Cardiac arrhythmias in infants and children

Cardiac A r r h y t h m i a s in Infants and Children By MILTON H. P,\UL

IlE G E N E R A L PRINCIPLES of mechanism, diagnosis and treatment of irregularity of the heart beat in infants and children are, similar in most respects to those in the adult but the successful management of these arrhythmias in the pediatric age group requires an awareness of some specific points. The important etiologic factors include congenital heart disease, rheumatic ]mart disease, viral iiffections, the pre-excitation (WPW) mechanism, drug toxicity and cardiac trauma related to cardiovascular surgery or cardiac cath('terization. As in adults, the causative factors are often not definit(dv ascertainable and no associated heart anomaly may be appar(,nt.

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In the healthy child the normal sino-atrial and atrioventrieular progression of impulses results in a regular cardiac rhythm with age-dependent rates wtrying fi:om about 80 to 180 t)(~ats/minute. The average resting heart rate is less than 140/minute during the first weeks of life, less than 120 during the first year, less than 100 by 5 or 6 years of age, and less than 90 as adolescence approaches. Sinus tachycardia is quite common in infancy anti chilclhood 1)(,ing r(,lat('d to crying, excitement, fear and febrile illness. Sinus tachyc'arclia r(3)rt'sc'nts an al)normally rapid discharge of the sinus node and the mechanism is consich'r(,d normal if" a normal sequence of P and QRS is maintained and the P wave is upright in leads I and II and the P-II interval is not shorter than about 0.10 second (Fig. 1). Sinus tachycardia may be suspected clinically when the rate is between 140 and 200 beats/minute and auscultation demonstrates some slight rate variation in contrast to the characteristic clock-like regularity of paroxysmal atrial taehyeardia with an ectopic pacemaker. In most instances sinus tachycardia is transitory but should such tachycarclia persist in the absence of heart disease, a diligent search should be undertaken for a causative underlying pathologic condition such as anemia, infection, thyrotoxicosis, or, in the older child, neuroeirculatory asthenia. Sinus bradycardia is much less common in healthy children and may be considered present when the heart rate is less than 100 in infants, and less than 80 in older children (Fig. 9.). Cerebral damage attendant upon birth and anoxia in the infant may result in sinus bradycardia (Fig. 3). In the normal infant breath holding or marked distension of the stomach may result in Aided in part by the Helen Fag Hunter Pediatric Cardiology Fund. MILTONH. PAUL, M.D.: Director, Division of Cardiology, The Willis J. Potts Children's Heart Center. The Children's Memorial Hospital, and Ass.oclate Professor of Pedlatries, Northwestern University Medical School, Chleago, Ill.

136 PROGRESS IN CARDIOVASCULARDISEASES, VOL, 9, No. 2. (SEPTEMBER), 1966

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Fig. 1.--Sinus taehyeardia in 4 month old infant with atrial septal defect and pneumonitis. (A) The diagnosis of normal impulse formation in the S-A node is based upon a normal sequence of P and QRST, normal (upright) P wave in leads I and II, and normal P-R interval (rate 200, P-R 0.13 sec.). (B) and (C) Thirty and 60 minutes after instituting aspirin and oxygen tent therapy.

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episodes of bradycardia. Sinus bradyeardia has also been noted in rheumatic earditis, although sinus tachycardia is the most frequent abnormality. Persistent bradyeardia in a newborn or infant should always raise the possibility of congenital complete atrioventricular heart block and the mechanism should b(' clarified by electrocardiography. Sinus arrhythmia is characterized by significant wtriations in the heart rate, usually phasic and related to respiration: Slow cardiac rates predispose to sinus arrhythmia and the irregularity can be readily diminished or abolished by exercise-induced tachycardia. This form of arrhythmia, presumably related to wtgal discharge,, may 1)e associated with slight wu:iations in electrocardiographic P wave configuration due to shifting (wandering) of the pacemaker, and the size, shape, or even direction of the P wave may wiry sinmltaneovsly with slowing of the rate and change in the P-I/interwd. PIIEM ATUIIIq ~ YST()I,I,;S

Premature systoles, supraventricular or ventricular in origin, are rather unconnnon in childhood, although these are the most fre
Paroxysmal supravcntricular tachycardia is the most common type of rapid heart action encountered in the young infant or child. In contrast, ventriculat paroxysmal tachycardia is extremely rare. Paroxysmal (supraventricular) taehycardia of infancy was recognized as a clinical entity by ttubbard, a It often presents as a cardiac emergency in infancy occurring during the first months of life and affecting primarily male infants without organic heart disease. The infant will become irritable and restless with a rapid respiration and may have a persistent cough as congestive heart failure develops. If the taehyeardia persists for 24 or 48 hours, peripheral vasoconstriction may result in striking skin pallor or cyanosis. Nadas 4 has emphasized that paroxysmal taehyeardia in children can be divided into clinical groups on the basis of age of onset, sex and etiologic factors. One group consists primarily of infant males less than 4 months of age without apparent heart disease, and the other group

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a constant interval (fixed coupling). (B) Sinus rhythm returned 2 days later. is composed of older infants and children of either sex who may or may not have associated heart disease. The taehyeardia in infancy is usually associated with rapid heart rates (250-300) but, fortunately, almost always responds to adequate digitalis therapy (Fig. 5). Reflex vagal stimulation by carotid sinus massage or eyeball pressure has rarely been of value in the infant age group, but in the older child with supraventrienlar taehyeardia these maneuvers as well as the valsalva maneuver can occasionally terminate the paroxysm. The most commonly employed digitalis preparation in pediatric usage is oral digoxin using 0.04 mg./pound of body weight as the digitalizing dose in infants under 1 year of age. One half of the calculated dose is given initially followed by one quarter of the calculated dose at 2 subsequent 4 or 6-hour intervals. If the arrhythmia has not been converted to a normal sinus mechanism with this dosage, an additional one sixth of the digitalizing dose may be administered every 4 to 6 hours until conversion is achieved or digitalis toxicity appears. If the clinical status warrants greater haste, intramuscular or intravenous digoxin can be administered using approximately two thirds of the oral dosage calculations. Nonspecifie supportive measures, including oxygen and antibiotics, should be employed when congestive heart failure is evident. In desperate or nonresponsive clinical situations, external electric countershoek should be employed and this technic has been demonstrated to be effective in terminating most forms of supraventrieular as well as ventrieular taehycardiaY ~ Even if the cardiac rhythm cannot be diagnosed with certainty, electric eountershoek should be utilized with the proper technic and supportive drug therapy. After successful termination of the taehyeardia, in the very young male infant particularly, it is usual to continue with daily digitalis maintenance therapy (one fourth of the digitalizing dosage for digoxin) for 3 to 6 months since re-

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Fig. 5.--Paroxysmal supraventricular tachycardia ill infant 5 weeks old with no apparent heart disease. (A) The precise regularity of the rapid rhyth.n (rate 310), the norlnal duration of QI~S, and the P wave (VI) preceding each ventrieular respon.,e establish the diaguosis. (B) Abrupt termination of tachvcardia with normal si,ms rlavthm after 12 hours of digoxin therapy.

currcnces may 1)e frequent during this period but are much less common beyond 1 vear after the initial attack. In contrast, ill the older infant and child, attacks may continue for several years, particularly if tilt; pre-exeitation (WPW) syndrome is evident. The older child with paroxysmal supraventricular tachycardia has a mow characteristic symptomatology and the attack is less likely to proceed unnoticed for days as in the infant. In the older child, reflex termination of an attack of supraventrieular tachycardia should be attempted since it may be effective particularly after initial digitalis administration. Here again, as in the infant, digitalis is the treatment of choice but in some instances quinidine has been required to terminate the taehycardia in the older child with recurrent episodes of supraventrieular tachycardia. Effective long-term prophylaxis may be accomplished with digitalis alone but often small doses of quinidine sulfate ;ire required (0.9, Gin., orally, 3 to 4 times/day) for optimum control. The pre-Excitation (WPW) syndrome v is characterized by specific electrocardiographic features and a tendency to recurrent attacks of paroxysmal taehyeardia (Fig. 6). The electrocardiographic characteristics o~ the pre-exeitation syndrome are present at some time in about 10 per cent of pediatric patients with supraventrieular tachycardia. About one half of the infants and children with these pre-excitation syndrome electrocardiographic features but without heart disease have episodes of paroxysmal supraventrieular taehyeardia. When concomitant congenital heart lesions are present, these are most commonly Ebstein's anomaly of the tricuspid valve or primary myocardial disease. Prognosis in the patient with isolated pre-exeitation (WPW) syndrome is good. In those patients with associated paroxysmal supraventricular taehy-

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Fig. 6.--Paroxysmal supraventricular taehycardia in 3 week old infant with no apparent heart disease. (A) Tachycardia, rate 275. (B) Sinus rhythm after 24 hours of digoxin therapy. Note pre-excitation syndrome with short P-R interval, distortion (slurring) of the initial segment of QRS, and widened QRS. (C) Normal sinus rhythm in same infant 2 weeks later without evidence of pre-excitation mechanism. eardia, digitalis is again the initial therapy of choice and when recurrent attacks are a problem, digitalis alone or in combination with quinidine constitutes the most effective prophylactic therapy. Traumatic supraventricular (or atrioventricular junctional) tachycardia associated with cardiac catheterization or intracardiac surgery is increasingly frequent in this era of aggressive cardiac diagnosis and therapy. Supraventricular taehycardia induced at catheterization is usually transient but when prolonged it responds readily to digoxin therapy. Although supraventricular (and atrioventrieular junctional) tachycardias are often observed following open heart surgery, 8 operative trauma is only one of several possible causes including electrolyte imbalance, anoxia, acidosis or digitalis toxicity. The important aspects of management here relate to the adequate correction of these abnormalities with specific therapy before resorting to the use of cardiac drugs. Persistent (chronic) ectopic atrial tachycardia is a term that has been applied to an arrhythmia with characteristic features that clearly distinguish it from the other forms of supraventricular tachycardia2 The usual form of paroxysmal atrial tachycardia is characterized by sudden onset and termination, taehyeardia lasting for hours or days, fixed cardiac rates usually greater than 180/ minute, and a response to digitalis therapy with abrupt return to normal sinus rhythm. The much less common persistent form of supraventrieular tachycardia may last weeks or months or years, often shows changes in heart rate

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Fig. 7.--Persistent (chronic) eetopic atrial taehycardia in 2 year old boy known to have been present intermittently since early infancy. (A) Atrial taehycardia, rate 170. (B) Digoxin therapy leads to control of ventricular rate with characteristie response for this arrhythinia, i.e., partial (second degree) atrioventricular block with 4:3 and 3:2 response and Wenekehach l)eriods. (C) Transient return to simls mechanism.

without an apparent change in pacemaker site, and the most common response to digitalis therapy is ventricular slowing due to partial atrioventrieular block (Fig. 7). It has been possible to suppress temporarily or to slow considerably the ectopic pacemaker in 3 patients by reserpine or guanethidine administration (reserpine 0.02 rag./Kg./24 hr. ) ( Fig. 8). Ventricular paroxysmal tachycardia is extremely rare in infants and children and occurs most frc(tuently as a result of trauma at cardiac catheterization or surgery or from digitalis or drug intoxication. In spontaneous repetitive ventricular paroxysmal tachycardia the attack may give rise to congestive heart failure or to syncope. As in the adult, parenteral quinidine or procaine amide are useful therapeutic agents in the acute emergency (Fig. 9), but it is important to note that very large oral doses of procaine amide have been required to prevent recurrences.l" ATRIAL FIBRILLATION AND FLU'/WER

Atrial fibrillation and flutter are rarely encountered in the pediatric patient, although each mechanism has been described as occurring even at birth and being congenital in origin. Atrial fibrillation is quite uncommon in rheumatic heart disease in the pediatric age group, occurring in only about 1 to 2 per cent of these children. It is of serious prognostie importance in the child since it often indicates recurrent attacks with the continuing presence of active carditis or a grossly enlarged left atrium. Atrial fibrillation is particularly infrequent in association with eongenital heart lesions but has been noted in some patients with advaneed idopathie hypertrophic subaortie stenosis and should be regarded as an ominous prognostic sign) 1 Atrial flutter, in contrast to its relative infrequeney in adults, is more eom-

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A B C D Fig. 9.--Paroxysmal ventrieular tachycardia in 10 month old male infant with (A) ventrieular rate 210, atrial rate 110. Prolongation of QRS complexes, irregularity of the ventricular rate and independence of atrial and ventricular rhythms illustrated here cannot be relied on completely in the differential diagnosis betwen supraventricular and ventricular tachycardia 17 but later presence of isolated ventricular beats and reciprocal beats verified this mechanism. (B, C, D) Response to intravenous procaine amide.

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B Fig. 10.--Atrial flutter in 6 year old boy first demonstrated on electrocardiogram at 2 months of age. (A) Atrial flutter with 4:1 A-V block. (B) Slow nodal rhvthm noted twenty-four hours after starting therapy with diphenylhydantoin (l)ilalltin) 25 rag. p.o. q8h. Atrial flutter rectored after discontinuing I)ilantin. mon than atrial fibrillation in the infant and young child. Atrial flutter may appear transiently as a postoperative complication of atrial septal defect surgery or as a result of catheterization trauma. In association with congenital heart disease the spontaneous occurrence of flutter is also of ominous prognosis since it is usually present with severe congestive heart failure or gross dilatation of the atria. Idiopathic (no congenital heart malformation demonstrated) atrial flutter (Fig. 10) in the newborn has been reported and reversion to normal rhythm can occur with digitalis treatm:~nt, v-' It is pertinent here to emphasize the dangers of cardiac ',m:est or ventrieular fitn'illation associated with the use of quinidine sulfate in the treatment of arrhythmias when the heart is markedly enlarged and dilated as in many instances of congenital heart disease, in contrast, external electric eountershoek has been particularly successful and safe when used for the termination of atrial flutter in the pediatric patient with congenital heart disease. ATRIOVENTRICULAR BLOCK

The normal upper limits for the P-R interval varies from about 0.14 second in infancy to 0.18 second in the adolescent. Prolongation of the P-R interval does not necessarily indicate heart disease; however, it is commonly noted in some forms of congenital heart disease (patent ductus arteriosus, atrial septal defect, Ebstein's anomaly of the tricuspid valve, L-[corrected] transposition of the great arteries ), and in association with rheumatic fever. Second degree A - V block is commonly noted in association with the surgical intracardiac trauma of atrial or ventricular septal defect repair, hypoxia or digitalis intoxication. It is also noted to occur spontaneously in L-[corrected] transposition of the great arteries where presumably the anatomic inversion of the atrioventrieular bundle leads to a specific vulnerability to A-V conduction defects (Fig. 11)? 3 In many instances of second degree A-V block, the failure of the ventrieular response is preceded by progressive delay in atrioventrieular conduction with the pattern constituting the classical Wenckebach period.

145

CARDIAC ARRttYTHMIAS IN INFANTS AND CHILDREN

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Third degree atrioventricular block is most commonly observed as congenital complete heart block in infants and children 14 although it has been noted to occur in relationship with viral myocarditis. 1~ A common present-day cause of complete A-V block is intracardiac surgical trauma. Long-term follow-up studies have indicated that congenital complete heart block often occurs as the only cardiac anomaly and may have a relatively good prognosis. In most children with congenital complete heart block the QllS complexes are of normal duration and configuration and it has been emphasized that the children who have had Stokes-Adams attacks have had slow ventricular heart rates and prolonged QRS complexes. Stokes-Adams attacks appear to be rare in patients with resting heart rates above 50/minute and, fortunately, in most children the pacemaker is faster (located above bifurcation of the common bundle) as opposed to the slower idioventricular pacemaker usually noted in the adult with acquired (atherosclerotic) complete heart block. Cardiac enlargement by x-ray and moderately loud systolic ejection and diastolic inflow murmurs may be present in patients with congenital heart block without septal defects. These findings suggest the presence of a left-to right shunt but they simply result from the markedly increased stroke

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v o l u m e . W h e n c o n g e n i t a l h e a r t lesions a r e a s s o c i a t e d w i t h c o m p l e t e h e a r t b l o c k , w e h a v e e n c o u n t e r e d t h e o s t i u m p r i m u m f o r m of a t r i a l s e p t a l d e f e c t a n d t h e L - [ c o r r e e t e d ] t r a n s p o s i t i o n of t h e g r e a t a r t e r i e s m o s t f r e q u e n t l y . Although most children with congenital complete heart block are asymptomatic in c h i l d h o o d , t h e o c c u r r e n c e of dizziness or s y n c o p e calls for e a r l y t h e r a p e u t i c c o n s i d e r a t i o n s , lI~ I s u p r e l is effective in a c c e l e r a t i n g t h e v e n t r i c u l a r p a c e m a k e r a n d artificial e l e c t r i c a l p a c e m a k e r s c a n b e e m p l o y e d . REFERENCES

1. Reeve, R., and DeBoer, K.: Sinus arrhythmia. Pediatrics 26:402, 1960. 2. l~yon, R. A., and Rauh, L. W.: Extrasystoles in children. Anicr. J. Dis, Chiht. 57:278, 1939. 3. tlublmrd, J. P.: Paroxysmal tachycardia and its treatnient in young infants. Anler. ], Dis. Chihl. 6l:687, 1941. 4. Nadas, A. S., Daeschner, C. W., Rotla, A., and Bhnnenthal, S. I,: Paroxysnlal taclaycardia in infants and ehildrc,n. Pediatrics 9:167. 1952. 5. I)aul, M. C , and Miller. R. A.: External electrical terlnination of snpraventrieuhlr arrhythmias in congenital heart disease. Circuhition 25:604, 1962. 6. Pryor, R., and Blount, S. (;.: Refractnrv snpraventricular tachycardia in infancy. Amer. J. Dis. Chihl. 107:428, 1964. 7. Swiderski, N., l,ees, M. II., and Nadas, A. S.: The Wolff-Parkinson-White syndrome in infancy and elaildhood. Brit. Heart J. 24:561, 1962. 8. Popper, 14. W., Selzer, A., Osborn, j. j., Kerth, W. J., Robinson, S. J., and Gerbode, F.: Arrhythmias after cardiac surgery. Airier. Iteart J. 68:32, 1964. 9. Morgan, C. L., and Nadas, A. S.: Chronic ectopic tachycardia in infancy and childhood. Amer. Heart J. 67:617, i964. 10. Mortimer, E. A., and Rakita, L.: Ventricular tachycardia in childhood controlled with large doses of procaine

amide. New Eng. J. Med. 262:615, 1960.

[1. Braunwahl, E., I,aml)rcw, C. T., Rockott', S. D., Ross, j., Jr., and Morrow, A. G.: Idiopathic 1Dlwrtrnphie subaortic stcnosis. Circulation Suppl. IV 30:20, 1964. 12. Ilasscnriiek, A., Chojnacki, B., and Barker, 1I. J.: Cardioversion of auricular tlntter in a newborn infant. Amer. J. Cardiol. 15:726, 1965. 13. l~ev, M., Licata, R. lI., and May, R. C.: The conduction system in mixed levocardia with ventricular inversion (corrected transposition). Circulation 28: 232, 1963. t4. Paul, M. 1I., ltndolph, A. M., and Nadas> A. S.: Congenital c(nnl)letl~ atrinventricuhn" 1)hick: l)rnlilenis of clinical assesslnent. Circulation 18:18;k 1958. 15. Sissinan, N. J.: Stokes-Adams syndronle in childhood. Amer. J. Dis. Child. 110:658, 1965. 16. Moltham, M. E., Miller, R. A,, Hastreiter, A. R., and Paul, M. II.: Congenital heart block with fatal AdamsStokes attacks in childhood. Pediatrics 30:32, 1962. 17. Langendorf, R., and Pick, A.: Cardiac arrhythmias in infants and children, Chapter 8. In Gasul, B., Arcilla, R. and Lev, M. (Eds.).: Heart Diseases in Children. Philadelphia, J. B. Lippincott Co., 1966.