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Management of Patients with CHF Emphasis on New Modalities of Treatment


Management of Patients with CHF Emphasis on New Modalities of Treatment GH Ajami MD. Professor of Pediatrics Pediatric Cardiology Shiraz University of Medical Sciences – PowerPoint PPT presentation

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Title: Management of Patients with CHF Emphasis on New Modalities of Treatment

Management of Patients with CHFEmphasis on New
Modalities of Treatment
  • GH Ajami MD.
  • Professor of Pediatrics
  • Pediatric Cardiology
  • Shiraz University of Medical Sciences

  • Objectives
  • The student at the end of the lecture should be
  • 1. To explain the mechanisms of CHF in patient
  • 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 deliverycardiac 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

  • 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

  • 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)

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)

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

Differential diagnosis of Heart Failure in
  • 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

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,
  • 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
  • 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)

What is the bodys reaction to CHF?
  • Symptoms signs of
  • 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

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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

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
  • Decreases WOB, supports myocardium
  • Even if sats are normal!
  • Correct predisposing factors
  • Fever, anemia, infection
  • Daily weight
  • 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
  • Arteriolar vasodilation
  • Decreases BP
  • Most common agent ?? ACE inhibitor
  • Captopril (oral)
  • Milrinone (IV infusion)

  • 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,
  • ß 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
  • 3. Causes K, Mg depletion which prone patients
    to arrhythmia
  • 4. Blunt baroreflex response.

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

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.

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 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
Table 2. Cardiac Malformations leading to heart
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
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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