M.Gorky Donetsk National Medical University Department No. 2 of Pediatrics Head of the Department Dr. Churilina A.V., Ph.D. C?NGESTIVE HEART FAILURE IN CHILDREN

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M.Gorky Donetsk National Medical
UniversityDepartment No. 2 of Pediatrics Head
of the Department Dr. Churilina A.V.,
Ph.D.C?NGESTIVE HEART FAILURE IN CHILDREN

• Associated professor Masyuta D.I.

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

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Clinical manifestations

• These depend on the degree of cardiac reserve
  under various conditions.
• A critically ill infant or child who has
  exhausted his compensatory, mechanisms to the
  point where he 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
  exercise to compromise cardiac function in
  children who have less severe heart disease (II
  degree).

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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.

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Clinical manifestations

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

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Clinical manifestations in children

• In children the 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.

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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.
  

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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.

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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.

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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.

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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 will have 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 in the course of their disease.
• Fluffy perihilar pulmonary markings suggestive of
  venous congestion and acute pulmonary edema are
  usually seen only with more severe degrees of
  heart failure.

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Diagnosis

• Chamber hypertrophy by electrocardiography may be
  helpful in assessing the etiology of congestive
  heart failure but does not establish the
  diagnosis.
• In cardiomyopathies, left or right ventricular
  ischemic 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
  inflammatory disease but can also be seen with
  pericarditis.
• The electrocardiogram is the best tool for
  evaluating rhythm disorders as a potential cause
  of heart failure.

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Diagnosis

• Echocardiographic techniques are very useful in
  assessing ventricular function.
• The most commonly used parameter is the ejection
  fraction, determined as the difference between
  end- and end-systolic volumes divided by the
  end-diastolic volume.
• The normal ejection fraction is between 55 and
  65 .

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Diagnosis

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

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Treatment

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

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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.

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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.

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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 feedings may be
  helpful.
• Small amount of food at frequent intervals is
  more acceptable than large bulks of the food at
  big gaps.

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Diet

• The use of very low sodium formulas in the
  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.

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Digitalis

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

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Digitalis

• Patients who are not critically ill may 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.

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Rapid digitalization

• Rapid digitalization of 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 immediately and the
  succeeding two one-quarter doses at 12 hr
  intervals later.

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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 a new rhythm
  disturbance is noted.
• A significant prolongation of the 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.

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Rapid digitalization

• Nausea and vomiting are somewhat less 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.

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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.

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Maintenance Digitalis Therapy

• Maintenance digitalis therapy 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.

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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.

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Diuretics

• These agents interfere with reabsorption of water
  and 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.

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Furosemide

• Furosemide is the most commonly used diuretic in
  patients 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.

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Furosemide

• Chronic furosemide therapy is then prescribed at
  a dose of 14 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.

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Spironolactone

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

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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 in divided
  doses.
• Potassium supplementation is often required it
  this agent is used alone.

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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
  to cardiomyopathy and in patients with severe
  mitral or aortic insufficiency.

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Afterload-Reducing Agents

• They may also be effective in 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.

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Nitroprusside

• Nitroprusside should he administered only in 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
  return to 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 hypotension
  pre-exists.

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Hydralazine

• Hydralazine is a direct arteriolar smooth 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).

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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.

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Captopril

• Captopril is an orally active angiotensin-converti
  ng-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.

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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.

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Isoproterenol

• Isoproterenol, an intravenous preparation used
  for treating low cardiac output has both central
  and peripheral ß-adrenergic effects, and
  therefore enhances myocardial contractility and
  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.

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Dopamine

• Dopamine has 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.

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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 a-adrenergic effects
  may result in vasoconstriction.
• At high doses dopamine may also cause an increase
  in pulmonary vascular resistance.

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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 in peripheral vascular resistance.

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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.

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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.

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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.