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Associated professor Masyuta D.I.

Associated professor Masyuta D.I.

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Associated professor Masyuta D.I.

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  1. M.Gorky Donetsk National Medical UniversityDepartment No. 2 of PediatricsHead of the Department Dr. Churilina A.V., Ph.D.CОNGESTIVE HEART FAILURE IN CHILDREN Associated professor Masyuta D.I.

  2. Heart failureis defined as a state in which the heart cannot deliver an adequate cardiac output to meet the metabolic needs of thebody. • In early stages of heartfailure, various compensatory mechanisms are evoked to maintain normal metabolic function (cardiac reserve). As these mechanisms become ineffective, increasingly severe clinical manifestations result.

  3. Clinical manifestations • These depend on the degree of cardiac reserveunder various conditions. • A critically ill infant or child who has exhausted his compensatory, mechanisms to the point wherehe can no longer achieve sufficient cardiac output to meet the basal metabolic needs of the body will be symptomatic at rest (IV degree). • Other patients may be comfortable when quiet but are incapable of increasing cardiac output in response to even mild activity without developing significant symptoms (III degree). • On the other hand, it may take rather vigorous exerciseto compromise cardiac function in children who have less severe heart disease (II degree).

  4. Clinical manifestations • There is the New York classification of heart failure (in summary): • Heart disease is present, but no undue dyspnoea from ordinary activity. • Comfortable at rest; dyspnoea on ordinary activities. • Less than ordinary activity causes dyspnoea, which is limiting. • Dyspnoea present at rest; all activity causes discomfort.

  5. Clinical manifestations • The three cardinal signs of congestive heart failure are: • Cardiomegaly. • Tachypnea (left side). • Hepatomegaly (right side).

  6. Clinical manifestations in children • In childrenthe signs and symptoms of congestive heart failure are similar to those in adults. These include • fatigue, • effort intolerance, • anorexia, • abdominal pain, and • cough. • Dyspnea is a reflection of pulmonary congestion.

  7. Clinical manifestations in children • Elevation of systemic venous pressure may be gauged by clinical assessment of the jugular venous pressure and liver enlargement. • Orthopnea and basilar rales may be present; edema is usually discernible in dependent portions of the body, or anasarca may be present. • Cardsomegaly is invariably noted. • A gallop-rhythm is common: other auscultatory findings are specific to the back cardiac lesion.

  8. Clinical manifestations in infants • In infants congestive heart failure may be more difficult to identity. • Prominent manifestations include • tachypnea, • feeding difficulties, • poor weight gain, • excessive perspiration, • irritability, • weak cry, and • noisy, labored respirations with intercostal and subcostal retractions as well as flaring of the alae nasi.

  9. Clinical manifestations in infants • The signs of cardiac pulmonary congestion may be indistinguishable from those of bronchiolitis, including wheezing as the most prominent finding. • Hepatomegaly nearly always occurs, and cardiomegaly is invariably present. • In spite of pronounced tachycardia, a gallop rhythm can frequently be recognized.

  10. Clinical manifestations in infants • The other auscultatory signs are those produced by the underlying cardiac lesion. • Clinical assessment of the jugular venous pressure in infants may be difficult because of the shortness of the neck and the difficulty of observing a relaxed state. • Edema may be generalized, usually involving the eyelids as well as the sacrum, and less often the legs and feet.

  11. Diagnosis • Roentgenograms of the chest show cardiac enlargement. • The pulmonary vascularity is variable depending on the etiology of the heart failure. • Infants and children having large left-to-right shunts willhave exaggeration of the pulmonary arterial vessels to the periphery of the lung fields, whereas patients having cardiomyopathy may have a relatively normal pulmonary vascular bed early inthe course of their disease. • Fluffy perihilar pulmonarymarkings suggestive of venous congestion and acute pulmonary edema are usually seen only with more severe degrees of heartfailure.

  12. Diagnosis • Chamber hypertrophy by electrocardiography may be helpful in assessing the etiologyof congestive heart failure but does not establish the diagnosis. • In cardiomyopathies, left or right ventricularischemic changes may correlate well with clinical and other noninvasive parameters of ventricular function Low-voltage QRS morphology with ST-T wave abnormalities may also suggest myocardial inflammatorydisease but can also be seen with pericarditis. • The electrocardiogram is the best tool for evaluating rhythm disorders as a potential cause of heart failure.

  13. Diagnosis • Echocardiographic techniques are very usefulin assessing ventricular function. • The most commonly used parameter is the ejection fraction, determined as the difference betweenend-and end-systolic volumes divided by the end-diastolic volume. • The normalejection fraction is between55 % and 65 %.

  14. Diagnosis • Arterial oxygen levels may bedecreased when ventilation/perfusion inequalities occur secondary to pulmonary edema. • When heart failure is severe, respiratory and/or metabolic acidosis may be present.

  15. Treatment • The underlying cause of cardiac failure must be removed or alleviated if possible.

  16. General Measures • Strict bed rest is rarely necessary except in extreme cases, but it is important that the child rest often and sleep adequately. • Most older patients feel better sleeping in a semi-upright position at an angle of 20-30 degree in bed to reduce venous return. • After patients begin to respond to treatment, restrictions on activities can often be modified within the context of the specific diagnosis and the patient's ability.

  17. Oxygen Therapy • Oxygen inhalation should be given to reduce anoxia and relieve dyspnea. • Oxygen should not be dry or oversaturated. • 40-50 % oxygen with 80 % humidity is preferred. • It may be administered by tent or catheter. Whichever is comfortable as well as acceptable to the child.

  18. Diet • Infants having congestive heart failure may fail to thrive because of both increased metabolic requirements and decreased caloric intake. Increasing daily calories is an important aspect of their management. • Severely ill infants may lack sufficient strength for effective sucking because of extreme fatigue, rapid respirations, and generalized weakness, in these circumstances, nasogastric feedingsmay behelpful. • Small amount of food at frequent intervals is more acceptable than large bulks of the food at big gaps.

  19. Diet • The use of verylow sodium formulasinthe routine management of infants with congestive heart failure is not recommended because these preparations are often poorly tolerated. • Most older children can be managed with "no added salt" diets and abstinence from foods containing large amounts of sodium. • A strict extremely low sodium diet is rarely required. • Water should be restricted moderately.

  20. Digitalis • Digoxin is the digitalis glycoside used most often in the pediatric patient.

  21. Digitalis • Patients who are not critically illmay be digitalized initially by the oral route, and in most instances digitalization is completed within 24 hr. • When slow digitalization is desirable, for example, in the immediate postoperative period, initiation of a maintenance digoxin schedule without a prior loading dose will achieve full digitalization in 3-5 days.

  22. Rapid digitalization • Rapid digitalizationof infants and children in congestive heart failure may be carried out intravenously. • The dose depends on the patient's age • (neonate ( 1 month) - 0.03 mg/kg, • infant or child - 0.05 mg/kg). • The recommended schedule is to give one half of the total digitalizing dose immediatelyand the succeeding two one-quarter doses at 12 hr intervals later.

  23. Rapid digitalization • The electrocardiogram must be closely monitored and rhythm strips obtained prior to each of the three digitalizing doses. • Digoxin should be discontinued if anew rhythm disturbance is noted. • A significant prolongation ofthe PR interval is not in itself an indication to withhold digitalis, but a delay in administering the next dose or a reduction in the dosage should be considered depending on the patient's, clinical status.

  24. Rapid digitalization • Nausea and vomiting are somewhatless frequent in the pediatric patient as features of digoxin toxicity. • Slowing of heart rate, • below 100/min in infants, • below 80 /min in young children, and • below 60/min in older children, indicates digoxin toxicity.

  25. Rapid digitalization • Baseline serum electrolyte levels should be measured prior to and after digitalization. • Hypokalemia and hypercalcemia exacerbate digitalis toxicity. • Because hypokalemia is relatively common in patients receiving diuretics, the potassium level should be followed closely in patients receiving a potassium-wasting diuretic, for example, furosemide, in combination with digitalis.

  26. Maintenance Digitalis Therapy • Maintenance digitalistherapy is started approximately 12 hr after full digitalization. • The daily dosage is divided in two and given at 12-hr intervals for more consistent blood levels and more flexibility in case of toxicity. • The dosage is one quarter or fifth of the total digitalizing dose. • For patients who are initially digitalized intravenously, maintenance digoxin can be given orally.

  27. Digitalis • With growth of the child, maintenance doses are to be increased to keep up with growth. • If the infant improves significantly on digitalis over a period of a few months and the need for the drug appears to be lessening (e.g., a ventricular septal defect that is becoming smaller), the dosage is not increased as the child gains weight. • If the clinical status warrants, the drug is eventually discontinued.

  28. Diuretics • These agents interfere with reabsorption of waterand sodium by the kidneys, which results in the reduction of circulating blood volume and thereby reduces pulmonary fluid overload and ventricular filling pressures. • They are most often used in conjunction with digitalis therapy in patients with severe congestive heart failure.

  29. Furosemide • Furosemide is the most commonly used diuretic inpatients with heart failure. • It inhibits the reabsorption of sodium and chloride in the distal tubules and the loop of Henle. • Patients requiring acute diuresis should be given intravenous or intramuscular furosemide at an initial dose of 1-2 mg/kg. This usually results in rapid diuresis and prompt improvement in clinical status, particularly if symptoms of pulmonary congestion are present.

  30. Furosemide • Chronic furosemide therapy is then prescribed at a dose of 1—4 mg/kg/24 hr given between 1 and 4 times a day. • Careful monitoring of electrolytes is necessary with long-term furosemide therapy, because there may be significant loss of potassium. • Potassium chloride supplementation is usually required unless the potassium-sparing diuretic spironolactone is given concomitantly.

  31. Spironolactone • Spironolactoneisan inhibitor of aldosterone and enhances potassium retention. • It is usually given orally in 2-3 divideddoses of 2-3 mg/kg/24 hr. • Combinations of spironolactone and chlorothiazide are commonly usedfor convenience and because they eliminate the need for potassium supplementation, which is often poorly tolerated.

  32. Chlorothiazide • Chlorothiazide is used occasionally for diuresis in children with less severe, chronic congestive heart failure. • It is less immediate in action and less potent than furosemide, and it affects the reabsorption of electrolytes only in the renal tubules. • The usual dose is 20-50 mg/kg/24 hr individed doses. • Potassium supplementation is often required it this agent is used alone.

  33. Afterload-Reducing Agents • This group of drugs reduces ventricular afterload by decreasing peripheral vascular resistance, thereby improving myocardial performance. • Some of these agents also decrease systemic venous tone, significantly reducing preload. • Afterload reducers are especially useful in children with congestive heart failure secondary tocardiomyopathy and in patients with severe mitral or aortic insufficiency.

  34. Afterload-Reducing Agents • They may also be effectivein patients with congestive heart failure secondary to left-to-right shunts. • They are usually not used in the presence of stenotic lesions of the left ventricular outflow tract. • Afterload-reducing agents are most often used in conjunction with other anticongestive drugs, such as digoxin and diuretics.

  35. Nitroprusside • Nitroprusside should he administered onlyin an intensive care setting and for as short a period of time as possible. • Its short intravenous half-life makes it ideal for titrating the dose in critically ill patients. • Peripheral arterial vasodilatation and afterload reduction are the major effects, but venodilatation causing a decrease in venous returnto the heart may also be beneficial. • Blood pressure must he continuously monitored by means of an intra-arterial line, as sudden hypotension can occur with overdose. • Nitroprusside is contraindicated when hypotensionpre-exists.

  36. Hydralazine • Hydralazineis adirect arteriolarsmooth muscle relaxant and has virtually no effects on preload. • It is occasionally administered together with a venodilating agent, such as one of the nitrate derivatives. • The usual oral dose of hydralazine is 0.5-7.5 rng/kg/24 hr in three divided doses. Many patients require increasing dosage with time in order to maintain the peripheral dilating effects (tachyphylaxis).

  37. Hydralazine • Adverse reactions with hydralazine include • headache, • palpitations, • nausea, and • vomiting, in addition, • systemic lupus erythematosus occasionally occurs after administration of large doses of hydralazine over prolonged periods; these manifestations arc reversible when the drug is discontinued.

  38. Captopril • Captopril is an orally active angiotensin-converting-enzyme (ACE) inhibitor that produces marked arterial dilatation by blocking the production of angiotensin 11, resulting in significant afterload reduction. • Venodilatation and consequent preload reduction have also been reported. • This agent also interferes with aldosterone production and thereby also helps control salt and water retention.

  39. Captopril • The oral dose is 0.5- 6 mg/kg/24 hr given in 2-3 divided doses. • The adverse reactions to captopril include hypotension and its sequelae (e.g., syncope, weakness, and dizziness). • A maculopapular pruritic rash is encountered in 5-8% of patients, but the drug may be continued because the rash often disappears spontaneously with time. • Neutropenia and renal toxicity also occur.

  40. Isoproterenol • Isoproterenol,an intravenous preparation used for treating low cardiac output has both central and peripheral β-adrenergic effects, and therefore enhances myocardial contractilityand also reduces cardiac afterload. • The drag is administered in an intensive care setting, where the dose is titrated between 0.01 and 0.5 μg/kg/min. • Because isoproterenol has a marked chronotropic effect, it should not be used in patients who already have significant tachycardia.

  41. Dopamine • Dopaminehas fewer chronotropic and arrhythmogenic effects than isoproterenol. • In addition, it results m selective renal vasodilatation, particularly useful in patients with the compromised kidney function that is often associated with low cardiac output.

  42. Dopamine • At a dose of 2-10 μg/kg/min, dopamine results in increased contractility with little peripheral vasoconstrictive effects. • However,if the dose is increased beyond 15 μg/kg/min, its peripheral α-adrenergic effects may result in vasoconstriction. • At high doses dopamine may also cause an increase in pulmonary vascular resistance.

  43. Dobutamine • Dobutamine,a derivative of dopamine, is also used to treat low cardiac output. • It causes direct inotropic effects with a moderate (albeit less than isoproterenol) reduction inperipheral vascular resistance.

  44. Dobutamine • Dobutamine can be used as an adjunct to dopamine therapy in order to avoid the vasoconstrictive effects of high-dose dopamine. • Dobutamine is also less likely to cause cardiac rhythm disturbances. • The usual dose is 2-20μg/kg/min.

  45. Manegment OfSevere Pulmonary Edema • For patients with severe pulmonary edema, positive-pressure ventilation may be required along with other drag therapy. • Beta-adrenergic agonists, such as dopamine, epinephrine, and dobutamine, along with afterload reducing agents (e.g., nitroprusside, captopil), may be required in an intensive care setting.

  46. Manegment OfSevere Pulmonary Edema • The most useful management of acute pulmonary edema are as follows: • Oxygen inhalation. • Propped up position. • Tourniquet application to extremities or venesection to reduce venous return. • Diuretics - best furosemid. • Digitalisation. • Salt and water restriction.