The document discusses patent ductus arteriosus (PDA), which is the failure of the ductus arteriosus to close after birth. It defines PDA, discusses its incidence, risk factors, embryology, fetal circulation, closure at birth, classification, natural history, clinical manifestations including signs and symptoms, investigations including echocardiogram and cardiac catheterization, and management including medical treatment with drugs and nonsurgical closure using devices. PDA is usually diagnosed using echocardiogram and can often be closed nonsurgically using devices like the Amplatzer duct occluder.
These are cardiac anomalies arising as a result of a defect in the structure or function of the heart and great vessels which is present at birth
These lesions either obstruct blood flow in the heart or vessels near it, or alter the pathway of blood circulating through the heart
A cyanotic heart defect is a group-type of congenital heart defects (CHDs). The patient appears blue (cyanotic), due to deoxygenated blood bypassing the lungs and entering the systemic circulation. This can be caused by right-to-left or bidirectional shunting, or malposition of the great arteries.
Cyanotic heart defects, which account for approximately 25% of all CHDs, include:
Tetralogy of Fallot (ToF)
Total anomalous pulmonary venous connection
Hypoplastic left heart syndrome (HLHS)
Transposition of the great arteries (d-TGA)
Truncus arteriosus (Persistent)
Tricuspid atresia
Interrupted aortic arch
Pulmonary atresia (PA)
Pulmonary stenosis (critical)
Eisenmenger syndrome(Reversal of Shunt due to Pulmonary Hypertension) .
Patent ductus arteriosus may cause cyanosis in late stage.
These are cardiac anomalies arising as a result of a defect in the structure or function of the heart and great vessels which is present at birth
These lesions either obstruct blood flow in the heart or vessels near it, or alter the pathway of blood circulating through the heart
A cyanotic heart defect is a group-type of congenital heart defects (CHDs). The patient appears blue (cyanotic), due to deoxygenated blood bypassing the lungs and entering the systemic circulation. This can be caused by right-to-left or bidirectional shunting, or malposition of the great arteries.
Cyanotic heart defects, which account for approximately 25% of all CHDs, include:
Tetralogy of Fallot (ToF)
Total anomalous pulmonary venous connection
Hypoplastic left heart syndrome (HLHS)
Transposition of the great arteries (d-TGA)
Truncus arteriosus (Persistent)
Tricuspid atresia
Interrupted aortic arch
Pulmonary atresia (PA)
Pulmonary stenosis (critical)
Eisenmenger syndrome(Reversal of Shunt due to Pulmonary Hypertension) .
Patent ductus arteriosus may cause cyanosis in late stage.
commonly used for medical students, and helpful to use this ppt to study for them, and also a common man can understand very easily what is coarctation of aorta.
A congenital heart defect is a problem with the structure of the heart. It is present at birth. Congenital heart defects are the most common type of birth defect. The defects can involve the walls of the heart, the valves of the heart, and the arteries and veins near the heart. They can disrupt the normal flow of blood through the heart. The blood flow can slow down, go in the wrong direction or to the wrong place, or be blocked completely.
Doctors use a physical exam and special heart tests to diagnose congenital heart defects. They often find severe defects during pregnancy or soon after birth. Signs and symptoms of severe defects in newborns include
Rapid breathing
Cyanosis - a bluish tint to the skin, lips, and fingernails
Fatigue
Poor blood circulation
Many congenital heart defects cause few or no signs and symptoms. They are often not diagnosed until children are older.
Many children with congenital heart defects don't need treatment, but others do. Treatment can include medicines, catheter procedures, surgery, and heart transplants. The treatment depends on the type of the defect, how severe it is, and a child's age, size, and general health.
Kindly leave your comment if you found this helpful ;)
Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
commonly used for medical students, and helpful to use this ppt to study for them, and also a common man can understand very easily what is coarctation of aorta.
A congenital heart defect is a problem with the structure of the heart. It is present at birth. Congenital heart defects are the most common type of birth defect. The defects can involve the walls of the heart, the valves of the heart, and the arteries and veins near the heart. They can disrupt the normal flow of blood through the heart. The blood flow can slow down, go in the wrong direction or to the wrong place, or be blocked completely.
Doctors use a physical exam and special heart tests to diagnose congenital heart defects. They often find severe defects during pregnancy or soon after birth. Signs and symptoms of severe defects in newborns include
Rapid breathing
Cyanosis - a bluish tint to the skin, lips, and fingernails
Fatigue
Poor blood circulation
Many congenital heart defects cause few or no signs and symptoms. They are often not diagnosed until children are older.
Many children with congenital heart defects don't need treatment, but others do. Treatment can include medicines, catheter procedures, surgery, and heart transplants. The treatment depends on the type of the defect, how severe it is, and a child's age, size, and general health.
Kindly leave your comment if you found this helpful ;)
Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
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Read| The latest issue of The Challenger is here! We are thrilled to announce that our school paper has qualified for the NATIONAL SCHOOLS PRESS CONFERENCE (NSPC) 2024. Thank you for your unwavering support and trust. Dive into the stories that made us stand out!
1. DR. SAYEEDUR RAHMAN KHAN RUMI
dr.rumibd@gmail.com
MD (CARDIOLOGY) FINAL PART STUDENT
NHFH&RI
PATENT DUCTUS
ARTERIOSUS
2. Definition
• Patent ductus arteriosus, the most common type of
extracardiac shunt, represents persistent patency of the
vessel that normally connects the pulmonary arterial
system and the aorta in a fetus.
3. Incidence
• PDA occurs in approximately 1 of 2,000 live births,
but it is relatively uncommon among the adult
population.
• In infants, it accounts for 10% to 12% of all
congenital heart disease
• PDAs are twice as common in female infants as in
male infants
• In rubella syndrome male female are affected
equally
4. Risk factors
• Maternal rubella infection
• Birth at high altitude
• Premature birth
• Female sex, and
• Genetic factors
• In infants born at < 28 weeks of gestation, there is a
60% incidence of PDA
5. Embryology
• The ductus arteriosus is a normal and essential component of
cardiovascular development that originates from the distal
sixth left aortic arch.
• A PDA is most commonly funnel shaped with the larger aortic
end (ampulla) distal to the left subclavian artery, then
narrowing toward the pulmonary end, with insertion at the
junction of the main and left pulmonary arteries
6. Fetal circulation
• The presence of the ductus
arteriosus in the fetal circulation is
essential to allow right-to-left
shunting of nutrient-rich,
oxygenated blood from the
placenta to the fetal systemic
circulation, thereby bypassing the
fetal pulmonary circuit
• In the fetus, the ductus arteriosus
is kept open by
Low arterial oxygen content
and
Placental prostaglandin E2
(PGE2)
7. Birth
• Several changes occur at birth to initiate normal
functional closure of the ductus arteriosus within the
first 15 to 18 hours of life.
• Spontaneous respirations result in increased blood
oxygen content.
• Prostaglandin levels decrease because of placental
ligation and increased metabolism of prostaglandins
within the pulmonary circulation by prostaglandin
dehydrogenase.
• Generally, the ductus arteriosus is hemodynamically
insignificant within 15 hours and completely closed by
2 to 3 weeks
8. Classification
Isolated PDAs, are often categorized according to the degree of
left-to-right shunting, which is determined by both the size and
length of the duct and the difference between systemic and
pulmonary vascular resistance, as follows:
• Silent: tiny PDA detected only by nonclinical means (usually
echocardiography)
• Small: continuous murmur common; Qp/Qs <1.5
• Moderate: continuous murmur common; Qp/Qs 1.5 to 2.2
• Large: continuous murmur present; Qp/Qs >2.2
• Eisenmenger: continuous murmur absent; substantial
pulmonary hypertension, differential hypoxemia, and
differential cyanosis (pink fingers, blue toes)
10. Natural History
• Unlike PDA in premature infants, spontaneous closure
of a PDA is rare in full-term infants and children.
• This is because the PDA in term infants results from a
structural abnormality of the ductal smooth muscle
rather than a decreased responsiveness of the ductal
smooth muscle to oxygen.
• CHF or recurrent pneumonia develops if the shunt is
large.
• Pulmonary vascular obstructive disease may develop if
a large PDA with pulmonary hypertension is left
untreated.
• Although rare, an aneurysm of PDA may develop and
possibly rupture in adult life.
12. History
• The history of the mother’s pregnancy and of
perinatal events may provide clues associated with
a high incidence of PDA, such as exposure to
rubella in the first trimester in a non immunized
mother.
• PDA is also more common in premature infants,
especially those with birth asphyxia or respiratory
distress
13. Symptoms
• Severity of symptoms depends on the degree of left-to-
right shunting; and it is determined by the size of the
PDA, ductal resistance, cardiac output, as well as the
systemic and pulmonary vascular resistances.
• Patients with small PDA are asymptomatic.
• With larger PDAs, symptoms may develop.
• The most common symptom is exercise intolerance
followed by dyspnea, peripheral edema, and
palpitations.
14. Signs
• Tachycardia and tachypnea may be present in
infants with CHF.
• Bounding peripheral pulses
• Wide pulse pressure
• Hyperactive precordium: With a large shunt
• Systolic thrill: may be present at the upper left
sternal border.
• The P2 is usually normal, but its intensity may be
accentuated if pulmonary hypertension is present.
15. • A grade 1 to 4 of 6 continuous (“machinery”) murmur is best
audible at the left infraclavicular area or upper left sternal
border.
• An apical diastolic rumble may be heard when the PDA shunt
is large.
• Patients with small ductus do not have the above findings.
16. • The duration of the diastolic murmur reflects
pulmonary artery pressures; elevated pulmonary
artery pressures lead to a decreased gradient for
left-to-right flow through the PDA during diastole,
which results in a shorter diastolic murmur.
• As pulmonary pressure increases, the systolic
component of the murmur shortens.
• Right-to-left flow may not generate a systolic
murmur.
• Differential cyanosis: If pulmonary vascular
obstructive disease develops, a right-to-left ductal
shunt results in cyanosis only in the lower half of
the body.
18. ECG
• With a small shunt the ECG is normal.
• Left ventricular hypertrophy of the volume
overload type, with deep Q waves and increased R-
wave voltage in the left precordial leads, is noted
with increasing shunt size with left ventricular
volume overload.
• Right ventricular hypertrophy is seen with
pulmonary hypertension.
19. CXR
• Chest radiographs may be normal with a small-shunt
PDA.
• Cardiomegaly of varying degrees occurs in moderate-
to large-shunt PDA with enlargement of the LA, LV, and
ascending aorta.
• Pulmonary vascular markings are increased.
• With pulmonary vascular obstructive disease, the
heart size becomes normal, with a marked
prominence of the PA segment and hilar vessels.
20. CXR P/A view of a 2-day-old infant demonstrating the
ductus bump (arrow).
21. Echocardiogram
TTE has a 42% sensitivity and 100% specificity for the
diagnosis of PDA.
• On 2-D echo, the left-sided chambers (LA and LV)
are dilated due to increased venous return from
the pulmonary circulation.
• This constitutes left ventricular volume overload.
• Due to dilatation of left atrium, the ratio between
size of the left atrium and proximal aorta (LA : Ao
ratio) exceeds 1.3.
22. Parasternal long axis showing LA
and left ventricular enlargement
Echocardiogram in parasternal
short axis demonstrating a patent
ductus arteriosus with color-flow
mapping indicating reversed flow
23. Continuous wave Doppler
echocardiogram positioned
through the PDA, showing
retrograde flow throughout the
cardiac cycle
Pulsed-Doppler echocardiogram
shows increased diastolic
flow in the branch pulmonary
artery
25. • Oxymetry:
Steps up of O2 saturation in PA in comparison to RA.
• Pressure study:
RV & PA pressure is normal, but elevated in large PDA.
PVR is normal in infant & children but elevated in adult.
• LV graphy: to see associated VSD
• Aortography: to see PDA & associated CoA
26. MRI & CT
• Magnetic resonance imaging (MRI) and computed
tomography may be useful in defining the anatomy
in patients with unusual PDA geometry and in
patients with associated abnormalities of the aortic
arch.
28. Medical
Pharmacological closure of duct:
• For premature infants, treatment with indomethacin is
usually the first-line therapy (0.2 mg/kg intravenously
every 12 hours for up to three doses).
• Indomethacin therapy has been associated with an
increased bleeding tendency resulting from platelet
dysfunction, decreased urine output secondary to renal
dysfunction, and necrotizing enterocolitis.
• Ibuprofen has achieved closure rates equivalent to those of
indomethacin with less renal toxicity.
Secondary measures:
• Prophylaxis against IE
• Treatment of HF
29. ACC/AHA 2008 Guidelines for the Management of
Adults With Congenital Heart Disease
Class I Recommendations for Closure of Patent Ducts Arteriosus
1. Closure of a PDA either percutaneously or surgically is indicated
for the following:
a. Left atrial and/or LV enlargement or if PAH is present, or in
the presence of net left-to-right shunting
b. Prior endarteritis
2. Consultation with ACHD interventional cardiologists is
recommended before surgical closure is selected as the method
of repair for patients with a calcified PDA.
3. Surgical repair by a surgeon experienced in CHD surgery is
recommended when:
a. The PDA is too large for device closure.
b. Distorted ductal anatomy precludes device closure (eg,
aneurysm or endarteritis).
30. Nonsurgical Closure
• Since the early 1990s,
transcatheter techniques have
become the first-line therapy
for most PDAs.
• Complications: Rare.
• The most common
complication is embolization of
the coil or device.
• Percutaneous coils were
developed in 1992 and are the
preferred treatment for older
children and adults with PDAs
< 3.5 mm in diameter
Duct-Occlud coil
31. Amplatzer Ductal Occluder
• The ADO, a cone-shaped plug occluder made of
thrombogenic wire mesh delivered with a 5F to 7F
venous system, is the preferred device for
percutaneous closure of moderate to large PDAs.
• The ADO stents the PDA, and blood is forced to flow
through the center of the device, which is lined with
thrombogenic wire mesh.
• The PDA then essentially clots off.
• Advantages include simple implantation, ability to
retract the ADO into the sheath and redeploy if
needed, and high success rates.
• There is an 89% occlusion rate on post procedure day 1
and 97% to 100% complete occlusion after 1month
33. Lateral angiogram showing coil occlusion of a patent ductus
arteriosus (PDA).
A. Small PDA allows shunting from descending aorta to
pulmonary artery (arrow).
B. Shunting is eliminated by an Amplatzer ductal occluder
device placed in the ductus arteriosus (arrow).
34. Surgical Closure
• In 1938, the first successful closure of a PDA was performed,
which was the first repair of a congenital heart defect.
• With continued advances in percutaneous closure devices,
surgery has become second-line therapy for most adults with
PDAs
Procedure:
1. Ligation and division through left posterolateral
thoracotomy without cardiopulmonary bypass is the
standard procedure.
2. The technique of video-assisted thoracoscopic surgery
(VATS) clip ligation has become the standard of care for
surgical management of ductus with adequate length (to
allow safe ligation), which is performed through three
small ports in the fourth intercostal space.
35. Mortality:
• The surgical mortality rate is <1% for both
techniques.
Complications:
• Injury to the recurrent laryngeal nerve (hoarseness)
• The left phrenic nerve (paralysis of the left
hemidiaphragm)
• The thoracic duct (chylothorax) is possible.
• Recanalization (reopening) of the ductus is possible,
although rare, occurring after ligation alone (without
division).
36. Complications of PDA
The most common complications of PDA include
• CHF
• Infective endocarditis
• Pulmonary hypertension
37. Differential diagnosis
• VSD associated with aortic insufficiency
• Aortopulmonary window
• Pulmonary atresia with systemic collateral vessels
• Innocent venous hum
• Arteriovenous communications such as
• pulmonary arteriovenous fistula
• coronary artery fistula
• systemic arteriovenous fistula
• Ruptured sinus of Valsalva aneurysm
38. Reproductive Issues
• Pregnancy is well tolerated in women with silent
and small PDAs and in patients who were
asymptomatic before pregnancy.
• In women with a hemodynamically important PDA,
pregnancy may precipitate or worsen heart failure.
• Pregnancy is contraindicated in those with
Eisenmenger syndrome because of the high
maternal (≈50%) and fetal (≈60%) mortality.