 Name : Mrs.

MA
 Age : 24 years old
 Gender : Female
 Address : Toloa, South Tidore
 Medical Record : 783092
 Admitted : December 20th, 2017
 Chief complaint : Shortness of breath
 Shortness of breath has been
experienced since childhood and
worsened since a few month before
admitted to the hospital. There is
shortness of breath during activity. No
shortness of breath while lying down. No
history of chest pain. Patient has known
her illness since childhood. No nausea
and vomitting
General Status :
› Moderate ill
› Nutritional Status : Good (BMI : 24,97 kg/m²)
 Weight : 60 kg
 Height : 1,55 m
› Consciousness : Conscious
Vital Sign
› Blood Pressure : 100/60 mmHg
› Pulse Rate : 90 bpm
› Respiratory Rate : 16 rpm
› Temperature : 36.4 °C
Head and Neck Examination
› Eye : conjunctia anemic (-/-), sclera icteric (-/-)
› Lip : cyanosis (-)
› Neck : no mass, no tenderness, JVP R+2 cmH2O
Chest Examination
› Inspection : symmetric left = right
› Palpation : no mass, no tenderness, vocal
fremitus left=right
› Percussion : sonor left=right, lung-liver border in
ICS VI right anterior
› Auscultation : breath sound:vesicular ; additional
sound: ronkhi (-), wheezing (-)
Cardiac Examination
› Inspection : apex was not visible
› Palpation : apex was not palpable
› Percussion : right heart border in right
parasternal line, left heart border in left
midclavicularl line ICS V
› Auscultation : heart sound : S I/II regular;
additional sound: continous murmur at
upper left sternal border
Abdominal Examination
› Inspection : flat, following breath movement
› Auscultation : peristaltic sound (+), normal
› Palpation : no mass, no tenderness, no
palpable liver and spleen
› Percussion : tympani (+), ascites (-)
Extremities Examination
› Pretibial edema (-/-)
› Dorsum pedis edema (-/-)
› Cyanosis (-)
 Interpretation
 Sinus rhytm
 HR: 83 bpm
 Regular
 P wave : 0,08”
 PR interval : 0,08”
 QRS complex :
0,10”, SV1+RV5=43
 Axis : normoaxis
(55,6°)
 ST segmen : normal
 T wave : normal

Conclussion : Sinus rhytm, HR:83 bpm, LVH

TEST RESULT NORMAL TEST RESULT NORMAL
VALUE VALUE
WBC 7,6 x 103/uL 4.0 – 11.0 x 103 SGOT 21 u/L <38
RBC 4,93 x 106/uL 4.0 – 6.0 x 106 SGPT 42 u/L <41
HGB 13,7 g/dL 12 – 16 Ureum 26 10-50
HCT 41 % 37 – 48 Creatinine 0,63 0,5-1,2
PLT 233 x 103/uL 150 – 400 x 103 Natrium 143 136 - 145
Kalium 3.1 3,5 - 5,1
Chloride 100 97 - 111
Patent Ductus Arteriosus
 IVFD  NaCL 0,9% 500 cc/24h/iv
 Antibiotic  Ceftazidine 1 g/12h/iv
 Diuretic  Furosemide 40 mg/24h/oral

 Duct closure  Amplatzer Duct

Occluder (ADO)
PATENT DUCTUS ARTERIOSUS
 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.
 1 in 2000 birth  5% to 10 % of all
congenital heart disease
 Include silent PDA  1 in 500 birth
 Female : male  2 : 1
 Premature
 Genetic abnormalities
 Infection and environmental factor
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.
 Left to Right Pulmonary Pulmonary
Shunt overcirculation edema

Hypertensive
Increase stroke Increase flow
Pulmonary
volume and return to left
vascular
hypertrophy LV heart
disease

Increased
Congestive
contractility
Heart Failure
and heart rate
 Silent: tiny PDA detected only by nonclinical means
(usually echocardiography)
 Small: continuous murmur common; Qp/Qs < 1.5 : 1
 Moderate: continuous murmur common; Qp/Qs of
1.5 to 2.2 : 1
 Large: continuous murmur present; Qp/Qs > 2.2 : 1
 Eisenmenger: continuous murmur absent;
substantial pulmonary hypertension, differential
hypoxemia, and differential cyanosis (pink fingers,
blue toes)
A. Type A (“conical”) ductus, with well-
defined aortic ampulla and constriction
near the pulmonary artery end.
B. Very large type B (“window”) ductus,
with very short length.
C. Type C (“tubular”) ductus, which is
without constrictions.
D. Type D (“complex”) ductus, which has
multiple constrictions.
E. Type E (“elongated”) ductus, with
theconstriction remote from the anterior
edge of the trachea.
Symptoms
 Small PDA  asymptomatic
 Moderate  fatigue, dyspnea, palpitation
 Large  CHF with tachycardia, poor feeding, slow
growth, recurrent lower respiratory tract infection

Physical Examination
 continuous, machine-like murmur
 lower extremity cyanosis and clubbing
 Chest Radiograph  Normal,
cardiomegaly , calcification of the
ductus
 ECG  Normal, sinus tachycardia, atrial
fibrillation, left ventricular hypertrophy,
left atrial enlargement
 Echocardiogram  Confirm diagnosis
and to characterize teh PDA
 MRI and CT  degree of calcification
 Cardiac Catheterization  unnecessary
for diagnostic purposes
 Angiography  abnormal flow of blood
through the PDA. Detailed assessment of
the ductal anatomy
 Congestive Heart Failure

 Hypertensive Pulmonary Vascular

Disease

 Endarteritis
 Infective arteritis was reported to be 1%
per year
 Improved availability of health care,
widespread use of antibiotics,
 Vegetations usually occur on the
pulmonary artery end of the ductus, and
embolic events are usually of the lung
rather than the systemic circulation
 Diuretic and digoxin
 After load reduction  ACE Inhibitor
 Antidysrhythmia
 Endarteritis prophylaxis
Transcatheter Surgical

 Treatment of choice  Ductal ligation or

 Amplatzer Duct division
Occluder (ADO)  Very Large PDA
 No device closure
 Examined periodically for possible
recanalization
 Silent residual shunts may be found by
transthoracic echocardiography.
 Endocarditis prophylaxis is
recommended for 6 months after PDA
device closure or for life if any residual
defect persists
 Isolated PDA  Excellent
 Adult  more dependent on the
condition and status of pulmonary
vascular and myocardium