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From medical students to other med students
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Heart Failure in ChildhoodHusna Najihah Dzulkarnain1213828
Contents
• Definition• Epidemiology• Pathophysiology• Causes• Clinical Features• Investigations• Management• Differential diagnosis
Definition
• Childhood: period from birth to being adolescents.
• Heart Failure is defined as the inability to provide adequate cardiac output to meet the metabolic demand of body.
( Nelson Textbook of Paediatrics, 19th edition)
Epidemiology
• Worldwide, congenital heart disease is the most common cause of pediatrics heart failure, followed by cardiomyopathy.
• CHD occurs in around 8 per 1000 live births, however, many of these children receive early surgical intervention and it has been estimated that the yearly incidence of heart failure as a result of congenital defects is between 1 and 2 per 1000 live births.
• Malaysia?
Why is it important?
• Childhood-a period of rapid growth, and high energy, nutrients need to be supplied adequately.
• Slower growth and development• Complications-emotional issues ,lifelong management
(follow up in CHD)
Physiology of the heart
Cardiac Output
Cardiac output = Heart Rate x Stroke volume
• Afterload• Preload• Contractility
(intrinsic myocardial function)
• Tachyarrhythmia-shorten the diastolic time interval for ventricular filling.
Physiology of the heart
Pressure-volume relationship
Normal heart
• In a healthy heart, the increase in preload which consequently increase in the ventricular end-diastolic volume will cause the augmentation of cardiac output.
• The increased stroke volume in this manner is possible due to the stretching of myocardial fibers which also result in increased wall tension.
Compensatory mechanism
• Frank-Starling Mechanism- The increased volume of blood stretches the
ventricular wall, causing cardiac muscle to contract more forcefully.
• Neurohormonal System activation
• Sympathoadrenal axis- increase in sympathetic tone secondary to
increase adrenal secretion of circulating epinephrine and increased
neural release of norepinephrine.
• Initially, increase heart rate and myocardial contractility.
• Later, hypermetabolism, increased afterload, arrythmogenesis,
increased myocardial oxygen requirements, and direct myocardial
toxicity.
• Activation of RAAS
• Myocardial structural changes-dilatation or hypertrophy
Compensatory mechanism
Pathophysiology
Low Output Failure
High Output Failure
Cardiac Output
Cardiac output = Heart Rate x Stroke volume
• Afterload• Preload• Contractility
(intrinsic myocardial function)
• Tachyarrhythmia-shorten the diastolic time interval for ventricular filling.
Preload and afterload
Heart Failure
• Myocontractility : cardiac muscle with a compromised intrinsic contractility requires a greater degree of dilatation to produce an increased stroke volume, and does not achieve the same maximal CO as normal myocardium
• Preload : If a dilated chamber is already dilated because of a lesion causing an increased preload (e.g: left to right shunt or valvular insufficiency) , there is only a little room left for further dilatation and augmentation of CO.
• Afterload : the presence of lesions that results in increased afterload to the ventricel (e.g: aortic or pulmonic stenosis, coarctation of aorta) decreases cardiac performance, leading to reduced CO.
• Abnormal rhythms : Tachyarrhythmia shorten the diastolic time interval for ventricular filling.
High output cardiac failure
• The CO is normal or increased, but because of
decreased systemic oxygen content (secondary to
anemia) or increased oxygen demand (secondary to
hyperventilation, hyperthyroidism, or
hypermetabolism), there is an inadequate amount of
oxygen delivered to meet the body’s needs.
• This will result in development of signs and symptoms
of heart failure when there is no basic abnormality in
myocardial function and the CO is greater
than normal.
Causes
• Congenital• Acquired
Causes
• Left to right shunt lesions : VSD,PDA,AVSD,ASD• Obstructive left heart lesions: Hypoplastic left
heart syndrome, coarctation of aorta, aortic stenosis• Common mixing unrestricted pulmonary flow :
Truncus arteriosus, TAPVD, tricuspid atresia, TGA, single ventricle, pulmonary atresia with VSD,large aortopulmonary collateral
• Valvular regurgitation: AV valve regurgitation, Eibstein anomaly, semilunar valve regurgitation
• Myocardial Ischemia : anomalous origin of left coronary artery from pulmonary artery.
Congenital
Causes
• Acquired valvular disease : chronic rheumatic valvular disease, post infective endocarditis
• Myocardial disease
Acquired
Causes: Myocardial disease (Acquired)
• Effect the heart’s contractility.
Primary cardiomyopath
y:
• Idiopathic• Familial
Secondary cardiomyopathy:
• Arrythmia-induced: congenital heart block, atrial etopic tachycardia
• Infection: post viral myocarditis, Chagas disease.
• Ischemic: Kawasaki disease• Myopathic : muscular
dystrophy• Pompe disease ,
mitochondrial disease• Metabolic: hypothyroidism• Drug-induced: anthtracycline• Others: iron overload
(thalassemia)
Acute myocarditi
s:
• Viral• Rheumatic• Kawasaki
disease
Etiology according to age group
• Fetal:
• Severe anemia (hemolysis,fetal-maternal
transfusion,parvovirus B19-induced
anemia,hypoplastic anemia)
• Supraventricular tachycardia
• Ventricular tachycardia
• Complete heart block
Premature Neonate:Fluid overloadPDAVSDCor Pulmonale
(bronchopulmonary dysplasia)
• Full-term neonate• Asphyxial cardiomyopathy• AVM• Left-sided obstructive lesions (coarctation of
aorta, hypoplastic left side of the heart)• Large mixing cardiac defects (single
ventricle,truncus arteriosus)• Viral myocarditis
Infant-ToddlerLeft-to-right cardiac shunts (VSD)HemangiomaAnomalous left coronary arteryMetabolic cardiomyopathyAcute hypertension (HUS)SVTKawasaki’s disease
• Child-adolescent• Rheumatic fever• Acute hypertension (glomerulonephritis)• Viral myocarditis• Thyrotoxicosis• Hemochromatosis-hemosiderosis• Cancer therapy • Sickle-cell anemia• Endocarditis• Cor pulmonale (cystic fibrosis)• Cardiomyopathy
Complications
• Metabolic acidosis• Cardiogenic shock
Approach to patient
• History• Physical Examination• Investigation• Treatment
History
• NEONATES & INFANTS • Poor feeding
• Tachypnoea worsening during feeding
• Sweating during feeding
• Poor weight gain
• Irritable
• Weak cry
• Wheezing
• Labored breathing
• Recurrent chest infections
• OLDER CHILDREN• Fatigue
• Exercise intolerance
• Dyspnoea –pulmonary congestion
• Pedal edema
• Growth failure
Physical Examination
1) Poor perfusion- cool extremities,
decreased capillary refill, decreased
peripheral pulses, and low systemic
blood pressure.
2) Pulmonary congestion- resting
tachypnea, respiratory distress (chest
retractions, use of accessory muscles,
infants with gruntings and nasal flaring).
Wheezing and crepitation are more
common in older children
3) Systemic congestion – hepatomegaly,
raised JVP (usually not in infants and
younger children), peripheral edema.
Others
• High blood pressure limited to upper extremities and/or feeble pulses in lower extremities are suggestive of aortic coarctation
• The presence of a systolic murmur may be seen in patients with outflow obstruction in hypertropic cardiomyopathy or aortic stenosis, congenital heart defects with left-to-right shunting (eg, ventricular septal defects), or mitral regurgitation.
• Precordial examination may reveal a “thrill” in patients with shunt lesions, whereas those with a long-standing cardiomyopathy may have a “heave” with a laterally displaced point of maximal impulse.
Investigation
• Blood tests• Chest X-Ray• ECG• Echocardiography• Doppler ultrasound
Blood Tests
1) Full blood count-anemia, leukocytosis
2) Liver function tests –elevated due to hepatic congestion with right-sided heart failure.
3) Serum electrolytes, blood urea nitrogen, and creatinine.
• Hyponatremia due to water retention.
• Hyperkalemia may represent tissue destruction due to low CO or renal compromises.
• High BUN and creatinine due to reduced RBF may suggest renal impairment.* Brain natriuretic peptide (BNP) - cardiac hormone
secreted by the ventricular cells in response to increased wall stress in volume or pressure overload
Chest X-Ray
e.g: Ventricular Septal Defect
Case courtesy of Dr Frank Gaillard, Radiopaedia.org
Findings:
• Cardiomegaly
• Pulmonary edema
ECG
• Sinus tachycardia• Varying degrees of heart block may sometimes
be observed in patients with rheumatic or lyme carditis, or in patients with neonatal lupus.
• Increased QRS voltage that meets criteria for ventricular hypertrophy may be seen in hypertrophic or dilated cardiomyopathy
• Decreased QRS voltage may suggest myocardial edema or pericardial effusion, and may be present in children with myocarditis
Transthoracic Echocardiography (TTE)
• Assess ventricular function
Fractional shortening
Cardiac output
“Eyeballing“ of LVF Cardiac Index
Ejection fraction (EF) - Simpson method
Contractility (dp/dt)
Stroke volume Tei index
• lower cost, less risk, and greater availability compared with cardiac magnetic resonance imaging or cardiac catheterization
Doppler ultrasound
• Estimate cardiac output• Assess cardiac function, wall motion abnormalities as it
records motion of blood inside the heart.• Obstruction in arteries• Measure degree of narrowing or leakage of heart valve
Management
• Aim:• Treat underlying causes• enhancing cardiac contractility• reducing the preload and afterload• improving oxygen delivery
Management- General Measures
• Oxygen supplementation, keep in propped up position
• Keep warm, gentle handling• Fluid restriction to ¾ normal maintenance if
not dehydrated• Correct anemia, electrolyte imbalance, treat
concomittant chest infections.• Diets-increased daily calorie intakes
• Total daily fluid requirement = Normal Maintenance Fluids + Deficit + Ongoing Abnormal Losses
• Factors that increase caloric requirements: Similar to adults, certain factors will increase daily caloric requirements in children.
AGE (yrs)
Kcal/kg/day
0 - 1 90 - 120
1 - 7 75 - 90
7 - 12 60 - 75
12 - 18 30 - 60
FACTOR INCREASE IN CALORIC NEED2
Fever 10 - 12 % for each degree > 37o C
Cardiac failure 15 - 25 %
Major surgery 20 - 30 %
Burns up to 100 %
Severe sepsis 40 - 50 %
Long term growth failure 50 - 100 %
Anti Failure Medications
• Diuretics –increased water and sodium loss, providing symptomatic relief in fluid overload• Loop diuretics (more powerful agents than thiazide)-
frusemide, bumetanide• Spironolactone-potassium-sparing diuretics, aldosterone
antagonist• ACE inhibitor : afterload-reducing agent, by
decreasing peripheral vascular resistance.• Captopril-greater stability in liquid formulation• Enalapril-require less frequent dosing
• Digoxin-useful in HF with excessive tachycardia, SVT• IV inotropic agents- dopamine, dobutamine,
adrenaline, milrinone• Use in acute HF, cardiogenic shock, post-op low output
syndrome
Specific management
• Aetiology establishment• Specific treatment for targeted aetiology• Congenital-surgery• Heart block- pacemaker• Post infectious glomerulonephritis- control BP• Acute rheumatic carditis – High dose aspirin
Mnemonic for management
Differential Diagnosis
• Respiratory distress
• Neonates-Respiratory distress syndrome, transient tachypnea of the newborn, meconium aspiration, congenital diaphragmatic hernia, pneumothorax, pneumonia, and pulmonary hypoplasia.
• Older infants and children – Pneumonia, asthma, and gastroesophageal reflux.
• Poor weight gain and FTT- Gastrointestinal causes include protein-milk allergy, cystic fibrosis, and celiac disease, Chronic infections, Hyperthyroidism, Metabolic disorders
• Fatigue in older children may be due to sleep apnea, depression
• Peripheral edema may be caused by renal failure or venous thrombosis
• Shock may be due to overwhelming sepsis or hypovolemia
References
• Nelson Textbook of Pediatric, 16th edition• Paediatric Protocols, 3rd edition• Heart Failure in children and young adults, Anthony
C.Chang, Jeffrey A.Towbin
Thank You !