Heart failure in children

Introduction

 HF occurs when the heart can no

longer meet the metabolic demands
of the body in case of normal venous
filling pressure.
 Cardiac output (CO) = stroke
volume (SV) X heart rate (HR)
 Compensatory mechanisms are:
◼ Increasing HR with neurohormonal controll
◼ Dilation of cardiac cavities
◼ Myocardial hypertrophy walls
Situations
 Low cardiac output – Congestive HF
 High output cardiac failure:
◼ Severe anemia,
◼ Sepsis with Gram -negative germs,
◼ Beriberi ( deficit vitamin B1) ,
◼ Thyrotoxicosis,
◼ Fistulas/arteriovenous malformations
 Pathophysiology
 Myocytes exhaustion – necrosis
 Stimulation of fibroblast proliferation
 Cardiac dilatation and systolic
dysfunction
 In the acute form:
◼ adrenergic systems and renin-angiotensin-
aldosteron system activation to maintain
flow.
◼ Increasing of the myocardial contractility
with peripheral vasoconstriction, fluid
retention to maintain BP
Classification

 Right/left
 Systolic/diastolic
 HF with low CO and increased
pulmonary vascular resistance (PVR)
or increased CO and low PVR.
 Functional - NYHA
NYHA functional classification

 Class I: no limitation of activity ;

without symptoms to normal activities .
 Class II: slight limitation of activity ;
rest without symptoms .
 Class III : marked limitation of any
activity ; rest without symptoms
 Class IV: any physical activity is
accompanied by discomfort and
symptoms are present at rest .
 Ross classification
Scor Infant Children
I asymptomatic asymptomatic
II Mild sweating, tachypnea at nutrition Mild dyspnea on
exertion

III Tachypnea and marked sweating at Dyspnea on exertion

nutrition
The prolongation of the nutrition time
Growth failure
IV Symptoms at rest Dyspnea at rest
 Etiology
Infant and small children
 CHD with left -right shunt - the most common
◼ VSD, AVSD , PDA , CTA , aorto-pulmonary window,
◼ Single ventricle without pulmonary flow obstruction,
◼ PA (pulmonary atresia) with VSD and large MAPCAs (major aorto -
pulmonary collateral arteries)
◼ TAPVR (total abnormal pulmonary venous return) without obstruction.
 Pulmonary flow increases with decreasing lung resistance
 ALCAPA ( abnormal left coronary artery from
pulmonary artery) - with worsening coronary
perfusion , myocardial ischemia and dysfunction.
 Cardiomyopathies - idiopathic endomyocardial
fibroelastosis, mitochondrial disease, storage disease ,
carnitine deficiency , hypertrophic cardiomiopathy,
myocarditis.
 Noncardiac causes: kidney failure, sepsis, severe
anemia, residual lesions after cardiac surgery - ventricular
dysfunction, great shunts significant valvular regurgitation,
arrhythmias.
Etiology
Elder children

Non-operated CHD
 Left heart insufficiency (LHI):
◼ AV valve insufficiency - AVSD,
congenitally corrected TGA,
◼ aortic insufficiency – VSD with Ao
prolapse, infectious endocarditis.
 Right heart insufficiency (RHI):
◼ Ebstein disease, associated or not with
cardiac arrhythmias,
◼ Eisenmenger syndrome,
◼ Tricuspid or pulmonary regurgitation
 Clinical evaluation

 Tachycardia - the first clinical

sign/exception bradyarrhythmias or AVB
 Signs of congestive vascular
 LHI - signs of pulmonary congestion and
RHI - signs of systemic congestion.
 In the final stage clinical - low CO signs
 In general, HF associated with normal CO is
called compensated and HF with low CO-
decompensated.
 Tachycardia – the first sign

◼ Right ◼ Left
 hepatomegaly  tachypnea
 intercostal retractions
 Ascites
 Beating the nasal
 pleural effusion wings
 edema  pulmonary crackles
 jugular distension  Pulmonary edema

Low CO
Tiredness/fatigue
Pallor
Sweating
Cold extremities
Poor growth
Dizziness / altered consciousness
Syncope
 In children the onset is rapid, with signs of
biventricular CHF.
◼ dyspnea with tachypnea
◼ tachycardia
◼ cough and wheezing
◼ irritability
◼ malnutrition,
◼ excessive sweating
◼ anorexia
◼ peripheral edema
◼ abdominal pains
◼ cold extremities
Investigations
 Oxygen saturation,
 blood count,
 ionogram,
 Urea/creatinine - kidney function
 hepatic function
 thyroid function
 Inflammatory acute phase reaction
 BNP - natriuretic peptide - grown specifically
for HF
Cardiomegaly

 Compensated HF –
cardiomegaly
 LHI –vascular
redistribution:
Kerley lines,
interstitial edem
Echocardiography
 Ejection Fraction (N: 50 – 70%, in HF - < 40%)
 Shortening Fraction
 Etiology HF - CHD/valvulopaty/pericarditis
ECG
 Arrhythmias
 Coronary ischemic disease/myocardial
infarction
 Left/right ventricular hypertrophy
 Conduction disturbances
 contractility

Treatment

preload

afterload
 Treatment
 It varies with age and type of disease.
1. Treatment pathogenic
◼ Emergency - Drug Therapy
◼ It is based on understanding the etiology
2. Etiological treatment
◼ Therapy/specific procedures for cardiac
arrhythmias.
◼ Cardiac surgery/transplantation - in CHD.
 Treatment patogenic-obiective
↑ contractility
↓ preload

Improvement
of
oxygenation
and nutrition
(hemoglobin)

↓ afterload
 Tratamentul patogenic-obiective
↑ contractility - inotropics: dopamin,
dobutamin, amrinone, milrinone, digoxin

Improvement
of
oxygenation
and nutrition
(hemoglobin)

↓ afterload ↓ preload
Diuretics PO / IV
ACEI, po
(furosemide,
Vasodilatators, IV: hydralazine,
thiazide).
nitroprusside or alprostadil
Venous dilators
 Pathogenic treatment
 Reducing preload
◼ Diuretics PO / IV (furosemide, thiazide).
◼ Venous dilators (nitroglycerin)
 Increase contractility
◼ Inotropic agents: dopamine, dobutamine,
amrinone, milrinone).
◼ Digoxin can be extremely useful in HF
 Decrease afterload
◼ ACEI po
◼ Vasodilators, IV: hydralazine, nitroprusside or
alprostadil.
 Agent Pediatric Dose Comment
Preload reduction
Furosemide 1 mg/kg/dose PO or IV May increase to qid
Hydrochlor 2 mg/kg/d PO divided bid May increase to qid
othiaz
ide
Metolazone 0.2 mg/kg/dose PO Used with loop diuretic, may
increase to bid
Inotropic
Digoxin Preterm infants: 0.005 mg/kg/d PO divided bid or 75% of this dose IV <10 y: 0.010
mg/kg/d PO divided bid or 75% of this dose IV>10 y: 0.005 mg/kg/d PO qd or 75%
of this dose IV
Dopamine 5-28 mcg/kg/min IV Gradually titrate upward to
desired effect

Dobutamin 5-28 mcg/kg/min IV Gradually titrate upward to

e desired effect
Inamrinone 5-10 mcg/kg/min IV Load: 1 mg/kg IV over 2-3 min
*
Milrinone 0.5-1 mcg/kg/min IV Load: 50 mcg/kg IV slowly over
15 min
Afterload reduction
Captopril 0.1-0.5 mg/kg/d PO divided q8h -
Enalapril 0.1 mg/kg/d PO divided qd/bid, not to exceed 0.5 mg/kg/d Adults: 2.5-5 mg/d PO qd-bid,
not to exceed 40 mg/d
Lisinopril Not established Adults: 10 mg PO qd
Nitroprussi 0.5-10 mcg/kg/min IV May need to monitor cyanide
de level
Alprostadil 0.05-0.1 mcg/kg/min IV -
†
 Etiological treatment

Structural diseases Rhythm disorders

Specific forms
HF in the newborn and infant
 Sepsis or duct-dependent CHD
 Initial management
◼ ABC, IV access;
◼ Empirical antibiotic therapy
◼ Low CO - IV dopamine 5-10 mcg/kg/min,
◼ Correction of acidosis by administering fluids and/or
bicarbonate
◼ Echocardiography - need for PGE1
 If echocardiography can not be performed
immediately, a CHD duct-dependent must be
considered - coarctation of the aorta, interrupted
aortic arch, total pulmonary venous return anomaly,
hypoplastic left heart syndrome, truncus arteriosus,
pulmonary atresia, transposition of the great vessels.
Specific forms
HF in the newborn and infant

 IV alprostadil (PGE 1) is recommended

for duct-dependent CHD or when they
can not be excluded.
 PGE1 can worsen the condition of
children with TAPVR or obstructive CHD
or sepsis.
 Pharmacological therapy or
cardioversion – in conduction and
rhythm disturbances associated with HF.
HF in elderly children

 Hospitalisation in PICU
 Diuretics IV - furosemide
 Inotropic - dopamine 5-10
mcg/kg/min to stabilize
 Central venous line for venous
pressure and CO monitoring.
 Chronic HF

 In mild forms of HF
◼ digoxin (0.008-0.010 mg/kg/d PO 2 doses) and
furosemide (1 mg/kg/dose PO X2)
◼ The dose of digoxin may present signs of toxicity
decreases: decreased appetite, frequent vomiting.
 In more severe forms of HF
◼ furosemide - 2 mg/kg/dose PO X 3/day, or associated with
hydrochlorothiazide.
 Afterload decrease - in patients with large shunts left/right
(VSD/PDA), left heart regurgitations or reduced systolic
function (myocarditis and dilated cardiomyopathy).
◼ ACE inhibitors are the first choice.
 For each patient who receives furosemide > 1
mg/kgX2/day without ACE inhibitors, this should be
associated with spironolactone.
 Potassium levels need to be monitored and eventually
supplemented orally.
 Beta-blockers in CHF in children

 beta1-selective blockers - metoprolol

 alpha 1/beta 2 blockers - carvedilol

 Encouraging results in chronic HF

associated with cardiomyopathy, with
increasing EF.
 Nutrition
 Treatment of anemia
 Malnutrition is an indicator for
medical management or surgical
intervetion.
Beyond the limit
Device Therapy for Heart Failure
 Cardiac resynchronization therapy (CRT)
 Implantable defibrillators (IDs)

 CRT:
◼ Clinical improvement, exercise tolerance, quality of life, echocardiographic
indices of LV performance,
◼ Increased survival in adults with HF and intraventricular conduction disorder
◼ In adults - recommendations: symptomatic HF and electric dyssynchrony
(intraventricular conduction disorder)
◼ In children - study on 7 children with CHD and RBBB with small but significant
improvement of CO and dp/dt for RV
 IDs
◼ In adults - ↓ 30% lower risk of sudden death (SD) in patients with a history of
malignant ventricular rhythm disturbancies
◼ There are no guidelines for children
◼ They are recommended in ventricular arrhythmias/resuscitated SD
Survival in HF

 It depends on the cause

 Structural anomaly - repaired - excellent.
 Eg: infants with VSD spontaneously
closed/surgically - normal life.
 Complex CHD - the results are variable
 Cardiomyopathy in elder children tend to
progress, unless there is a reversible cause
Va multumesc!