Congestive heart failure revised

Congestive Heart failure full details by Dr.Anup,Department of Pediatrics

1. Congestive Heart Failure Dr.Anup John Thomas Assistant Professor Department of Pediatrics,MGMCRI

2. DEFINITION It is a Clinical syndrome in which heart is unable to provide the output required to meet the metabolic demands of the body Inability to dispose systemic or pulmonary venous return adequately Combination of above two

3. Factors Affecting Cardiac Performance Cardiac output depends on: stroke volume and heart rate. Stroke volume is dependent on three important factors: preload, afterload and contractility. 

4. Preload = volume of blood received by the heart. Basically, preload is  stretch . Afterload = pressure or resistance the heart has to overcome to eject blood. Afterload is  squeeze .

5. Preload: Preload ( volume overload). preload (such as in VSD, or valvular insufficiency). Afterload: Afterload is the resistance (pressure) against which the heart must pump blood: e.g.; systemic vascular resistance. Afterload (such as with aortic stenosis, pulmonary stenosis, or coarctation of the aorta) Contractility Contractility (Cardiac Performance Independent of Preload or Afterload) Volume overload is the most common cause of CHF in children

6. Compensatory mechanisms in heart failure (1) Cardiac compensation increased HR and cardiac contractility Cardiac dilatation (The Frank-Starling mechanism) Myocardial hypertrophy ( 2) Systemic compensation Increase the blood volume Redistribution of blood flow Increase of erythrocytes Increased ability of tissues to utilize oxygen (3) neurohormonal compensation Sympathetic nervous system Renin-angiotensin system Atrial natriuretic peptide; endothelin

7. Etiology of Heart Failure Fetus Premature Neonate Severe anemia (hemolysis, fetal-maternal transfusion) Fluid overload Supraventricular tachycardia PDA Ventricular tachycardia VSD Complete heart block Full-Term Neonate Infant-Toddler Asphyxial cardiomyopathy Left-to-right cardiac shunts (VSD) Left-sided obstructive lesions (coarctation of aorta) Metabolic cardiomyopathy Transposition of great arteries Acute hypertension (hemolytic-uremic syndrome) Viral myocarditis Supraventricular tachycardia Anemia Kawasaki disease Supraventricular tachycardia Complete heart block Child-Adolescent Rheumatic fever Acute hypertension (glomerulonephritis) Viral myocarditis Thyrotoxicosis Endocarditis Cor pulmonale (cystic fibrosis) Arrhythmias Chronic upper airway obstruction (cor pulmonale) Cardiomyopathy

8. Classification of heart failure (1) According to the course of disease 1) Acute HF 2) Chronic HF 2)According to the cardiac output (CO) 1)   Low-output HF : due to volume overload, pressure overload & contractility problems. 2) High-output HF: Heart Rate is primarily affected; 3A (Anemia, Arrhythmia, AV Fistula)

9. (3) According to the location of heart failure 1) Left -side heart failure (LHF) 2) Right-side heart failure (RHF) 3) Biventricular failure (whole heart failure) ( 4)According to the function impaired 1) systolic failure :Myocarditis, hypertension 2) Diastolic failure: restrictive cardiomyopathy, cardiac tamponade.

10. WHEN TO SUSPECT CCF Poor wt. gain Difficulty in feeding Breathes too fast Persistent cough and wheezing Excessive perspiration, irritability, restlessness Puffiness of face Pedal edema Diaphoresis

11. APPROACH TO PATIENT HISTORY PHYSICAL EXAMINATION INVESTIGATION TREATMENT

12. Clinical History NEONATES & INFANTS Poor feeding Tachypnea worsening during feeding Cold sweat on forehead Poor weight gain OLDER CHILDREN Fatigue Exercise intolerance Dyspnea Puffy eyes & pedal edema Growth failure

13. CLINICAL MANIFESTATIONS The physical examination findings depend on whether pulmonary venous congestion, systemic venous congestion, or both are present. Tachycardia, a gallop rhythm, and thready pulses may be present with either cause. If left-sided failure is predominant, tachypnea, orthopnea, wheezing, and pulmonary edema are seen. If right-sided failure is present, hepatomegaly, edema, and distended neck veins are present.

14. IMAGING STUDIES chest x-ray: cardiomegaly. Pulmonary edema ECG : Arrhythmias An echocardiogram assesses the heart chamber sizes, measures myocardial function accurately, and diagnoses congenital heart defects when present. Pulse-oximetry, CBG, hyperoxia test CBC, U&E, calcium, creatinine, and LFT Blood tests Thyroid function

15. Clinical diagnosis of CHF E c h o c a r d i o g r a m Structural diagnosis (e.g. myopathy, valvular) Pathophysiological diagnosis Systolic dysfunction (LVEF < 40% ) Diastolic dysfunction ( LVEF > 40%) Proceed to treatment guidelines

16. NYHA CHF classification for infants NYHA I - NO SIGN NYHA II - RR>50 , WITH OR WITHOUT HEPATOMEGALY NYHA III- ALL ABOVE WITH RIB RETRACTION NYHA IV- RR>60/min H/R>160/ min, WITH HEPATOMEGALY,RIB RETRACTION WITH OR WITHOUT POOR PERFUSION.

17. Treatment principles (1) Correct the underlying causes of HF (2) Diet ; (low salt and high calories) (3) Digitalis ; Improve the cardiac contractility ( 4) Diuretics ; Reducing preload: frusemide ( 4) Dilators ; Reducing afterload; ACE Remember 4 D

18. Treatment of Heart Failure General Care Rest Reduces cardiac output Oxygen Improves oxygenation in presence of pulmonary edema Sodium, fluid restrictions Decreases vascular congestion; decreases preload Other Treatment of underlying causes Closure of defects like ASD or VSD Transplantation Removes diseased heart

19. Precipitating factors Hypertension Anemia Arrhythmia Hyperthyroidism Infection Fever

20. Diuretics ; Reducing preload Diuretics Furosemide Salt excretion by ascending loop of Henle; reduces preload Spironolactone Potassium-sparing diuretic

21. Improve the cardiac contractility Inotropic Agents Digitalis Inhibits membrane Na + , K + -ATPase and increases intracellular Ca 2+ , improves cardiac contractility, increases myocardial oxygen consumption Dopamine Releases myocardial norepinephrine plus direct effect on β-receptor, may increase systemic blood pressure; at low infusion rates, dilates renal artery, facilitating diuresis

22. Dilators ; Reducing afterload Afterload Reduction Hydralazine Arteriolar vasodilator Nitroprusside Arterial and venous relaxation; vasodilation reduces preload Captopril/enalapril Inhibition of angiotensin-converting enzyme; reduces angiotensin II production

23. ß BLOCKERS Effacious in CHF in children due to CHD, Anthracycline induced cardiomyopathy , dilated cardiomyopathy. Improved left ventricular function & exercise tolerance, decreased need for heart transplant. It has been shown to improve clinical symptoms & neurohormonal markers in infants with CHF due to Lt to Rt shunts. Dose should titrated upwards Avoid in decompensated heart failure. Carvedilol(initial dose0.08 →0.46mg/kg)

24. Nonpharmacological treatment modalities Cardiac resynchronization therapy: BiVP cardiomyopathy LBBB LV assist device Surgery: (depends on the type of defect) Blalock Tausig shunt Balloon septoplasty Mustard Senning Jatene’s switch

25. HEART FAILURE IN SPECIAL CONDITION Ductus dependent circulation- PGE 2 Rheumatic carditis -Steroids Kawasaki’s disease-IG Preterm PDA-Indomethacin

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