Conversion of Paroxysmal Supraventricular Tachycardia in a Child With a Slow Verapamil Infusion: Case Report and Literature Review GARY P. YOUNG, MD, ANTHONY The investigators present the case of a lbmonth-old female with Down’s syndrome and an endocardial cushion defect who presented acutely ill in paroxysmal supraventrlcular tachycardla (PSYY). Unsuccessful vagal maneuvers were followed by a slow intravenous infusion of verapamll, during which the rhythm converted. The discussion which follows highlights the many issues to be addressed in the acute management of pediatric PSVT including the varied presentations, underlying etiologies, differential diagnosis, electrocardiographic findings, electrophyslologic mechanisms, and prognosis. The literature review concludes with a discussion of the many different therapies available for pediatric PSVT including vagal maneuvers, cardioversion, overdrive pacing, and pharmacologic therapies. In particular, the relative merits of verapamil and adenoslne are discussed. (Am J Emerg Med 1991;9:603-608. Copyright 0 1991 by W.B. Saunders Company)

Paroxysmal supraventricular tachycardia (PSVT) is the most frequently encountered sustained arrhythmia in infants and children.‘,’ In pediatric patients, PSVT usually presents initially during infancy;3 PSVT has even been documented in utero.4 The diagnosis of PSVT may be difficult because of a nonspecific or an unstable presentation in an infant or child. There are many therapeutic options in the management of pediatric PSVT, dependent upon the condition of the child and other underlying conditions which may have precipitated the episode of PSVT.’ We present the case of an infant with Down’s syndrome and congenital heart disease (CHD) who presented with nonspecific symptoms secondary to PSVT. Because the child was relatively stable, different therapeutic options were available to her physicians in the emergency department (ED). This case highlights many of the issues that an emergency physician must address in the evaluation and management of infants and children in PSVT. CASE REPORT A 12-month-old female was brought to the ED by her mother for the chief complaint of coughing and vomiting. She had a history of Down’s syndrome associated with an endocardial cushion repair. Hours prior to presentation she began to vomit and not tolerate feedings; then she became irritable and inconsolable. There was no From the Emergency Medicine Service, Portland Veterans Affairs Medical Center, Oregon Health Sciences University, Portland, OR; and the *Department of Emergency Medicine, Calgary General Hospital, University of Calgary, Alberta, Canada. Manuscript received April 18, 1991; accepted May 29, 1991. Address reprint requests to Dr Young, Emergency Medicine Service, Portland Veterans Affairs Medical Center, PO Box 10341 lC4, Portland, OR 97207. Key Words: Paroxysmal supraventricular tachycardia, pediatric cardiac arrhythmias, verapamil, adenosine. Copyright 0 1991 by W.B. Saunders Company 07358757/91/0908-0019$5.00/O

S. TAYLOR,

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history of fever, but there was contact with a case of gastroenteritis 1 week prior. Her medications were furosemide 7 mg orally every other day and digoxin 0.035 mg orally twice a day. On initial presentation, she was very irritable and ill in appearance with an ashen color. Her vital signs were pulse 2201min and respirations 48/min. She vomited upon arrival and her heart rate decreased to 120-130/min. Her color improved. The physical examination revealed no focus of infection. Lungs were clear. Cardiac auscultation during the heart rate of 120/min revealed a 3/6 harsh pansystolic murmur over the precordium. Abdominal palpation revealed a liver edge 2.5 cm below the costal margin. During an intravenous access attempt and blood draw, the patient went back into a rapid tachycardia of 220/min. She became pale and clammy. The electrocardiogram (ECG) revealed a wider QRS complex (0.09 set; Fig l), suggestive of an incomplete right bundle branch block pattern. However, a diagnosis of SVT was made based upon the fact that the QRS complex was morphologically similar to when the patient was in normal sinus rhythm. Vagal maneuvers (gag and diving reflex) failed. Pediatric intensivists were consulted for possible cardioversion. A verapamil infusion was elected. Intravenous verapamil (0.1 mg/kg in 20 mL of normal saline) was started slowly until the SVT converted after a total of 0.3 mg over 3 minutes. A repeat ECG revealed a narrower QRS (0.06 set) with similar morphology (Fig 2). There was no recurrence of the SVT. Propran0101maintenance therapy was initiated at 0.5 mg orally twice a day. The diagnostic workup was negative, including a digoxin level of 1.5 ng/mL.

DISCUSSION Campbell and associates found PSVT to be the cause of tachyarrhythmia in 94 of 101 children without associated CHD; the other seven children had ventricular tachycardia (VT).6 Half of infantile PSVT is idiopathic (Table l), 20% is related to CHD, and 10% is associated with pre-excitation syndromes, such as the Wolff-Parkinson-White syndrome (WPW). 7,8 Importantly, 20% of cases are related to underlying conditions (eg, infection, fever, volume depletion, electrolyte or acid-base disturbance, and medication or drug effect).5 The most common symptoms at the time of presentation are nonspecific, including upper respiratory tract infection, fussiness and irritability, feeding difftculties, vomiting, pallor, lethargy, and failure to thrive. However, tachypnea, hypotension, syncope, and cyanosis can occur. In the differential diagnosis, the emergency physician must consider the possibility of VT (see below), sepsis and congestive heart failure (CHF), or problems caused by any underlying condition responsible for setting off the PSVT. Febrile infants may have sinus tachycardia rates up to 220/min, and acutely ill preadolescent children may have sinus tachycardia rates up to 200/min.9 In infantile PSVT, the heart rate ranges from 220 to 320/min; in l- to 603

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FIGURE 1.

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2-year olds, 180 to 300/min, and in older children, 150 to 250/min.‘~376~8A narrow QRS width is a consistent finding on the ECG in cases of pediatric PSVT; SVT with aberration occurs in only 2% of children with PSVT.9 Thus, in writing about medicolegal cases involving children with PSVT, Garson states that VT should be the presumptive diagnosis when the QRS width “. . . is at the upper limits of normal duration for age (certainly greater than 0.09 seconds at any age) and if the QRS morphology is different from the QRS that had been present in sinus rhythm. ‘19In children, as in adults, there is a significant risk to the patient associated with the use of antiarrhythmic agents which are usually effective for PSVT (eg, digitalis or verapamil) when these agents are administered to patients in VT.9 As in adults, re-entrant circuits are the most common electrophysiologic mechanisms responsible for pediatric PSVT.’ Nevertheless, the mechanisms underlying pediatric PSVT are more varied than in adults, especially with regard to the increased frequency of ectopic rhythms (enhanced automaticity). 7,10-12The re-entrant circuits involve both the atrioventricular nodal re-entry (AVNR) and accessory pathways (eg, WPW).” The ectopic foci are either atrial (atrial ectopic tachycardia [AET]) in approximately 10% of cases” or junctional (junctional ectopic tachycardia [JET]) in an additional S%.‘* Gillette and Garson studied the electrophysiologic and pharmacologic characteristics of AET and JET.“*‘* They found that the surface ECG revealed atrial P waves in AET (as opposed to AVNR rhythms) and a narrow QRS tachy-

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cardia with evidence of AV dissociation. Nevertheless, Gillette stresses that the ECG is not reliable in differentiating AET and JET from AVNR.’ This is important therapeutically because only AVNR reliably responds to verapamil and because there is an increased risk of adverse responses to the administration of verapamil in patients with AET and JET (see below). In children, as in adults, there is also a risk to the patient associated with the use of digitalis or verapamil for PSVT secondary to the WPW syndrome.‘3 In contradistinction to the course of the great majority of adults with PSVT, pediatric PSVT is not a benign cardiac arrhythmia. In different series, the mortality from pediatric PSVT has ranged from 2% to 11%,‘.2*6-8related to complications of therapy, CHF, or associated underlying conditions. The presence and severity of associated CHF is related to the duration of the episode of PSVT, the heart rate, and underlying congenital cardiac anomalies. The different therapies available for the conversion of pediatric PSVT include interventions such as vagal maneuvers,‘T9 application of military antishock trousers, l4 synchronized electrical cardioversion,” and transvenous’6 or transesophageal” atria1 overdrive pacing. Pharmacologic therapies which have been used successfully include digitalis,’ a-adrenergic agents,’ l3 blockers,” calcium-channel blockers,‘8‘26 and, most recently, adenosine (Table 2).27-29 Prior to admission of the hemodynamically unstable infant or young child to a neonatal or pediatric intensive care unit, ED treatment will be necessary to convert PSVT (assuming

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that the proper diagnosis is not VT). If time allows, the emergency physician may be able to secondarily treat the PSVT by primarily treating the underlying condition responsible for the arrhythmia (see above). In the sickest patients (ie, shock, acidosis, pulmonary edema), immediate synchronized DC cardioversion with 051.0 J/kg may be necessary (less than the l-2 J/kg dose reserved for ventricular arrhythmias).9*‘4 Some investigators’ also recommend cardioversion be used in neonates and very young infants because they are less responsive to other therapies or more prone to adverse responses to drug administration. Furthermore, they are often more unstable than the clinical picture would indicate to the unsuspecting clinician (eg, displaying only tachypnea or hepatomegaly as signs of CHF).9 If the patient received intravenous digitalis or is chronically digitalized, then Garson’ recommends the administration of 1 mg/kg of intravenous lidocaine immediately before cardioversion. Other investigators’ recommend pretreatment with phenytoin (10-E mg/kg intravenously over 20-30 minutes), if time permits. Another more invasive procedure for an unstable patient would be transvenous’” or transesophageal” overdrive atrial pacing. The goal of atrial pacing is to produce a slower ventricular rate with a 2:l atrioventricular block in order to improve perfusion. In stable patients with few symptoms, there is more time to apply vagal maneuvers or administer antiarrhythmic agents. Although increasing vagal tone via simple Valsalva maneuvers (ie, pressing on an infant’s abdomen, carotid si-

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nus massage, or gagging) are relatively simple and safe, they are often unsuccessful in children, particularly those younger than 4 years of age. In this age group, pressing on the eyeballs to increase vagal tone is contraindicated. The

TABLE 1. Characteristics of Paroxysmal Tachycardia in Infants and Children

Supraventricular

Etiology (Infants) Idiopathic (50%) Congenital heart disease (20%) Pre-excitation (10%) Secondary to acute illness (20%) (eg, infection, dehydration, medication) Presenting symptoms and signs Symptoms: viral illness, irritability, lethargy, feeding difficulties, failure to thrive, congestive heart failure, syncope Signs: none or tachypnea, hypotension, cyanosis, rales, murmur, hepatomegaly, lethargy, irritability Heart rates Infants: 220-320/min 1-2 years old: 180-300/min Older children: 150-250/min Electrophysiology Atrioventricular nodal re-entry (75%) Accessory pathways (10%) Atrial ectopic tachycardia (10%) Junctional ectopic tachycardia (5%)

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TABLE 2. Recommended Therapies Available Paroxysmal Supraventricular Tachycardia

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Vagal maneuvers: abdominal pressure, carotid sinus massage, gagging, diving reflex (ie, cold wet washcloth or ice bag to face) Electrical cardioversion: 0.5-l J/kg synchronized Digitalis: 0.01 mg/kg intravenously over 5 minutes, then 0.005 mg/kg intravenously every 6 hours for 2 doses Cautions: WPW, VT, cardioversion delayed Verapamil: 0.1 mg/kg intravenously over 1 minute (consider slow infusion at a rate of 0.1 mg/min) Cautions: WPW, VT, f3 blockers, CHF, sinus node disease, hypotension, and under 6-12 mo old Adenosine: 0.0375-0.05 mgikg (37.5-50 pgikg) IVP, repeat incremental doses every 2 minutes to maximum dose of 0.25-0.375 mglkg Cautions: short duration of action or adverse effects of bradycardia, heart block, asystole, atrial fibrillation or flutter, PVCs WPW, Wolff-Parkinson-White syndrome; VT, tachycardia; CHF, congestive heart failure; IVP, inpush; PVCs, premature ventricular contractions.

ABBREVIATIONS:

ventricular travenous

vagal maneuver is to elicit the diving reflex (eg, in an infant, by placing a cold wet washcloth or an ice bag on the face for 15-30 seconds). In patients with moderate hypotension, increasing the blood pressure with an u-adrenergic agent (ie, phenylephrine 0.01 mg/kg intravenously) may increase vagal tone by stimulating baroreceptors. However, in children younger than 18 months old, (Yagents are not effective and they may result in hypertension or worsening heart failure. If vagal maneuvers fail to convert the stable infant in PSVT, Garson’ next recommends the administration of 0.01 mg/kg digitalis intravenously over 5 minutes; conversion of the SVT will usually not occur for at least 2 hours, or even until half-doses are administered at 6 and 12 hours later. Digitalis is the traditional antiarrhythmic for infants and children in PSVT; presently, it is reserved for stable non-lifethreatening episodes. The major drawback with using digoxin is that it may take up to 10 hours before the PSVT converts. Digoxin is potentially hazardous in patients with WPW, especially if they are in atria1 fibrillation, in which case conduction through accessory AV pathways may be increased. Following the administration of intravenous digitalis, WPW patients in atria1 fibrillation may progress to ventricular fibrillation. Digoxin is not likely to be of value in VT patients who may also progress to ventricular fibrillation. The traditional B-blocking agent has been propranolol at an intravenous dose of 0.1 mg/kg; it also prolongs AV nodal conduction and it can be administered to patients unresponsive to digitalis. However, both bradycardia and hypotension may result. For this reason, the newer rapid acting, short duration parenteral B-blocking agent esmolol may be preferred; the recommended dose range is 500 pgikg over 1 minute, followed by a 4-minute infusion, usually starting with 50 &kg/min, increasing by 50 pg/kg/min every 5 minutes up to 200 Fg/kg/min. 3o However, a literature search failed to find any published reports of the use of esmolol in pediatric PSVT. recommended

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The availability of newer antiarrhythmic agents has increased the success, speed, and safety with which PSVT is converted in infants and children. The calcium-channel blocking agent verapamil at an initial intravenous dose of 0.1 mg/kg has replaced digitalis and propranolol as an effective, rapid, and relatively safe antiarrhythmic for PSVT.‘8-2” Initial case series were supportive of the use of verapamil in children. Pediatric cardiologists extrapolated its efficacy and safety from the adult population to younger patients. In comparison with digitalis, verapamil has a faster onset of action (minutes): however, it shares the same caveats concerning contraindications to its use in most patients with WPW and in all VT patients. In comparison with B-blocker therapy. verapamil is more specific in its effect upon AV nodal conduction of the rapid PSVT cycles; however, it shares similar problems as do B blockers with regard to potential for bradyarrhythmias and cardiac depression. The initial consensus from the pediatric literature was that as long as the patient was not on B-blocker therapy, verapamil was safe, rapid, and effective.‘8-‘h However, there have since been many case reports of decompensation following the use of verapamil in infants with PSVT.‘,3’-33 Most of these cases involved infants less than or very close to 6 months of age. Epstein et a13’ described three infants with PSVT and CHF treated with verapamil. Each of the infants demonstrated hemodynamic decompensation with cardiovascular collapse and respiratory arrest requiring aggressive resuscitative measures; none of the three infants died. Radford3* described two infants with PSVT and poor peripheral perfusion who were treated with verapamil 0.1 mg/kg intravenous push over 30 seconds. Both infants initially converted to sinus rhythm before becoming very bradycardic and hypotensive requiring aggressive resuscitation. A mottled 4-month old in PSVT with an unobtainable blood pressure developed cardiovascular collapse after receiving verapamilO.1 mg/kg intravenously; autopsy showed myocarditis. Kirk et a133reported cardiovascular collapse following intravenous verapamil in five infants between 2 and 4 weeks of age. Although recommending it as the pediatric drug of choice for PSVT, Porter and colleagues*’ suggested that verapamil may not work in children younger than 6 months of age. They also recommended against the use of verapamil in the presence of any potential contraindications (ie, P-blocker therapy, sinus node disease, CHF, hypotension). In particular, Garson’ does not use verapamil in infants younger than 1 year of age. Other investigators34 recommend against using verapamil in children under 2 years of age. What are the reasons for the increased risk of complications from verapamil in children? Epstein and co-workers3i explained that the infant’s autonomic nervous system is immature. Cardiac output is more dependent upon heart rate than on stroke volume. Hence, the immature myocardium is unable to increase its stroke volume by increasing catecholamine output in response to the negative inotropic effects of verapamil. Extrapolating from experimental data collected in the immature animal model,35 an alternative explanation is an increased sensitivity to the direct cardiac depressant effect of verapamil. Acidosis and hypoxemia may contribute to this inability to compensate for the negative inotropic, chronotropic, dromotropic, and vasodilatory effects of verapamil.

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A safer method of administering verapamil may be suggested by our own case report in which an infusion rather than a bolus was administered to a 12-month old in PSVT. At present there are no published case series to suggest when or how verapamil infusions should be administered. We recommend that the same dose of verapamil be administered (0.1 mg/kg intravenously), but not as a conventional intravenous push over 30 seconds. Instead, we place that amount of verapamil (0.1 mg/kg) in 20 ml of normal saline and slowly administer the full dose at a rate of 0.1 mg/min until the PSVT terminates. A different technique using pretreatment with intravenous calcium prior to the administration of verapamil has been described in adults;36.37 the result has been a decrease in the incidence and severity of hypotension associated with the use of verapamil without compromising its antiarrhythmic efficacy. Adenosine, a purine nucleoside, has been approved by the Food and Drug Administration for the conversion of PSVT. Like verapamil, adenosine slows AV nodal conduction to terminate re-entrant SVT involving the AV node (whether or not the re-entrant circuit also involves a bypass pathway) or to transiently slow down supraventricular tachyarrhythmias crossing the AV node. The mechanism of action of adenosine accounts for its lack of efficacy in converting pediatric patients with ectopic foci underlying their tachycardia (eg, AET or JET).” In the reported series of the use of adenosine in pediatric patients with PSVT,28-30 an average initial dose of 0.0375-0.05 mg/kg (37.5-50 kg/kg) was administered as an intravenous bolus. If cardioversion did not occur, repeat intravenous bolus doses (with the doses increased in increments equivalent to the initial dose) were administered as often as every 2 minutes until an effect was seen (range of effective doses, 0.0375-0.375 mg/kg)29 or a maximum dose of 0.25 mg/kg was reached (range of effective doses, 0.025-0.25 mg/kg intravenously). 3o Adenosine has a success rate similar to that of verapamil (90%) in adults in PSVT secondary to AVNR or WPW, but adenosine is successful in some patients who are unresponsive to verapamil and it is safer in hemodynamically compromised patients. Adenosine has the following advantages over verapamil: (1) a lack of significant negative hemodynamic effects; (2) a lack of interactions with other cardiac drugs (ie, verapamil and digitalis or p blockers); (3) it is safe when administered to patients with widecomplex tachycardias (it may be helpful diagnostically in distinguishing VT from SVT with aberrancy); and (4) because it is metabolized by circulating adenosine deaminases with rapid transport into cells, adenosine has a very short half-life of 5-15 seconds. Thus, when successful, adenosine terminates PSVT in less than 20 seconds; even if conversion is not successful, the resultant transient increase in AV block may facilitate the diagnosis of the arrhythmia’s mechanism. Till et al29 reported that 90 of 117 episodes of PSVT in infants and children were terminated. However, the short effect of adenosine resulted in ‘Ye-initiation” of the PSVT within 5 seconds in 13 of these 90 initially terminated episodes. Overholt et a12’ reported that all 25 of their infants and children either had termination of the PSVT or transient increased AV block. Six of their 25 infants and children experienced side effects, usually minor and always short-lived. However, one of their patients with diffuse cardiac conduction disease developed prolonged sinus bradycardia which

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required temporary pacing. The reported adverse effects associated with the administration of adenosine include atria1 flutter and atrial fibrillation, premature ventricular contractions (PVCs) and transient asystole prior to conversion of PSVT, and transient bradycardia and heart block after conversion of PSVT. Adenosine has a weak bronchoconstrictor effect when inhaled; this has not been seen following intravenous infusion. Concurrent treatment with dipyridamole potentiates the effect of adenosine, whereas theophylline is a known adenosine antagonist. Because of its obvious advantages as compared with verapamil, adenosine has been recommended for safe administration in unstable and stable pediatric patients in PSVT. 28-3oHowever advantageous the use of adenosine for PSVT may appear, the clinical experience with its use is still limited, especially in pediatric patients. CONCLUSION The emergency treatment for the infant or child in PSVT must be individualized, especially because there is not one appropriate response to each clinical situation. In neonates (less than 1 month of age), most investigators seem to agree that cardioversion is the treatment of choice. In hemodynamically unstable infants or those with signs of severe CHF or pulmonary edema, cardioversion is also preferred. In infants and children with mild CHF, digoxin has been the traditional choice, and verapamil has recently become a controversial choice because of its negative hemodynamic effects. But verapamil should not be administered to those under 6 months to 1 year of age, and perhaps it should be reserved for stable infants and children in whom adenosine has failed. In stable children, either digoxin, verapamil, or adenosine might be appropriate. Although its use in pediatric patients is limited at this time, adenosine appears to have many advantages and few disadvantages to its use for pediatric PSVT. The authors would like to thank the contribution bourne, MD, for reviewing the case report.

of John Ash-

REFERENCES 1. Nadas AS, Daeschner CW, Roth A, et al: Paroxysmal tachycardia in infants and children. Pediatrics 1952;9:167-181 2. Langendorf R, Pick A: Cardiac arrhythmias in infants and children. Pediatr Clin North Am 1954;1:215-234 3. Gaum WE, Kaplan S: Supraventricular tachycardia in infancy. Am J Cardiol 1984;54:664-665 4. Newburger J, Keane J: Intrauterine supraventricular tachvcardia. J Pediatr 1979:95:780-783 5: Binder LS, Boeche d, Atkinson D: Evaluation and management of supraventricular tachycardia in children. Ann Emerg Med 1991;20:51-54 6. Campbell RM, Dick M, Rosenthal A: Cardiac arrhythmias in children. Ann Rev Med 1984:35:397-410 7. Gillette PC: The mechanism of supraventricular tachycardia in children. Circulation 1976;54:133-139 6. Garson A, Gillette PC, McNamara DG: Supraventricular tachycardia in children-Clinical features, response to treatment, and long-term follow-up in 217 patients. J Pediatr 1981;98:875-882 9. Garson A: Medicolegal problems in the management of cardiac arrhythmias in children. Pediatrics 1987;79:84-88 10. Gillette PC, Garson A, Kugler JD: Wolff-Parkinson-White syndrome in children-Electrophysiologic and pharmacologic characteristics. Circulation 1979;60:1487-1496 11. Gillette PC, Garson A: Electrophysiologic and pharmaco-

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logic characteristics of automatic ectopic atrial tachycardia. Circulation 1977;56:571-579 12. Garson A, Gillette PC: Junctional ectopic tachycardia in children-Electrocardiography, electrophysiology, and pharmacologic response. Am J Cardiol 1979;44:289-298 13. Gulamhusein S, Patrick K, Klein GJ: Ventricular fibrillation following verapamil in the Wolff-Parkinson-White syndrome. Am Heart J i983;106:145-147 14. Walker LA. MacMath TL. Chioman H. et al: MAST aoolication in the treatment of paroxysmal’supraventricular tachydardia in a child. Ann Emerg Med 1988;17:529-531 15. Gutgesell HP, Taker WA, Geddes LA, et al: Energy dose for ventricular defibrillation of children. Pediatrics 1976;58:898-904 16. Gillette PC, Shannon C, Blair H, et al: Transvenous pacing in pediatric patients. Am Heart J 1983;105:843-847 17. Dick M, Scott WA, Serwer GS, et al: Acute termination of supraventricular tachycardia in children by transesophageal atrial pacing. Am J Cardiol 1988;61:925-927 18. Silberbach M, Dunningham A, Benson DW: Effect of intravenous propranolol or verapamil in infant orthodromic reciprocating tachycardia. Am J Cardiol 1989;63:438-441 19. Greco R, Musto B, Arienzo V, et al: Treatment of paroxysmal supraventricular tachycardia in infancy with digitalis, adenosineQ’-triphosphate and verapamil-A comparative study. Circulation 1982;66:504-508 20. Porter CJ, Gillette PC, Garson A, et al: Effects of verapamil on supraventricular tachycardia in children. Am J Cardiol 1981;48:487-491 21. Porter CJ, Garson A, Gillette PC: Verapamil-An effective calcium blocking agent for pediatric patients. Pediatrics 1983; 711748-755 22. Sapire DW, Mongkolsmai C, O’Riordan AC: Control of chronic ectopic supraventricular tachycardia with verapamil. J Pediatr 1979;94:312-314 23. Sapire DW, O’Riordan AC, Black AFS: Safety and efficacy of short and long term verapamil therapy in children with tachycardia. Am J Cardiol 1981;48:1091-1096 24. Shahar E, Barzilay Z, Frand M: Verapamil in the treatment

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of paroxysmal supraventricular tachycardia in infants and children. J Pediatr 1981;98:323-326 25. Shakibi JG, Aryanpun I: Electrophysiologic effects of verapamil in children. JpnHeart J 1979;20:789-861 26. Soler-Soler J. Saarista-Savieda J. Cabrera A, et al: Effect of verapamil in infants with paroxysmal supraventricular tachycardia. Circulation 1979;59:876-879 27. Clarke B, Rowland E, Barnes PJ et al: Rapid and safe termination of supraventricular tachycardia in children by adenosine. Lancet 1987;1:299-301 28. Overholt ED, Rheuban KS, Gutgesell HP, et al: Usefulness of adenosine for arrhythmias in infants and children. Am J Cardiol 1988;61:336-340 29. Till J, Shinebourne EA, Rigby ML, et al: Efficacy and safety of adenosine in the treatment of supraventricular tachycardia in infants and children. Br Heart J 1989;62:204-211 30. Esmolol-A short-acting IV beta-blocker. Med Lett Drugs Ther 1987;29:57-58 31. Epstein ML, Kiel EA, Victorica BE: Cardiac decompensation following verapamil therapy in infants with supraventricular tachycardia. Pediatrics 1985;75:737-740 32. Radford D: Side effects of verapamil in children. Arch Dis Child 1983;58:465-469 33. Kirk CR, Gibbs JL, Thomas R, et al: Cardiovascular collapse after verapamil in supraventricular tachycardia. Arch Dis Child 1987;62:1265-1282 34. McCrory JH: Heart Disease. In Tintinalli JE, Krome RL, Ruiz E (eds): Emergency MedicineA Comprehensive Study Guide. New York, NY, McGraw-Hill, 1988, pp 412-415 35. Gibson R, Driscoll D, Gillette P: The comparative electrophysiologic and hemodynamic effects of verapamil in puppies and adult dogs. Dev Pharmacol Ther 1981;2:164-110 36. Weiss AT, Lewis BS. Halon DA, et al: The use of calcium with verapamil in the management of supraventricular tachyarrhythmias. Int J Cardiol 1983;4:275-280 37. Haft JI, Habbab MA: Treatment of atrial arrhythmiasEffectiveness of verapamil when preceded by calcium infusion. Arch Intern Med 1986;146:1085-1089