2 Congestive heart failure (CHF) refers to a clinical state of systemic and pulmonary congestion resulting from inability of the heart to pump as much blood as required for the adequate metabolism of the body.Clinical picture of CHF results from a combination of “relatively low output” and compensatory responses to increase it
3 PATHOPHYSIOLOGYUnmet tissue demands for cardiac output result in activation ofRenin-aldosterone angiotensin systemSympathetic nervous systemCytokine-induced inflammation“signaling” cascades that trigger cachexia.
5 Longstanding increases in myocardial work and myocardial oxygen consumption (MVO2) ultimately worsen HFsymptoms and lead to a chronic phase that involves cardiac remodeling
6 CARDIAC REMODELING? Maladaptive cardiac hypertrophy Expansion of the myofibrillar components of individual myocytes (new cells rarely form)An increase in the myocyte/capillary ratioActivation and proliferation of abundant nonmyocyte cardiac cells, some of which produce cardiac scarringProduce a poorly contractile and less compliant heart
7 Endogenous mechanisms defend progressive HF Stimulation of insulin like growth factor and GHANP and BNP are hormones secreted by the heart in response to volume and pressure overload that increase vasodilation and diuresis acutely and chronically prevent inflammation, cardiac fibrosis and hypertrophy.
8 CLINICAL MANIFESTATIONS IN INFANTS WITH HF Variety of age dependent clinical presentationsIn neonates, the earliest clinical manifestations may be subtle
9 CLINICAL MANIFESTATIONS IN INFANTS WITH HF Pulmonary ralesPeripheral edemaEasy fatigability.SweatingIrritabilityfailure to thrive.Feeding difficultiesRapid respirationsTachycardiaCardiac enlargementGallop rhythm (S3)Hepatomegaly
10 Feeding difficulties & increased fatigability Important clue in detecting CHF in infantsOften it is noticed by motherInterrupted feeding (suck- rest -suck cycles)Infant pauses frequently to rest during feedingsInability to finish the feed, taking longer to finish each feed (> 30 minutes)Forehead sweating during feeds –due to activation of sympathetic nervous system –a very useful signIncreasing symptoms during and after feedings
11 Rapid respirations Tachypnea > 60/min in 0-2mth >50/mt in 2mth to 1yr>40/mt 1-5 yr in calm childHappy tachypnea- tachypnea with out much retractionsGrunting (a form of positive end-expiratory pressure)In cyanotic heart disease rapid respirations may be due to associated brain anoxia and not CHF -treatment for these two conditions is entirely differentFever especially with a pulmonary infection may produce rapid respirations.
12 Tachycardia Rate is difficult to evaluate in a crying or moving child Tachycardia in the absence of fever or crying when accompanied by rapid respirations and hepatomegaly is indicative of HFPersistently raised heart rate > 160 bpm in infants> 100 bpm in older children.Consider SVT if heart rate > 220 bpm in infants and > 180 bpm in older children.
13 CardiomegalyConsistent sign of impaired cardiac function, secondary to ventricular dilatation and/or hypertrophy.May be absent in early stages, especially with myocarditis, arrhythmias, restrictive disorders and pulmonary venous obstruction(obstructed TAPVC)Apex 4th space 1cm outside MCL in newborn
14 HepatomegalyLower edge of the liver is palpable 1 to 2 cms below right costal margin normally in infancyIn the presence of respiratory infection increased expansion of the lungs displace liver caudallyUsually in such circumstances the spleen is palpableHepatomegaly is a sign of CHFDecrease in size is an excellent criterion of response to therapy
15 Pulmonary rales Of not much use in detecting CHF in infants Rales may be heard at both lung basesWhen present are difficult to differentiate from those due to the pulmonary infection which frequently accompanies failure
16 Peripheral edemaEdema is a very late sign of failure in infants and childrenPresacral and posterior chest wall edema in young infantsIt indicates a very severe degree of failure.Daily wt monitoring is useful in neonates -- rapid increase in wt > 30 gm /day may be a clue to CCF and is useful in monitoring response to treatment.
17 Cold extremity, low blood pressure, skin mottling are signs of impending shock Pulsus alternans (alternate strong and weak contractions of a failing myocardium),or pulsus paradoxus (decrease in pulse volume and blood pressure with inspiration) are frequently observed in infants with severe CHF
18 CLASSIFICATION NYHA Heart Failure Classification is not applicable Ross Heart Failure Classification was developed for global assessment of heart failure severity in infantsModified to apply to all pediatric agesModified Ross Classification incorporatesFeeding difficultiesGrowth problemsSymptoms of exercise intolerance
19 MODIFIED ROSS HEART FAILURE CLASSIFICATION FOR CHILDREN AsymptomaticClass IIMild tachypnea or diaphoresis with feeding in infantsDyspnea on exertion in older childrenClass IIIMarked tachypnea or diaphoresis with feeding in infantsMarked dyspnea on exertionProlonged feeding times with growth failureClass IVSymptoms such as tachypnea, retractions, grunting, or diaphoresis at rest
20 The time of onset of CHF holds the key to the etiological diagnosis in this age group
21 Parallel circulation becomes series at birth Cardiac anomalies present at that point areCritical ASHLHSMitral atresia
22 Functional closure PDA 1 to 2weeks PDA dependent lesions ,depend on patent duct for eitherpulmonary blood flow- Fallots with pulmonary atresiasystemic blood flow-IAA/COAmixing of systemic and pulmonary blood-TGAPresent at 1 to 2weeks
23 Anatomic closure of PDA by 2to4 weeks Coarctation of aorta
24 Pulmonary vascular resistance falls 4to 6weeks Congestive heart failure due to L-R shuntLarge VSDPDAALCAPA
25 CHF in the fetusDisorders that are fatal in the immediate neonatal period are often well tolerated in the fetus due to the pattern of fetal blood flow (e.g. TGA)Causes of CHF in the fetusSVTSevere bradycardia due to CHBAnemiaSevere TR due to Ebstein’s anomaly or MR from AV canal defectMyocarditis
27 Most of these are recognized by fetal echo Severe CHF in the fetus produces hydrops fetalis with ascites, pleural and pericardial effusions and anasarca.Digoxin or sympathomimetics to the mother may be helpful in cases of fetal tachyarrhythmia or CHB respectively.
29 CHF on first day of lifeMyocardial dysfunction secondary to asphyxia, hypoglycemia, hypocalcaemia or sepsis are usually responsible for CHF on first dayFew structural heart defects cause CHF within hours of birthHLHS, severe TR or PR, Large AV fistulaTR secondary to hypoxia induced papillary muscle dysfunction or Ebstein’s anomaly of the valveImproves as the pulmonary artery pressure falls over the next few days
30 CHF in first week of life Serious cardiac disorders which are potentially curable but carry a high mortality if untreated often present with CHF in the first week of lifeA sense of urgency should always accompany evaluation of the patient with CHF in the first weekClosure of the ductus arteriosus is often the precipitating eventProstaglandins E1 should be utilised
31 Peripheral pulses and oxygen saturation (pulse oximeter) should be checked in both the upper and lower extremitiesA lower saturation in the lower limbs means right to left ductal shunting due to PAH or AAIASD or VSD does not lead to CHF in the first two weeks of life, an additional cause must be sought (eg.COA or TAPVC).
32 TGAno VSD -1ST weekVSD and no PS-6-8 weeksCritical AS or PSObstructive TAPVCAdrenal insufficiency due to enzyme deficiencies or neonatal thyrotoxicosis could present with CHF in the first few days of life
33 ALPROSTODIL Prostaglandins E1 Maintain patency of ductus Cyanotic lesions TGALT sided obstructive lesions HLHS, critical AS,COA,IAAAvailable as inj 500microgm/mlIV 0.05 to0.1microgm /kg/min0.01 to 0.05 microgm /kg/min maintainanceVasodilation of all arteries including ductus
34 Monitor spo2,RR, HR,BP,ECG,temp Complicationsapnea,SeizureHypotensionBradycardiaTachycardiacardiac arrestfeverExtravasation may cause sloughing and necrosis
35 CHF beyond second week of life Most common cause of CHF in infants is VSDPresents around 6-8 weeks of age.Left to right shunt increases as the PVR fallsMurmur of VSD is apparent by one weekFull blown picture of CHF occurs around 6-8 weeks.Other left to right shunts like PDA present similarlyFall in PVR is delayed in presence of hypoxic lung disease and at high altitude and can alter the time courseSpontaneous improvement in CHF -development of obstructive pulmonary arterial hypertension even in early childhood
36 ALCAPA a rare disease in this age group It is curableAs the pulmonary artery pressure decreases in the neonatal period, these babies suffer from episodes of excessive crying with sweating (angina) and myocardial infarction.ECG shows pathologic q wavesOften misdiagnosed as having “dilated cardiomyopathy”
39 VOLUME OVERLOAD (EXCESSIVE PRELOAD) Left-to-right shuntingVSDPDAAP windowAVSDASD(rare)Total/Partial Anomalous Pulmonary Venous ConnectionAV or semilunar valve insufficiencyAR in bicommissural aortic valve/after valvotomyMR after repair of AVSDPR after repair of TOFSevere TR in Ebstein anomaly
40 Right-sided volume loading Large ASD or anomalous pulmonary vein connectionsCongenital or surgically acquired PR especially if downstream pulmonary arterial narrowingHighly compliant RV accepts significant volume -without increasing filling pressureRarely causes HF early in life
41 PRESSURE OVERLOAD (EXCESSIVE AFTERLOAD) Left sided obstructionCongenital ASAortic coarctationLethal arrhythmias - severe afterload stress??HTNRight-sided obstructionSevere PS
42 Left heart obstructive lesions First postnatal week-ductus arteriosus closesIncreased LVEDP and a decreased pressure gradient between the aorta and ventricle at end-diastole produce subendocardial ischemia due to inadequate coronary flowIncreased afterload and subendocardial ischemia result inHF syndrome
44 Often combined volume and pressure overload Both systemic and pulmonary circulations can be affectedCyanosis in CCHD-risk of subendocardial ischemia contributing to impaired ventricular performanceMolecular abnormalities in transcription factors that lead to congenital structural abnormalities – also associated with abnormal myocardial performance and arrhythmias
45 ABNORMAL RVIn pediatric heart disease much of the pathology is due to an abnormal RVRV myocytes appear to be structurally identical to LV myocytesDifferences in contraction compared to the LV are due to the shape of the RV and myocardial organization
46 Gene expression patterns are different in the RV and the LV, which may affect function. Genes that affect angiotensin and adrenergic receptor signaling showed lower expression in the RV than the LVGenes that contribute to maladaptive signaling showed higher expression in the RV
47 Hypoplastic right heart syndromes -3 parts of the RV do not form normally or may be missing entirely.Defects in the IVS or abnormal LV function- Adversely affect the third phase of normal RV contraction through its interdependence on normal septal function
48 Volume overload of the RV Can arise through significant PR or TRCompensatory dilation to decompensated dilation occur slowly
49 Increased RV afterload RVOT obstructionRV serving as the systemic ventricleUsually can adapt if present at birthOnce the RV assumes a mature, thin-walled configuration, it cannot always mount a hypertrophic responseRV is able to support the systemic circulation for many years but function often deteriorates over time
50 SINGLE VENTRICLE PHYSIOLOGY Ventricular morphology (left, right, indeterminate, or unbalanced) results in a single functional pumping chamberAt birth presentation depends on the morphologyRange from well-tolerated cyanosis to decompensated heart failure and cardiogenic shockdouble inlet ventricle(SV), HLHS , Tricuspid atresia, isomerism
53 These factors can occur individually or in various combinations Pathophysiological factors associated with heart failure in SV physiology in the newborn period areUnobstructed pulmonary blood flowObstruction to systemic flowObstruction to pulmonary venous returnInsufficiency of the atrioventricular valveMyocardial abnormalities or dysfunctionCoronary hypoperfusion.These factors can occur individually or in various combinations
54 Functional single ventricle heart is volume-loaded because of the need to supply the pulmonary and systemic circulations, until the creation of the cavo-pulmonary anastomosis at 6 months of age.Elevated BNP levels before the surgery; afterward, they return to normal
55 After the Fontan procedure Diastolic filling properties often remain abnormal for some timeVentricular function depend on morphologySingle RV has a lower mass: volume ratio which creates a relative increase in wall stress -poorer performanceSingle RV does not have the functional benefit of the interdependence with the LV and interventricular septum that the RV has in 2-ventricle physiology
57 Conduction and rhythm abnormalities is relatively high after Fontan procedure Fontan procedure is often well-tolerated for many yearsAs increasing numbers of these patients survive to adulthood, the prevalence of so-called Fontan failure is increasing
58 CHF WITH NO CARDIAC MALFORMATIONS PRIMARY CARDIACCardiomyopathyMyocarditisCardiac ischemiaAcquired valve disordersHypertensionKawasaki syndromeArrhythmia(bradycardia or tachycardia)NONCARDIACAnemiaSepsisHypoglycemiaDiabetic ketoacidosisHypothyroidismOther endocrinopathiesArteriovenous fistulaRenal failureMuscular dystrophies
59 DISORDERS OF CONTRACTILITY Cardiomyopathy is a genetically triggered or acquired diseaseOccurs in approximately 1.13 in 100,000 childrenHF (less commonly, dysrhythmia) is the presenting featureDCMCharacterized by enlarged ventricular chambers and impaired systolic and diastolic functionUsually idiopathicInfection (myocarditis viral-enterovirus)Operative injuryConsequence of degenerative or metabolic diseasesMuscular dystrophiesMitochondriopathy,Hyperthyroidismcarnitine deficiency
60 Restrictive cardiomyopathy IdiopathicInfiltrative or storage diseaseshemochromatosisPompe diseaseHypertrophic cardiomyopathyIdiopathic hypertrophic subaortic stenosis, rarely associated with pediatric HF.
61 ARRHYTHMIASArrhythmias cause HF when the heart rate is too fast or too slow to meet tissue metabolic demands
62 TACHYCARDIADiastolic filling time shortens to and cardiac output is decreased.Most common childhood tachyarrhythmia is SVTOften presents in the first few months of lifeRarely cause heart failureOccasionally PJRT ,ectopic atrial tachycardia and VT
63 CHRONIC BRADYCARDIAS LV enlarges to accommodate larger stroke volumes Chamber dilation reaches a limit that cannot be compensated without increase in heart rateFebrile states are particularly stressfulCongenital CHB may be well-tolerated in uteroDysfunction cause hydrops and intrauterine demiseAfter birth, progression to HF depends on the ventricular rate and the speed of diagnosis and interventionChildren with congenital CHB who are pacemaker dependent are at risk of subsequent pacemaker-mediated cardiomyopathy
64 CARDIAC ISCHEMIA Relatively rare in children ALCAPA Palliative surgery that requires reconstruction of or near the coronary arteriese.g. Ross procedure, arterial switch operation
65 HIGH OUTPUT HF +EXCESSIVE PRELOAD Septic shock causesVolume load on both sides of the heartIncreased SV associated with hyperdynamic systolic functionElaboration of vasoactive molecules such as endotoxin and cytokines such as TNF-alpha leads to decreased SVRCardiac output is increasedPrecapillary shuntingDecreased tissue perfusion and lactic acid productionIncreased vascular permeability -increased total body fluid volumeToxin or direct microbial actions -negative inotropic effectsStresses produce demands for cardiac output and MVO2
67 CXRSize of the heart is difficult to determine radiologically, particularly if there is a superimposed thymic shadow.Enlarged cardiac shadow unassociated with signs of CHF- suspect that shadow noncardiacAbsence of cardiomegaly in a good inspiratory film (with diaphragm near the 10th rib posteriorly) practically excludes CHF except due to a cause like obstructed total anomalous pulmonary venous connection (TAPVC)
68 CT Ratio method, > 60%Massive cardiomegalyRA dilationPulm plethoraLV Dialatation
69 ECHOCARDIOGRAPHYNot useful for the evaluation of HF, which is a clinical diagnosisEssential for identifyingCauses of HF such as structural heart diseaseVentricular dysfunction (both systolic and diastolic)Chamber dimensionsEffusions (both pericardial and pleural)
70 Assessment of right and single ventricular function is more complicated because of altered geometry RV tissue Doppler imaging correlates with measurements of RVEDP obtained during cardiac catheterizationDoppler myocardial performance index has been used to assess function in children with SVs and abnormal RVsSingle (left) ventricle physiology-remodeling to a spherical shape associated with deterioration
71 CMR- Geometric assessment of RV and SV function 3D echo -additional detail of intracardiac anatomy
72 Worse EF and FS at presentation -poor outcome in children with DCM LV remodeling to a more spherical shape -predict a poorer prognosis in children with DCMMyocarditis- children can present with severely depressed ventricular function but recover normal function within a few weeks to monthsLack of improvement in EF % over time –correlate worse outcome.
73 HF BIOMARKERS Released primarily in response to atrial stretching Sensitive marker of cardiac filling pressure and diastolic dysfunctionBNP levels can distinguish between cardiac and pulmonary causes of respiratory distress in neonates and children
74 In acute decompensated heart failure due to cardiomyopathy a BNP level 300 pg/Ml strongly correlate with poor outcome than symptoms or echocardiographic findingsBNP levels can be different in children with DCM and congenital heart disease despite similar NYHA class, EF, and MVO2
75 PRINCIPLES OF MANAGING HEART FAILURE Recognition and treatment of underlying systemic diseaseTimely Surgical Repair of Structural AnomaliesAfterload ReductionACE inhibitorsARBMilrinone Type 4 phosphodiesterase inhibitorsNitratesRecombinant BNP
77 MEDICAL THERAPYMedical management aims to maximize cardiac output and tissue perfusion while minimizing stresses that increase MVO2Goals are accomplished by reducing afterload stress and preloadTreatments that “rest” the heart such as vasodilators are preferred to inotropic agents that increase MVO2
78 Few drugs have evidence based efficacy compared to adults Pediatric dosing is necessaryScaling adult doses for pediatric use solely based on weight can result in either inadequate or excessive drug levels
79 GENERAL MEASURES Bed rest and limit activities Nurse propped up or in sitting positionControl feverExpressed breast milk for small infantsFluid restriction in volume overloadedOptimal sedationCorrection of anemia ,acidosis, hypoglycemia and hypocalcaemia if presentOxygen –caution in LT-RT shunt as pulmonary vasodilation my increase shuntCPAP or mechanical ventilation as necessary
81 CONGENITAL HEART DISEASE: VOLUME OVERLOAD General therapeutic approach is to minimize symptoms and optimize growth until a definitive procedure can be performed.Mainstays of medical therapy are digitalis and diuretics.
82 DIGITALIS Digitalis considered as essential component Evidence for efficacy is less in volume-overload lesions with normal function where the mild inotropic effect of digitalis is unnecessarySympatholytic properties may modulate pathological neurohormonal activation
83 LOOP DIURETICSFurosemide improved clinical symptoms on a background of digitalis administrationDecrease pulmonary congestion and thus decrease the work of breathingIt is one of the least toxic diuretics in pediatricsAssociated with sensorineural hearing loss after long-term administration in neonatal respiratory distressDeafness related to speed of infusionTorasemide is also safe and effective in this group
84 26. Faris R FM, Purcell H, Poole‐Wilson PS, Coats AJS 26. Faris R FM, Purcell H, Poole‐Wilson PS, Coats AJS. Diuretics for heart failure. Cochrane Database of Systematic Reviews27. Ward OC, Lam LK. Bumetanide in heart failure in infancy. Arch Dis Child Nov;52(11):877‐82.28. Muller K, Gamba G, Jaquet F, Hess B. Torasemide vs. furosemide in primary care patients with chronic heart failure NYHA II to IV‐‐efficacy and quality of life. Eur J Heart Fail Dec;5(6):793‐801.29. Senzaki H, Kamiyama MP, Masutani S, Ishido H, Taketazu M, Kobayashi T, et al. Efficacy and safety of Torasemide in children with heart failure. Arch Dis Child Mar 12.30. Lowrie L. Diuretic therapy of heart failure in infants and children. Prog Pediatr Cardiol Nov 4;12(1):45‐55.31. Arnold WC. Efficacy of metolazone and furosemide in children with furosemide‐resistant edema. Pediatrics Nov;74(5):872‐5.32. Rosenberg J, Gustafsson F, Galatius S, Hildebrandt PR. Combination therapy with metolazone and loop diuretics in outpatients with refractory heart failure: an observational study and review of the literature. Cardiovasc Drugs Ther Aug;19(4):301‐6.
85 ACE INHIBITION Improved growth was seen in some children with CHF Captopril and enalaprilConcerning incidence of renal failure particularly in premature and very young infants.No efficacy data on ARBs in children with heart failure
89 SPIRONOLACTONELiterature supporting the role in paediatric HF is limited61. Hobbins SM, Fowler RS, Rowe RD, Korey AG. Spironolactone therapy in infants with congestive heart failure secondary to congenital heart disease. Arch Dis Child Dec;56(12):934‐8.62. Buck ML. Clinical experience with spironolactone in pediatrics. Ann Pharmacother May;39(5):823‐8.
90 NESIRITIDE Recombinant form of BNP Promotes both diuresis and vasodilationDrug reduces both preload and afterloadDirectly inhibits the sympathetic nervous system, mineralocorticoid expression, and cardiac fibroblast activation and promotes myocyte survival.Studies in the pediatric age group are lacking
91 INTRACARDIAC REPAIREarly transcatheter or surgical intervention, often before age 6 months is possibleMinimizes time of significant symptoms or medicationMinimizes the risk of pulmonary vascular disease.Contemporary data indicate that early repair of a VSD, even in the first month of life and at weights 4 kg, does not confer increased risk compared with older, larger infants.
92 TRANSCATHETER DEVICE CLOSURE Transcatheter device closure of muscular VSDWeight atleast 5.2 kg.
93 CONGENITAL HEART DISEASE PRESSURE OVERLOAD Ventricular response to pressure overload is determined by the severity and duration of the loadCritical AS can cause acute LV failure in early infancy“Critical "implies a requirement for maintaining PDA with prostaglandin infusion
94 Optimizing hemodynamics until urgent intervention Balloon valvuloplasty, first described in neonates in replaced surgical valvotomy, as the first-line intervention in uncomplicated AS, including critical AS.Ventricular function improves and usually normalizes after catheter based or surgical intervention.
95 Higher AV gradient -associated with lower FS, decreased exercise capacity, increased risk of SCD and serious arrhythmiasSevere AS (Doppler MG 50 mm Hg(40)) - intervention to prevent or ameliorate symptomsMild AS (Doppler MG 25 mm Hg) could be followed upThese criteria continue to guide contemporary management along with other criteria such as symptoms, exercise capacity, ventricular hypertrophy, wall stress, and evidence of arrhythmia.
96 COMPLEX CONDITIONS RV failure in children There is no systematic clinical evidence for anticongestive therapyFurosemide- relieve the clinical symptomsRV dysfunction - betablocker therapy did not improve ventricular functionSuggest a different pathophysiological process in RV failure and thus a requirement for novel treatment strategies
97 RV functioning as systemic ventricle If symptomatic ventricular dysfunction occursISHLT Guidelines recommend diuretics, digitalis, and ACE inhibition, based solely on expert consensus
98 Fontan procedureSystemic and pulmonary circulations are separated and SV is pumping to the systemic circulationA large cross-sectional study of 546 Fontan survivors aged 6 to 18 years found normal ejection fraction in 73% of subjects but abnormal diastolic function in 72%.Diastolic function was significantly worse in the group with RV compared with LV or mixed ventricular morphology.Overt heart failure after the Fontan operation is relatively infrequent in the pediatric population but increases in the adultIdentifying and treating underlying causes of HF such as conduction or rhythm abnormalities or residual structural lesions is initial strategy.
99 Single ventricleNo compelling data to guide medical treatmentISHLT guidelines recommend diuretics, digitalis, and ACE inhibition but not beta blockade, based on expert consensus.
100 CARDIOMYOPATHIES Primary or acquired DCM ISHLT Guidelines reflect only data from studies in adults in recommending both digitalis and diuretics only for symptomatic LV dysfunction in childrenTorasemide, a newer loop diuretic with potassium-sparing properties, significantly improved New York University Pediatric Heart Failure Index, decreased BNP levels, and improved fractional shorteningSenzaki etal Efficacy and safety of Torasemide in children with heart failure. Arch Dis Child Mar 12
101 ISHLT Guidelines recommend ACE inhibition for moderate or severe degrees of LV dysfunction regardless of symptomsARB therapy if ACE inhibitor is indicated but not tolerated
103 Although the carvedilol trial did not demonstrate efficacy based on the primary end point improvement in FS and clinical outcome seen in DCM patients who received carvedilol has led to the empirical use of carvedilol in this group of patients.long-term responses to BB therapy have not been studied in childrenClose monitoring of potential adverse effects is essential
106 Systemic exposure to carvedilol amongst paediatric heart failure patients and has indicated that higher doses relative to body weight are required to provide exposure comparable to adultsPaediatric carvedilol doses1mg/kg/day for adolescents2mg/kg/day for children aged to 11 years3mg/kg/day for infants (aged 28 days to 23 months)Carvedilol used in many of the studies have been lower than these recommendations
107 Treatment of primary diastolic heart failure in children with hypertrophic or restrictive cardiomyopathy are limited to the judicious use of diuretics to decrease the degree of pulmonary congestion.
108 Inotropes in acute cardiac failure Routine use of in children cannot be recommendedUsed in treatment of exacerbating conditions and as a bridging therapy pending transplantationDopamine as it possesses both the cardiac and renal effects is more useful
109 Practice guidelines for pediatric heart failure, developed by the International Society for Heart and Lung Transplantation (ISHLT)None of the 49 recommendations is level A evidence7 are level B evidenceRemainder are level C (expert consensus).
111 NUTRITION AND EXERCISE IN PEDIATRIC HEART FAILURE Important as medical therapy, particularly in infantsIncrease the caloric density of feeds as soon as a diagnosisSodium restriction is not recommended in infants and young children.Sodium restriction can result in impaired body and brain growth
112 There is evidence that regular physical activity can result in sustained improvements in physical functioning even in children with complex congenital heart disease.Significant, sustained improvements in exercise function, behavior, self-esteem and emotional state.