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The pediatric electrocardiogram 2
The pediatric electrocardiogram 2
The pediatric electrocardiogram 2
The pediatric electrocardiogram 2
The pediatric electrocardiogram 2
The pediatric electrocardiogram 2
The pediatric electrocardiogram 2
The pediatric electrocardiogram 2
The pediatric electrocardiogram 2
The pediatric electrocardiogram 2
The pediatric electrocardiogram 2
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The pediatric electrocardiogram 2

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  • 1. Diagnostics The pediatric electrocardiogram Part II: Dysrhythmias Matthew O'Connor MDa , Nancy McDaniel MDb , William J. Brady MDc,⁎ a Department of Pediatrics, Children's Medical Center, University of Virginia Health System, Charlottesville, VA 22908, USA b Division of Cardiology, Department of Pediatrics, Children's Medical Center, University of Virginia Health System, Charlottesville, VA 22908, USA c Department of Emergency Medicine, University of Virginia Health System, Charlottesville, VA 22908, USA Received 27 July 2007; accepted 31 July 2007 Abstract The following article in this series will describe common arrhythmias seen in the pediatric population. Their definitions and clinical presentations along with electrocardiogram (ECG) examples will be presented. In addition, ECG changes seen in acute toxic ingestions commonly seen in children will be described, even if such ingestions do not produce arrhythmias per se. Disturbances of rhythm seen frequently in patients with unrepaired and corrected congenital heart disease will be more fully discussed in the third article of this series. Numerous classification schemes for arrhythmias exist; in this article arrhythmias will be grouped based upon their major ECG manifestations. © 2008 Elsevier Inc. All rights reserved. 1. Introduction The following article in this series will describe common arrhythmias seen in the pediatric population. Their defini- tions and clinical presentations along with ECG examples will be presented. In addition, ECG changes seen in acute toxic ingestions commonly seen in children will be described, even if such ingestions do not produce arrhyth- mias per se. Disturbances of rhythm seen frequently in patients with unrepaired and corrected congenital heart disease will be more fully discussed in the third article of this series. Numerous classification schemes for arrhythmias exist; in this article arrhythmias will be grouped based upon their major ECG manifestations. 2. Bradyarrhythmias Bradyarrhythmias are uncommon causes of ECG abnormalities in children without congenital heart disease; they are seen frequently in patients with congenital heart disease who have undergone surgical manipulation of the atria (eg, Fontan procedure, atrial septal defect repair, atrioventricular [AV] canal repair, and older “atrial switch” operations for transposition of the great arteries). Sinus bradycardia is defined by the presence of a sinus rhythm that is abnormal only in that it is slower than expected for the child's age (Fig. 1). Specific age-related norms were described in the previous article, but in general a heart rate less than 100 beats per minute (bpm) in children younger than 3 years old, less than 60 bpm in children 3 to 9 years old, less than 50 bpm in children 9 to 16 years old, and less than 40 in older children and adolescents should entertain the diagnosis of sinus bradycardia [1]. As in adults, several factors must be considered before making this ⁎ Corresponding author. E-mail address: wb4z@virginia.edu (W.J. Brady). www.elsevier.com/locate/ajem 0735-6757/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.ajem.2007.07.034 American Journal of Emergency Medicine (2008) 26, 348–358
  • 2. diagnosis, particularly with regard to sleeping vs the waking state and level of athletic training. Sinus arrest (also known as sinus pause) reflects the failure of the sinoatrial node to propagate impulses. If the period of arrest is prolonged, escape rhythms may “take over” the function of the sinoatrial, and these escape rhythms may occur at the AV nodal, bundle of His, or ventricular level. In children, the mean maximum duration of sinus pause (F2 SD) was found to be 1.82 seconds [2]. 3. Atrioventricular block The generic term AV block implies a disturbance of impulse conduction from the atria to the ventricles. The anatomic locations of such disturbances vary depending on the underlying mechanism of the arrhythmia. Generally, AV block is categorized into first-degree (1°), second-degree (2°), and third-degree (3°) subtypes. First-degree block (Fig. 2) is identified electrocardiographically by a prolonged Fig. 1 Sinus bradycardia in a child with hypothyroidism. The heart rate varies between 30 and 40 bpm. Fig. 2 First-degree AV block in a young boy undergoing Holter monitoring. Note the markedly prolonged PR interval. 349The pediatric ECG
  • 3. PR interval for age. The reader is referred to age-related pediatric norms as discussed in Part I and other age-related norms discussed in this article [3]. First-degree block is typically asymptomatic and generally does not imply underlying disease of the conduction system. It may be seen in the sleeping state [4], in trained athletes with low resting heart rates [5], and rarely in Lyme disease and myocarditis [6]. Second-degree AV block is divided into 2 categories: type I (Wenkebach), in which there is progressive prolongation of the PR interval until failure of AV conduction occurs (Fig. 3A), and type II (Möbitz), in which random “dropping” or failure of AV conduction occurs without PR prolongation (Fig. 3B). Of the two, type II block is more ominous and may progress to complete (3°) heart block. Type I 2° block is again a common variant of normal, particularly in trained athletes [5]. It is also common after repair of structural congenital heart disease [7]. The presence of Möbitz block or any symptomatic 2° block warrants pediatric cardiology consultation with consideration given to pacing. Complete or 3° heart block is defined by the absence of conduction between the atria and ventricles. Complete heart Fig. 3 A, Type I second-degree AV block from a Holter recording in a 7-year-old boy with congenital complete heart block. B, Type II second-degree AV block with wide QRS complex. Fig. 4 Third-degree AV block seen in the same patient as in Fig. 3A. Note that there is no relationship between P waves and QRS complexes. 350 M. O’Connor et al.
  • 4. block is manifested by AV dissociation in which regularly spaced P waves are not related temporally to the ventricular escape rhythm (Fig. 4). The QRS duration may be normal or prolonged depending on the location of the block; more proximal blocks (ie, near the AV node) will typically result in a normal QRS duration. Congenital complete heart block occurs in infants of mothers carrying anti-Ro and anti-La antibodies; mothers may or may not have clinical symptoms of lupus [8]. Complete heart block is also a known complication of surgery for congenital heart disease and has a significant effect on morbidity and mortality [9]. Complete heart block is almost always symptomatic and usually requires dual-chamber pacemaker implantation. The bundle branches are the downstream limbs of the bundle of His and allow for nearly synchronous depolariza- tion of the left and right ventricles, which is important in maintaining cardiac synchrony. Prolongation of conduction through the bundle branches results in QRS prolongation and is known as bundle branch block (BBB). Bundle branch block can affect the right or left bundle branches (RBBB, LBBB) and be classified as complete or incomplete, based upon whether there is QRS prolongation for age. Incomplete RBBB is commonly seen in pediatric ECGs and is manifested by an rSR′ pattern in lead V1 and a small S wave in lead V6; the initial upstroke of the QRS is normal with a delay in the terminal portion of the QRS complex (Fig. 5). Right bundle branch block is detected in V1; the Fig. 5 Incomplete RBBB in a 3-week-old male infant after tetralogy of Fallot repair. Note the rSR′ pattern in leads V1 and V2 with minimal QRS prolongation. Fig. 6 Complete RBBB in a 19-year-old adolescent girl with repaired tetralogy of Fallot. Note the similarity of the rSR′ pattern to the previous figure, with this ECG manifesting QRS prolongation. Fig. 7 Left bundle branch block. Note the prolonged QRS duration in the lateral precordial lead V5. 351The pediatric ECG
  • 5. initial upstroke of the QRS is delayed (Fig. 6) with the terminal portion of normal duration, whereas LBBB is typically manifested by QRS prolongation in V6 (Fig. 7). Bundle branch blocks may be seen in a variety of conditions and is a frequent finding after surgery for congenital heart disease, particularly in which there has been a ventriculot- omy (ie, tetralogy of Fallot) [10]. 4. Normal QRS duration tachycardias Numerous schemes exist for classifying tachycardias; a useful and simple way is to categorize them based upon the QRS duration. In general, tachycardias with a normal QRS duration for age can be considered as originating superior to the AV node, whereas tachycardias associated with QRS prolongation typically originate at locations inferior to the AV node. This scheme is not perfect but allows for ease of organization. Sinus tachycardia is usually simple to recognize on the ECG (Fig. 8). For the diagnosis of sinus tachycardia to be established, a P wave must precede every QRS complex and the P waves must have a normal axis (discussed previously). In adults, a heart rate greater than 100 bpm is considered tachycardia. In children, this rate is age dependent but general guidelines exist; heart rates greater than 160 bpm in infants and greater than 140 bpm in children suggest sinus tachycardia [11]. Sinus tachycardia often reflects anxiety, dehydration, or fever, and can be considered an “appropriate” physiologic response to the underlying disturbance. “Inap- propriate” sinus tachycardia implies underlying primary cardiac disturbance and is often seen in myocarditis or congestive heart failure. Although a wide range of heart rates may be seen in sinus tachycardia, the sinus node rarely paces at heart rates greater than 220 bpm; when greater heart rates are seen, sinus tachycardia is uncommon. Ectopic atrial tachycardias can be difficult to distinguish from so-called supraventricular tachycardias (SVTs; see below), particu- larly at high rates in which the P wave is “buried” within the T wave of the preceding QRS complex (Fig. 9). Atrial flutter and atrial fibrillation are quite rare in pediatric patients. However, a form of atrial flutter can be seen after surgery for congenital heart disease, particularly in patients with Fontan-type operations and atrial switch procedures for transposition of the great arteries [12]. Atrial flutter is identified by so-called sawtooth waves representing the rapid atrial rate with typically normal QRS duration. Atrial fibrillation demonstrates chaotic irregular atrial activity with an “irregularly irregular” ventricular rate; QRS is usually normal in duration (Fig. 10). Supraventricular tachycardia is one of the most common arrhythmias encountered in pediatric patients (Fig. 11). The term supraventricular tachycardia is confusing and does not imply a single mechanism, however. Supraventricular tachycardia includes any arrhythmia that requires atrial or AV nodal tissue for their initiation and propagation, and includes atrial tachycardias, atrial fibrillation, atrial flutter, nodal tachycardia, junctional ectopic tachycardia, and others [13] For the purposes of this discussion, SVT will be defined as a paroxysmal tachyarrhythmia manifested by the absence of P waves and by the presence of normal QRS complexes. In children, there are 2 common mechanisms of SVT [14]. Both involve reentry mechanisms. In AV nodal reentry tachycardia the reentry mechanism involves the AV node, and in AV reentry tachycardia reentry proceeds via an accessory pathway near, but not including, the AV node. Two mechanisms are often indistinguishable via ECG. Preexcita- tion syndromes are more common in children with AV reentry tachycardia and are discussed below. The treatment of SVT involves vagal maneuvers, adenosine, and in rare cases synchronized cardioversion and is discussed in further detail elsewhere [15]. Two additional SVTs occasionally encountered in pedia- trics include junctional ectopic tachycardia and permanent junctional reciprocating tachycardia (Fig. 12). Junctional ectopic tachycardia is a common and frequently hemodyna- mically deleterious rhythm seen in postoperative patients and is discussed in a subsequent article. Permanent junctional reciprocating tachycardia is a chronic, incessant form of tachycardia involving an accessory pathway that presents in infants and is electrocardiographically manifested by a Fig. 8 Sinus tachycardia detected on Holter monitoring of a 6-year-old girl with near syncope. The heart rate is regular at 157 bpm. 352 M. O’Connor et al.
  • 6. prolonged R-P interval [16]. It frequently causes a cardio- myopathy which responds to rate control, although achieve- ment of normal sinus rhythm can be extremely difficult. 5. Abnormal QRS duration tachycardias Tachycardias demonstrating prolonged QRS duration for age imply a ventricular origin to the arrhythmia. Ventricular arrhythmias also demonstrate “bizarre” QRS morphologies. Ventricular arrhythmias are uncommon in children and usually arise in the setting of severe electrolyte disarray, ingestion, or rare inherited disorders of cardiac conduction. Ventricular arrhythmias, however, are poorly tolerated hemodynamically so prompt recognition and initiation of therapy are vital. Premature ventricular contractions (PVCs) are a frequent finding in children and may be cause for concern in rare cases (Fig. 13). They are manifested on the ECG by bizarrely shaped, wide QRS complexes with the associated T wave usually pointing in the opposite direction of the QRS complex. A compensatory pause after the PVC will be seen. Premature ventricular contractions of uniform morphology are less concerning than those of multiple forms. Ventricular tachycardia consists of 3 or more successive PVCs at a regular rate of 120 to 180 bpm (Fig. 14). As in adults, it can degenerate into ventricular fibrillation, a usually lethal rhythm unless promptly treated. Several special conditions associated with ventricular tachycardia in children should be Fig. 10 Atrial flutter in a neonate without structural congenital heart disease. Note the rapid ventricular rate and distinctive flutter waves seen best in leads aVR and aVF. Fig. 9 Ectopic atrial tachycardia captured on Holter monitoring of a young girl. Note how the P waves are difficult to separate from the QRS complex owing to the high heart rate. 353The pediatric ECG
  • 7. mentioned. The Brugada syndrome is a rare, autosomal dominant, and frequently lethal disorder associated with bouts of ventricular tachycardia and sudden death. A peculiar “saddle-form” ST-segment elevation in the right precordial leads with a family history suggests the diagnosis [17]. Arrhythmogenic right ventricular dysplasia is another rare inherited disorder causing ventricular tachycardia and sudden death in affected individuals due to the replacement Fig. 12 Narrow complex tachycardia in an 8-month-old infant presenting with feeding difficulties, poor weight gain, and cardiomyopathy. Electrophysiologic study revealed the diagnosis of permanent junctional reciprocating tachycardia. Fig. 11 Supraventricular tachycardia in a 10-year-old boy with palpitations and a rapid heart rate. Note the regular rate, narrow QRS complex, and absence of P waves. The tachycardia resolved with intravenous adenosine. Final diagnosis was orthodromic reciprocating tachycardia due to an accessory pathway. 354 M. O’Connor et al.
  • 8. of right ventricular myocardium with fatty and fibrous tissue. Patients with this disorder typically present after puberty with ventricular tachycardia, and the interval ECG is notable for a persistent juvenile pattern of T-wave inversion and a widened QRS complex in right precordial leads. 6. Ventricular preexcitation syndromes The term preexcitation refers to ventricular depolarization that is earlier than expected. Preexcitation can occur via either a reentry pathway or an accessory pathway [18]. In either case, the potential for sustained and dangerous tachycardia exists because the AV node no longer “protects” the ventricles from excessively high atrial rates. The electrocardiographic appearance of preexcitation (Fig. 15) consists of (a) normal P-wave morphology and axis, (b) shortened PR interval, (c) prolonged QRS complex with initial “slurring” (delta wave), and (d) Q waves and T-wave abnormalities in what is termed a pseudoinfarction pattern. The most common syndrome associated with preexcitation in children and adults is the Wolff-Parkinson-White (WPW) syndrome. In patients with WPW, the most commonly encountered arrhythmia is a paroxysmal reentry SVT. Detection of the “WPW pattern” (ie, delta wave with a Fig. 14 Unprovoked ventricular tachycardia from Holter monitoring in a 13-year-old adolescent girl with syncope. Fig. 13 Multiple PVCs in a 17-year-old adolescent boy with a history of transposition of the great vessels after arterial switch procedure. Note the bizarre, wide QRS complexes interspersed with QRS complexes of normal configuration. 355The pediatric ECG
  • 9. prolonged QRS complex) in an asymptomatic child warrants cardiology referral, although the actual risk of sudden death in this population is likely quite low [19]. 7. Tachycardias associated with a prolonged QT interval Evaluation of the QT interval is an essential aspect of ECG interpretation. Norms for the corrected QT interval have been published and were discussed in the previous article of this series. Prolongation of the QT interval is often asymptomatic but puts the patient at risk of ventricular arrhythmias, the most common of which is torsades de pointes. Torsades de pointes is a form of polymorphic ventricular tachycardia that has the ECG appearance of “twisting along a string.” Prolongation of the QT interval can be due to a multitude of factors, congenital and acquired. QT prolongation is associated with hypokalemia and hypocalcemia; it is also seen with administration of antiarrhythmic agents. Many medications are associated Fig. 16 Prolonged QT interval in an 18-year-old adolescent girl with familial long QT syndrome and a history of cardiac arrest. The QT interval calculated by Bazett's formula is 506 milliseconds. Fig. 15 Delta waves seen in a child with WPW syndrome who presented with SVT; preexcitation did not manifest until the tachycardia resolved. 356 M. O’Connor et al.
  • 10. with QT prolongation as well, particularly antibiotics and older antipsychotics. Congenital forms of the long QT syndrome warrant discussion in pediatric patients. Congenital long QT syndrome is a cause of pediatric sudden death and has been associated with sudden death during sleep, exercise, and perhaps a small subset of infants dying of sudden infant death syndrome [20]. The 2 most common inherited long QT syndromes are known eponymously as the Romano-Ward and Jervell/Lange-Nielsen syndromes and are caused by known mutations in cardiac ion channels. Congenital long QT syndrome is a common cause of sudden death attributable to cardiac causes in children; in an international registry of long QT patients, 8% died suddenly during 5 years of follow-up [21]. Certainly, identification of a prolonged QT interval in a pediatric patient warrants pediatric cardiology referral and close follow-up (Fig. 16). 8. Toxicology Children frequently present to EDs after ingestion of medications or other toxins, unintentionally or otherwise. Obtaining an ECG is an important aspect of evaluating these patients. A number of agents cause QRS prolongation, mainly via blockade of the sodium channels responsible for depolarization during phase 0 of the myocardial action potential. Examples of such agents include tricyclic antidepressants, diphenhydramine, propanolol, hydroxy- chloroquine, and many antiarrhythmic agents [22]. QRS prolongation in the setting of sodium channel blockade, when severe, may lead to asystole unless therapy with saline or sodium bicarbonate is administered. Tricyclic antidepressant ingestion warrants special attention owing to the multitude of effects on the ECG [23]. The ECG presentation of such toxicity is dependent on the specific medication ingested as well as the ingested dose. Tricyclic antidepressants have 4 important effects: (1) inhibition of presynaptic neurotransmitter reuptake; (2) α-adrenergic receptor blockade; (3) anticholinergic effects; and (4) sodium channel blockade. Collectively, these can lead to tachycardia, QRS prolongation, and QT prolonga- tion (Fig. 17). β-Blockers and calcium-channel blockers are commonly used medications in adults that not infrequently are unintentionally ingested by children. β-Blockers are phar- macologically heterogeneous with each agent exerting single or multiple effects at β1, β2, and α1 receptors. Some β-blockers contain sodium-channel blocking ability and may prolong the QRS interval. Sotalol, a class III antiarrhythmic agent, contains potassium channel blocking ability and can cause QT interval prolongation [24]. β1 Receptors, however, located in the myocardium, are largely responsible for the cardiovascular sequelae of β-blocker overdose. Electrocar- diogram manifestations of ingestion generally include bradycardia, various grades of AV block, and QRS complex widening. [25]. Calcium channel blockers cause predictable but non- specific changes in the ECG. Common changes include hypotension, bradycardia, and AV blocks [26]. Because many current formulations of calcium channel blockers are of the extended-release variety, symptoms may be delayed for up to several hours postingestion [27]. Another consideration in evaluating calcium channel overdose is the cardioselectivity of the agent. Older agents such as nifedipine may exert a predominantly vascular effect at lower doses, resulting in hypotension with reflex bradycardia. Newer Fig. 17 Sinus tachycardia with widened QRS complex, deep S wave in lead I, and prominent R wave in lead aVr. This ECG was recorded in a lethargic adolescent with tricyclic antidepressant ingestion. 357The pediatric ECG
  • 11. agents such as verapamil or diltiazem may result in bradycardia and conduction disturbances without hypoten- sion. At sufficient doses, however, selectivity is lost. In summary, arrhythmias in otherwise healthy children are relatively uncommon in the pediatric population but prompt recognition will prevent excess morbidity and mortality. The incidence of arrhythmias in patients with a history of congenital heart disease is markedly higher and the ECG manifestations of such arrhythmias in this patient population will be described in the next article of this series. References [1] Martin AB, Kugler JD. Sinus node dysfunction. In: Gillette PC, Garson Jr A, editors. Clinical pediatric arrhythmias. Philadelphia: W.B. Saunders; 1999. p. 51-62. [2] Southall DP, Richards J, Mitchell P, et al. Study of cardiac rhythm in healthy newborn infants. Br Heart J 1980;43:14-20. [3] Davignon A, Rautaharju P, Boiseelle E, et al. Normal ECG standards for infants and children. Pediatr Cardiol 1979;1:123-52. [4] Nagashima M, Matsushima M, Ogawa A, et al. Cardiac arrhythmias in healthy children revealed by 24-hour ambulatory ECG monitoring. Pediatr Cardiol 1987;8:103-8. [5] Viitasalo MT, Kala R, Eisalo A. Ambulatory electrocardiographic findings in young athletes between 14 and 16 years of age. Eur Heart J 1984;5:2-6. [6] Chan TC, Brady WJ, Pollack M. Electrocardiographic manifestations: acute myopericarditis. J Emerg Med 1999;17:865-72. [7] Ross BA, Gillette PC. Atrioventricular block and bundle branch block. In: Gillette PC, Garson Jr A, editors. Clinical pediatric arrhythmias. Philadelphia: W.B. Saunders; 1999. p. 63-77. [8] Brucato A, Franceschini F, Gasparini M, et al. Isolated congenital complete heart block: longterm outcome of mothers, maternal antibody specificity and immunogenetic background. J Rheumatol 1995;22: 533-40. [9] Weindling SN, Saul JP, Gamble WJ, et al. Duration of complete atrioventricular block after congenital heart disease surgery. Am J Cardiol 1998;82:525-7. [10] Gelband H, Walso AL, Kaiser GA, et al. Etiology of right bundle- branch block in patients undergoing total correction of tetralogy of Fallot. Circulation 1971;44:1022-33. [11] Park MK, Gunteroth WG. How to read pediatric ECGs. St. Louis: Mosby; 1992. p. 110-30. [12] Ghai A, Harris L, Harrison DA, et al. Outcomes of late atrial tachyarrhythmias in adults after the Fontan operation. J Am Coll Cardiol 2001;37:585-92. [13] Fish FA, Benson Jr DW. Disorders of cardiac rhythm and conduction. In: Allen HD, Gutgesell HP, Clark EB, et al, editors. Heart disease in infants, children, and adolescents, including the fetus and young adult. Philadelphia: Lippincott Williams & Wilkins; 2001. p. 482-533. [14] Van Hare GF. Supraventricular tachycardia. In: Gillette PC, Garson Jr A, editors. Clinical pediatric arrhythmias. Philadelphia: W.B. Saun- ders; 1999. p. 97-120. [15] Chun TU, Van Hare GF. Advances in the approach to treatment of supraventricular tachycardia in the pediatric population. Curr Cardiol Rep 2004;6:322-6. [16] Vaksmann G, D'Hoinne C, Lucet V, et al. Permanent junctional reciprocating tachycardia in children: a multicentre study on clinical profile and outcome. Heart 2006;92:101-4. [17] Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the second consensus conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. Circulation 2005;111:659-70. [18] Lindbergh JR, Brady WJ. Preexcitation syndromes. In: Chan TC, Brady WJ, Harrigan RA, et al, editors. ECG in emergency medicine and acute care. Philadelphia: Elsevier/Mosby; 2005. p. 112-7. [19] Sarubbi B, Scognamiglio G, Limongelli G, et al. Asymptomatic ventricular pre-excitation in children and adolescents: a 15 year follow up study. Heart 2003;89:215-7. [20] Schwartz PJ, Stramba-Badiale M, Segantini A, et al. Prolongation of the QT interval and the sudden infant death syndrome. N Engl J Med 1998;338:1709-14. [21] Garson Jr A, Dick M, Fournier A, et al. The long QT syndrome in children: an international study of 287 patients. Circulation 1993;87: 1866-72. [22] Holstege CP, Baer AB. Other preexcitation syndromes. In: Chan TC, Brady WJ, Harrigan RA, et al, editors. ECG in emergency medicine and acute care. Philadelphia: Elsevier/Mosby; 2005. p. 274-8. [23] Harrigan RA, Brady WJ. ECG abnormalities in tricyclic antidepressant ingestion. Am J Emerg Med 1999;17:387-93. [24] Link MS, Foote CB, Sloan SB, et al. Torsade de pointes and prolonged QT interval from surreptitious use of sotalol: use of drug levels in diagnosis. Chest 1997;112:556-7. [25] Barry JD, Williams SR. Beta-adrenergic blocking agents. In: Chan TC, Brady WJ, Harrigan RA, et al, editors. ECG in emergency medicine and acute care. Philadelphia: Elsevier/Mosby; 2005. p. 260-2. [26] Offerman SR, Ly BT. Calcium channel antagonists. 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