Heart Failure in

Childhood
Husna Najihah Dzulkarnain
1213828
 Definition
Epidemiology
Pathophysiology
Causes
Clinical Features
Investigations
Management
Differential diagnosis

Contents
 Childhood: period from birth to being adolescents.

Heart Failure is defined as the inability to provide adequate

cardiac output to meet the metabolic demand of body.
( Nelson Textbook of Paediatrics, 19th edition)

Definition
 Worldwide, congenital heart disease is the most
common cause of pediatrics heart failure, followed by
cardiomyopathy.
CHD occurs in around 8 per 1000 live births, however,
many of these children receive early surgical
intervention and it has been estimated that the yearly
incidence of heart failure as a result of congenital
defects is between 1 and 2 per 1000 live births.
Malaysia?

Epidemiology
 Childhood-a period of rapid growth, and high energy,
nutrients need to be supplied adequately.
Slower growth and development
Complications-emotional issues ,lifelong management
(follow up in CHD)

Why is it important?
Physiology of the heart
Cardiac output = Heart Rate x Stroke volume

Tachyarrhythmia-shorten Afterload
the diastolic time interval Preload
for ventricular filling. Contractility
(intrinsic
myocardial
function)

Cardiac Output
Pressure-volume relationship

Physiology of the heart

 In a healthy heart, the increase in preload which
consequently increase in the ventricular end-diastolic
volume will cause the augmentation of cardiac
output.
The increased stroke volume in this manner is
possible due to the stretching of myocardial fibers
which also result in increased wall tension.

Normal heart
 Frank-Starling Mechanism- The increased volume of blood stretches
the ventricular wall, causing cardiac muscle to contract more forcefully.
Neurohormonal System activation
Sympathoadrenal axis- increase in sympathetic tone secondary to
increase adrenal secretion of circulating epinephrine and increased
neural release of norepinephrine.
Initially, increase heart rate and myocardial contractility.
Later, hypermetabolism, increased afterload, arrythmogenesis, increased
myocardial oxygen requirements, and direct myocardial toxicity.
Activation of RAAS
Myocardial structural changes-dilatation or hypertrophy

Compensatory mechanism
Compensatory mechanism
 Low Output Failure

High Output Failure

Pathophysiology
Cardiac output = Heart Rate x Stroke volume

Tachyarrhythmia-shorten Afterload
the diastolic time interval Preload
for ventricular filling. Contractility
(intrinsic
myocardial
function)

Cardiac Output
Preload and afterload
 Myocontractility : cardiac muscle with a compromised
intrinsic contractility requires a greater degree of dilatation
to produce an increased stroke volume, and does not achieve
the same maximal CO as normal myocardium
Preload : If a dilated chamber is already dilated because of a
lesion causing an increased preload (e.g: left to right shunt
or valvular insufficiency) , there is only a little room left for
further dilatation and augmentation of CO.
Afterload : the presence of lesions that results in increased
afterload to the ventricel (e.g: aortic or pulmonic stenosis,
coarctation of aorta) decreases cardiac performance, leading
to reduced CO.
Abnormal rhythms : Tachyarrhythmia shorten the diastolic
time interval for ventricular filling.

Heart Failure
 The CO is normal or increased, but because of decreased
systemic oxygen content (secondary to anemia) or increased
oxygen demand (secondary to hyperventilation,
hyperthyroidism, or hypermetabolism), there is an inadequate
amount of oxygen delivered to meet the bodys needs.
This will result in development of signs and symptoms of heart
failure when there is no basic abnormality in
myocardial function and the CO is greater
than normal.

High output cardiac failure

 Congenital
Acquired

Causes
 Left to right shunt lesions : VSD,PDA,AVSD,ASD
Obstructive left heart lesions: Hypoplastic left heart
syndrome, coarctation of aorta, aortic stenosis
Common mixing unrestricted pulmonary flow :
Truncus arteriosus, TAPVD, tricuspid atresia, TGA,
single ventricle, pulmonary atresia with VSD,large
aortopulmonary collateral
Valvular regurgitation: AV valve regurgitation,
Eibstein anomaly, semilunar valve regurgitation
Myocardial Ischemia : anomalous origin of left
coronary artery from pulmonary artery.

Congenital
Causes
 Acquired valvular disease : chronic rheumatic valvular
disease, post infective endocarditis
Myocardial disease

Acquired
Causes
 Effect the hearts contractility.
Secondary cardiomyopathy:
Arrythmia-induced: Acute
Primary congenital heart block, atrial myocarditis:
cardiomyopathy: etopic tachycardia
Infection: post viral Viral
Idiopathic myocarditis, Chagas disease. Rheumatic
Familial Ischemic: Kawasaki disease Kawasaki
Myopathic : muscular disease
dystrophy
Pompe disease ,
mitochondrial disease
Metabolic: hypothyroidism
Drug-induced: anthtracycline
Others: iron overload
(thalassemia)

Causes: Myocardial disease (Acquired)

 Fetal:
Severe anemia (hemolysis,fetal-maternal
transfusion,parvovirus B19-induced
anemia,hypoplastic anemia)

Supraventricular tachycardia
Premature Neonate:
Ventricular tachycardia
Fluid overload
Complete heart block
PDA
VSD
Cor Pulmonale
(bronchopulmonary dysplasia)

Etiology according to age

group
 Full-term neonate
Asphyxial cardiomyopathy
AVM
Left-sided obstructive lesions (coarctation
of aorta, hypoplastic left side of the heart)
Large mixing cardiac defects (single
ventricle,truncus arteriosus)
Viral myocarditis

Infant-Toddler
Left-to-right cardiac shunts (VSD)
Hemangioma
Anomalous left coronary artery
Metabolic cardiomyopathy
Acute hypertension (HUS)
SVT
Kawasakis disease
 Child-adolescent
Rheumatic fever
Acute hypertension (glomerulonephritis)
Viral myocarditis
Thyrotoxicosis
Hemochromatosis-hemosiderosis
Cancer therapy
Sickle-cell anemia
Endocarditis
Cor pulmonale (cystic fibrosis)
Cardiomyopathy
 Metabolic acidosis
Cardiogenic shock

Complications
 History
Physical Examination
Investigation
Treatment

Approach to patient
 NEONATES & INFANTS
Poor feeding
Tachypnoea worsening during feeding
Sweating during feeding
Poor weight gain
Irritable
Weak cry
Wheezing
Labored breathing
Recurrent chest infections

OLDER CHILDREN
Fatigue
Exercise intolerance
Dyspnoea pulmonary congestion
Pedal edema
Growth failure

History
1) Poor perfusion- cool extremities, decreased
capillary refill, decreased peripheral pulses, and
low systemic blood pressure.
2) Pulmonary congestion- resting tachypnea,
respiratory distress (chest retractions, use of
accessory muscles, infants with gruntings and
nasal flaring). Wheezing and crepitation are
more common in older children
3) Systemic congestion hepatomegaly, raised JVP
(usually not in infants and younger children),
peripheral edema.

Physical Examination
 High blood pressure limited to upper
extremities and/or feeble pulses in lower extremities
are suggestive of aortic coarctation
The presence of a systolic murmur may be seen in
patients with outflow obstruction in hypertropic
cardiomyopathy or aortic stenosis, congenital heart
defects with left-to-right shunting (eg, ventricular
septal defects), or mitral regurgitation.
Precordial examination may reveal a thrill in patients
with shunt lesions, whereas those with a long-standing
cardiomyopathy may have a heave with a laterally
displaced point of maximal impulse.

Others
 Blood tests
Chest X-Ray
ECG
Echocardiography
Doppler ultrasound

Investigation
1) Full blood count-anemia, leukocytosis
2) Liver function tests elevated due to hepatic congestion
with right-sided heart failure.
3) Serum electrolytes, blood urea nitrogen, and creatinine.
Hyponatremia due to water retention.
Hyperkalemia may represent tissue destruction due to low CO
or renal compromises.
High BUN and creatinine due to reduced RBF may suggest
renal impairment.
* Brain natriuretic peptide (BNP) - cardiac hormone secreted by the
ventricular cells in response to increased wall stress in volume or
pressure overload

Blood Tests
 e.g: Ventricular
Septal Defect

Findings:

Cardiomegaly
Pulmonary edema

Case courtesy of Dr Frank Gaillard, Radiopaedia.org

Chest X-Ray
 Sinus tachycardia
Varying degrees of heart block may sometimes be
observed in patients with rheumatic or lyme carditis,
or in patients with neonatal lupus.
Increased QRS voltage that meets criteria for
ventricular hypertrophy may be seen in hypertrophic
or dilated cardiomyopathy
Decreased QRS voltage may suggest myocardial
edema or pericardial effusion, and may be present in
children with myocarditis

ECG
 Assess ventricular function

Fractional Cardiac
shortening output

Eyeballing
Cardiac Index
of LVF

Ejection
fraction (EF) Contractility
- Simpson (dp/dt)
method
lower cost, less risk, and greater
availability compared with cardiac Stroke
magnetic resonance imaging or Tei index
volume
cardiac catheterization

Transthoracic Echocardiography (TTE)

 Estimate cardiac output
Assess cardiac function, wall motion abnormalities as it
records motion of blood inside the heart.
Obstruction in arteries
Measure degree of narrowing or leakage of heart valve

Doppler ultrasound
 Aim:
Treat underlying causes
enhancing cardiac contractility
reducing the preload and afterload
improving oxygen delivery

Management
 Oxygen supplementation, keep in propped up
position
Keep warm, gentle handling
Fluid restriction to normal maintenance if not
dehydrated
Correct anemia, electrolyte imbalance, treat
concomittant chest infections.
Diets-increased daily calorie intakes

Management- General Measures

 Total daily fluid requirement = Normal Maintenance
Fluids + Deficit + Ongoing Abnormal Losses
Factors that increase caloric requirements: Similar to
adults, certain factors will increase daily caloric
requirements in children.
FACTOR INCREASE IN CALORIC
NEED2
AGE Kcal/kg/da
(yrs) y Fever 10 - 12 % for each degree >
37o C
0-1 90 - 120
Cardiac failure 15 - 25 %
1-7 75 - 90
Major surgery 20 - 30 %
7 - 12 60 - 75
Burns up to 100 %
12 - 18 30 - 60
Severe sepsis 40 - 50 %
Long term growth failure 50 - 100 %
 Diuretics increased water and sodium loss, providing
symptomatic relief in fluid overload
Loop diuretics (more powerful agents than thiazide)-
frusemide, bumetanide
Spironolactone-potassium-sparing diuretics, aldosterone
antagonist
ACE inhibitor : afterload-reducing agent, by decreasing
peripheral vascular resistance.
Captopril-greater stability in liquid formulation
Enalapril-require less frequent dosing
Digoxin-useful in HF with excessive tachycardia, SVT
IV inotropic agents- dopamine, dobutamine, adrenaline,
milrinone
Use in acute HF, cardiogenic shock, post-op low output
syndrome

Anti Failure Medications

 Aetiology establishment
Specific treatment for targeted aetiology
Congenital-surgery
Heart block- pacemaker
Post infectious glomerulonephritis- control BP
Acute rheumatic carditis High dose aspirin

Specific management
Mnemonic for management
 Respiratory distress
Neonates-Respiratory distress syndrome, transient tachypnea of
the newborn, meconium aspiration, congenital diaphragmatic
hernia, pneumothorax, pneumonia, and pulmonary hypoplasia.
Older infants and children Pneumonia, asthma, and
gastroesophageal reflux.
Poor weight gain and FTT- Gastrointestinal causes include
protein-milk allergy, cystic fibrosis, and celiac disease, Chronic
infections, Hyperthyroidism, Metabolic disorders
Fatigue in older children may be due to sleep apnea, depression
Peripheral edema may be caused by renal failure or venous
thrombosis
Shock may be due to overwhelming sepsis or hypovolemia

Differential Diagnosis
 Nelson Textbook of Pediatric, 16th edition
Paediatric Protocols, 3rd edition
Heart Failure in children and young adults, Anthony
C.Chang, Jeffrey A.Towbin

References
Thank You !