1. Congestive Heart Failure
in Infants and Children
Dr A.N Patnaik
Additional professor of Pediatrics,
NIMS,Hyderabad.

2. Objectives
Understand the path physiology of heart failure because it serves as the
rationale for management and drug therapy.
Highlight on the different way of classification of heart failure in infants
and children.
Stress on management of acute/ chronic heart failure in neonates, infants
and children

3. Background
In children, cardiac failure is most often caused by congenital heart disease and
cardiomyopathy. These causes are significantly different from those usually
responsible for the condition in adults, which include coronary artery disease and
hypertension.
Literature review: Pub Med, the Cochrane Library, BMJ Clinical Evidence, National
Guideline Clearinghouse and EMLc - There is a large amount of research published on
the management of heart failure in adults but a fewer studies in children and those
which do exist are often small, retrospective and use a diverse range of measures to
assess efficacy.
The management of cardiac failure in children has largely evolved based on clinical
experience and the application of adult data, supported by the more limited pediatric
literature.

4. Anatomy of Heart.

5. Burdon of Heart Failure in
Children.
In adults, cardiac failure usually involves failure of the left ventricle, with the most
common causes in developed nations being coronary artery disease; hypertension-induced
cardiac stress, arrhythmias and valvular disease. In developing nations, it has been reported that
other causes are frequently implicated, including rheumatic heart disease (20.1%) and
cardiomyopathy (16.8%).
In children for developed countries, the causes of cardiac failure :congenital malformations,
such as left-to-right shunts(the function of both the right and the left ventricles will be affected
and these children suffer from high-output cardiac failure),cardiomyopathy , anthracycline
toxicity. In developing nations, many cases are caused or exacerbated by anemia, often
secondary to malaria , malnutrition and hypocalcaemia and vitamin D deficiency.
Heart failure in post surgical or cardiac procedures (61.4%) compared to adults with heart
failure (0.28%).
Congenital heart disease occurs in around 8 per 1000 live births; many of these children
receive early surgical intervention and the yearly incidence of heart failure as a result of
congenital defects is between 1 and 2 per 1000 live births . Hence cardiomyopathy contributes
to a .lot

6. Definition of CHF
Congestive heart failure (CHF) occurs when the heart can no longer meet the
metabolic demands of the body at normal physiologic venous pressures either
in lungs or systemic veins or both.

7. Compensatory Mechanisms of CHF
Typically, the heart can respond to increased demands
by means of one of the following:
Increasing the heart rate, which is controlled by neural and humoral input
Increasing the contractility of the ventricles, secondary to both circulating
catecholamine's and autonomic input
Augmenting the preload, medicated by constriction of the venous capacitance vessels
and the renal preservation of intravascular volume

8. Compensatory Mechanisms of CHF

9. Contributary Factors of CHF
 Systolic dysfunction is characterized
by diminished ventricular
contractility resulting in an impaired
ability to increase the stroke volume
to meet systemic demands.
 Factors such as anatomic stresses (eg,
coarctation of the aorta) that
contribute to an increased afterload
(end-systolic wall stress) and those
resulting from neurohormonal factors
that increase systemic vascular
resistance also lead to increased
systolic dysfunction

10. Contributary Factors of CHF
 Diastolic dysfunction results from decreased
ventricular compliance, necessitating an
increase in venous pressure to maintain
adequate ventricular filling.
 Causes of primary diastolic dysfunction
include an anatomic obstruction that prevents
ventricular filling (eg, pulmonary venous
obstruction), a primary reduction in
ventricular compliance (eg,cardiomyopathy),
external compression (eg, pericardial
effusion).

11. Path physiology in AHF
During acute CHF, the sympathetic nervous system and renin-angiotensin system act to
maintain flow and pressure to the vital organs.
Increased Neurohormonal activity results in increased myocardial contractility, selective
peripheral vasoconstriction, salt and fluid retention, and blood pressure maintenance.
 As a chronic state of failure ensues, these same mechanisms cause adverse effects.
The myocardial oxygen demand that exceeds the supply increases because of an increase in the
heart rate, in contractility, and in wall stress.
Alterations in calcium homeostasis and changes in contractile proteins occur, resulting in a
hypertrophic response of the myocytes.
Neurohormonal factors may lead to direct cardio toxicity and necrosis.

12. Path physiology in CHF
In chronic heart failure, myocardial cells die from energy starvation, from cytotoxic
mechanisms leading to necrosis.
Necrosis stimulates fibroblast proliferation, which results in the replacement
of myocardial cells with collagen.
The loss of myocytes leads to cardiac dilation and an increased after load and wall
tension, which results in further systolic dysfunction.
In addition, the loss of mitochondrial mass leads to increased energy starvation.

13. Signs /Symptoms of CHF
Tachycardia
Venous congestion
Right-sided Left-sided
Hepatomegaly Tachypnea
Ascites Nasal flaring or grunting
Pleural effusion Retractions
Edema Pulmonary edema
Jugular venous distension
Low cardiac output
Fatigue or low energy
Pallor
Sweating
Cool extremities
Poor growth
Dizziness
Altered consciousness
Syncope

14. Signs /Symptoms of CHF
CHF with normal cardiac output is called compensated CHF.
CHF with inadequate cardiac output is considered decompensa

15. Ross Classification of Cardiac Failure
in children

16. Physical Examination
Ross score was 7
Diaphoresis of head/body =2
Frequent tachypnea=2
Retraction=1
RR<50/min=0
HR<160/min=0
Hepatomegaly >3cm =2
His weight and length are in 10th centile for age.
BP= 90/45mmHg.
Cardiomegaly ,normal intensity of sounds, no audible murmurs

17. NYHA Classification of CHF
This system relates symptoms to everyday activities and the patient's quality of life.
Patient Symptoms:
 Class I
Asymptomatic; no limitation of physical activity. Ordinary physical activity does not cause
undue fatigue, palpitation, or dyspnea (shortness of breath ).
Class II
Symptoms with moderate exertion; slight limitation of physical activity. Comfortable at
rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea.
 Class III
Symptoms with minimal exertion; marked limitation of physical activity. Comfortable at
rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea.
Symptoms at rest; unable to carry out any physical activity without discomfort. Symptoms
of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is
increased.
 Class IV
Symptom at rest.

18. Causes of Heart failure
Finding Causes
Cardiac rhythm disorders CHB,SVT,SND
Volume overload Structural heart disease (e.g., VSD, PDA, AR,
MR) ,Anemia, Sepsis
Pressure overload Structural heart disease (e.g., AS, PS, COA )
Hypertension
Systolic ventricular dysfunction or failure Myocarditis
Dilated cardiomyopathy
Malnutrition
Ischemia
Diastolic ventricular dysfunction or failure Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Pericardial or cardiac tamponade

20. Work-up in CHF
Thorough history taking and physical examination, including an assessment of the
upper- and lower-extremity blood pressures
Laboratory testing : CBC
Electrolyte levels
Calcium level,
BUN level, creatinine level
Chest/Heart X-ray: Increase C/T ratio (except TAPVR with obstruction)
Pulmonary blood flow and congestion
A 12-lead ECG: Hypertrophy of ventricles
Arrhythmia.
Echocardiography Etiology of CHF
Assess systolic and diastolic functions
Pulse oximetry, and a hyperoxia of arterial test in newborns distinguishing
intracardiac
mixing malformations from pulmonary disease in the setting of hypoxia.
Blood gas abnormalities Respiratory alkalosis (mild forms of CHF)
Metabolic acidosis (low cardiac output or ductal-dependent
lesions

21. Left ventricular/LA enlargement
Pulmonary venous congestion grade I

23. Echocardiograghy
Segmental Approach-to establish pathology.

24. Treatment of CHF
The management of CHF is difficult and sometimes dangerous without knowledge of
 the underlying cause.
The goals of medical therapy for CHF include reducing the preload, enhancing cardiac
contractility, reducing the after load, improving oxygen delivery, and enhancing nutrition.
Preload reduction can be achieved with oral or intravenous diuretics (e.g., furosemide,
thiazides, metolazone). Venous dilators (e.g., nitroglycerin) can be administrated.
 Contractility can be supported with intravenous agents (e.g., dopamine) or mixed
agents (e.g., dobutamine, inamrinone, milrinone). Digoxin appears to have some benefit
in CHF,
After load reduction is obtained orally by administration of angiotensin-converting
enzyme (ACE) inhibitors or intravenously by administration of other agents such as
hydralazine, nitroprusside, and alprostadil.

25. Pharmaceutical Agents used in the Treatment of CHF
Preload reduction
Furosemide 1 mg/kg/dose qid (PO or IV)
Hydrochlorothiazide 2 mg/kg/d bid-qid
Metolazone 0.2 mg/kg/dose bid (PO)
Inotropic
Digoxin Preterm infants: 0.005 mg/kg/d PO bid or 75% of this dose IV
<10 y: 0.010 mg/kg/d PO bid or 75% of this dose IV
>10 y: 0.005 mg/kg/d PO qd or 75% of this dose IV
Dopamine 5-28 mcg/kg/min IV
Dobutamine 5-28 mcg/kg/min IV
Milrinone 0.5-1 mcg/kg/min IV Load: 50 mcg/kg IV slowly over 15 min

26. Pharmaceutical Agents used in the
Treatment of CHF
Afterload reduction
Captopril 0.1-0.5 mg/kg/d PO tid
Enalapril 0.1 mg/kg/d PO qd/bid
Nitroprusside 0.5-10 mcg/kg/min IV monitor cyanide

27. Acute CHF in the neonate or infant
Cardiac lesions that may appear early and that should be considered include coarctation or
interruption of the aortic arch, total anomalous pulmonary venous return, hypoblastic left-heart
syndrome. More chronic conditions to consider in young infants with CHF include a large VSD.
PGE1 infusion is indicated when ductal-dependent cardiac lesions are diagnosed or when they
cannot be ruled out in a timely fashion. Absent femoral pulses or the inability to increase the
systemic arterial PaO2 to above 150 mm Hg with a fraction of inspired oxygen (FiO2) of 1
suggests a ductal-dependent lesion, and treatment with PGE1 is mandatory.
Nonstructural cardiac problems that occur during this stage include tachyarrhythmia's (usually
supraventricular tachyarrhythmia [SVT]) and complete heart block. Pharmacologic or electrical
cardio version is needed in any patient with a tachyarrhythmia who presents with CHF.

28. Acute CHF in the older child
In older children with acute CHF, admission to ICU for diuresis with IV furosemide and
IV dopamine infusion at a rate of 5-10 mcg/kg/min are appropriate until stabilization is
achieved.
 Older children may require the placement of a central venous catheter to monitor venous
pressure and cardiac output during stabilization.

29. Chronic or stable CHF
For more severe CHF, diuretic therapy with oral furosemide may be increased to 2 mg/kg/dose
PO tid, or a second agent, such as hydrochlorothiazide can be added.
After load reduction is indicated in patients who have large Lt-Rt shunt, left-sided regurgitant
lesions or poor systolic function .
In any patient taking more than 1 mg/kg of oral furosemide bid without ACE inhibitors,
spironolactone should be added for its potassium-sparing effect. Alternatively, their serum
potassium levels should be monitored, and appropriate supplementation should be provided

30. Chronic stable CHF
The selective beta1-blocker metoprolol and the nonselective beta1- and beta2-blocker
carvedilol, used primarily in adults have generally shown encouraging results in select patients
with cardiomyopathy and mild or moderate chronic CHF in children.
Carvedilol has been shown to decrease pulmonary artery mean and wedge pressures, decrease
cardiac nor epinephrine levels, and increase peripheral vasodilatation by means of alpha1-
blockade. For these reasons, in part, increased use of carvedilol has progressed in recent years,
particularly in cardiomyopathy.
An increased ejection fraction has been demonstrated in children and adults using both drugs.
Adults using these beta blockers have demonstrated an increased stroke volume during exercise,
along with a decreased heart rate and LV chamber size.

31. Chronic or stable CHF
In a patient who is haemodynamically stable, outpatient management can be initiated by
using several agents.
In mild forms of CHF, Digoxin and low-dose furosemide may be initiated.
The dose of Digoxin is almost never increased, either for effect or according to Digoxin
levels, which are notoriously unreliable. However, the dose may be decreased in the presence
of signs of toxicity. The suspicion of Digoxin toxicity should increase if an infant is
uninterested in feedings, gags, or vomits frequently. These symptoms are typically due to an
overdose or renal failure.

32. Management of Chronic CHF
Nutrition is crucial in the management of chronic CHF. Particularly during infancy, CHF
increases the metabolic demands while making feeding itself more difficult. Enhanced caloric
content feedings and, in some cases, nasogastric feedings may be necessary to maintain the
patient's growth.
Anemia aggravates CHF by increasing the demands for cardiac output, and often, careful
attention to iron stores or the administration of red cell transfusions results in a significant
improvement the oxygen-carrying capacity of the blood.
The success of medical therapy of CHF in infants and small children is judged according to the
child's growth. The failure to gain weight in the setting of marked CHF signifies that the current
regimen is not sufficient. A failure to thrive is an indication for increased medical management
or surgical repair.