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Chapter 1
INTRODUCTION
1.1. Background
Congestive heart failure (CHF) refers to a clinical state of systemic and pulmonary
congestion resulting from inability of the heart to pump as much blood as required for the
adequate metabolism of the body. The clinical picture of CHF results from a combination of
relatively low output and compensatory responses to increase it. Excellent reviews on CHF
in infants and children are available.1 The diagnosis of CHF in older children is often straight
forward, but it may be difficult at times, to diagnose CHF or to distinguish it from pulmonary
disease or sepsis in the neonate. Feeding difficulties and excessive sweating are the usual
presenting features. Tachycardia >150/min is common, and heart rates >180/min are
abnormal even in the setting of respiratory distress and suggests CHF. Thus, the grading of
the severity of CHF in infants should include an accurate description of these historical and
clinical variables.2
In developing countries structural heart defects are the most common cause of heart
failure in infants and children. The incidence of congenital heart disease in children is
approximately 8 per 1000 live births, or 0.8%. 3 About one third to one half of these defects
are severe enough to produce symptoms that prompt treatment, catheterization or surgery, or
to cause death in the first year of life. Only about one half of these severe defects results in
CHF; interventions are performed in there maining defects because of cyanosis or potential or
actual circulatory collapse related to closure of the ductus arteriosus. Thus the yearly
incidence of heart failure from structural defects is about 0.1% to 0.2% of live births. The
defects most likely to cause heart failure include left-to-right shunt lesions (eg, ventricular
septal defect, common atrioventricular canal defect, patent ductus arteriosus,
aorticopulmonary window, truncus arteriosus), left heart obstructive lesions (eg, critical
aortic stenosis, severe aortic coarctation, congenital mitral stenosis), and congenital
atrioventricular or semilunar valve regurgitation.4
A ventricular septal defect (VSD) is a hole or a defect in the septum that divides the 2
lower chambers of the heart, resulting in communication between the ventricular cavities. A
VSD may occur as a primary anomaly, with or without additional major associated cardiac
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defects. A VSD occurs in approximately 2-6 of every 1000 live births and accounts for more
than 20% of all congenital heart diseases. The symptoms and physical findings associated
with ventricular septal defects (VSD) depend on the size of the defect and the magnitude of
the left-to-right shunt. Chest radiography, magnetic resonance imaging (MRI), andelectrocardiography (ECG) may all provide useful information in the workup of a VSD.
Although cardiac catheterization was a standard part of the evaluation in the past, detailed
echocardiography is now preferred in most institutions.5
Children with small VSD are asymptomatic and have an excellent long-term prognosis.
Neither medical therapy nor surgical therapy is indicated. In children with moderate or large
VSD, a trial of medical therapy is indicated to manage symptomatic congestive heart failure
(CHF) because many VSD may become smaller with time. Uncontrolled CHF with growth
failure and recurrent respiratory infection is an indication for surgical repair. Neither the age
nor the size of the patient is prohibitive in considering surgery.5
1.2. Objective
The aim of writing this paper is in order to complete the assignment in following the doctors
professional education program in the department of pediatrics. In addition, providing
knowledge to the author and readers about congestive heart failure ec ventricular septal
defect.
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Chapter 2
LITERATURE REVIEW
2.1. Congestive Heart Failure
2.1.1. Defenition
Congestive heart failure (CHF) refers to a clinical state of systemic and pulmonary
congestion resulting from inability of the heart to pump as much blood as required for the
adequate metabolism of the body. The clinical picture of CHF results from a combination of
relatively low output and compensatory responses to increase it.1
Over time, decreased cardiac output leads to a cascade of compensatory responses
that are aimed directly or indirectly at restoring normal perfusion to the body's organs and
tissues. For most adults, heart failure (HF) results from diminished myocardial contractility
caused by ischemic heart disease. In contrast, decreased contractile states account for a
smaller percentage of causes of pediatric HF. Instead, the various triggers of HF in children
can be categorized broadly as syndromes of excessive preload, excessive afterload, abnormal
rhythm, or decreased contractility, which all can lead to a final common HF pathway. 1,2
2.1.2. Prevalence
The over all incidence and prevalence of pediatric HF is unknown, largely because
there is no accepted universal classification applied to its many forms. The largest HF burden
comes from children born with congenital malformations. It has been estimated that 15% to
25% of children who have structural heart disease develop HF. 1 Although cardiomyopathy is
relatively rare, approximately 40% of patients who experience cardiomyopathy develop heart
failure of such severity that it leads to transplantation or death.6
2.1.3. Etiology
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Heart failure can result from cardiac and noncardiac causes. Cardiac causes include
those associated with congenital structural malformations (Table 2.1.) and those involving no
structural anomalies (Table 2.2.).
Table 2.1. Cardiac Malformations Leading to Heart Failure1,5
Shunt Lesions
Ventricular septal defect
Patent ductus arteriosus
Aortopulmonary window
Atrioventricular 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/subaortic stenosis/supravalvular aortic stenosis
Aortic coarctation
Table 2.2. Sources of Heart Failure With a Structurally Normal Heart1,5
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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2.1.4. Pathophysiology
Unmet tissue demands for cardiac output result in activation of the renin-aldosteroneangiotensin system, the sympathetic nervous system, cytokine-induced
inflammation, and recently appreciated signaling cascades that trigger cachexia.7 A vicious
cycle begins when decreased cardiac output leads to increased metabolite production in
downstream organ systems. These metabolites, in turn, stimulate local vasodilation and
decreased blood pressure. Falling blood pressure stimulates angiotensin and
mineralocorticoid release further, inducing fluid-retaining mechanisms in the kidney and
stimulating increases in systemic vascular resistance. Stimulation of the sympathetic nervous
system and increased release of catecholamines cause tachycardia, enhanced myocardial
contractility, and maladaptive forms of cardiac hypertrophy.
Initially, these effects help to improve cardiac output and maintain blood pressure. The
Pediatric Advanced Life Support course offered by the American Heart Association terms
this stage of HF compensated shock. However, HF occurs in diseases that are not readily
reversible. In these situations, long standing increases in myocardial work and myocardial
oxygen consumption (MVO2) ultimately worsen HF symptoms and lead to a chronic phasethat involves cardiac remodeling (Fig. 1).8
Cardiac remodeling is a structural transformation in which the normally elliptical heart
increases in mass and becomes more spherical. This increase in cardiac mass (maladaptive
cardiac hypertrophy) involves an expansion of the myofibrillar components of individual
myocytes (new cells rarely form), an increase in the myocyte/ capillary ratio, and activation
and proliferation of abundant nonmyocyte cardiac cells, some of which produce cardiac
scarring. Taken together, these processes produce a poorly contractile and less compliant
heart, resulting in increased filling pressures, pulmonary or systemic edema, hypoxia,
redistribution of blood flow away from skeletal muscle and the splanchnic circulation, tissue
lactic acidosis, and loss of lean body mass (cachexia). Cachexia is a state of
catabolic/anabolic imbalance leading to weight loss and disordered homeostasis and involves
inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukins, as
well as neurohormonal activation. Recent
work suggests That activation of cachexia
pathways may drive worsening HF.8
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Figure 2.1. Heart failure results from an interaction of beneficial and deleterious pathways
that ultimately modulate cardiac output and remodeling.8
Although decreased cardiac output stimulates deleterious neuroendocrine
mechanisms, endogenous mechanisms defend the heart from progressive HF. Thesemechanisms include stimulation of insulin-like growth factor and growth hormone and
secretion of atrial and brain natriuretic peptides (ANP and BNP). For example, growth
hormone deficiency and low insulin-like growth factor concentrations have been associated
with poor HF outcomes in adults, and increased concentrations appear to be protective. 9
2.1.5. Clinical Manifestation and Diagnosis
In infants, the symptoms of heart failure most commonly exhibited include tachypnea,
tachycardia, poor feeding, and failure to thrive. Other signs of heart failure in this group of
patients include hepatomegaly,diastolic gallop on physical examination, and cardiac
enlargement with or without pulmonary edema on chest radiograph. Toddlers and older
children may also exhibit tachycardia and tachypnea but typically manifest symptoms of
fatigue and exercise intolerance; poor appetite and growth failure are typical of this age
groupas well. In older children, venous distension and peripheral edema may be apparent as
well.
Until 1987, the only system available for grading HF in children was the New York
Heart Association (NYHA) classification. However, this system was based on limitations to
physical activity for adults, which did not translate well for use with children, particularly
infants. Therefore, we developed a symptom-based classification using more age-appropriate
variables (Table 3) and demonstrated that plasma norepinephrine correlated in a stepwise
fashion with this new Ross HF classification from grades I to IV. 10
Tabel 2.3 Original Ross classification10
I: No limitations or symptoms
II: Mild tachypnea or diaphoresis with feedings in infants, dyspnea at exertion in older
children; no growth failure
III: Marked tachypnea or diaphoresis with feedings or exertion and prolonged feeding
times with growth failure from CHF
IV: Symptomatic at rest with tachypnea, retractions, grunting, or diaphoresis
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2.1.6. Laboratory Studies
Because knowledge of the specific underlying disease is critical in the understanding ofthe pathophysiology, management, and response to therapy for HF, certain laboratory tests
are essential. Pulse oximetry is helpful in identifying cyanosis in infants who have HF caused
by increased pulmonary blood flow (left-to-right shunts) because recognizing cyanosis in an
infant is nearly impossible by physical examination alone. Decreased percutaneous oxygen
saturation never is associated with acyanotic heart disease unless poor tissue perfusion or
intrapulmonary right-to-left shunting occurs. The 12- lead electrocardiogram is essential to
assess arrhythmia induced HF. The chest radiograph may demonstrate cardiac enlargement,
increased pulmonary blood flow, venous congestion, or pulmonary edema. However, chest
radiographs generally have a high specificity but low sensitivity for detecting cardiac
enlargement. Although not useful for the evaluation of HF, which is a clinical diagnosis,
echocardiography is essential for identifying causes of HF such as structural heart disease,
ventricular dysfunction (both systolic and diastolic), chamber dimensions, and effusions (both
pericardial and pleural).11
2.1.7. Management
The first goal of HF care is to treat the specific cause. Prompt treatment of noncardiac
causes of HF such as anemia or endocrinopathies as well as timely referral for surgical
corrections of structural cardiac anomalies can prevent or ameliorate HF. Examples closing a
ventricular septal defect or patent ductus arteriosus, repairing a coarctation, or relieving a
valve obstruction.12
HF-causing cardiac malformations usually can be approached surgically. Accordingly,
medical management of HF serves as a temporizing measure if surgery must be delayed.
Because there is no cure for primary childhood cardiomyopathies, the goal of medical
management is to delay or eliminate the need for cardiac transplantation. 13
Medical management (Table 2.4) aims to maximizecardiac output and tissue perfusion
while minimizing stresses that increase MVO2. These goals are accomplished by reducing
the amount of force the heart needs to generate to eject blood (reducing afterload stress) and
by reducing overfilling of the heart (preload). Thus, treatments that rest the heart, such as
vasodilators, are preferred to inotropic agents that increase MVO2.14
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Afterload reduction is accomplished by using drugs that decrease the systemic vascular
resistance. These agents include angiotensin-converting enzyme inhibitors and type 4
phosphodiesterase inhibitors (milrinone) or systemic nitrates (nitroprusside).12,13 Another
approach to resting the failing heart is through inhibition of the sympathetic nervous system.Beta-blocker therapy is a cornerstone of the medical management of HF in adults.
Diuretics reduce preload, theory improving Frank- Starling relationships in the heart.
Decreased preload helps to prevent pulmonary edema-producing high cardiac filling
pressures. Besides loop diuretics such as furosemide, other classes of diuretics are used,
including thiazides and mineralocorticoid inhibitors (spironolactone). Recent data suggest
that aldosterone inhibition also helps to
prevent maladaptive cardiac remodeling and interstitial fibrosis.14
Digoxin is the only commonly used oral inotropic agent. However, itsmost important
mechanism of action may be its ability to blunt the sympathetic nervous system, slow the
heart rate, and increase cardiac filling time.
Table 2.4. Principles of Managing Heart Failure13
Recognition and Treatment of Underlying Systemic Disease
Timely Surgical Repair of Structural Anomalies
Afterload Reduction
Angiotensin-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
Mineralocorticoid inhibitors Inotropy
Digoxin
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2.1.8. Prognosis
The outcome for patients experiencing HF depends largely on its cause. Whennoncardiac disorders are responsible, the improvement in HF is related to successful
treatment of the systemic disease. For many cardiac malformations (preloading and
afterloading conditions), surgical correction can be curative. Unfortunately, surgery for many
congenital heart lesions only palliates the underlying disease.13
In general, too little is known about HF risk assessment in children to permit confident
statements about prognosis and response to treatment. The New York Heart Association
Classifications, routinely used in adult studies, fail in pediatric applications because of the
unique presentations of HF in children. Alternatives, such as the Ross classification or the
New York University Pediatric HF Index also have not gained wide acceptance.12,14
2.2. Ventricular Septal Defect
2.2.1. Definition and Classification
A ventricular septal defect (VSD) is a hole or a defect in the septum that divides the 2
lower chambers of the heart, resulting in communication between the ventricular cavities.
The defect can be small or large . A VSD may occur as a primary anomaly, with or without
additional major associated cardiac defects.6
Many classifications of VSD have been proposed:6
a. Perimembranous (infracristal, conoventricular) VSDs lie in the LV outflow tract just
below the aortic valve. Because they occur in the membranous septum with defects in the
adjacent muscular portion of the septum, they are subclassified as perimembranous inlet,
perimembranous outlet, or perimembranous muscular. These are the most common types
of VSD and account for 80% of such defects.
b. Supracristal (conal septal, infundibular, subpulmonic, subarterial, subarterial doubly
committed, outlet) VSD account for 5-8% of isolated VSDs in the United States but 30%
of such defects in Japan. These defects lie beneath the pulmonic valve and communicate
with the RV outflow tract above the supraventricular crest and are associated with aortic
regurgitation secondary to the prolapse of the right aortic cusp.
c. Muscular VSDs (trabecular) are entirely bounded by the muscular septum and are often
multiple. The term Swiss-cheese septum has been used to describe multiple muscular
VSD. Other subclassifications depend on the location and include central muscular or
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midmuscular, apical, and marginal (when the defect is along the RV-septal junction).
These VSDs account for 5-20% of all defects. Any single defect observed from the LV
aspect may have several openings on the RV aspect.
d. Posterior (canal-type, endocardial cushiontype, AV septumtype, inlet, juxtatricuspid)VSDs lie posterior to the septal leaflet of the tricuspid valve. Although the locations of
posterior VSDs are similar to those of VSDs observed with AV septal defects, they are
not associated with defects of the AV valves. About 8-10% of VSDs are of this type.
2.2.2. Epidemiology
The most frequent types of congenital malformations affect the heart. It is estimated that
approximately eight in 1,000 newborns have CHD. A VSD is the most frequent of the various
types of CHD (25%-30% of all CHD). Approximately one infant in 500 will be born with a
VSD. The most common form of congenital heart disease in childhood is the VSD, occurring
in 50% of all children with congenital heart disease and in 20% as an isolated lesion. 15
2.2.3. Etiology
The definitve cause of any individual congenital heart defect is rarely determined.
Congenital heart defects are believed to be multifactorial with both environmental and
genetic components. Genetic risk factors include the presence of certain chromosomal
syndromes including: trisomies 13, 18, 21 or a family history of cardiac defects.
Environmental factors include: maternal diabetes or phenylketonuria, exposure to disease or
teratogens within in the first 8 weeks of gestation. It should be mentioned that a recent study
in Northern Ireland found that the risk of VSD was not increased by maternal smoking,
alcohol consumption or maternal age. Parent/family education should include the complexity
of cardiac development and medical sciences's limited inability to ascertain causality.16,17
2.2.4. Pathophysiology
The size of the VSD, the pressure in the right and left ventricular chambers, and
pulmonary resistance are factors that influence the hemodynamic significance of VSDs. A
VSD may not be apparent at birth because of the nearly equal pressures in the right and left
ventricles and a lack of shunting. With increasing shunt corresponding to the increasing
pressure difference between the ventricles, these defects become clinically apparent.
Exceptions to this rule are patients with Down syndrome who may not undergo the natural
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drop in pulmonary resistance and do not manifest signs of a VSD. Routine screening of all
Down syndrome patients is the standard of care.18
The shunt volume in a VSD is determined largely by the size of the defect and the
pulmonary vascular resistance. Without pulmonary hypertension or obstruction to the rightventricle, the direction of shunt is left to right, with corresponding pulmonary artery, left
atrial, and left ventricular volume overload. In the setting of elevated pulmonary vascular
resistance, right ventricular obstruction resulting from muscle bundles, or pulmonary
stenosis, the shunt volume is limited and may be right to left, depending on the difference in
pressure. Eisenmenger syndrome results from long-term left-to-right shunt, usually at higher
shunt volumes. The elevated pulmonary artery pressure is irreversible and leads to a reversal
in the ventricular level shunt, desaturation, cyanosis, and secondary erythrocytosis.
Muscular VSDs can undergo spontaneous closure as a result of muscular occlusion.
Perimembranous defects can close by tricuspid valve aneurysm formation. Infundibular
defects can close by prolapse of the right aortic cusp. A reduction in the size of the defect by
any of these mechanisms results in changes in the hemodynamic significance of the defect.
The integrity of structures immediately adjacent to ventricular defects is a concern. For
example, the development of aortic insufficiency in the case of infundibular defects is a result
of the deficiency of the support apparatus of the aortic valve and results in damage to the
aortic valve leaflets.19
2.2.5. Clinical Feature
VSDs can be detected by auscultation. The murmurs are typically described as
holosystolic or pansystolic. The grade of murmur depends on the velocity of flow; the
location of murmur is dependent on the location of the defect. Smaller defects are loudest and
may have a thrill. Muscular defects can be heard along the lower left sternal border and may
vary in intensity as the defect size changes with muscular contraction throughout systole.
Infundibular defects shunt close to the pulmonary valve and can be heard best at the left
upper sternal border. Perimembranous defects may have an associated systolic click of a
tricuspid valve aneurysm.20
In the setting of low pulmonary vascular resistance, larger defects have murmurs of
constant quality that vary little throughout the cardiac cycle and less commonly have an
associated thrill. These defects will have a corresponding increase in mitral flow, resulting in
a diastolic rumble at the apex. There may be evidence of left ventricular volume overload on
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palpation of the precordium with a laterally displaced impulse. Elevated pulmonary pressure
causes an increase in the pulmonary component of the second heart sound. Large defects with
no shunt and defects with Eisenmenger physiology and right-to-left shunt often do not have a
VSD murmur.
18,19
2.2.6. Diagnostic Evaluation
Electrocardiography
The ECG is most likely normal in patients with small VSDs. With increasing
shunt, there may be evidence of left ventricular volume load and hypertrophy. Left atrial
enlargement may be present. In cases of elevated pulmonary artery pressure, right axis
deviation, right ventricular hypertrophy, and right atrial enlargement may be evident on
ECG.
Chest Radiography
Small defects have no apparent radiographic abnormality. With larger defects,
chamber enlargement is present to various degrees, depending on the volume of the shunt.
Increased pulmonary vascularity is present. As patients develop Eisenmenger syndrome
or increasing pulmonary resistance, there is loss of pulmonary vascularity and pruning of
the vasculature. In these patients, there is evidence of right heart enlargement and a
dilated main pulmonary artery.
Echocardiography
Echocardiographic evaluation of VSDs is a noninvasive tool that accurately
delineates the morphology and associated defects. Hemodynamic evaluation of the defect,
the presence of elevated pulmonary artery pressure, obstruction of the right ventricular
outflow tract (double chamber physiology), insufficiency of the aortic valve, and
distortion of the valve apparatus are all evaluated by echocardiography. When limitations
in image quality of transthoracic echocardiography prevent evaluation of these aspects of
the cardiovascular physiology, transesophageal imaging can be performed. Three-
dimensional echocardiography has proved accurate for quantifying shunt and can provide
accurate visualization of defects that otherwise are difficult to evaluate by 2-dimensional
imaging alone.
Magnetic Resonance Imaging
Magnetic resonance imaging can be used to delineate VSDs in patients with
complex associated lesions.
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Cardiac Catheterization
Catheterization can give accurate measurements of pulmonary vascular resistance,
pulmonary reactivity, and volume of shunting. Response to pulmonary vasodilators can
be determined and can guide therapy. Angiography can provide information on thelocation of a defect, number of defects, and the degree of aortic insufficiency. The aortic
valve can be inspected for integrity.
2.2.7. Management
Medical Management of of Symptomatic CHF:5
Therapies used to manage symptomatic CHF in children with moderate or large VSDs may
include the following:
Increased caloric density of feedings to ensure adequate weight gain - Occasionally,
oral feeds must be supplemented with tube feeds because a baby in CHF may be
unable to consume adequate calories for appropriate weight gain
Diuretics (eg, furosemide) to relieve pulmonary congestion - Furosemide is usually
given in a dosage of 1-3 mg/kg/d divided in 2 or 3 doses; long-term furosemide
treatment results in hypercalcemia and renal damage and electrolyte disturbances
Angiotensin-converting enzyme (ACE) inhibitors (eg, captopril and enalapril) - Thesemedications reduce both the systemic and pulmonary pressures (the latter to a greater
degree), thereby reducing the left-to-right shunt
Digoxin (5-10 g/kg/d) - This may be indicated if diuresis and afterload reduction do
not relieve adequately symptoms.
Surgical Closure5
At present, direct surgical repair using cardiopulmonary bypass is the preferred
surgical therapy in most centers. Most perimembranous and inlet VSDs are repaired via a
transatrial surgical approach. Defects in the outlet septum are approached through the
pulmonary valve. Multiple muscular defects, especially near the apex, pose a difficult
problem. Initial pulmonary banding or left ventricular (LV) approach through an apical left
ventriculotomy and closing the defect with a single patch are the standard techniques.
Short-term results of video-assisted cardioscopy for intraventricular repair of VSD have led
to its wide adoption as a means of reducing surgical trauma. Short-term results are
excellent.
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Transcatheter therapy (see below) remains an experimental approach. A hybrid operation is a
joint procedure involving the interventional cardiologist and the cardiac surgeon, who
concomitantly optimize surgical management of complex congenital heart disease. This
approach may be used for multiple VSDs where the perimembranous VSD is repairedsurgically and the muscular VSDs are closed with a transcatheter device.
Transcatheter closure
Muscular VSDs have been closed with transcatheter devices for the past 15 years.
Perimembranous VSDs, though relatively common, can be difficult to close percutaneously.
With previous devices (eg, Rashkind or button devices), attempts to close the VSDs have
been unsuccessful, because of the proximity of the defects to the aortic valve and potential
aortic valve damage.
Most procedures are performed with the patient under general anesthesia and with
echocardiographic guidance. Reported complications have included aortic and tricuspid
regurgitation, device embolization, complete heart block, transient left bundle-branch block
(LBBB), hemolysis, small residual shunts, and perforation.
In a phase I study, Fu et al reported 3 adverse events of complete heart block, perihepatic
bleeding, and rupture of tricuspid valve chordae tendineae. In a previous article, they reported
2 cases of transient heart block that responded to high-dose steroids. Subsequent studies
found that the Amplatzer membranous VSD occluder resulted in excellent closure rates but
had an unacceptably high rate of complete heart block.
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Chapter 3
CASE REPORT
IDENTITY
Name : FR
Age : 4 months
Sex : Female
RM : 54.14.51
Address : Jl. Brigjen Katamso Gg. Pemuda No. 35 Medan
Date of Admission : December, 17th 2012
Major Complaint : Shortness of breath
History :
FR, 4- month- year old girl, weight 4200 gram, height 60 cm, was admitted to Pediatric
Department at Haji Adam Malik General Hospital on December17th 2012 with the main
complaint of shortness of breath.
It has already been experienced since the birth of patient. This shortness of breath is not
related to the weather. The complaint is not accompanied with a wheezing soundor bluish
around the mouth or on the fingertips of hands and feet. According to her mother, she has
drinking problems since birth, sweating a lot during feeding and also crying. Coughing is
found for 2 weeks by now, with white phlegm. Fever has been found for these two weeks,
fever is up and down, fever is down when she is given a febrifuge.
History of Previous Illness : FR previously went to MitraSejati Hospital with the same
complain and was diagnosed with Acyanotic Congenital Heart Disease + pneumoniae by
pediatrician.
History of Previous Medication: Asering, Inj. Ceftriaxone, duminsupp
History of Pregnancy: The age of mother was 27 years. History of fever and sore throat was
found. She took aspirin and herbal when the first month of pregnancy. There is no history of
diabetes mellitus, hypertension, smoking, and alcohol consumption. History of stillbirth was
not found.
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History of birth: Patient is the fourth child. Patient was born spontaneously by the midwife
and not immediately crying, and motion was positive. Birth weight was 3900 grams, birth
length was 50 cm, and history of cyanosis was not found.
Feeding History
From birth to 2 months : Breast milk only
From 2 months to 3 months 3 weeks : Breast milk and rice porridge
From 3 months 3 weeks to now : Breast milk and SGM 1 milk
Physical Examination
Generalized status
Body weight : 4200 g
Body length : 60 cm
Body weight in 50th percentile according to age : 6200 g
Body length in 50th percentile according to age : 62 cm
Body weight in 50th percentile according to body length : 5800 g
BW/age :6,2
4,2x 100% = 67,74 %
BL/age : 62
60
x 100% = 96,7 %
BW/BL :5,8
4,2x 100% = 72,41 %
Presence Status
Sensorium: alert, BP= 100/50 mmHg, HR= 140 bpm, RR= 60 x/min, temperature: 36.5oC.
Anemic (-), dyspnea (+), cyanotic (-), edema (-), icteric (-). Body weight (BW): 4200 g. Body
length (BL): 60 cm. CDC: BW/Age = 67,74 %, BL/Age = 96,7 %, BW/BL = 72,41 %
Localized Status
Head : Eye: light reflex (+/+), isochoric pupil, 3 mm, pale inferiorcon-
junctivapalpebra (-/-) Old man face (+),
Nose: Nostril breathing (+), NGT (+). Mouth: within normal limit. Ear :
within normal limit.
Neck : Lymph node enlargement (-), TVJ R-2 cm H2O
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Thorax : Symmetric fusiform, retraction (+) suprasternal, intercostals, epigastrial,
bulging (+), HR: 140 bpm, regular, pansystolic murmur(+), RR: 60 x/minute,
regular, ronchi (+/+), wheezing (+/+)
Abdomen : Soepel (+), peristaltic (+), liver and spleen not palpable.Extremities : Pulse = 140 bpm, regular, adequate pressure/volume, warm axilla, capillary
refill time(CRT) < 3, clubbing finger (-).
Genitalia : Female, within normal limit.
Chest X-Ray AP 17 December 2012:
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Laboratory Result : December 17, 2012
HEMATOLOGY
Test Result Unit ReferralHb 9,0 gr% 10,7 17,1
WBC 7,6 x 103/mm 6,0 17,5
RBC 3,4 x 106/mm 3,75 4.95
Hematocrite 26,5 % 38 52
PLT 373 x 10/mm 217 497
MCV 77,9 fL 93 115
MCH 26,5 Pg 29 35
MCHC 34 g% 28 34
RDW 15,2 % 14.9 18.7Neutrophil 51,3 % 37 48
Lymphocyte 34,3 % 20 40
Monocyte 14,2 % 2 8
Eosinophil 0,10 % 1 6
Basophil 0,100 % 0 1
CLINICAL CHEMISTRY
Test Result Unit Referral
Analysis of the gas blood
pH 7,460 7,35 7,45
pCO2 46,3 mmHg 38 42
pO2 179,9 mmHg 85 100
HCO3 32,1 mmol/L 22 26
Total CO2 33,6 mmol/L 19 25
BE 7,2 mmol/L (-2) (+2)
Saturation O2 99,3 % 95 100
Metabolism of CarbohidrateBlood glucose 70 mg/dl
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Differential Diagnosis:
1. CHF ec. Acyanotic CHD ec. VSD + Bronkhopneumonia + Marasmus type malnutrion
2. CHF ec. Acyanotic CHD ec. ASD + Bronkhopneumonia + Marasmus type malnutrion
3. CHF ec.Acyanotic CHD ec. PDA + Bronkhopneumonia + Marasmus type malnutrion
Working Diagnosis: CHF ec. Acyanotic CHD ec. VSD + Bronkhopneumonia + Marasmus
type malnutrion
Management:
- O2 1 2 L/i
- IFVD D5% NaCl 0,225% 5 gtt/i micro
- Inj. Ceftriaxone 100 mg/12 h/IV (skin test)
- Inj. Gentamicine 20 mg/24 h/IV (skin test)
- Furosemide 2 x 4 mg
- Spironolactone 2 x 6,25 mg
- NebuleNaCl 0,9% 2,5 cc/8 h
- Diet of Breast milk/supplementary of breast milk 60 cc/3h from NGT
- Chest Fisioteraphy
- Fluid balance/ 6 h
Diagnostic Planning:
Echocardiografi
Picture of FR:
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FOLLOW UP
December 18, 2012
S Shortness of breath (+)
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O
Sensorium : Compos mentis Temp : 37.3oC
BW : 4200 g BL : 60 cm
Head : Eye: light reflex (+/+), isochoric pupil, 3 mm, pale inferior
conjunctiva palpebra (-/-) Old man face (+), Ear and mouth : within
normal limit, Nose: Nostrils breathing (+), NGT (+).
Neck : lymph node enlargement (-)
Thorax : symmetric fusiform, retraction (+) suprasternal,intercostals,
epigastrial, bulging (+), HR: 144 bpm, regular,
pansystolicmurmur(+), RR: 60 bpm, regular, ronchi (+/+),
wheezing (+/+)
Abdomen : Soepel, Peristaltic (+) N, Liver/Spleen : not palpable
Extremity : Pulse : 144 bpm, regular, p/v adequate, acral warm, CRT < 3
BP : 100/60 mmHg
ACHF ec. Acyanotic CHD ec 1. VSD 2. ASD 3. PDA + Bronkhopneumonia +
Marasmus type malnutrion
P
- O2 1 2 L/I
- IFVD D5% NaCl 0,225% 5 gtt/i micro
- Inj. Ceftriaxone 100 mg/12 h/IV (skin test)aff.
- Inj. Gentamicine 20 mg/24 h/IV
- Furosemide 2 x 4 mg
- Spironolactone 2 x 6,25 mg
- Nebule NaCl 0,9% 2,5 cc/8 h
- Diet of Breast Milk/supplementary of breast milk 60 cc/3h from NGT
- Chest Fisioteraphy
- Fluid balance/ 6 h
Planning : Echocardiografi
Balance 06.00
December 19, 2012
S Shortness of breath (+)
Input : 80cc Output : 100 cc Balance : -20cc
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O
Sensorium : Compos mentis Temp : 37.4oC
BW : 4200 g BL : 60 cm
Head : Eye: light reflex (+/+), isochoric pupil, 3 mm, pale inferior
conjunctiva palpebra (-/-) Old man face (+), Ear and mouth : within
normal limit, Nose: Nostril breathing (+), NGT (+).
Neck : lymph node enlargement (-)
Thorax : symmetric fusiform, retraction (+) suprasternal, intercostals,
epigastrial, bulging (+), HR: 180 bpm, regular,
pansystolicmurmur(+), RR: 56 bpm, regular, ronchi (+/+),
wheezing (+/+)
Abdomen : Soepel, Peristaltic (+) N, Liver/Spleen : not palpable
Extremity : Pulse : 180 bpm, regular, p/v adequate, acral warm, CRT < 3
BP : 100/60 mmHg
A CHF ec. Acyanotic CHD ec 1. VSD 2. ASD 3. PDA + Bronkhopneumonia +Marasmus type malnutrion
P
- O2 1 2 L/I
- IFVD D5% NaCl 0,225% 5 gtt/i micro
- Inj. Gentamicine 20 mg/24 h/IV
- Inj. Ampicillin 100 mg/6 h/IV
- Furosemide 2 x 4 mg
- Spironolactone 2 x 6,25 mg
- NebuleNaCl 0,9% 2,5 cc/8 h
- Diet of Breast milk/supplementary of breast milk 60 cc/3h from NGT
- Chest Fisioteraphy
- Fluid balance/ 6 h
Planning : Echocardiograf
Balance 06.00
December 20, 2012
Input : 450 cc Output : 192 cc Balance : 258 cc
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S Shortness of breath (+)
O
Sensorium : Compos mentis Temp : 37.4oC
BW : 4200 g BL : 60 cm
Head : Eye reflex : +/+; pupil isochor; pale inferior conjunctiva palpebra (-/-).
Old man face (+), Ear/Nose/Mouth: within normal limit, O2 nasal kanul(+), NGT (+)
Neck : lymph node enlargement (-)
Thorax : symmetric fusiform, retraction (+) suprasternal,intercostals,
epigastrial, bulging (+), HR: 140 bpm, regular,
pansystolicmurmur(+), RR: 60 bpm, regular, ronchi (+/+),
wheezing (+/+)
Abdomen : Soepel, Peristaltic (+) N, Liver/Spleen : not palpable
Extremity : Pulse : 140 bpm, regular, p/v adequate, acral warm, CRT < 3
BP : 100/60 mmHg
ACHF ec. Acyanotic CHD ec 1. VSD 2. ASD 3. PDA + Bronkhopneumonia +
Marasmus type malnutrion
P
- O2 1 2 L/I
- IFVD D5% NaCl 0,225% 5 gtt/i micro
- Inj. Gentamicine 20 mg/24 h/IV
- Inj. Ampicillin 100 mg/6 h/IV
- Furosemide 2 x 4 mg
- Spironolactone 2 x 6,25 mg
- NebuleNaCl 0,9% 2,5 cc/8 h
- Diet of Breast milk/supplementary of breast milk 60 cc/3h from NGT- Chest Fisioteraphy
- Fluid balance/ 6 h
Echocardiografi: Mod- Large PMO VSD 5,7 mm
Balance 06.00
December 21, 2012
S Shortness of breath (+) cough (+)
Input : 200cc Output : 142 cc Balance : 58 cc
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O
Sensorium : Compos mentis Temp : 37oC
BW : 4300 g BL : 60 cm
Head : Eye reflex : +/+; pupil isochor; pale inferior conjunctiva palpebra (-/-).
Old man face (+), Ear/Nose/Mouth: within normal limit, O2 nasal kanul
(+), NGT (+)Neck : lymph node enlargement (-)
Thorax : symmetric fusiform, retraction (+) suprasternal, intercostals,
epigastrial, bulging (+), HR: 142 bpm, regular, pansystolic
murmur(+), RR: 46 bpm, regular, ronchi (+/+), wheezing (+/+)
Abdomen : Soepel, Peristaltic (+) N, Liver/Spleen : not palpable
Extremity : Pulse : 142 bpm, regular, p/v adequate, acral warm, CRT < 3
BP : 100/60 mmHg
ACHF ec Mod-Large PMO VSD + Bronkhopneumonia + Marasmus type
malnutrion
P
- O2 1 2 L/I
- IFVD D5% NaCl 0,225% 4 gtt/i micro
- Inj. Gentamicine 20 mg/24 h/IV
- Inj. Ampicillin 100 mg/6 h/IV
- Furosemide 2 x 4 mg
- Spironolactone 2 x 6,25 mg
- NebuleNaCl 0,9% 2,5 cc + ventoline /8 h
- Diet of Breast milk/supplementary of breast milk 60 cc/3h from NGT
- Chest Fisioteraphy
Planning : Catheterization
Balance 06.00
December 22, 2012
S Shortness of breath (+) cough (+)
Input : 100cc Output : 522 cc Balance : -422 cc
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O
Sensorium : Compos mentis Temp : 37,3oC
BW : 4300 g BL : 60 cm
Head : Eye reflex : +/+; pupil isochor; pale inferior conjunctiva palpebra (-/-).
Old man face (+), Ear/Nose/Mouth: within normal limit, O2 nasal kanul
(+), NGT (+)Neck : lymph node enlargement (-)
Thorax : symmetric fusiform, retraction (+) suprasternal, intercostals,
epigastrial, bulging (+), HR: 134 bpm, regular, pansystolic
murmur(+), RR: 56 bpm, regular, ronchi (+/+), wheezing (+/+)
Abdomen : Soepel, Peristaltic (+) N, Liver/Spleen : not palpable
Extremity : Pulse : 134 bpm, regular, p/v adequate, acral warm, CRT < 3
BP : 100/60 mmHg
ACHF ec Mod-Large PMO VSD + Bronkhopneumonia + Marasmus type
malnutrion
P
- O2 1 2 L/I
- IFVD D5% NaCl 0,225% 4 gtt/i micro
- Inj. Gentamicine 20 mg/24 h/IV
- Inj. Ampicillin 100 mg/6 h/IV
- Furosemide 2 x 4 mg
- Spironolactone 2 x 6,25 mg
- Folat Acid 1x 5 mg
- Cotrimoxazole 2 x 120 mg
- Becefort syrup 1 cthI
- Vitamin A 1 x 50.000 IU- NebuleNaCl 0,9% 2,5 cc/8 h
- Diet F75 50 cc/ 3 h + 1,2 cc mineral mixed
- Chest Fisioteraphy
- Planning : Catheterization
December 23, 2012
S Shortness of breath
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O
Sensorium : Compos mentis Temp : 36,7oC
BW : 4300 g BL : 60 cm
Head : Eye reflex : +/+; pupil isochor; pale inferior conjunctiva palpebra (-/-).
Old man face (-), Ear/Nose/Mouth: within normal limit, O2 nasal kanul
(+), NGT (+)Neck : lymph node enlargement (-)
Thorax : symmetric fusiform, retraction (+) epigastrial, bulging (+), HR: 128
bpm, regular, pansystolic murmur(+) grade 3/6, RR: 32bpm,
regular, ronchi (-/-), wheezing (-/-)
Abdomen : Soepel, Peristaltic (+) N, Liver/Spleen : not palpable
Extremity : Pulse : 128 bpm, regular, p/v adequate, acral warm, CRT < 3
A CHF ec Mod-Large PMO VSD
P
- O2 1 2 L/I
- IFVD D5% NaCl 0,225% 4 gtt/i micro- Inj. Gentamicine 20 mg/24 h/IV
- Inj. Ampicillin 100 mg/6h/IV
- Furosemide 2 x 4 mg
- Spironolactone 2 x 6,25 mg
- Folat Acid 1x 1 mg
- Cotrimoxazole 2 x 120 mg
- Becefort syrup 1 cthI
- Diet F100 modification with LLM 104 g mixed in 500 cc water 65 cc/3
h + 1,3 cc mineral mix
- Chest Fisioteraphy
Planning : Catheterization
December 24, 2012
S Shortness of breath
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O
Sensorium : Compos mentis Temp : 36,5oC
BW : 4300 g BL : 60 cm
Head : Eye reflex : +/+; pupil isochor; pale inferior conjunctiva palpebra(-/-).
Old man face (-), Ear/Nose/Mouth: within normal limit, NGT (+)
Neck : lymph node enlargement (-)Thorax : symmetric fusiform, retraction (-) suprasternal, intercostals,
epigastrial, bulging (+), HR: 120 bpm, regular, pansystolic
murmur(+) grade 3/6, RR: 40 bpm, regular, ronchi (-/-), wheezing
(-/-)
Abdomen : Soepel, Peristaltic (+) N, Liver/Spleen : not palpable
Extremity : Pulse : 120 bpm, regular, p/v adequate, acral warm, CRT < 3
A CHF ec Mod-Large PMO VSD
P
- IFVD D5% NaCl 0,225% 4 gtt/i micro
- Inj. Gentamicine 20 mg/24 h /IV- Inj. Ampicillin 100 mg/6 h/IV
- Furosemide 2 x 4 mg
- Spironolactone 2 x 6,25 mg
- Folat Acid 1x 1 mg
- Cotrimoxazole 2 x 120 mg
- Becefort syrup 1 cthI
Diet F100 modification with LLM 104 g mixed in 500 cc water 65 cc/3
h + 1,3 cc mineral mix
- Chest Fisioteraphy
Planning : Catheterization
December 25, 2012
S Shortness of breath (-)
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O
Sensorium : Compos mentis Temp : 37oC
BW : 4400 g BL : 60 cm
Head : Eye reflex : +/+; pupil isochor; pale inferior conjunctiva palpebra (-/-).
Old man face (-), Ear/Nose/Mouth: within normal limit, NGT (+)
Neck : lymph node enlargement (-)Thorax : symmetric fusiform, retraction (-) suprasternal, intercostals,
epigastrial, bulging (+), HR: 122 bpm, regular, pansystolic
murmur(+) grade 3/6, RR: 30 bpm, regular, ronchi (-/-), wheezing
(-/-)
Abdomen : Soepel, Peristaltic (+) N, Liver/Spleen : not palpable
Extremity : Pulse : 122 bpm, regular, p/v adequate, acral warm, CRT < 3
A CHF ec Mod-Large PMO VSD
P
- IFVD D5% NaCl 0,225% 4 gtt/i micro
- Inj. Gentamicine 20 mg/24 h/IV- Inj. Ampicillin 100 mg/6h/IV
- Furosemide 2 x 4 mg
- Spironolactone 2 x 6,25 mg
- Folat Acid 1x 1 mg
- Cotrimoxazole 2 x 120 mg
- Becefort syrup 1 cthI
Diet F100 modification with LLM 104 g mixed in 500 cc water 65 cc/3
h + 1,3 cc mineral mix
- Chest Fisioteraphy
Planning : Catheterization
December 26, 2012
S Shortness of breath (-)
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O
Sensorium : Compos mentis Temp : 37,1oC
BW : 4200 g BL : 60 cm
Head : Eye reflex : +/+; pupil isochor; pale inferior conjunctiva palpebra (-/-).
Old man face (+), Ear/Nose/Mouth: within normal limit, NGT (+)
Neck : lymph node enlargement (-)Thorax : symmetric fusiform, retraction (-) suprasternal,intercostals,
epigastrial, bulging (+), HR: 120 bpm, regular,
pansystolicmurmur(+) grade 3/6, RR: 28 bpm, regular, ronchi
(-/-), wheezing (-/-)
Abdomen : Soepel, Peristaltic (+) N, Liver/Spleen : not palpable
Extremity : Pulse : 120 bpm, regular, p/v adequate, acral warm, CRT < 3
A CHF ec Mod-Large PMO VSD
P
- IFVD D5% NaCl 0,225% 4 gtt/i micro
- Furosemide 2 x 4 mg
- Spironolactone 2 x 6,25 mg
- Folat Acid 1x 1 mg
- Cotrimoxazole 2 x 120 mg
- Becefort syrup 1 cthI
- Diet F100 modification with LLM 104 g mixed in 500 cc water 65 cc/3 h
+ 1,3 cc mineral mix
Planning : - Catheterization (waiting for the schedule, there is no injector)
- Home medical treatment
Chapter 4
DISCUSSION AND SUMMARY
4.1. Discussion
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FR, 4 month-year old girl, weight 4200 gram, height 60 cm, was admitted to Pediatric
Department at Haji Adam Malik General Hospital on December17st 2012 with the main
complaint of shortness in breath and was diagnosed with Congstive Heart Failure. The
diagnose was established based on history taking and clinical manifestations where shortnessof breath experienced since thebirth, she has drinking problems since birth, sweating and
crying when feeding. The initial treatment given were, O2, IVFD D5% NaCl 0,225% 5 gtt/i
micro, Inj. Ceftriaxone 100 mg/12 h/IV, Inj. Gentamicine 20 mg/24 h/IV Furosemide,
Spironolactone, NebuleNaCl 0,9% 2,5 cc/8 h, Diet of ASI/PASI 60 cc/3h, Chest Fisioteraphy,
Fluid balance/ 6 h.
Congestive heart failure (CHF) refers to a clinical state of systemic and pulmonary
congestion as result of the inability of heart to pump as much blood as required for the a
dequate metabolism of the body. In developing countries, structural heart defects are the most
common cause of heart failure in infants and children. The incidence of congenital heart
disease in children is approximately 8 per 1000 live births, or 0.8%. The most common form
of congenital heart disease in childhood is the VSD, occurring in 50% of all children with
congenital heart disease and in 20% as an isolated lesion.
In infants, the symptoms of heart failure most commonly exhibited include tachypnea,
tachycardia, poorfeeding, and failure to thrive.The grades of HF in children were shown inthe Ross classification (tabel 2.3.) In this patient, tachypnea, poor feeding, failure to thrive
and retraction found are classified as grade IV in Ross Classification. If patient has VSD, it
can be detected by auscultation. The murmurs are typically described as holosystolic or
pansystolic. This patient has pansystolic murmur graded 3/6.
The chest radiograph of HF may demonstrate cardiac enlargement, increased pulmonary
blood flow, venous congestion, or pulmonary edema. However, chest radiographs generally
have a high specificity but low sensitivity for detecting cardiac enlargement. Although it is
not useful for the evaluation of HF, which is a clinical diagnosis, echocardiography is
essential for identifying causes of HF such as structural heart disease, ventricular dysfunction
(both systolic and diastolic), chamber dimensions, and effusions (both pericardial and
pleural). Chest x-ray of this patient demonstrate cardiac enlargement (CTR 54%). Result of
the echocardiography is Mod- Large PMO VSD 5,7 mm, therefore the patient is diagnosed
with CHF ec mod-large PMO VSD 5,7 mm.
The first goal of HF care is to treat the specific cause. HF-causing cardiac malformationsusually can be approached surgically. Medical management (Table 2.4.) aims to
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maximizecardiac output and tissue perfusion while minimizing stresses that increase MVO2.
These goals are accomplished by reducing the amount of force the heart needed to generate to
eject blood (reducing afterload stress) and by reducing the overfilling of heart (preload). This
patient was given Furosemide 2 x 4 mg and Spironolactone 2 x 6,25 mg as diuretic to reducethe preload. This patient was planned to get catheterization and surgery.
4.2. Summary
FR, 4-month-year old girl, weight 4200 gram, height 60 cm, was admitted to Pediatric
Department at Haji Adam Malik General Hospital on December17st 2012 with the main
complaint of shortness of breath and was diagnosed with Congstive Heart Failure ec mod-
large PMO VSD. The diagnose was established based on history taking and clinical
manifestations where shortness of breath has been experienced since thebirth, shehas drinking
problems since birth, sweating and crying when feeding. From the physical diagnostic
tachypnea, failure to thrive and retraction are found and by Ross classification, it is classified
in grade IV. From auscultation, this patient has pansystolic murmur grade 3/6. Chest x-ray of
this patient demonstrates cardiac enlargement (CTR 54%). Result of the echocardiography is
Mod- Large PMO VSD 5,7 mm. The initial treatment given were, O2 1 2 L/I, IVFD D5%
NaCl 0,225% 5 gtt/i micro, Inj. Ceftriaxone 100 mg/12 h/IV (skin test), Inj. Gentamicine 20
mg/24 h/IV (skin test), Furosemide 2 x 4 mg, Spironolactone 2 x 6,25 mg, NebuleNaCl 0,9%
2,5 cc/8 h, Diet of ASI/PASI 60 cc/3h from NGT, Chest Fisioteraphy, Fluid balance/ 6 h.
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