Congestive cardiac failure (CCF) is defined as the inability of the heart to maintain an output required to sustain the metabolic needs of the body at rest or during stress (systolic failure) without evoking certain compensatory mechanisms.1 In addition, inability of the heart to receive blood into ventricular cavities at low pressure during diastole (diastolic failure).2 Presence of myocardial failure distinguishes CCF from peripheral circulatory congestion resulting from mechanical obstruction as in constrictive pericarditis.
Congestive cardiac failure by itself is not a diagnosis. It is a manifestation of an underlying anatomical or pathological cause affecting the heart.
HEART FAILURE SYNDROMES
Clinically, heart failure syndromes are of 3 types:
- Shock: This is a situation of acute circulatory collapse (low output state) which has to be treated immediately. The etiological factors include septicemia, gastroenteritis, hypoplastic left heart syndrome, aortic atresia, cardiomyopathies, etc.
- Acute heart failure: This is an emergency when there is acute decompensation of left ventricle due to fuid overload, hypertensive crisis, rupture of papillary muscle, severe mitral stenosis, etc.
- Chronic heart failure: This is that situation when there is stable balance between diminished systemic fow and activation of compensatory hemodynamic and neurohormonal responses.
ETIOPATHOGENESIS
Though diastolic failure was not recognized earlier, systolic failure however is much more common. The causes of systolic cardiac failure can be divided into two groups according to age (Table 1.1). The commonest cause of CCF in infants is congenital heart disease, whereas in older children, it is rheumatic fever and rheumatic heart disease.2
Congenital Heart Disease (CHD)
Infants with CHD have a relatively healthy myocardium and if they do not manifest with CCF in the first year of life, they are not likely to do so in the next 10 years unless complicated by anemia, infection, arrhythmias or bacterial endocarditis. Congenital heart disease with volume or pressure overload is the most common cause of CCF in the pediatric age group. Lesions with volume overload such as ventricular septal defect (VSD), patent ductus arteriosus (PDA) and endocardial cushion defect (ECD) are the commonest cause of CCF in the first 6 months of life. Infants with left to right shunt tend to develop CCF around 6-8 weeks of life. At birth, the pulmonary vascular resistance is high but there is a gradual fall during the first few weeks of life. Patients with transposition of great arteries (TGA) with intact ventricular septum and total anomalous pulmonary venous connection (obstructed) manifest with CCF within the first week of life, otherwise TGA with ventricular septal defect or unobstructed anomalous pulmonary venous connection, the CCF develops by the age of 6-8 weeks following physiological fall in pulmonary vascular resistance.
Acquired Heart Diseases
- Myocardial disease: Viral myocarditis usually occurs in children more than 1 year of age. The commonest cause of myocarditis is Coxsackie B virus infection leading on to dilated cardiomyopathy. There are other viral infections, e.g. adenoviruses, cytomegaloviruses, etc. which also give rise to myocarditis.3 The primary myocardial disease causing CCF include glycogen storage disease, endocardial fibroelastosis, medial necrosis of coronary arteries and anomalous origin of left coronary artery.
Arrhythmias
Three fourths of patients with arrhythmias leading on to CCF are below 4 months of age. Heart rates above 180 per minute tend to precipitate CCF and if the tachycardia persists for 24 hours, 20% of patients develop CCF and after 48 hours, 50% go into CCF. There is a tendency for the recurrence of arrhythmias if the onset is after 4 months of age.
Anemia
In children with normal hearts, protracted decrease of hemoglobin levels of around 5 gm/dl can result in CCF, whereas higher hemoglobin level (7-8 gm%) can precipitate CCF in children with diseased cardiac status. Infants are more prone to CCF because of prolonged anemia.
Rheumatic Fever and Rheumatic Heart Disease
Rheumatic carditis and valvular involvement of rheumatic etiology are the commonest cause of CCF in older children.4
Hypertension
Systemic hypertension due to acute glomerulonephritis and aorto-arteritis are the next common causes leading on to CCF in older children and adolescents.
PATHOPHYSIOLOGY
The manifestations of CCF are caused largely by the physiological compensations called into play to combat the inadequate oxygen delivery. The oxygen delivery is dependent on the oxygen content of blood and the cardiac output, while the cardiac output in turn is determined by the preload, afterload, myocardial contractility and the heart rate (Flow chart 1.1).
- Preload— Filling volume of the heart. It is basically a function of venous return and compliance of ventricles.
- Afterload— The resistance the ventricles face on ejection of blood. It can be described as the intra-venous wall stress that develops during ejection and is determined by ventricular pressure, diameter and wall thickness. The simplest approximation of afterload can be obtained by the magnitude of aortic pressure.
- Myocardial contractility— Signifes the efficiency and vigour of the contraction of the myocardium. A decrease in the contractility, the reserve of the ventricles as a pump becomes insuffcient to meet body requirement and therefore CCF is the systemic manifestation of inadequate pump function of heart. The fall in cardiac output leads to activation of several neurohormonal compensatory mechanisms aimed at improving the mechanical environment of the heart.Flow chart 1.1: Neurohormonal and compensatory mechanisms in heart failure5Activation of sympathetic system tries to maintain cardiac output with an increase in heart rate increased myocardial contractility and peripheral vasoconstriction. Similarly stimulation of renin - angiotensin system (RAS) also helps to improve the cardiac output and maintain perfusion of vital organs with retention of salt and water which sometimes unfortunately overreacts and this results in further deterioration of cardiac contractility, establishing a vicious cycle of failure begetting failure.6
- Heart rate is directly related to the cardiac output and is used as a compensatory mechanism by the body to maintain optimal cardiac output by increasing or decreasing the heart rate. The cardiac output is the net product of heart rate and the stroke volume per beat. If the stroke volume falls, the heart rate increases in response to increased catecholamine secretion to compensate for the fall in cardiac output.6
CLASSIFICATION
The classifcation of heart failure as per NYHA and Ross is given in Tables 1.2 and 1.3 respectively.
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CLINICAL FEATURES
Neonates
- In newborn infants, CCF manifests with respiratory distress and feeding difficulty.
- Early onset of poor perfusion—seen as pale, sallow or cyanotic grey complexion.
- Tachycardia and rhythm disturbances due to hypoxia.
- Critical coarctation or other ductus dependent lesions present between 3-10 days of life as the ductus begins to close, leading on to poor peripheral perfusion.
- Hyperactive precordium, abnormal heart sounds and murmurs indicate an underlying large shunt leading on to CCF.
Infants
- Poor feeding with easy fatiguability leading on to failure to thrive, respiratory distress, baseline tachypnea and diaphoresis—features of increased pulmonary fow.
- Cyanosis, hypotonia and shock—are late manifestations.
- Slow weight gain—manifesting as facial puffiness, pedal edema.
- Ventricular septal defect (large)—most common acyanotic heart disease to present in this age group. The two most common models of presentation are:
- Progressive CCF in early infancy.
- Recurrent episodes of chest infection.
- Relatively uncommon causes in later infancy, e.g. TAPVR (unobstructed) and anomalous origins of coronary artery from pulmonary artery—lead onto myocardial dysfunction and ventricular dilatation manifesting with features of CCF.
Children and Adolescents
- Classical manifestations include—progressive exertional dyspnea, anorexia, easy fatigability, abdominal pain, anasarca and pedal edema.
- Physical examination—tachycardia, gallop rhythm, tachypnea, elevated JVP, enlarged tender liver, pulsatile precordium, cardiomegaly and presence of basal crepitations in the lungs.
MANAGEMENT
The general aims of management are to achieve increase in cardiac performance, augment peripheral perfusion and decrease pulmonary and systematic venous congestion. The initial therapy is aimed at stabilizing the infant's condition for diagnostic purposes, e.g. echocardiography and possibly an angiocardiography also, because in all situations, the decision to intervene surgically or to continue with medical management requires a definitive anatomical diagnosis.
Before starting treatment, a few investigations have to be carried out, which include:
Electrocardiogram: Helpful in diagnosis of underlying heart disease by revealing selective chamber enlargement or hypertrophy.
Echocardiogram: Assessing ventricular function and diagnosing underlying heart defects.
Serum electrolytes/ABG: May be altered in critically ill patients. The serum sodium may be low, however total body sodium and water are increased.
Cardiac catheterization: Preoperative assessment of complex and complicated cardiac lesions.
MRI: Accurate assessment in complex congenital heart disease.
Myocardial biopsy: It helps in clinching diagnosis in myocarditis.
TREATMENT
Treatment of chronic heart failure includes:
- Medical
- Devices
- Surgical
Medical Therapy—Aims:
- To reduce morbidity and hospitalization.
- Improve quality of life, enhance exercise capacity and improved long term survival.
- To maintain normal growth.
- To decrease neurohormonal activation and halt or delay the progression of heart failure.
Medical Therapy
- Non-pharmacological and pharmacological.
Non-Pharmacological-General Therapy
- Counselling—Making parents and patients understand the disease and principles of treatment.
- Fluid—Fluid intake to be restricted in severe cases of CCF.
- Salt—High salt content to be avoided, e.g. pickle, chips, papad, etc.
- All immunizations should be given.
- Regular exercises—Physiotherapy should be encouraged.
- Nutrition—Diet
Nutrition has to be emphasized upon, because in chronic CCF failure to thrive and finally growth failure ultimately result because of prolonged undernutrition.
Calorie and Protein Requirement
Caloric requirement is greater than a normal child—120-160 Kcal/Kg/day.
Caloric density has to be increased to 24-36 Kcal/ounce. This can be achieved by adding corn oil and sugar to the milk or formula in phases. If the patient is not able to accept feeds, then nasogastric feeding may have to be resorted to. Because of its long half life, serum pre-albumin is a more reliable parameter of nutritional status compared to albumin. The children should be advised to avoid the use of extra salt and high sodium containing foods.10
Precipitating and aggravating factors in CCF include anemia, hypertension, infective endocarditis, myocarditis, thyrotoxicosis, drug toxicity, fever, infections, arrhythmias and pulmonary embolism. If the patient is not responding well, the aggravating factors should be looked for and managed.
There is some evidence that immunosuppressive therapy may be useful in patients with active myocarditis.
Pharmacological Therapy
Myocardial performance begins to decrease when approximately 20% of the contractile units of the heart are impaired. With further destruction, decompensation sets in rapidly. Renal blood fow is decreased in direct proportion to the reduction in cardiac output. Reduction in renal fow causes increased tubular reabsorption of sodium and water causing an increase in blood volume which results in increased venous pressure (preload) and edema formation. There is an increase in intracellular and extracellular sodium content. The reduced cardiac output is associated with increased ventricular diastolic pressures, the atrial pressure and the systemic vascular resistance, which is related to increased vascular stiffness. The management of CCF consists of a “four pronged attack” for the correction of inadequate cardiac output.
- Augment myocardial contractility.
- Improve myocardial performance by reducing the heart size.
- Reduce cardiac work and thus improve cardiac function.
- Correct the underlying cause.
Augmenting Myocardial Contractility
Inotropic Drugs
Inotropic drugs improve the myocardial contractility in an acute crisis by the use of dopamine or dobutamine. In a chronic situation using digoxin is an important component of CCF management. The use of inotropic agents has often been disputed using the argument that stimulating the failing myocardium may further damage it and that the heart is already exposed to potent inotropic agents in CCF. On the other hand, an increase in myocardial contractility decreases the preload and refexly the afterload with consequent diminished oxygen consumption which is benefcial for the failing heart. Digitalis has been demonstrated to be superior to captopril in improving the quality of life. Some of the other non-digitalis ionotropic agents and diuretics are described in Table 1.4.
Digitalis
The digitalis group of drugs act by the inhibition of Na- K ATPase which in turn leads to an increase in intracellular sodium which is exchanged for Ca by the sarcolemmal membrane resulting in better excitation-contraction coupling.11
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Digoxin augments myocardial contractility, reduces preload, afterload and also myocardial O2 consumption. It is useful in controlling heart rate in paroxysmal atrial tachycardia and atrial fibrillation. Digoxin has half-life of 36 hours and the initial effect is after 30 minutes and a peak percent is excreted unchanged in the urine. Therapeutic levels of the drug should be maintained between 0.08-0.16 microgram/dl (Table 1.5).
Though rapid digitalization is considered safe in children, slow digitalization may be considered in a less sick child whereby 7 to 10 days would be required to achieve the desired levels by daily maintenance dosing. Special care needs to be taken when administering digoxin with diuretics as hypokalemia induced by loop diuretics precipitates digitalis toxicity. Anorexia, nausea and vomiting are amongst the earliest signs of digitalis intoxication. The most frequent arrhythmia caused by digitalis is premature ventricular beats. First-degree heart block in the form of prolongation of P-R interval necessitates withdrawal of the drug. Any new arrhythmias developing on the drug should be considered to be digoxin related, until proved otherwise. When tachyarrythmias develop from digitalis intoxication, withdrawal of the drug and treatment with oral potassium, phenytoin and lidocaine are indicated.
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Potassium is preferably given orally and must not be given in the presence of hyperkalemia.
Sympathomimetic Agents
Dopamine and dobutamine are the most effective of the sympathomimetic amines used in the management of CCF especially with a view to tide over an acute crisis in patients with compromised peripheral perfusion. Dopamine is a naturally occurring precursor of norepinephrine with actions on dopaminergic and adrenergic receptors. At doses of 1 to 2 μg/kg/min it dilates the renal and mesenteric blood vessels causing an increase in renal blood fow and sodium excretion. At doses of 10 μg/kg/min, it has an inotropic effect on the heart whereas at doses of 10 to 20 μg/kg/min peripheral vasoconstrictive action dominates raising the blood pressure. Higher doses cause generalized vasoconstriction and hence are not useful. A major problem with all sympathomimetics is that of progressive loss of responsiveness which may become evident within 8 hours of continuous infusion. Dobutamine is a synthetic catecholamine with a potent inotropic but poor vasoconstrictive action. It is given in continuous infusions of 2.5 to 10 μg/kg/min and is considered especially useful in cardiogenic shock as it causes no increase in the afterload. These drugs combine inotropic effect with peripheral vasodilatation.7
Phosphodiesterase Inhibitors
These drugs combine inotropism with peripheral vasodilatation—reduce afterload and decrease myocardial oxygen demand. They also increase cardiac output, reduce ventricular pressure, enhance ventricular emptying without altering heart rate.
Amrinone is a bipyridine with both positive inotropic effect with peripheral vasodilatation thus reducing after1oad. They act by selectively inhibiting a specific phosphodiesterase. They increase the cardiac output, reduce ventricular filling pressure and enhance the ventricular emptying without a change in heart rate and blood pressure. Thus the myocardial oxygen demand is decreased. The drug is administered in dosage of 0.075 mg/kg intravenously initially and then by an infusion of 5-10 μg/kg/min. Side effects include hypotension and reversible thrombocytopenia. It is useful only to tide over an acute situation.
Milrinone is an analog which has been tried orally for prolonged use. It increases exercise capacity and cardiac output. However some studies have shown an increase in long-term mortality precluding its routine use. It is said to be 30-50 times more potent than amrinone and useful in treating those patients who are refractory to standard therapy.
Levosimendan—Most useful drug but is under research trial—will probably replace inotropes in future.13
Reducing the Heart Size
Diuretics
The drugs to achieve this objective are diuretics (Table 1.6). By reducing the circulating blood volume, the venous return is decreased causing a reduction in the preload and the ventricular end-diastolic volume. Following the reduction in heart size, myocardial function improves and the cardiac output tends to increase. By reducing the sodium and water content of the arterial wall, its stiffness is reduced. Moreover, loss of sodium and water results in decrease in blood pressure and thus the afterload. It must be kept in mind, however, that the decrease in blood volume by diuretics leads to decreased renal perfusion. If this is achieved vigorously it may result in hypotension and increase in blood urea nitrogen.
The commonest diuretics being used are:
Loop diuretics
- Furosemide (Lasix): It does not reduce renal fow. It can be used alone or in combination with a potassium sparing diuretic like spironolactone or amiloride.
- Side effects—hyponatremia, hypokalemia and hypochloremic alkalosis.
- Bumetanide—an analogue of furosemide.
Table 1.6 Diuretics AgentsClassActionDoseSide effectsLoop diureticsLoopInhibitPO 4 mg/kg/dosehyponatremiaNa+ 2Cl- K+CotransportI/V 1-2 mg/kg/dosehypokalemiaUp to 6 mghypochloremic alkalosisBumetanide0.015-0.1 mg/kg/doseEthacrynic acid, torsemideThiazide/Thiazide like diureticsChlorothiazideInhibit Na+Cl- Cotransport10-20 mg/kg/dosehyponatremic alkalosisHydrochlorothiazideDistal tubule1-2 mg/kg/dose↑glucoseMetolazone-do-Indapamide-do-0.2-0.4 mg/kg/24 hrs↑ uric acidAldosterone Receptor Antagonists (K+ Sparing)Spironolactonecollecting duct↑ Na, ↑Cl1-4 mg/kg/dayGynecomastiaEplerenone-do-↑ K - Torsemide—Loop diuretic with anti-aldosterone properties. It is better tolerated than f urosemide and has comparatively less hypokalemic effect.
In infants, diuretics cause an increase in plasma renin levels in those with a large left to right shunt. To get better results, a thiazide diuretic may be added to an already administered loop diuretic. The thiazide diuretic metolazone, administered in conjunction with a loop diuretic (Furosemide/ Torsemide) can be uniquely successful in effecting a diuresis in edematous or diuretic resistant patients.
Although spironolactone and eplerenone are potassium sparing diuretics, their benefcial effects in heart failure are probably less related to their diuretic effects than other effects. Though spironolactone is a drug well established in pediatric practice, eplerenone is a drug in research studies in adults and has not yet been used in children.
Reducing Cardiac Work and Improving Working Environment
With the pump dysfuction, compensatory neurohumoral mechanisms initiate a vicious cycle. Peripheral arteriolar constriction leads to increased wall stress (after load) whereas venoconstriction results in increased venous return (preload) and high ventricular filling pressure. The normal heart can easily cooperate with increased pre and afterloads, but the failing myocardium working on the lower segment of the Starling's law curve is unable to do so. The rationale for using vasodilators is to improve the working environment of the heart (Table 1.7). Vasodilators make the pump function more efficiently by reducing the workload and ventricular filling pressures without augmenting the contractility and thus the oxygen requirements. The sites of action and doses of various vasodilators are given in Table 1.8.
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The drugs (nitroglycerin) acting on veins-increases venous capacitance,10 thereby reducing venous return, ultimately relieving pulmonary and systemic venous congestion. Arterial dilators (hydralazine) reduce systemic impedance (afterload), thereby increasing cardiac output.
Vascular smooth muscle has certain unique properties. Intracellular calcium ion concentration is increased predominantly by the receptor operated channels and minimally by the potential dependent channels, as most blood vessels resist depolarization. The intracellular calcium regulates the contractile process probably by myosin light chain kinase via calmodulin to phosphorylate myosin light chain.
Despite different mechanisms of action, all vasodilators favorably alter the short term hemodynamic response. Long term trials of some of these drugs have shown continued benefits. Captopril and isosorbide dinitrate improve symptomatic status and exercise capacity. Hydralazine and prazosin, however, were not found consistently more effective than placebo during long term use. There is a higher incidence of tolerance with the use of latter drugs because they ultimately stimulated vasoconstrictor mechanisms that offset the acute vasodilatory response. The long term effcacy of isosorbide dinitrate persists due to its venodilator effect on pulmonary vasculature even though tolerance develops to the arteriolar vasodilation. Angiotensin converting enzyme inhibitors execute multi-pronged action like preventing the degradation of bradykinin and stimulating prostaglandin production thus providing the long term effcacy.916
Angiotensin Converting Enzyme Inhibitors (ACE-inhibitors)
The vasodilators also redistribute the blood fow to regional beds. Reduced hospitalization and mortality has been shown with ACE-1 as vasodilator therapy. ACE inhibitors produce their effects through at least three mechanism; inhibition of the angiotension-converting enzyme, inhibition of norepinephrine release from sympathetic nerve endings. ACE-1 are at present considered to be the first line of therapy in mild, moderate, severe or very severe CCF and can be used in monotherapy in mild congestive heart failure. In pediatric practice, patients of CCF showing adequate response with diuretics and digoxin should receive ACE-l as the third drug.11 Uncommonly, dry irritating cough can be a significant and troublesome side effect of ACE-1 therapy. Since ACE-1 or Losartan cause potassium retention, supplements of potassium and potassium sparing diuretics like triamterene or amiloride should not be given at the same time. The safer diuretic would be furosemide combined with metolazone in a small dose. Combining two agents acting at different vascular beds with variable mechanisms like isosorbide dinitrate and hydralazine has been found to provide additive benefit.12 ACE-inhibitors are contraindicated in renal vascular disorders, e.g. renal artery stenosis, coarctation of aorta and aorto-arteritis.
Angiotensin II Receptor Blockers (ARB)
Losartan Potassium-non peptide selective at 1 receptor antagonist, has hemodynamically same effects as ACE-inhibitors. They are more benefcial in elderly patients because, they lack brady kinin potentiating activity—so there is no cough as a side effect. In salt depleted patients, it can cause hypotension.
Calcium Channel Blockers
Nifedipine and diltiazem have also been used in CCF. The trials have shown hemodynamic benefits although less favorable as compared to other vasodilators. Nifedipine cannot be recommended as the initial vasodilator agent except when additional indications like systemic hypertension coexists. Its predominant effect is on the resistance of vessels and hence needs to be combined with diuretics and venodilators. It's use should be avoided with other negative inotropic agents in patients with left ventricular failure and also with relatively low blood pressure. However, most studies do not favor use of calcium channel blockers in CCF since they do not improve short term or long term exercise capacity. Nifedipine, diltiazem and verapamil have been shown to have a negative inotropic effect which can lead to clinical or hemodynamic deterioration. In long term use, calcium channel blockers activate sympathetic and renin angiotensin system thus adversely affecting CCF and have been found to increase mortality in CCF due to systolic dysfunction.17
Beta Adrenergic Antagonists
These drugs are carvedilol, bisoprolol, metoprolol XL and they are reserved for those patients who are clinically stable on ACE inhibitors, diuretic and digitalis. These drugs reduce afterload, and also reduce adrenergic drive.
It is widely recognized that myocardial cell loss irrespective of the basic cause precipitates in a vicious cycle where excessive sympathetic activity causes myocardial beta receptor “down regulation” in addition to the peripheral vasoconstriction. The prognosis of patients with CCF is inversely related to the circulating catecholamine levels. If catecholamines indeed contribute to pathogenesis of CCF, it will be worth while trying a beta blocker. The improvement in ventricular function occurs slowly over a period of months. Other studies lend support to this concept, including one where cardiac transplantation for end-stage CCF could be avoided with the use of beta blockers.
Correcting the Underlying Cause
It is outside the scope of this review to cover this aspect of management of CCF except to emphasize that CCF is a manifestation of an underlying disease and the primary aim should be to identify and correct the pathological basis of CCF.
Device Therapy
Two major advances in treatment of heart failure and prevention of sudden cardiac death in adults is to use devices in adults. Experience with use of cardiac re-synchronization therapy in children with systemic ventricular dysfunction and heart failure is small but increasing.
- Mechanical device used in heart failure include:
- Intra-aortic balloon pump—this is the most commonly used device to improve cardiac function and maintain circulation, especially in the preoperative stage before valve replacement or cardiac transplantation (Figs. 1.2A and B).
- Ventricular assist device—this device is under investigation as an alternate to cardiac transplantation (Fig. 1.3).
- Cardiac resynchronization-Biventricular Pacing—this is an emerging mode of therapy in resistant chronic CCF. The installed pacemaker synchronizes left ventricular contraction, which leads to increase in left ventricular ejection fraction and cardiac index. This ultimately leads on to improved quality of life.
- Implantable cardiac defibrillator—Treatment of choice in those who have survived sudden cardiac arrest. This is programmed when the heart rate goes beyond a certain rate. Other investigational devices are in an experimental state.
- External pneumatic counter pulsation prevents ventricular remodeling therapy and preventing further ventricular dilatation. This is an electric motor driven artifcial heart which can be implanted in the thoracic cage with all its attachments (Fig. 1.4).
Surgical Therapy
- Mitral valve reconstruction: This surgery is indicated in patients with gross mitral regurgitation with left ventricular dysfunction where medical therapy is unable to correct remodeling.
- Ventricular reduction surgery-Batista procedure: Surgical removal of 20-40 % akinetic wall of left ventricle to reshape LV. But this has not given good results and later LV assist devices will be required.
- Coronary artery bypass grafting (CABG)—indicated in young patients with established coronary artery disease and also in those children with anomalous origin of coronary artery from pulmonary artery (ALCAPA). This surgery gives favorable results in those with severe left ventricular dysfunction (LVEF < 30%).
- Cardiac transplantation: Ideal for late stage heart disease but the biggest limitation is lack of donors.Indications
- End stage heart failure
- Dilated cardiomyopathy, restrictive cardiomyopathy, hypoplastic left heart syndrome.
Contraindications- Malignancy,
- Systemic medical disorders—Hypertension, diabetes mellitus, bleeding disorders, etc.
- Active infection—HIV, HBB, HBC.
GUIDELINES FOR MANAGEMENT OF CCF
- Bed rest—Propped up position
- Humified oxygen
- Diet-Salt restricted
- Infants—Nasogastric feeding, calorie dense formula (0.8 cal/ml)
- Control of precipitating factors—Anemia, arrhythmias, hypertension, infective endocarditis, electrolyte disturbance.
- Pharmacological
- Digoxin-Inotropic drug
- Diuretics
- Furosemide, spironolactone,
- Vasodilators - hydralazine
- ACE inhibitors - captopril, enalapril
- Angiotensin receptor antagonists - losartan
- Beta blockers - atenolol, carvedilol
- Devices and surgery
- IABP, pacemaker/defibrillator,
- Ventricular assist devices
- Valve replacement
- Heart transplantation
REFERENCES
- Behram RE. The cardiovascular system. In: Textbook of pediatrics (16th Edn) Behram RE, Kleighmen RM, Nelson WE, Vaughan VC. WB Saunders Company, Philadelphia. 2000 pp.
- Francis GS. Neurohormonal Mechanisms involved in congestive heart failure. Am J Cardiol 1985;55:15A–21A.
- Perloff WH. Physiology of Heart and Circulation. In: Cardiovascular problems in Pediatric Critical Care. Eds. Swedlow DB, Raphaely Rc. Churchill Livingstone New York. 1986; 1–85.
- Eugene Braunwald. Heart Failure. In: Harrison's Principles of Internal Medicine. (13th Edn). Isselbacher KJ. Braunwald E, Wilson ill Martin JB Fauci AS Kasper DL. WB Saunders Company 1994:998–1009.
- Lejemtel TH, Sonnenblick EH. Should the failing myocardium be stimulated? N Engl J Med 1984;310: 1384–86.
- Unverferth DE, Megorein RD, Levis RP. Long term benefit of dobutamine in patient with congestive cardiomyopathy. Amer Heart J 1980;100:622–25.
- Young B, et al. Prospective randomized study of ventricular failure and effcacy of digoxin. J Am Coil Cardio 1992;19:259A–262A.
- Packer M, et al. Comparison of Vasodilatation and ACE inhibition (Enalapril) on exercise capacity and quality of life in chronic CHF. N Eng J Med 1987;317:799–801.
- Vaksmann G, Khayat P, Godart F, et al. Effects of transdermal Nitroglycerine in children with congestive heart failure: A Doppler Echo-cardiography study. Pediatr Cardiol 2001-02;22:11–13.
- Tripathi KD. Plasma Kinins, Angiotensins and ACE Inhibitors in Essentials of Medical Pharmacology (3rd edn) 1994;176–85.
- Nasser A, Dietz JR, Siddique M, et al. Effects of Kaliuretic peptide on sodium and Water Excretion in persons with Congestive Heart Failure. Am J Cardiol 2001;88:23–29.