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Heart Failure in infants and neonates Dr Sanmath Shetty K Senior Resident, Dept of Cardiology Medical College, Calicut
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Definition of Heart Failure Brief review of Pathophysiology Unique features of heart failure in neonates. Clinical features Fetal circulation and its changes after birth Classification and Etiology Management of heart failure in neonates
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Congestive Cardiac Failure is a clinical syndrome in which the heart is unable to pump enough blood to the body to meet its needs, to dispose off systemic or pulmonary venous return adequately, or a combination of the two. Clinical manifestations of heart failure due to a combination of “low output state” and compensatory responses to increase it.
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Heart failure syndromes Acute postnatal cardiac failure: inability of heart to maintain a cardiac output necessary to maintain oxygenation of tissues. Manifest as shock or pulmonary edema. Low cardiac output, low systemic blood flow High cardiac output, low systemic blood flow: large AV shunts, vein of galen malformation. Subacute or Chronic heart failure: may follow improvement from acute cardiac failure or may have an insidious onset due to progressive ventricular dysfunction. Features: Diaphoresis, failure to thrive, weight loss, feeding difficulties, increased respiratory effort.
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pathophysiology Unmet tissue demands for cardiac output result in activation of The renin-aldosterone angiotensin system The sympathetic nervous system Cytokine-induced inflammation “Signaling” cascades that trigger cachexia
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Initially these compensatory effects help to improve cardiac output and maintain blood pressure. STAGE OF “COMPENSATED SHOCK” Long standing increases in cardiac workload and myocardial O2 consumption leads to cardiac “REMODELING”
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Cardiac remodeling Increase in cardiac mass ( maladaptive hypertrophy) Expansion of myofibrillar components of individual myocytes (new cells rarely formed). Increase in the myocyte/capillary ratio. Activation and proliferation of nonmyocyte cardiac cells (may produce scarring). Ultimately causes: a poorly contractile and less compliant heart
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HF in neonates: UNIQUE FEATURES The neonatal heart is more liable to develop HF because of the following factors: The neonatal cardiac output. The number of contractile units. Preload, afterload and Frank Starling’s law Sympathetic innervations and catecholamines. Myocardial metabolism, Ca2+ and fetal Hb. Hypoxemia and acidosis
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Neonatal cardiac output Fetal life ------ combined biventricular cardiac output is 450 ml/kg/min, “parallel circulation” RV= 300 ml/kg/min, LV= 150 ml/kg/min Extrauterine life ------- Series circulation. LV output= 150 450 ml/kg/min. Cardiac output gradually reduces to adult value of 70 ml/kg/min over 6 – 12 mths.
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Contractile units Neonatal heart has less contractile units per mm2 than adult hearts. Inside the neonatal myocyte, contractile units are restricted to 30% (70% in adults) Advantage of neonatal myocardium: ability to produce hyperplasia.
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Preload, afterload, frank-starling’s law In neonates, venous return is high because of increased cardiac output. Frank Starling law is fully acknowledged leaving little margin for tolerating additional overload. Afterload is directly related to radius of ventricular cavity and inversely related to wall thickness Wall stress=pressure x radius/2 x wall thickness In infants, radius high due to increased LVEDV and LV wall is thinner than in adults-------------- high afterload.
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Sympathetic innervations and catecholamines Infants with HF: Higher concentrations of catecholamines in circulation----- stores are depleted. Decrease in density and number of beta receptors in myocardium. Limits the action of exogenously administered catecholamines.
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Myocardial metabolism, ca2+, fetal Hb Neonatal myocyte can use only glucose 6 phosphate as fuel. Newborn glycogen stores are limited------ hypoglycemia causes HF. Poor sarcoplasmic reticulum in neonates---- hypocalcemia causes HF. Fetal Hb has high affinity to oxygen. Hence , only way of increasing oxygen to tissues is by increasing cardiac output.
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Hypoxemia and acidosis: Frequently seen in sick newborns. Significantly reduce cardiac contractility.
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CLINICAL MANIFESTATIONS IN INFANTS WITH HF Feeding abnormalities Tachypnoea Tachycardia Cardiomegaly Gallop rhythm (S3) Hepatomegaly Pulmonary rales Peripheral edema Sweating Irritability Failure to thrive
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Feeding difficulties Important clue for presence of CHF in infants Usually first noticed by the mother Interrupted feeding (suck-rest-suck cycles) Inability to finish feeds, excessive time for each feed (> 30 mins) Forehead sweating during feeds --- due to activation of sympathetic system
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Rapid respirations Tachypnea > 60/min in 0-2 mth >50/mt in 2 mth to 1 yr >40/mt 1-5 yr in calm child Cardiac neonatal tachypnea: due to Increased pulmonary venous pressure (due to left to right shunt) Pulmonary venous obstruction Increased LVEDP. ? Neurohormonal basis Two breathing patterns in heart disease in neonates: Tachypnea with retractions and deep breaths: almost always seen with HF. Tachypnea with shallow breaths: seen with reduced pulmonary flow without HF. Happy Tachypnea: Tachypnea without significant increased work of breathing at rest, seen in infants with CHD with mild to moderate pulmonary overcirculation.
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tachycardia Persistently raised heart rate > 160 bpm in infants > 100 bpm in older children. Tachycardia in the absence of fever or crying when accompanied by rapid respirations and hepatomegaly is indicative of HF Consider SVT if heart rate > 220 bpm in infants and > 180 bpm in older children.
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cardiomegaly Consistent sign of impaired cardiac function, secondary to ventricular dilatation and/or hypertrophy. Very few cases of HF do not show cardiomegaly. rapidly fatal cardiomyopathies supra-ventricular tachycardia in its early stages total anomalous pulmonary venous return infra diaphragmatic type with obstruction.
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hepatomegaly This sign is present in almost all cases of neonatal HF. The normal neonatal liver appears large on palpation and it is found about 2 cm below the right costal edge. In the presence of respiratory infection increased expansion of the lungs displace liver caudally. Usually in such cases, the spleen is also palpable.
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Failure to thrive In chronic HF, there is inadequate growth Causes: Poor feeding, frequent respiratory infections, increased metabolic requirements, decreased absorption from gut due to congestion. Boys>girls, Acyanotic heart disease, weight gain more affected than height. Cyanotic heart disease, weight and height equally affected. In acute heart failure, weight gain may be seen. Weight gain> 30 gm/day --- suggestive of CCF
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Other signs of neonatal heart failure Peripheral edema: Late sign, indicates severe heart failure, presacral and posterior chest wall edema. Pulmonary rales: not useful, difficult to differentiate from pulmonary infections which frequently accompanies heart failure. Pulsus alternans: seen in severe HF. S3 or gallop rhythm: frequently seen. S3 may not indicate HF in neonates.
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Fetal blood flow
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Landmark events in postnatal life
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At birth Parallel circulation becomes series soon after birth Lesions that present during first few days of life: Critical AS HLHS Critical PS Mitral atresia
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Closure of the ductus arteriosus Term infant Two phases: Functional closure: 18 t0 24 hours after birth Anatomic closure: over next 2 – 3 weeks Preterm infant Remains open for many days following birth. Cause: Immature ducts have high threshold of response to oxygen. Immature ducts are more sensitive to PGE2 and NO PGE2 fail to get metabolized by immature lungs. MECHANISM Removal of PGE2 based relaxing system Activation of constrictor mechanism by rise in blood oxygen tension
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Cardiac lesions that manifest during closure of the ductus Functional closure: Depend for pulmonary flow (TOF with pulmonary atresia) Depend for systemic flow (IAA/CoA) Depend for mixing of systemic and pulmonary blood (TGA) Anatomic closure: CoA
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Pulmonary Vascular resistance falls further after birth between 3 to 6 weeks Large VSD PDA ALCAPA
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Classification NYHA Heart Failure Classification: Not well translated for use in infants. The Original Ross Classification Ross Scoring system for heart failure in infants Modified Ross score: for older children New York University Paediatric heart failure index
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Original ross Classification Class I : No Limitations or symptoms Class II: Mild tachypnea or diaphoresis with feedings in infants Dyspnea in older children No growth failure Class III: Marked tachypnea or diaphoresis with feedings Prolonged feeding times Growth failure from CCF Class IV Symptomatic at rest with tachypnea, retractions, grunting or diaphoresis
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Ross scoring system in infants
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New York university paediatric heart failure index– Connelly et al.
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Proposed HF staging for infants and children by the International Society for Heart and Lung Transplantation Modified from the American College of Cardiology/American Heart Association guidelines and complementing the Ross classification system Stage A: Patients with increased risk of HF but normal cardiac function and no evidence of cardiac chamber volume overload Examples: previous exposure to cardiotoxic agents, family history of heritable cardiomyopathy, congenitally corrected transposition of the great arteries Stage B: Patients with abnormal cardiac morphology or cardiac function, with no symptoms of HF, past or present Examples: history of anthracycline with LV dysfunction, Aortic insufficiency with LV dysfunction. Stage C: Patients with underlying structural or functional heart diseases and past or current symptoms of HF Stage D: Patients with end-stage HF requiring continuous infusion of inotropic agents, mechanical circulatory support, cardiac transplantation, or hospice care
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Heart failure in the fetus CHF in utero is manifested as right heart failure– pericardial or pleural effusions, ascites and peripheral (skin,placental) edema. Fetal Hydrops: nonspecific term, two or more fluid collection in the fetus. Fetal heart failure causes 26-40% of nonimmune hydrops. Echo: Cardiomegaly. Cardiothoracic area > 0.3 Cardiothoracic circumference > 0.5 Systolic dysfunction: Fractional shortening (N=28-40%) Diastolic dysfunction: small or absent E wave
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NEONATAL HEART FAILURE Etiology- cardiac causes
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Etiology- non cardiac causes Metabolic abnormalities- Severe hypoxia, acidosis, hypoglycemia, hypocalcemia Endocrinopathies: Hyperthyroidism Severe Anemia: Hydrops fetalis Bronchopulmonary dysplasia Sepsis Arteriovenous fistula, vein of galen malformation
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Etiology of Neonatal Heart Failure by Age of presentation
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Investigations Blood tests: CBC, creatinine. Glucose, Calcium Pulse oximetry ECG ABG Radiological tests: CXR Echo Biomarkers Cardiac catheterization: in patients with heart failure following repair or palliation of congenital heart disease ( residual disease, assessment of shunt function)
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Hyperoxia test Administer 100 % oxygen for > 10 min PaO2 > 100 mmHg: pulmonary disease likely PaO2 < 70 mmHg, rise by < 30 mmHg or SaO2 unchanged: cardiac cause (R-L shunt) likely Exceptions: Total anomalous pulmonary venous return may respond Pulmonary disease with a massive intrapulmonary shunt may not respond
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CXR Cardiomegaly: Absence rules out CHF (exception: obstructed TAPVC) Upper limit 0.55 in infants and 0.6 in neonates. Thymic shadow may mimic mediastinal widening in infants. Features of pulmonary venous hypertension:
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Echocardiography Essential for identifying Causes of HF such as structural heart disease Ventricular dysfunction (both systolic and diastolic) Chamber dimensions Effusions (both pericardial and pleural)
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HF Biomarkers ANP (atrial strain) BNP (ventricular strain) Troponins (cardiomyocyte compromise) BNP and NT pro BNP levels rise at birth in normal healthy infants, level off at 3-4 days and then fall steadily. Normal values for these biomarkers in infants has not been adequately established.
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Management approach based on physiologic considerations General circulatory models Series Circulation Left to right shunt Circulation Right to left shunt Circulation Parallel Circulation Venous Obstruction Ventricular Dysfunction
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Series circulation Normal circulatory pattern Absence of mixing between oxygenated and deoxygenated blood Eg:Structural malformations causing obstruction to blood flow (AS,PS) Hypoxia : due to V/Q mismatch Treatment: Improve pulmonary status using diuretics, supplemental O2 and positive pressure ventilation Inotropic support in cases of pump dysfunction.
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Left to right shunt circulation Characterised by a certain volume of oxygenated blood that recirculates between the lungs and the heart never making it to the systemic circulation. Eg: ASD,VSD,PDA Volume depends on : size of shunt, SVR and PVR, presence and degree of outflow tract obstruction Hypoxemia: Pump Failure, LRTIs Treatment: Adequate oxygenation Diuretics. Maintaining adequate cardiac pump function with inotropes
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Right to left shunt circulation Characterised by the presence of deoxygenated blood which circulates between the heart and the body without passing through the pulmonary circulation. Volume depends on shunt size, SVR and PVR , the degree of obstruction to pulmonary circulation and the presence, absence and status of pulmonary arteries. Hypoxemia: Due to reduced Pulmonary blood flow. Treatment: In severe hypoxemia and low Qp: PGE1 therapy (change to left to right shunt, oxygenation at the expense of systemic circulation) In elevated Qp: Diuretics.
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Parallel circulation Blood recirculates through the pulmonary circuit, never providing oxygenated blood to the body, and another pool circulates through the body, never providing deoxygenated blood to the lungs. Not compatible with life unless there is some volume of pulmonary blood that enters the systemic circulation. Eg: TGA, DORV with malpositioned great vessels, single ventricle physiology. Hypoxemia: postnatally due to closure of PDA and Foramen ovale. At birth- shunts are bidirectional (Qs is maintained) As PVR reduces, Qp>Qs, however saturation paradoxically worsens despite pulmonary overcirculation. Treatment: No role for oxygenation. Shunts across atrial septum- provide palliation.
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Venous obstruction In neonates with TAPVC or single ventricle physiology due to tricuspid atresia, cardiac output and oxygenation is dependent on right to left shunting at atrial level. In such conditions, obstruction to pulmonary or systemic venous return reduces cardiac output. Treatment: Maintenance of preload to maintain right to left shunt. CVP monitoring, judicious use of fluids and diuretics. Inotropes with chronotropic effect avoided- shortens diastolic filling time.
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Ventricular dysfunction Both systolic and diastolic dysfunction seen in neonates. Eg: ALCAPA: ischemic cardiomyopathy Treatment: Reducing preload (diuretics) and afterload (ACE inhibitors/ ARBs) conditions. Inotropic support
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TREATMENT--general measures Bed rest and limit activities Nurse propped up or in sitting position Control fever Expressed breast milk for small infants Fluid restriction in volume overloaded Optimal sedation Correction of anemia ,acidosis, hypoglycemia and hypocalcaemia if present
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Ventilation- cardiopulmonary interactions Non invasive ventilation ( Mask, CPAP) Invasive ventilation Positive pressure ventilation: Reduces work of breathing Reduces filling of right side of the heart Reduces left ventricular transmural pressure (reduced afterload)
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Nutritional support Goals: Provide sufficient calories and proteins to allow normal growth and prevent breakdown of lean body mass. To make up for the past deficiencies and allow “catch-up” growth. Approx 150 kcal/kg/day Increase calorie density of feeds due to restricted fluid intake Babies on diuretics: supplementation of electrolytes (Na, K, Cl)
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Drug therapy Three major classes of drugs: Diuretics Inotropic agents Afterload reducing agents
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diuretics Prinicipal therapeutic agent to reduce pulmonary and systemic congestion. Side effects: Hypokalemia (except spironolactone), hypochloremic alkalosis
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Rapid acting inotropic agents Useful in critically ill infants with hypotension, those with renal dysfunction and postoperative patients in HF. Milrinone: noncatecholamine agent, PDE inhibitor, inotropic + vasodilator effect.
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digitalis Inotropic action Parasympathomimetic action (slows heart rate and AV conduction) Mild diuretic action. Decreases myocardial oxygen consumption in failing heart. Uses: DCM to increase CO CHF from L to R shunts: after diuretic and afterload reducing agent, if further improvement is needed Therapeutic range: 0.8-2 ng/ml
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Digitalization 1.) Baseline ECG and serum electrolytes 2.)Calculate the oral total digitalizing dose Maintenance dose is 25% of the total dig.dose. I.V. dose is 75% of the oral dose. 3.) Give one half of the TDD immediately ,then 1/4th & then the final 1/4th at 6- to 8-hr intervals. 4.) Start the maintenance dose 12 hrs after the final TDD
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Afterload reducing agents Augments the stroke volume without a great change in contractile state, i.e, without increasing myocardial oxygen demand.
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Beta blockers Small scale studies have shown benefit of using beta blockers in some children with chronic CHF who were symptomatic after being treated with standard drugs (digoxin, diuretics and ACEI) . Should not be used in decompensated heart failure. Starting dose: Metoprolol: 0.1-0.2 mg/kg per dose twice daily. Carvedilol: 0.09 mg/kg per dose twice daily.
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carnitine Cofactor for transport of long chain fatty acids into mitochondria for oxidation. Improved myocardial function and reduced cardiomegaly in patients with DCM. Dosage: 50-100 mg/kg/day twice to thrice daily (max 3 g)
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Pharmacologic management of chronic reduced ef heart failure
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Pharmacologic management of “preserved Ef” failure
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Surgical treatment Pacemaker and implantable defibrillator therapy Biventricular pacing Ventricular assist devices Cardiac Transplantation
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REFERENCES: 1.) Paediatric Heart Failure. Robert E Shaddy, Gil Wernovsky: Chapters 6, 7, 14, 15, 16; Taylor and Francis group, 2005. 2.) Heart Failure in congenital heart disease; from fetus to adult. Robert E Shaddy: Chapter 2; Springer, 2011. 3.) Park’s paediatric cardiology for practitioners. Myung K Park, 6th edition: Chapter 27; Saunders, 2014. 4.) Madriago E, Silberbach M, Heart failure in infants and children: Paediatrics in review , 2010; 31; 4-12. 5.) Hsu TD, Pearson GD. Heart Failure in Children: Part I: History, Etiology, and Pathophysiology. Circ Heart Fail. 2009;2:63-70. 6.) Hsu TD, Pearson GD. Heart Failure in Children: Part II: Diagnosis, Treatment, and Future Directions. Circ Heart Fail. 2009;2:490-498. 7.) Sharma M, Nair MNG, Jatana SK, Shahi BN. Congestive Heart Failure in Infants and Children: MJAFI 2003; 59 : 228-233 8.) Anderson’s Paediatric cardiology, 3rd edition, chapter 14.
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thank you