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The list of antiarrhythmic drugs is constantly changing. Here's how to keep all the different classes and their indications straight.
Have you noticed how challenging it is to keep pace with the changing beat of pharmacology? Just as you learn the latest drugs and classifications, new classes are developed and new drugs are added to classes. Even drugs that have been on the market a long time can have dosing and indication changes.
Today's antiarrhythmic drugs are no exception: The tune is always changing. In this article, I'll bring you up-to-date on the antiarrhythmics now available.
Most antiarrhythmic drugs used to slow a rapid heart rate are classified according to the Vaughn Williams classification system. See Classifying antiarrhythmics the Vaughn Williams way. These drugs fall into four general groups in this classification system, with each group having several subgroups. Drugs are assigned to classes I through IV according to their effects on the heart's action potential; each class acts on a difference phase. For details on cardiac conduction, see Conducting impulses.
Of course, it's not completely straightforward: The classes can be confusing because they include some types of drugs that have properties of more than one class; others don't fit into any class at all. Let's break it down, class by class.
Sodium channel blockers stop the flow of sodium into the cell during the initial phase of the action potential. The blocking action slows the exchange of ions through the sodium-potassium channel, resulting in conduction and repolarization delays.
Drugs in Class I are further broken down into three subcategories:
* Class IA agents, which moderately block the effect of the sodium channels, reducing conductivity and prolonging repolarization and the action potential
* Class IB agents, which cause a minimal blocking effect and shorten repolarization
* Class IC agents, which have marked sodium channel blocking effects and significantly reduce conductivity.
Procainamide, a Class IA drug, is used to convert atrial fibrillation (AF) or flutter to normal sinus rhythm and to control the rate if the ventricular function is preserved. Procainamide can also be used for paroxysmal supraventricular tachycardia uncontrolled by vagal maneuvers and adenosine, or for stable wide-complex tachycardia of unknown origin, as long as cardiac function is preserved.
Because procainamide may cause dysrhythmias, use it cautiously, especially if the patient's had an acute myocardial infarction (MI), if he's hypokalemic or hypomagnesemic, or if he's receiving other drugs that prolong the QT interval, such as amiodarone or sotalol. Reduce the dosage if he has renal impairment.
Lidocaine, a Class IB agent, may be used to treat hemodynamically stable VT or cardiac arrest from VT or VF.
Lidocaine isn't recommended in acute MI to prevent ventricular dysrhythmias.
Flecainide, a Class IC antiarrhythmic, is approved only in oral form in the United States. This drug is indicated to treat ventricular dysrhythmias, as well as supraventricular tachycardia (SVT) in patients without coronary artery disease (CAD). It has also been found to terminate AF, atrial flutter, SVT, and AV nodal reentry tachycardia associated with an accessory pathway. Because this drug has significant negative inotropic effects, it shouldn't be used in patients with impaired left ventricular function.
Propafenone is another Class IC antiarrhythmic that's approved only for oral use in the United States. It's indicated to treat ventricular and supraventricular dysrhythmias.
Don't give propafenone to patients who've have an MI or who have CAD; this drug's been found to increase the risk of death in patients who've had an MI. Be sure to frequently check digoxin levels and the international normalized ratio (INR) when propafenone is taken with digoxin or warfarin, because it can increase digoxin and warfarin levels. Propafenone also has significant negative inotropic effects, so don't use it if left ventricular function is impaired.
The conduction system of the heart, shown below, begins with the heart's natural pacemaker, the sinoatrial (SA) node. When an impulse leaves the SA node, it travels through the atria along Bachmann's bundle and the internodal pathways on its way to the atrioventricular (AV) node. After the impulse passes through the AV node, it travels to the ventricles, first down the bundle of His, then along the bundle branches and, finally, down the Purkinje fibers.
Beta-receptor blockers decrease SA nodal automaticity, increase AV nodal refractoriness, and decrease AV nodal conduction velocity. These drugs are used to control ventricular response and to convert the rhythm in PSVT, AF, and atrial flutter. The cardiac conduction effects of beta-blockers are similar to those of the calcium channel blockers diltiazem and verapamil.
Beta-blockers are divided into three categories:
* nonselective beta-adrenergic receptor blockers, includiing propranolol. This drug decreases heart rate and contractility, but also blocks beta-receptors in the lungs.
* cardiac selective beta-adrenergic receptor blockers, which include atenolol and metoprolol. They block beta-receptors in the heart only.
* combination alpha-beta receptor blockers, such as labetalol, which block alpha-receptors in the peripheral blood vessels, resulting in vasodilation, and beta-receptors in the heart.
Potassium channel blockers inhibit the movement of potassium during the third phase of the action potential-cell membrane recovery-prolonging repolarization and the refractory period.
Ibutilide is used to convert recent-onset AF and atrial flutter. Ibutilide prolongs the action potential and increases atrial and ventricular refractoriness.
Be alert for potential adverse reactions when administering ibutilide. Ventricular dysrhythmias, such as torsades de pointes, occur in about 3% of patients who receive ibutilide. Patients with significantly impaired left ventricular function are at greatest risk for these dysrhythmias. Monitor the patient's cardiac rhythm during the infusion and for 4 to 6 hours postinfusion.
Amiodarone is an example of a Class III agent that has properties of all four Vaughn Williams classes. Patients may develop hypotension from this drug, so monitor blood pressure frequently. Also watch for compatibility with other drugs being given; amiodarone can prolong the QT interval, so don't use it with other drugs that prolong the QT interval. Amiodarone is given I.V. or orally, depending on the indication. The drug is administered I.V./IO in emergencies or when the patient can't take the drug orally. It's used orally in nonemergency situations and for maintenance therapy.
If your patient is on maintenance oral therapy, tell him to avoid the sun and to use sunblock. Sun exposure will give the skin a blue or grayish tint.
Calcium channel blockers inhibit the movement of calcium through the slow calcium channels of the SA and AV nodes during the second phase of the action potential. Calcium channel blockers decrease conduction velocity, increase the refractory period at SA and AV nodes, and decrease the strength of contraction.
Diltiazem and verapamil are examples of calcium channel blockers that are often used to treat rapid AF and atrial flutter. By slowing conduction through the AV node, these drugs decrease ventricular response, reducing myocardial oxygen consumption. These drugs shouldn't be used in the presence of second- or third-degree heart block or sick sinus syndrome without a pacemaker, and should be avoided in patients with a history of heart failure. Use them with extreme caution in older adults. Calcium channel blockers shouldn't be given to patients with Wolff-Parkinson-White syndrome and AF or atrial flutter.
Some antiarrhythmics don't fall into one of the classes I've just discussed. Let's take a closer look.
Atropine is typically used to treat symptomatic bradycardias while awaiting transcutaneous pacing. It blocks the effects of acetylcholine on the SA and AV nodes, increasing heart rate. If the patient is experiencing myocardial isch-emia or hypoxia, remember that atropine increases myocardial oxygen demand.
Atropine should be avoided if the patient is experiencing bradycardia as a result of hypothermia. In that situation, the hypothermic heart may not respond to the drug, and drug metabolism is reduced, which may let the drug accumulate to toxic levels.
Atropine can be administered through an endotracheal tube in an emergency when I.V. or IO routes aren't possible.
If the patient doesn't respond to atropine, epinephrine or dopamine infusion may be considered while awaiting pacer or if pacing ineffective. Dopamine may be used to increase the heart rate.
Both epinephrine and dopamine may cause tachydysrhythmias or excessive vasoconstriction. These drugs should be given through a central venous access device whenever possible to minimize the risk of extravasation.
Digoxin can be used to slow the ventricular rate in patients with AF or atrial flutter. This drug decreases heart rate and conduction velocity through the AV node, and increases cardiac contractility.
Digoxin is often combined with another agent. It isn't used for acute treatment of dysrhythmias because it takes time to develop a therapeutic digoxin level. Unfortunately, digoxin toxicity causes many adverse reactions, including conduction abnormalities, nausea, vomiting, fatigue, generalized muscle weakness, yellow-green halos around images, and blurred vision.
Adenosine is the treatment of choice for most forms of narrow-complex PSVT. It's also a naturally occurring amino acid found in all body cells. Adenosine slows conduction through the AV node and can interrupt the reentry pathways through the AV node.
Adenosine has an extremely short half-life of less than 10 seconds. Transient effects of adenosine include brief periods of asystole, bradycardia, and ventricular ectopy.
Magnesium sulfate can be another treatment option for certain ventricular dysrhythmias. Because magnesium is essential for the function of the sodium-potassium pump and myocardial cell depolarization, magnesium deficiency is associated with a high incidence of cardiac dysrhythmias.
By understanding the mechanisms of action and indications for antiarrhythmic drugs, you'll be better prepared to effectively manage emergency situations and get your patient back on the beat.
Aehlert B. ECGs Made Easy, 2nd edition. C.V. Mosby, 2002.
Cummins R, et al. ACLS Provider Manual. American Heart Association, 2005.
Drug Facts and Comparisons 2008. Lippincott Williams & Wilkins, 2007.
Nursing2008 Drug Handbook. Lippincott Williams & Wilkins, 2007.
Palatnik A. And the beat goes on[horizontal ellipsis]. Nursing Made Incredibly Easy!! 3(1):30-41, January/February 2005.
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