HEART FAILURE

HEART FAILURE(HF):

 Definition.
 Etiology
 Pathogenesis and Pathology
 Clinical manifestations.
 Management.
Definition:

“It’s a clinical syndrome in which heart is not

able to pump enough blood to the body to
meet it’s metabolic needs,
to dispose off the venous return adequately (
or a combination of the two),
or can sustain normal output only by
compensatory mechanisms.”
HF v/s Cardiogenic shock.
CAUSES:

BY MECHANISM:
 Volume overload.

 Pressure overload.

 Primarily abnormal myocardial function.

BY AGE:
 Fetal.

 Neonatal.

 Infants.

 Children.
VOLUME OVERLOAD:

 Shuntlesions.
 Regurgitant lesions.

 Severe anemia.
 Renal failure.
 Excessive intravenous infusion.
PRESSURE OVERLOAD:

 Severe AS, coarctation of aorta.

 TAPVD with obstruction.
 Mitral atresia.
 Systemic hypertension.
 Severe pulmonary hypertension (immediate
newborn period).
Myocardial failure with normal
loads:
 Myocarditis.
 Cardiomyopathy.
 Myocardial infarction.
 Metabolic.
 Arrhythmias.
 Severe anemia.
Causes in fetus:

 Anemia. (Rh sensitization)

 Arrhythmias. (SVT, VT, heart block, AF)
 Severe regurgitant lesions.
 Myocarditis.
Neonatal Period:
 Myocardial  Volume overload:
dysfunction:
Shunt lesions.
Asphyxia.
A-V fistulas.
Sepsis.
 Arrhythmias:
Hypoglycemia and other
metabolic SVT, AF, AFl.
abnormalities. Congenital complete heart
Myocarditis. block.
 Pressure overload:

AS.
Coarctation.
Severe PHT.
Infants:

 Volume overload:  Secondary heart failure:

Shunt lesions: Renal disease.
Ventricular level, atrial Hypertension.
level, great vessel level. Sepsis.
 Myocardial failure:

Endocardial fibroelastosis
Pompe’s disease,
myocarditis, Kawasaki’s
disease
Childhood:
 Palliated CHDs.
 A-V valve regurgitation.
 Rheumatic fever.
 Viral myocarditis.
 Cardiomyopathy.
 Bacterial endocarditis.
 Secondary causes: AGN, Sickle cell anemia,
drug induced cardiomyopathy.
PATHOPHYSIOLOGY:

Manifestations of HF are secondary to:

 Compensatory mechanisms.

 Low cardiac output.

 Venous congestion.
Compensatory Mechanisms:
Sympathetic over-activity:
Leads to:
Occurs due to:
Increased α stimulation:
I. Stimulation of atrial Reduced blood flow to
and venous stretch limbs, splanchnic
circulation and kidneys.
receptors.
Increased β stimulation:
II. Stimulation of aortic Increased cardiac activity,
and carotid tachycardia.
baroreceptors. Increased cholinergic
sympathetic activity:
Increased generalized
sweating, particularly in
infants, more with
exertion.
Long Term Effects:

 Hypermetabolism.
 Potential for arrhythmia.
 Increased myocardial oxygen requirements.
 Peripheral vasoconstriction.
 Down regulation of β adrenergic receptors and
direct myocardial cell damage secondary to
circulating catecholamines.
Fluid retention in HF:
Due to decreased renal excretion of sodium and
secondary water retention.
3 mechanisms:
 Decreased GFR: Due to
↓ RBF,↑ renal vascular resistance, ↑ angiotensin.
 Increased aldosterone: Due to
↑ adrenal secretion, ↓ hepatic degradation.
 Increased Renin: Due to
↓ GFR
Sodium retention intensified by exercise.
Myocardium:
 Systolic dysfunction.
 Diastolic dysfunction.
 Chamber dilatation followed by hypertrophy.
 Dilation occurs due to volume overload and
impaired function of myocardium.
 Oxygen requirement increases; may further
increase myocardial dysfunction.
Ventricles:

 Protodiastolic gallop (S3).

 Mitral and tricuspid regurgitation.
 Pulsus alternans.

Atria:
 Dilatation and hypertrophy; S4.
 Increase in venous pressures.
Pulmonary veins:
 Increased pulmonary venous pressure:
Respiratory difficulty.
Orthopnea, pulmonary edema.
 Increased bronchial venous pressure:

Cough, wheezing, rhonchi.

 Systemic Arteries:
Increased sodium and water content: stiffness.
Systemic veins:

Increased systemic venous pressure leads to:

 Increased JVP.

 Hepatomegaly.

 Splenomegaly.

 G.I. venous congestion.

 Pitting edema less common due to large

venous capacitance.
 Ascites (usually with right sided heart failure
and tricuspid valve dysfunction).
CLINICAL MANIFESTATIONS:
Infancy:
Symptoms:
 Feeding difficulties.

 Failure to thrive.

 Excessive perspiration.

Signs:
 Tachycardia.

 Tachypnea.

 Cool extremities, low BP with narrow pulse pressure.

 Edema.
CVS:
 Active precordium. CARDINAL
 Gallop rhythm. SIGNS
 Cardiomegaly. Tachypnea
Other signs:
Mild wheezing. Tachycardia
Rales.
Hepatomegaly. Hepatomegaly
Children:
Symptoms:
 Breathlessness.
 Orthopnea.
 Chronic hacking cough.
 Fatigue, weakness.
Signs:
 Tachycardia.
 Tachypnea.
 Coolness and pallor of exrtremities.
 Low BP, narrow pulse pressure.
CVS:
 Edema.
 Cardiomegaly.
 Gallop rhythm.
SUMMARY OF CLINICAL
FEATURES:  Low cardiac output
 Fatigue or low energy
 Tachycardia
 Pallor
 Cardiomegaly  Sweating
 Venous congestion  Cool extremities
 Right-sided  Poor growth
Hepatomegaly,Ascites  Dizziness
Pleural effusion Edema  Altered consciousness
Jugular venous
 Syncope
distension
 Left-sided
 Tachypnea,Retractions,
Rales
 Pulmonary edema
INVESTIGATIONS:
X- Ray chest:
 Cardiomegaly.
 Pulmonary edema: butterfly
pattern around hila.
ECG:
Abnormal.
Echocardiography:
 Helpful in evaluating
myocardial function (EF).
 Reveals structural
abnormalities.
Serum B type Natriuretic
Peptide (SBNP)
Treatment:
Definitive treatment:
Treating the underlying cause.
General Measures:
 Rest, semi reclining position, infant chair.

 Supplemental oxygen, mechanical ventilation.

 Correction of anemia, treatment of infection, fever.

Diet:
 Extra calorie.

 No added salt diet; low sodium diets are not

palatable.
Pharmacological Treatment:
Diuretics.

Afterload reducers.
Cardiac glycosides.
Diuretics:

Furosemide 1-3 mg/kg, 1-4 Chlorthiazide 25-50

times/day mg/kg/day

Hydrochlorthiazi 1-2 mg/kg/day

Bumetanide 0.015-0.1 mg de
/kg, 1-2
times/day
Spironolactone 1-2 mg/kg/day

Metolazone 0.2-0.4 mg/kg

OD Triamterene 2-4 mg/kg/day
After load reducers:
General Features:
Specially useful for patients with
 Cardiomyopathy

 Severe MR, AR and

 Left-to-right shunts;

Not generally used in the presence of stenotic lesions

ACEIs and ARBs:
May have additional beneficial effects on cardiac
remodelling.
 Intravenously administered agents such as nitroprusside
should be administered only in an intensive care setting
and for as short a time as possible.
AFTERLOAD-REDUCING AGENTS:
 Captopril:
Prematures: Start at 0.01 mg/kg/dose; 0.1-0.4 mg/kg/day, divided q6-
24h
Infants: 1.5-6 mg/kg/day, divided q6-12h.
Children: 2.5-6 mg/kg/day, divided q6-12h.

 Enalapril:
0.08-0.5 mg/kg/day, divided q12-24h

 Hydralazine:
IV: 0.1-0.5 mg/kg/dose (maximum, 20 mg)
PO: 0.75-5 mg/kg/day, divided q6-12h.

 Nitroglycerin:
IV: 0.25-0.5 µg/kg/min start; increase to 20 µg/kg/min max.

 Nitroprusside (Nipride):
IV: 0.5-8 µg/kg/min.
Cardiac Glycosides:
Less frequently used nowadays.
Usually used in conjunction with ACE
inhibitors and diuretics.
Age TDD (mcg/kg) Maitenance
(mcg/kg/day)
Prematures 20 5

Term 30 8

< 2 years 40-50 10-12

> 2 years 30-40 8-10

How to digitalize?

 Oral or intravenous.
 Calculate TDD.
 ½ TDD at ‘0’ hrs.
 ¼ TDD at ‘12’ hrs.
 ¼ TDD at ’24’ hrs.
 Maintenance: 24 hours after last dose.
 ECG monitoring.
Toxicity/poisoning:

 Vomiting.
 Abdominal pain.
 arrhythmias; supraventricular, ventricular
bigeminy, A-V blocks.
Management of digitalis
toxicity/poisoning:
 Stomach wash.
 Charcoal.
 SVT, PMC: KCl.
 Tachyarrhythmias: lidocaine, phenytoin.
 Heart block: atropine.
 Digibind ( digoxin immune Fab)
Intravenous inotropic agents:

Dobutamine : 2-20 µg/kg/min.

Dopamine : 2-20 µg/kg/min.
Isoproterenol : 0.01-0.5 µg/kg/min.
Epinephrine : 0.1-1.0 µg/kg/min.
Norepinephrine: 0.1-2.0 µg/kg/min.
Phosphodiesterase inhibitors:
Milrinone:
 Useful in refractory patients, low-output state
children after open heart surgery.
 Milrinone has both positive inotropic effects and
peripheral vasodilatory effects.
 Generally been used as an adjunct to dopamine or
dobutamine therapy in the intensive care unit.
 Dose: Intravenous infusion at 0.25-1 µg/kg/min,
sometimes with an initial loading dose of 50 µg/kg.
Chronic treatment with β blocker:
β-adrenergic blocking agents (Metoprolol and
Carvedilol)
 Improve exercise tolerance,

 Decrease hospitalizations,

 Reduce overall mortality in adults with dilated

cardiomyopathy.
Used only for the chronic treatment of patients
with heart failure.
 Clinical studies in children show mixed
results, potentially due to the significant
heterogeneity of the populations being
studied.
Newer Approaches
Biventricular Resynchronization Pacing:
 Tried in adults with dilated cardiomyopathy.

 Results in better synchronization of right and

left ventricle contraction.
 Showing early success in children also.

Ventricular Assist Device:

 Mechanical device, augments pumping of
heart.
Cardiac Transplantation
Key Takeaways:

 Etiology of HF in pediatric age group

depends on the age.
 Signs and symptoms are due to failing heart
and compensatory mechanisms.
 Management includes supportive care and
pharmacotherapy in addition to the
treatment of the underlying cause.