Tutorial
Patent Ductus Arteriosus (PDA)
Closure timing nuance, the three ductal Doppler flow patterns, hemodynamically-significant-PDA criteria, and distinguishing PDA flow from aortic regurgitation.
Published . Last reviewed .
The ductus arteriosus is a normal fetal vessel connecting the main pulmonary artery to the descending aorta, allowing blood to bypass the fluid-filled fetal lungs. Persistence of ductal patency beyond the normal postnatal closure window is called patent ductus arteriosus (PDA) — a common, but genuinely heterogeneous, lesion whose clinical significance ranges from an incidental, hemodynamically trivial finding to the sole source of pulmonary or systemic blood flow in a critically ill neonate.
Normal Anatomy and Closure Timing
In a normal left aortic arch, the duct arises from the left pulmonary artery near the bifurcation of the pulmonary trunk and inserts at the transition from the aortic arch to the descending aorta — anterolaterally in the newborn, shifting more medially with growth. It typically measures 7–11 mm in length, runs posteroinferior to the left main bronchus, and is crossed anteriorly by the vagus nerve, whose recurrent laryngeal branch loops beneath the duct near its aortic end. Shape varies — cylindrical, hourglass, funnel-shaped (usually narrowing at the pulmonary end), aneurysmally dilated, or occasionally a “window duct” with essentially no length, just an oval opening between the opposed aortic and pulmonary walls.
Closure isn’t a single event at one fixed time — several distinct milestones occur in sequence, and it’s worth knowing all of them rather than a single oversimplified number:
- Functional closure begins within roughly 10–15 hours of birth in most full-term infants.
- Doppler studies in healthy newborns show ductal flow no longer detectable in nearly all subjects by 4–7 days.
- The lumen is typically anatomically occluded by the second or third week.
- Full conversion to a fibrous ligament — via progressive intimal proliferation — can take up to 3 months.
- A duct still patent beyond 3 months of age in a term infant is considered persistently patent, the clinical threshold for calling a PDA truly abnormal in that population.
In preterm infants, by contrast, ductal patency is common and is generally regarded as a functional immaturity of the closure mechanism rather than a structural cardiac anomaly.
Epidemiology and Etiology
PDA accounts for roughly 10–18% of all congenital heart disease and shows a notable female predominance (male-to-female ratio of about 1:2–3) — distinct from lesions like VSD or tetralogy of Fallot, which occur roughly equally by sex. Incidence rises sharply with prematurity and lower birth weight. Recognized associations include congenital rubella, high-altitude residence (chronic hypobaric hypoxia), isolated genetic mutations, chromosomal and genetic syndromes, and pharyngeal-arch gene variants associated with cardiovascular defects resembling those seen in 22q11 deletion. Char syndrome is a specific familial form of PDA with characteristic facial dysmorphism and hand anomalies, worth recognizing as a distinct entity rather than an incidental combination.
Anatomic Variants Worth Recognizing
- Right aortic arch (about 0.1% of the population, more common with tetralogy of Fallot, truncus arteriosus, and tricuspid atresia, and strongly associated with 22q11 deletion) changes where the duct inserts: directly into the right descending aorta, into the proximal left subclavian artery, or both (bilateral duct). Recognizing duct location here matters because it can be a component of a vascular ring.
- Reverse-oriented (“vertical”) duct — in critical right heart obstruction (tricuspid atresia, pulmonary atresia with intact septum, severe tetralogy of Fallot physiology), flow direction reverses to aorta-to-MPA in fetal life, changing the ductal arch’s shape (concave portion facing upward rather than downward) and producing a duct that’s typically long and tortuous.
- Ductal aneurysm — reported incidence varies widely (0.8% to nearly 9%, depending on the population and diagnostic criteria), with real associations to chromosomal abnormalities or syndromes (~25%) and connective tissue disorders (~13%). The clinical course is usually benign, with roughly 70% closing by 3 days of age; surgery is reserved for aneurysms persisting beyond the neonatal period or developing complications (compression, thrombus, airway erosion).
Ductal-Dependent Lesions: A Distinct Clinical Category
This is worth understanding as a category, not just a severity label. Some forms of congenital heart disease depend entirely on ductal patency for survival: right heart obstructive lesions make the PDA the primary source of pulmonary blood flow, while left heart obstructive lesions make it the primary source of systemic perfusion. This is fundamentally different from an isolated PDA in an otherwise normal heart, both in urgency and in management — closing the duct in a ductal-dependent lesion before the underlying obstruction is addressed can be catastrophic.
Pathophysiology
With normal pulmonary vascular resistance, flow runs left-to-right (aorta to pulmonary artery), increasing pulmonary blood flow and volume-loading the left heart — over time, left atrial and ventricular dilation, and potentially secondary mitral regurgitation. A large shunt can cause diastolic aortic “run-off” into the pulmonary circulation, lowering aortic diastolic pressure — combined with increased intramyocardial tension from LV dilation and increased oxygen demand, this can produce genuine subendocardial ischemia in significant cases. PDA also carries a real, quantified infective endocarditis risk of roughly 1% per year.
Clinical Findings
- Auscultation — the classic continuous “machinery” murmur, loudest at the second left intercostal space, extending from systole into diastole.
- ECG — left atrial enlargement and LV hypertrophy, the same left-sided volume-overload pattern seen with VSD (both volume-load the left heart directly, unlike ASD’s right-sided pattern).
- Chest X-ray — may be normal with a small PDA; larger shunts show pulmonary congestion, prominent pulmonary vessels, an enlarged main pulmonary artery, and — in chronic, longstanding cases — ductal calcification.
- Cardiac catheterization — an oxygen step-up at the pulmonary artery level compared with the right ventricle localizes the shunt, distinct from the RV-level step-up of a VSD or the RA-level step-up of an ASD.
Echocardiographic Findings
In infancy, one of the most common indications for an echocardiogram is simply to screen for a PDA, and echo is necessary for early diagnosis — especially in the preterm infant, where the finding has direct management implications.
A View-by-View Approach
- High left parasternal window — the “ductal view.” This is the view where the transducer sits closest to the duct and lines up best with flow, so it yields the most accurate Doppler signal. A useful way to get there: from the parasternal long-axis view, angle the transducer leftward and superiorly toward the distal RVOT to demonstrate ductal flow; then move up to the high left parasternal window and rotate clockwise to bring the pulmonary artery bifurcation into view; finally, rotating counterclockwise toward 12 o’clock shows the entire length and width of the typical PDA, from the underside of the descending aorta to the left pulmonary artery. This is what’s often called the ductal view.
- Parasternal short-axis view. The PDA can be seen by 2D along the left lateral border of the main pulmonary artery, leftward of the left pulmonary artery, with a cranial tilt of the transducer. In a typical left-to-right PDA, flow is directed toward the transducer.
- Suprasternal window. With the aortic arch in view, a slight leftward tilt shows the left pulmonary artery, and a slight clockwise rotation brings the left pulmonary artery and descending aorta into the same plane — once both are seen together, the PDA, if present, will be visualized in that plane. This is also the best window for evaluating a PDA in older children, along with the high left parasternal view.
- Subxiphoid and apical views. In most infants, ductal flow can be picked up by color Doppler from these windows as well. The subxiphoid view also lets you check the abdominal aorta for diastolic flow reversal, and the apical view is where LA and LV size and function are assessed.
In older children, transthoracic imaging can be difficult because of poor acoustic windows, which is why the high left parasternal and suprasternal notch views matter most in that age group.
A Normal Flow Pattern That Can Mimic a PDA
It isn’t unusual to see a color Doppler flow pattern in normal individuals that can be mistaken for PDA flow. In the parasternal short-axis view, a flow signal directed toward the transducer can sometimes be seen along the medial aspect of the main pulmonary artery in early systole. This most likely represents helical flow within the MPA — a consequence of flow in a curved tube. The medial location and the systolic-only timing distinguish it from true ductal flow, which runs along the lateral aspect and, in a left-to-right PDA, continues into diastole.
Two Specific Signs — and One Pitfall
Diastolic ductal flow along the lateral wall of the main pulmonary artery, distal to the pulmonic valve, is a specific and well-quantified sign — 96% sensitivity and 100% specificity for PDA. Suprasternal notch interrogation of the descending aorta typically shows holodiastolic flow reversal from antegrade ductal runoff — but this must be distinguished from the diastolic flow reversal of aortic regurgitation, since the two conditions can genuinely coexist in the same adult patient, and conflating them leads to a missed or incorrectly attributed diagnosis. See Aortic Regurgitation for the broader AR severity picture this needs to be distinguished from. In adults, where direct visualization of the duct is often limited, the chronic volume-overload consequences (LA and LV dilation) frequently carry as much diagnostic weight as the duct itself.
A Right-to-Left PDA Is Easy to Miss
A PDA with right-to-left flow can be genuinely difficult to identify, because its flow profile can look similar to the flow in the descending aorta or left pulmonary artery. Anatomic assessment by 2D with color Doppler is the most important step in these cases, along with the clinical context. Supporting evidence includes severe pulmonary hypertension and an oxygen saturation differential with upper extremities higher than lower. If the right-to-left duct is restrictive, the Doppler profile can resemble coarctation of the aorta, and the RV should be considered suprasystemic.
Special Situations Worth Knowing How to Image
- PDA with a right aortic arch. Begin by determining arch sidedness — the suprasternal coronal view is the best window for arch sidedness and the branching order of the brachiocephalic vessels. A right-sided PDA runs from the proximal descending aorta to the origin of the right pulmonary artery; a left-sided PDA runs from the left subclavian artery to the origin of the left pulmonary artery. Both sites must be interrogated with 2D, color, and spectral Doppler, and the PDA followed along its whole course from a high parasternal or suprasternal view. A right aortic arch with an aberrant left subclavian artery and a left-sided PDA is highly likely to be a vascular ring.
- Reverse-oriented (vertical) PDA. Its tortuous course is best seen with the aortic arch in view on the suprasternal long-axis, following the duct with color Doppler — though it’s often hard to see its whole length in a single plane because of the tortuosity. If a reverse-oriented PDA is found, the RVOT and pulmonary arteries need detailed assessment to exclude stenosis or atresia, and the pulmonary artery segment at or just beyond the duct insertion should be checked specifically for discrete stenosis or discontinuity.
- Bilateral PDA. This needs a high index of suspicion — think of it with a right aortic arch and aberrant left subclavian artery, or when mediastinal branch pulmonary arteries are absent or discontinuous. Every possible site of ductal insertion should be checked with color Doppler, and when discontinuous pulmonary arteries are a concern, MRI, CT, or angiography may be needed, particularly in the newborn when prostaglandin therapy is being started or stopped.
- Ductal aneurysm. On a high left parasternal transverse view, suspect it when unusual flow is seen from the PDA into the MPA and a large vessel is visualized leftward and superior to the left pulmonary artery, with the restricted portion of the duct at its insertion — three large vessels then line up from medial to lateral: ascending aorta, MPA, and the ductal aneurysm. From the suprasternal short-axis view, angling posteriorly to the descending aorta gives the characteristic “rabbit-ear sign”: the right-sided ear is the transverse arch and descending aorta, and the left-sided ear is the aneurysm. Look-alikes include mirror-image aliasing of the pulmonary artery, the normal soft-tissue shadow of the superior PDA, a left superior vena cava, a dilated left atrial appendage, and a vertical duct.
- Prenatal assessment. In the fetus the PDA is a normal, generally large structure carrying flow from the pulmonary artery to the aorta, and it’s assessed as part of a complete fetal echocardiogram. A reverse-oriented PDA in a fetus with right heart obstruction heralds severe disease.
- Adults. PDA is uncommon in adults, but when present it’s associated with calcification, endocarditis, aneurysm formation, dissection, rupture, left heart volume overload, and pulmonary vascular disease. Transthoracic imaging is challenging because of restricted acoustic windows and is best performed from the suprasternal view using the same techniques as in children. CT and MRI can help when echo is inconclusive; cardiac MRI is preferred because it also shows the hemodynamic effect — biventricular size and function, and an estimate of the pulmonary-to-systemic flow ratio.
How to Diagnose It: A Practical Sequence
- Look for the duct with color Doppler in the high left parasternal (“ductal”) view, then confirm on 2D that a channel connects the underside of the descending aorta to the left pulmonary artery. In infants, screen from the suprasternal, subxiphoid, and apical windows too.
- Confirm with spectral Doppler. Note the pattern (left-to-right, bidirectional, or right-to-left — see below), and look for diastolic flow along the lateral wall of the MPA (96% sensitive, 100% specific for PDA).
- Exclude the look-alikes: helical MPA flow (medial, early systolic only) and, in a suspected right-to-left duct, flow in the descending aorta or left pulmonary artery.
- Measure the narrowest diameter of the duct, and its length and the size of the aortic and pulmonary ends if closure is being planned.
- Decide whether it’s hemodynamically significant: LA and LV dilation, holodiastolic flow reversal in the descending aorta, increased branch pulmonary artery diastolic flow, and pulmonary vein velocity (see the preterm checklist below).
- Estimate pulmonary artery pressure from the ductal peak gradient subtracted from simultaneous systolic blood pressure.
- Define arch sidedness and screen for ductal-dependent or associated lesions — coarctation, RVOT or LVOT obstruction, and other defects — before assuming the PDA is isolated.
The Three Ductal Doppler Flow Patterns
Ductal flow resolves into one of three recognizable patterns, and identifying which one is present is itself diagnostically informative about pulmonary and systemic vascular resistance:
- Dominant left-to-right — continuous flow with a late-systolic peak, continuing into diastole. Seen in an isolated PDA without significant LVOT obstruction or pulmonary hypertension (PVR < SVR).
- Bidirectional — right-to-left in systole, left-to-right in diastole. Can be a normal transitional pattern in the first hours of life before PVR falls, or can reflect LVOT/arch obstruction or pulmonary hypertension of intermediate severity.
- Dominant right-to-left — continuous or near-continuous right-to-left flow with an early-systolic peak. Reflects either a ductal-dependent lesion with significant LVOT obstruction and atrial septal restriction, or severe pulmonary hypertension with PVR at or exceeding SVR.
Pulmonary artery systolic pressure can be estimated directly: the peak late-systolic gradient across the duct (via CW Doppler and the modified Bernoulli equation) is subtracted from simultaneously recorded systemic systolic blood pressure. This correlates well with catheterization-measured peak instantaneous gradients, though sample volume position, adjacent branch pulmonary artery flow, and ductal anatomy can all limit accuracy.
Distinguishing a restrictive right-to-left PDA from coarctation matters clinically and can be done reliably: confirm an unobstructed aortic arch and isthmus, demonstrate flow clearly originating in the main pulmonary artery and coursing to the descending aorta via the duct, look for evidence of severe pulmonary hypertension, and correlate clinically (normal lower-extremity pulses, no upper-to-lower blood pressure gradient). An oxygen saturation differential (upper extremities higher than lower) also supports a right-to-left PDA specifically.
Hemodynamically Significant PDA in the Preterm Infant
Because a hemodynamically insignificant PDA is common and expected in preterm infants, a defined echocardiographic checklist — not a single measurement — is used to establish when a PDA is actually significant enough to warrant treatment:
- Smallest ductal diameter ≥1.4 mm/kg
- Left ventricular dilation
- Holodiastolic flow reversal in the descending aorta
- Increased antegrade diastolic flow in the branch pulmonary arteries, with a mean velocity >0.5 m/s
- Increased pulmonary venous flow velocity, with a preserved normal phasic pattern
A Complete Echocardiographic Assessment
Beyond confirming the duct itself, a full PDA study should also: demonstrate its position, size, and course by 2D and color Doppler; measure its narrowest diameter; determine flow direction; measure peak systolic velocity for PA pressure estimation (with simultaneous blood pressure); demonstrate aortic arch sidedness and branching; screen for coarctation (transverse arch, isthmus, and descending aorta dimensions, plus the left subclavian artery origin); evaluate the abdominal aorta for diastolic flow reversal; assess the branch pulmonary arteries for stenosis or discontinuity (particularly the left PA); evaluate LA and LV size and function; and look for any associated lesions.
Echocardiography Before, During, and After Closure or Stenting
- Before closure. A complete echocardiogram is needed to define the size and type of the PDA and to make sure there is no other structural heart defect — particularly ductal-dependent disease. The aortic and pulmonary ends of the PDA and its length are measured to choose the right device.
- During device closure. Echo can guide the procedure in infants, limiting radiation and contrast. It focuses on the device after deployment but before final release, checking for impingement of the left pulmonary artery or descending aorta; the high left parasternal view shows the device, the aortic arch, and the left pulmonary artery, and each should be checked with 2D, color, and spectral Doppler for obstruction to flow.
- After closure. The immediate post-procedure study looks for residual ductal flow, pericardial effusion, and new valvular regurgitation. Follow-up studies look for residual flow and for narrowing of the left pulmonary artery or descending aorta, in addition to routine ventricular and valve assessment. Echo is also useful for device position and inadvertent migration — a device causing near-complete occlusion of the proximal left pulmonary artery is one recognized complication.
- After medical closure in preterm infants. Closure can be induced pharmacologically, but even after documented cessation of ductal flow, the duct can reopen — worth rechecking rather than assuming it stays shut.
- PDA stenting (an alternative to a systemic-to-pulmonary shunt in ductal-dependent cyanotic lesions) requires echo evaluation of the duct’s origin from the aorta, insertion into the pulmonary artery, and course — long and tortuous versus short and straight — since this determines feasibility. After stenting, echo first checks for inadvertent occlusion of the pulmonary artery or descending aorta, then follows the stent for occlusion by thrombus or neointimal proliferation.
Transesophageal and 3D Echocardiography
TEE is useful when transthoracic windows are inadequate — most often in older children or adults — and for preoperative or preprocedural planning. 3D echocardiography adds detailed spatial visualization of the duct and its relationship to adjacent structures, particularly valuable ahead of transcatheter device closure.
Treatment Considerations
- Pharmacologic closure (indomethacin, or other prostaglandin-synthesis inhibitors) is most effective in preterm infants, working by promoting the same physiologic closure mechanism that’s simply immature in this population.
- Transcatheter coil or device closure is now the most common approach outside the immediate neonatal period and has largely replaced surgery for older, asymptomatic patients with an isolated PDA.
- Surgical ligation is reserved for cases unresponsive to medical or catheter-based treatment, or where ductal anatomy is unsuitable for device closure.
- Endocarditis prophylaxis guidance, like that for VSD, has narrowed considerably from older teaching — current society guidelines reserve it for specific higher-risk situations rather than treating every small, unrepaired PDA as an automatic indication. Consult current guideline-specific criteria directly rather than a blanket rule.
- Postoperative or post-device-closure follow-up should use Doppler to screen for residual shunting and any device-related complications.
Clinical Importance
The clinical spectrum of PDA runs from a trivial incidental finding to a life-sustaining connection in ductal-dependent congenital heart disease — recognizing which situation applies is the single most important judgment a PDA diagnosis requires. See Atrial Septal Defect and Ventricular Septal Defect for the parallel shunt-lesion frameworks at the atrial and ventricular levels, and Right Ventricle Evaluation for how the resulting volume and pressure changes are assessed.
References
- 1. Ho SY, Rigby ML, Anderson RH. The Arterial Duct. In: Echocardiography in Congenital Heart Disease Made Simple. Singapore: World Scientific; 2005.
- 2. Caris E, Arya B. Abnormalities of the Ductus Arteriosus and Pulmonary Arteries. In: Lai WW, Mertens LL, Cohen MS, Geva T, eds. Echocardiography in Pediatric and Congenital Heart Disease: From Fetus to Adult. 3rd ed. Hoboken, NJ: Wiley; 2022.
- 3. Systematic Approach to Adult Congenital Heart Disease; and Common Congenital Heart Defects Associated With Left-to-Right Shunts. In: Lang RM, Khandheria BK, Goldstein SA, Kronzon I, Saric M, Mor-Avi V, eds. ASE's Comprehensive Echocardiography. 3rd ed. Philadelphia, PA: Elsevier; 2021.
- 4. Otto CM. The Adult With Congenital Heart Disease. In: Textbook of Clinical Echocardiography. 7th ed. Philadelphia, PA: Elsevier; 2022.