1. DR SARIKA GUPTA (MD,PHD) ASST. PROFESSOR CLINICAL APPROACH & MANAGEMENT OF CHF

2. DEFINITION  A clinical syndrome  Occurs when  The heart is unable to pump enough blood to the body to meet its needs  The heart is unable to dispose of systemic or pulmonary return adequately  Or a combination of the two

3. PATHOPHYSIOLOGY  Systemic oxygen transport = cardiac output X systemic oxygen content  Cardiac output = heart rate X stroke volume  The primary determinants of stroke volume: afterload (pressure work) preload (volume work) contractility (intrinsic myocardial function)

4. PATHOPHYSIOLOGY  The heart can be viewed as a pump with an output proportional to its filling volume and inversely proportional to the resistance against which it pumps

5. PATHOPHYSIOLOGY  As ventricular end-diastolic volume increases, a healthy heart increases cardiac output until a maximum is reached The increased stroke volume obtained in this manner is due to stretching of myocardial fibers Resulting in increased wall tension, elevating myocardial oxygen consumption Cardiac muscle with compromised intrinsic contractility requires a greater degree of dilatation to produce increased stroke volume & does not achieve the same maximal cardiac output as normal myocardium does

6. PATHOPHYSIOLOGY Lesion causing increased preload (left-to-right shunt or valvular insufficiency) Cardiac chamber is already dilated Little room for further dilatation as a means of augmenting cardiac output Lesions that result in increased afterload to the ventricle (aortic or pulmonic stenosis, coarctation of the aorta) decreases cardiac performance

7. PATHOPHYSIOLOGY  Abnormalities in heart rate: compromise cardiac output Tachyarrhythmias shorten the diastolic time interval for ventricular filling.  High-output failure: NO basic abnormality in myocardial function Cardiac output is greater than normal Alterations in the oxygen-carrying capacity of blood (anemia or hypoxemia) & increased oxygen demands (secondary to hyperventilation, hyperthyroidism, or hypermetabolism)

8. PATHOPHYSIOLOGY

9. ETIOLOGY FETAL Severe anemia (hemolysis, fetal-maternal transfusion, parvovirus B19–induced anemia, hypoplastic anemia) Supraventricular tachycardia Ventricular tachycardia Complete heart block Severe Ebstein anomaly or other severe right-sided lesions Myocarditis

10. ETIOLOGY PREMATURE NEONATE Fluid overload Patent ductus arteriosus Ventricular septal defect Cor pulmonale (bronchopulmonary dysplasia) Hypertension Myocarditis Genetic cardiomyopathy

11. ETIOLOGY FULL-TERM NEONATE Asphyxial cardiomyopathy Arteriovenous malformation (vein of Galen, hepatic) Left-sided obstructive lesions (coarctation of aorta, hypoplastic left heart syndrome) Large mixing cardiac defects (single ventricle, truncus arteriosus) Myocarditis Genetic cardiomyopathy

12. ETIOLOGY INFANT-TODDLER Left-to-right cardiac shunts (ventricular septal defect) Hemangioma (arteriovenous malformation) Anomalous left coronary artery Genetic or metabolic cardiomyopathy Acute hypertension (hemolytic-uremic syndrome) Supraventricular tachycardia Kawasaki disease Myocarditis

13. ETIOLOGY CHILD-ADOLESCENT Rheumatic fever Acute hypertension (glomerulonephritis) Myocarditis Thyrotoxicosis Hemochromatosis-hemosiderosis Cancer therapy (radiation, doxorubicin) Sickle cell anemia Endocarditis Cor pulmonale (ILD, cystic fibrosis) Genetic or metabolic cardiomyopathy

14. CLINICAL FEATURES  Depend on the degree of the child's cardiac reserve  A critically ill infant or child who has exhausted the compensatory mechanisms- symptomatic at rest  Other patients may be comfortable when quiet but are incapable of increasing cardiac output in response to even mild activity without experiencing significant symptoms

15. CLINICAL FEATURES  History:  Poor feeding, poor weigh gain, tachypnea (worsening during feeding), cold sweat on the forehead- CHF in infants  Shortness of breath, specially with activities, easy fatigability, puffy eyelids or swollen feet-older children

16. CLINICAL FEATURES  Examination:  Tachycardia, gallop rhythm, weak & thready pulses  Growth failure, perspiration, cold & wet skin  Cardiomegaly  Tachypnea  Dyspnea on exertion  Orthopnea  Wheezing & pulmonary crackles COMPENSATORY RESPONSE PULMONARY VENOUS CONGESTION

17. CLINICAL FEATURES  Examination:  Hepatomegaly  Puffy eyelids  Distended neck veins  Ankle edema SYSTEMIC VENOUS CONGESTION Clinical assessment of jugular venous pressure in infants may be difficult because of the shortness of the neck & the difficulty of observing a relaxed state; palpation of an enlarged liver is a more reliable sign Edema may be generalized & involves the eyelids & sacrum & less often the legs and feet

18. CLINICAL FEATURES

19. INVESTIGATION  X-RAY Study:

20. INVESTIGATION  X-RAY Study:

21. INVESTIGATION  ECG: not helpful  ECHO:  Standard technique for assessing ventricular function  The most commonly used parameter in children is fractional shortening (impaired LV systolic function)  Difference between end-systolic & end-diastolic diameter divided by end-diastolic diameter (N=28%- 42%)  Ejection fraction (impaired LV systolic function)  Enlargement of ventricular chambers  Doppler tissue imaging (impaired LV systolic & diastolic function)

22. INVESTIGATION  Magnetic resonance angiography  Cardiac catheterization-evaluation of biopsy specimens  Decreased arterial oxygen levels; respiratory or metabolic acidosis  Hyponatremia  Serum B-type natriuretic peptide (BNP)  Cardiac neurohormone released in response to increased ventricular wall tension  Elevated in patients with heart failure due to systolic dysfunction (cardiomyopathy)  Elevated in children with volume overload (left-to- right shunts such as ventricular septal defect)

23. MANAGEMENT  PRINCIPAL:  Elimination of the underlying causes  Treatment of the precipitating or contributing causes (infection, anemia, arrhythmias, fever)  Control of the heart failure state

24. MANAGEMENT  Control of the heart failure– GENERAL MEASURES  Bed rest  Humidified oxygen  Adequate calories & fluid 1. Calorie dense food 2. Frequent small feeding 3. Nasogastric feeding 4. Salt restrictions  Patients with pulmonary edema- positive pressure ventilation  Daily weight measurement in hospitalized children

25. MANAGEMENT  Control of the heart failure state- Drug therapy  Inotropic agents  Diuretics  Afterload reducing agents DIURETICS: interfere with reabsorption of water & sodium by the kidneys results in a reduction in circulating blood volume thereby reduces preload & control pulmonary & systemic venous congestive symptoms

26. MANAGEMENT INOTROPIC AGENTS:  Rapidly acting Inotropic agents Dopamine, dobutamine, isoproterenol, epinephrine & amrinone Additional vasodilator actions Used for critically ill infants with CHF, those with renal dysfunction & postoperative cardiac patients with CHF  Digoxin

27. MANAGEMENT AFTERLOAD REDUCING AGENTS:  Arteriolar vasodilator Augments cardiac output by acting primarily on the arteriolar bed Reduction of afterload Hydralazine  Venodilators Dilate systemic veins & redistribute blood from the pulmonary to the systemic circuits Decrease in pulmonary symptoms Nitriglycerine, isosorbide dinitrate

28. MANAGEMENT AFTERLOAD REDUCING AGENTS:  Mixed vasodilator Act on both arteriolar & venous beds ACE inhibitors, nitroprusside & prazosin ACEIs have additional beneficial effects on cardiac structure & function that may be independent of their effect on afterload

29. MANAGEMENT AFTERLOAD REDUCING AGENTS:  Afterload reducers: especially useful in children with heart failure secondary to cardiomyopathy & in patients with severe mitral or aortic insufficiency  Effective in patients with heart failure caused by left- to-right shunts  Not used in the presence of stenotic lesions of the left ventricular outflow tract because of concern over coronary perfusion

30. MANAGEMENT β-ADRENERGIC BLOCKERS:  β-Blockers are used for the chronic treatment of patients with heart failure who were symptomatic despite being treated with standard anticongestive drugs

31. MANAGEMENT