs being given; amiodarone can prolong rine or dopamine infusion may be considered while the the QT interval, so don’t use it with other drugs that pro- patient awaits pacing or if pacing is ineffective. Dopamine long the QT interval. Amiodarone is given intravenously may be used to increase the heart rate. (I.V.) or orally, depending on the indication. The drug is Both epinephrine and dopamine may cause tachydys- administered I.V. in emergencies or when the patient rhythmias or excessive vasoconstriction. These drugs can’t take it orally. It’s used orally in nonemergency situa- should be given through a central venous access device tions and for maintenance therapy. whenever possible to minimize the risk of extravasation. If your patient is on maintenance therapy, tell him to Digoxin can be used to slow the ventricular rate in avoid the sun and to use sunblock. Sun exposure will give patients with AF or atrial flutter. This drug decreases the skin a blue or grayish tint. heart rate and conduction velocity through the AV node, and increases cardiac contractility. Class IV Digoxin is often combined with another drug. It isn’t Calcium channel blockers inhibit the movement of cal- indicated for acute treatment of dysrhythmias because cium through the slow calcium channels of the SA and building to a therapeutic digoxin level takes time. Moni- AV nodes. But only two calcium channel blockers affect tor the patient for signs and symptoms of digoxin toxicity, heart rate by inhibiting the movement of calcium during including conduction abnormalities, , vomiting, the second phase of the action potential: diltiazem and , generalized muscle weakness, yellow-green halos verapamil. Calcium channel blockers decrease conduc- around images, and blurred vision. tion velocity, increase the refractory period at the SA Adenosine, a naturally occurring amino acid found in and AV nodes, and decrease the strength of contraction. all body cells, is the treatment of choice for most forms of Diltiazem and verapamil are often used to treat rapid narrow-complex PSVT. Adenosine slows conduction AF and atrial flutter. By slowing conduction through the through the AV node and can interrupt the reentry path- AV node, these drugs decrease ventricular response, ways through the AV node. reducing myocardial oxygen consumption. These drugs Adenosine has an extremely short half-life, less than 10 should be used in the presence of second- or third-degree seconds. Transient effects of adenosine include brief peri- heart block or sick sinus syndrome without a pacemaker, ods of asystole, , and ventricular ectopy. and should be avoided in patients with a history of heart Magnesium sulfate can be another treatment option failure. Use them with extreme caution in older adults. for ventricular dysrhythmias. Because magnesium is Diltiazem and verapamil shouldn’t be given to patients essential for the function of the sodium-potassium pump with Wolff-Parkinson-White syndrome (a dysrhythmia and cell depolarization, magnesium deficiency is associat- caused by an extra abnormal electrical pathway in the ed with a high incidence of cardiac dysrhythmias. heart) and AF or atrial flutter. Ready for steady rhythm Unclassified antiarrhythmics By understanding the mechanisms of action and indica- Some antiarrhythmics don’t fall into any of the classes tions for antiarrhythmic drugs that may be ordered in mentioned above. Let’s take a closer look. an emergency, you’ll be better prepared to manage your Atropine is typically used to treat symptomatic brady- patient’s care and help get him back on the beat. LPN cardias while the patient awaits transcutaneous pacing. It blocks the effects of acetylcholine on the SA and AV Selected references Cummins R, et al. ACLS Provider Manual. Dallas, Tex., American Heart nodes, increasing heart rate. If the patient is experiencing Association, 2005. myocardial ischemia or hypoxia, remember that atropine Drug Facts and Comparisons 2008. Philadelphia, Pa., Lippincott Williams & increases myocardial oxygen demand. Wilkins, 2007. Atropine should be avoided if the patient is experienc- Nursing2008 Drug Handbook. Philadelphia, Pa., Lippincott Williams & Wilkins, 2007. ing bradycardia as a result of hypothermia. In that situa- Palatnik A. And the beat goes on…Nursing2008. 38(2):56cc1-55cc3, February tion, the hypothermic heart may not respond to the drug. 2008.

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