Heart failure in children Flashcards
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
Low cardiac output
Congestive HF
High output cardiac failure:
◼ Severe anemia,
◼ Sepsis with Gram -negative germs,
◼ Beriberi ( deficit vitamin B1) ,
◼ Thyrotoxicosis,
◼ Fistulas/arteriovenous malformations
Low output failure
Causes
Normal -> 5 l/min
Failure -> 3 l/min
1.Hypertensive
2.Ischaemic heart disease
3.Valvular heart disease
4.Myocarditis
High ouput failure
Pre-existing high output to meet body requirements -> 9 l/min
Failure -> 7 l/min , output still greater than normal
Diseases associated with increased blood volume :
1.Chronic Anaemia
2.Arteriovenous shunting or increased vascularity of tissues e.g. PAGET’S DISEASE OF BONE, HYPERTHYROIDISM following TRANSFUSION OVERLOAD
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
Score
Infant
I Asymptomatic
II Mild sweating, tachypnea at nutrition
III Tachypnea and marked sweating at nutrition
The prolongation of the nutrition time
Growth failure
IV Symptoms at rest
Children
I Asymptomatic
II Mild dyspnea on exertion
III Dyspnea on exertion
IV 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
Etiology
Infant and small children
ALCAPA
( abnormal left coronary artery from
pulmonary artery) - with worsening coronary
perfusion , myocardial ischemia and dysfunction.
Etiology
Infant and small children
Cardiomyopathies
- idiopathic endomyocardial fibroelastosis,
- mitochondrial disease,
- storage disease ,
- carnitine deficiency ,
- hypertrophic cardiomiopathy, myocarditis.
Etiology
Infant and small children
Noncardiac causes:
kidney failure, sepsis, severe
anemia, residual lesions after cardiac surgery - ventricular
dysfunction, great shunts significant valvular regurgitation,
arrhythmias.
Etiology
elder children
LHI , RHI
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
Right
hepatomegaly
Ascites
pleural effusion
edema
jugular distension
Tachycardia – the first sign
Left
tachypnea
intercostal retractions
Beating the nasal wings
pulmonary crackles
Pulmonary edema
Tachycardia – the first sign
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
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
↓ afterload
Improvement of oxygenation
and nutrition (hemoglobin)
↑ contractility
inotropics:
- dopamin,
- dobutamin,
- amrinone,
- milrinone,
- digoxin
Digoxin can be extremely useful in HF
↓ afterload
ACEI po
Vasodilatators, IV: hydralazine,
nitroprusside or alprostadil
↓ preload
Diuretics PO / IV
(furosemide, thiazide).
Venous dilators (nitroglycerin)
Specific forms
HF in the newborn and infant
SOS
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
Treatment
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.
Chronic HF
In more severe forms of HF
◼ furosemide - 2 mg/kg/dose PO X 3/day, or associated with hydrochlorothiazide.
Chronic HF
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.
Chronic HF
About furosemide and potassium
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.
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
