This document provides an overview of heart failure in pediatrics. It discusses that heart failure is a clinical syndrome caused by low cardiac output, characterized by symptoms and signs associated with circulatory, neurohormonal and molecular abnormalities. The pathophysiology involves compensatory mechanisms like activation of the sympathetic nervous system and renin-angiotensin-aldosterone system in response to the initial reduction in cardiomyocyte contractility that can eventually become maladaptive. Clinical features in infants include difficulties feeding and cyanosis, while older children may experience fatigue, shortness of breath, and exercise intolerance. Investigations and therapeutic approaches aim to eliminate the underlying cause and control symptoms and disease progression.

1. CMT05211: Paediatrics and Child
Health II
Heart Failure
Presenter Diana Lawrence

2. Introduction
Heart failure is a clinical syndrome caused by low cardiac output.
 It is a clinical syndrome characterized by typical symptoms and signs
associated with specific circulatory, neurohormonal and molecular
abnormalities.

3. ETIOLOGY

4. PATHOPHYSIOLOGY
• The index event, regardless of the cause, produces an initial reduction of
cardiomyocyte contractility in HF. The initial injury results in a reduction in
cardiac output that is, in turn countered with two major compensatory
mechanisms.
• The first of these mechanisms is the activation of the sympathetic nervous
system, resulting in increased release and decreased uptake of
norepinephrine, with peripheral vasoconstriction to maintain( by increasing
systemic vascular resistance) mean arterial pressure and organ perfusion.
Enhanced catecholamine levels, however lead to further cardiomyocyte
injury, dysfunctional intracellular signaling and ultimately cardiomyocyte
death

5. cont…
• The second mechanism is the stimulation of rennin- angiotensin
aldosterone system, consisting of increased circulating levels of
rennin, angiotensin II and aldosterone. Renin is responsible of
cleaving angiotensinogen in angiotensin I, which is converted into
angiotensin II by angiotensin converting enzyme. Angiotensin II is a
potent vasoconstrictor that preserves end-organ perfusion. Aldosterone
causes salt and water retention, resulting in increased preload and then
cardiac output according to Frank- Starling mechanism. However the
elevation of both aldosterone and angiotensin II promotes cardiac
fibrosis and apoptosis. These mechanisms may temporary contribute
to circulatory stability, but over time become maladaptive and promote
the progression of HF

6. CLINICAL FEATURES
In infants and young children
• Difficult in feeding( from prolonged feeding time intake to frank
intolerance)
• Cyanosis
• Tachypnea
• Sinus tachycardia
• Diaphoresis

7. cont.…
In older children
• Fatigue
• Shortness of breath
• Tachypnea
• Exercise intolerance
• Abdominal pain
• Oliguria
• Leg pitting edema

8. MODIFIED ROSS CLASSIFICATION

9. INVESTIGATIONS
• Electrocardiogram
• Chest radiography
• Echocardiogram
• Complete blood count
• Electrolytes
• Renal function test
• Liver function test
• Natriuretic peptides
• Thyroid function test

10. • Arterial blood gas
• Cardiac magnetic resonance
• Cardiac catheterization
• Endomyocardial biopsy

11. Therapeutic approaches
Treatment of paediatric heart failure aims to
Eliminate the cause
Control the symptoms and disease progression
 ELIMINATE THE CAUSE
• Correct treatment should be performed in CHDs
• Systemic diseases (such as sepsis) or electrolytic imbalance ( such as
hypocalcaemia) must be carefully researched and treated

12. CONTROL OF SYMPTOMS AND
DISEASE PROGRESSION