Can Patent Ductus Arteriosus Cause Pulmonary Hypertension?
Yes, patent ductus arteriosus (PDA) absolutely causes pulmonary hypertension, and this is one of its most serious complications that can progress to irreversible pulmonary vascular disease and Eisenmenger syndrome if left untreated. 1
Mechanism and Pathophysiology
The left-to-right shunt through a PDA directly exposes the pulmonary vasculature to increased blood flow and pressure, leading to elevated pulmonary artery pressures. 1 The severity depends on PDA size and duration:
- Moderate to large PDAs result in elevated pulmonary pressures from the outset 1
- In patients reaching adulthood with moderate PDA, either left ventricular volume overload or pulmonary arterial hypertension may predominate, with genetic predisposition playing a role 1
- Adult patients with large PDAs typically develop Eisenmenger physiology with reversal of shunt direction (right-to-left) 1
Clinical Evidence of the PDA-Pulmonary Hypertension Link
The relationship is well-documented across multiple studies:
- 96% of surgical PDA patients had pulmonary hypertension in one surgical series 2
- A direct correlation exists between ductus diameter and pulmonary artery pressure—as ductus diameter increases, pulmonary artery pressure increases significantly 2
- Patients with PDA and severe pulmonary hypertension can have near-systemic or systemic right ventricular pressures 3, 4
Clinical Presentations Based on Severity
Small PDA
- Normal pulmonary artery pressure 1, 5
- No left ventricular volume overload 5
- Continuous machinery murmur present 1
Moderate PDA
- Two distinct phenotypes:
Large PDA
- Eisenmenger physiology with differential cyanosis and clubbing 1
- Lower extremities cyanotic (sometimes left arm too) because unoxygenated blood from the ductus enters the aorta distal to the left subclavian artery 1
- Only systolic murmur may be heard (continuous murmur disappears) 1
Critical Diagnostic Pitfall
Do not miss differential cyanosis—always check oxygen saturation in all four extremities to detect right-to-left shunting at the ductal level. 1, 5 Upper extremities may have normal saturation while lower extremities are cyanotic and clubbed. 1
Implications for Management
When Closure is Indicated
PDA should be closed when pulmonary hypertension is present BUT pulmonary artery pressure remains less than 2/3 of systemic pressure or pulmonary vascular resistance is less than 2/3 of systemic vascular resistance. 1, 5
When Closure is Contraindicated
PDA closure is absolutely contraindicated in patients with established Eisenmenger physiology (net right-to-left shunt), as closure would be harmful. 1, 6 In cases of doubt, pulmonary vascular resistance testing is mandatory. 1
Staged Approach for Severe Pulmonary Hypertension
For patients with severe but potentially reversible pulmonary hypertension:
- Aggressive medical treatment of pulmonary hypertension first creates a window of opportunity for safe PDA closure 3
- Balloon test occlusion during cardiac catheterization is critical to determine safety of closure 3
- Successful closure requires mean pulmonary arterial pressures to decrease markedly after trial occlusion (e.g., from 78 mmHg to 41 mmHg) and systemic oxygen saturation to remain >90% 4
- If pulmonary arterial pressure increases by >10 mmHg after trial occlusion or oxygen saturation drops significantly, closure should not proceed 4
Reversibility After Closure
When PDA is closed before irreversible pulmonary vascular disease develops, pulmonary artery pressures decrease significantly postoperatively. 2 However:
- The decrease is faster in isolated PDA compared to PDA with congenital heart disease and right-left shunt 2
- Follow-up shows pulmonary artery pressure normalizes or reaches upper normal limits in most successfully closed cases 7
- Left untreated, the large PDA inevitably results in irreversible pulmonary vascular disease 3