VENTRICULAR SEPTAL DEFECT

Zaipullah S
C111 13 046

Supervisor
dr. Andi Alief Utama Armyn, M.Kes, Sp.JP

Department Of Cardiology And Vascular Medicine

Medical Faculty Of Hasanuddin University
Makassar
2016
 Patient Identity

Name : Tn. PS
Age : 37 years old
Gender : male
Address : Fak-Fak papua
Medical Record : 791272
Admitted : April 6th, 2017
 History Taking
Chief complaint : Shortness of breath and fatigue
Shortness of breath has been experienced since two days ago before
admitted to the hospital. It was experienced while doing activities,
intermitten and not influence by position. Patient complained fatigue, left
chest feels full while doing activities, sometimes stabbing left chest pain
but improved with rest.
PND (-), fever (-), nausea and vomitting (-), palpitate (-), cold sweat (-)
Patient was hospitalized with the same complaint on february 2017.
History of smoking since over 10 years ago
The patient denial history of hypertension, diabetes mellitus and renal
disease
No history of heart disease in family
 Physical Examination
General moderate illness/well
Nourished/composmentis
status GCS E4M6V5

Blood pressure 130/80 mmHg

Vital status Heart rate 90 bpm

Respiratory rate 22 tpm
Temperature 36,7 oC

Head and anemic (-), Icteric (-/-)

Neck JVP R+2 cm H2O

 Thorax

inspection Normochest, Symmetry left = right

Mass (-), tenderness (-), cracless (-),

palpation normal vocal fremitus

sonor, lung liver border in ICS VI right

percussion anterior.

auscultation Vesicular, ronchi -/-, wheezing -/-

 Cor
inspection Ictus cordis not visible

palpation Thrill (+) ICS III-IV left parasternal line and ICS V
left midclavicula line, ictus cordis not palpable

Upper border 2nd ICS sinistra, Right border 4th ICS

percussion linea parasternalis dextra, Left border 5th ICS linea
axillaris anterior sinistra

auscultation S1/SII reguler, : systolic murmur ICS III-IV left

parasternal line and ICS V left midclavicula line
 Abdomen

inspection Flat, follow breath movement

auscultation Peristaltic (+) normal

Mass (-), Hepar and lien not

palpation palpable

percussion Ascites (-)

Extremities examination

Pretibial edema -/-

cyanosis (-)
X-ray Thoracs
Interpretation:

Cardiomegaly and
pulmonary oedema
sign
 Electrocardiography
Interpretation
Sinus rhytm
HR: 83 bpm
Regular
P wave : 0,08
PR interval : 0,20
QRS complex : 0,06,
SV1+RV5=41
Axis : normoaxis
ST segmen : normal
T wave : normal

Conclussion : Sinus rhytm, HR:75 bpm, LVH

Electrocardiography
 Laboratory Finding

TEST RESULT NORMAL VALUE TEST RESULT NORMAL VALUE

WBC 8.3 x 103/uL 4.0 11.0 x 103 SGOT 22 u/L <38
RBC 5.11 x 106/uL 4.0 6.0 x 106 SGPT 30 u/L <41
HGB 15 g/dL 12 16 Ureum 26 10-50
HCT 43 % 37 48 Creatinine 1.09 0,5-1,2
PLT 199 x 103/uL 150 400 x 103 Natrium 134 136 - 145
Kalium 3.9 3,5 - 5,1
Chloride 96 97 - 111
Echocardiographi
Normaly of systolic function ,
EF 57 %
Dilatasi LV and LA
VSD subaortic diameter 0.5
cm, L-R shunt
Hipertrofi LV eksentrik
 Diagnosis

Ventricular Septal Defect

 Management & Planning

O2 3 LPM via nasal kanul

IVFD NaCL 0,9% 500 cc/24h/iv
Antibiotic Ceftriaxon 2 g/24h/iv
diuretic Furosemide 40 mg/24h/iv

Plan :
VSD closure Amplatzer muscular VSD Occluder
(AMVO)
DISCUSSION
WHAT IS HEART FAILURE ?

A syndrome in which the patients should have the following features:

symptoms of HF, typically shortness of breath at rest or during
exertion, and/or fatigue; signs of uid retention such as pulmonary
congestion or ankle swelling, and objective evidence of an
abnormality of the structure or function of the heart at rest.
Physiology
Aetiology
CAUSE
Pathophysiology
Cardiac Output

Compensation mechanism :
1. Adrenergic system
2. Neurohormonal
activation
3. Myocyte growth HEART
FAILURE
 How to Diagnose
Framingham Heart Study
MAJOR CRITERIA MINOR CRITERIA

Paroxysmal nocturnal Edema extremities

dyspnea Cough at night
Rhonchi Hepatomegaly
HEART FAILURE if 2 major criteria or
1 major criteria and 2 minor criteria Lung edema Dyspnea d effort
Cardiomegaly Pleural effusion
Gallop S3 Tachycardia
Venous distention
Hepatojugular reflux
Increase vena jugularis
pressure
How to Diagnose
- Laboratory
- Electrocardiography
- Chest X-Ray
- Echocardiography
- Biomarker
Classification
Treatment

The aims of treatment

Treating the cause of heart failure
improving contractile performance (by enhancement of the
intrinsic contractile properties or by decreasing afterload);
decreasing peripheral demands for cardiac output.
Treatment

Lifestyle changes
Modify daily activities and get enough rest to avoid stressing the heart
Eat a heart-healthy diet that is low in sodium and fat
Don't smoke and avoid exposure to second-hand smoke
Don't drink alcohol or limit intake to no more than one drink two or three times a week
Lose weight
Avoid or limit caffeine intake
Get regular exercise, which may include a physical rehabilitation program, once symptoms are stable
Reduce stress
Weigh yourself daily, for a sudden increase may signal fluid build-up
Keep track of symptoms and report any changes
Have regular checkups to monitor the condition
Treatment
Medication
Angiotensive converting enzyme (ACE) inhibitors
Beta-blockers.
Diuretics
Potassium and magnesium supplements Digoxin.
Anti-arrhythmic
Medication for underlying disease
Treatment
Surgery
Heart transplantation
Surgery for underlying disease
Ventricular Septal Defect

Defenition

This type lesion consists of an opening between left

ventricel (LV) and the right ventricel (RV), caused by a defect in
the wall that separates these two cambers, the interventricular
septum (IVS)
Anatomy

The ductus arteriosus derives from the

left sixth primitive aortic arch and
connects the proximal left pulmonary
artery to the descending aorta, just distal
to the left subclavian artery.
classification
 Pathophysiology

Hypertensive
Pulmonary
Left to Right Pulmonary Pulmonary
overcirculatio
Shunt edema vascular
n
disease

Increase
Increased
stroke Increase flow
Congestive contractility
volume and return to left
Heart Failure and heart
hypertrophy heart
rate
LV
 Clinical Features

Sign and Symptom

fatigue
Short of breath, takipneu
cyanosis ( late sign ) ( Eisenmenger Sindrom)

Physical Examination
systolik murmur ICS III-IV left parasternal line and
ICS V left midclavicula line ( apeks )
 Examination
Chest Radiograph Normal in small defects, cardiomegaly and
increased pulmonary vascular markings in moderate defects,
marked cardiomegaly and pulmonary oedema seen in large
defects.
ECG ECG is normal in small VSDs, shows signs of LA dilatation
and LV hypertrophy in moderate VSDs, and evidence of
biventricular hypertrophy in large VSDs.
Echocardiogram It is usually the only imaging modality
required to determine the diagnosis, size and location of a VSD,
and can also provide information about chamber size, wall
thickness, estimates on right ventricular and pulmonary artery
pressures, as well as any associated anomalies.
 Examination
Cardiac Catheterization Not routinely necessary, can be
performed when there are remaining questions about
anatomy and pulmonary vascular resistance and its response
to therapy.
Haematoly Typically normal, except for patients with
Eisenmenger syndrome, who may develop polycythaemia,
thrombocytopenia and coagulopathy as complications of
cyanosis.
 Complication

Congestive Heart Failure

Hypertensive Pulmonary Vascular Disease

Endocarditis
 Treatment

30-40% of muscular and membranous VSDs close within

the first 6 months or become smaller with age. Inlet and
outlet VSDs do not close spontaneously or get smaller with
age.
Medications, such as diuretics and ACE inhibitors,
VSDs can be closed surgically . Some muscular VSDs may
be closed with a device in the cath lab.
No activity restrictions or long-term medications are
needed for children who have spontaneous closure or
surgical repair of their VSDs in the absence of other heart
disease.
 Closure of VSD
Transcatheter

Treatment of choice
Amplatzer Muscular VSD Occluder (AMVO)

Surgical
THANK
YOU