CLASSIFICATION

& MANAGEMENT
OF HEART
FAILURE IN
CHILDREN
 BACKGROUND
HEART FAILURE IN CHILDREN

• A serious public health concern.

• Etiology and pathogenesis are different than adults
• A major cause of morbidity and mortality.
• A greater understanding of the pathophysiology of
heart failure may help inform therapeutic strategies
• The overall outcome is better than adults
CARDIAC PHYSIOLOGY
CARDIAC PHYSIOLOGY

Figure
20.20
CARDIAC PHYSIOLOGY

Figure
20.23
 Heart Failure
Determinants of Ventricular Function

CONTRACTILITY

PRELOAD AFTERLOAD

STROKE

VOLUME
- Synergistic contraction
- Valvular competence
HEART
RATE

CARDIAC OUTPUT
ETIOLOGY OF PHF
PATHOPHYSIOLOGI

• Pediatric Heart failure cause by :

-> Ventricular pump dysfunction
-> Volume overload (preload)
-> Pressure overload (afterload)
 PATHOPHYSIOLOGI
• The heart is unable to pump sufficient blood ,
provided the venous return is normal

• Insufficient oxygen and nutrient supply to the

tissues,and cells+ insufficient removal of the
metabolic endproducts

• Is aclinical syndrome that develops as a final

common pathway of diverse cardiac
injuries.
.
->Decrease myocardial performance

->Myoacardium metabolic demand unmet

->Compensatory mechanism take place

->Initially compensated, at the end become

decompensated

->Functional and structural disturbance of the

heart
 There are two main categories
of causes of pediatric heart
failure

• the heart muscle pumps well, but the route

that blood takes is very inefficient.

• where the structure of the heart is normal, it

is usually due to a weakening of the heart
muscle
Compensatory mechanism
Compensatory Responses
Compensatory mechanisms

• Increasing the heart rate

• Hypertrophy of muscle
• Dilatation of heart
• Increasing the preload

As the demands on the heart exceed the

normal range of physiologic
compensatory mechanisms, signs of
CHF occur.
 NEUROHUMORAL COMPENSATION
N/H changes Favorable effect Unfavor. effect

 Sympathetic  HR , contractility, Arteriolar constriction 

activity vasoconst.   V return, After load  workload
 filling  O2 consumption

 Renin-Angiotensin – Salt & water retention Vasoconstriction 

Aldosterone VR  after load
 Vasopressin Same effect Same effect
Prostaglandin
Prostasiklin
 GFR
 interleukins May have roles in myocyte Apoptosis
&TNF hypertrophy
 Endothelin Vasoconstriction VR  After load
Common signs and symptoms of heart failure
 NYHA and modified Ross classification of heart
failure in children
illustrates a
useful construct to assist the clinician in their evaluation, based on the presence of abnormal perfusion
and increased fluid congestion
NEW YORK HEART ASSOCIATION CLASSIFICATION FOR OLDER
CHILDREN AND ADULTS

• Class 1 : No limitation of physical activity, ordinary physical activity doesn’t

cause undue fatique, palpitation,or dyspnoe

• Class 2 (mild): Slight limitation of physical activity. Comfortable at rest, but

ordinary physical activity results in fatique, palpitations, or dyspnoe.

• Class 3 (moderate) : Marked limitation of physical activity. Comfortable at

rest, but less than ordinary activity causes fatique, palpitations, or dyspnoe.

• Class IV (severe) : Unable to carry out any physical activity without

discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is
undertaken, discomfort is increased
CLASIFICATION OF PHF
 • Eliminate the causes of PHF
• Control the symptoms and disease progression.
-General measures
-Medical therapy
-Diuretics
-ACE inhibitors
Therapeutic approach -b blockers
-Inotropes
-Sympathomimetic amines
-Phosphodiesterase type III inhibitors
-Calcium sensitizer
-Vasodilators
-Promising new therapies
-. Device therapy
-Heart transplantation
OPTIMAL TREATMENT
• -> Ensuring an accurate
diagnosis

• ->Defining etiology
Treatment of PHF
• Based on clinical experience
• Extrapolation of adult data
• Supported by by the more limited pediatric
literature

The Goal of treatment

1. To maintain stability
2. Prevent progression
3. To allow somatic growth and optimal
development
Pharmacologic Treatment of Heart Failure
weakness of heart muscle
 workload 1. Increase  workload
4. I n c r ea s e u r i ne
iproduction
n s u f f ic i e n contraction
t
f or c e o f
blood
salt & fluid p u m p ed blood vessels
retention 2. Block the contract
RAAS

Activates the
Renin-Angiotensin Aldosterone System
Sympathetic Nervous System

3. Block the SNS

The drugs which are still
investigational include

• Natriuretic peptides
• Vasopressin antagonist
• Renin inhibitor endothelin antagonis oral
phosphoddiesteras inhibitors
• Anti inflammatory molecules
• Nitric oxide agonists neuropeptidase
antagonist
DEVICE THERAPY IN PHF
• Pacemaker
• CRT (CARDIAC RESYNCHRONIZATION THERAPY)
• Mechanical circulatory support
• Implantable cardioverter defibrillator (ICD)
• ECMO(extracorporeal membrane
• Ventricular Assist Device (VAD)
• Heart transplant remains the therapy of choice for
end stage PHF refractory to surgical and medical
therapy
FUTURE CHALLENGES