Transcript Surgical Treatment of Patients with CHF

Management of Patients with CHF
Emphasis on New Modalities of Treatment
GH Ajami MD.
Professor of Pediatrics
Pediatric Cardiology
Shiraz University of Medical Sciences
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 .
Definition of CHF: Inadequate blood supply and
delivery of oxygen to tissues for metabolic
needs of body
Systemic O2 delivery=cardiac output × Hb × O2%
Cardiac output = stroke volume × heart rate
Stroke volume depends on:
Preload
Afterload
Contractility
Myocardial Contractility
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Definition
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Force generated by the myocardium
Squeeze
Reflects chemical or hormonla influences
Catecholamines
↑Contractility  ↑ SV
 ↑ Cardiac output
Afterload
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Definition
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The resistance the ventricle needs to overcome to
empty its contents
Can be estimated by arterial systolic BP
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If no obstruction btwn ventricle and aorta
Decreased by arterial vasodilators
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ACE inhibitors
↓ Afterload (resistance)  ↑ SV
 ↑ Cardiac output
Preload
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Definition
Amount of myocardial stretch at the end of
diastole (relaxation phase)
 Distention of ventricle before the “
squeeze”
 Frank and starling
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, 19th century
 Frank-starling curve
(ventricular function curve)
 Physiological
Compensatory mechanisms in patients
with CHF
I.
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
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Mechisms
1.
Volume overload
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2.
Pressure overload
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3.
After too high
Myocardial insufficiency
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4.
Preload is too high
Poor contractility
Other
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Arrhytmia,anemia
Differential diagnosis of Heart
Failure in children
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Congenital Heart Defects
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Cordimyopathies
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Genetic – inbom errors of metabolism, neuromuscular,
familial
Other Acquired conditions
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Volume load-large left to right shunts or severe valvular
regurgitation
Pressure load-left heart obstructive lesions
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, hepatic)
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 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)
Cardiomyopathy (hypertrophic, dilated)
What is the body’s reaction to
CHF?
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Symptoms & signs of :
1.
2.
3.
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
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Gallop rhythm
The Role of Investigations
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Primarily clinical diagnosis
CXR
- Cardiomegaly
- Pulmonary edema
Blood Gas
- Metabolic acidosis
- Elevated lactate
The Role of Investigations
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ECG
– helpful in determining underlying defect
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Echo
– Ventricular function/size
– Identify structural defects
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e.g. large VSD
Approach to Management
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Initial stabilization
Supportive management
Identify cause of CHF
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ECG, Echo, laboratory investigations
Infectious work up
Treatment for underlying cause
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– e.g. Surgical correction of structural defects
Initial Stabilization
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Airway
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Breathing
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Supplemental Oxygen
CPAP / Ventilation
Circulation
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Fluid Management
Ionotropic support
General Measures
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Oxygen
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Correct predisposing factors
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Fever, anemia, infection
Daily weight
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Decreases WOB, supports myocardium
Even if sats are normal!
Hospitalized patients
Maximize nutrition
Medical Rx: Preload
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Diuretics
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Optimize preload
Ideal portion of Frank-Starling curve
Promotes fluid loss via kidney (renal tubules)
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Lasix, aldactazide, acetazolamide
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Medical Rx: Contractility
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Myocardial support
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Increase the contractility of heart muscle
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Improve the “squeeze”
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Used primarily in severe CHF
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IV administration
Ionotropic infusions
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epinephrine, dobutamine…
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)
Beta-Blockers
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Latest research
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Increased sympathetic drive in CHF
myocardial cell death
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B-Blockers impair the process
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decreased cell death → improved outcomes
Long-term therapy
Introduced when patients are stable
Most common---Carvedilol
Carvedilol has 1, adrenergic blocking,
β 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 arrhythmia
3.
Causes K, Mg depletion which prone patients to
arrhythmia
4. Blunt baroreflex response.
Surgical Treatment of Patients with CHF
1.
2.
3.
4.
Heart and heart-lung transplant for
cardiomyopathies or complex CHD not
operable
Repair of underlying CHD in patient with
intractable CHF
Intractable CHF in patients with endocarditis
New surgical procedures such as Dor or
Batissta technique for patients with dilated
cardiomyopathy
Why is heart failure in children important
While adult heart failure is clearly a more compelling
health problem:
1.
The cost are higher for children became of the
frequent surgical or catheter-intervention which my
be needed.
2.
The demands of medical care adversely affect
parental economic productivity
3.
Loss of a child with heart failure has economic
impact because of loss of potentially productive years
per death.
4.
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
Class II
Class III
Class IV
Asymptomatic
Mild tachypnea or diaphoresis with feeding in
infants
Dyspnea on exertion in older children
Marked tachypnea or diaphoresis with feeding
in infants
Marked dyspnea on exertion
Prolonged feeding times with growth failure
Symptoms such as tachypnea, retractions,
grunting, or diaphoresis at rest
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
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
Stage
Interpretation
Clinical Examples
A
At risk for developing HF
Congenital heart defects
Family history of cardiomyopathy
Anthracycline exposure
B
Abnormal cardiac structure of function
No symptoms of HF
Univentricular hearts
Asymptomatic cardiomyopathy
Repaired congenital heard disease
C
Abnormal cardiac structure or function
Past or present symptoms of HF
Repaired and unrepaired congenital
heart defects
Cardiomyopathies
D
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
Same as stage C