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Management of Patients with CHF Emphasis on New Modalities of Treatment GH Ajami MD. Professor of Pediatrics Pediatric Cardiology Shiraz University of Medical Sciences CHF Objectives: The student at the end of the lecture should be able: 1. To explain the mechanisms of CHF in patient with A. obstructive lesions B. Left to right shunt C. Regurgitant lesion D. Myocardial disease E. arrhythmia 2. To understand and discuss the compensatory mechanisms used by the patient with CHF 3. To explain the symptoms of the patient on the basis of hemodynamic changes in CHF 4. To appreciate the role of PE and chest X-ray for diagnosis of CHF 5. To know how the following medications can improve the condition of patient with CHF: O2, diuretics, digoxin, dopamine, angiotensin converting enzymes inhibitor (captopril), Pace maker . Definition of CHF: Inadequate blood supply and delivery of oxygen to tissues for metabolic needs of body Systemic O2 delivery=cardiac output × Hb × O2% Cardiac output = stroke volume × heart rate Stroke volume depends on: Preload Afterload Contractility Myocardial Contractility Definition Force generated by the myocardium Squeeze Reflects chemical or hormonla influences Catecholamines ↑Contractility ↑ SV ↑ Cardiac output Afterload Definition The resistance the ventricle needs to overcome to empty its contents Can be estimated by arterial systolic BP If no obstruction btwn ventricle and aorta Decreased by arterial vasodilators ACE inhibitors ↓ Afterload (resistance) ↑ SV ↑ Cardiac output Preload Definition Amount of myocardial stretch at the end of diastole (relaxation phase) Distention of ventricle before the “ squeeze” Frank and starling , 19th century Frank-starling curve (ventricular function curve) Physiological Compensatory mechanisms in patients with CHF I. Renin-Angio-Ald. (R.A.A.) syst.: Low CO → low renal perfusion R.A.A. syst. Salt and water retension →↑ Preload Starling law ↑ contractility ↑C.O Angiotension II → vasoconstriction →↑ after load ↑ perfusion to brain & heart ↑ R.A.A. system activity causes cardiac remodeling which is a pathological process (hypertrophy, fibrosis and change in receptors) II. Sympathetic system overactivity: causes ↑heart rate, ↑contractility and ↑ of blood pressure, the end result is cardiac remodeling (hypertrophy, fibrosis and accumulation of calcium in myocytes leading to cell death) III. Cardiac muscle hypertrophy IV: ↑ In level of 2-3 DPG Etiology of heart failure Mechisms 1. Volume overload 2. Pressure overload 3. After too high Myocardial insufficiency 4. Preload is too high Poor contractility Other Arrhytmia,anemia Differential diagnosis of Heart Failure in children Congenital Heart Defects Cordimyopathies Genetic – inbom errors of metabolism, neuromuscular, familial Other Acquired conditions Volume load-large left to right shunts or severe valvular regurgitation Pressure load-left heart obstructive lesions Pericarditis/ tamponade Sepsis Coronary artery disease Arrhythmia Causes of CHF Fetal Severe anemia (hemolysis, fetal-maternal transfusion, parvovirus B 19-induced anemia, hypoplastic anemia) Supraventricular tachycardia Ventricular tachycardia Complete beart block Premature neonate Fluid overload Patent ductus arteriosus Ventricular septal defect Cor pulmonale (bronchopulmonary dysplasia) Hypertension 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) Viral myocarditis Causes of CHF Infant-Toddler Left to right cardiac shunts (ventricular septal defect) Hemangioma (arteriovenous malformation) Anomalous left coronary artery Metabolic cardiomyopathy Acute hypertension (hemolytic-uremic syndrome) Supraventricular tachycardia Kawasaki disease Viral myocarditis Child-adolescent Rheumatic fever Acute hypertension (glomerulonephritis) Viral myocarditis Thyrotoxicosis Hemochromatosis-hemosiderosis Cancer therapy (radiation, doxorubicin) Sickle cell anemia Endocarditis Cor pulmonale (cystic fibrosis) Cardiomyopathy (hypertrophic, dilated) What is the body’s reaction to CHF? Symptoms & signs of : 1. 2. 3. Pulmonary venous congestion Systemic venous congestion Sympathetic overload CHF is a clinical diagnosis Pulmonary Venous Congestion Symptoms Poor feeding Poor Growth Shortness of Breath Cough Exercise intolerance New York Classification Signs Tachypnea Increased WOB Nasal flaring Subcostal indrawing Grunting Crackles – fine Rales 02 requirement Symptoms Venous Congestion Symptoms Puffiness Abdominal swelling Abdominal pain - RUQ Signs Peripheral edema Jugular venous distention Hepatomegaly Cardiomegaly Symptoms Overload Symptoms Sweating Pallor Decreased urine output Signs Tachycardia Decreased perfusion Gallop rhythm The Role of Investigations Primarily clinical diagnosis CXR - Cardiomegaly - Pulmonary edema Blood Gas - Metabolic acidosis - Elevated lactate The Role of Investigations ECG – helpful in determining underlying defect Echo – Ventricular function/size – Identify structural defects e.g. large VSD Approach to Management Initial stabilization Supportive management Identify cause of CHF ECG, Echo, laboratory investigations Infectious work up Treatment for underlying cause – e.g. Surgical correction of structural defects Initial Stabilization Airway Breathing Supplemental Oxygen CPAP / Ventilation Circulation Fluid Management Ionotropic support General Measures Oxygen Correct predisposing factors Fever, anemia, infection Daily weight Decreases WOB, supports myocardium Even if sats are normal! Hospitalized patients Maximize nutrition Medical Rx: Preload Diuretics Optimize preload Ideal portion of Frank-Starling curve Promotes fluid loss via kidney (renal tubules) Lasix, aldactazide, acetazolamide Medical Rx: Contractility Myocardial support Increase the contractility of heart muscle Improve the “squeeze” Used primarily in severe CHF IV administration Ionotropic infusions epinephrine, dobutamine… Medical Rx: Afterload Afterload reduction ●Decreases the resistance the heart is pumping against ●Arteriolar vasodilation •Decreases BP ●Most common agent ACE inhibitor •Captopril (oral) •Milrinone (IV infusion) Beta-Blockers Latest research Increased sympathetic drive in CHF myocardial cell death B-Blockers impair the process decreased cell death → improved outcomes Long-term therapy Introduced when patients are stable Most common---Carvedilol Carvedilol has 1, adrenergic blocking, β antagonist effect and anti-oxidant activity. This medication with dosage of 0.1 mg/kg up to 1 mg/kg in divided dose can block over activity of sympathetic system and so prevents progression or severity of remodeling of the heart which is a pathological process, in patients with CHF. Aldosterone Blockade in Cardiovascular Disease Heart 2004; 90 1229-1234 Allan D Struthers Division of Medicine, therapeutics Nine well Hospital, Dundee, UK Adverse effects of aldosterone are: 1. Vascular endothelial dysfunction by reducing (NO) production 2. ↑Inflammatory response with increased expression of cytokines such as osteopontin and so its blockade reduces tissue injury and fibrosis in myocardium, kidney and brain So progression of myocardial remodeling is slowed down and also patchy fibrosis of myocardium is prevented which can be a focus for arrhythmia 3. Causes K, Mg depletion which prone patients to arrhythmia 4. Blunt baroreflex response. Surgical Treatment of Patients with CHF 1. 2. 3. 4. Heart and heart-lung transplant for cardiomyopathies or complex CHD not operable Repair of underlying CHD in patient with intractable CHF Intractable CHF in patients with endocarditis New surgical procedures such as Dor or Batissta technique for patients with dilated cardiomyopathy Why is heart failure in children important While adult heart failure is clearly a more compelling health problem: 1. The cost are higher for children became of the frequent surgical or catheter-intervention which my be needed. 2. The demands of medical care adversely affect parental economic productivity 3. Loss of a child with heart failure has economic impact because of loss of potentially productive years per death. 4. Grawing numbers of children with heart failure are reaching adult hood. Historical perspective 1. William Harvey indentified the heart as an organ that pumping the blood rath generating heart (17th century). 2. Ippolito Albertini first described the clinical picture of congestive heart failure (17th century). 3. From the latel 1890, for the first time in predicative textbooks a chapter on heart disease were included. 4. In mid-20th century the most common cause of childhood heart failure remained rheumatic fever. 5. Since 1950 the novel concept that congenital heart disease disproportionally causes heart failure in children appreciated. Table 1. Modified Ross Heart Failure Classification for Children Class I Class II Class III Class IV Asymptomatic Mild tachypnea or diaphoresis with feeding in infants Dyspnea on exertion in older children Marked tachypnea or diaphoresis with feeding in infants Marked dyspnea on exertion Prolonged feeding times with growth failure Symptoms such as tachypnea, retractions, grunting, or diaphoresis at rest Table 2. Cardiac Malformations leading to heart failure Shunt lesions - Ventricular septal defect - Patent ductus arteriosus - Aorto pulmonary window - Atrio ventricular septal defect - Single ventricle without pulmonary stenosis - Atrial septal defect (rare) Total / partial anomalous pulmonary venous connection Valvular regurgitation - Mitral regurgitation - Aortic regurgitation Inflow obstruction - Cor triatriatum - Pulmonary vein stenosis - Mitral stenosis Outflow obstruction - Aortic valve stenosis/ sub aortic stenosis/spravalvular aortic stenosis -Aortic Coarctation Table 3. Sources of heart failure with a structurally normal heart Primary cardiac - Cardiomyopathy Myocarditis Myocardial infarction Acquired valve disorders Hypertension Kawasaki syndrome Arrhythmia ( bradycardia or tachycardia) Noncardiac - Anemia - Sepsis - Hypoglycemia - Diabetic ketoacidosis - Hypothyroidism - Other endocrinopathies - Arteriovenous fistula - Renal failure - Muscular dystrophies Table 4. Principles of Management Heart Failure Recording and Treatment of Underlying Systemic disease Timely Surgical repair of structural anomalies After load reduction - anogiotensin- converting enzyme inhibitors - Angiotensin receptor blockers - Milrinone - Nitrates - Brain natriuretic peptide (BNP) Preload reduction -Diuretics -BNP Sympathetic inhibition -Beta blockers - BNP - digoxin Cardiac remodeling prevention - Mineral corticoid inhibitors Inotropy Digoxin Table 5. Heart Failure Staging in Pediatric Heart Disease Stage Interpretation Clinical Examples A At risk for developing HF Congenital heart defects Family history of cardiomyopathy Anthracycline exposure B Abnormal cardiac structure of function No symptoms of HF Univentricular hearts Asymptomatic cardiomyopathy Repaired congenital heard disease C Abnormal cardiac structure or function Past or present symptoms of HF Repaired and unrepaired congenital heart defects Cardiomyopathies D Abnormal cardiac structure or function Continuous infusion of intravenous inotropes of prostaglandin E1 to maintain patency of a ductus arteriosus Mechanical ventilatory and/or mechanical circulatory support Same as stage C