Although certain arrhythmias are more common in neonates and young infants compared to older children and adults, all types of arrhythmias can occur. Many are benign and do not cause hemodynamic compromise. Others may diminish cardiac output and cause decreased blood pressure and decreased perfusion. Sustained tachyarrhythmias may eventually cause myocardial dysfunction, which is known as tachycardia-induced cardiomyopathy. The purpose of this chapter is to review diagnosis and management of common arrhythmias in neonates and young infants.
The electrical impulse normally originates in the sinoatrial (SA) node. The atrioventricular (AV) node, His bundle, and bundle branches provide the only normal pathway for transmission of impulses between the atria and ventricles. Generation of impulses from the SA node is modulated by many factors, including body temperature, blood pressure, autonomic nervous system, and circulating catecholamines. Abnormalities in any of these factors can result in bradycardia or tachycardia that are not related to any specific cardiac disorder.
Conduction through the AV node is slowed so that atrial contraction is complete before ventricular contraction occurs. If the SA node fails to depolarize, the AV node can function as an escape pacemaker.
Abnormalities in impulse formation result in sinus bradycardia and tachycardia, premature atrial and ventricular contractions, and ectopic or automatic rhythms from the atria, AV node, or ventricles. Automatic tachycardias are usually incessant (ie, they are almost always present). Increased automaticity occurs when atrial, nodal, or ventricular cells display autonomous repetitive depolarization at a higher rate than is normal. This type of tachycardia is sometimes associated with fever, hypoxemia, electrolyte disturbances, or infusion of intravenous sympathomimetic agents. Sinus tachycardia can be considered an automatic tachycardia, but it is rarely spontaneous and characteristically resolves when the abnormal stimulus resolves. In contrast, other forms of automatic tachycardia, such as atrial ectopic tachycardia, junctional ectopic tachycardia, and the automatic form of ventricular tachycardia, may be spontaneous or triggered by the aforementioned stimuli. Regardless of site of origin, onset and termination are often gradual rather than abrupt. The rate of an automatic tachycardia is often sensitive to changes in autonomic tone. Therapies that produce only transient effects, such as direct current (DC) cardioversion and administration of adenosine, do not terminate automatic tachycardias.
Block within the normal conduction system is the most obvious form of abnormal impulse conduction. Block can occur at any location, but atrioventricular block is the most common site.
Re-entry, the other form of abnormal impulse conduction, is an important mechanism underlying supraventricular tachycardia in infants. The re-entrant circuit involves two functionally distinct pathways that have different conduction velocities and refractory periods (Figure 10-1). Under the right circumstances (often in response to a premature atrial contraction), an electrical impulse arrives when one of the pathways is refractory. The impulse traverses the other pathway, and conduction is delayed enough so that the impulse is able to “reenter” the blocked pathway from the other direction, thus completing the re-entrant circuit. Re-entry mechanisms usually cause paroxysmal tachycardias, which may start and stop multiple times in the course of the day. Re-entrant tachycardias start and stop abruptly, and they often terminate in response to interventions that produce only transient effects (eg, adenosine) because interruption of the re-entrant circuit usually terminates the tachycardia.
FIGURE 10-1.
Re-entrant tachycardia. Two pathways, one conducting slowly and one conducting rapidly, are shown. A. Normal sinus rhythm. The impulse is traveling down both pathways but is blocked at the slow pathway. B. A premature atrial contraction is blocked in the fast pathway because this pathway remains refractory after the previous beat. The impulse is able to travel down the slow pathway and then retrograde up the fast pathway, which is no longer refractory. C. Supraventricular tachycardia. Conduction of the impulse up the fast pathway creates a re-entrant circuit.
Sinus arrhythmia is a normal phasic variation in impulse formation from the SA node that is often in cycle with respiration (Figure 10-2). This is the most common cause of an irregular heart rate, especially in older infants. The P-wave axis is usually normal. If substantial slowing occurs, junctional tissue depolarizes first, and junctional escape beats may be seen. Sinus arrhythmia is more common at slower heart rates and is therefore more frequent in sleeping infants and in any patient with increased vagal tone (Table 10-1). This rhythm is a normal variant, and no special monitoring or intervention is indicated.
The definition of sinus bradycardia depends on the method used to record the rhythm. An infant is usually stimulated by placement of the leads for a standard electrocardiogram (ECG), so bradycardia is usually defined as a heart rate <100 beats per minute. In contrast, the infant is much less stimulated during recording of a 24-hour electrocardiogram and sleeps during portions of the recording. During wakeful times, the average heart rate in young infants is 105 to 110 beats per minute, and the average minimum rate is in the low 90s. Based on these data, bradycardia in a neonate, defined as two standard deviations below the mean, is a heart rate of less than 80 beats per minute while awake and less than 60 beats per minute while asleep. This information has important implications for infants placed on apnea monitors. The alarm for low heart rate should not be set too high.
The most common cause of sinus bradycardia in neonates is increased vagal tone (Table 10-1). The next most common, especially in premature infants, is hypoxemia related to apnea. Hypoxemia in the fetus causes apnea and bradycardia, and the apnea of prematurity is a postnatal manifestation of this response. Conversely, hypoxemia not caused by apnea stimulates tachypnea after birth, and this is associated with tachycardia rather than bradycardia. Other causes of sinus bradycardia include hypothermia, drug therapy, and hypothyroidism. Infants with long QT syndrome often have slower heart rates, so the QT interval corrected for heart rate (QTc) interval should be assessed carefully in all neonates with sinus bradycardia.
Rarely, infants with sinus bradycardia have familial bradycardia or tachycardia-bradycardia (sick sinus) syndrome. These infants may need antiarrhythmic medication and/or pacemaker placement.
First-degree atrioventricular (AV) block is characterized by an abnormally long PR interval for age and heart rate. In neonates with normal heart rates, the upper limit of normal is 160 ms on the first day of life and 140 ms thereafter. According to these criteria, first-degree AV block is present in about 6% of normal newborn infants and most often can be considered a normal variant. First-degree AV block also results from prolonged AV nodal conduction, which is usually the result of medication (eg, digoxin) or from trauma/ischemia in patients who have had cardiac surgery. Treatment is not necessary, but further evaluation to exclude higher degrees of AV block may be required.
Second-degree AV block is defined as intermittent loss of AV conduction (failure of a normal atrial impulse to conduct to the ventricles). Mobitz type I (Wenckebach) block is characterized by gradual lengthening of the PR interval eventually followed by a P wave without a subsequent QRS complex (“dropped beat”). This results in the typical “grouped QRSs” (Figure 10-3). Mobitz type I block is typically seen during sleep and in patients who have increased vagal tone (Table 10-1). This pattern usually can be considered a normal variant. No further evaluation is necessary unless this pattern is noted during times of increased catecholamine state.
Mobitz type II block is characterized by intermittent loss of conduction of P waves to the ventricles without prolongation of the PR interval and is always considered pathologic. Every other P wave is conducted in 2:1 block. Conduction may be lost for more than one P wave (eg, 3:1 block); this is called high-grade second-degree AV block and may progress to complete AV block. This rhythm is uncommon in newborn infants and is thought to be related to block in the bundle of His. It can occur in infants born to mothers with connective tissue disease, in infants with congenital cardiovascular disease (eg, l-looped ventricles, heterotaxy syndrome [left atrial isomerism]), and in infants who have had cardiac surgery. Mobitz type II block may progress to complete AV block, and for this reason, these patients must be observed closely. Patients with Mobitz type II block and a wide QRS complex should be considered for permanent pacemaker placement.
At times, an electrocardiographic pattern of 2:1 AV block is associated with marked prolongation of the QTc interval and is caused by the very prolonged ventricular refractory period associated with the long QT interval (Figure 10-4). This can be caused by electrolyte disorders, especially hypocalcemia. Alternatively, although rare, patients may have congenital long QT syndrome and will need aggressive treatment because the risk of sudden death is high even in asymptomatic patients.
Complete, or third-degree, AV block is characterized by failure of all atrial impulses to be conducted to the ventricle. Generally, the atrial rhythm (P wave) is completely dissociated from the ventricular rhythm (QRS complex) (Figure 10-5). The atrial rate is normal for age and responds to chronotropic stimuli, such as pain and arousal, and can be used as a marker of hemodynamic stress caused by the AV block. The QRS complexes are regular, and the heart rate, which varies little, is usually 60 to 80 beats per minute in neonates. The QRS complexes may be narrow if the escape rhythm originates near the AV node and impulses flow down the normal ventricular conduction system or wide if the escape rhythm originates from below the bundle of His.
The onset of complete AV block in neonates is usually during fetal life and the condition is called congenital complete AV block (CCAVB). If the heart is structurally normal, CCAVB is often associated with maternal collagen vascular disease, such as systemic lupus erythematosus or Sjögren syndrome. Maternal autoantibodies to SSA/Ro and SSB/La proteins cross the placenta and interact with the developing conduction system. The exact mechanism for antibody-mediated AV block remains to be defined, but it appears that a series of immune-mediated inflammatory events results in fibrosis of the AV node and distal conduction system. In addition to CCAVB, affected infants may show signs of neonatal lupus, including discoid lesions, leukopenia, thrombocytopenia, and hemolytic anemia. Many mothers have no signs or symptoms, so all mothers who have offspring with CCAVB without structural cardiovascular abnormalities should be evaluated for connective tissue diseases. The incidence of CCAVB is 1% to 2% in offspring of mothers who have anti-Ro and anti-La antibodies. The risk of CCAVB is 15% to 20% in subsequent pregnancies after the birth of one child with CCAVB.
CCAVB diagnosed during fetal life that is associated with hydrops fetalis and cardiac enlargement carries a poor prognosis. Therapy for this condition is discussed in Chapter 4. Newborns with CCAVB are often asymptomatic because stroke volume increases to compensate for the decreased ventricular rate, and thus cardiac output is maintained. Infants with structurally normal hearts who are born with or develop congestive heart failure often respond well to supportive therapy. Inotropic agents, such as isoproterenol, and pacemaker placement are often necessary. Although rare, bradycardia may be severe at birth and produce signs and symptoms of inadequate cardiac output. In those cases, emergency pacing is necessary in the delivery room. This can be accomplished by placement of a temporary transvenous pacemaker or pacing by use of transcutaneous pacing electrodes until a permanent pacemaker is placed.
Criteria for pacemaker placement in neonates and young infants with CCAVB include congestive heart failure, cardiomegaly and/or ventricular dysfunction, premature ventricular contractions or ventricular tachycardia, prolonged pauses, prolonged QTc interval, and a wide complex (ventricular) instead of narrow complex (junctional) escape rhythm. Controversy exists as to whether a pacemaker should be placed in neonates solely because of a slow ventricular rate (<55 beats per minute). As many as 20% of those with CCAVB diagnosed during fetal life or shortly after birth may be at risk of developing dilated cardiomyopathy during childhood; the presence of maternal antibodies is likely a risk factor. Serial follow-up of ventricular function is important in these patients.
Congenital cardiovascular defects associated with CCAVB include l-looped ventricles (eg, corrected transposition of the great arteries), heterotaxy syndrome (left atrial isomerism), and atrioventricular septal defects. Such defects are present in about 50% of infants with CCAVB. These infants occasionally develop nonimmune hydrops. Despite aggressive treatment, the prognosis is poor in infants with complex heart disease and CCAVB.
Complete AV block may also occur after cardiac surgery, especially in those patients with l-loop or in those who have had surgery involving the ventricular septum (eg, tetralogy of Fallot, ventricular septal defect, or atrioventricular septal defect). Permanent pacemaker placement is always indicated for postoperative patients in whom complete AV heart block related to cardiac surgery does not resolve within 10 to 14 days. Temporary pacing (transvenous, transcutaneous, temporary pacing wires) may be indicated, and, rarely, isoproterenol infusion is necessary before a permanent pacemaker is placed. The threshold for the temporary pacer lead must be checked daily; a patient who has an inadequate underlying rhythm and high-pacing threshold should be considered for immediate permanent pacemaker placement.
Sinus tachycardia is characterized by a normal P-wave axis (upright in lead II) and a rate up to 240 beats per minute in neonates (Figure 10-6). Variability in the rate is common. Sinus tachycardia is usually caused by some other problem in neonates, such as hypovolemia, fever, hypoxemia, sympathomimetic medications, anemia, pain, and inadequate sedation. When the heart rate is >170 to 180 beats per minute, P waves may be difficult to see because they are superimposed on the preceding T wave. Sometimes, vagal maneuvers (see following text) will transiently decrease the heart rate enough that sinus rhythm can be more easily identified. Neither vagal maneuvers, administration of adenosine, nor DC cardioversion will terminate sinus tachycardia. Instead, treatment should address the underlying cause of tachycardia. For example, administration of analgesia to a postoperative patient in pain will decrease the heart rate and confirm sinus rhythm.
Premature atrial contractions (PACs; also known as supraventricular premature contractions) are caused by premature heart beats originating in the atria; early P waves are seen on electrocardiographic recordings (Figure 10-7). They are most commonly an incidental finding in infants who have been placed on cardiac monitors for other reasons. The morphology of the P wave may be different than that of the normal sinus P wave and reflects the ectopic origin of the impulse within the atrium. At times, the P wave may be superimposed on the preceding T wave. Most often, PACs are conducted normally to the ventricles, and the QRS complex is normal. Occasionally, there is conduction with aberrancy; a bundle branch pattern with a wide QRS complex is seen because the bundle branch is still refractory from the previous depolarization. If the premature P wave is very early, it will not be conducted to the ventricles because the AV node or proximal His bundle is refractory; this is called a blocked PAC. This will tend to slow the heart rate, and frequent blocked PACs can cause bradycardia (Figure 10-8). Iatrogenic causes include endocardial irritation from an intracardiac catheter or extracorporeal membrane oxygenation cannula and effects of pharmacologic agents, such as caffeine, theophylline, dopamine, epinephrine, and isoproterenol. Rarely, electrolyte or metabolic abnormalities, cardiac tumors, myocarditis, or structural heart disease are present. Possible predisposing conditions should be treated, but a specific etiology is not determined in most cases. Even if frequent, PACs do not cause hemodynamic compromise and do not need to be treated. A healthy newborn infant who does not have any risk factors and who has a normal physical examination does not require further work-up. PACs may occur in up to one-third of neonates and usually disappear within the first 3 months of life.
FIGURE 10-8.
Premature atrial contractions. Lead II rhythm strip showing frequent blocked premature atrial contractions. P waves falling at the end of the T wave (arrow) are conducted to ventricles with aberration. The premature P waves falling within the ST segment or on the upstroke of the T wave are not conducted to the ventricles or blocked (*). The frequent blocked premature beats caused asymptomatic bradycardia in this neonate.
Supraventricular tachycardia (SVT) is an abnormal tachycardia that requires atrial or AV nodal tissue for initiation and maintenance. Excluding sinus tachycardia, re-entrant SVT is the most common arrhythmia in infants and children, and the incidence has been estimated to be as low as 1 in 25 000 and as high as 1 in 250 infants.
More than 75% of SVT in infants is related to an accessory AV pathway. Accessory pathways are anomalous bands of tissue that form an extra electrical conduction pathway between the atrium and the ventricle. Many accessory pathways will conduct from the atrium to the ventricle (antegrade) and from the ventricle to the atrium (retrograde). Patients in whom conduction occurs antegrade across the accessory pathway have ventricular pre-excitation with a short PR interval and a delta wave. SVT and pre-excitation is known as Wolff-Parkinson-White syndrome (WPW; Figure 10-9). Pre-excitation may be difficult to see on the electrocardiogram in infants because of the rapid conduction through the AV node. In addition, up to one-third of patients with WPW show intermittent pre-excitation, and thus some of their tracings may appear normal. The electrical impulse from the SA node passes through both the AV node and the accessory AV pathway. Impulses passing through the AV node are delayed as in normal conduction; the impulse passing through the accessory pathway is not delayed, and thus the early (“pre-excited”) ventricular activation is reflected by the short PR interval and the slurred early QRS delta wave (Figure 10-10B). In other patients, the accessory pathway does not conduct in an antegrade manner. These patients have a normal ECG and what is known as a “concealed” accessory pathway (Figure 10-10C). This mechanism is responsible for more than half the SVT that occurs in infants. Most infants (60% to 90%) will not have recurrent SVT beyond 1 year of age.
FIGURE 10-10.
Mechanisms for conduction. A. Normal. Conduction in sinus rhythm. B. Wolff-Parkinson-White syndrome. The impulse from the sinoatrial node passes through both the AV node and the accessory pathway. There is no delay within the accessory pathway, so the early, or “pre-excited,” ventricular activation produces a short PR interval, and the delta wave as seen on the ECG. C. “Concealed” accessory AV pathway. If the accessory pathway is blocked during sinus rhythm, the ECG is normal because conduction is antegrade through the normal conduction system. D. Orthodromic reciprocating tachycardia. Normal antegrade conduction through the AV node results in a normal QRS complex. The re-entrant circuit is completed by retrograde conduction through the accessory AV pathway, resulting in atrial activation shortly after ventricular depolarization (note the abnormal P waves just after the QRS complexes). E. Antidromic reciprocating tachycardia. Conduction is antegrade through the accessory pathway and retrograde through the AV node. The abnormal sequence of ventricular depolarization causes a wide QRS complex, and P waves are often difficult to see on the surface ECG. This rhythm can be mistaken for ventricular tachycardia. F. AV node re-entry tachycardia. Typically, slow antegrade conduction occurs through a posterior “pathway” of atrial tissue (wavy line), and retrograde conduction travels via a “fast” pathway involving more anterior aspects of the AV node. The P waves are not seen; they are buried in the QRS complex because atrial and ventricular activation occur simultaneously. Abbreviations: AVN, atrioventricular node; His, His bundle; LBB, left bundle branch; RBB, right bundle branch; SN, sinoatrial node.
During an episode of abnormal tachycardia, a re-entry circuit forms between the AV node and the accessory pathway (Figure 10-10D). This is often triggered by a premature atrial contraction that travels normally through the AV node but is blocked in the accessory pathway. The impulse from the ventricle is then conducted retrograde in the accessory pathway back to the atrium, thus completing the re-entrant circuit. The atrium is reactivated by the retrograde impulse, and in this manner, the re-entrant circuit becomes self-perpetuating and thus sustains the abnormal tachycardia. The QRS complex is normal because the normal pathway is used for antegrade conduction, producing the normal sequence of ventricular activation. The accessory pathway is used for retrograde conduction to maintain the re-entry loop. This is the most common form of re-entrant SVT and is called orthodromic reciprocating tachycardia (Figure 10-10D). When the impulse travels in the other direction (ie, forward through the accessory pathway and retrograde through the AV node), the QRS is wide because of the abnormal sequence of ventricular activation. This is called antidromic reciprocating tachycardia and can be mistaken for ventricular tachycardia because of the wide QRS complex (Figure 10-10E).
The re-entrant circuit in AV nodal re-entrant tachycardia also involves two pathways, but in this case, one pathway is within the AV node, and the other is a distinctly different pathway that may be within the AV node or a few millimeters outside the AV node (Figure 10-10F). The effective refractory period of one pathway is longer than that of the other pathway. This allows initiation of re-entrant tachycardia when a premature atrial contraction is blocked in the pathway with the longer refractory period. This occurs rarely in infants but is the most common mechanism for SVT in adult patients.
In the permanent form of junctional reciprocating tachycardia (PJRT), the accessory pathway is concealed and conducts slowly in the retrograde direction. The rate in neonates is usually slower than typical SVT with rates of 160 to 200 beats per minute. PJRT may be present as an incessant tachycardia during fetal life. The rate is more variable than most re-entrant tachycardias because both limbs of the circuit are influenced by autonomic tone. Initially, this tachycardia is fairly well tolerated because of the slower heart rate and may not be detected in normal neonates and young infants. Eventually, a tachycardia-induced dilated cardiomyopathy may develop. The ECG shows an abnormal superior P-wave axis, usually a negative P wave in lead II and an upright P wave in lead aVL. During tachycardia, the interval from the R wave to the next P wave is relatively long; the P wave is located closer to the subsequent QRS complex than the previous one (Figure 10-11). This form of re-entrant SVT responds less well to the usual medications (see following text). Flecainide and other medications may be efficacious in some patients, but others are refractory to medical management and will need to undergo ablation by a pediatric electrophysiologist.
Typically, the onset of re-entrant tachycardia is sudden. If the tachycardia converts to sinus rhythm (either spontaneously or in response to therapy), there is an abrupt cessation of tachycardia rather than a gradual slowing in heart rate. In infants, the heart rate is usually >250 beats per minute and is often about 300 beats per minute but can be as low as 150 beats per minute. Infants will generally tolerate these rapid heart rates initially, but after 36 to 72 hours, signs and symptoms of heart failure develop. Cardiac output becomes compromised in part because the decreased duration of diastole interferes with coronary arterial flow to the myocardium. Infants with SVT rarely present in cardiogenic shock.
Patients with accessory bypass pathways typically have structurally normal hearts. However, 8% to 25% have structural heart disease, most commonly Ebstein malformation of the tricuspid valve or levo- or corrected transposition of the great arteries.
The typical ECG shows a regular and narrow QRS tachycardia (Figure 10-12). P waves are often not visible. If visible, the P waves located just before the QRS complex are usually less prominent than normal and often are negative in leads II, III, and aVF (typical findings in PJRT). Retrograde P waves (seen within or just after the QRS complex) are also sometimes present (Figure 10-13). Sometimes, the first few beats of SVT are wide because of aberrant conduction, and then the QRS complex becomes narrow.
The most important differential diagnosis is sinus tachycardia. The maximal heart rate is usually <240 beats per minute in patients with sinus tachycardia. A normal P wave (upright in lead II) is suggestive of sinus tachycardia (Figure 10-6). Any patient with an increased heart rate should be evaluated for remediable causes of sinus tachycardia, such as fever, anemia, pain, sympathomimetic medications, and so on. Variability in the heart rate, such as during crying or blood drawing, is consistent with sinus tachycardia. Sometimes, administration of adenosine will transiently decrease the heart rate enough that sinus rhythm can be more easily identified. Other causes of narrow QRS tachycardia are discussed in the following text (Table 10-5).
The AV node is an essential part of the re-entry circuit in many patients with SVT, and thus therapy directed toward slowing conduction through the AV node is often effective in breaking the tachycardia. Even if the AV node is not involved, slowing conduction through the AV node may decrease the ventricular rate, thereby revealing the mechanism of the tachycardia. In either case, it is very important to record a rhythm strip during all attempts to terminate an episode of tachycardia.
Vagal maneuvers are the simplest, quickest, and safest way to terminate an episode of re-entrant tachycardia. For patients <12 months of age, application of ice slurry to the forehead induces strong vagal stimulation (diving reflex). Ice and water are put in a glove or washcloth that is placed over the patient’s forehead, eyes, and bridge of the nose. It is important not to cover the nose or mouth and not to press on the eyes. Contact between the ice slurry and upper face is maintained for 10 to 20 seconds. This may be repeated several times, but if this maneuver is performed correctly, it usually is effective on the first or second attempt. Repeated ice applications may cause skin damage in neonates, so care should be taken. Nasogastric stimulation or stimulation of a gag reflex may also be effective, but carotid massage is a much less effective vagal maneuver in young infants. Pressure should never be applied to the eyes because of the risk of retinal detachment.
Synchronized DC cardioversion is the treatment of choice for SVT in critically ill infants (very low or not measurable blood pressure, nonpalpable pulses, poor perfusion, and altered level of consciousness). The initial energy is 0.5 J/kg and should be delivered synchronized to the QRS complex. This may be increased to 1 to 2 J/kg if there is no response to the first attempt. If however, this higher discharge energy is not effective or tachycardia recurs immediately, DC cardioversion should not be repeated. Instead, pharmacologic therapy or overdrive pacing should be considered.
For infants in whom vagal maneuvers, adenosine, and/or cardioversion have resulted in only transient or no termination of the arrhythmia, drugs such as β-adrenergic blocking agents (eg, esmolol or propranolol), class I antiarrhythmic agents (eg, procainamide or flecainide), or class III agents (eg, sotalol or amiodarone) may be useful. Administration of intravenous verapamil is contraindicated in patients younger than 1 year of age (see following text).
Placing an electrode in the esophagus to record an atrial electrogram can be helpful in defining the precise mechanism of SVT and can also be used by a pediatric cardiologist to terminate SVT by overdrive pacing (pacing the atria at a rate somewhat higher than the rate of the SVT for a brief period of time). This method of terminating SVT can be very effective while waiting for plasma concentrations of antiarrhythmic medications to become high enough to prevent reinitiation of tachycardia and can be performed repetitively with low risk of adverse effect.
Prophylactic antiarrhythmic therapy is indicated for most infants with SVT because 20% to 30% will have more than one episode of SVT. Digoxin is commonly used in patients without evidence of pre-excitation. In adults and older children with WPW (SVT and pre-excitation), digoxin is contraindicated because it may increase conduction through the accessory pathway, thereby permitting a very rapid ventricular rate during atrial fibrillation. Although atrial fibrillation is rare in newborns, some cardiologists prefer to use β-adrenergic blocking agents, such as propranolol or atenolol, as initial therapy for newborns with pre-excitation. Some patients may require treatment with more than one agent. Administration of both digoxin and atenolol is very useful in patients who do not have pre-excitation. Patient refractory to therapy may be treated with sotalol, flecainide, or amiodarone. All of these agents have important toxicities (see following text).
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