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Heart failure in children.pptx
- 1. CONGESTIVE HEART FAILUREIN CHILDREN Dr. Sabona Lemessa (Assistant professor in pediatrics and child health, JUMC) 8/12/2022 1
- 2. Outline Definition Pathophysiologyof Heart failure Etiologies Clinical manifestation Diagnosis Management Reference 8/12/2022 2
- 3. Definition Heart failureis a clinical syndrome in which the heart unable to pump enough blood to the body to meet its needs to dispose of systemic or pulmonary circulation or venous return adequately or a combination of the two. accompanied by molecular abnormalities cause progressive deterioration of the failing heart premature myocardial cell death 8/12/2022 3
- 4. Cont.. It isa clinical condition that results from Ventricular dysfunction volume or pressure overload alone or in combination Typical symptoms and signs associated with specific circulatory, neurohormonal and molecular abnormalities. systolic HF” with reduced ejection fraction, Systolic dysfunction Diastolic HF with preserved systolic function, poor relaxation combined systolic and diastolic HF 8/12/2022 4
- 5. Pathophysiology of HeartFailure HF may be viewed as a progressive disorder that is initiated after an index event either; Damages the heart muscle loss of functioning cardiac myocytes or Disruption of the ability of the myocardium to generate force preventing the heart from contracting normally. 8/12/2022 5
- 6. Cont… In HF,low cardiac output leads to reduced baroreceptor stimulation, sensed by baroreceptors in the left ventricle, aortic arch, carotid sinus, and renal afferent arterioles Activation of the sympathetic nervous system Increases heart rate and cardiac contractility vasoconstriction. These mechanisms provide helpful support for the heart as a transitory compensation when the myocardium starts to fails. 8/12/2022 6
- 7. Cont… Chronically increasedsympathetic stimulation can have deleterious effects Hypermetabolism increased afterload Arrhythmogenesis and increased myocardial oxygen requirements. Peripheral vasoconstriction decreased renal, hepatic and GIT function. Decreased blood flow to hypertrophied heart muscle direct myocardial cell damage. promotes myocardial fibrosis which is maladaptive response. 8/12/2022 7
- 8. Cont… 8/12/2022 8 Frank-Starling principle CO=SV x HR LVED increase CO increase but when maximum reached, no augmentation pulmonary or systemic venous congestion induce neurohormonal responses
- 9. Cont… Fig-2 Pathophysiology ofchronic Heart Failure 8/12/2022 9 Dec CO Dec arterial pressure Dec pulse pressure Modify carotid and aortic BR discharge
- 10.
- 11. Etiologies FETAL PRETERM NEONATEFULL TERM NEONATE INFANT-TODDLER CHILD-ADOLESCENT Severe anemia SVT Ventricular tachycardia Complete heart block Severe Ebstein anomaly Myocarditis Fluid overload PDA VSD Corpulmonale (BPD) Hypertension Myocarditis cardiomyopathy Asphyxial cardiomyopathy Arteriovenous malformation Left-sided obstructive lesions Large mixing cardiac defects Myocarditis cardiomyopathy Left-to-right cardiac shunts (VSD) cardiomyopathy Hypertension SVT Kawasaki disease Myocarditis CHD RF Acute HTN Myocarditis Thyrotoxicosis Endocarditis Cor pulmonale cardiomyopathy (hypertrophic, dilated) 8/12/2022 11
- 12. Precipitating factors HTN Infective endocarditis Anemia Rheumatic recurrence Thyrotoxicosis Arrhythmia Infections Drug discontinuation 8/12/2022 12
- 13. Clinical Features Theclinical picture of HF is directly related to age Symptoms of HF depend upon whether there is congestion due to chronic right HF or hypo-perfusion due to acute left HF. 8/12/2022 13
- 14. Cont… Table-2 shows NYHAand modified Ross classification of HF in children. 8/12/2022 14
- 15. Stages of heartfailure in infants and children Stage A patients who are at high risk for HF Cardio toxic chemotherapeutic agents CKD requiring dialysis Stage B Patients with abnormal cardiac morphology or cardiac function no symptoms of HF, past or present 8/12/2022 15
- 16. Cont… Stage C Patientswith functional heart disease with prior or current symptoms of heart failure goals of therapy are to provide symptomatic relief and limit progression of the disease. Stage D Symptomatic HF that is refractory to optimized oral therapies characterized by frequent hospitalizations for fluid overload or low cardiac output Has comorbidities such as anemia, renal impairment and hyponatremia long-term survival requires cardiac transplant and/or mechanical circulatory support (MCS) 8/12/2022 16
- 17. Table-3 Stages ofheart failure in infants and children Stage Definition Example A Patients with increased risk of developing HF normal cardiac function and chamber size Exposure to cardiotoxic agents, family history of heritable cardiomyopathy, univentricular heart, congenitally corrected transposition of the great arteries B Patients with abnormal cardiac morphology or function, with no symptoms of HF, past or present Aortic insufficiency with LV enlargement, history of anthracycline exposure with decreased LV systolic function C Patients with structural or functional heart disease, and past or current symptoms of HF Symptomatic cardiomyopathy or congenital heart defect with ventricular pump dysfunction D Patients with end-stage HF requiring specialized interventions Marked symptoms at rest despite maximal medical therapy 8/12/2022 17
- 18. Diagnosis History Physicalexamination Laboratories- CBC, RFT, serum electrolyte, LFT Imaging- CXR, ECG, ECHO 8/12/2022 18
- 19. Management of HeartFailure The underlying cause of cardiac failure must be removed or alleviated if possible. Treatment of the precipitating or contributing causes. General Measures bed rest Oxygen supplementation Fluid intake restriction to 80% of basal metabolic requirements Nutritional support CHF follow chart(V/s, UOP, Liver size, Daily weight…) Medical therapy Surgical management 8/12/2022 19
- 20. Nutrition in childrenwith HF Growth impairment caused by Insufficient caloric intake(amino acids, carbohydrates and lipids) Malabsorption of the ingested calories Causing an increase in energy expenditure of patients with the disease FTT and malnutrition Increased metabolic rate Repeated vomiting Increased caloric requirement 8/12/2022 20
- 21. Nutritional support Therequired calorie intakes may be as high as 150 to 160 kcal/kg/day for infants in CHF. In children and adolescents, current recommendations suggest that 25-30 kcal/kg/d is a reasonable target for most patients. Human milk fortifier (Enfamil, Mead Johnson), 1 packet per 25 mL of breast milk = 24 kcal/oz Formula concentration to 24 kcal/oz by:- 1 cup powdered formula + 3 cups water or 4 oz ready-to-feed + ½ scoop powdered formula 8/12/2022 21
- 22. Medical therapy Diuretics- areusually the first mode of therapy initiated in patients with CHF. 8/12/2022 22
- 23. 8/12/2022 23 AfterloadArterial dilation Preload Venous dilation Improve myocardial activity Reduce myocardial fibrosis Inhibit reabsorption of Na, k and Cl At loop of henle and distal tubules Anti‐arrhythmic effects Improve exercise tolerance Free radical scavenging
- 24.
- 25. Diuretic resistant heartfailure Braking phenomenon that occurs when the magnitude of natriuresis following each diuretic dose declines. 1. ECF volume contraction- caused by all diuretics Increase in filtration fraction (GFR/renal blood flow) stimulating the vascular mechanism of renin secretion also inhibits the secretion of atrial natriuretic peptide fluid reabsorption in the proximal tubule Enhances proximal solute and fluid reabsorption by decreasing the renal interstitial pressure 2. Stimulation of efferent sympathetic nerves reduces urinary NaCl excretion stimulating tubule NaCl reabsorption. 8/12/2022 25
- 26. Cont… 3. Loop diureticsstimulate renin secretion by inhibiting NaCl uptake into macula densa cells. stimulates renin secretion directly leading to a volume-independent increase in Ang II and aldosterone secretion. 4. Diuretics increase solute delivery to distal segments Cause epithelial cells to undergo both hypertrophy and hyperplasia at DCT increased reabsorption of sodium in this segment blunting the natriuretic effect and shifting the dose-response curve downward and to the right 8/12/2022 26
- 27. Treatment noncompliance shouldbe excluded Restriction of sodium intake higher doses and more frequent administration of loop diuretics Combination therapy. DCT diuretics to loop diuretics Prevent or attenuate postdiuretic NaCl retention Inhibit salt transport along the proximal tubule. Inhibit NaCl transport along the renal distal tubule Continuous Diuretic Infusion(furosemide 0.1-0.4mg/kg/hr) avoid troughs of diuretic concentration prevent postdiuretic NaCl retention. 8/12/2022 27
- 28. Cardiogenic Shock Cardiacpump impairment that results in Insufficient delivery of blood flow to tissues to meet resting metabolic demands Considered the most severe expression of left ventricular failure End-organ dysfunction can mimic other forms of severe shock Tachycardia, cold peripheral, impaired mental status, fast breathing, cyanosis, hyperventilation due to acidosis. Oliguria (less than 1 mL/kg/h) Hypotension is typically a late finding. 8/12/2022 28
- 29. Cont… Causes:- Myocarditis Cardiomyopathy congenital heartdisease Arrhythmias Following cardiac surgery septicemia severe burns anaphylaxis 8/12/2022 29
- 30. Treatment ABC oflife Oxygen supplementation Elevate head of bed to reduce pulmonary pooling (infant chair) Boluses of fluid (5-10 mL/kg/hr) To replace deficits (preload) shouldn’t be given if there is pulmonary edema If deteriorate restrict fluid and salt. 8/12/2022 30
- 31. Cont… Positive pressureventilation Improve blood gas tension and Reduce work of breathing Reduction in afterload. CPAP can be used Heart transplantation A history of repeated hospitalizations for HF Escalation in the intensity of medical therapy Refractory cardiogenic shock Continued dependence on intravenous inotropes to maintain adequate organ perfusion…. 8/12/2022 31
- 32. Cont… In advancedHF, ACEI therapy introduction:- should occur after stabilization of HF symptoms with diuretic simultaneous to inotropic support withdrawal. Up titration can proceed safely over 3-10 days in most inpatients Can be more gradual in outpatients. 8/12/2022 32
- 33.
- 34.
- 35. Cont… Drugs Dose(μg/kg/min) effectadvantage Dopamine 0.5-2 Renal vasodilation NE release from cardiac adrenergic nerve endings 2-10 ↑Cardiac index >10-20 Vasoconstriction Dobutamine 1-20 ↑Cardiac index Vasoconstriction not dependent on the release of stored norepinephrine Milrinone Loading 10–50 μg/kg over 10 min; then 0.1–1 μg/kg/min ↑Cardiac index ↓SVR, PVR ↓= Filling pressures Arrhythmia, ↓BP Epinephrine 0.05–0.3 Positive inotrope ↑HR, ↓ renal flow ↑O2 consumption Arrhythmia In the treatment of shock and hypotension unresponsive to fluid resuscitation useful in patients with accompanied bradycardia preferable to dopamine in cases with marked circulatory instability, particularly in infants Sodium nitroprusside 0.5–10 Vasodilator Arteries and veins ↑Cardiac index 8/12/2022 35
- 36. Heart failure inSAM Has a reduced output and impaired contractility Results from- Electrolyte disturbance like Hypokalemia, Hypomagnesiumia Selenium deficiency- degeneration and necrosis of cardiac muscle, necrotizing cardiomyopathy Anemia Infection Fluid overload Treatment complication 8/12/2022 36
- 37. Cont… DIAGNOSIS Physical deteriorationwith weight gain, sudden increase in liver size, tenderness of the liver Increased respiratory rate, ‘grunting’ breathing, crepitation in lungs, prominent superficial and Increased edema or reappearance of edema. When weight gain precedes or is associated with signs of respiratory distress, heart failure should be the first than pneumonia. 8/12/2022 37
- 38. Treatment Stop allintake of oral or IV fluids. No fluid or food should be given until heart failure has improved (even if this takes 24 to 48 hrs) Small amounts of sugar-water can be given orally to prevent hypoglycemia Give Furosemide (1 mg/kg) single dose, repeat if necessary If it is due to severe anemia, manage accordingly. 8/12/2022 38
- 39. Monitoring of Childrenwith chronic heart failure 8/12/2022 39
- 40. Routine Investigations formonitoring of patients with chronic heart Failure 8/12/2022 40
- 41. Reference Joseph W.Rossano, heart failure Nelson 21st edition. Myung K. Park, MD, FAAP, FACC, park Cardiology 5th edition. Bibhuti B. Das, Review Current State of Pediatric Heart Failure, 2018(PubMed). Jack F. Price, Congestive Heart Failure in Children, Pediatrics in Review 2019. Rosenthal et al, Journal of Heart and Lung Transplantation Rosenthal Volume 23, Number 12. CATHERINE A. LEITCH, Section of Neonatal–Perinatal Medicine, pediatric Heart Failure, 2015. Dr Lode De Bruyne, Department of Cardiology article review. Paul F. Kantor & Luc L. Mertens, Heart failure in children,February, 2010 Robert E. Shaddy, Daniel J. Penny, Andersons pediatric Cardiology, 4th Edition Kantor et al, Canadian Journal of Cardiology 29, Canadian Cardiovascular Society Guidelines, 2013. 8/12/2022 41
- 42.
Editor's Notes
- #9 Mechanical Factors The ability of heart muscle to increase contraction in response to stretching of its fibers was demonstrated in intact heart preparations by Frank in 1895 (17) and by Starling in 1918 (21). They first described the relationship between ventricular diastolic volume and pressure and stroke output. Subsequently, the concept of the ventricular function curve was developed to define cardiac function (19) and the important role of sympathetic nerve stimulation in increasing cardiac contractility was demonstrated by showing an upward shift of the function curve (20). When myocardial damage or disease occurs and inotropy is impaired, increasing ventricular filling provides only a limited increase in cardiac output and at relatively high end-diastolic pressure, no further increase in output is achieved. The high end-diastolic pressure results in an increase of atrial and venous pressures. An increase in afterload on the normal ventricle reduces stroke volume, but in the presence of myocardial dysfunction, the reduction of stroke volume with elevation of afterload is greatly exaggerated (21). In congenital cardiac lesions with left-to-right shunts, an excessive volume load is placed on the ventricle. Depending on the lesion, the output of the left or right or both ventricles is increased. To achieve this increased output, ventricular end-diastolic volume and pressure are increased, based on the Frank–Starling mechanism. Although myocardial performance may be normal, the elevated diastolic pressure may result in pulmonary or systemic venous congestion and may induce neurohormonal responses (see below). Lesions that obstruct ventricular outflow impose a pressure load on the ventricle. The increased afterload produced by the obstruction reduces ventricular stroke volume. In an attempt to maintain systemic blood flow, based on the Frank–Starling mechanism, ventricular end-diastolic pressure is raised to increase stroke volume. Although not as common in infants and children as in adults, diastolic filling of the ventricle may be impaired. This Heart Failure—A Historical Perspective 9 altered lusitropy may result from myocardial fibrosis or marked hypertrophy, and from restraint on the ventricle from external factors. Systolic function may be normal, but interference with filling of the ventricle restricts stroke volume. Ventricular diastolic volume enhancement is achieved only by very large increases in diastolic pressure, resulting in atrial distension and venous congestion.
- #10 The observations indicating that cardiac output is extremely sensitive to the increased afterload in patients with cardiac failure, and that afterload is often markedly increased as a result of the increased sympathetic activity and the effect of A II, introduced the concept that the reducing afterload could decrease loading on the ventricle and possibly improve output. Several vasodilators have been used, but inhibition of production of A II by administering inhibitors of ACE has been favored in recent years. Several studies in adults, using captopril or enalapril, in addition to digitalis and diuretic therapy, have shown symptomatic improvement and prolongation of survival (51,52). The ACE inhibitors have also been administered to infants and children with cardiac failure with beneficial effect (53,54). Although the reduction of afterload may be responsible for the effects of ACE inhibitors, it is now evident that they may influence the effect of A II on cardiac muscle. A II, which is produced locally in cardiac myocytes in response to stretch, has been shown to induce hypertrophy of myocytes, unrelated to any general hemodynamic effect, as well as apoptosis (55,56). A II directly stimulates fibroblasts and also increases fibrosis in cardiac muscle (57). Restriction of A II production by use of ACE inhibitors, or blockade of A I receptors with losartan limits the development of cardiac hypertrophy, as well as apoptosis and fibrosis. Furthermore, inhibition of A II effects may not only limit myocardial damage, but may reverse it by inducing regression of fibrosis (58).
- #18 CARDIAC Cardiomyopathy Arrhythmias Chemotherapy: • Daunorubicin • Doxorubicin • Idarubicin Female sex Age <5 yr at time of treatment Higher doses of chemotherapy (≥300 mg/m2) Higher doses of cardiac radiation (≥30 Gy) Combined-modality therapy with cardiotoxic chemotherapy and irradiation
- #20 <10kg….100ml/kg/day 10-30kg….600ml-1L/day >30kg…1-2L/day
- #23 A creatinine rise of greater than 50% over baseline value in any patient requires a reassessment of fluid balance and diuretic therapy, and consideration for a dosage reduction or withdrawal of ACEi therapy Aldosterone antagonist SIDE EFFECT- Hyperkalemia - painful Gynacomastia - worsening of RF. CONTRA Ix – Cr- > 2.5mg/dl - serum K+ > 5.5 mmol/lit - worsening of RFT=> STOP
- #24 Restriction of A II production by use of ACE inhibitors, or blockade of A I receptors with losartan limits the development of cardiac hypertrophy, as well as apoptosis and fibrosis. Furthermore, inhibition of A II effects may not only limit myocardial damage, but may reverse it by inducing regression of fibrosis (58)
- #25 Simplified decision-making in symptomatic acute decompensated heart failure management. Groups A-D correspond to those designated in Figure 1. It is usual to admit all patients who are symptomatic at their initial presentation. Those with mild symptoms and no vomiting/ gastrointestinal symptoms might respond to oral therapy, although IV diuretics are typically required. It is usual to reserve IV inotropic/vasodilator therapy for those who have underperfusion and volume overload. Most patients should be able to achieve oral maintenance therapy, at least on a temporary basis. , with or without; ACEi, angiotensin-converting enzyme inhibitor; BNP, brain natriuretic peptide; EF, ejection fraction; IV, intravenous; LV, left ventricular; NPPV, noninvasive positive pressure ventilation; RV, right ventricular.
- #29 PATHOPHYSIOLOGY Cardiogenic shock results from an impairment of cardiac output (CO), elevated systemic vascular resistance (SVR), orboth. Recall that cardiac output is equal to the product of heart rate (HR) and stroke volume (SV) (Eq 1). Stroke volume is influenced by contractility and left ventricular filling pressure. In infants and children, cardiac output is primarily driven by heart rate due to a lack of ventricular muscle mass and thus a lack of improved contractility. Elevations in SVR hinder left ventricular ejection through increased afterload [5]. CO = HR x SV (Eq. 1) There are four major determinants of ventricular function: contractility, heart rate, preload, and afterload. The Frank-Starling relationship is a series of curves detailing the relationship between preload and ventricular function (Fig. 1). As preload increases, so then must cardiac output. At the point when the myocytes are stretched beyond their ability to generate increased force, ventricular function worsens. At the extremes of impaired ventricular function, the heart failure may result in cardiogenic shock. In the normal heart, intracellular calcium shifts determine contractility. In the case of decreased myocardial performance, calcium handling is abnormal, leading to both systolic and diastolic dysfunction. Compensatory responses that protect the body in other forms of shock can contribute to worsening of heart failure by further depressing cardiac function. The body naturally responds to a low output state by increasing systemic vascular resistance. However, this increase in systemic vascular resistance imparts an increase in ventricular afterload, adding to increased cardiac work and further decreasing function. In an effort to increase blood flow to end-organs, the renin-angiotensin II-aldosterone pathway is activated, thereby encouraging renal juxtaglomerular cells to increase reabsorption of water and salt. This process furtherincreases preload and in a cardiogenic shock state, contributes to pulmonary and peripheral edema via excessive ventricular end diastolic volume. Another effect of decreased cardiac output is the activation of the sympathetic nervous system, releasing catecholamines. The immediate effect of this in early shock is to increase heart rate, thereby increasing cardiac output. In the long-term, however, the vasoconstrictive properties of endogenous catecholamines increase afterload, thereby contributing to heart failure and further organ dysfunction.