Patent Ductus Arteriosus PDA

Slide 1 · Patent ductus arteriosus

Congenital cardiac shunt • fetal physiology • pulmonary vascular pathology

Anatomy → closure → shunt physiology → clinical consequences

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · What this lecture will explain

Identify the ductus and describe its fetal function

Explain normal closure and causes of persistence

Predict shunt direction, pulmonary pathology, and treatment logic

Anatomy

Closure

Shunting

Consequences

Slide 3 · PDA is a persistent fetal arterial connection

The ductus connects pulmonary artery to aorta

Persistence after birth permits abnormal communication

Unlike ASD and VSD, this is an extracardiac vascular shunt

AORTA

Pulmonary

Artery

Distal to left

Subclavian origin

DUCTUS

Persistent arterial connection

Slide 4 · PDA belongs to left-to-right shunt lesions

The common group includes ASD, VSD, and PDA

They increase flow into pulmonary circulation after birth

Initial shunt direction does not produce cyanosis

ASD

VSD

PDA

Different locations of abnormal communication

Slide 5 · CHD becomes apparent as circulation changes

Structural anomalies can be tolerated before delivery

The fetal-to-neonatal transition alters pressure gradients

Clinical effects may therefore emerge after birth

Fetal circulation

Birth transition

Postnatal hemodynamics

Slide 6 · Ductus anatomy: A pulmonary-to-aortic channel

The ductus originates from the pulmonary artery

It joins the aorta on the descending side of the arch

This route bypasses the fetal pulmonary vascular bed

AORTA

Pulmonary

Artery

Distal to left

Subclavian origin

DUCTUS

Persistent arterial connection

Slide 7 · The aortic insertion lies beyond the left subclavian

Robbins locates the entry just distal to left subclavian origin

The ductus therefore connects great vessels, not chambers

The position matters when explaining flow direction

AORTA

Pulmonary

Artery

Distal to left

Subclavian origin

DUCTUS

Persistent arterial connection

Slide 8 · A patent ductus is normal before birth

Fetal lungs are not yet oxygenating the circulating blood

The ductal pathway conveys blood away from the lungs

Pulmonary arterial blood enters the aorta via the ductus

Pulmonary artery → ductus → aorta

Fetal physiology

Slide 9 · Fetal shunting is pulmonary artery to aorta

Pulmonary artery supplies the ductal inflow

The aorta receives the bypassing blood

The channel reduces dependence on fetal pulmonary flow

AORTA

Pulmonary

Artery

Distal to left

Subclavian origin

DUCTUS

Fetal direction: Pulmonary → systemic

Slide 10 · Postnatal survival changes ductal requirements

Oxygenation rises after ventilation begins

Pulmonary vascular resistance decreases

Ductal patency is no longer required in normal anatomy

Ventilated lungs

Changed resistance

Ductal constriction

Slide 11 · Increasing arterial oxygen favors constriction

A rise in oxygenation is a closure stimulus

This response follows the onset of extrauterine respiration

Hypoxic conditions can delay the constrictive response

Higher arterial O₂

Ductal constriction

Functional closure

Slide 12 · Declining prostaglandin E₂ favors closure

Local prostaglandin E₂ levels fall after birth

The fall contributes to ductal constriction

Prostaglandin regulation explains therapeutic opportunities

Lower PGE₂

Less patency support

Ductal constriction

Slide 13 · Falling pulmonary resistance changes flow

Birth reduces pulmonary vascular resistance

The postnatal circulation favors aorta-to-pulmonary shunting if ductus remains open

Direction is therefore not fixed across life

Fetus: Pulmonary → aorta

After birth: Aorta → pulmonary

Slide 14 · Normal closure integrates multiple signals

Higher arterial oxygenation

Lower local prostaglandin E₂

Reduced pulmonary vascular resistance accompanies transition

Higher O₂

Lower PGE₂

Lower PVR

Slide 15 · Functional closure usually occurs in 1–2 days

In healthy term infants the ductus constricts rapidly

The lumen becomes functionally closed within one or two days

Functional closure precedes tissue-level obliteration

Birth

Functional

Closure

Structural

Closure

Slide 16 · Anatomic obliteration takes longer

The ductal structure undergoes permanent obliteration

Complete closure develops over the first few postnatal months

The resulting remnant is the ligamentum arteriosum

Birth

Functional closure

Ligamentum

Slide 17 · The ligamentum arteriosum marks closure

A persistent fetal blood conduit becomes a fibrous remnant

The remnant no longer carries blood between the vessels

Structural closure differs from transient smooth-muscle constriction

Patent channel

Obliterated ductus

Ligamentum arteriosum

Slide 18 · Functional and structural closure are distinct

Early constriction stops flow

Later obliteration removes the arterial channel

Confusing these time frames obscures the meaning of “persistent”

Phase

Principal change

Functional

Constricted ductus; Blood flow ceases

Structural

Permanent obliteration; Fibrous remnant

Slide 19 · PDA means closure has not been completed

Patency retains a channel between great vessels

Persistence may be delayed or absent altogether

The defect must be interpreted in its physiological setting

Persistent lumen

Arterial shunting

Clinical consequences

Slide 20 · Hypoxia can prevent timely ductal closure

Hypoxia with delayed or absent closure

Respiratory distress is one relevant clinical context

Other heart disease can also sustain hypoxemia

Hypoxia

Delayed constriction

Persistent ductus

Slide 21 · Other defects can sustain ductal patency

Coexisting congenital lesions alter pressure and flow

VSDs that elevate pulmonary pressures

An apparently simple PDA may coexist with a complex circulation

VSD

Higher pulmonary pressure

Delayed closure

Slide 22 · Genetic context: Char syndrome

The congenital heart disease gene table associates PDA with Char syndrome

TFAP2B is the listed gene

The gene product is a transcription factor

Char syndrome

TFAP2B

Transcription factor

Slide 23 · Genetic context: CHARGE syndrome

PDA can occur among multiple cardiac malformations

CHD7 for CHARGE syndrome

The table identifies CHD7 as a helicase-binding protein

CHARGE syndrome

CHD7

PDA among cardiac features

Slide 24 · Syndromic associations do not explain every PDA

Many congenital anomalies occur without identified mutations

One genotype may be associated with several phenotypes

A syndromic association is not a universal cause of PDA

Genetic susceptibility

Variable expression

Clinical phenotype

Slide 25 · PDA contributes about 7% of CHD cases

The Robbins congenital malformation table lists PDA at 7%

It is one of the common congenital shunt abnormalities

This is a proportion among classified CHD cases, not all newborns

PDA: 7% of CHD

Table 12.2

Denominator matters

Slide 26 · Most PDAs are isolated lesions

About 90% as isolated defects

Isolation does not imply a uniformly benign course

Large isolated channels can still damage pulmonary vessels

90% isolated

Size matters

Pulmonary vascular risk

Slide 27 · The direction of flow reverses after birth

Fetal flow: Pulmonary artery to aorta

Uncomplicated postnatal PDA: Aorta to pulmonary artery

Late pulmonary vascular disease may reverse it again

Stage

Typical ductal flow

Fetal

Pulmonary artery → aorta

Postnatal PDA

Aorta → pulmonary artery

Advanced disease

Pulmonary artery → aorta

Slide 28 · Postnatal PDA follows the pressure gradient

Blood moves from the systemic to the pulmonary circuit

This is the initial left-to-right shunt pattern

Shunt direction reflects relative vascular pressures

AORTA

Pulmonary

Artery

Distal to left

Subclavian origin

DUCTUS

After birth: Systemic → pulmonary

Slide 29 · PDA connects systemic and pulmonary flow

Aortic blood re-enters the pulmonary arterial circulation

Pulmonary flow is increased without an intracardiac defect

The lungs must accommodate recirculated blood

Aorta

PDA

Pulmonary arteries

Lungs

Slide 30 · A small PDA may have little physiological impact

Ductal diameter influences shunt volume

A narrow channel may not impair growth or development

Anatomic patency does not always mean severe disease

Small channel

Limited shunt

Minimal clinical effect

Slide 31 · A large PDA may create substantial overload

A wide duct permits more communication

Additional pulmonary blood volume and pressure impose stress

Severity is not determined by the term “PDA” alone

Wide channel

Major shunt

Pulmonary overload

Slide 32 · Cardiovascular status modifies PDA severity

The same opening can behave differently under different hemodynamics

Pulmonary vascular conditions affect the gradient

Associated malformations must be interpreted together

Ductal diameter

Pulmonary resistance

Associated disease

Clinical impact

Slide 33 · PDA is commonly asymptomatic at birth

Robbins explicitly describes initial asymptomatic presentation

Early tolerance does not exclude a persistent shunt

Clinical findings can become evident as physiology evolves

Birth

Initially silent

Later recognition

Slide 34 · A characteristic finding is a continuous murmur

PDA classically produces a harsh, machinery-like murmur

The murmur is continuous rather than limited to a single cardiac phase

Auscultation must be interpreted with the whole hemodynamic picture

Continuous

Harsh

Machinery-like

Slide 35 · Continuous flow explains the murmur pattern

A persistent arterial communication allows ongoing flow

In a typical postnatal shunt, aortic-to-pulmonary flow is sustained

The persistent flow supports a continuous auscultatory sound

Patent conduit

Sustained flow

Continuous murmur

Slide 36 · Initial left-to-right PDA is not cyanotic

Oxygenated systemic blood travels toward the lungs

Systemic arterial blood is not diluted by venous blood initially

Acyanotic presentation does not exclude a major shunt

Aorta → pulmonary artery

No initial cyanosis

Slide 37 · The first major risk is pulmonary overcirculation

Large left-to-right shunts elevate pulmonary blood flow

Both volume and pressure loading may increase

Downstream pulmonary vessels adapt to the increased load

Large PDA

↑ Pulmonary flow

Vascular overload

Slide 38 · Pulmonary arteries respond to chronic overload

Pulmonary muscular arteries initially remodel

Medial hypertrophy is an adaptive change

The response occurs within a normally low-resistance vascular bed

Chronic load

Medial hypertrophy

Vascular remodeling

Slide 39 · Pulmonary vasoconstriction is an early response

Narrowing helps regulate distal capillary pressure

It simultaneously increases pulmonary vascular resistance

Persistent stimulus can promote further vascular damage

Elevated flow/pressure

Vasoconstriction

↑ Resistance

Slide 40 · Obstructive intimal lesions mark progression

Prolonged abnormal pressure/flow promotes arterial injury

Irreversible intimal obstruction can develop

The vascular pathology may persist even if the initial communication is addressed

Persistent overload

Intimal obstruction

Irreversible disease

Slide 41 · The right ventricle responds to rising resistance

Progressive pulmonary resistance increases right ventricular workload

The right ventricle undergoes hypertrophy

This ventricular adaptation reflects pulmonary vascular disease

↑ PVR

↑ RV workload

RV hypertrophy

Slide 42 · Pulmonary resistance may approach systemic levels

The pressure advantage sustaining left-to-right flow diminishes

Shunt volume and direction can change over time

Advanced disease may create right-to-left flow

↑ Pulmonary resistance

Gradient narrows

Flow reverses

Slide 43 · Eisenmenger physiology is late shunt reversal

A prior left-to-right shunt becomes right-to-left

Irreversible obstructive pulmonary vascular disease is the driver

The resulting systemic desaturation is clinically consequential

Longstanding PDA

Pulmonary vascular disease

Right-to-left reversal

Slide 44 · Right-to-left flow introduces venous blood systemically

Pulmonary arterial blood can pass into the aorta

This bypasses oxygenation through the lungs

Cyanosis becomes possible after reversal

AORTA

Pulmonary

Artery

Distal to left

Subclavian origin

DUCTUS

Late reversal: Pulmonary → systemic

Slide 45 · Cyanosis is a late warning in uncomplicated PDA

No cyanosis is expected with the initial left-to-right shunt

Cyanosis after reversal indicates advanced pulmonary vascular pathology

The timing and mechanism differ from primary cyanotic CHD

Early PDA

Advanced reversal

Left → right

Right → left

No initial cyanosis

Cyanosis can develop

Pulmonary overload

Obstructive vascular disease

Slide 46 · Pulmonary vascular irreversibility changes management

Longstanding obstruction may make the defect irreparable

This is why large shunts require early attention

A simple “close every duct” rule is unsafe in advanced physiology

Reversible overload

Obstructive disease

Irreparable shunt state

Slide 47 · Three clinical trajectories should be separated

Small PDA: Little or no developmental impact

Large PDA: Pulmonary flow and pressure overload

Longstanding major shunt: Reversal with cyanotic consequences

Narrow

Large

Advanced

Minimal symptoms

Overcirculation

Shunt reversal

Limited impact

Pulmonary remodeling

Cyanosis

Slide 48 · ASD, VSD, and PDA share but differ

Each can begin with a left-to-right shunt

ASD typically adds right ventricular/pulmonary volume

VSD and PDA can elevate both pulmonary flow and pressure

Lesion

Principal communication

Physiology

ASD

Between atria

RV/pulmonary volume

VSD

Between ventricles

Pulmonary flow + pressure

PDA

Between great vessels

Pulmonary flow + pressure

Slide 49 · PDA is not the same as a septal defect

The ductus is a connection between great arteries

An ASD or VSD is within the cardiac septa

Physical location changes anatomical interpretation

ASD: Atria

VSD: Ventricles

PDA: Great vessels

Different locations of abnormal communication

Slide 50 · Clinical evaluation starts with physiology

Ask whether the infant is symptomatic or thriving

Determine whether a characteristic continuous murmur is present

Assess whether pulmonary overload or late cyanosis is suspected

Presentation

Auscultation

Hemodynamic interpretation

Slide 51 · Echocardiography provides structural context

The parent CHD discussion describes echocardiographic detection of defects

Imaging can evaluate a suspected congenital communication

Interpret the visible anatomy together with shunt physiology

Suspected CHD

Echocardiography

Anatomy + physiology

Slide 52 · Early closure addresses the cause of overload

An isolated PDA is generally closed as early as feasible

Removing the communication stops abnormal recirculation

The objective is to prevent progressive pulmonary injury

Persistent PDA

Eliminate shunt

Prevent vascular injury

Slide 53 · Prostaglandin synthesis inhibition can close PDA

Prostaglandin synthesis inhibitors as therapy

The intervention exploits the role of prostaglandins in patency

Selection depends on individual clinical circumstances

Reduce prostaglandin support

Ductal constriction

Closure

Slide 54 · Percutaneous closure offers a mechanical option

Interventional closure is a recognized strategy

It interrupts communication between the great vessels

This option when needed after medical measures

Evaluate PDA

Percutaneous intervention

Obliterate channel

Slide 55 · Surgery is another route to closure

Surgical treatment can interrupt ductal blood flow

Its use depends on lesion and patient circumstances

Treatment should match anatomy and clinical risk

Patent communication

Surgical intervention

Stop shunting

Slide 56 · Treatment decisions cannot ignore pulmonary disease

A large patent shunt can progress to irreversible lesions

Shunt reversal signals that simple closure reasoning has changed

Intervention is most useful before fixed severe vascular disease

Before vascular injury

After fixed vascular injury

Aimed at prevention

Risk requires reassessment

Early closure feasible

Simple closure not assumed

Slide 57 · Some congenital lesions need an open ductus

A duct may serve as the only route to vital blood flow

This occurs in lesions obstructing systemic or pulmonary output

Ductal preservation can be lifesaving

Outflow atresia

Duct-dependent perfusion

Maintain patency

Slide 58 · Aortic valve atresia: Ductus supports systemic flow

Normal ventricular-to-aortic egress is obstructed

Ductal connection can supply the systemic circulation

Closing that channel may eliminate essential perfusion

Pulmonary artery → PDA → aorta

Systemic flow depends on duct

Slide 59 · Pulmonary valve atresia: Ductus supports lung flow

Normal right ventricular-to-pulmonary egress is obstructed

The ductal channel can supply the pulmonary circulation

Maintaining patency preserves an essential flow route

Aorta → PDA → pulmonary artery

Pulmonary flow depends on duct

Slide 60 · Prostaglandin E₁ can maintain ductal patency

Robbins explicitly describes PGE₁ administration

The goal in duct-dependent lesions is to keep the channel open

This is the opposite of treating an isolated large PDA

Duct-dependent defect

Administer PGE₁

Preserve perfusion

Slide 61 · The treatment paradox is physiology-dependent

Isolated PDA with harmful shunting: Aim for closure

Outflow obstruction with duct-dependent supply: Preserve patency

The identical vessel may be pathologic or lifesaving

Isolated PDA

Duct-dependent CHD

Abnormal recirculation

Vital bypass pathway

Close when appropriate

Maintain patency with PGE₁

Slide 62 · Case: Asymptomatic infant with small PDA

A narrow PDA is detected without growth impairment

Explain why observation of mild impact does not negate anatomy

Identify which change would raise concern about future risk

CLINICAL REASONING

Small ductal diameter

No growth effect

Evaluate shunt burden

Slide 63 · Case: Large PDA with changing physiology

A persistent large shunt exposes pulmonary arteries to overload

Name the expected arterial and ventricular adaptations

Explain why intervention timing matters

CLINICAL REASONING

Pulmonary overcirculation

Arterial remodeling

Prevent irreversible changes

Slide 64 · Case: Cyanosis after a longstanding shunt

A formerly acyanotic patient develops cyanosis

Infer what happened to pulmonary vascular resistance

Explain why shunt direction may have reversed

CLINICAL REASONING

↑ Pulmonary resistance

Right-to-left reversal

Eisenmenger physiology

Slide 65 · Case: Duct-dependent outflow obstruction

An infant has pulmonary valve atresia

The ductus may be essential for pulmonary blood supply

Determine why routine ductal closure would be dangerous

CLINICAL REASONING

Atretic pulmonary outflow

Duct supplies lungs

Preserve PDA

Slide 66 · Integrating PDA pathogenesis

A fetal conduit persists after the normal closure window

Left-to-right flow causes pulmonary volume and pressure loading

Chronic vascular disease can reverse shunting and cause cyanosis

Persistent conduit

Pulmonary overload

Vascular obstruction

Reversal

Slide 67 · Four questions determine the clinical meaning

What is the anatomical connection and direction of flow?

How large is the duct and what is the pulmonary vascular state?

Is the communication harmful or supplying essential flow?

Would closure prevent injury or interrupt perfusion?

Anatomy

Magnitude

Vascular disease

Duct dependence

Slide 68 · Primary textbook reference

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th edition (2026).

Congenital heart disease: left-to-right shunts and patent ductus arteriosus.