Heart failure

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5.2 Heart failure

Robin Choong

Essentials

1 Congestive heart failure (CHF) is a clinical syndrome and may result from:

• excessive workload caused by increased pressure or volume, usually increased pulmonary blood flow, and/or
• normal workload faced by a damaged myocardium.

2 Clinical signs may include tachycardia, tachypnoea, increased work of breathing, sweatiness, cardiomegaly and hepatomegaly. In addition, infants may have failure to thrive, recurrent lower respiratory tract infections and respiratory distress.
3 In older children, new onset heart failure may be less overtly symptomatic. Malaise, decrease in the level of daily activity, abdominal pain, nausea, anorexia and weight loss may be present.
4 Current medications used in heart failure include diuretics, digoxin and angiotensin-converting enzyme inhibitors.

Causes of congestive heart failure1–4

Most cases of congestive heart failure in childhood result from congenital heart defects.

Left-to-right shunts with increased pulmonary blood flow, e.g. ventricular septal defect (VSD), atrioventricular septal defect (AVSD), patent ductus arteriosus (PDA). atrioventricular septal defect, patent ductus arteriosus.
Acute left heart obstruction, e.g. aortic stenosis, coarctation of the aorta, interrupted aortic arch, hypoplastic left heart syndrome.

A smaller number of cases may be from:

Primary myocardial dysfunction, e.g. myocarditis, cardiomyopathy, anomalous left coronary artery.
Other causes, e.g. anaemia, metabolic, toxic, dysrhythmia.

Age-based

The causes of congestive heart failure change with age. Congenital heart defects generally present in the first days or months of life. Acquired cardiac disease may occur at any age. The following lists the likely causes at particular ages.

First days of life

Asphyxia, left heart obstruction, metabolic, sepsis.

One day to one week of age

Left heart obstruction in duct-dependent lesions, e.g. aortic stenosis, coarctation of the aorta.

Large left-to-right shunt lesions, e.g. large VSD, AVSD, truncus arteriosus.

First month

Large left-to-right shunt, e.g. large VSD, AVSD, truncus arteriosus.

First three months

Large left-to-right shunt, e.g. large VSD, AVSD, truncus arteriosus.

Metabolic disease.

Acquired heart disease may occur at any age due to:

• inflammatory/infective, e.g. viral myocarditis, Kawasaki disease, pleuropericarditis, rheumatic fever;
• metabolic genetic, e.g. inherited cardiomyopathy;
• dysrhythmia, e.g. sustained SVT, ventricular tachycardia (VT);
• severe anaemia.

Clinical manifestations and investigations1–4

Presentation

Infants may present with problems related to feeding, such as sweating, tachypnoea, reduced volume of feeds leading to failure to thrive. Respiratory problems, such as cough, recurrent respiratory infections, tachypnoea and increased work of breathing are prominent. Lower respiratory tract infection may have features in common with congestive cardiac failure (CCF). Cardiac failure should be considered in atypical, persistent or recurrent cases of lower respiratory tract infection (LRTI), particularly in infants.

General features

• Tachycardia – due to fixed stroke volume.
• Tachypnoea – due to decreased compliance with increased lung water.
• Gallop rhythm, weak pulse.
• Failure to thrive – from decreased energy intake, increased energy expenditure.
• Cardiomegaly – may be due to left heart obstruction with left-to-right shunt or left ventricular dysfunction.
• Sweaty (cold sweat) – prominent with feeding.
• Fatigue/lethargy.
• Hepatomegaly – not specific to right heart failure unlike in adults, may occur with any aetiology.

Investigations

Routine

• Chest X-ray

Cardiomegaly (in an AP film the normal cardiothoracic ratio is <0.6). Pulmonary plethora in left-to-right shunt. Pulmonary venous congestion in left heart obstruction/left ventricular dysfunction. Radiologic features include reticulogranular pattern, fluid in lung fissures, pleural effusions, pulmonary oedema.

• ECG

Assess rhythm, myocarditis (voltages), ischaemia (ST-T wave).

Specialized

• Echocardiography.
• Cardiac catheterisation.
• Others: angiography (computerised tomography and magnetic resonance imaging), viral studies (blood, throat swab, faeces), chromosomal analysis, urine metabolic screen, myocardial tissue biopsy.

Referral

The diagnosis of cardiac failure in an infant or child mandates urgent review by a paediatrician or paediatric cardiologist.

Management1–3,5–15

Current medications used in heart failure include diuretics, digoxin and angiotensin-converting enzyme inhibitors.

Acute management

Resuscitate with ventilatory support if required.
If desaturated consider supplemental oxygen. Caveat: large left-to-right shunt lesions (e.g. truncus arteriosus) may worsen with high FiO2. Consult early in these cases.
Fluid restriction and diuretic therapy.
Infants with left heart obstruction may present with cardiorespiratory failure when the ductus arteriosus closes. Prostaglandin infusion may reopen the ductus and assist systemic perfusion.

Diuretics

Acutely: furosemide 1 mg kg–1 dose–1 intramuscular (IM) or intravenous(IV) (anticipate hypokalaemia).
Chronically: furosemide 1–3 mg kg–1 day–1 in divided doses, with spironolactone, 1 mg kg–1 dose–1 po q12h. Beware potassium-sparing effect of angiotensin-converting enzyme inhibitors.

Digoxin

• Severe congestive heart failure treated with initial IV administration. Early failure in less distressed infants can be treated orally. All patients should have oral therapy as soon as possible. IV dosage is only 70–80% of amount used orally.
• The total digitalising dose (premature: 20 mcg kg–1; infant: 30–40 mcg kg–1; over 2 years: 30 mcg kg–1) may be given as 1/2 stat, 1/4 in 6–12 hr, and 1/4 in another 12–18 hr.
• Maintenance dose (IV, oral) is 3 to 5 mcg kg–1 12-hourly (maximum of 200 mcg (IV) to 250 mcg (oral)). If heart failure is not severe, then may start with a maintenance dose only.
• Digoxin is contraindicated in complete heart block, pericardial tamponade, hypertrophic cardiomyopathy and other outflow tract obstructions. Reduce dose in renal failure.
• Monitor with ECG and serum digoxin level (keep below 2.5 nmol L–1 [2.0 ng L–1]).

Angiotensin-converting enzyme inhibitors

Angiotensin-converting enzyme inhibitors are used in heart failure due to large left-to-right shunts and heart failure caused by ventricular failure. Oral captopril (0.1–1 mg kg–1 dose–1 8-hourly) or lisinopril (0.1 mg kg–1 daily, increasing to 0.2–0.4 mg kg–1 daily over 4–6 weeks) may be used.

β-blockers

β-blockers have a role in paediatric heart failure though doses are extrapolated from adult data. However, their role in children with heart failure remains to be fully defined.

Levosimendan

Levosimendan is an IV calcium sensitiser used in acutely decompensated severe congestive cardiac failure. It has inotropic, vasodilatory and cardioprotective properties. In adults with severe cardiac failure, improvement in 31-day survival compared with dobutamine has been shown.

References

1 Park M.K. Congestive heart failure. In Park M.Y., editor: Pediatric cardiology for practitioners, 5th ed., Philadelphia: Mosby Elsevier, 2008.

2 Shaddy R.E., Tani L.Y. Chronic Congestive Heart failure. In Allen H.D., Driscoll D.J., Shaddy R.E., et al, editors: 2007 Moss and Adams’ heart disease in infants, children and adolescents: Including the fetus and young adult, 7th ed., Philadelphia: Lippincott Williams & Wilkins, 2007.

3 Abelson W.H., Garth Smith R. Residents handbook of pediatrics, 7th ed. Toronto: The Hospital for Sick Children, Toronto, Canada, BC Decker Inc; 1987.

4 Guzman M.F., Hedley Brown A., Been M., et al. Manual of cardiorespiratory critical care. Sevenoaks, Kent: Butterworth; 1989.

5 Chang A.C., Hanley F.L., Wernovsky G., Wessel D.L. Pediatric cardiac intensive care. Baltimore, MD: Williams & Wilkins; 1998.

6 Shaddy R.E. Optimizing treatment for chronic congestive heart failure in children. Crit Care Med. 2001;29(Suppl):S237-S240.

7 Schwartz S.M., Duffy J.Y., Pearl J.M., Nelson D.P. Cellular and molecular aspects of myocardial dysfunction. Crit Care Med. 2001;29(Suppl.):S214-S219.

8 Clark B.J.IIIrd. Treatment of heart failure in infants and children. Heart Dis. 2000;2(5):354-361.

9 Buchhorn R., Hammersen A., Bartmus D., Bursch J. The pathogenesis of heart failure in infants with congenital heart disease. Cardiol Young. 2001;11(5):498-504.

10 Kay J.D., Colan S.D., Graham T.P.Jr. Congestive heart failure in pediatric patients. Am Heart J. 2001;142(5):923-928.

11 Wernovsky G., Hoffman T.M. Pediatric heart failure management: Solving the puzzle. Crit Care Med. 2001;29(10 Suppl.):S212-S213.

12 Shaddy R.E. Beta-adrenergic receptor blockers as therapy in pediatric chronic heart failure. Minerva Pediatr. 2001;53(4):297-304.

13 Shekerdemian L. Nonpharmacologic treatment of acute heart failure. Curr Opin Pediatr. 2001;13(3):240-246.

14 De Luca L., Colucci W.S., Nieminen H.S., et al. Evidence-based use of levosimendan in different clinical settings. Eur Heart J. 2006;27:1908-1920.

15 Egan J.R., Clarke A.J.B., Williams S., et al. Levosimendan for low cardiac output: A pediatric experience. J Intensive Care Med. 2006;21(3):183-187.

Further reading

Allen H.D., Driscoll D.J., Shaddy R.E., et al. Moss and Adams’ heart disease in infants, children and adolescents, 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2007.

Archer N., Burch M. Paediatric cardiology. An introduction. London: Chapman & Hall Medical; 1998.

Park M.K. Congestive heart failure. In Park M.Y., editor: Pediatric cardiology for practitioners, 5th ed., Philadelphia: Mosby Elsevier, 2008.

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