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VENTRICULAR SEPTAL DEFECT

Present By
Nur Kurnia Putri Halim

Supervisor
dr. Akhtar Fajar M , SpJP, FIHA
PATIENT’S IDENTITY

• Name : Mrs. KM
• DOB : March 29th 1994(21 yo)
• Adress : Pangkep
• Medical Record :479121
• Admission Date : November 12th 2015
HISTORY TAKING

• Chief Complaint : Shortness of breath


• Present Illness History :
• Suffered since 1 week before admitted to Wahididn
general hospital, intermittent. Other complaint includes
heart throb, fatigue and lack of appetite Pain at
epigastrium (+), DOE (+) , PND (-), ortopneu (-),chest
pain (-).Fever (-) ,Nausea (+), vomiting (-),cough (-),
heartburn (-) . Defecation and urination is normal
HISTORY TAKING

• Past Illness History :


• No past illness

• Famly illness history :


• No family with history of heart disease
PHYSICAL EXAMINATION

• General Status
• Moderate illness/ Normoweight/ Compos Mentis
• Vital Status
• Blood pressure : 100/70 mmHg
• Heart rate : 88 x/m
• Respiratory rate : 20 x/m
• Temperature : 36,5 oC
HEAD AND NECK
• No anemic, no icteric
• No cyanosis
• JVP R+1cmH20

LUNG
• Inspection : Symmetry left=right
• Palpation : Mass (-), no tenderness
• Percussion : Sonor
• Auscultation : Vesicular
Rhonchi -/-, wheezing-/-
HEART
• Inspection : Ictus cordis invisible
• Palpation : Ictus cordis isn’t palpable
• Percussion : normal heart size
• Upper border 2nd ICS sinistra
• Right border 4th ICS linea parasternalis dextra
• Left border 5th ICS linea axillaris anterior sinistra
• Auscultation : Heart sound I/II regular, murmur (+) sistolik gr 4/6
LLSB

ABDOMEN
• Inspection : flat, follows breath movement
• Auscultation : peristaltic (+), normal
• Palpation : liver and spleen not palpable
• Percussion : tympani, ascites (-)

EXTREMITIES
• No edema
ELECTROCARDIOGRAM
• Heart rate : 87x/min, reguler
• P wave : 0.08’
• PR interval : 0.12’
• Axis :normoaxis
• QRS complex
• Duration : 0.08’
• ST segment : Normal
• T wave : Normal

• conclusion :
• Sinus rhythm , HR 87 bpm, normoaxis
RADIOLOGY (CXR)
• Cardiomegaly (cti 0.54
) with left to right shunt
ECHOCARDIOGRAPHY

• Sistolyc and diastoloc


function of left ventricle is
good
• Sistolic function of right
ventricle is good
• Moderate tricuspid
regurgitation
• Modarate pulmonal
hypertenison
• VSD Perimembran
• MSA (+)
Result Normal Values

RBC 4,18.106/mm3 (4,5 - 6,5).106/mm3

HGB 13.0 g/dL 12 - 16 g/dL

WBC 8.2/mm3 (4 - 10).103/mm3

PLT 228.103/mm3 (150 - 500).103/mm3

GDS 97 mg/dl 140 mg/dL

Ureum 28 mg/dL 10 - 50 mg/dL

Kreatinin 0.67 mg/dL < 1,3 mg/dL

SGOT 14 U/L < 38 U/L

SGPT 3 U/L < 41 U/L

Natrium 141 mmol/L 136-145 mmol

Kalium 3,7 mmol/L 3.5-5.1 mmol

Klorida 110 mmol/L 97-111mmol


RESUME
• A girl 21 years old came to the hospital with shortness of breath
since 1 week before admitted to hospital, intermittent.Other
complaint inculude heart throb, fatigue, and lack of appetite. Pain at
epigastrium (+), DOE (+),Nausea (+).

• From physical examination of the heart it is found a systolic murmur


gr 4/6 at the LLSB.

• The additional diagnostic test shows radiology result cardiomegaly


(CTI 0,54) with left to right shunt. Echocardiogram result Sistolyc
and diastoloc function of left ventricle is good, Sistolic function of
right ventricle is good ,Moderate tricuspid regurgitation, Modarate
pulmonal hypertenison, VSD Perimembran, MSA (+).
WORKING DIAGNOSIS

• Ventricular Septal Defect


• Dispepsia
INITIAL MANAGEMENT

• O2 2-4 L/min ( via nasal canule )


• NaCl 0,9% 500 cc/24 hours/iv
• Ranitidin 50 mg/12 hours/ iv
• Domperidone 1 tab/ 8 hours/ oral
PLANNING

• Evaluation of vital signs


• Angiography coroner
VENTRICULAR SEPTAL DEFECT
Definition • 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.
ANATOMY
CLASSIFICATION
Small VSD :

• defect smaller than 1/3 of anulus aorta

Moderate VSD :

• defect ½ of annulus aorta.

Large VSD :

• defect more equal to annulus aorta


• At present, a multifactorial etiology based on an
interaction between hereditary predisposition and
environmental influences is assumed to cause the
defects.
Maternal factors
• Maternal diabetes
• Alcohol consumption

Genetic risk factors


• A family history of a cardiac or noncardiac defect
• Familial congenital heart defects
Pansistolik murmur

Increase RV vol
LV pressure > RV Left to right
VSD (hipertrophy,dila
pressure shunt
tation)

Increase
RV pressure > LV Pulmonary Increase vessel
pulmonary
pressure hipertension resistance
blood flow

cyanosis
Right to left
shunt LV volume
(esenmenger overload
syndrome)
Small defects

• asymptomatic

Medium defects (uncommon)

• associated with protective valvular or subvalvular pulmonary


stenosis
• dyspnea

Large VSDs (infancy)

• heart failure surgery


• pulmonary stenosis
• pulmonary hypertension (the Eisenmenger syndrome).
• Cyanosis, dyspnea, and syncope .
• diastolic murmur of aortic regurgitation
Eisenmenger
Small VSDs Moderate VSDs Large VSDs
syndrome/VSD +
severe pulmonary
• normal vital signs • thrill • signs of CHF vascular disease
• Physiologic • pansystolic harsh • tachycardia, • tachypnea only
splitting of S2 murmur lower tachypnea, and with exercise and
• harsh, pansystolic LSB , lower pitch hepatomegaly, not at rest.
murmur compare to small • cardiomegaly • mildly cyanotic at
LSB(well VSD • pansystolic rest but profound
localized) murmur (poorly cyanosis with
• Small defects  localized) + exercise.
high pitched or diastolic rumble.
squeaky noise
Chest
radiography

Magnetic
resonance
Echocardiography imaging

Additional (MRI)

Examinati
on

Cardiac Electrocardiography
catheterization (ECG)
Observation & follow up
• Small VSDs

Medical management
• Medium sized vsd
• CHF- treat with diuretics, ACEI
• 2-3 months follow up
• RV & PAH pressures assessed

Surgical
• Large vsd
• Furosemide 1–3 mg/kg per day
• Digoxin 10-20mcg/kg per day
• Captopril 0.5–2 mg/kg per day
• Large VSD with pulmonary hypertension
• VSD with aortic regurgitation
• VSD with associated defects
• Failure of congestive cardiac failure to respond to
medications
THANK YOU

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