DR J P SONI Professor and Head of the Department Pediatrics Division of Pediatric Cardiology DR S N Medical College Jodhpur Doc_jpsoni@yahoo.com

1. DR J P SONI
Professor and Head of the Department Paediatrics
Division of Pediatric Cardiology
DR S N Medical College
Jodhpur
Doc_jpsoni@yahoo.com

2. P D A

3. Acyanotic CHD’s
ACYANOTIC
CHDS
PURE
ACYANOTIC
POTENTIALLY
CYANOTIC

4. Acyanotic
CHD
Without shunt(normal
or decreased flow)
Right side of heart
PULMONARY
STENOSIS
Left side of heart
AORTIC STENOSIS
COARCTATIONOF
AORTA
L-> R SHUNT ↑ PBF
ASD
VSD
P.D.A.
Aorto-pulmonary
Window

5. The human embryonic period proper is divided into 23 Carnegie stages
covering the first 8 weeks post-ovulation
The arterial duct exists bilaterally on both right and
left sides at Carnegie stage 16 (37-40 days of post
embryonic gestation).
After stage 16, the right-sided arterial duct is atrophied
and the right dorsal aorta is obliterated at stage 18 (44-
48 days).
At the end of arch development (stage 23; 56-60 days)
the arterial duct connects to the aortic arch just distal
to the left subclavian artery.

6. The ductus embryologically originates from the distal portion of one of the six aortic arches and
its persistence, site, and course are closely associated with the development of the aortic arch.
Commonly seen on the left side even in a patient with right sided arch, the ductus can connect
either the proximal right or left pulmonary artery to virtually any location on the aortic arch or
proximal portion of the brachiocephalic artery. Rarely right sided ductus between the right
brachiocephalic and right pulmonary artery forms PDA.
In fetus PDA is kept open by -
1. Low PO2 in ductus arteriosus Pao2 18mmHg
2. Prostaglandin E produce by placenta
3. Local production of Prostaglandin PGE2 and PGI2
4. Nitrous Oxide (NO) produce by vasa vasorum of ductus arteriosus
5. High intra luminal pressure in Ductus because of solid lung
Intra-uterine fetal PDA can contract if mother ingest Nonsteroidal anti inflammatory drugs
Like indomethacin, ibuprofen, Rubia cardifolia and Polyphenols – Chocolates, grape and red wine.
This will produce PAH, PR, TR, dilated RV and RA and hepatomegaly at birth.

7. Functional closure of the ductus arteriosus occurs in almost 50% of full-term infants
by 24 hours, in 90% by 48 hours, and in all by 72 hours after birth. In healthy preterm
infants of ≥30 weeks’ gestation, duct closure occurs by the fourth day after birth,
while preterm infants of <30 weeks’ gestation, with severe respiratory distress, have a
65% incidence of PDA beyond the fourth day of life.
A prospective study demonstrated a spontaneous closure of the PDA in the first 10
days of life in at least 35% of extremely low-birth-weight (ELBW) infants and up to
70% in neonates of >28 weeks’ gestation.
There was a direct relationship between gestational age and spontaneous closure and
for each additional week above 23 weeks, the odds of spontaneous closure increased
by a ratio of 1.5. Among infants of <27 weeks’ gestation with a persistent PDA at the
time of hospital discharge, 75% of the infants will spontaneously close their PDA by
the end of the first year

8. The main provider of nutrients to the DA is the lumen; however, the vasa vasorum is also a
substantial provider to the outer wall of the ductus. The vasa vasorum grows toward the lumen and
extends 400–500 μm from the outer wall of the ductus. The distance between the lumen and the
vasa vasorum (40–500 μm) is referred to as the avascular zone and represents the maximum
distance allowable for effective nutrient diffusion. In full-term infants, this avascular zone is
expanded beyond the effective diffusion distance, therefore contributing to cell death. In preterm
infants, the avascular zone does not sufficiently expand, resulting in cell survival and maintenance of
ductal patency.

9. As the ductus constricts, the luminal area is diminished, resulting in a thickened vessel
wall and obstructed flow through the vasa vasorum, the essential capillary network
nourishing the outer cells of the vessel. This causes an increased distance of diffusion
for oxygen and nutrients, including glucose, glycogen, and adenosine triphosphate
(ATP), which results in nutritional deficit and oxygen starvation, leading to cell death.
Ductal constriction in preterm infants is not sufficiently profound. Consequently,
preterm infants are resistant to smooth muscle hypoxia, which is paramount in
triggering the cell death and remodeling required for permanent closure of the DA.
Inhibition of prostaglandin and nitric oxide resulting from tissue hypoxia is not as
extensive in the preterm neonate in comparison to the term infant, further
contributing to resistance to DA closure in the preterm infant. the levels of circulating
PGE2 and other prostaglandins are decreased through COX inhibition, closure is
facilitated.

10. Patent ductus arteriosus (PDA) constitutes 5%–10% of all congenital heart defects with a
prevalence of “symptomatic” PDA being 0.5/1000 live births. Clinical manifestations depend on
the diameter and length of PDA and the relative systemic and pulmonary vascular resistances.
Frequency of patent ductus increases with decreasing gestational age and decreasing birth
weight.
After birth PDA closes because of -
1. High PO2 in ductus arteriosus PaO2 100 mmHg
2. Placenta is cut & removed thus Prostaglandin E produced by placenta is not there.
3. Local production of Prostaglandin PGE2 and PGI2 also decreases
4. Nitrous Oxide (NO) produce by vasa vasorum of ductus arteriosus decreases
5. Intra luminal pressure in Ductus decreases because 1. Lung Expands 2. Pulmonary vasculature
dilates and Pulmonary flow increases.

11. It is a connection between the aorta and the pulmonary artery.
During intrauterine life, 10% of the cardiac output passes through the lungs. The remaining 90%
is shunted via the ductus arteriosus (DA) to the aorta and systemic circulation.
After birth, most of the right ventricular output pass through the lungs to facilitate proper gas
exchange. In order to make this possible, the ductus undergoes spontaneous constriction and
functional closure soon after birth in term neonates.
Eighty percent (80%) of the DA in term infants close by 48 hours and nearly 100% by 96 hours.
Among preterm babies it usually closes by the first 2 weeks of life.
Failure of this normal closure results in problems especially in preterm neonates.
Frequency of patent ductus decreases with increasing gestational age and increasing birth
weight.

12. Almost all healthy new born’s of 30 weeks of gestational age and greater, duct closure will
occurred by fourth day after birth.
GESTATIONAL
AGE WEEKS
INCIDENCE PDA OPEN HEALTHY NEW BORN
24 24 - 48 48 - 72 72 - 96
≤ 29 80 40 20 7
30-33 97 31 13 0
34-37 96 42 12 4
38-40 85 50 5 0
≥ 40 55 0 0 0
Patent ductus arteriosus (PDA) is a major morbidity encountered in preterm neonates, especially in babies less than 28 weeks
gestation or 1000g. It may close spontaneously in preterm neonates. However, failure to close spontaneously in preterm
neonates results in significant mortality and morbidity.

13. In preterm infant the incidence of PDA depend on how small is the infant and the respiratory
condition after birth.
Every third preterm infant with a birth weight (BW) of 501 to 1500 g (very low birth weight -
VLBW) is expected to have a persistent PDA . Furthermore, 55% of infants who weigh <1000 g
(extremely low birth weight, ELBW) have been described to have a symptomatic PDA that needs
medical treatment.
Spontaneous permanent ductus arteriorsus closure occurs in about 34% of ELBW neonates
between 2 to 6day postnatal days and in the majority of VLBW neonates within the first year of
life.
Spontaneous closure rate of PDA in preterm neonates varies from 35% to 75% in the 1st year of
life.
Small PDAs in full-term neonates may close up to 3 months of age, whereas large PDAs are
unlikely to close spontaneously.
Rate of spontaneous closure of PDA after infancy is 0.6% per year.

14. Patent ductus arteriosus (PDA) constitutes 5%–10% of all congenital heart defects
with a prevalence of “symptomatic” PDA being 0.5/1000 live births
Clinical manifestations depend on the diameter and length of PDA and the relative systemic and
pulmonary vascular resistances.
In the historic study by Dr. Paul Wood’s, 79% of patients with large PDA had onset of
Eisenmenger syndrome in infancy.

15. PDA : median ductal diameter in infant < 29 weeks with increasing postnatal age
POST NATAL AGE hours MEDIAN DUCT DIA METER
mm
TWO 2 mm
SIX 1.8 mm
NINE 1.6 mm
TWELVE 1.3 mm

16. P D A Epidemiology
The incidence of PDA in children who are born prematurely is 20% in premature infants > 32 weeks' gestation
up to 60% in those < 28 weeks' gestation, children with a history of perinatal asphyxia, and, possibly, children
born at high altitude.
In addition, up to 30% of low birth weight infants (< 2500 g) develop a patent ductus arteriosus (PDA).
Siblings also have an increased incidence.
Perinatal asphyxia usually only delays the closure of the ductus, and, over time, the ductus typically closes
without specific therapy.
As an isolated lesion, patent ductus arteriosus (PDA) represents 5-10% of all congenital heart lesions. It occurs
in approximately 0.008% of live premature births.
There is a female preponderance (female-to-male ratio, 2:1).
In patients in whom the patent ductus arteriosus (PDA) is associated with a specific teratogenic exposure, such
as congenital rubella, the incidence is equal between the sexes.

17. • Symptoms :
• a) None if small
b) If large can cause CHF at 6-8 weeks in a term infant
c) In a preterm baby increasing respiratory support usually occurs after day 3 of life.

18. PDA
Pul A.
Pul V.
LA
LV
Aorta
Enlargement
of LV
Enlargement
of LA, MV
>LA/AO
MR
Plethora
Enlargement
of PA
Machinery
murmur
Diastolic Murmur
systolic Murmur
Loud P2
Haemodynamic of PDA
Low PA pressure
High PA
pressure
Descending
Aorta
Mixing Fall
SPO2
Differential Cyanosis
RV
RA
Enlargement
of RV
Enlargement
of RA
TR
PPHN PA pressure < systemic pressure
PR

20. Clinical signs in preterm baby
▪ Increase respiratory rate, breathlessness
▪ Early tiring while breast feeding – Suck and rest phenomenon
▪ RDS – increase respiratory support with high pco2.
▪ wide pulse pressure – bounding
▪ Tachycardia; s3 gallop; hyperactive precordium.
▪ Continuous systolic murmur
▪ Hepatomegaly

21. Effects of ductal shunting:
• Steal from ascending aorta & arch
Neurological : ICH, apnea & decreased svc flow
Coronary steal : decreased ventricular function
▪ Steal from descending aorta
Neonatal enterocolitis
Decreased renal perfusion
Decreased lower limb pulses.

22. Auscultation
• Sounds : S1－Accentuated, loud Mitral & delayed closure of mitral valve sound S2-Splitting
• Murmurs :In 1898, Gibson described the classic murmur. Subsequently, the hallmark
physical finding of patent ductus arteriosus (PDA) has been described to as a
machinery murmur, which is continuous. The murmur may be accentuated in systole.
Typically, the murmur is loudest at the left upper chest.
• If the pulmonary-to-systemic blood ratio approaches or exceeds 2:1, a diastolic
rumble, caused by high flow across mitral valve, is frequently present.
• Also, because of high flow through the left ventricle into the aorta , an aortic ejection
murmur is also produced.
• If PDA is small, the amplitude of the murmur may increase with inspiration as
pulmonary impedance drops.

23. Classification according to the size of PDA
Large PDA:
Associated with significant left heart volume overload (left ventricular end-diastolic dimension
>+2Z score for weight), congestive heart failure, and severe pulmonary arterial hypertension.
PDA murmur is unlikely to be loud or continuous.
ii. Moderate PDA: Some degree of left heart overload, mild-to-moderate pulmonary artery
hypertension, and no/mild congestive heart failure. Murmur is continuous.
iii. Small PDA: Minimal or no left heart overload. No pulmonary hypertension or congestive
heart failure. Murmur may be continuous or only systolic.
iv. Silent PDA: Diagnosed only on echo Doppler. These are hemodynamically insignificant,
produce no murmur and there is no pulmonary hypertension.

24. X-ray chest
Cardiac enlargement with a LV silhouette
May be LA enlargement
Prominent ascending aorta and aorta
knuckle
Plethoric lung field
Prominent PA segment

25. There is presence of signs of left ventricular volume overload, hypertrophy
[tall R waves and tall peaked T waves in inferior leads (II, III and aVF)
and lateral leads (V5-V6), with prominent q waves in V5-V6] and
left atrial enlargement (broad notched P waves in leads I and II, with a
broad, deep terminal force in lead V1) in those with a large left-to-right
shunt.
Right ventricular hypertrophy is seen if the PVR is elevated. In small
PDA, ECG is normal.
ECG

27. P D A
▪ After first week, the murmur is reasonably accurate for detection of PDA.
▪ The presence of hyperdynamic precordium and bounding pulse are suggestive of
hemodynamically significant PDA.
▪ Echocardiography is required before intervention ( Medical or Surgical) to rule out
association of duct dependent lesions is there or not.

28. Echocardiography
This is the key tool for
The diagnosis of PDA
Assessment of its size and anatomy of PDA for suitability of device closure
Cardiac function - Left atrial and left ventricular dimensions
Estimation of the direction of shunt, Pulmonary artery pressure and quantification of
shunt
Evaluation for associated other cardiac defects.

29. Echocardiographic view For diagnosis &
evaluation of PDA
Parasternal long axis view PLAX - M Mode and 2 D
Parasternal short axis view PSAX & ductal arch view
Apical 4 Chamber view with E/A doppler assessment
Supra sternal long, short axis view and modified ductal arch view

30. “M” MODE PSLA VIEW 2D VIEW
PV
RV
IVS
LV
AO
LA
DAO
LA
LA
AO
AO
RV
LA
AO
RV
LV
IVS
Parasternal
long axis view
PLAX

31. PLAX VIEW

32. PSAX BASAL

33. Ductal arch view
This uses the high parasternal window
just beneath the left clavicle. After
obtaining the short axis cut of the great
vessel visualizing the pulmonary artery
bifurcation the transducer is rotated
anticlockwise in gradual motion. At one
point the left pulmonary artery goes away
from view and the duct with adjacent
descending aorta opens. This view in
neonates and infants also visualizes the
origin of the left subclavian artery. In
patients with associated coarctation the
posterior shelf is also well visualized.

34. Apical 4 ”C” View
DAO
PV

35. SUPRA STERNAL LONG AXIS
This is the best view for visualizing
the vertical duct arising from the
undersurface of the transverse
arch in patients with pulmonary
atresia. The origin of such ductii is
well seen but the insertion point at
the pulmonary artery required
further anterior tilt. This is
because of the tortuous nature of
such ductii.
In patients with discordant
ventriculo-arterial connection (e.g.
transposition of great vessels), the
duct can be visualized very well in
its entire length in this view.

36. SUPRA STERNAL SHORT AXIS

37. Supra sternal short axis view
Suprasternal short axis view – this is the classical short axis arch view and can visualize those
rare duct which arises form the base of the left subclavian artery and descends straight down
to insert into the left pulmonary artery.
If aortic arch is right sided and the patient has pulmonary stenosis physiology. The entire
length of the duct can be seen in one view because unlike in those patients with vertical duct it
does not follow a tortuous course

38. Modified ductal arch view
Modified ductal view – this a less well described view to visualize the usual duct. It has
the advantage of visualizing the duct in its entire length and most closely mimics the
lateral angiogram performed during cardiac catheterization. From the usual suprasternal
long axis view the transducer is rotated anticlockwise. A slight anterior tilt then shows
the duct from its ampullary part to its insertion and accurate measurements can be
made.

39. In PSAX and Supra sternal view - PDA location, size and blood flow is evaluated
In PLAX and Apical 4 C view - Left side Volume load is assessed
M mode, 2D and Doppler Echo is performed in all these views to assess cardiac status

40. Evaluation of PDA
PLAX view
PULMONARY HYPER PERFUSION LA/AO > 1.6, INCREASE PUL
VENOUS RETURN
LA/AO < 1.4
LA/AO >1.4

41. Apical 4 C view
Haemodynamically significant PDA - yes /no
Left side volume over load Enlarge LA & LV, MR E/A = 1 or > 1
LA/AO < 1.4
LA/AO >1.4

42. PSAX view
AO
DAO
DAO
AO
RVOT
RVOT
PA
PA
PDA
PDA
Tripod sign PDA connecting to LPA

43. PSAX view PDA connecting to LPA

45. PSAX view

46. LA
PA
DAO
Pulsatile PDA flow
A
O
PSAX Ductal view Check ductal patency and direction of
flow
The most accurate view for measuring the size of the DA is the high left parasternal short axis window, also called “ductal
view.” Concentrating on the main pulmonary artery, the origin of the right pulmonary artery, which is not always visible, and of
the left pulmonary artery can be visualized; the DA is positioned to the left of it. The DA should be measured at its narrowest
point, before its entry into the main pulmonary artery

47. Supra sternal long axis view

48. PDA CHARACTERISTICS DUCTAL SIZE > 2MM
PULSATILE PDA DOPPLER
NO PDA CONTRICTION
NON RESTRICTIVE L-> R
BIDIRECTIONAL
RESTRICTIVE L-> R
Tiny PDA
PDA reversal Right -> Left
PA
DAO
NON RESTRICTIVE L-> R

49. Non restrictive PDA with high pressure gradients show Doppler velocity spectral display of
PDA flow from left-to-right only.
The tracing shows a Peak than decrease in gradient from aorta to MPA.

50. Characteristic Doppler velocity spectral display of PDA flow in patients with left-to-right
shunting only. Restrictive PDA with high pressure gradients. The superimposed simultaneous
pressure tracing shows a continuous gradient from aorta to MPA.

51. Doppler spectrum shows bidirectional shunt across PDA with pulmonary hypertension, low
pressure gradients between MPA and aorta. Flow below the zero line is simultaneously recorded
from the descending aorta by the continuous-wave Doppler
Flow during diastole from AO to PA
Flow during systole from PA to AO

52. Doppler spectrum shows unidirectional shunt across PDA with severe pulmonary hypertension.

53. “very small” to include clinically silent PDAs and “small” to refer to PDAs that may or may not
have a characteristic PDA murmur but are not associated with hemodynamic consequences.

54. Tiny PDA

55. Rubella – Cataract with large PDA

56. RVH
PV
POST STENOTIC
DILATATION
PS
PDA
LEFT CATRACT RIGHT

57. Rubella PPHN

59. CMV -PDA

60. Critical PUL. Stenosis Valvular with PDA

61. PDA – Eissenmenger

62. TGA - PDA
d - TGA PDA L - TGA PDA

63. D TGA PDA
PSSX PLAX

64. Dextrocardia d TGA PDA
Subcostal

65. Thrombosus in PA with PDA

66. LA
LA
PA
AO AO
AO
AO
AO
PA
PA
PA
PA
PDA SHOWING BIDIRECTION BLOOD FLOW

67. PDA Right to left flow
PFO Bidirectional flow
TR OR PR PULMONARY ARTERIAL SYSTOLIC PRESSURE
RV function Tricuspid annular plane systolic excursion – TAPSE
Myocardial performance index- MPI RV
RV systolic/diastolic ratio
Pulmonary Arterial Systolic Hypertension
Right to left flow
PAH flow from RV -> PA -> PDA -> DAO

68. PPHN PDA REVERSAL
RV
RA TR
TR
AO
PDA FLOW

69. Conical PDA
Window PDA
Tubular PDA
Aneurysmal PDA
Elongated PDA
Krichenko Angio-graphic type of PDA

70. Conical PDA

71. Tortuous PDA

72. Suprasternal view PSAX
Tortuous PDA

73. Vertical PDA

74. Stepwise evaluation of PDA
•Visualize the ductus ostium and aortic isthmus from the parasternal short axis, high parasternal short axis
and suprasternal views)
•Determine the direction of shunt by color flow mapping and Doppler
•Take the peak velocity of the PDA signal which will give the pressure difference between the aorta and
pulmonary artery and obtain the aortic, RVOT and PA velocities
•Take the measurements of the left ventricle and left atrium as these will reflect the volume of the left to
right shunt
•Specifically look for associated defects like coarctation of aorta (suprasternal view), aortic interruption and
aortopulmonary window (communication between the ascending aorta and pulmonary artery)

75. Haemodynamically significant - hs PDA
PDA CHARACTERISTICS DUCTAL SIZE > 2MM
PULSATILE PDA DOPPLER
NO PDA CONTRICTION
PULMONARY HYPER
PERFUSION
LA/AO > 1.6, INCREASE PUL
VENOUS RETURN
SYSTEMIC
HYPOPERFUSION
RETRO GRADE FLOW IN -
DESCENDING AORTA
CELIAC AXIS OR SMA
MCA

76. Echocardiography parameter No PDA Mild Moderate Large
Features of ductus arteriosus
Transductal diameter (mm) – <1.5 1.5-3.0 >3.0
Ductal velocity Vmax (cm/sec) – >2 1.5-2.0 <1.5
Antegrade PA diastolic flow (cm/sec) – >30 30-50 >50
Pulmonary overcirculation
Left atrial /aortic root width ratio 1.1 ± 0.2 <1.4:1 1.4-1.6 >1.6:1
Left ventricular/aortic root width ratio 1.9 ± 0.3 – 2.2 ± 0.4 2.27 ± 0.27
E wave/A wave ratio <1 <1 1-1.5 >1.5
IVRT(ms) <55 46-54 36-45 <35
LVSTI 0.34 ± 0.09 – 0.26 ± 0.03 0.24 ± 0.07
Systemic hypoperfusion
Retrograde diastolic flow (%) 10 < 30 30-50 >50
Aortic stroke volume (mL/kg) £2.25 – – £2.34
Left ventricular output (mL/kg/min) 190-310 – – >314
LVO/SVC flow ratio 2.4 ± 0.3 – – 4.5 ± 0.6
LVO = left ventricular output, SVC = superior vena cava, LVSTI = left ventricular stroke volume index, IVRT = isovolumic relaxation time, PWD =
pulse wave Doppler, CWD = continuous wave Doppler, PA =pulmonary artery.

77. Cardiac catheterization:
Rarely required for diagnosing a PDA.
Cardiac catheterization is indicated in older children and adults with pulmonary hypertension
and suspected pulmonary vascular disease.
Besides conventional methods to test operability in catheterization laboratory, balloon occlusion
of PDA may help decide whether PDA should be closed or not. Those showing pulmonary artery
systolic pressure/aortic systolic pressure ratio <0.5 on balloon occlusion testing may be suitable
for closure.
The main indication for cardiac catheterization currently is for performing device closure of
the PDA.

78. Where is shunt ?
What is the direction of shunt ?
What is diagnosis?
What is Qp/Qs
74
78
74
95
74
74 95
95
80
90

79. Where is shunt ?
What is the direction of shunt ?
What is diagnosis?
What is Qp/Qs
74
78
74
95
74
74 95
95
80
90
Qp= 1/PAO2-PVO2 X 100= 1/90-95 X100 = 20
Answer : At arterial level
Left to right from AO to PA
P D A
Qs=
𝟏
𝑺𝑨𝑶𝟐
− 𝑴𝑽𝑶𝟐 𝑿 𝟏𝟎𝟎 =
𝟏
𝟗𝟓
− 𝟕𝟒𝑿 𝟏𝟎𝟎 = 𝟓
Qp/Qs=
𝟐𝟎
𝟓
= 4 : 1
QeS = 1/PAO2-MVO2 X 100 = 1/90-74 X 100= 5
LEFT TO RIGHT SHUNT = Qp - QeS = 20 -5 = 15

80. Where is shunt ?
What is the direction of shunt ?
What is diagnosis?
What is Qp/Qs
74
78
74
95
74
74 95
95
80
90
Qp/Qs=
𝑺𝑨𝑶𝟐−𝑴𝑽𝑶𝟐
𝑷𝑽𝑶𝟐−𝑷𝑨𝑶𝟐
Answer : At PULMONARY LEVEL
Left to right from AO to PA
P D A
Qp/Qs=
𝟗𝟓−𝟕𝟒
𝟗𝟓−𝟗𝟎
Qp/Qs=
𝟐𝟏
𝟓
= 4.2 : 1

81. Where is shunt ?
What is the direction of shunt ?
What is diagnosis?
What is Qp/Qs
74
78
74
90
74
74
100
100
100

82. Where is shunt ?
What is the direction of shunt ?
What is diagnosis?
What is Qp/Qs
74
78
74
90
74
74
100
100
100
at Arterial level
Right to left
PDA
Qp=1/PAO2-PVO2 X 100= 1/74-100 X 100 = 1/26 X 100 = 4 L
Qs = 1/SAO2-MVO2X 100 = 1/90-74 X 100 = 1/16 X 100 = 6.6L
QeS = 1/PVO2-MVO2 X 100 = 1/100-74 X 100 = 1/26 X100 = 4
Qp /Qs = 4/6 = 0.6.6
RT to LT shunt = Qs –QeS = 6-4 = 2
LT to Rtshunt = Qp-QeS = 4-4 = 0

83. Medical Management
It include administration of –
Oxygen – Hood/ CPAP/ Ventilatory therapy
Diuretic -
Vasodilator -
Dopamine or Dobutamine
If PPHN - milrinone and nitric oxide can be given

84. Indomethacin group: Oral indomethacin (3 doses at 12 hourly intervals) with starting dose of
0.2mg/kg followed by 0.1mg/kg for babies less than 2 days of age, 0.2 mg/kg for 2-7 days of
postnatal life, 0.25mg/kg for >7 days of postnatal life.
Ibuprofen group: Oral ibuprofen at the initial dose of 10mg/kg followed by 5 mg /kg after 24
and 48 hr.
Paracetamol group: Intravenous paracetamol at 15 mg/kg every 6 hourly for 3 consecutive
days.
after the completion of first-course baby is assessed clinically as well as by echocardiography to confirm PDA
closure within 24 hours of the last dose. If PDA remained open, a second course of the same drug can be
repeated and repeat clinical as well as echo assessment was is within 24 hours of the last dose.

85. PDA
LARGE/MODERATE MODERATE SMALL SILENT
Rx – CHF & PAH
PLAN CLOSURE
IN NEXT 3-6 MTHS
CLASS I
NO CHF
PLAN CLOSURE
IN NEXT 6-12 MTHS
CLASS I
PLAN CLOSURE
IN NEXT 6-12 MTHS
CLASS I
NO CLOSURE
CLASS III

86. Those presenting beyond 6 months of life with large PDA, significant pulmonary
hypertension and suspected elevated PVR should be referred to a center for further
evaluation to assess operability.
PDA associated with severe pulmonary arterial hypertension with irreversible pulmonary
vascular occlusive disease and silent PDA (Class III) are not advisable to under go any
kind intervention.
All patients with PDA must be advised to maintain Good oro-dental hygiene.

87. Method of closure
i. Weight >6 kg – Can be individualized. Device closure (preferred as less invasive), coil
occlusion, or surgical ligation (Class I).
ii. Weight <6 kg – Surgical ligation (Class I), device/ coils (off-label use; Class IIb)
iii. Surgical ligation is recommended in cases of progressively enlarging or symptomatic ductal
aneurysm, endarteritis, and PDA with unusual shape not considered suitable for device
(Class I).
iv. Drug therapy with indomethacin/ibuprofen/ paracetamol not to be used in term babies
( classIII)