This document defines pediatric heart failure and reviews its pathophysiology, clinical manifestations, common causes, and treatment. Pediatric heart failure is characterized by insufficient cardiac output to meet metabolic demands, leading to compensatory responses aimed at restoring perfusion. Common causes include excessive preload/afterload, arrhythmias, or decreased contractility. Clinical manifestations vary by age but include feeding difficulties, dyspnea, edema, and hepatomegaly. Treatment focuses on reducing preload and afterload, enhancing contractility and nutrition, and may include ACE inhibitors, beta-blockers, diuretics, or heart transplantation in severe cases.

1. Heart Failure
Henok Tadele
Associate Professor
Pediatrics and child health
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2. Learning Objectives
1. Define Pediatric heart failure (HF) and review its
Pathophysiology.
2. Describe the clinical manifestations of Pediatric HF
3. Identify common Pediatric HF syndromes.
4. Recognize the differences between Pediatric and adult HF
5. Discuss the treatment of Pediatric HF
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3. Definition: Heart failure
• A syndrome
• Cardiac output is insufficient to meet the metabolic
demands of the body.
• Decreased cardiac output leads to a cascade of
compensatory responses that are aimed directly or indirectly
at restoring normal perfusion to the body's organs and
tissues.
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4. • Cardiac output--- Stroke volume X Heart rate
• Heart rate varies with age
• Stroke volume is the amount of blood ejected per beat
• Preload– the amount of blood returning to the heart during diastole
• After load— the amount of pressure exerted against ventricular
ejection during systole
Definition: Heart failure
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5. Causes of Pediatric heart failure
•Excessive preload
•Excessive afterload
•Abnormal rhythm
•Decreased contractility
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6. Pathophysiology
• Unmet tissue demands for cardiac output result in activation
• Renin—angiotensin-aldosterone system
• Sympathetic nervous system
• “Signaling” cascades that trigger cachexia
• Stimulation of the sympathetic nervous system and increased release
of catecholamines cause tachycardia, enhanced myocardial
contractility, and maladaptive forms of cardiac hypertrophy.
• Initially quite helpful.
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7. Cardiac remodeling
• Structural transformation in which the normally elliptical heart increases
in mass and becomes more spherical
• Maladaptive cardiac hypertrophy
These processes result in a poorly contractile and less compliant heart
leading to
• Increased filling pressures
• Pulmonary or systemic edema
• Hypoxia
• Redistribution of blood flow away from skeletal muscle and the splanchnic
circulation, lactic acidosis, and loss of lean body mass (cachexia).
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8. Cardiac Cachexia
• Cachexia is a state of catabolic/anabolic imbalance leading to
• weight loss and disordered homeostasis
• involves inflammatory cytokines such as tumor necrosis factor-alpha (TNF-
alpha) and interleukins, as well as neurohormonal activation.
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9. Assessment
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10. Clinical manifestations
• Infants
• Feeding difficulties associated with loss of appetite (anorexic
hormones)
• Dyspnea
• Increased fatigability
• Failure to thrive
• Respiratory distress, gallop rhythm, hepatomegaly
• Older children (similar to adults)
• Edema
• JVD
• Cough, wheezing, crackles etc.
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11. Causes of heart failure: Structurally abnormal
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12. Causes of heart failure: structurally normal
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13. Disorders of Contractility
• Dilated cardiomyopathy is characterized by enlarged ventricular
chambers and impaired systolic and diastolic function.
• Idiopathic
• Infection (myocarditis)
• Operative injury
• Chemotherapy (most commonly due to anthracyclines),
• Degenerative or metabolic diseases (certain muscular dystrophies,
mitochondriopathy, hyperthyroidism).
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14. Restrictive cardiomyopathy
• Idiopathic
• Infiltrative or storage diseases (hemochromatosis, Pompe disease).
• The hallmark of restrictive cardiomyopathy is abnormal diastolic function.
• The echocardiographic image shows enlarged atria and nondilated, mildly hypertrophied
ventricles with abnormal tissue Doppler indices.
• Hypertrophic cardiomyopathy, such as idiopathic hypertrophic subaortic stenosis, seldom is
associated with pediatric HF.
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15. Management
Treat the cause!!!!!
• Structural heart disease
• Arrhythmia
• Cardiomyopathy
• Systemic disorder
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16. General Principles of treatment
• Reducing the preload
• Enhancing cardiac contractility
• Reducing the afterload
• Improving oxygen delivery
• Enhancing nutrition
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17. Principles of management of heart
failure
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18. Treatment options
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19. Angiotensin-Converting Enzyme Inhibitors
• ACEI improve survival and slow progression of heart failure
• Should be used in all patients with heart failure
• Should not be stopped unless side effects are intolerable
• Beneficial in shunt lesions
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20. Beta-blocker therapy
• Another approach to resting the failing heart is through
inhibition of the sympathetic nervous system.
• Beta-blocker therapy is a cornerstone of the medical
management of HF in adults.
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21. Diuretics
• reduce preload, thereby improving Frank- Starling relationships in the
heart.
• Decreased preload helps to prevent pulmonary edema-producing high
cardiac filling pressures.
• Besides loop diuretics such as furosemide, other classes of diuretics are
used, including thiazides and mineralocorticoid inhibitors
(spironolactone).
• Recent data suggest that aldosterone inhibition also helps to prevent
maladaptive cardiac remodeling and interstitial fibrosis.
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22. Digoxin
• The only commonly used oral inotropic agent
• most important mechanism of action may be its ability to blunt the
sympathetic nervous system, slow the heart rate, and increase cardiac
filling time
• Despite its wide usage in treating pediatric HF, no studies have
demonstrated its efficacy.
• close therapeutic/toxic ratio demands close surveillance, especially if the
patient is in renal failure
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23. Heart transplantation
• The ultimate therapy for HF
• The decision to proceed with heart transplantation is based on the
likelihood of successful medical therapy, quality of life, donor
availability, and institutional preference
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