CASE REPORT

“A 26 Years Old Adult With Ventricle Septum Defect (VSD)”

By :
Lale Sirin Rifdah Salsabila
H1A322107

Supervisor:
Dr. dr. Yusra Pintaningrum, Sp.Jp(K), FIHA, FAPSC,FAsCC,FAPSIC

DALAM RANGKA MENGIKUTI KEPANITERAAN KLINIK MADYA

BAGIAN/SMF ILMU PENYAKIT DALAM
RUMAH SAKIT UMUM DAERAH PROVINSI NTB
RUMAH SAKIT UNIVERSITAS MATARAM
FAKULTAS KEDOKTERAN UNIVERSITAS MATARAM
2023
 PREFACE

I thank Allah SWT because only with His blessings, I was able to complete
the assignment of a case report entitled "26 Year Old Adult with Ventricular Septal
Defect (VSD)". This case report was prepared in order to fulfill an assignment
during the process of attending clinical clerkship in the Internal Medicine
Department at the Regional General Hospital of West Nusa Tenggara Purovince –
Faculty of Medicine, University of Mataram. I express my deepest gratitude to Dr.
dr. Yusra Pintaningrum, Sp.JP(K), FIHA, FAPSC, FAsCC, FAPSIC. The author
hopes that the preparation of this case report can be useful in increasing the reader's
understanding.
The author realizes that this case report is not perfect. Therefore, the authors
really hope for constructive criticism and suggestions to improve this report.

Mataram, August 2023

Author

1
 LIST OF CONTENTS

Preface…………………………………………………………………...... 1
List of Contents……………………………. 2
……………………………………...
List of Figures...………………….………………………………………... 3
BAB I Introduction.……………………………………………………….. 4
BAB II Literature Review ….…………………………………………….. 5
BAB III Case Report…………………………………………………..….. 20
BAB IV Discussion…..………………………………………………….... 34
BAB V Conclusion……………………………………………………….. 39
References…….………………………………………………………...… 40

2
 LIST OF FIGURES

..................................................................................
Figure 1. Septum interventricular components11 5
7.........................................................................
Figure 2. Interventricular communication and VSD 6
.....................................................................................................................................
Figure 3. Types of VSD17 9
Figure 4. Pathophysiology Schematic of Ventricular septal defect (VSD)...........10
Figure 5. AP chest radiograph in a patient with VSD............................................12
.................................
Figure 6. ECG of a patient with a biventricular hypertrophic VSD8 13
Figure 7. Echocardiogram showing VSD..............................................................13
Figure 8. Trans-esophageal echo (TEE) from VSD...............................................14
Figure 9. MRI in a patient with VSD.....................................................................15
Figure 10. CTA in VSD.........................................................................................15
......................................................................
Figure 11. Cardiac catheterization showing VSD 20 16
Figure 12. USG Thorax Marker examination.........................................................26
Figure 13. Patient’s ECG ......................................................................................27

3
 BAB I
INTRODUCTION

Cardiovascular disease is the leading cause of worldwide death and

significantly contributes to morbidity and increased health costs 1 . Structural heart
disease accounts for a sizeable proportion of the overall burden of cardiovascular
disease, especially in low- and middle-income countries. Without prevention or
surgical therapy, structural heart disease has a history of progressive disease.
Ventricular septal defect (Ventricular Septal Defect, VSD) is one of the structural
abnormalities of the heart characterized by a defect in the partition that separates
the two chambers of the heart (interventricular septum) 3. Most VSDs are
congenital, but a small proportion can be acquired due to trauma , surgery, or
complications of other diseases such as myocardial infarction and infective
endocarditis4–6. As part of congenital heart disease, VSD is also the most common
type of congenital heart disease7. In Indonesia, it is estimated that of all cases of
congenital heart disease, 30 % of cases in children and 23% of adult cases are
VSD. In other words, VSD is the most common congenital heart anomaly in
children as well as being the second most common congenital abnormality in
adults8.
Regardless of the cause, the presence of an abnormal connection between
the right and left ventricles with gout formation is the main mechanism of
hemodynamic compromise in VSDs. Most VSDs close spontaneously, but if they
do not close, large defects can lead to adverse complications such as pulmonary
arterial hypertension (PAH), ventricular dysfunction, and an increased risk of
arrhythmias9. Other complications that can occur include insufficiency aorta,
infective endocarditis, or supraventricular arrhythmias10.

4
 BAB II
LITERATURE REVIEW

2.1 Definition
Ventricular septal defect (VSD) is one of the structural abnormalities of the
heart characterized by a defect in the partition that separates the two chambers of
the heart (interventricular septum). it consists of the following four components
(Figure 1):11
1. Inlet (atrioventricular canal septum). The inlet is a smooth-walled
passage that extends inferiorly and posteriorly adjacent to the leaflet

tricuspid valve septum to the distal attachment of the septum to the

papillary muscle of the tricuspid valve. This portion extends posteriorly
from the membranous portion to the posterior wall of the heart thereby
closing the gap between the two atrioventricular valves.

Figure 1. Schematic of the components of the interventricular septum 11

2. Trabecular. This structure is characterized by the presence of

trabeculations which are then divided into three parts, namely apical,
mid muscular, and high muscular.
3. Outlet (infundibular or conal). Extends anteriorly from the membranous
pars to the superventricular crest.

5
 4. Membranose. This portion is fibrous and faces the tricuspid valve as
well as the small portion of the right atrium on the right and the left
ventricular outflow tract, slightly below the aortic valve and adjacent to
the right coronary-noncoronary commissure of the aortic valve on the
left side.
However, VSD needs to be differentiated from other disorders that also
cause interventricular communications (Figure 2). Figure A shows a cardiac
structure with a double outlet right ventricle with the aorta arising exclusively from
the right ventricle with a cranial margin formed by a fibrous continuity between the
aortic and mitral valve outlets. The space between this boundary and the apex of
the apical muscular septum is the true interventricular communication. The
chamber (arrow), however, can never be closed because such a closure would block
the aorta from the left ventricle. In contrast to image B, the yellow dots in the
image indicate the edges of the defect can be closed thereby placing the aortic root
in continuity with the left ventricular cavity. It is this curved surface that represents
a true ventricular septal defect

Figure 2. Interventricular communication and VSD 7

2.2 Etiopathogenesi
The interventricular septum is an asymmetrical curved structure due to
pressure differences in the ventricular chambers. This septum consists of five
sections: membranous, muscular (often referred to as trabecular), infundibular,
atrioventricular, and inlet. Failure of the development or fusion of one of these
components during embryonic cardiac morphogenesis results in a VSD in the
respective component9.
Most VSDs are congenital, but some small amounts may be acquired as a
result of trauma, surgery, or complications of other diseases such as myocardial
infarction and infective endocarditis4–6.
6
 Congenital VSD results from developmental abnormalities or impaired
formation of the interventricular septum during cardiac organogenesis. VSD often
occurs alone, but sometimes it can coexist with other congenital heart defects such
as atrial septal defect (ASD), patent ductus arteriosus (PDA), right aortic arch, and
pulmonary stenosis. VSD can also be a component of more complex congenital
heart disease such as tetralogy of Fallot (ToF) and transposition of the great
arteries (TGA). Several genetic factors have been identified to cause VSD
including chromosomal, single gene, and polygenic inheritance. TBX5 mutations
were recently found to cause septal defects in patients with Holt-Oram syndrome.
Other non-heritable risk factors include maternal infections (rubella, influenza,
and febrile illness), maternal diabetes mellitus, and phenylketonuria. Exposure to
toxic substances such as alcohol, marijuana, cocaine, and certain drugs such as
metronidazole and ibuprofen are also associated with VSD9.
VSD on the other hand can also be a sequela of blunt trauma. Cardiac
compression between the sternum and vertebrae which causes a sudden increase
in intrathoracic pressure at the end of diastole or early systole is thought to be the
basis of the mechanism for the occurrence of VSD in this case 12. In this condition,
the ventricles are filled while the valves are being closed 13,14. Furthermore, the
myocardial contusion (most commonly), coronary artery dissection or adventitial
bleeding occurs. These conditions can lead to necrosis and rupture of the
interventricular septum soon or later12. The most common site of injury is the
interventricular septum pars muscularis near the apex of the heart. In addition,
significant blunt chest trauma can also reopen closed septal defects in patients
with congenital VSDs13,14.
VSD in cases of infective endocarditis occurs due to destruction of the
septal leaflet of the tricuspid valve which also opens the VSD which has closed
spontaneously in congenital VSD patients. In addition, there is the possibility of
subaortic fistula formation from left to right ventricle due to involvement of the
aortic and tricuspid valves15.
VSD is also one of the main complications of myocardial infarction. The
associated risk factors are age, hypertension, lack of thrombolysis and
collaterals16.

7
2.3 Epidemiology
VSD is a relatively common structural cardiac abnormality with an incidence
of 1.5-3.5 per 1000 live births (in congenital VSD)11. Isolated VSD accounts for
37% of all congenital heart disease in children. The incidence of isolated VSD is
approximately 0.3% of newborns. The incidence of VSD is lower in adults because
as many as 90% of cases of VSD can eventually close spontaneously 9. However,
VSD is the most common congenital heart anomaly in children as well as being the
second most common congenital abnormality in adults8. VSD does not have a sex
predilection9. VSD most often affects the membranous part of the interventricular
septum (70%), while the rest are located on the muscularis part (30%)11.

2.4 Klasifikasi
According to The International Congenital Heart Surgery
Nomenclature, VSD is classified into four major groups (Figure 3), including:9,17
- Type 1: (infundibular, outlet) This VSD is located below the semilunar
(aortic and pulmonary) valves in the right ventricular outlet septum above
the supraventricular crista, and is therefore also sometimes referred to as
supracristal. This type is the most unusual type representing only 6% of
all VSDs with the exception of the Asian population which accounts for
around 30%. Aortic valve prolapse and regurgitation often occurs due to
loss of right valve support and/or aortic valve noncoronary valves. This
defect cannot close spontaneously.
- Type 2: (membrane) This VSD, by far the most common type, accounts
for 80% of all defects. The defect is located in the membranous septum
inferior to the supraventricular crista and often involves the muscular
septum commonly known as the perimembrane. The septal leaflet of the
tricuspid valve sometimes forms a "pocket" which reduces the shunt and
can result in spontaneous closure.

8
 - Type 3: (canal or atrioventricular inlet) This VSD is located just below
the inlet valves (tricuspid and mitral) within the inlet portion of the right
ventricular septum. This type represents only 8% of all defects and is
seen in patients with Down syndrome.
- Type 4: (muscular, trabecular) This VSD is located in the muscular
septum, bounded by muscle usually in the apical, central, and outlet
interventricular septum. Can be multiple resulting in a "Swiss Cheese"
appearance. These VSDs represent up to 20% of VSDs in infants.
However, the incidence is lower in adults because of the tendency for
spontaneous closure.

Gambar 3. Types of VSD17

Apart from being classified by location, VSDs can also be classified by size.
This size is compared with the diameter of the aortic annulus. A VSD is considered
small if it measures ≤25% of the aortic annulus diameter, moderate VSD if it
measures >25% but <75%, and a large VSD if it measures >75% of the aortic
annulus diameter9.

2.5 Patophysiology
The main pathophysiological mechanism of VSD is the creation of a shunt
between the right and left ventricles (Figure 4). The amount of blood and the
direction the blood is passing through
9
 This threshold determines the hemodynamic significance of the VSD. These
factors are governed by the size, location of the VSD, and the relative resistance
of the pulmonary and systemic vessels9,18.
In small-sized defects, the resistance to blood flow through these defects is
less than that of the pulmonary and systemic vessels, therefore significantly
inhibiting gout and left-to-right. In contrast, in larger defects, the volume of gout
is determined by the relative resistance of the pulmonary and systemic vessels. In
the perinatal period, pulmonary vascular resistance nearly approaches systemic
vascular resistance, resulting in minimal gout formation between the ventricles.
After birth, as pulmonary vascular resistance increases, gout increases from left to
right. Thus there can be excess volume relative to the right ventricle, pulmonary
circulation, left atrium, and left ventricle. Initially, increased blood flow to the
ventricles now increases stroke volume through the Frank-Starling mechanism.
However, over time, an increase in volume load can lead to dilatation of the
cardiac chambers, systolic dysfunction, and symptoms of heart failure18.

Figure 4. Pathophysiology Schematic of Ventricular septal defect (VSD) A | Streamline flow

from left to right ventricle (arrow). B | Schematic view of blood flow through an uncomplicated
VSD, dotted line indicates increased blood return to the left side of the heart due to gout,
resulting in left atrial and left ventricular enlargement. Ao, aorta; IVC, inferior vena cava; PA,
pulmonary artery; RA, right atrium; SVC, superior vena cava.18

In cases of prolonged left-to-right gout, the endothelium of the pulmonary vessels

undergoes irreversible changes resulting in persistent PAH. When the pressure in
the pulmonary circulation exceeds the pressure in the systemic circulation, the
direction of gout reverses and becomes a right-to-left shunt. This condition is

10
known as Eisenmenger syndrome, and occurs in 10% to 15% of patients with
VSD9.

2.6 Diagnostic Enforcement

2.6.1 Symptoms
The clinical manifestations of an unrepaired VSD are highly dependent on
the presence of hemodynamically significant piarie; because it is directly related
to the size of the defect. Small VSDs cause only minimal left-to-right gout
without left ventricular (LV) fluid overload or PAH and are usually asymptomatic
or discovered incidentally on physical examination9.
Moderate VSDs cause moderate LV volume overload and mild to
nonexistent PAHs. Patients may come seeking treatment in late childhood with
mild congestive heart failure (CHF). Patients with large VSDs develop CHF in
early childhood due to LV fluid overload and severe PAH. 9 Symptoms include
rapid breathing, refusal to feed, failure to thrive, and frequent lower respiratory
tract infections. VSD patients with complications of pulmonary vascular disease
and right-to-left gout may experience symptoms of tightness and cyanosis.
Infective endocarditis can occur regardless of the size of the defect18.
2.6.2 Physical Examination
VSD murmurs are usually pan-systolic best heard at the left lower sternal
border; sounds harsher and louder on small defects but softer and less intense on
large defects. The clenching motion increases the afterload thereby increasing the
power of the murmur. The infundibular defect is best heard over the pulmonary
area. Diastolic decrescendo murmurs and a wide pulse pressure can be detected in
cases of aortic regurgitation. An increase in LV outflow may cause a mid-diastolic
rumbling sound at the left lower sternal border. A septal aneurysm systolic click
may occasionally occur with a membranous defect. Eisenmenger syndrome
manifests with cyanosis, desaturation, dyspnea, syncope, secondary
erythrocytosis, and clubbing; in such cases, the characteristic VSD murmur may
be muted and a prominent pulmonary component of the second heart sound may
be heard9.

11
 Systolic thrill can most often be palpated over the murmur region. Once
pulmonary vascular disease has developed, the holosystolic murmur may
disappear as the pressure gradient decreases across the defect. In these patients
there will be obvious RV heave, loud lung closing sounds (P2) and cyanosis18.
2.6.3 Supporting Examination
Chest radiography (CXR). CXR is useful in estimating blood flow to the
lung and therefore the significance of the defect. CXR is often normal in patients
who have small defects. Cardiomegaly and increased bronchovascular markings
can be observed in patients who have larger defects and increased LV size (Fig.
5). An increased bronchovascular pattern indicates left-to-right gout and excess
pulmonary circulation. RV enlargement and increased lung diameter with
peripheral tapering can be observed in patients with PAH. Likewise,
hyperinflation of the lungs, manifested by air trapping in the lower airways, is
another sign of significant gout and requires surgical intervention8,9,18.

Figure 5. AP chest radiograph in a patient with a VSD

AP chest radiograph in a patient with a VSD showing cardiomegaly, increased bronchovascular
markings, and atelectasis of the left lower lung lobe8.

Electrocardiography (EKG). The ECG is completely normal in half of the

patients with VSD18. The electrocardiogram may show left or right ventricular
hypertrophy, but more commonly shows hypertrophy of both ventricles (Fig. 6) 8.
In patients with PAH, the EKG may show right bundle branch block, right axis
deviation, and right ventricular (RV) hypertrophy and dilatation9.

12
 Figure 6. ECG of a patient with a biventricular hypertrophic VSD 8

Echocardiography with Color Doppler. This test can accurately determine

the location of the defect, the direction and magnitude of gout, and estimate the
right ventricular systolic pressure (Fig. 7) 18. This difference in pressure gradient
may indicate a restriction of the defect. The defect can also be shown in relation to
adjacent cardiac structures, as well as whether there is a valve abnormality, eg
prolapse of the aortic valve. The presence of dilatation of the left atrium indicates
a large gout8.

Figure 7. Echocardiogram showing VSD

A cross-sectional echocardiogram taken in a 4-chamber projection shows the apical VSD (white
arrow) on the left side of Figure A. The right side shows color Doppler of the restrictive
hemodynamic state of the muscular VSD. The apical 5-space view in image B shows color
Doppler of the apical muscular VSD (white arrow).8

Color Doppler transthoracic echocardiography (TTE) is the most important tool

for diagnosis because of its high sensitivity. Color Doppler TTE can detect up to
95% of VSDs, especially non-apical lesions >5 mm and provides morphological
information such as size, location, and number of defects as well as hemodynamic

13
 information such as jet size, severity, and estimation of pulmonary artery pressure
(Fig. 8). TTE is useful in detecting associated aortic insufficiency and other
associated congenital heart defects. Lastly, TTE is also helpful in evaluating the
size and function of the right and left ventricular chambers. Limitations of this
modality include operator dependency and poor acoustic windows. When the
results of conventional TTE are unclear, transesophageal echo (TEE) is
recommended.9

Figure 8. Trans-esophageal echo (TEE) from VSD (a) VSD in mid esophageal RV inflow-outflowview. (b)
VSD Inlet VSD in 4-chamber mid esophageal view. (c) Subarterial (supracristal/outlet) VSD on the long
axis view of the LV mid esophageal showing right coronary cusp herniation of the aortic valve. (d)
Muscular VSD in 4-chamber mid-esophageal view.19

Cardiac magnetic resonance imaging (MRI) and computed tomography

(CT) are useful in cases with complex anatomic challenges such as a VSD
accompanied by other congenital cardiac anomalies as well as defects in unusual
locations that are difficult to visualize by conventional TTE (Figs. 9 and Fig. 10) 9.

14
 Figure 9. MRI in a patient with a VSD
MRI in a patient with a massive membranous VSD has not corrected the widening of the inlet
that causes Eisenmenger's syndrome20.

Figure 10. CTA on VSD

CTA in a massive membranous VSD patient (long arrow). There is a levo-transposition of the
large arteries and a substantial dilatation and morphology of the left ventricle, which is the origin
of the pulmonary artery. After failed gout revision, a PTPE graft (short arrow) is inserted
laterally from the left atrium.20

Cardiac catheterization. Cardiac catheterization provides additional

information regarding hemodynamics, especially if there is suspicion of increased
pulmonary vascular resistance (Fig. 11)8. This examination is very useful in patients
who have high pulmonary pressures in order to measure pulmonary vascular
resistance. This study provides further detail about concomitant aortic regurgitation,
in cases of multiple VSDs, and when coronary artery disease is suspected 8,9. In this
case, there may be an increase in oxygen saturation in the right ventricle compared
to the right atrium due to gout from the highly oxygenated blood moving from the
left ventricle to the right ventricle.

15
 Figure 11. Cardiac catheterization showing VSD20

2.7 Differential Diagnosis

As part of acyanotic heart disease, the following is the differential diagnosis
of VSD:9,21

- Atrioventricular septal defect

- Atrial septal defect
- Aortopulmonary window
- Coarctation of the aorta
- Pulmonary stenosis
- Cor triatriatum

2.8 Theraphy
Historically, surgery to repair the VSD was the only option, however, recent
technological advances have made percutaneous VSD closure possible9.
2.8.1 Medikamentosa
In VSD patients with gout producing symptoms such as failure to thrive,
difficulty feeding, diaphoresis, or tachypnea, diuretics are the first line of medical
palliative treatment. When diuretics are used in high doses, side effects, especially
hypokalemia, need to be considered, and potassium-sparing diuretics are selected.
Afterload reduction is also required to promote direct systemic flow from the left
ventricle, thereby reducing the amount of left-to-right gout through the defect.
Afterload reduction is achieved using angiotensin converting enzyme inhibitors
(ACEI). Inotropic agents such as digoxin are useful in patients with large gout and
left ventricular volume overload. Inotropy with afterload reduction can also be
16
 achieved by administering milrinone intravenously. However, the provision of
such therapy is limited to patients awaiting surgery.8
2.8.2 Prophylaxis Antibiotic
Patients with unrepaired ventricular septal defects should not be routinely
prescribed prophylactic antibiotics for infective endocarditis. 9 Endocarditis is a
rare problem and is more frequently found in hemodynamically restrictive defects.
This is because the presence of a high-velocity jet through the defect causes a
Venturi effect, with the potential for platelet adhesion and subsequent vegetation
on the endocardial surface of the septal defect or the septal leaflets of the tricuspid
valve.8 Endocarditis prophylaxis is especially indicated in cyanotic congenital
heart disease, previous episodes of endocarditis, and in patients who have
prosthetic heart valves or have been repaired with prosthetic materials.9
2.8.3 Surgery
In general, VSD closure is indicated in moderate to large defects with
significant hemodynamic compromise as well as in patients who are symptomatic
and have left ventricular dysfunction. Intervention should also be considered in
cases of progressive aortic insufficiency or after an episode of endocarditis. 9 In
congenital VSDs, surgical correction is recommended in the first month of life
especially in children with concomitant heart failure or pulmonary hypertension.
Defects of moderate size without pulmonary vascular disease but with significant
left-to-right gout can be corrected in childhood.18
Indications for surgical closure according to ACC/AHA guidelines are
summarized below:9
- Patients suffering from episodes of endocarditis.

17
- Ratio of pulmonary blood flow to systemic blood flow (Qp/Qs) ≥2 plus clinical
evidence of fluid overload in the LV.
- In milder gouts such as Qp/Qs above 1.5, intervention may be considered if there
is evidence of systolic or diastolic LV dysfunction, or if pulmonary artery
pressure and pulmonary vascular resistance are <2/3 of systemic pressure and
systemic vascular resistance respectively.

Surgery reduces the risk of endocarditis, may improve PAH, and overall
improves survival. Without PAHs, the operative mortality rate is approximately
1%. Complications include residual or recurrent VSD, valvular incompetence such
as tricuspid regurgitation and aortic insufficiency, arrhythmias, LV dysfunction,
and the development of PAH. Arrhythmias accompanying VSD repair include
atrial fibrillation, complete heart block, and less commonly, ventricular
tachycardia. The main contraindication for surgical VSD closure is the presence of
irreversible PAH; This is due to high perioperative surgical mortality and
pulmonary complications.9
2.8.4 Cutaneous closure
VSD closure with percutaneous devices is an alternative for patients whose
surgery is particularly risky because of severe PAH, multiple comorbidities, and
patients who have had previous cardiothoracic surgery such as residual or
recurrent VSDs. Muscular VSDs are the main type amenable to this procedure,
this is because in other types of VSDs, the proximity of the inlet valve defect
makes this technique difficult. The outcome of this procedure is excellent with
complete closure and low mortality. The most frequent complication is complete
atrioventricular block which is mostly associated with perimembrane defects. 9

2.9 Prognosis
The prognosis of patients with isolated defects is considered good. Some
patients with a muscular VSD may experience spontaneous valve closure. In
addition, a perimembranous VSD can also be expected to close spontaneously due
to apposition of adjacent tissues from the tricuspid valve leaflet. Only doubly
committed defects often require repair because failure to close these defects
increases the risk of aortic valve prolapse. 8 Approximately 85% to 90% of
isolated small VSDs close spontaneously during the first year of life. Patients with

18
asymptomatic small VSDs in the absence of PAH have an excellent prognosis
without any intervention. However, unrepaired defects >2 cm in diameter are
associated with a mortality rate of 71% or late cardiovascular complications such
as pulmonary arterial hypertension.3 Conversely, the prognosis is good in VSD
patients who have undergone repair. However, these patients still have a higher
long-term risk of arrhythmias, endocarditis, and congestive heart failure compared
to the general population.9 In contrast, VSD complicated by Eisenmenger
syndrome and pulmonary hypertension has a poor prognosis and is characterized
by activity intolerance, hypoxia, and right ventricular dysfunction.8
Traumatic VSD is often life threatening with a mortality rate of 19%.
Therefore, this case was mainly diagnosed post mortem. 12 However, some cases
can also close spontaneously.13,14

2.10 Complication
Beberapa komplikasi yang dapat ditemukan pada pasien yang mengidap
VSD, antara lain:9,10
- Sindrom Eisenmenger
- Insufisiensi aorta akibat prolaps leaflet katup aorta
- Endokarditis infeksi
- Embolisasi
- Aritmia supraventrikular

19
 BAB III
CASE REPORTS

3.1 PASIEN IDENTITY

Name : Tn. AAG
Sex : Male
Age : 26 years old
Religion : Islam
Tribe : Sasak
Last Education : SMA
Address : Praya, Lombok Tengah
MR No. : 2268xx
Hospitalized : 1 July 2023 (16.00 WITA)
Examination : 4 July 2023

3.2 ANAMNESIS
A. Main Complaint
Shortness of breath
B. Current Medical History
The patient came to the IGD RSUDP NTB on July 1 2023 with
complaints of shortness of breath since 8 am (8 hours of SMRS). Since you
feel it comes and goes and it gets worse when you start doing activities,
even when you walk a few steps. The patient feels more comfortable in a
supine position with the pillow elevated. The patient also had felt nauseous
since this morning but now has improved. Patients often complain of
intermittent chest pain. The patient also complained about his stomach
getting bigger and feeling bloated since 1 month ago.

During the examination on July 4 2023 (4th day of treatment) there

were no complaints from the patient. Other complaints such as fever,
headache, convulsions, vomiting, abdominal pain, bluish lips were denied.
The patient's BAK is normal, yellow in color. The patient has never had a
bowel movement since entering the hospital.

20
 C. Past Medical History
- The patient has a history of VSD since a year ago. According to the
patient's statement, this was due to having hit a blunt object in the chest.
Currently the patient is taking furosemide and ramipril. The patient had a
history of checking his condition at Praya Hospital and planned to have
an echocardiography examination at the heart polyclinic at the NTB
General Hospital on July 3 2023, but the patient's condition was getting
worse so he was taken to the emergency room first.
- History of previous diseases such as high blood pressure, diabetes, high
cholesterol, asthma, stroke, liver disease, kidney disease, lung disease,
history of infection and malignancy is denied.
- The patient has a history of allergy to demacolin. The patient has no
history of food allergies.
- History of previous operations denied.

D. Family Medical History

Similar complaints of tightness in the family were denied. Denied
history of high blood pressure, diabetes, asthma, heart disease, lung
disease, kidney disease, liver disease, and malignancy.
E. Social History
The patient is an active smoker. The patient has a history of
smoking since high school (1-2 packs per day), and frequently drinks
coffee (2-3 cups per day).
3.3 PHYSICAL EXAMINATION
3.4 GENERAL STATUS
General condition: Moderate
Awareness : compos mentis (GCS E4V5E6)
Vital Signs
Blood Pressure : 120/80 mmHg
Pulse : 89x/s
Respiration Rate : 20x/s

21
Temperature : 36,5oC
SpO2 : 99% RA

LOCAL STATUS
Head
- Inspection: Normocephali, normal distribution of hairs, lesions (-)
- Palpation : Mass (-), tenderness (-), cephalhematoma (-)
Eyes
- Inspection: Conjunctiva anemic (-/-), icteric sclera (-/-), exopthalmus
(-/-), eyelid edema (-/-), direct pupillary reflex (+/+), indirect pupillary
reflex (+/+ ), isochor, photophobia (-/-)

- Palpation : Tenderness (-/-), palpebral edema (-/-)

Ears
- Inspection: Normal shape, symmetrical, normal mucosa, hyperemia (-)
- Palpation : Tenderness (-/-)
Nose
- Inspection: normal shape, symmetrical, septal deviation (-), rhinorrhea (-),
bleeding (-), normal mucosa, hyperemia (-), nostril breathing (-)
- Palpation : Tenderness (-)

Mouth
- Inspection: Symmetrical, central cyanosis (-), moist lip mucosa, corner lip
lesion (-), stomatitis (-)
Neck
- Inspection: Tracheal deviation (-), mass (-), distended, jugular vein
dilation (-), use of the SCM accessory muscles (-), hypertrophy of the
SCM muscles (-)

- Palpation: Trachea is in the middle, lymph node enlargement (-), thyroid

enlargement (-), neck stiffness (-)
Thorax
- Inspection:
o Chest shape and size: symmetrical when static, pectus excavatum (-)
o Chest wall movement: Symmetrical
o Surface of chest wall: scar (-), lesion (-), mass (-), spider nevi (-),
gynecomastia (-)

22
 o Use of accessory respiratory muscles: intercostal muscles (-),
intercostal hypertrophy (-), active abdominal accessory muscles (-)
o Ribs and between the ribs: symmetrical, widening between the ribs (-)
o Supraclavicular and infraclavicular fossa: concave, symmetrical
o Jugular fossa: trachea in the middle (+)
o Respiratory type: Thoracoabdominal
- Palpation:
o Anterior surface of chest wall: tenderness (-), mass (-), deformity (-),
crepitus (-) vibration (-), thrill (-)

o Raba noise : normal symmetrical

o Mediastinal position: tracheal deviation (-), palpable ictus cordis at

ICS V MCLS

o Front and back focal fremitus: normally symmetrical

- Percussion
o Heart boundary:

▪ Right border: right parasternal ICS IV

▪ Left border : left midclavicular ICS V

o Front :
Sonor Sonor
Sonor Sonor
Sonor Sonor
o Back :
Sonor Sonor
Sonor Sonor
Sonor Sonor
- Auscultation
o Cor: single regular S1S2, pansystolic murmur on ICS 3-4 (+), gallop
(-)

23
 o Pulmo:

▪ Breathing sound (front and back)

Vesicular Vesicular
Vesicular Vesicular
Vesicular Vesicular

▪ Rhonki (front and back)

- -
- -
- -

▪ Wheezing (front and back)

- -
- -
- -

Abdomen

- Inspection : Distended (+) undulation (+), mass (-), injury (-),

dilation of veins (-), darm countor (-), striae (-)
- Auscultation : Bowel sounds (+) 8x/minute,metallic sound (-)
- Percussion : Tympany over the entire abdominal field

- Palpation : mass (-), tenderness (-), hepatosplenomegaly (-), CVA

tapping pain (-)
Extremities
- Superior : warm acral (+/+), edema (-/-), deformity (-/-), cyanosis (-/-),
CRT< 2 seconds,clubbing finger (-/-)
- Inferior : warm acral (+/+), edema (-/-), deformity (-/-), cyanosis (-/-),
CRT < 2 seconds,clubbing finger (-/-)

24
 3.5 SUPPOERTING EXAMINATION
A. Laboratory Examination
01/07/2023 Satuan Nilai Rujukan
Darah Lengkap
Hemoglobin 11.7 g/dL 12,0-16,0
Leukosit 7.190 /uL 4.000-10.000
Eritrosit 3.88 juta/uL 3,50-5,00
Trombosit 375000 /uL 150.000-400.000
Hematokrit 34 % 25-42
MCV 86,9 fL 80-100
MCH 30,2 Pg 26-34
MCHC 34,8 g/dL 32-36
RDW-SD 50,3 fL 35-47
PDW 15,9 fL 9-13
MPV 8.4 fL 7.2-11.1
PCT 0,32 % 0.15-0.40
Basofil 0.09 103/uL 0.00-0.10
Eosinofil 0.46 103/uL 0.00-0.40
Neutrofil 4,83 103/uL 1.50-7.00
Limfosit 1.15 103/uL 1.00-3.70
Monosit 0.66 103/uL 0.00-0.70
Fungsi Ginjal
Ureum 40 mg/dL 10-50
BUN 18,69 mg/dL 8,90-20,60
Kreatinin 0,6 mg/dL 0,6-1,3
eGFR 162 ml/mnt/1,73m2 >90
Fungsi Hati
SGOT 51 U/l 0-40
SGPT 75 U/l 0-41
Albumin 2.8 mg/dL 3,5-5,2
Bilirubin Total 0.8 mg/dL <1,00
Bilirubin Direk 0.34 mg/dL <0.20
Elektrolit
Natrium 132 mmol/L 135-146
Kalium 4.2 mmol/L 3.4-5.4
Klorida 100 mmol/L 95-108
Serologi
HIV Rapid Non reaktif - Non reaktif

25
B. USG Thorax + Marker
Examination date : 3 July 2023

Figure 12. USG Thoraks Marker

Interpretation:
Bilateral plueral effusion
- Right : volume ± 810 cc, marked on the midscapular line with a
minimum punctum of ± 2 cm, punctum optinum of ± 2.4 cm.

- Left : volume ± 845 cc, marked on the linea midscapula with a

minimum punctum of ± 1.3 cm, punctum optinum of ± 2.8 cm

C. Echocardiography (RS Praya)

Result :
- VSD subarterial doubly comitted (SADC) diameter 1.5-1.7 cm
- RA-RV dilatation
- TR minimal, TVs 35-40

26
 D. EKG
Examination date : 1 July 2023

Figure 13. Patient’s EKG examination

Interpretation:
Rhythm : Sinus rhythm
Pulse Frequency : 102 x/minute
Axis : Deviation of the axis to the right
P wave : >120 msec
QRS complex : Narrow, S/R at V5 = 1.55, SV6 = 8 mm
ST segment : isoelectric
T wave : T inversion at AVR, V1, V2
QT interval : Normal
Impression: Right axis deviation, Left Atrial Enlargement, Biventricular
Hypertrophy

3.6 ASSESMENT
- Ventricular septal defect (VSD) SADC
- Efusi pleura bilateral

27
 3.7 PLANNING
A. Diagnostic
Echocardiography
B. Medicamentosa
- Inj. Ceftriaxone 1 gr/12 hour IV
- Inj. Furosemide 20 mg/8 hour IV
- Inj. Lansoprazole 1 x 30 mg IV
- Spironolacton pO 1 x 25 mg
- Ramipril pO 1 x 2,5 mg
- Bisoprolol pO 1,25 mg-0-0
- Revatio (Sildenafil) pO 3 x 20 mg
- Vipalbumin pO 3 x 1
C. Non Medicamentosa
- O2 nasal canule 2 lpm
- IVFD NaCl 0,9% 500 cc/24 hour (7 tpm)
- Monitor urin output/24 hour
- Minum maksimal 1000 cc/day
D. Monitoring
- Monitoring complaints and vital signs
- Radiology: AP/lateral Chest X-Ray
E. Education
- Explain to patients and families regarding the disease they are
experiencing
- Explain the risk factors for the patient's disease
- Explain the diagnostic approach, management and complications of
the patient's disease
- Explain the prognosis of the disease in patients and families
-

3.8 PROGNOSIS
- Ad Vitam : dubia ad malam
- Ad Functionam : dubia ad malam
- Ad Sanationam : dubia ad malam

28
 BAB IV
DISCUSSION

This case report discusses a 26 year-old man who was diagnosed

withventricular septal defect with suspected ADC and bilateral pleural effusion. In
Indonesia, it is estimated that of the total cases of congenital heart disease, 23% of
adult cases are VSD. Thus, VSD is the second most common congenital heart
anomaly in adults.8 VSD does not have a sex predilection.9

Congenital VSD can be congenital and acquired (acquired) due to trauma,

surgery, or complications of other diseases such as myocardial infarction and
infective endocarditis.4–6 In this case there are two possible causes of VSD. First,
congenital VSD that was newly diagnosed in adulthood, and secondly, VSD was
acquired through a blunt trauma mechanism. The possibility of both tendencies is
quite small because traumatic VSD often has a poor prognosis which causes
immediate death.11 In addition, traumatic VSDs often involve the muscularis
septum near the apex,12,13 whereas in patients, the location of the VSD is in the
pars infundibular.

Findings in Echocardiography previously demonstrated the presence of a

VSD subarterial doubly comitted (SADC). SADC VSD is also known as VSD
type 1 (infundibular/outlet) which is characterized by a defect just below the
valves of the two major arteries above the supraventricular crest (aortic and
pulmonary arteries).21 This type is an uncommon type that represents only 6% of
all VSDs. However, in Asians the proportion can reach 30%. This defect does not
close spontaneously.9

Based on the size comparison with the aortic annulus, VSD can also be
divided into small, medium, and large. A VSD is considered small in size

≤25% of the aortic annulus diameter, moderate VSD if >25% but <75%, and large
VSD if >75% of the aortic annulus diameter. 9 In this case, the diameter of the
VSD was found to be 1.5-1.7 cm. This size then needs to be compared with the
normal value of the aortic annulus in adult males. Something

29
research on the normal value of dimensionsaortic rootthrough trans-esophageal
echocardiography in the adult male population of Thailand (as part of Southeast
Asia) showed the normal aortic annulus diameter in males is equal to

22.3 ± 3.4 mm.22 If using these references, it is estimated that the size of the VSD
in patients is in the moderate to severe range.

Several mechanisms have been proposed to explain the tricuspid

regurgitation associated with peri-membrane VSDs. First, it can be induced by the
high speed of the VSD which results in distortion ofleaflet anterior to the tricuspid
valve directs flow toward the right atrium; second, aneurysmleaflet The septum is
induced by the Venturi effect of gout and partially closes the gout but results in
complete loss of tricuspid valve closure during systole with subsequent tricuspid
regurgitation. Closure of the peri-membrane VSD by either surgery or an
occlusion device is usually associated with total resolution of tricuspid
regurgitation.23

In this case, the patient has come with symptoms of shortness of breath and
activity intolerance. This corresponds to the size of the septal defect in moderate
to severe patients. Moderate VSDs result in moderate LV volume overload and
mild PAHs or none at all. As is the case, patients with these defects may seek
treatment at an older age with clinical mild congestive heart failure (CHF). 9

Smoking is a risk factor for major cardiovascular disease. Congenital heart

disease (CHD) patients who smoke even have an increased risk of dangerous
consequences such as coronary heart disease, hospitalization, and premature
mortality.24,25 Studies show the prevalence of smoking in adolescent and adult
patients with this disease is 5-28%. 25 In this case, the patient was known to be an
active smoker, and therefore, adverse side effects might have been influenced by
this factor.

Physical examination showed normal results and only found a pansystolic

murmur on ICS 3-4. VSD murmurs are usually pan-systolic best heard at the left
lower sternal border; sound rough and hard on

30
small defects but softer and less intense on large defects. However, defects in the
infundibular area are best heard in the pulmonary area.9

Physical examination also shows abdominal distention which is suspected

as ascites. Ultrasound examination of the thorax markers showed bilateral pleural
effusions with a volume of 800 cc each. Ascites is an abnormal accumulation of
fluid in the peritoneal space. One of the causes is congestive heart failure. Venous
return is impaired in heart failure, thereby causing expansion of venous volume,
increased hydrostatic pressure, and filtration of fluid into the peritoneal spaces. 26
On the other hand, pleural effusion is also common in patients with congestive
heart failure. This process results from a type of left ventricular function that
causes an increase in pulmonary venous and left atrial pressure.27

Complete blood laboratory examination, renal function, liver function,

electrolytes and serology were within normal limits. Hypoalbumin was found
(Albumin = 2.8 mg/dL). Hypoalbuminemia in patients with heart failure occurs
primarily as a result of decreased albumin synthesis and protein loss due to
hemodilution, chronic inflammatory conditions, hepatic congestion, malnutrition,
cachexia due to fluid overload and proteinuria, or intestinal disease. Albumin is
associated with many important biological processes involved in heart failure and
causes poor outcomes. Low albumin further triggers and encourages congestion
due to decreased intravascular colloid osmotic pressure, increased oxidative stress,
inflammation, and susceptibility to infection.28

The patient's EKG revealed right axis deviation, left atrial enlargement,
and biventricular hypertrophy. The electrocardiogram may show left or right
ventricular hypertrophy, but more often it shows hypertrophy of both ventricles. 8
In patients with PAH, the EKG may show right bundle branch block, right axis
deviation, and right ventricular (RV) hypertrophy and dilatation.9

Treatment consists of pharmacological and non-pharmacological. Non-

pharmacological treatment consists of administering oxygen supplementation,
supplementation

fluids and monitor fluid balance. Pharmacological treatment consists of

administering antibiotics, diureticsloop (furosemide), lansoprazole, potassium-
31
sparing diuretics (spironolactone), ACEI (ramipril), bisoprolol, sildenafil and
vipalbumin. In VSD patients with gout that causes symptoms, diuretics are the
first line of medical palliative treatment. Plus, reductionafterload it is also needed
to promote direct systemic flow from the left ventricle, thereby reducing the
amount of left-to-right gout through the defect. Afterload reduction is achieved
using angiotensin converting enzyme inhibitors (ACEI).8

Furosemide inhibits tubular reabsorption of sodium and chloride in the

proximal, distal tubule and thick ascending loop of Henle by inhibiting the
sodium-chloride cotransport system resulting in excessive excretion of water
along with sodium, chloride, magnesium, and calcium.The Food and Drug
Administration (FDA) has approved furosemide to treat conditions with volume
overload and edema secondary to exacerbations of congestive heart failure. In
addition, diuretic therapy is recommended in patients with liver cirrhosis and
ascites, accompanied by dietary sodium restriction. The recommended diuretic is a
combination of spironolactone and furosemide, starting with a ratio of 100 mg of
spironolactone and 40 mg of furosemide. Drugs are titrated to an adequate
response or maximum dose of 400 mg of spironolactone plus 160 mg of
furosemide.29

The current ESC guidelines for HF indicate that diuretics, renin-

angiotensin-aldosterone system (RAAS) inhibitors, β-blockers, and
mineralocorticoid receptor antagonists may be used in patients with congenital
heart disease, especially when neurohormonal and cardiac autonomic activity is
increased. In these patients ventricular filling is significantly impaired. β-Blockers
can increase functional capacity and can improve outcomes such as the severity of
systemic AV valve regurgitation and RV remodeling.30

Sildenafil is a selective phosphodiesterase-5 inhibitor that enhances the

bioavailability of cyclic guanosine monophosphate and thereby supports
endogenous vasodilation. Sildenafil has beneficial effects on pulmonary arterial
hypertension in both children and adults.31

Markhazard ratio the age-related mortality in patients with uncorrected

VSD was 2.7 (95% CI: 2.4–3.0). One third of these causes of death originate from

32
the heart in patients with uncorrected defects. Although one-third of these causes
are from ischemic conditions, heart failure is the most common non-ischemic
cause.32

33
 BAB V
CONCLUSION

Ventricular septal defect (VSD) is a disorder in the form of a defect in the

interventricular septum. VSDs are partially congenital, but can also be acquired from
conditions such as myocardial infarction, trauma, or infectious endocarditis. VSDs are
divided into 4 types based on the location of the defect (infundibular, muscular,
membranous, and inlet) and divided into 3 based on the size of the defect (small,
moderate, severe). ). Smaller VSDs are sometimes diagnosed in adulthood due to
symptoms of congestive heart failure. Echocardiographic examination is used as the
main basis for the diagnosis of VSD. Correction of VSD either surgically or
percutaneously is the mainstay of treatment. VSD conditions that have been
accompanied by pulmonary vascular disease or Eisenmenger syndrome have a poor
prognosis.

34
 REFERENCES

1. Vaduganathan M, Mensah GA, Turco JV, Fuster V, Roth GA. The Global
Burden of Cardiovascular Diseases and Risk: A Compass for Future Health.
J Am Coll Cardiol [Internet]. 2022 Dec 20 [cited 2023 Jul 30];80(25):2361–
71. Available from: https://www.jacc.org/doi/10.1016/j.jacc.2022.11.005
2. Watkins DA, Hasan B, Mayosi B, Bukhman G, Marin-Neto JA, Jr AR, et al.
Structural Heart Diseases. Curr Opin Obstet Gynecol [Internet]. 2017 Nov
17 [cited 2023 Jul 30];2(2):223–5. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK525139/
3. Doshi U, Wang-Giuffre E, Doshi U, Wang-Giuffre E. Ventricular Septal
Defects: A Review. Congenit Hear Defects - Recent Adv [Internet]. 2022
May 5 [cited 2023 Jul 30]; Available from:
https://www.intechopen.com/chapters/81658
4. Juneau D, Hermann D, Wells GL, Juneau D, Hermann D, Wells GL.
Penetrating Trauma Resulting in Ventricular Septal Defect. World J
Cardiovasc Surg [Internet]. 2014 May 14 [cited 2023 Jul 30];4(5):77–80.
Available from: http://www.scirp.org/Html/1-1960123_45867.htm
5. Durden R, Turek J, Reinking B, Bansal M. Acquired ventricular septal
defect due to infective endocarditis. Ann Pediatr Cardiol [Internet]. 2018
Jan 1 [cited 2023 Jul 30];11(1):100. Available from:
/pmc/articles/PMC5803962/
6. Singh N, Gupta RK, Multani MK, Singh S. A Case of Acquired Ventricular
Septal Defect Complicating Silent Myocardial Infarction: An Unusual
Presentation. Hear India [Internet]. 2015 [cited 2023 Jul 30];3(1):24.
Available from: https://www.heartindia.net/article.asp?issn=2321-
449x;year=2015;volume=3;issue=1;spage=24;epage=26;aulast=Singh
7. Spicer DE, Hsu HH, Co-Vu J, Anderson RH, Fricker FJ. Ventricular septal
defect. Orphanet J Rare Dis [Internet]. 2014 Dec 19 [cited 2023 Jul
30];9(1):144. Available from:
https://ojrd.biomedcentral.com/articles/10.1186/s13023-014-0144-2
8. Ismail MT, Hidayati F, Krisdinarti L, Noormanto, Nugroho S, Wahab AS.

35
 Epidemiological Profile of Congenital Heart Disease in a National Referral
Hospital. J Acta Cardiol Indones. 2015;1(2):66–71.
9. Dakkak W, Oliver T. Ventricular Septal Defect. StatPearls [Internet]. 2023
[cited 2023 Jul 23]; Available from: https://www.statpearls.com/point-of-
care/31090
10. Nayak, S., Patel, A., Haddad, L., Kanakriyeh, M., & Varadarajan, P. (2020).
Echocardiographic evaluation of ventricular septal defects.
Echocardiography, 37(12), 2185–2193. doi:10.1111/echo.14511
11. Al-Hijji MA, Kelle AM, Park JY, Dearani JA, Taggart NW. Delayed
Repercussions of Blunt Trauma: Isolated Muscular Ventricular Septal
Defect. CASE [Internet]. 2017 Feb 1 [cited 2023 Jul 30];1(1):11–3.
Available from:
http://www.cvcasejournal.com/article/S2468644116300226/fulltext
12. Ryan L, Skinner DL, Rodseth RN. Ventricular septal defect following blunt
chest trauma. J Emerg Trauma Shock [Internet]. 2012 Apr [cited 2023 Jul
30];5(2):184. Available from: /pmc/articles/PMC3391845/
13. Tochii M, Watanuki H, Sugiyama K, Futamura Y, Ishikawa H, Matsuyama
K. Ventricular septal rupture after blunt chest trauma: a case report. Surg
Case Reports 2022 81 [Internet]. 2022 May 12 [cited 2023 Jul 30];8(1):1–4.
Available from:
https://surgicalcasereports.springeropen.com/articles/10.1186/s40792-022-
01448-z
14. Durden R, Turek J, Reinking B, Bansal M. Acquired ventricular septal
defect due to infective endocarditis. Ann Pediatr Cardiol [Internet]. 2018
Jan 1 [cited 2023 Jul 30];11(1):100. Available from:
/pmc/articles/PMC5803962/
15. Singh N, Gupta RK, Multani MK, Singh S. A Case of Acquired Ventricular
Septal Defect Complicating Silent Myocardial Infarction: An Unusual
Presentation. Hear India [Internet]. 2015 [cited 2023 Jul 30];3(1):24.
Available from: https://www.heartindia.net/article.asp?issn=2321-
449x;year=2015;volume=3;issue=1;spage=24;epage=26;aulast=Singh
16. Bradley, Scott M. "Ventricular Septal Defects (VSD)." Adult and Pediatric

36
 Cardiac Surgery. STS Cardiothoracic Surgery E-Book, Chicago: Society of
Thoracic Surgeons, 2022. STS Surgery, ebook.sts.org.
17. Lilly L. Pathophysiology of Heart Disease. 6th editio. Lilly L, editor.
Philadelphia: Wolters Kluwer; 2015. 479 p.
18. Han Yee Yu M, Roubertie F, Henaine R, Iriart X, Jalal Z, Thambo JB, et al.
Surgical closure of ventricular septal defect in adults: A multicenter study.
Arch Cardiovasc Dis Suppl. 2018 Jan 1;10(1):133.
19. Elsaka, Omar & GHAZALI, MOSTAFA & AL-RAZIK, ASHRAF &
HISHAM, DALIA & ALGAMAL, ABDULSALAM. (2021).
PATHOPHYSIOLOGY, INVESTIGATIONS, AND MANAGEMENT OF
VENTRICULAR SEPTAL DEFECT. 10.5281/zenodo.6408962.
20. Sreedhar R. Acyanotic congenital heart disease and transesophageal
echocardiography. Ann Card Anaesth. 2017 Jan;20(Supplement):S36-S42.
doi: 10.4103/0971-9784.197795. PMID: 28074821; PMCID: PMC5299826.
21. Ivander A, Adriansyah R, Tanjung ICD, Raynaldo AH. Perbandingan
Penutupan Ventricular Septal Defect secara Transkateter dengan
Pembedahan pada Anak: Telaah Sistematis dan Meta Analisis. Scr SCORE
Sci Med J. 2022;3(2):159–73.
22. Maisat W, Sawasdiwipachai P, Aroonrat W, Lapmahapaisan S.
Measurement of aortic root dimensions by transesophageal
echocardiography in adult patients undergoing cardiac surgery. Ann Card
Anaesth. 2020 Oct-Dec;23(4):409-413. doi: 10.4103/aca.ACA_114_19.
PMID: 33109795; PMCID: PMC7879907.
23. Abdelnabi M, Almaghraby A. Ventricular septal defect causing tricuspid
regurgitation with consequent pulmonary hypertension and right ventricular
hypertrophy. The Southwest Respiratory and Critical Care Chronicles
2021;9(40):77–78
24. Fox, K.R., Hardy, R.Y., Moons, P. et al. Smoking among adult congenital
heart disease survivors in the United States: Prevalence and relationship
with illness perceptions. J Behav Med 44, 772–783 (2021).
https://doi.org/10.1007/s10865-021-00239-5
25. Moons, P., Luyckx, K., Kovacs, A. H., Holbein, C. E., Thomet, C., Budts,

37
 W., … Apers, S. (2019). Prevalence and effects of cigarette smoking,
cannabis consumption and co-use in adults with congenital heart disease
from 15 countries. Canadian Journal of Cardiology.
doi:10.1016/j.cjca.2019.07.635
26. Trongtorsak A, Kittipibul V, Antala D, Meng Q, Puwanant S. Heart Failure-
Related Ascites With Low Serum-Ascites Albumin Gradient: Diagnostic
Clues From Triphasic Abdominal Computed Tomography. Cureus. 2022
Jan 14;14(1):e21251. doi: 10.7759/cureus.21251. PMID: 35178310;
PMCID: PMC8842280.
27. Rajyaguru, C., Kalra, A., Samim, A., Abeije, B., Wessel, R., & Vempilly, J.
J. (2017). Mechanism of Pleural Effusion in Heart Failure: The Role of
Diastolic Dysfunction and Misconception of Systolic Function. Journal of
Cardiac Failure, 23(8), S42. doi:10.1016/j.cardfail.2017.07.116
28. Chao, P., Cui, X., Wang, S. et al. Serum albumin and the short-term
mortality in individuals with congestive heart failure in intensive care unit:
an analysis of MIMIC. Sci Rep 12, 16251 (2022).
https://doi.org/10.1038/s41598-022-20600-1
29. Khan TM, Patel R, Siddiqui AH. Furosemide. [Updated 2023 May 8]. In:
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-.
Available from: https://www.ncbi.nlm.nih.gov/books/NBK499921/
30. Werner Budts and others, Treatment of heart failure in adult congenital
heart disease: a position paper of the Working Group of Grown-Up
Congenital Heart Disease and the Heart Failure Association of the European
Society of Cardiology, European Heart Journal, Volume 37, Issue 18, 7
May 2016, Pages 1419–1427, https://doi.org/10.1093/eurheartj/ehv741
31. Bhasin S, Gogia P, Nair R, Sahoo TK. Perioperative sildenafil therapy for
children with ventricular septal defects and associated pulmonary
hypertension undergoing corrective surgery: A randomised clinical trial.
Indian J Anaesth. 2017 Oct;61(10):798-802. doi: 10.4103/ija.IJA_210_17.
PMID: 29242651; PMCID: PMC5664884.
32. Eckerström F, Nyboe C, Maagaard M, Redington A, Hjortdal VE. Survival
of patients with congenital ventricular septal defect. Eur Heart J. 2023 Jan

38
1;44(1):54-61. doi: 10.1093/eurheartj/ehac618. PMID: 36418929; PMCID:
PMC9805405.

39