Management of Patients with CHF Emphasis on New Modalities of Treatment

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Management of Patients with CHFEmphasis on New
Modalities of Treatment

• GH Ajami MD.
• Professor of Pediatrics
• Pediatric Cardiology
• Shiraz University of Medical Sciences

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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 .

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• Definition of CHF Inadequate blood supply and
  delivery of oxygen to tissues for metabolic needs
  of body
• Systemic O2 deliverycardiac output Hb O2
• Cardiac output stroke volume heart rate
• Stroke volume depends on
• Preload
• Afterload
• Contractility

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Myocardial Contractility

• Definition
• Force generated by the myocardium
• Squeeze
• Reflects chemical or hormonla influences
• Catecholamines
• ?Contractility ? ? SV
• ? ? Cardiac output

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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

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Preload

• Definition
• Amount of myocardial stretch at the end of
  diastole (relaxation phase)
• Distention of ventricle before the squeeze
• Frank and starling
• Physiological , 19th century
• Frank-starling curve
• (ventricular function curve)

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Compensatory mechanisms in patients with CHF

• 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)

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• 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

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Etiology of heart failure

• Mechisms
• Volume overload
• Preload is too high
• Pressure overload
• After too high
• Myocardial insufficiency
• Poor contractility
• Other
• Arrhytmia,anemia

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Differential diagnosis of Heart Failure in
children

• Congenital Heart Defects
• Volume load-large left to right shunts or severe
  valvular regurgitation
• Pressure load-left heart obstructive lesions
• Cordimyopathies
• Genetic inbom errors of metabolism,
  neuromuscular, familial
• Other Acquired conditions
• Pericarditis/ tamponade
• Sepsis
• Coronary artery disease
• Arrhythmia

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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

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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)

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What is the bodys reaction to CHF?

• Symptoms signs of
• Pulmonary venous congestion
• Systemic venous congestion
• Sympathetic overload
• ? CHF is a clinical diagnosis

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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
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Symptoms Venous Congestion
Symptoms Puffiness Abdominal swelling Abdominal pain - RUQ Signs Peripheral edema Jugular venous distention Hepatomegaly Cardiomegaly
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Symptoms Overload
Symptoms Sweating Pallor Decreased urine output Signs Tachycardia Decreased perfusion Gallop rhythm
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The Role of Investigations

• Primarily clinical diagnosis
• CXR
• - Cardiomegaly
• - Pulmonary edema
• Blood Gas
• - Metabolic acidosis
• - Elevated lactate

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The Role of Investigations

• ECG
• helpful in determining underlying defect
• Echo
• Ventricular function/size
• Identify structural defects
• e.g. large VSD

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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

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Initial Stabilization

• Airway
• Breathing
• Supplemental Oxygen
• CPAP / Ventilation
• Circulation
• Fluid Management
• Ionotropic support

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General Measures

• Oxygen
• Decreases WOB, supports myocardium
• Even if sats are normal!
• Correct predisposing factors
• Fever, anemia, infection
• Daily weight
• Hospitalized patients
• Maximize nutrition

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Medical Rx Preload

• Diuretics
• Optimize preload
• Ideal portion of Frank-Starling curve
• Promotes fluid loss via kidney (renal tubules)
• Lasix, aldactazide, acetazolamide

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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

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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)

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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

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• Carvedilol has ?1, adrenergic blocking,
• ß antagonist effect and anti-oxidant activity.

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• 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.

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Aldosterone Blockade in Cardiovascular Disease

• Heart 2004 90 1229-1234
• Allan D Struthers
• Division of Medicine, therapeutics
• Nine well Hospital, Dundee, UK

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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.

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Surgical Treatment of Patients with CHF

1. Heart and heart-lung transplant for
   cardiomyopathies or complex CHD not operable
2. Repair of underlying CHD in patient with
   intractable CHF
3. Intractable CHF in patients with endocarditis
4. New surgical procedures such as Dor or Batissta
   technique for patients with dilated
   cardiomyopathy

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Why is heart failure in children important

• While adult heart failure is clearly a more
  compelling health problem
• The cost are higher for children became of the
  frequent surgical or catheter-intervention which
  my be needed.
• The demands of medical care adversely affect
  parental economic productivity
• Loss of a child with heart failure has economic
  impact because of loss of potentially productive
  years per death.
• Grawing numbers of children with heart failure
  are reaching adult hood.

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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.

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Table 1. Modified Ross Heart Failure
Classification for Children
Class I Asymptomatic
Class II Mild tachypnea or diaphoresis with feeding in infants
Class II Dyspnea on exertion in older children
Class III Marked tachypnea or diaphoresis with feeding in infants
Class III Marked dyspnea on exertion
Class III Prolonged feeding times with growth failure
Class IV Symptoms such as tachypnea, retractions, grunting, or diaphoresis at rest
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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
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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
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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
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Table 5. Heart Failure Staging in Pediatric
Heart Disease
Clinical Examples Interpretation Stage
Congenital heart defects Family history of cardiomyopathy Anthracycline exposure At risk for developing HF A
Univentricular hearts Asymptomatic cardiomyopathy Repaired congenital heard disease Abnormal cardiac structure of function No symptoms of HF B
Repaired and unrepaired congenital heart defects Cardiomyopathies Abnormal cardiac structure or function Past or present symptoms of HF C
Same as stage C 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 D
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