What is the effect of a patent ductus arteriosus (PDA) on blood flow in newborns, particularly those born prematurely?

What Does a Patent Ductus Arteriosus Do?

A patent ductus arteriosus (PDA) creates a persistent left-to-right shunt between the aorta and pulmonary artery, causing pulmonary overcirculation and left ventricular volume overload, with severity depending on the size of the defect. 1

Hemodynamic Effects of PDA

Normal Fetal vs. Postnatal Physiology

• During fetal life, 85% of circulation bypasses the lungs through the ductus arteriosus, maintained by high pulmonary vascular resistance 2
• At birth, oxygen inhalation triggers reduced pulmonary vascular resistance and ductal closure, though the ductus may remain open for up to 6 weeks in full-term infants without being pathological 2
• In preterm infants (25-28 weeks gestation), delayed closure occurs in up to 80% of cases due to immaturity and altered physiologic mechanisms 3, 4

Primary Hemodynamic Consequences

Left-to-right shunting through the PDA exposes the pulmonary vasculature to increased blood flow and pressure, leading to elevated pulmonary artery pressures. 5 The magnitude of these effects depends directly on PDA size and duration:

• Small PDA: Normal left ventricle, normal pulmonary artery pressure, typically asymptomatic with continuous murmur 1, 5
• Moderate PDA: Two distinct phenotypes emerge:
  • Predominant LV volume overload with dilated left ventricle and potential left heart failure 1, 5
  • Predominant pulmonary arterial hypertension with pressure-overloaded right ventricle and potential right heart failure 1, 5
• Large PDA: Eisenmenger physiology develops with shunt reversal (right-to-left), causing differential cyanosis affecting lower extremities and sometimes the left arm 1, 5

Organ-Specific Effects

The PDA causes pulmonary overcirculation and systemic hypoperfusion through blood flow redistribution. 3, 6 This manifests as:

• Pulmonary system: Increased pulmonary blood flow leads to interstitial pulmonary edema, prolonged ventilation risk, and bronchopulmonary dysplasia 7
• Systemic circulation: Decreased systemic perfusion affects multiple organs, particularly in premature infants 3, 6
• Cardiovascular: Volume load to the left heart with potential congestive heart failure, tachycardia, and bounding peripheral pulses 4

Clinical Presentations by Severity

Asymptomatic Small PDA

• Continuous murmur on auscultation (though "silent" PDAs exist without audible murmur) 1
• Normal ventricular size and function 1
• Normal pulmonary artery pressures 5

Symptomatic Moderate-to-Large PDA

• Signs of volume overload: tachycardia, bounding pulses, wide pulse pressure 4
• Congestive heart failure symptoms when LV dysfunction develops 1, 4
• Elevated pulmonary pressures from the outset in moderate-to-large defects 5

Eisenmenger Physiology (Advanced Stage)

Adult patients with large untreated PDAs typically develop Eisenmenger physiology with differential cyanosis and clubbing. 5 This represents:

• Shunt reversal from right-to-left due to severe pulmonary vascular disease 8
• Differential cyanosis: lower extremities cyanotic, sometimes left arm affected 1
• The ductus now serves as essential decompression for the failing right ventricle 8

Associated Morbidities in Premature Infants

Hemodynamically significant PDA increases risk for multiple serious complications: 7

• Necrotizing enterocolitis or focal intestinal perforation 7, 6
• Intraventricular hemorrhage 7, 6
• Chronic lung disease/bronchopulmonary dysplasia 3, 7
• Retinopathy of prematurity 3
• Neurodevelopmental delay 3
• Increased mortality risk 7

Critical Diagnostic Considerations

Always check oxygen saturation in all four extremities to detect right-to-left shunting at the ductal level, as differential cyanosis may be present. 5, 2 This is essential because:

• Differential cyanosis indicates shunt reversal and Eisenmenger physiology 1, 5
• Clinical examination alone is insufficient; echocardiography must confirm hemodynamic significance 2
• Serious complications like pulmonary vascular disease can develop despite stable clinical appearance 2

Progression to Irreversible Disease

If left untreated, PDA can progress to irreversible pulmonary vascular disease and Eisenmenger syndrome. 5 The European Society of Cardiology emphasizes that:

• Moderate-to-large PDAs result in elevated pulmonary pressures from onset 5
• Chronic exposure to increased pulmonary blood flow and pressure causes vascular remodeling 5
• Once Eisenmenger physiology develops, PDA closure becomes contraindicated as the ductus provides necessary right ventricular decompression 1, 8

Management Implications Based on Hemodynamic Effects

Indications for Closure

PDA should be closed when there are signs of LV volume overload or when pulmonary hypertension is present but pulmonary artery pressure remains less than 2/3 of systemic pressure. 1, 5

Contraindications to Closure

• PDA closure is contraindicated (Class III) in patients with established Eisenmenger physiology (net right-to-left shunt) 1, 5, 8
• In this setting, the patent ductus serves as a necessary pop-off valve for the failing right ventricle 8
• Management should instead focus on rate control for arrhythmias and optimization of heart failure therapy 8

Common Pitfalls to Avoid

• Never assume stability based solely on clinical examination—always confirm with echocardiography as pulmonary vascular disease can develop silently 2
• Do not overlook differential cyanosis—check oxygen saturation in all four limbs to detect ductal-level shunting 5, 2
• Avoid closure in Eisenmenger physiology—the PDA provides essential right ventricular decompression in this setting 1, 8
• Do not dismiss "silent" PDAs—very small PDAs without murmur generally do not require closure, but moderate PDAs may be hemodynamically significant despite minimal auscultatory findings 1