mechanism of HF in CHILDREN

1. Heart Failure in Pediatrics
Dr.Mariam Mahmoud Hassan
Specialist Pediatrician
Cairo University , Cairo, Egypt

2. • The heart is the central pump of the cardiovascular system that
drives blood through the blood vessels.
• It is a muscular structure, which is made up of four chambers.
Two atria (right and left) which are separated from each other by
the interatrial septum.
Two ventricles (right and left) which are separated from each other
by the interventricular septum
The human heart contains four valves
Two atrioventricular valves (AV valves) between the atria and the
ventricles:
o Tricuspid valve between the right atrium and the right ventricle.
o Mitral valve between the left atrium and there left ventricle.
Two semilunar valves:
o Aortic valve between the left ventricle and the aorta.
o Pulmonary valve between the right ventricle and the pulmonary
trunk.
The heart

3. Blood flow from the heart
• During ventricular systole, blood is pumped into
the circulation.
• During diastole, the pumping of blood stops and
the ventricles get filled with blood.

4. Cardiac output
 Cardiac output is the blood flow generated by
ventricles per minute.
• The cardiac output is equal; to the volume of blood
pumped by ventricles per beat × the number of beats
per minute:
Q = SV × HR
Where Q = cardiac output, SV = stroke volume, and HR =
heart rate.

5. Factors Affecting Cardiac Performance
• Cardiac output depends on: stroke volume
and heart rate.
• Stroke volume is dependent on three
important factors:
• Preload,
• Afterload and
• contractility.

6. • Preload = volume of blood received by the heart.
• Basically, preload is stretch. The amount of volume
being returned to the heart.
• Afterload = pressure or resistance the heart has to
overcome to eject blood.
• Afterload is squeeze. The amount of resistance that
the heart has to overcome in order to eject blood.

7. • Preload:
• Preload (volume overload).
• preload (such as in VSD, or valvular insufficiency).
• Afterload:
• Afterload is the resistance (pressure) against which the
heart must pump blood: e.g; systemic vascular resistance.
• Afterload (such as with aortic stenosis, pulmonary stenosis,
or coarctation of the aorta)
• Contractility
• Contractility (Cardiac Performance Independent of Preload or
Afterload)
• Volume overload is the most common cause of CHF in
children

9. PATHOPHYSIOLOGY OF HEART
FAILURE

10. Definition of Heart Failure:
is a clinical syndrome in which an abnormality of
cardiac structure or function which is responsible
for the inability for the heart to eject or fill with the
blood at a rate to meet the requirements of the
metabolizing body tissue and maintain hydrostatic
relationship at normal levels.

11. MECHANISM OF HEART
FAILURE:
Systolic and diastolic heart
failure:
In systolic heart failure-impairment of
myocardial contractility causes weak
systolic contraction and leads to reduced
stroke volume and cardiac output and
unable to propel blood to aorta.

12. In diastolic heart failure –
there is impaired relaxation and filling of ventricles
and leads to elevated Ventricular diastolic pressure.
Diastolic heart failure is in those with ejection
fraction >50%.
In diastolic HF the cardiac output may be normal
Or well maintained with exercise but may be
symptomatic with filling pressure

13. CAUSES OF ADAPTIVE AND
MALADAPTIVE MECHANISMS:
1.Excessive work load in normal
myocardium—in congenital/acquired heart
disease
2.A normal work load faced by a damaged
myocardium eg inflammation.

14. FRANK-STARLING MECHANISM:
Increase in end diastolic volume of ventricle
is associated with stretching of heart muscle
and enhancing contraction .
But the ventricular dilatation becomes
maladaptive when excessive-- as increased
wall stress reduces shortening (Laplace’s
Law).

18. The muscle contraction may weaken due
to over loading during diastole.
In healthy person over loading
Causes muscle contraction to raise cardiac
output (Frank-Starlings Law).
In heart failure weak cardiac
Fails to pump adequate amount of blood.

19. To compensate lowered cardiac output heart rate
increases.
Stroke volume reduces as the contractions start to
fail.
If the volume of blood at the end of systole rises
means less blood is ejected or if the volume
decreases after diastole means less blood enters the
heart

20. The cardiac reserve may reduce.
The heart needs to cope with normal metabolic
demands, elevated demands
During exertion.
In heart failure the reserve is lowered.

21. With time the heart starts to enlarge leading to
hypertrophy.
Initially heart muscle fibers increase
In size to improve contractility but
with time become stiff and of no benefit.
The arterial blood Pressure falls with reduced
flow to kidneys.

22. Compensatory mechanisms in heart failure
(1) Cardiac compensation
– increased HR and cardiac contractility
– Cardiac dilatation (The Frank-Starling mechanism)
– Myocardial hypertrophy
(2) Systemic compensation
– Increase the blood volume
– Redistribution of blood flow
– Increase of erythrocytes
– Increased ability of tissues to utilize oxygen
(3) Neurohormonal compensation
– Sympathetic nervous system
– Renin-angiotensin system
– Atrial natriuretic peptide; endothelin

23. Etiology of Heart Failure
Fetus Premature Neonate
Severe anemia (hemolysis, fetal-maternal
transfusion)
Fluid overload
Supraventricular tachycardia PDA
Ventricular tachycardia VSD
Complete heart block
Full-Term Neonate Infant-Toddler
Asphyxial cardiomyopathy Left-to-right cardiac shunts (VSD)
Left-sided obstructive lesions (coarctation of aorta) Metabolic cardiomyopathy
Transposition of great arteries Acute hypertension (hemolytic-uremic syndrome)
Viral myocarditis Supraventricular tachycardia
Anemia Kawasaki disease
Supraventricular tachycardia
Complete heart block
Child-Adolescent
Rheumatic fever Acute hypertension (glomerulonephritis)
Viral myocarditis Thyrotoxicosis
Endocarditis Cor pulmonale (cystic fibrosis)
Arrhythmias Chronic upper airway obstruction (cor pulmonale)
Cardiomyopathy

24. CLINICAL MANIFESTATIONS
• Clinical presentation of CHF in infants includes poor
feeding, failure to thrive, tachypnea, and excessive
sweating with feeding.
• Older children may present with shortness of breath, easy
fatigability, and edema.
• The physical examination findings depend on whether
pulmonary venous congestion, systemic venous
congestion, or both are present.
• Tachycardia, a gallop rhythm, and thready pulses may be
present with either cause.
• If left-sided failure is predominant, tachypnea, orthopnea,
wheezing, and pulmonary edema are seen.
• If right-sided failure is present, hepatomegaly, edema, and
distended neck veins are present.

25. IMAGING STUDIES
• chest x-ray: cardiomegaly.
• ECG: Arrhythmias
• An echocardiogram assesses the heart
chamber sizes, measures myocardial function
accurately, and diagnoses congenital heart
defects when present.

26. Treatment principles
• (1) Correct the underlying causes of HF
• (2) Diet; (low salt and high calories)
• (3) Digitals; Improve the cardiac contractility
• (4) Diuretics; Reducing preload: frusemide
• (4) Dilators; Reducing afterload; ACE
• Remember 4 D

27. Treatment of Heart Failure
General Care
Rest Reduces cardiac output
Oxygen Improves oxygenation in presence of
pulmonary edema
Sodium, fluid restrictions Decreases vascular congestion; decreases
preload
Other
Treatment of underlying causes Closure of defects like ASD or VSD
Transplantation Removes diseased heart

28. Diuretics; Reducing preload
Diuretics
Fruosemide Salt excretion by ascending loop of Henle;
reduces preload
Spironolactone Potassium-sparing diuretic

29. Improve the cardiac contractility
Inotropic Agents
Digitalis Inhibits membrane Na+, K+-ATPase and
increases intracellular Ca2+, improves
cardiac contractility, increases myocardial
oxygen consumption
Dopamine Releases myocardial norepinephrine plus
direct effect on β-receptor, may increase
systemic blood pressure; at low infusion
rates, dilates renal artery, facilitating
diuresis

30. Dilators; Reducing Afterload
Afterload Reduction
Hydralazine Arteriolar vasodilator
Nitroprusside Arterial and venous relaxation;
venodilation reduces preload
Captopril/enalapril Inhibition of angiotensin-converting
enzyme; reduces angiotensin II
production