Arrhythmias and Conduction Disturbances

Carol Jacobson

MECHANISMS OF ARRHYTHMIAS

Cardiac arrhythmias result from abnormal impulse initiation, abnormal impulse conduction, or both mechanisms together. Abnormal impulse initiation includes enhanced normal automaticity, abnormal automaticity, and triggered activity resulting from afterdepolarizations; abnormal impulse conduction includes conduction block and reentry.¹, ², ³, ⁴, ⁵ Although all of these mechanisms have been shown to cause arrhythmias in the laboratory, it is not possible to prove which mechanism is responsible for a particular arrhythmia using currently available diagnostic tools in the clinical setting. However, it is possible to postulate the mechanism of many clinical arrhythmias based on their characteristics and behavior and to list rhythms most consistent with known electrophysiologic mechanisms.³, ⁴, ⁵, ⁶ Some arrhythmias, such as atrioventricular nodal reentry tachycardia (AVNRT), atrial flutter, some ventricular tachycardias (VTs), and reentry tachycardias involving accessory pathways, have been proven to be caused by reentry. This section describes the major mechanisms of arrhythmias and lists arrhythmias suggested or proven to be caused by each mechanism whenever possible. Knowledge of the cardiac action potential is essential in understanding concepts presented here (see Chapter 1).

Abnormal Impulse Initiation

Abnormal impulse initiation can be due to enhanced normal automaticity, abnormal automaticity, or afterdepolarizations. It is important to understand the property of normal automaticity before considering these other mechanisms.

Automaticity

Automaticity is the ability of certain cardiac cells to spontaneously depolarize and initiate an electrical impulse without external stimulation. The sinus node (or sinoatrial [SA] node) is the normal pacemaker of the heart because it has the fastest rate of automaticity. Other cells in the heart also have the property of automaticity, including cells in several areas of the atria, coronary sinus, pulmonary veins, atrioventricular (AV) junction, AV valves, and Purkinje system. The rates of these other pacemakers are slower than the rate of the SA node; therefore, they are suppressed by the SA node under normal conditions, a phenomenon known as overdrive suppression. The site of fastest impulse initiation is referred to as the dominant pacemaker, whereas sites of impulse formation that are suppressed by the dominant site are called subsidiary or latent pacemakers.

Enhanced Normal Automaticity.

Impulse initiation can be shifted from the SA node to other parts of the heart if the rate of the SA node drops below that of a subsidiary pacemaker or if the automatic rate of a subsidiary pacemaker rises above that of the SA node. Increased vagal tone, drugs, electrolyte abnormalities, or disease of the SA node can decrease its rate of automaticity or can cause exit block of its impulse, thus allowing subsidiary pacemakers to assume control of the heart. Examples of clinical arrhythmias due to shifting of the pacemaker from the SA node include atrial, junctional, or ventricular escape rhythms that occur due to sinus bradycardia or AV block. Such “escape” pacemaker activity cannot be considered abnormal because it is a manifestation of the normal automaticity of these cells. Sinus tachycardia is due to enhanced normal automaticity, and accelerated ventricular rhythm following myocardial infarction (MI) may be due to enhanced automaticity.¹,³

Subsidiary pacemaker activity can be enhanced by factors that decrease the transmembrane resting potential (TRP), decrease the threshold potential, or increase the rate of diastolic phase 4 depolarization of the subsidiary pacemaker cells. Figure 16-1 illustrates how these mechanisms can change the rate of firing of pacemaker cells.⁷

Enhanced normal automaticity can occur with enhanced sympathetic activity; drugs such as digitalis and sympathomimetic agents; ischemia; stretch that occurs in heart failure (HF), cardiomyopathy, and ventricular aneurysms; and with genetic mutations that alter the function of ion channels in the cardiac membrane.³, ⁴, ⁵,⁸,⁹ Clinical arrhythmias that may be due to enhanced normal automaticity include sinus tachycardia, some atrial tachycardias (ATs), junctional tachycardia, accelerated ventricular rhythm, and ventricular parasystole. Automaticity is not the mechanism of most rapid tachycardias but it can precipitate or trigger reentrant tachycardias that can occur at very rapid rates.⁴

Abnormal Automaticity.

Atrial and ventricular myocardial cells that do not normally have automaticity can develop abnormal automaticity when their TRP is reduced and is referred to as depolarization-induced automaticity.¹,⁴ Subsidiary pacemakers like those in the Purkinje system that are normally overdrive suppressed by the faster SA node can also develop abnormal automaticity when their TRP is reduced. This abnormal automaticity is thought to be mediated by the slow inward current carried mainly by calcium (slow channels) because the normal fast sodium channels are inactivated at reduced membrane potentials.¹,³,⁴ However, both sodium and calcium channels may play a role in the development of abnormal automaticity. Abnormal automaticity that develops at more negative diastolic potentials, between −70 and −50 mV, can be suppressed by sodium channel blockers, indicating that a sodium current is involved, whereas automaticity that develops at less negative diastolic potentials, from −50 to −30 mV, can be suppressed by calcium channel blockers.²,⁴

The resting potential of a cell can be reduced (e.g., from −90 to −70 mV) and the cell partially depolarized by anything that increases the extracellular potassium concentration, decreases the intracellular potassium concentration, increases the permeability of the membrane to sodium, or decreases the membrane permeability to potassium.¹, ², ³, ⁴ Ischemia, hypoxia, acidosis, hyperkalemia, digitalis toxicity, chamber enlargement or dilation, stretch, and other metabolic abnormalities or drugs can reduce the resting potential and result in abnormal automaticity. Hypoxia and ischemia affect the TRP by decreasing the amount of oxygen available to supply adenosine triphosphate in amounts sufficient to operate the sodium—potassium pump efficiently. Anything that interferes with proper operation of this pump, such as digitalis, reduces normal resting ionic gradients across the cell membrane and results in reduction of the resting potential. When the TRP is reduced at rest, the cell is partially depolarized and the time required for spontaneous diastolic depolarization to reach threshold is reduced, thus increasing pacemaker activity (see Fig. 16-1). For the same reason, automaticity is increased when the threshold potential is reduced (e.g., from −40 to −50 mV) by ischemia or drug effects because less time is required for phase 4 depolarization to reach the lower threshold. The rate of phase 4 depolarization can be increased by several factors, including local norepinephrine release at ischemic sites, systemic catecholamine release, reduced vagal tone, and drugs.

Figure 16-1 Diagram illustrating the principal mechanisms underlying changes in the frequency of discharge of a pacemaker fiber. The upper diagram shows a reduction in rate caused by a decrease in the slope of diastolic, or pacemaker, depolarization from a to b, and thus an increase in the time required for the membrane potential to decline to the threshold potential (TP) level. The lower diagram shows the reduction in the rate associated with a shift in the level of the threshold potential from TP-1 to TP-2, and a corresponding increase in cycle length (b to c); also illustrated is a further reduction in rate due to an increase in the maximal diastolic potential level (Compare a with c and d with e). (From Hoffman, B. F., & Cranefield, P. F. [1960]. Electrophysiology of the heart. New York: McGraw-Hill. Used with permission of the McGraw-Hill Book Company.)

Clinical arrhythmias that may be due to abnormal automaticity include some ATs, accelerated junctional or ventricular rhythm, parasystole, and some VTs associated with acute MI.¹, ², ³, ⁴ The rate of a rhythm due to abnormal automaticity is related to the membrane potential from which it arose: the less negative the membrane potential (i.e., the greater the depolarization), the faster the rate. Rhythms due to abnormal automaticity tend to occur at faster rates than rhythms due to normal automaticity.¹,²

Triggered Activity Due to Afterdepolarizations

Afterdepolarization is a transient depolarization of the cell membrane that occurs at some time during or right after repolarization of an action potential. Early afterdepolarizations (EAD) occur during the repolarization of an action potential. Delayed afterdepolarizations (DADs) occur after repolarization is complete but before the next action potential is due to occur. Figure 16-2 shows both EAD and DAD.¹⁰

Early Afterdepolarizations.

EADs that occur early in phase 2 at potentials positive to −30 mV are called phase 2 EADs; those that occur at more negative potentials are called phase 3 EADs.⁴ EADs are thought to be due primarily to a calcium current, although sodium channel activity during the plateau phase of the action potential may also play an important role in inducing EADs.⁴ If an EAD is large enough to reach threshold, a second upstroke occurs, causing an “early” beat. This second upstroke is called a triggered beat because it depends on and arises as a result of the preceding action potential. The triggered beat may be followed by its own afterdepolarization, which initiates yet another upstroke. This activity may be sustained for several beats and may terminate only when the membrane finally repolarizes to a high enough level to extinguish the rhythmic activity. This mechanism of abnormal impulse formation differs from abnormal automaticity in that automatic beats result from spontaneous initiation of each impulse, whereas beats due to afterdepolarizations depend on a preceding impulse.

EADs have been shown to occur most often in Purkinje fibers and midmyocardial M cells in the ventricles.⁴ EADs are caused by conditions that delay repolarization of the action potential and occur in the presence of hypoxia, acidosis, hypokalemia, hypomagnesemia, hypothermia, high PCO₂, catecholamines, many drugs, and in ventricular hypertrophy and HF.²,⁴ Gene mutations that alter sodium and potassium ion channel activity and result in prolonged action potential duration have been identified and shown to cause EADs. The congenital long QT syndrome (LQTS) associated with torsades de pointes (TdP), a polymorphic VT (PVT) associated with sudden cardiac death (SCD), has been shown to be due to genetic mutations that affect ion channel function and prolong repolarization, thus leading to EAD formation. Triggered activity due to EADs occurs at slow heart rates, and arrhythmias thought to be due to EAD often occur during bradycardia or after a pause in rhythm. The proarrhythmic effects of many drugs, especially class IA and class III antiarrhythmics, are due to their ability to prolong repolarization in cardiac cells and cause EADs. Clinical arrhythmias thought to be due to EAD include both the acquired and congenital types of TdP, and many arrhythmias that occur with hypertrophy and HF.

Figure 16-2 (A) An early afterpolarization (arrow). (B) A single triggered action potential caused by this afterdepolarization (arrow). (C) A train of triggered action potentials (arrow). (D,E) Action potentials caused by propagating impulses (indicated by vertical lines), followed by DAD (arrow in D). (E) Triggered activity caused by the afterdepolarization (arrow). (From Wit, A. L., & Rosen, M. R. [1981]. Cellular electrophysiology of cardiac arrhythmias: Part I. Arrhythmias caused by abnormal impulse generation. Modern Concepts in Cardiovascular Disease, 50, 5. Used with permission of the American Heart Association.)

Delayed Afterdepolarizations.

DADs occur after the membrane has repolarized to its original level after an action potential but before the next propagated impulse. Subthreshold afterdepolarizations do not result in triggered activity, but, if the DAD is large enough to reach threshold, a triggered impulse arises. This triggered impulse may also be followed by its own afterdepolarization, leading to trains of triggered beats. Again, the mechanism differs from automaticity in that afterdepolarizations depend on and arise as a result of preceding action potentials. DADs occur in association with increased intracellular calcium levels. There is a direct relation between amplitude of DAD and heart rate: as the heart rate increases, so does afterdepolarization amplitude. Thus, triggered activity tends to occur after premature beats or at rapid heart rates. Factors that increase DAD amplitude and contribute to triggered arrhythmias include high concentrations of catecholamines and digitalis and hypokalemia.¹, ², ³, ⁴ Clinical arrhythmias that may be due to DAD include digitalis toxic rhythms like accelerated junctional rhythm and AT, idiopathic VT originating in the right ventricular outflow tract (RVOT), accelerated idioventricular rhythm after MI, and tachycardias originating in the coronary sinus.

Abnormal Impulse Conduction

Abnormal impulse conduction can result in bradyarrhythmias or aberrancy when impulses are blocked, or premature beats and tachyarrhythmias when reentrant excitation occurs.

Conduction Block

The electrical impulse can be prevented from propagating through the heart for a variety of reasons. If the propagating impulse is not strong enough to excite the tissue ahead of it, conduction will fail (see section below titled “Decremental Conduction”). If an impulse arrives at an area where the tissue is still refractory after a previous depolarization, it will not be able to conduct further (see section below titled “Phase 3 Block”). If an impulse reaches tissue that is abnormally depolarized due to ischemia, disease, or drugs, it may not be able to conduct at all or will conduct with delay (see section below titled “Phase 4 Block”). Scar tissue from previous MI, surgery, or catheter ablation also prevents conduction.

Decremental Conduction.

Decremental conduction is the progressive decrease in conduction velocity of an impulse as it travels through a region of myocardium and occurs when an action potential loses its ability to stimulate the tissue ahead of it. Decremental conduction is a normal function of the AV node, delaying the impulse in the AV node long enough for atrial contraction to contribute to ventricular filling. Decremental conduction normally occurs in areas of the heart where resting potentials are low and action potentials depend on slow channels, such as the AV and SA nodes. It can also occur in areas where resting potentials are low due to ischemia, disease, or drugs. Under such circumstances, conduction velocity is slow because of the slower rate of rise of the action potential that occurs when cells are stimulated at reduced resting potentials. At times, decremental conduction can be so pronounced that the impulse fails to conduct, thus leading to block. This failure of conduction can occur in the SA node, leading to sinus exit block; in the AV node, leading to AV block; or in the bundle-branch system, causing bundle-branch block.

Phase 3 Block.

When a cell is stimulated during phase 3 of the action potential, conduction is impaired because the membrane has not yet returned to its resting level. Whenever a cell is stimulated at a less negative membrane potential, the rate of rise of the action potential, and thus conduction velocity, is slow because most sodium channels are inactivated at reduced membrane potentials. Figure 16-3 illustrates phase 3 block occurring in the right bundle branch, resulting in aberrant conduction of the impulse with a right bundle-branch block (RBBB) pattern.

Phase 3 block, also called short-cycle aberrancy¹¹ or tachycardia-dependent block,³ can occur in normal hearts if impulses are premature enough to reach fibers during their normal refractory period, resulting in aberrant conduction of premature beats. It is also responsible for rate-dependent bundle-branch blocks and for the aberration that commonly occurs when cycle lengths are very irregular, as in atrial fibrillation (AF). Phase 3 block can occur pathologically if the refractory period is abnormally prolonged by drugs or disease.

Phase 4 Block.

Phase 4 block, also called long-cycle aberrancy¹¹ or bradycardia-dependent block,³ occurs late in diastole when fibers are stimulated at reduced membrane potentials secondary to spontaneous phase 4 depolarization. In this case, the membrane has begun to depolarize spontaneously during its normal phase 4. By the time a stimulus arrives, the resting potential has been reduced enough to cause slow conduction. Again, whenever a cell is stimulated at a reduced membrane potential, only some of the sodium channels are available, and slow conduction results. Figure 16-4 shows a normal right bundle-branch action potential followed by spontaneous phase 4 depolarization. By the time the second impulse arrives in that bundle, membrane potential has been reduced enough to cause slow conduction and RBBB.

Phase 4 block is responsible for abnormal conduction that occurs only at the end of long cycles or for so-called bradycardia-dependent bundle-branch block. Phase 4 block is uncommon and is considered pathologic when it occurs.

Reentry

Reentry is a type of conduction abnormality that leads to the occurrence of premature beats or sustained tachycardias rather than to a block. Reentry can occur in areas of the heart where conduction velocity is abnormally slow because of ischemia, electrolyte abnormalities, drugs, or disease. Reentry means that an impulse can travel through an area of myocardium, depolarize it, and then reenter the same area to depolarize it again. For anatomic reentry to occur, there must be an area of unidirectional block in which an impulse can conduct in one direction but not in the opposite direction. In addition, conduction velocity must be slow enough relative to tissue refractoriness and circuit length to allow the impulse to continue propagating in a circular manner.³, ⁴, ⁵ Figure 16-5A illustrates normal conduction of an impulse through an area of myocardium, and Figure 16-5B shows reentry occurring as a result of an area of unidirectional block and slow conduction.¹²

Figure 16-3 Phase 3 block. The ECG on the bottom shows a normal beat followed by a premature atrial beat that conducts with RBBB. The action potentials on top illustrate that the early beat entered the right bundle during phase 3, when the membrane potential was still reduced. The resulting action potential is a slow channel response and conduction fails. (From Conover, M. [2003]. Understanding electrocardiography [8th ed., p. 172]. St. Louis, MO: CV Mosby.)

For reentry to occur, an area of unidirectional block is necessary to allow an impulse to conduct in one direction and to provide a return pathway by which the original stimulus can reenter a previously depolarized area. Conduction velocity must be slow enough and the refractory period short enough to allow time for the previously stimulated area to recover its ability to conduct. If the refractory period of the previously stimulated tissue is long or conduction velocity is fast, the impulse dies out because it encounters tissue that is unable to conduct.

Figure 16-4 Phase 4 block. The ECG on the bottom shows a normal beat followed by a pause and a second beat that conducts with RBBB. The action potential on top illustrates that the pause after the first normal action potential allowed sufficient time for spontaneous phase 4 depolarization to occur in the RBBB. The impulse after the pause enters the RBBB at a time when its membrane potential is reduced, resulting in conduction failure. (From Conover, M. [2003]. Understanding electrocardiography [8th ed., p. 173]. St. Louis, MO: CV Mosby.)

Based on these general concepts, three main types of reentry have been described.³, ⁴, ⁵,¹³ Anatomic reentry (see Fig. 16-5) involves an anatomic obstacle around which the circulating wave of depolarization can travel. Functional reentry does not require an anatomic obstacle but depends on local differences in conduction velocity and refractoriness among neighboring fibers that allow an impulse to circulate repeatedly around the area. Anisotropic reentry is caused by structural differences among adjacent fibers that cause variations in conduction velocity and repolarization between these fibers. An impulse conducts more rapidly when it travels along the length of fibers than it does when it travels in the transverse direction across fibers. These differences in conduction velocity can result in unidirectional block and slow conduction, leading to reentry.

Figure 16-5 (A) Normal conduction of an impulse through Purkinje fibers and ventricular muscle. A Purkinje fiber (1) dividing into two branches (2 and 3) and carrying the impulse into ventricular muscle (4). Normally, impulses from all Purkinje fibers “collide” in the ventricle and extinguish themselves, resulting in one ventricular depolarization. (B) Reentry due to an area of unidirectional block and slow retrograde conduction (shaded area). The impulse enters through Purkinje fiber 1 and depolarizes fiber 2 normally but is blocked from stimulating fiber 3 at point A. It continues down fiber 2 to depolarize ventricular muscle (4) and enters fiber 3 from the area below unidirectional block. The impulse is able to conduct slowly backward through the depressed segment (dashed arrow) and reenter fiber 2 at point C to stimulate it again. (Adapted from Rosen, M. R., & Danilo, P. [1979]. Electrophysiological basis for cardiac arrhythmias. In O. S. Narula [Ed.], Cardiac arrhythmias: Electrophysiology, diagnosis, management [p. 9]. Baltimore: Williams & Wilkins.)

When an impulse travels the reentry loop only once, a single premature beat results. If conduction velocity is slow enough and the refractory period of normal tissue is short enough, a single impulse could travel the loop numerous times, resulting in a run of premature beats or in a sustained tachycardia. Reentry that occurs in small loops of tissue, such as the AV node or Purkinje tissue, is called microreentry. If the reentry loop involves large tracts of tissue, such as AV bypass tracts or the bundle-branch system in the ventricles, it is called macroreentry.

Many clinical arrhythmias are thought to be due to reentry, including most VT, AF, atrial flutter, and some AT. Arrhythmias that are known to involve discrete reentry circuits are atrial flutter, AVNRT, circus movement tachycardia (CMT) using an accessory pathway in Wolff-Parkinson-White (WPW) syndrome, and bundle-branch reentry VT.

BASIC ARRHYTHMIAS AND CONDUCTION DISTURBANCES

An arrhythmia is any cardiac rhythm that is not normal sinus rhythm at a normal rate. The debate continues regarding whether the term dysrhythmia should be used instead of arrhythmia, because many believe that arrhythmia means total absence of rhythm whereas dysrhythmia means a disturbance in rhythm. In this chapter, arrhythmia will be used because it is a more commonly used term and continues to be used in the most recent medical textbooks on the subject.

Table 16-1

CLASSIFICATION OF ANTIARRHYTHMIC DRUGS

Class	Action	ECG Effect	Examples
IA	Sodium channel blockade	↑ QRS, ↑ QT	Quinidine
	Prolong repolarization time		Procainamide
	Slow conduction velocity		Disopyramide
	Suppress automaticity
IB	Sodium channel blockade	↓ QT	Lidocaine
	Accelerate repolarization		Mexiletine
IC	Sodium channel blockade	↑↑ QRS	Flecainide
	Marked slowing of conduction		Propafenone
	No effect on repolarization		Moricizine (has IA and IB effects too)
II	β-Blockade	↓ HR, ↑ PR	Acebutolol, atenolol, esmolol, metoprolol, propranolol, timolol
			Sotalol
			(Other β-blockers are available but not usually used as antiarrhythmics)
III	Potassium channel blockade	↑ QT, ↓ HR, ↑	Amiodarone
	Prolong repolarization time	QRS	Sotalol
			Ibutilide
			Dofetilide
IV	Calcium channel blockade	↓ HR, ↑ PR	Verapamil
			Diltiazem
			(Other calcium channel blockers are available but not usually used as antiarrhythmics)
↑ = increased, ↓ = decreased, HR = heart rate, PR = PR interval, QRS = QRS width, QT = QT interval.

Arrhythmias can be due to abnormal impulse initiation, either at an abnormal rate or from a site other than the SA node, or abnormal impulse conduction through any part of the heart. This section focuses on arrhythmias that originate in the SA node, atria, AV junction, and ventricles, as well as basic AV conduction disturbances. Refer to Tables 16-1 and 16-2 for information related to antiarrhythmic drugs, and Tables 16-3, 16-4 and 16-5 for current guidelines for the management of specific arrhythmias. The Advanced Cardiac Life Support (ACLS) algorithms for current recommendations for the acute treatment of arrhythmias can be found in Chapter 27.

Rhythms Originating in the SA Node

The SA node is the normal pacemaker of the heart because it has the highest rate of automaticity of all potential pacemaker sites. The arrhythmias that originate in the SA node are sinus bradycardia, sinus tachycardia, sinus arrhythmia, sinus arrest, sinus exit block, and sick sinus syndrome.

Table 16-2

DRUGS USED FOR HEART RATE AND RHYTHM CONTROL

Drug (Class)	Indication	Dose/Administration Therapeutic Level/Half-Life		Side Effects	Comments
Adenosine (Adenocard)	First-line therapy to terminate AV nodal active SVT (AVNRT, CMT)Can be diagnostic in AV nodal passive rhythms by causing AV block and revealing underlying atrial mechanism, and in wide complex tachycardias of uncertain originVT arising in the RVOT that is due to after depolarizations may respond to adenosine	6 mg given very rapidly IV followed by rapid saline flushMay follow with 12 mg if needed and repeat 12 mg if no effectHalf-life = 9 seconds		Acute onset of AV block usually lasting a few seconds. May result in brief period of asystole or bradycardia that is not responsive to atropineTorsades can occur in patients who are susceptible to bradycardia-dependent arrhythmiasFlushing, hot flash, acute dyspnea lasting a few seconds, chest pressureCan precipitate bronchoconstriction in asthmatic patients	Very short half-life so side effects are transientWarn patients about side effects before giving drug—especially dyspnea. It may be helpful to have patient take a deep breath while injecting drug to ↓ dyspneic sensationShould not be used when arrhythmia is known to be atrial fib or flutterMonitor ECG during administration and be prepared for cardioversionMay accelerate accessory pathway conduction and should not be used when antegrade conduction is occurring over accessory pathwayMay rarely accelerate ventricular rate in atrial flutterDrug interactions: Theophylline (and related drugs) and caffeine antagonize effects of adenosine and make it ineffectiveDipyridamole and carbamazepine potentiate effects of adenosine
Amiodarone (Cordarone)(Classified as a class III antiarrhythmic but has powerful class I sodium channel blocking effects, moderate class II β-blocking effects, and weak class IV calcium channel blocking effects)	Life-threatening ventricular arrhythmias: recurrent VF, recurrent hemodynamically unstable VTAlso widely used for:Conversion of atrial fib to sinus rhythm and maintenance of NSRSlowing conduction through accessory pathways in atrial fib or CMT	PO: 800-1,600 mg q.d. for 1-3 weeks, then 400-800 mg q.d. for 1-3 weeksMaintenance: 100-400 mg/dayMay be given as single daily dose or bid if GI intolerance occursIV: 1,000 mg over first 24 hours given as follows:First rapid infusion: 150 mg over first 10 minutes (15 mg/min)(Add 3 mL [150 mg] to 100 mL D5W) Infuse 100 mL over 10 minutesFollowed by slow infusion: 360 mg over next 6 hours (1 mg/min) (Add 18 mL [900 mg] to 500 mL D5W) Infuse at 33.6 mL/hMaintenance infusion: 540 mg over next 18 hours (0.5 mg/min)(Decrease rate of slow loading infusion to 0.5 mg/min) Infuse at 16.8 mL/hMay continue with 0.5 mg/min for 2-3 weeks if needed. Central line recommended for long-term infusionsIf breakthrough VT occurs, may give supplemental doses of 150 mg over 10 min. (150 mg added to 100 mL D5W)		Bradycardia, heart blockProarrhythmia (VF, incessant VT, torsades)Hypotension with IV formPulmonary fibrosis, corneal microdeposits, photosensitivity, blue skin, thyroid dysfunction (hypo and hyper), liver dysfunctionTremor, malaise, fatigue, GI upsets, dizziness, poor coordination, peripheral neuropathy, involuntary movementsLiver enzyme elevations are common but occur in patients with MI, HF, shock, multiple defibrillations, and so forth. It is unknown if elevations in liver enzymes are due to amiodarone or to associated conditions commonly present in these patientsHepatocellular necrosis has occurred in patients who received IV amiodarone at rates higher than recommended	Give with meals to ↓ GI intoleranceBaseline chest x-ray, renal, liver, thyroid, and pulmonary function testsTakes several weeks to achieve therapeutic blood levels and for effects to decrease after stopping drugIs not dialyzable. Monitor K⁺ and Mg²⁺ levelsMonitor QTcDrug interactions: Additive proarrhythmic effects with many drugs (1A antiarrhythmics, phenothiazines, tricyclic antidepressants, thiazide diuretics, sotalol)↑ Protime with coumadin↑ Serum levels of digoxin, quinidine, procainamide, cyclosporineMay double flecainide levelCimetidine ↑ serum amiodarone levelsCholestyramine and phenytoin (Dilantin) ↓ serum amiodarone levelsAdditive effects on ↓ HR and ↓ AV conduction with β-blockers and Ca²⁺ blockers
		IV to PO transition:			Special precautions with IV form: Physically incompatible with aminophylline, heparin, cefamandole, cefazolin, mezlocillin, sodium bicarbonateMust be delivered using a volumetric pump (not drop counter) because drop size is altered by drug
		Duration of IV	PO dose
		<1 week	800-1600 mg q.d.
		1-3 weeks	600-800 mg q.d.
		>3 weeks	400 mg q.d.
		Therapeutic level = 0.5-2 mcg/mLVery long half-life (26-107 days; average 53 days)
Atenolol (Tenormin)(Cardioselective β-blocker)	Ventricular rate control in atrial fib/flutterSlow conduction through AV node in AVNRT and CMT	Initial dose: 12.5-25 mg PO q.d. Maintenance dose: 50-100 mg PO q.d.IV: 5 mg over 5 minutes, may repeat in 5 minutesHalf-life = 6-7 hours		Hypotension, bradycardia, AV block. Diarrhea, wheezing, HF	Cardioselective β-blocker used primarily for hypertension and anginaDrug interactions: Additive effects on HR, AV conduction, BP, and ↑ potential for HF when given with negative inotropic drugs, Ca²⁺ blockers, digoxin
Atropine(Anticholinergic, parasympatholytic)	Treatment of symptomatic bradycardia (sinus, junctional, AV block) and asystole	Symptomatic bradycardia: 0.5 mg IV. May repeat q 3-5 minutes to a total of 3 mgAsystole: 1 mg IV, repeat q 3-5 minutes to a total vagolytic dose of 0.04 mg/kgMay be given down ET tube during cardiac arrest if no IV available: use 2-2.5 mgHalf-life = 2-5 hours		CV: tachycardia, chest pain, VT/fibrillation (rare)CNS: drowsiness, confusion, dizziness, insomnia, nervousnessGI: dry mouth, ↓ GI motility, constipation, nauseaOther: urinary retention, hot flushed skin, rash	Doses (0.5 mg may cause paradoxical bradycardiaCauses pupils to dilate (significant when checking pupils during cardiac arrest situation)Drug interactions: Incompatible with aminophylline, metaraminol, norepinephrine, pentobarbitol, sodium bicarbonate
Digoxin	Ventricular rate control in atrial fib/flutterRarely used as an antiarrhythmic anymoreUsed as an inotropic agent in HF	PO loading dose: 0.5-1 mg divided into three or four doses at 6-8-hour intervalsPO maintenance dose: 0.125-0.5 mg q.d.IV loading dose: 0.5-1 mg divided into three or four doses given at 4-8-hour intervalsTherapeutic level = 0.8-2 ng/mLHalf-life = 36-48 hours		CV: bradycardia, AV blockDigoxin toxicity: sinus exit block, AV block, AT with block, bidirectional VT, fascicular tachycardia, accelerated junctional rhythm, regularization of ventricular response to atrial fibVisual disturbances (halo vision), anorexia, nausea, vomiting, malaise, headache, weakness, disorientation, seizures	Contraindicated in patients with WPWDigoxin toxicity is more common in the presence of hypokalemia, renal failure, pulmonary or thyroid disease, and in older peopleDrug interactions: The following drugs ↓ digoxin levels: cholestyramine, antacids, kaopectate, neomycin, sulfasalazine, para-aminosalicylateThe following drugs ↑ digoxin levels: Erythromycin, tetracycline, quinidine, amiodarone, verapamil, spironolactone, nicardipine, indomethacin
Diltiazem (Cardizem)(Calcium channel blocker: nondihydropyridine, “heart rate lowering” Ca²⁺ blocker)	Ventricular rate control in atrial fib/flutterSlow conduction through AV node in AVNRT and CMT	120-360 mg/day in divided dosesIV: 0.25 mg/kg bolus over 2 minutesIf needed, repeat with 0.35 mg/kg over 2 minutesIV infusion: 5-15 mg/hTherapeutic level = 50-200 ng/mLHalf-life = 4-6 hours		Bradycardia, heart block, HF, hypotension, flushing, angina, syncope, insomnia, ringing ears, edema, headache, nauseaLess depression of contractility than with verapamil but watch for HF	Contraindicated in patients with accessory pathways (WPW, short PR syndrome)Drug interactions: Additive effects on HR, AV conduction, BP, and ↑ potential for HF when given with negative inotropic drugs, β-blockers, digoxin
Disopyramide (Norpace)(Class IA antiarrhythmic)	Used to prevent recurrence of VT or VFEffective in preventing atrial fib and flutterSlows conduction through accessory pathways	Total daily dose = 400-800 mg in divided doses, usually 150 mg q 6 hoursSR form = 300 mg q 12 hoursTherapeutic level = 3-6 mcg/mLHalf-life = 4-10 hours		Anticholinergic effects: dry mouth, urinary retention, constipation, precipitation or exacerbation of glaucomaCV: marked negative inotropic effects, HF, prolongs QT interval, proarrhythmic (less than quinidine or procainamide), ↑ SVR	Monitor QT interval and watch for torsadesDrug Interactions: May potentiate effect of coumadinAdditive negative inotropic effects with β-blockers or Ca²⁺ blockers. Phenobarbitol, dilantin, rifampin ↓ disopyramide levels. Quinidine ↑ disopyramide level
Dofetilide (Tikosyn)(Class III antiarrhythmic)	Conversion of atrial fibrillation or flutter to NSR and maintenance of NSR after conversion	Dose based on creatinine clearance: if normal renal function, 500 mcg b.i.d. If abnormal renal function, 250 mcg b.i.d.Do not give if creatinine clearance <20 mL/min Half-life = 9.5 hours		TdP (up to 3% incidence), usually occurs within 3 days after initiating therapyHas no negative inotropic effects and does not lower BP	Patient must be on telemetry during initiation of therapy or with increase in dosage (recommendation is for 3 days monitoring)Monitor QT interval every 2-3 hours: if QTc increases >15% or if QTc is >500 milliseconds, reduce dose. If QTc after second dose is >500 milliseconds, drug should be discontinuedDrug Interactions: Drugs that increase dofetilide levels include verapamil, ketoconazole, cimetidine, macrolide antibiotics, ritonavir, prochlorperazine, megestrolMaintain normal K⁺ and Mg²⁺ levels
Epinephrine (Adrenalin)	Treatment of any cardiac arrest situation requiring CPR: VF, pulseless VT, asystole, PEA	1 mg IV bolus every 3-5 minutes during resuscitation effortsMay be given by way of ET tube if IV access not available: use 2-2.5 mgMay be infused at 2-10 mcg/min to maintain BP during symptomatic bradycardia		CV: tachycardia, hypertension, arrhythmias, anginaCNS: restlessness, headache, tremor, strokeOther: nausea, ↓ urine output, transient tachypnea	Drug Interactions: Has potential to cause arrhythmias when given with digoxin, other sympathomimetic agentsPhysically incompatible with aminophylline, ampicillin, cephapirin, sodium bicarbonate, and other alkaline solutions
Esmolol (Brevibloc)(Cardioselective β-blocker)	Rapid control of ventricular rate in atrial fib/flutter	Loading infusion: 500 mcg/kg/min for 1 minuteMaintenance infusion: 50-100 mcg/kg/minUse dosing chart that comes with drug.β-Blocking plasma concentration = 0.15-1 mcg/mLHalf-life = 9 minutes		Hypotension, dizziness, diaphoresis, nausea	Short half-life so effects reversed within 10-20 minutes after stopping drug
Flecainide (Tambocor)(Class IC antiarrhythmic)	In absence of structural heart disease:Conversion of atrial fib to sinus rhythm and maintenance of NSRTreatment of SVT: AVNRT, CMTSlow conduction through accessory pathways in atrial fib or CMTLife-threatening ventricular arrhythmias (sustained VT)	100-200 mg PO q 12 hoursTherapeutic level = 0.2-1 mcg/mL (Plasma levels do not correlate with efficacy, but incidence of CV toxicity greater when levels >1 mcg/mL)Half-life = 12-27 hours		CV: marked proarrhythmia, marked negative inotropic effects (HF), bradycardia, heart blockCNS: blurred vision, dizziness, flushing, ringing ears, drowsiness, headache.Other: bad taste, constipation, edema, abdominal pain	Drug interactions: May increase digoxin levelAdditive effects on HR, AV conduction, BP, and ↑ potential for HF when given with negative inotropic drugs, Ca²⁺ blockers, digoxinIncompatible with sodium bicarbonate, Lasix, Valium, thiopentalHigher mortality rate in post-MI patients when studied in CAST. Safest in patients with normal LV functionShould not be used in patients with recent MIProlongs QT interval, potential for proarrhythmia (TdP)Monitor for HFFull therapeutic effect may take up to 5 daysDrug Interactions: ↑ digoxin levels.Cimetidine, amiodarone, propranolol increase flecainide levelsAdditive negative inotropic effects with β-blockers, Ca²⁺ blockers, disopyramide
Ibutilide (Corvert)(Class III antiarrhythmic)	Conversion of atrial fib or flutter to sinus	IV infusion of 1 mg over 10 minutesMay repeat same dose in 10 minutes if neededIn patients <60 kg: 0.01 mg/kgHalf-life = 6 hours		Hypotension, VT, torsades, bundle-branch block, AV block, nausea, headache	Prolongs QT interval: up to 6% incidence of torsades. Proarrhythmia usually occurs within 40 minutes. Monitor ECG continuously during administration and at least 4 hours afterConversion to NSR usually occurs within 20-30 minutes of infusionDrug interactions: Do not give other class I or class III agents within 4 hours
Lidocaine (Xylocaine)(Class IB antiarrhythmic)	Treatment of ventricular arrhythmias: VT, VFEffective for PVC suppression but PVC suppression not usually recommended	For VT: 1 mg/kg IV bolus over 3 minutes followed by infusion at 2-4 mg/min. Repeat bolus of 0.5-0.75 mg/kg in 10 minutes to maintain therapeutic level. May repeat to total of 3 mg/kgFor VF or pulseless VT: 1.5 mg/kg IV bolus. May repeat with same amount and follow with infusion at 2-4 mg/minMay be given down ET tube during cardiac arrest if no IV available.Therapeutic level = 1.4-5 mcg/mLHalf-life of bolus = 10 minutesHalf-life once therapeutic level reached = 1.5-2 hours		Side effects relatively rareCNS: lightheadedness, dizziness, tremor, agitation, tinnitus, blurred vision, convulsions, respiratory depression and arrestCV: bradycardia, asystole, hypotension, shock	↓ Dose to half if liver disease or low liver blood flow (shock)Drug Interactions:β-Blockers and cimetidine increase lidocaine levelsGlucagon and isoproterenol may increase liver blood flow and ↓ lidocaine levels
Magnesium	May be useful for treatment or prevention of both supraventricular and ventricular arrhythmias after MI or cardiac surgery. Treatment of choice for TdP and may be useful in VF or pulseless VT refractory to other drugs	1-2 g diluted in 10 mL D5W over 1-2 minutes. May be given IV push for VF or torsadesInfusion of 0.5-1 g/h for up to 24 hours		CV: hypotension, bradycardia, heart block, cardiac arrestCNS: weakness, drowsiness, peripheral neuromuscular blockade, absent deep tendon reflexesOther: ↓ respiratory rate, respiratory paralysis	Drug Interactions: CNS depression when used with general anesthetics, barbiturates, opiate analgesicsAdditive effects with neuromuscular blocking agentsIncompatible with calcium, sodium bicarbonate, ciprofloxacin
Metoprolol (Lopressor)(Cardioselective β-blocker)	Ventricular rate control in atrial fib/flutterSlow conduction through AV node in AVNRT and CMT	PO: 100-450 mg q.d. in divided dosesIV: 5 mg q 2-5 minutes for three doses (used in acute MI)β-Blocking plasma concentration = 50-100 ng/mLHalf-life = 3-7 hours		Hypotension, bradycardia, AV block	Drug interactions: Additive effects on HR, AV conduction, BP, and ↑ potential for HF when given with negative inotropic drugs, Ca²⁺ blockers, digoxin
Mexiletine (Mexitil)(Class IB antiarrhythmic)	Acute and chronic treatment of symptomatic VTSometimes used in combination with Quinidine or sotalol to increase efficacyMay be useful in congenital LQTS	PO loading dose = 400 mgMaintenance dose = 100-300 mg q 8 hours. Up to 400 mg q 8 hours if needed and no intolerable side effectsTherapeutic level = 0.5-2 mcg/mLHalf-life = 10-17 hours		GI: nausea, vomiting, heartburn, anorexia, diarrheaCNS: tremor, dizziness, ataxia, slurred speech, paresthesias, seizures, hallucinations, emotional instability, insomnia, memory impairmentCV: bradycardia, hypotension, HF, proarrhythmia (rare compared to other agents)Other: thrombocytopenia, fever, rash, positive antinuclear antibody	Often given in combination with other antiarrhythmics with increased effectiveness (quinidine, disopyramide, propafenone, amiodarone)Drug interactions: Phenobarbitol, dilantin, rifampin ↓ mexiletine levelsCimetidine ↑ mexiletine levelsMexiletine ↑ theophylline levels
Procainamide (Pronestyl)(Class IA antiarrhythmic)	Conversion of atrial fib to sinus and maintenance of NSRTreatment of AT, atrial flutter and fibSlows conduction through accessory pathways in WPWTreatment of monomorphic VT	PO dose (regular release form): loading dose of 1,000-1,200 mg; maintenance dose 50 mg/kg/day in divided doses three to four times a day (never more than 6 hour between doses)SR forms: 750-1,500 mg q 6 hoursIV loading dose: 17 mg/kg at 20 mg/min. If rapid loading is needed, give 100-mg doses over 5 minutes to total of 1gIV drip 2-4 mg/minTherapeutic level = 4-10 mcg/mL (may be as high as 5-32 mg/L to prevent sustained VT)Half-life = about 3.5 hoursActive metabolite is NAPA: therapeutic level = 9-12 mg/L		GI: nausea, vomiting, anorexiaCV: bradycardia, heart block, proarrhythmia (less than that with quinidine). Prolongs QT intervalHypotension. With IV useCNS: headache, insomnia, dizziness, psychosis, hallucinations, depressionLupus-like syndrome with long-term use (15%-25% of patients who take drug >1 year)Other: rash, fever, swollen joints, agranulocytosis, pancytopenia	Monitor QT interval, QRS width, PR.Monitor NAPA level (active metabolite)Watch for hypotension with IV useDrug Interactions: Amiodarone, cimetidine, ranitidine increase procainamide levelsAlcohol ↓ procainamide levelsAdditive effects on conduction system disease when given with other class IA, class IC, tricyclic antidepressants, or Ca²⁺ blockers
Propafenone (Rythmol)(Class IC antiarrhythmic, also has β-blocker effects)	Conversion of atrial fib to sinus and maintenance of NSRSlow conduction through accessory pathwaysLife-threatening ventricular arrhythmias (sustained VT)	150-300 mg t.i.d.Therapeutic level = 0.2-3 mcg/mLHalf-life = 2-10 hours in normal metabolizers, up to 32 hours in slow metabolizers		GI: nausea, anorexia, constipation, metallic tasteCNS: dizziness, headache, blurred visionCV: HF, bradycardia, AV block, bundle-branch block, proarrhythmia	Was not included in CAST but is same class as drugs shown to cause higher mortality post-MIWatch for proarrhythmiaDrug interactions: ↑ digoxin levels.Potentiates coumadinHas mild β-blocker and Ca²⁺ blocker effects↑ Cyclosporin levelsQuinidine and cimetidine increase propafenone levels
Propranolol (Inderal)(Noncardioselective β-blocker)	Ventricular rate control in atrial fib/flutterTreatment of SVT (slow AV node conduction): AVNRT, CMTEffective in some types of VT: exercise induced, digitalis inducedEffective in reducing incidence of VF and sudden death post-MI	PO: 10-30 mg three to four times a dayIV: 1-3 mg at rate of 1 mg/minβ-Blocking plasma concentration = 50-100 ng/mLHalf-life = 3-5 hours		GI: nausea, vomiting, stomach discomfort, constipation, diarrheaCNS: dreams, hallucinations, insomnia, depressionOther: bronchospasm, exacerbation of peripheral vascular disease, fatigue, hypoglycemia, impotence	Drug interactions: Additive effects on HR, AV conduction, BP, and ↑ potential for HF when given with negative inotropic drugs, Ca²⁺ blockers, digoxin
Quinidine(Class IA antiarrhythmic)	Not used much anymore due to high incidence of proarrhythmiaConversion of atrial fib to NSR and maintenance of NSRMay be used for other SVTs: AT, AVNRT, accessory pathwaysHas been used for VT	Sulfate: 200-400 mg q 6-8 hoursGluconate: 324 mg SR tabs, 1-2 q 8-12 hoursTherapeutic level = 2-6 mcg/mL Half-life = 7-9 hours		GI: nausea, diarrhea, abdominal painCV: hypotension, bradycardia, tachycardias, TdP, HF prolongs QTc interval, proarrhythmiaCNS: cinchonism (tinnitus, hearing loss, confusion, delirium, visual disturbances, psychosis)	Give with food.Monitor QT interval, QRS width, PRWatch for proarrhythmia (torsades)IV use rare (hypotension)Drug Interactions:↑ Digoxin levelsIncreased bleeding when used with coumadin
				Other: fever, headache, rashes, leukopenia, thrombocytopenia	Dilantin, phenobarbital, rifampin, nifedipine, sodium bicarbonate, thiazide diuretics all ↓ quinidine levelsCimetidine, amiodarone, verapamil all increase quinidine levels
Sotalol (Betapace)(Class III antiarrhythmic; and noncardioselective β-blocker)	Maintenance of NSR after conversion from atrial fib/flutter. Not recommended for pharmacological conversion of atrial fib/flutterTreatment of SVTSlow conduction through accessory pathwaysLife-threatening VT, VF	Should be used only in patients without heart disease or bradycardia when serum electrolytes are normalContraindicated if baseline QTc >450 milliseconds or CrCl <40 mL/min.80 mg b.i.d. × 3 days, then 160 mg b.i.d. × 3 days. Decrease dose or discontinue if QT prolongs to 500 milliseconds or moreMaximum recommended dose is 160 mg b.i.dTherapeutic level = 1-4 mcg/mL (not clinically useful)Half-life = 8-17 hours with normal renal function; up to 6 days with severe renal failure		CV: bradycardia, heart block, HF, proarrhythmiaOther: bronchospasm, fatigue, weakness, GI symptoms, dizziness, dyspnea, hypotension	Prolongs QT interval, potential for proarrhythmia. Monitor QT 2-4 hours after each dose when initiating therapyWatch for bradycardia, AV block, and new or worsening HF
Verapamil (Calan)(Calcium channel blocker: nondihydropyridine “heart rate lowering” Ca²⁺ blocker)	Ventricular rate control in atrial fib/flutterSlow conduction through AV node in AVNRT and CMT	PO: 80-120 mg t.i.d. or q.i.d.IV: 2.5-5 mg over 2 minutesMay repeat with 5-10 mg if neededTherapeutic level = 80-400 ng/mLHalf-life = 3-7 hours		Bradycardia, heart block, HF, hypotension, fatigue, headache, edema, constipation	Contraindicated in patients with accessory pathways (WPW, short PR syndrome)Drug interactions: Additive effects on HR, AV conduction, BP, and ↑ potential for HF when given with negative inotropic drugs, Ca²⁺ blockers, digoxin
CAST, Cardiac Arrhythmia Suppression Trial; CMT, circus movement tachycardia using an accessory pathway; ET, endotracheal, NAPA, N-acetylprocainamide; NSR, normal sinus rhythm, PEA, pulseless electrical activity, SVR, systemic vascular resistance, SR, sustained release.
↑ = increases, ↓ = decreases.

Table 16-3

GUIDELINES FOR MANAGEMENT OF AF AND ATRIAL FLUTTER

Pharmacological Rate Control During AF
Class I:	1.	Control of rate using either a β-blocker or nondihydropyridine CCB (in most cases) for patients with persistent or permanent AF. (Level B)
	2.	Administration of AV nodal blocking agents is recommended to achieve rate control in patients who develop postoperative AF. (Level B)
	3.	In the absence of preexcitation, IV administration of β-blockers (esmolol, metoprolol, or propranolol) or nondihydropyridine CCBs (verapamil, diltiazem) to slow ventricular response to AF in the acute setting, exercising caution in patients with hypotension or HF. (Level B)
	4.	IV administration of digoxin or amiodarone to control heart rate in patients with AF and HF who do not have an accessory pathway. (Level B)
	5.	Oral digoxin is effective to control heart rate at rest and is indicated for patients with HF, LV dysfunction, or for sedentary individuals. (Level C)
	6.	IV amiodarone is recommended to slow a rapid ventricular response to AF and improve LV function in patients with acute MI. (Level C)
	7.	IV β-blockers and nondihydropyridine CCBs are recommended to slow a rapid ventricular response to AF in patients with acute MI who do not have clinical LV dysfunction, bronchospasm, or AV block. (Level C)
Class IIa	1.	A combination of digoxin and either a β-blocker or nondihydropyridine CCB to control heart rate at rest and during exercise in patients with AF. Choice of medication should be individualized and the dose modulated to avoid bradycardia. (Level B)
	2.	It is reasonable to use ablation of the AV node or accessory pathway to control heart rate when pharmacological therapy is insufficient or associated with side effects. (Level B)
	3.	IV amiodarone can be useful to control heart rate when other measures are unsuccessful or contraindicated. (Level C)
	4.	In patients with an accessory pathway, when electrical cardioversion is not necessary, IV procainamide or ibutilide is a reasonable alternative. (Level C)
	5.	IV digitalis is reasonable to slow a rapid ventricular response and improve LV function in patients with acute MI and severe LV dysfunction and HF. (Level C)
Class IIb	1.	Oral amiodarone may be used to control heart rate when ventricular rate cannot be adequately controlled using a β-blocker, nondihydropyridine CCB, or digoxin, alone or in combination. (Level C)
	2.	IV procainamide, disopyramide, ibutilide, or amiodarone may be considered for hemodynamically stable patients with AF involving conduction over an accessory pathway. (Level B)
	3.	Catheter ablation of the AV node may be considered when the rate cannot be controlled with pharmacological agents or when tachycardia-mediated cardiomyopathy is suspected. (Level C)
Preventing Thromboembolism
Class I	1.	Antithrombotic therapy is recommended for all patients with AF except those with lone AF or contraindications. (Level A)
	2.	For patients without mechanical heart valves at high risk of stroke (prior stroke, TIA, or systemic embolism; rheumatic mitral stenosis), chronic oral anticoagulant therapy with a vitamin K antagonist is recommended in a dose to achieve the target INR of 2.0 to 3.0 unless contraindicated. (Level A)
	3.	Anticoagulation with a vitamin K antagonist is recommended for patients with more than one moderate risk factor (age ≥ 75 years, hypertension, HF, LVEF < 35%, diabetes). (Level A)
	4.	INR should be determined at least weekly during initiation of therapy and monthly when anticoagulation is stable. (Level A)
	5.	Aspirin 81-325 mg daily is an alternative to vitamin K antagonists in low-risk patients or those with contraindications to anticoagulation. (Level A)
	6.	For patients with mechanical heart valves, the target intensity of anticoagulation should be based on the type of prosthesis, maintaining an INR of at least 2.5. (Level B)
	7.	For patients with AF of ≥ 48 hours duration, or when the duration is unknown, anticoagulation (INR 2.0 to 3.0) is recommended for at least 3 weeks prior to and 4 weeks after cardioversion (electrical or pharmacological). (Level B)
	8.	For patients with AF of more than 48 hours duration requiring immediate cardioversion, heparin should be administered concurrently (unless contraindicated) by an initial IV bolus followed by a continuous infusion in a dose adjusted to prolong the aPTT to 1.5 to 2 times the reference control value. Oral anticoagulation (INR 2.0 to 3.0) should be given for at least 4 weeks after cardioversion. Limited data support SQ administration of LMWH in this indication. (Level C)
	9.	For patients with AF of less than 48 hours duration and hemodynamic instability (angina, MI, shock, or pulmonary edema), cardioversion should be performed immediately without delay for prior anticoagulation. (Level C)
Class IIa	1.	For primary prevention in patients with nonvalvular AF who have just one of the following risk factors (age ≥ 75 years, HTN, HF, impaired LV function, diabetes), therapy with ASA or a vitamin K antagonist is reasonable. (Level A)
	2.	For patients with nonvalvular AF who have one or more of the following less well-validated risk factors (age 65-74 years, female, or CAD), therapy with either ASA or a vitamin K antagonist is reasonable. (Level B)
	3.	As an alternative to anticoagulation prior to cardioversion, it is reasonable to perform TEE in search of thrombus in the left atrium or left atrial appendage. If no thrombus is identified, cardioversion is reasonable immediately after anticoagulation with UFH (aPTT 1.5 to 2 times control), followed by continuation of oral anticoagulation for at least 4 weeks. (Level B) Limited evidence to support use of SQ LMWH in this indication. (Level C)
	4.	If thrombus is identified by TEE, oral anticoagulation is reasonable for at least 3 weeks prior to and 4 weeks after restoration of sinus rhythm. A longer period of anticoagulation may be appropriate after successful cardioversion because the risk of thromboembolism remains elevated. (Level C)
	5.	It is reasonable to administer antithrombotic medication in patients who develop postoperative AF, as for nonsurgical patients. (Level B)
	6.	For patients with AF who do not have mechanical prosthetic heart valves, it is reasonable to interrupt anticoagulation for up to 1 week without substituting heparin for surgical or diagnostic procedures that carry a risk of bleeding. (Level C)
Class IIb	1.	In patients ≥ 75 years of age at increased risk of bleeding but without frank contraindications to oral anticoagulant therapy, and in other patients with moderate risk factors for thromboembolism who are unable to safely tolerate an INR 2.0-3.0, a lower INR target of 2.0 (range 1.6 to 2.5) may be considered. (Level C)
	2.	When surgical procedures require interruption of oral anticoagulant therapy for longer than one week in high-risk patients, UFH may be administered or LMWH given by SQ injection. (Level C)
	3.	Following PCI or revascularization surgery in patients with AF, low-dose ASA and/or clopidogrel may be given concurrently with anticoagulation to prevent myocardial ischemic events. (Level C)
Cardioversion of AF
Class I	1.	Administration of flecainide, dofetilide, propafenone, or ibutilide is recommended for pharmacological cardioversion. (Level A)
	2.	Immediate electrical (direct-current) cardioversion is recommended for patients with AF involving preexcitation when very rapid tachycardia or hemodynamic instability occurs. (Level B)
	3.	When a rapid ventricular response does not respond promptly to pharmacological measures in patients with myocardial ischemia, symptomatic hypotension, angina, or HF, immediate r-wave synchronized cardioversion is recommended. (Level C)
	4.	Electrical cardioversion is recommended in patients without hemodynamic instability when symptoms of AF are unacceptable to the patient. In case of early relapse of AF after cardioversion, repeated electrical cardioversion attempts may be made following administration of antiarrhythmic medication. (Level C)
	5.	Electrical cardioversion is recommended for patients with acute MI and severe hemodynamic compromise, intractable ischemia, or inadequate rate control with drugs. (Level C)
Class IIa	Pharmacological Cardioversion:
	1.	Amiodarone is a reasonable option for pharmacological cardioversion of AF. (Level A)
	2.	A single oral bolus dose of propafenone or flecainide (“pill-it-the-pocket”) can be administered to terminate persistent AF outside the hospital once treatment has proved safe in hospital for selected patients without sinus or AV node dysfunction, BBB, QT-interval prolongation, Brugada syndrome, or structural heart disease. Before antiarrhythmic medication is initiated, a β-blocker or nondihydropyridine CCB should be given to prevent rapid AV conduction in the event atrial flutter occurs. (Level C)
	3.	Amiodarone can be beneficial on an outpatient basis in patients with paroxysmal or persistent AF when rapid restoration of sinus rhythm is not deemed necessary. (Level C)
	4.	It is reasonable to restore sinus rhythm by pharmacological cardioversion with ibutilide or electrical cardioversion in patients who develop postoperative AF. (Level B)
	Electrical Cardioversion:
	5.	Electrical cardioversion can be useful to restore sinus rhythm as part of a long-term management strategy. (Level B)
	6.	Patient preference is a reasonable consideration in the selection of infrequently repeated electrical cardioversions for the management of symptomatic or recurrent AF. (Level C)
	Pharmacological Enhancement of Electrical Cardioversion:
	7.	Pretreatment with amiodarone, flecainide, ibutilide, propafenone, or sotalol can be useful to enhance the success of electrical cardioversion and prevent recurrent AF. (Level B)
	8.	In patients who relapse to AF after successful cardioversion, it can be useful to repeat the procedure following prophylactic administration of antiarrhythmic medication. (Level C)
Class IIb	1.	Quinidine or procainamide might be considered for pharmacological cardioversion, but the usefulness of these agents is not well established. (Level C)
	2.	For patients with persistent AF, administration of β-blockers, disopyramide, diltiazem, dofetilide, procainamide, or verapamil may be considered, although the efficacy of these agents to enhance the success of electrical cardioversion or to prevent early recurrence of AF is uncertain. (Level C)
	3.	Out-of-hospital initiation of antiarrhythmic medications may be considered to enhance the success of electrical cardioversion in patients without heart disease or in patients with certain forms of heart disease once the safety of the drug has been verified for the patient. (Level C)
Maintenance of Sinus Rhythm
Class I	1.	An oral β-blocker to prevent postoperative AF is recommended for patients undergoing cardiac surgery (unless contraindicated). (Level A)
	2.	Before initiating antiarrhythmic drug therapy, treatment of precipitating or reversible causes of AF is recommended. (Level C)
Class IIa	1.	Preoperative administration of amiodarone reduces the incidence of AF in patients undergoing cardiac surgery and is appropriate prophylactic therapy for patients at high risk for postoperative AF. (Level A)
	2.	In patients with lone AF without structural heart disease, initiation of propafenone or flecainide can be beneficial on an outpatient basis in patients with paroxysmal AF who are in sinus rhythm at the time of drug initiation. (Level B)
	3.	Drug therapy can be useful to maintain sinus rhythm and prevent tachycardia-induced cardiomyopathy. (Level C)
	4.	Infrequent, well-tolerated recurrence of AF is reasonable as a successful outcome of antiarrhythmic drug therapy. (Level C)
	5.	Outpatient initiation of antiarrhythmic drug therapy is reasonable in patients who have no associated heart disease when the agent is well tolerated. (Level C)
	6.	Sotalol can be beneficial in outpatients in sinus rhythm with little or no heart disease, prone to paroxysmal AF, if the baseline uncorrected QT interval is less than 460 milliseconds. Serum electrolytes are normal, and risk factors associated with class III drug-related proarrhythmia are not present. (Level C)
	7.	Catheter ablation is a reasonable alternative to drug therapy to prevent recurrent AF in symptomatic patients with little or no left atrial enlargement. (Level C)
Class IIb	1.	Prophylactic administration of sotalol may be considered for patients at risk of developing AF following cardiac surgery. (Level B)
Classification of Recommendations:
Class I: Benefit >>> risk, procedure/treatment should be performed/administered
Class IIa: Benefit >> risk, it is reasonable to perform procedure/administer treatment
Class IIb: Benefit ≥ Risk, Procedure/treatment may be considered
Level of Evidence Definitions:
Level A: Data derived from multiple randomized clinical trials or meta-analyses
Level B: Data derived from a single randomized trial or nonrandomized studies
Level C: Only consensus opinion of experts, case studies, or standard of care
aPTT, activated partial thromboplastin time; ASA, aspirin; BBB, bundle-branch block; CAD, coronary artery disease; CCB, calcium channel blocker; HTN, hypertension; INR, international normalized ratio; LMWH, low molecular weight heparin; LV, left ventricular; LVEF, left ventricular ejection fraction; PCI, percutaneous coronary interventions; SQ, subcutaneous; TEE, transesophageal echocardiography; TIA, transient ischemic attack; UFH: unfractionated heparin.
Adapted from Fuster, V., Ryden, L. E., Asinger, R. W., et al. (2006). ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: Executive summary: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation). Circulation, 114, 700-752.

Table 16-4

GUIDELINES FOR MANAGEMENT OF SUPRAVENTRICULAR ARRHYTHMIAS

Acute Management of Hemodynamically Stable and Regular Tachycardia
Class I:	Narrow QRS (SVT) and SVT with BBB:
	1.	Vagal maneuvers (Valsalva, CSM) (Level B)
	2.	Adenosine (Level A)
	3.	Verapamil, diltiazem (Level A)
	Preexcited SVT/AF
	1.	Flecainide (Level B)
	2.	Ibutilide (Level B)
	3.	Procainamide (Level B)
	4.	Electrical cardioversion (Level C)
	Wide QRS Tachycardia of Unknown Origin:
	1.	Procainamide (Level B)
	2.	Sotalol (Level B)
	3.	Amiodarone (Level B)
	4.	Electrical cardioversion (Level B)
	Wide QRS Tachycardia of Unknown Origin in Patients with Poor LV Function:
	1.	Amiodarone (Level B)
	2.	Lidocaine (Level B)
	3.	Electrical cardioversion (Level B)
Class IIb	Narrow QRS (SVT) and SVT with BBB:
	1.	β-Blockers (Level C)
	2.	Amiodarone (Level C)
	3.	Digoxin (Level C)
	Wide QRS Tachycardia of Unknown Origin:
	1.	Lidocaine (Level B)
	2.	Adenosine (Level C)
Long-Term Treatment of Recurrent AVNRT
Class I:	1.	Catheter ablation (Level B)
	2.	Verapamil for recurrent symptomatic AVNRT (Level B)
	3.	Diltiazem or β-blockers for recurrent symptomatic AVNRT (Level C)
	Infrequent, well-tolerated episodes of AVNRT:
	1.	Vagal maneuvers (Level B)
	2.	Pill-in-the-pocket (single dose oral diltiazem plus propranolol) (Level B)
	3.	Verapamil, diltiazem, β-blockers, catheter ablation (Level B)
Class IIa	1.	Verapamil, diltiazem, β-blockers, sotalol, amiodarone (Level C)
	2.	Flecainide, propafenone in patients with no coronary artery disease, LV dysfunction, or other significant heart disease (Level C)
Class IIb	1.	Digoxin (Level C)
	2.	Amiodarone (Level C)
Focal and Nonparoxysmal Junctional Tachycardia Syndromes
Class I:	Nonparoxysmal junctional tachycardia:
	1.	Reverse digitalis toxicity (Level C)
	2.	Correct hypokalemia (Level C)
	3.	Treat myocardial ischemia (Level C)
Class IIa	1.	β-Blockers, flecainide, catheter ablation (Level C)
	2.	Propafenone, sotalol, amiodarone in pediatric patients (Level C)
Long-Term Therapy of Accessory Pathway-Mediated Arrhythmias
Class I:	1.	Catheter ablation for WPW syndrome (preexcitation and symptomatic arrhythmias) that are well tolerated; or with AF and rapid conduction or poorly tolerated CMT (Level B)
	2.	Vagal maneuvers for single or infrequent episodes (Level B)
	3.	Pill-in-the-pocket (verapamil, diltiazem, β-blockers) for single or infrequent episodes (Level B)
		Contraindicated: verapamil, diltiazem, digoxin
Class IIa	1.	Flecainide, propafenone, sotalol, amiodarone, β-blockers (Level C)
	2.	Catheter ablation for single or infrequent episodes, or asymptomatic preexcitation (Level B)
Class IIb	1.	β-Blockers in poorly tolerated episodes (Level C)
	2.	Sotalol, amiodarone for single or infrequent episodes (Level B)
	3.	Flecainide, propafenone for single or infrequent episodes (Level C)
Treatment of Focal AT
Class I:	Acute Treatment:
	1.	Electrical cardioversion if hemodynamically unstable (Level B)
	2.	β-Blockers, verapamil, diltiazem for rate control (in absence of digitalis therapy) (Level C)
	Prophylactic Therapy:
	1.	Catheter ablation for recurrent symptomatic or incessant AT (Level B)
	2.	β-Blockers, verapamil, diltiazem (Level C)
Class IIa	Acute Treatment:
	1.	Adenosine, β-blockers, verapamil, diltiazem, procainamide, flecainide, propafenone, amiodarone, sotalol for hemodynamically stable patients (Level C)
	Prophylactic Therapy:
	1.	Disopyramide, flecainide, propafenone for recurrent symptomatic AT (these drugs should be combined with an AV nodal blocking agent to prevent rapid ventricular rate if atrial fib or flutter should occur) (Level C)
	2.	Sotalol, amiodarone for recurrent symptomatic AT (Level C)
Class IIb	1.	Digoxin for rate control (Level C)
Classification of Recommendations:
Class I:	Benefit >>> Risk, procedure/treatment should be performed/administered.
Class IIa:	Benefit >> risk, it is reasonable to perform procedure/administer treatment.
Class IIb:	Benefit ≥ risk, procedure/treatment may be considered.
Level of Evidence Definitions:
Level A:	Data derived from multiple randomized clinical trials or meta-analyses.
Level B:	Data derived from a single randomized trial or nonrandomized studies.
Level C:	Only consensus opinion of experts, case studies, or standard of care.
BBB, bundle-branch block; LV, left ventricular.
Adapted from Blomstrom-Lundqvist, C., Scheinman, M. M., Aliot, E. M., et al. (2003). ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—Executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation, 108, 1871-1909.

Normal Sinus Rhythm

The SA node normally fires at a regular rate of 60 to 100 beats per minute. The impulse spreads from the SA node through the atria and to the AV node, where it encounters a slight delay before it travels through the bundle of His, right and left bundle branches, and Purkinje fibers into the ventricles. The spread of this wave of depolarization through the heart gives rise to the classic surface electrocardiogram (ECG), which can be monitored at the bedside. Chapter 15 presents information on the origin of the waves and intervals of the cardiac cycle.

The characteristics of normal sinus rhythm include the following:

Rate: 60 to 100 beats per minute

Rhythm: Regular

P waves: Precede every QRS complex and are consistent in shape

PR interval: 0.12 to 0.20 second

QRS complex: 0.04 to 0.10 second

Table 16-5

GUIDELINES FOR MANAGEMENT OF VENTRICULAR ARRHYTHMIAS

Sustained Monomorphic VT
Class I:	1.	Wide QRS tachycardia should be presumed to be VT if the diagnosis is unclear. (Level C)
	2.	Electrical cardioversion with sedation is recommended with hemodynamically unstable sustained monomorphic VT. (Level C) CONTRAINDICATED: Calcium channel blockers (verapamil, diltiazem) should not be used to terminate wide QRS tachycardia of unknown origin, especially with history of myocardial dysfunction.
Class IIa	1.	IV procainamide is reasonable for initial treatment of patients with stable VT. (Level B)
	2.	IV amiodarone is reasonable for VT that is hemodynamically unstable, refractory to conversion with countershock, or recurrent despite procainamide or other agents. (Level C)
	3.	Transvenous catheter pace termination can be useful for VT that is refractory to cardioversion or is frequently recurrent despite antiarrhythmic medication. (Level C)
Class IIb	1.	IV lidocaine might be reasonable for initial treatment of monomorphic VT associated with acute myocardial ischemia or infarction. (Level C)
Repetitive Monomorphic VT
Class IIa	1.	IV amiodarone, β-blockers, and IV procainamide (or IV sotalol or ajmaline in Europe) can be useful for repetitive monomorphic VT in the context of coronary disease and idiopathic VT. (Level C)
PVT
Class I:	1.	Electrical cardioversion with sedation is recommended for sustained PVT with hemodynamic compromise. (Level B)
	2.	IV β-blockers are useful if ischemia is suspected or cannot be excluded. (Level B)
	3.	IV amiodarone is useful for recurrent PVT in the absence of QT prolongation (congenital or acquired). Level C
	4.	Urgent angiography and revascularization should be considered with PVT when myocardial ischemia cannot be excluded. (Level C)
Class IIb	1.	IV lidocaine may be reasonable for PVT associated with acute myocardial ischemia or infarction (Level C)
TdP
Class I:	1.	Withdrawal of any offending drugs and correction of electrolyte abnormalities are recommended for TdP. (Level A)
	2.	Acute and long-term pacing is recommended for TdP due to heart block and symptomatic bradycardia. (Level A)
Class IIa	1.	IV magnesium sulfate is reasonable for patients who present with LQTS and few episodes of TdP. (Level B)
	2.	Acute and long-term pacing is reasonable for recurrent pause-dependent TdP. (Level B)
	3.	β-Blockade combined with pacing is reasonable acute therapy for TdP and sinus bradycardia. (Level C)
	4.	Isoproterenol is reasonable as temporary acute treatment for recurrent pause-dependent TdP who do not have congenital LQTS. (Level B)
Class IIb	1.	Potassium repletion to 4.5-5 mM/L may be considered for TdP. (Level B)
	2.	IV lidocaine or oral mexiletine may be considered for LQT3 and TdP. (Level C)
Incessant VT
Class I:	1.	Revascularization and β-blockade followed by IV antiarrhythmic drugs such as procainamide or amiodarone are recommended for recurrent or incessant PVT. (Level B)
Class IIa	1.	IV amiodarone or procainamide followed by VT ablation can be effective in recurrent or incessant monomorphic VT. (Level B)
Class IIb	1.	IV amiodarone and IV β-blockers separately or together may be reasonable for VT storm. (Level C)
	2.	Overdrive pacing or general anesthesia may be considered for frequently recurring or incessant VT. (Level C)
	3.	Spinal cord modulation may be considered for some patients with frequently recurring or incessant VT. (Level C)
Classification of Recommendations:
Class I: Benefit >>> Risk, Procedure/Treatment should be performed/administered.
Class IIa: Benefit >> Risk, it is reasonable to perform procedure/administer treatment.
Class IIb: Benefit ≥ Risk, Procedure/treatment may be considered.
Level of Evidence Definitions:
Level A: Data derived from multiple randomized clinical trials or meta-analyses.
Level B: Data derived from a single randomized trial or nonrandomized studies.
Level C: Only consensus opinion of experts, case studies, or standard-of-care.
This table covers pharmacological and electrical cardioversion for treatment of VT. Guidelines for ICD implantation are covered in Chapter 28, and guidelines for catheter ablation are presented in Chapter 18.
Adapted from Zipes, D. P., Camm, J. A., Borggrefe, M., et al. (2006). ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death—Executive summary: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines. Circulation, 114, 1088-1132.

Example: Normal sinus rhythm. Rate, 65 beats per minute; PR interval, 0.14 second; QRS interval, 0.06 second

Sinus Bradycardia

Sinus bradycardia is discharge of the SA node at a rate slower than 60 beats per minute. It can be a normal variant, especially in athletes and during sleep. Sinus bradycardia may be a response to vagal stimulation, such as carotid sinus massage (CSM), ocular pressure, coughing, or vomiting. Pathological sinus bradycardia can occur with inferior wall MI, hypothyroidism, hypothermia, sleep apnea, increased intracranial pressure, glaucoma, myxedema, hypoxia, infections, and sick sinus syndrome.⁵,¹⁴,¹⁵ Sinus bradycardia can be a response to several medications, including digitalis, β-blockers, calcium channel blockers, and antiarrhythmics.

The following are ECG characteristics of sinus bradycardia:

Rate: Less than 60 beats per minute

Rhythm: Regular

P waves: Precede every QRS, consistent shape

PR interval: Usually normal (0.12 to 0.20 second)

QRS complex: Usually normal (0.04 to 0.10 second)

Conduction: Normal through atria, AV node, bundle branches, and ventricles

Example: Sinus bradycardia, rate 40 beats per minute

Sinus bradycardia does not require treatment unless the patient is symptomatic. If the arrhythmia is accompanied by hypotension, restlessness, diaphoresis, chest pain, or other signs of hemodynamic compromise or by ventricular ectopy, atropine 0.5 mg intravenously (IV) is the treatment of choice. Attempts should be made to decrease vagal stimulation, and, if bradycardia is due to medications, they should be held until their need has been reevaluated. See Chapter 27 for the ACLS algorithm for treatment of symptomatic bradycardia.

Sinus Tachycardia

Sinus tachycardia is sinus rhythm at a rate faster than 100 beats per minute. It is a normal response to anything that stimulates the sympathetic nervous system, including sympathomimetic drugs, exercise, and emotion. Sinus tachycardia that persists at rest usually indicates some underlying problem, such as fever, blood loss, anxiety, pain, HF, hypermetabolic states, or anemia. Sinus tachycardia is a normal physiologic response to a decrease in cardiac output. Drugs that can cause sinus tachycardia include atropine, isoproterenol, epinephrine, dopamine, dobutamine, norepinephrine, nitroprusside, and caffeine.

The rate of sinus tachycardia should not exceed 220 minus the patient’s age. For example, a 40-year-old patient can have sinus tachycardia up to a rate of 180 beats per minute, but a 70-year-old patient should not have sinus tachycardia at a rate faster than 150 beats per minute. If the heart rate exceeds these upper limits, some other mechanism of tachycardia should be suspected.

The ECG characteristics of sinus tachycardia include the following:

Rate: Greater than 100 beats per minute

Rhythm: Regular

Example of sinus tachycardia

P waves: Precede every QRS; have consistent shape; may be buried in the preceding T wave

PR interval: Usually normal, may be difficult to measure if P waves are buried in T waves

QRS complex: Usually normal

Conduction: Normal through atria, AV node, bundle branches, and ventricles

Example: Sinus tachycardia rate, 107 beats per minute

Treatment of sinus tachycardia is directed at the cause. Because this arrhythmia is a physiologic response to a decrease in cardiac output, it should never be ignored, especially in the cardiac patient. Because the ventricles fill with blood and the coronary arteries perfuse during diastole, persistent tachycardia can cause decreased stroke volume, decreased cardiac output, and decreased coronary perfusion secondary to the decreased diastolic time that occurs with rapid heart rates. Carotid sinus pressure may slow the heart rate temporarily and thereby help in ruling out other arrhythmias. β-Blockers are used to treat tachycardia in patients with acute MI without signs of HF or contraindications to β-blocker therapy.

Sinus Arrhythmia

Sinus arrhythmia occurs when the SA node discharges irregularly. It occurs as a normal phenomenon, especially in the young, and decreases with age. Sinus arrhythmia is commonly associated with the phases of respiration: during inspiration, the SA node fires faster; during expiration, it slows. Other than this phasic increase and decrease in rate, sinus arrhythmia looks like normal sinus rhythm and it does not require treatment. The following characteristics are typical of sinus arrhythmia:

Rate: 60 to 100 beats per minute

Rhythm: Irregular; phasic increase and decrease in rate, which may be related to respiration

P waves: Precede every QRS; have consistent shape

PR interval: Usually normal

QRS complex: Usually normal

Conduction: Normal through atria, AV node, bundle branches, ventricles

Example: Sinus arrhythmia

Sinus Arrest

Sinus arrest occurs when the SA node automaticity is depressed and impulses are not formed when expected. This delay results in the absence of a P wave at the time it is expected to occur, and unless there is escape of a junctional or ventricular pacemaker, the QRS complex is also missing. If only one sinus impulse fails to form, the term sinus pause is usually used, whereas if more than one sinus impulse in a row fails to form, sinus arrest has occurred. Because the SA node has depressed automaticity and does not form impulses regularly as expected, the P-P interval in sinus arrest is not an exact multiple of the sinus cycle. Causes of sinus arrest include vagal stimulation, carotid sinus sensitivity, MI interrupting the blood supply to the SA node, and drugs such as digitalis, β-blockers, and calcium channel blockers. Sinus arrest is characterized by the following ECG changes.

Example of sinus arrest

Rate: Atrial—usually within normal range but may be in bradycardic range if several sinus impulses fail to form. Ventricular—usually within normal range but may be in bradycardic range if several sinus impulses fail to form and there are no junctional or ventricular escape beats. Occasionally, the ventricular rate may be faster than the atrial rate because of junctional or ventricular escape beats that occur during the period of sinus arrest.

Rhythm: Irregular due to the absence of SA node discharge

P waves: Present when SA node is firing and absent during periods of sinus arrest. When present, they precede every QRS complex and are consistent in shape. If junctional escape beats occur, P waves may be inverted either before or after the junctional QRS.

PR interval: Usually normal when P waves are present. If junctional escape beats occur, the PR interval is short when the P wave precedes the QRS.

QRS complex: Usually normal when SA node is functioning and absent during periods of sinus arrest unless escape beats occur. If ventricular escape beats occur, QRS complex is wide.

Conduction: Normal through atria, AV node, bundle branches, and ventricles when SA node is firing. When the SA node fails to form impulses, there is no conduction through the atria. If a junctional escape beat occurs, ventricular conduction is usually normal, whereas if a ventricular escape beat occurs, conduction through the ventricles is abnormally slow.

Example: (A) Sinus pause and (B) sinus arrest with a junctional escape beat (5th beat)

Treatment of sinus arrest is aimed at the cause and at increasing ventricular rate if the patient is symptomatic. Any offending drugs should be discontinued, and vagal stimulation should be minimized. If periods of sinus arrest are frequent and cause hemodynamic compromise, atropine 0.5 mg IV may increase the ventricular rate. Pacemaker therapy may be necessary if all other forms of management fail.

Example of sinus exit block

Sinus Exit Block

Sinus exit block occurs when the impulse is formed in the SA node normally but fails to exit the node to excite atrial tissue. Sinus exit block can be type I, type II, or complete. The section in this chapter titled “Complex Arrhythmias and Conduction Disturbances” contains a discussion of sinus Wenckebach, which is type I sinus exit block. Type II sinus exit block looks exactly like sinus arrest except for the P-P intervals, which are multiples of the basic sinus cycle length. Complete sinus exit block exists when no impulses reach the atria from the SA node and no P waves occur. In this case, either a junctional or ventricular pacemaker emerges to take over pacing duties, or asystole occurs.

Rate: Atrial—usually within normal range but may be in bradycardic range if several sinus impulses fail to exit the SA node. Ventricular—usually in normal range but may be in bradycardic range if no junctional or ventricular escape beats occur during periods of sinus exit block.

Rhythm: Irregular due to pauses caused by sinus exit block

P waves: Present except when impulse fails to exit SA node. When present, they precede every QRS and are consistent in shape. The P-P interval is an exact multiple of the sinus cycle because impulses are formed regularly but occasionally fail to exit the SA node.

PR interval: Usually normal when P waves are present but may be prolonged if AV node conduction is slow.

QRS complexes: Usually normal when sinus impulse conducts and absent when exit block occurs. If ventricular escape beats occur, QRS is wide.

Conduction: Normal through atria, AV node, bundle branches, and ventricles when impulse exits SA node normally.

Example: Sinus exit block. The length of the pause is exactly double the sinus rate

Treatment of sinus exit block depends on the resulting ventricular rate and its hemodynamic significance. Atropine may cause an increase in rate if bradycardia is symptomatic. Pacing may be necessary, especially with complete sinus exit block. Otherwise, the treatment is similar to that of sinus arrest.

Sick Sinus Syndrome

The term sick sinus syndrome is used to describe rhythms in which there is marked sinus bradycardia, sinus pauses, or periods of sinus arrest alternating with paroxysms of rapid atrial arrhythmias, especially atrial flutter or AF. The term brady-tachy syndrome is commonly used to describe the same arrhythmias. During periods of sinus bradycardia or arrest, junctional escape rhythms commonly occur, and AV block is also often associated with the SA node dysfunction that causes sick sinus syndrome. Causes of sick sinus syndrome include coronary artery disease, inflammatory or infiltrative cardiac disease, cardiomyopathy, sclerodegenerative processes involving both the SA and AV nodes, and drugs such as β-blockers, calcium channel blockers, digitalis, amiodarone, propafenone, and adenosine.⁵,¹⁵,¹⁶ ECG characteristics of sick sinus syndrome include the following:

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Tags: Cardiac Nursing

Jan 10, 2021 | Posted by drzezo in NURSING | Comments Off

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