POSTGRAD. MED. J. (1964), 40, 428

THE TREATMENT OF CARDIACEMERGENCIES IN INFANCY

ELTON GOLDBLATT, B.SS., M.R.C.P.(Ed.), D.C.H.

Consultant Paediatrician, Cardiac Clinic, Royal Liverpool Children's Hospital, Liverpool 7;Part-time lecturer, Department of Child Health, University of Liverpool.

THE treatment of cardiac emergencies ininfancy is concerned mainly with the treat-ment of cardiac failure, cyanotic attacks.arrhythmias and cardiac arrest. The vastmajority of infants requiring such treatmenthave some underlying congenital cardiac ab-normality. Cardiac failure, if not associatedwith a congenital heart lesion, may be due toinfections acquired in the perinatal period,such as viral myocarditis, toxic myocarditis inan overwhelming bacterial infection, to par-oxysmal tachycardia, metabolic disorders suchas glycogen storage disease, or may occur inthe respiratory distress syndrome of the newborn.

All congenital cardiac abnormalities maycause cardiac faiilure, the treatment of whichsbould be thorough and intensive to enablefurther diagnostic investigations to be carriedout, if indicated, with a view to curative orpalliative surgery. In the infective and meta-bolic lesions there is no place for surgery andsupportive medical treatment offers the onlyhope for the infant. Accurate diagnosis, how-ever, is essential as unwarranted surgicalinterference in some cases may lead tountimely and avoidable death.

Cardiac Failure in InfancyMost cases of cardiac failure are associated

with some congenital cardiac abnormality,but, as mentioned, may be due to factors otherthan an anatomical abnormality.

Physical Signs and SymptomsWhere a congenital lesion is present there

are usually the physical signs of the lesion,whereas in infective conditions or metabolicdisorders there are often no specific diagnosticsigns. A discussion on the treatment of con-gestive cardiac failure in infancy is incompletewithout briefly reviewing the signs andsymptoms.

In comparing the signs of cardiac failurewith the familiar pattern seen in older childrenand adult patients, certain differences are

apparent and stress should be laid on thefollowing:

(i) Hepatic enlargement:This is the most important sign of cardiac

failure in infancy. It is easily and accuratelyelicited and changes in size are a good indica-tion of response to therapy.

(ii) Oedema and excessive weight gain:Infants in cardiac failure may gain excessive

weight although their food intake may be belowaverage. This is due to fluid retention thoughoedema is not unusually apparent until thecardiac failure is severe. Again, by accuratedaily weight records the infant's response totreatment may be assessed. Unless excessiveweight gain is checked by treatment oedemawill become manifest. This is usually mostapparent on the dorsum of the feet, and asperiorbital oedema.

(iii) Dyspnwea and tachypncea:This occurs in most infants in cardiac failure

and may be associated with indrawing of thelower intercostal spaces and movement of theale nasi. It is often one of the earliest signsof decompensation. Dyspnoea is a frequentsymptom. Mothers may volunteer the in-formation that the infant is breathless whenfeeding or even at rest. This is sometimesnot noticed but there is a history of poor anddifficult feeding, probably due to shortness ofbreath.

(iv) Tachycardia:Usually there is a heart rate of 140-180 per

minute, but occasionally decompensated infantsmay present with a bradycardia due, in some,to congenital atrioventricular block. The heartrate may also be used as a guide to responseof the infant to therapy.

(v) Cyanosis:Peripheral cyanosis may be caused by cardiac

failure. Central cyanosis may be due to an

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intracardiac right to left shunt resulting froma congenital malformation. Cyanosis is there-fore not necessarily a sign of cardiac failure.The degree of cyanosis is not a good indicationof the severity of the cardiac failure, but maybe helpful in the differential diagnosis of theunderlying cardiac lesion.

(vi) Signs in the lungs:In many cases the lungs may be clear

clinically, and crepitations so frequently heardin the adult in cardiac failure are absent inthe infant. If present, it may be impossibleto differentiate between those sounds whichare due solely to cardiac failure and those dueto pulmonary infection, which may have preci-pitated the cardiac failure. Similarly, whereinspiratory and expiratory rhonchi are present,they may be due to pulmonary oedema, bronch-ial infection, or both.(vii) Raised jugular venous pressure:

This is not an easily elicited sign in infantsdue to their short, and often fat, necks. It isalso difficult to elicit in the crying and strugglinginfant. Because of these factors, it should notbe regarded as an essential for the diagnosisto be made. If, however, an elevated jugularvenous pressure is noted, this is additionalevidence of cardiac failure.(viii) Signs of the cardiac abnormality:

If the underlying cause of cardiac failureis a congenital anatomical abnormality, thesigns of this lesion may be apparent.

(ix) Heart size:Accurate clinical evaluation of heart size is

difficult unless there is marked cardiac enlarge-ment. Cardiac enlargement alone is notevidence of cardiac failure.(x) Failure to thrive:

This is a frequent symptom. Infants withcongenital heart disease, although not in cardiacfailure, may not thrive even if their intake isapparently adequate. On the other hand, thedyspnoeic infant cannot take normal require-ments because of the effort needed to feedproperly and fails to thrive because of in-adequate intake. There is a history of normalfeeding in only a small proportion of cases.(Goldblatt, 1962).

Medical ManagementIn discussing the medical management certain

general measures should be considered beforedetailing the drug therapy. Intensive therapy

is essential to improve the infant's conditionas rapidly as possible to enable further in-vestigations to be carried out in suitable caseswith a view to surgical treatment.There have been many studies in which the

medical management of cardiac failure in in-fancy has been outlined. Although minordifferences are noticeable in these studies, thegeneral principles are similar in all and thesewill now be reviewed. (Kreidberg, Harvey andLopez, 1963; Goldblatt, 1962; McCue andYoung, 1961; Nadas, Rudolph & Reinhold,1953; Gasul and Arcilla, 1960; Keith, Roweand Vlad, 1958).A. General Measures(i) Oxygen therapy: Infants in acute cardiacfailure should be nursed in an incubator oroxygen tent with an oxygen saturation of ap-proximately 50%1, or higher if necessary.A high humidity is desirable to prevent plugsof mucus causing airway obstruction. This is

an essential precaution due to the drying effectof tachypnoea on respiratory secretions.(ii) Posture: For maximum comfort andrespiratory excursion, the infant should benursed on a tilted board which is placed in thecot. Various methods have been used to main-tain the infant in this position such as strappingapplied to the infant's back or some form ofharness. (Goldblatt, 1962). In this positionvenous return is reduced and ventilatory move-ments are assisted by allowing free descent ofthe diaphragm. Propping up with pillows doesnot allow this as the flexed thighs pressingagainst the abdomen may restrict diaphragmaticmovement.

(iii) Feeding: To prevent overdistension ofthe stomach which may further embarrassrespiration, frequent small feeds are preferableto the normal feeding regime. Feeding requiresgreat effort by the infant, and this is avoidedby using a nasogastric tube. (A useful tube isthe Argyle Premature Infant Feeding Tube,size 5 Fr.*). It can be left in situ for manydays without causing undue discomfort or nasalirritation and infection. Feeds can be givenvia this tube even when the infant is asleep.By using a 1-2 ml. syringe feeds cannot be givenmore rapidly than if taken orally by a normalinfant, and this prevents sudden overdistensionof the stomach which may embarrass respira-tion even further.

*Manufactured by Aloe, Division of Brunswick,St. Louis.

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Usual feeding formulae are recommended,but in the acutely ill infant it may be necessaryto use a low-salt milk ('Edosol'). When thisis used careful electrolyte control should bemaintained. Fluid restriction is never necessary,and maintenance of adequate hydration isessential particularly in cyanotic types of heartdisease.(iv) Travelling: When infants in cardiacfailure have to be moved to centres for special-ised treatment, it is essential to keep them coolby light clothing and few blankets. If necessarythey should be sedated prior to transfer. Beforedeparture the infant should be fed and, inthe cases of long journeys, fed on the way.Arriving in an overheated, hungry state mayaggravate the clinical condition because of theincreased metabolic demands created by acrying, hungry, pyrexial infant. The failingheart may not be able to cope with the extrademands created by this state. When theabove simple rules are observed these infantstravel remarkably well.B. Drug Therapy(i) Digoxin ('Lanoxin') is the drug of choiceas it is uniformly effective, easily administered,and serious toxic effects are rarely seen. Manydoctors do not give large enough doses, andthis leads to delay in adequate treatment andmay complicate full digitalisation in a specialcentre. It is usually given orally, but may begiven by the intramuscular or intravenous routewhen indicated.

Digitalising dose: 0.04-0.05 mg. per lb. bodyweight. (0.08-0.1 mg. per kg.). This is givenin the first twenty-four hours in four equaldivided doses. If given parenterally, a quarteror half the calculated digitalising dose is giveninitially, and the remainder in three equal dosesat six-hourly intervals.

Maintenance dose: Various authors recom-mend a sixth or more often a quarter of thedigitalising dose as maintenance. No singledose, however, should be less than 0.0625 mg.,except in premature infants or neonates, whenthe dose should be calculated according toweight. Tablets containing digoxin 0.0625 mg.are available. To avoid errors in dispensingthese tablets are coloured blue.The heart rate is a good rough guide to

dosage, and treatment should be discontinuedfor 12-48 hours if the rate falls below 100 permin. in the infant under three months, and 80-90per min. in infants between three and twelvemonths of age.

Vomiting Imay indicate overdosage, but maybe due to gastric irritation due to cardiac failurewhen the drug may have to be given parenter-ally. The generaIl condition of the infant shouldbe assessed before discontinuing treatment.(ii) Sedation: To ensure that the ill infanthas as much rest as possible sedation is anextremely important part of the treatment. Inthe acutely ill infant morphine is the drug ofchoice. The recommended initial dose is1/600 gr. per lb. body weight (0.1 mg per lb.or 0.2 mg. per kg.). In the premature infantand neonate approximately two-thirds to three-quarters of this dose is used. Subsequent dosescan be altered after assessing the response tothe initial dose and should be given every fourto six hours as required.

After the acute stage, to maintain mild seda-tion phenobarbitone should be given every sixto eight hours. The recommended dose is gr.1/8-1/6 (8-10 mg.) for infants up to sixmonths and gr. 1/4 (15 mg.) for older infants.For sedation for purposes of physical exam-

ination, recording of electrocardiograms andphonocardiograms, and accurate blood pres-sure measurement, chloral hydrate is a usefuldrug. The dose used is gr. 1/6-1/8 per lb.body weight (10-20 mg. per kg.).

Toilet procedures should be carried out andinjections given preferably during periods ofmaximal sedation.(iii) Diuretics: In cases of acute pulmonaryoedema mercurial diuretics, such as mersalyl,are the most efficient, and therefore the drugof choice. The recommended daily dose is0.2-0.5 ml. given intramuscularly.

In less severe cases, and for maintenancetherapy, chlorothiazide is given in a daily doseof 20 mg. per lb. body weight. This dose maybe increased to 50 mg. per lb. if necessary.When using diuretics careful watch should bekept on electrolyte levels as low as serum potas-sium predisposes the myocardium to digoxinintoxication. In practice, however, potassiumsupplements are rarely necessary.(iv) Aminophylline: Bronchodilators are in-dicated in the presence of pulmonary oedemawith bronchospasm. Aminophylline supposi-tories in a dose of 12.5-50 mg., depending onthe weight of the infant, every four to sixhours are often effective. In addition, ephedrinehydrochloride may be useful in a dose of gr.1/8-1/4 (8-15 mg.), depending on age, givensix to eight hourly.(v) Antibiotics: It is extremely difficult, if

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not impossible, to determine whether pulmonarysigns are due to cardiac failure, to infection,or both. (Simpson, 1958). Infection may haveprecipitated cardiac failure or complicated it.For this reason antibiotics, usually penicillinand streptomycin, should be used in the acutestage. It may be necessary to use other anti-biotics where indicated by bacteriological stud-ies. Long term maintenance antibiotics maybe necessary when recurrent infections precipi-tate repeated episodes of cardiac failure.(vi) Correction of anaemia: Anaemia maybe a precipitating factor in cardiac failure andif present should be treated, preferably by oraliron therapy, but a slow transfusion of packedcells in the severely anaemic infant may benecessary. In the case of cyanotic lesions itshould be remembered that the "normal"haemoglobin is high and relative anaemia shouldbe corrected.

C. Surgical ManagementIdeally every congenital malformation should

be corrected completely, but in a large numberof cases this is not possible. In some it maybe practical later but the best that can be offeredin infancy is palliative surgery which will tidethe infant over the acute emergency until older,when definitive corrective surgery may be under-taken with a much 'lower operative risk.A frequent difficulty is to decide the optimum

time for operation. In every case intensivemedical treatment should first be given in anattempt to get the infant into the best possiblecondition, but sometimes, when response is notsatisfactory an emergency thoracotomy shouldbe undertaken without further delay. Responseto treatment is assessed by falling respiratoryand pulse rates, diminishing size of the liverand normal weight gain.A detai;led diagnosis of the malformation is

of course desirable before surgical treatment isundertaken, and this should be established bycardiac catheterisation and angiocardiography,if the infant's condition -permits. In the illinfant, however, these procedures carry adefinite mortallity risk or may worsen the in-fant's general condition. In such cases it maybe preferable to rely upon clinical diagnosisand to carry out an exploratory thoracotomywith a view to corrective or palliative surgery.Diagnostic pressures at the time of surgerymay be of some help but the difficulties ofmaking an accurate diagnosis at the time ofoperation should be borne in mind.At present, the operations done in this clinic

and in many other centres for the more commonlesions are as follows:1. Patent ductus arteriosus-ligation, but oc-casionally it is necessary to divide the ductus.2. Ventricular septal defect with pulmonaryhypertension-banding of the pulmonary artery.By narrowing the pulmonary artery, thepressure distal to the constriction is reducedto approximately a half or a third of the proxi-mal pressure. By this procedure left to rightshunting is diminished. In some centres closureis attempted in the first instance.3. Atrio-ventricular canal with pulmonaryhypertension-banding, but the results are notas good or encouraging as in "uncomplicated"ventricular septal defects.4. Fallot's tetralogy-one of several proced-ures may be carried out. These includeBlalock-Taussig, or Potts anastomosis, infundi-bular dilatation and/or resection. The purposeof these procedures is to increase pulmonaryblood flow which in turn increases coronaryand systemic arterial oxygen saturation.5. Tricuspid atresia-cavo-pulmonary anasto-mosis, Blalock-Taussig or Potts anastomosis.6. Pulmonary atresia-cavo-pulmonary anas-tomosis, Blalock-Taussig or Potts anastomosis.7. Coarctation-resection. This is usuallypossible in the juxta and post-ductal type ofcoarctation, but not in the long preductal typeof coarctation. In any case where surgery isindicated the arch of the aorta should be ex-plored. (Waldhausen, King, Nahrwold, Lurie& Schumaker, 1964).8. Transposition of the great vessels-creationof atrial septal defect-Blalock-Hanlon proced-ure.9. Total anomalous pulmonary venous drain-age-an anastomosis is made between the pul-monary venous trunk and the left atrium. Insome centres the trunk is tied off and the atrialseptal defect closed at a second operation.(Williams, Richardson and Campbell, 1964).10. Severe pulmonary stenosis -pulmonaryvalvotomy.11. Aortic stenosis-aortic valvotomy shouldbe attempted, but the mortality may be highbecause there is often an extremely small valvering associated with a small left ventricle andhypoplastic ascending aorta.The overall mortality rate of infants with

cardiac failure is approximately 50%. (Gold-blatt, 1962). With improving surgical andanaesthetic techniques this will be reduced but

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there will always be a relatively high mortalitybecause of the number of complicated lesionscausing cardiac failure which are not amenableto surgical correction.Cyanotic AttacksMany paediatricians interpret the term

"'cyanotic attack" as an episode in which aninfant with a cyanotic cardiac lesion becomesincreasingly cyanosed on crying, feeding orwhen cold. This is a common occurrence inthese infants and it should be remembered thata change in colour alone is "physiological" andnot necessarily serious.True cyanotic attacks are spontaneous and

apparently occur in infants with cyanotic cardiaclesions associated with pulmonary oligaemiasuch as Fallot's tetralogy, pulmonary andtricuspid atresia and transposition of the greatvessels with pulmonary stenosis. They havebeen shown to be due to temporarily increasedobstruction of the right ventricular outflow tractwith an increased right to left shunt. Duringthe attack, because of the diminished flowthrough the right ventricuilar outflow tract, thesystolic murmur may become shorter, softer,or may entirely disappear. (Wood, 1958;Braudo and Zion, 1959 and 1960).

Clinically a cyanotic attack is usually charac-terised by a shrill cry or scream which isdifferent to the normal cry of the infant. It isdifficult to pacify the infant and he may con-tinue crying until exhausted, when he fallsinto a heavy sleep. On waking he may be aswell as prior to the attack.

Associated with the cry there is a change incolour, often to a deeper cyanosis or there maybe a greyish blue colouration of the lips andface. In addition the infant may sweat excess-ively. The respiratory rate increases, the eyesmay roll upwards and the infant may loseconsciousness for a variable period. Sometimes,there is a twitching. Although recovery usuallytakes place, an occasional attack is fatal.The treatment is urgent. In the first place

morphia should be administered as rapidly aspossible as this shortens the attack and enablesthe infant to rest. Oxygen should be admin-istered to relieve the associated anoxia, althoughthe attacks are not relieved by oxygen alone.Procaine hydrochloride given intravenously hasan immediate but short lived effect. (Braudoand Zion, 1959). Cyclopropane anaesthesiahas also been shown to be effective (Wood,1958), but for obvious reasons is not a practic-able method of treatment in the majority ofcases.

Increasing frequency or severity of attacksshould be regarded as an indication for im-mediate surgical treatment. As the attacksusually occur in infants with cyanotic heartlesions with pulmonary oligaemia, the surgicalapproach usually consists of an operationdesigned to increase pulmonary blood flowsuch as a systemic-pulmonary anastomosis, orinfundibular dilatation or resection where pos-sible. Cyanotic attacks should cease after asucessful operation. Even in the best handshowever, results of anastomotic procedures ininfants under the age of three months areuniformly bad.

AffhythmiasAll types of arrhythmia seen in adults and

older children may occur in infancy, but arenot common. For the purpose of this discus-sion the most frequent arrhythmias encounteredare paroxysmal tachycardia and complete heartblock. The former is usually a supraventricu-lar tachycardia. In fifty per cent of the seriesdescribed by Nadas (1957) there was no obviousexplanation for the tachycardia, whilst the re-mainder were associated with some congenitalcardiac abnormality, the Wolff-Parkinson-White syndrome or other factors which mayhave precipitated the arrhythmia.A few of the infants were not ill, but the

majority were extremely ill, the clinical pictureresembling severe pneumonia or septicaemia.Infants with paroxysmal tachycardia may berestless and irritable or present with feedingdifficulty with associated vomiting. Othersbecome dyspnoeic, pale and clammy.The majority of cases present in the first

few months of life. Of those without any knownpredisposing factors, the majority are males.The development of cardiac failure depends

on the heart rate, the duration of the tachy-cardia and the age of the infant (the younger,the greater the risk of cardiac failure develop-ing).The treatment should begin with reflex vagalstimulation such as carotid sinus or eyeball

pressure. If this is not successful, prostigminemay be tried but if there is evidence of cardiacfailure the principles of treatment are similarto those already discussed. Maintenancedigoxin should be continued for at least amonth, and longer if further attacks occur. Incases with the Wolff-Parkinson-White syn-drome, if the tachycardia does not respond todigoxin, quinidine may be the drug of choiceto control the tachycardia, and maintenancetherapy may be necessary. The dose is 100-200

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mg. every two hours for eight doses. Thedose should be increased each day until thetachycardia is abolished or toxic effects arenoted. Maintenance therapy given three orfour times a day may have to be continued forsome months.Complete congenital heart block does not

usually constitute a medical emergency as theremay be no symptoms due to compensatorymechanisms of an otherwise normal heart.There may, however, be symptoms of an under-lying cardiac malformation. Except for theoccurrence of Stokes-Adams attacks, which arerare, there is no indication to attempt to in-crease the heart rate.

Cardiac ArrestCardiac arrest may be regarded as the most

serious of all arrhythmias. It may occur ininfants with cardiac lesions in heart failure,during investigation or surgery or with someintercurrent illness. It may also occur in infantswith normal hearts who have severe infections,are dehydrated, have been accidentally poisonedor have inhaled vomit often related to feeding.The management in all cases is similar and

based on well established principles. Theseinclude:(i) Maintenance of an adequate airway;when possible intubate the infant.(ii) Maintenance of an adequate cardiac out-put by external massage is easy in an infant.At the same time, artificial respiration is carriedout. This is essential until the infant has beenintubated and is respired by intermittent posi-tive pressure.(iii) Correction of the metabolic acidosis,which occurs rapidly, by sodium bicarbonate(2.5% solution) intravenously. The amountgiven should be calcuilated according to thebase deficit, but as an emergency measure10-20 ml. should be infused and repeated ifnecessary at 10-30 minute intervals until thedeficit is corrected.

Intracardiac injections of adrenaline andcalcium chloride may also be useful in re-establishing cardiac action.Once cardiac action has returned it may be

necessary to use a mechanical ventilator fora period.

DiscussionThere have been several reviews of the in-

cidence, signs, symptoms and treatment ofcardiac failure in infancy. (Keith, 1956; Gold-blatt, 1962; Kreidberg and others, 1963).

It is common experience that the mortalityof both medical and surgical treatment ofcongenital heart lesions is extremely high inthe first three months of life, and it is duringthis time that the largest percentage of infantswith such malformations develop cardiacfailure. (Goldblatt, 1962).Among the most frequent lesions causing

cardiac failure in infancy are transposition ofthe great vessels, coarctation of the aorta,aortic atresia, atrioventricularis communis,ventricular septal defect, patent ductus arterio-sus, single ventricle, and other complicatedcyanotic lesions. A high mortality is to beexpected because of the complexity of someof the lesions which are not amenable to pallia-tive or curative surgery. There is, however, aneed for improved diagnostic and surgicaltechniques to reduce further this mortality.Where facilities for investigation and treat-

ment are not available, early transfer to aspecialised paediatric cardiological unit isdesirable in order to institute intensive therapywith minimail delay with a view to earlydiagnosis and operative treatment. This willhelp to reduce the high mortality.With the recent development of relatively

simple methods of determining pH, pCO2 andstandard bicarbonate levels, increasing attentionis being paid to the correction of acid-basedisturbance which sometimes occurs in infantswith cardiac failure, and this may be anextremely important addition to the treatmentoutlined above0(Jones, 1964).

SummaryThe signs, symptoms and management of

cardiac failure, cyanotic attacks and cardiacarrhythmias are discussed. General principlesof surgical treatment are mentioned.

Standard diagnostic procedures have theirlimitations in these ill infants, and the mortalityrate following surgery is still high, although itis falling with improved surgical and anaesthetictechniques. Considerable further improvementin both diagnostic and surgical methods isrequired if more of these infants are to survive.

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GOLDBLATr, E. (1962): The treatment of cardiac failure in infancy-Review of 350 cases. Lancet, ii, 212.JoNEs, R. S. (1964): Personal communication.KEiTH, J. D. (1956): Congestive Heart Failure, Pediatrics, 18, 491.KEITH, J. D., ROWE, R. D., VL.AD, P. (1958): Heart Disease in Infancy and Childhood. New York: Mac-

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ment of coarctation in infancy. J. Amer. med. Ass. 187, 270.WILLIAMS, G. R., RICHARDSON, W. R., CAMPBELL, G. S. (1964): Repair of total anomalous pulmonary

venous drainage in infancy. J. thorac. cardiovasc. Surg. 47, 199.WOOD, P. (1958): Symposium on congenital heart disease-attacks of deeper cyanosis and loss of cos

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