Opening in the interatrial septum producing left-to-right shunt, fixed split S2, and risk of paradoxical embolism.
Also known as: ASD, atrial septal defect, secundum ASD, primum ASD, sinus venosus defect
Overview
Congenital communication between the left and right atria allowing left-to-right shunting of oxygenated blood, with progressive right heart volume overload. Anatomical subtypes include ostium secundum (most common, ~75%), ostium primum (associated with AV canal defects and Down syndrome), sinus venosus (often with anomalous pulmonary venous drainage), and unroofed coronary sinus.
Epidemiology
Accounts for ~10% of congenital heart disease; female predominance ~2:1. Most common congenital heart defect diagnosed in adulthood. Patent foramen ovale (a flap-valve, not a true ASD) is present in 25-30% of the general population and is implicated in cryptogenic stroke.
Try two board-style Atrial Septal Defect questions
Real questions from the FirstPassPA bank, with the full explanation. Pick an answer — no signup, no email.
Question 1CardiovascularEasy
A 5-year-old girl is referred for evaluation of a murmur. On auscultation, there is a wide, fixed split S2 and a soft systolic ejection murmur at the upper left sternal border. ECG shows incomplete right bundle branch block. Which lesion best accounts for these findings?
AMild valvular pulmonary stenosis
BOstium secundum atrial septal defect
CBicuspid aortic valve with mild stenosis
DSmall perimembranous ventricular septal defect
EPatent ductus arteriosus
Reveal answer & full explanation
Correct answer: B — Ostium secundum atrial septal defect
AMild valvular pulmonary stenosis
BOstium secundum atrial septal defect✓
CBicuspid aortic valve with mild stenosis
DSmall perimembranous ventricular septal defect
EPatent ductus arteriosus
Why Ostium secundum atrial septal defect is correct
A wide, fixed (non-variable with respiration) splitting of S2 is the classic auscultatory hallmark of an atrial septal defect, due to chronic right-sided volume overload and fixed prolongation of right ventricular (RV) ejection.
The soft pulmonic flow murmur reflects increased flow across a normal pulmonary valve.
Incomplete right bundle branch block (RBBB) pattern is also typical of atrial septal defect.
Why the others are wrong
Bicuspid aortic valve with mild stenosis — bicuspid aortic valve gives an ejection click and a right upper sternal border murmur, not fixed S2 splitting.
Patent ductus arteriosus — patent ductus arteriosus (PDA) produces a continuous machinery murmur, not wide fixed S2 splitting.
Small perimembranous ventricular septal defect — ventricular septal defects (VSDs) produce a holosystolic murmur at the lower left sternal border without fixed splitting.
Mild valvular pulmonary stenosis — pulmonary stenosis also causes a systolic ejection murmur at the upper left sternal border and can widen S2 splitting, but the split still varies with respiration and an ejection click is often heard; fixed splitting points to the atrial-level shunt
Question 2CardiovascularMedium
A 32-year-old woman with a known atrial septal defect presents with acute left-arm weakness and aphasia. Imaging confirms an embolic stroke. Lower-extremity ultrasound reveals a deep vein thrombosis. Which mechanism best explains the relationship between her cardiac anatomy and the stroke?
ALeft atrial enlargement predisposing to in situ atrial thrombosis
BTumor embolization from a left atrial myxoma on the septum
CSeptic embolization from infective endocarditis vegetations
DParadoxical embolization through a right-to-left interatrial shunt
ECardioembolism from new-onset atrial fibrillation
Reveal answer & full explanation
Correct answer: D — Paradoxical embolization through a right-to-left interatrial shunt
ALeft atrial enlargement predisposing to in situ atrial thrombosis
BTumor embolization from a left atrial myxoma on the septum
CSeptic embolization from infective endocarditis vegetations
DParadoxical embolization through a right-to-left interatrial shunt✓
ECardioembolism from new-onset atrial fibrillation
Why Paradoxical embolization through a right-to-left interatrial shunt is correct
Paradoxical embolism occurs when a venous thrombus crosses an interatrial communication (atrial septal defect, ASD, or patent foramen ovale, PFO) into the systemic circulation.
Although ASDs typically shunt left-to-right at rest, transient right-to-left shunting occurs during Valsalva, coughing, or any rise in right atrial pressure, allowing emboli access to the brain.
The proven deep vein thrombosis (DVT) in this scenario points specifically to paradoxical embolism as the mechanism.
Why the others are wrong
Septic embolization from infective endocarditis vegetations — endocarditis is uncommon in isolated secundum ASD, and there is no clinical suggestion of infection here.
Cardioembolism from new-onset atrial fibrillation — left atrial enlargement and atrial fibrillation (AF) are downstream consequences of long-standing ASDs and can also cause stroke, but the proven DVT points specifically to paradoxical embolism rather than in situ atrial thrombus.
Left atrial enlargement predisposing to in situ atrial thrombosis — same reasoning as above; the DVT source makes paradoxical embolism the more direct explanation.
Tumor embolization from a left atrial myxoma on the septum — myxoma is the most common primary cardiac tumor in adults, usually arises from the interatrial septum near the fossa ovalis, and can cause embolic stroke in young patients, but an ASD is a defect rather than a mass, no atrial tumor is described, and the proven DVT supplies a venous embolus that crosses the defect to reach the brain.
That's 2. Get 7,700+ more.
Unlock the full FirstPassPA bank: 7,700+ board-style questions, flashcards, and an AI tutor that explains every answer. Your 7-day free trial includes everything, and there's no credit card required.
You've read your 2 free diagnosis previews. Create your free account to unlock the full Atrial Septal Defect (ASD) outline — plus all 514 diagnoses, 7,700+ board-style questions, flashcards, and an AI tutor. Your 7-day free trial includes everything, and there's no credit card required.
Left atrial pressure exceeds right atrial pressure in normal physiology, producing left-to-right shunting through the defect with right-sided volume overload, RA and RV dilation, and increased pulmonary blood flow. Compliance of the RV (greater than LV in adults) further drives shunt magnitude. Over decades, sustained pulmonary overcirculation can lead to pulmonary vascular remodeling and shunt reversal (Eisenmenger syndrome), though this is now uncommon with modern care. PFOs allow transient right-to-left shunting during Valsalva or coughing, enabling paradoxical embolism.
Clinical presentation
Symptoms
Often asymptomatic in childhood; diagnosed in adulthood after decades of right heart volume overload
Recurrent respiratory infections in larger defects
Cryptogenic stroke or TIA (especially PFO with paradoxical embolism)
Migraine with aura — associated with PFO, though closure does not consistently improve symptoms
Signs / physical exam
Wide and fixed splitting of S2 — the auscultatory hallmark (the shunt keeps RV volume high and RV ejection prolonged; the split stays fixed because the inspiratory rise in systemic venous return is offset by a reciprocal fall in left-to-right shunt flow, so RV volume and P2 timing do not vary with respiration)
Soft mid-systolic flow murmur at upper left sternal border (pulmonic outflow)
Mid-diastolic rumble at lower left sternal border in large shunts (increased tricuspid flow)
Right ventricular heave at the lower left sternal border
Loud P2 if pulmonary hypertension develops
Classic findings
Wide and fixed split S2 with pulmonic flow murmur in an otherwise asymptomatic adult.
Differential diagnosis
VSD — Holosystolic murmur at LLSB, no fixed split S2; pulmonary congestion and HF in infancy if large
Innocent flow murmur — Soft, mid-systolic, no fixed split, no chamber enlargement on echo
Anomalous pulmonary venous return (partial or total) — Often coexists with sinus venosus ASD; right heart dilation out of proportion to ASD size
Pulmonic stenosis — Systolic ejection murmur at ULSB, click, no fixed split; isolated lesion on echo
Pulmonary embolism (in adult with new RV dilation) — Acute onset, hypoxia, D-dimer elevation, CTPA confirms
Diagnostic workup
Diagnostic criteria
Hemodynamically significant ASD warranting closure: right heart (RA/RV) enlargement on imaging with Qp/Qs ≥1.5, without severe pulmonary hypertension. Closure may also be considered after documented paradoxical embolism or for platypnea-orthodeoxia. Closure is generally contraindicated if pulmonary vascular resistance is severely elevated and irreversible.
Labs
Basic labs typically unremarkable
BNP may be elevated if symptomatic HF
Imaging
Transthoracic echocardiography with agitated saline (bubble study) and color Doppler — visualizes defect, direction and magnitude of shunt, RA/RV size, RV function, and estimates pulmonary pressures
Transesophageal echocardiography for better characterization of sinus venosus and sinus coronarius defects and to evaluate suitability for percutaneous closure
ECG: incomplete or complete right bundle branch block (RBBB), right axis deviation in secundum ASD; LEFT axis deviation is characteristic of primum ASD due to abnormal AV node anatomy; atrial arrhythmias
CXR: cardiomegaly with prominent RA and RV, increased pulmonary vascular markings, prominent main pulmonary artery
Cardiac catheterization with shunt run (Qp/Qs) and pulmonary vascular resistance assessment if pulmonary hypertension or closure decision is uncertain
Diagnostic algorithm
ASD Subtype
Frequency
Location
ECG Axis
Closure Strategy
Secundum
~75%
Mid-septum (fossa ovalis)
Right axis deviation, RBBB pattern
Transcatheter device (preferred) or surgical
Primum
~15-20%
Inferior septum, near AV valves
LEFT axis deviation
Surgical (often with AV valve repair)
Sinus venosus
~5-10%
Superior or inferior septum near vena cavae
Variable, often abnormal P-wave axis
Surgical (often with PAPVR repair)
Coronary sinus
<1%
Unroofed coronary sinus
Variable
Surgical
Anatomic subtypes of ASD and key distinguishing features.
Treatment
First-line
Secundum ASD: percutaneous transcatheter device closure (e.g., Amplatzer septal occluder) is the preferred approach when anatomy is suitable (adequate rims, defect <38 mm)
Primum, sinus venosus, and unroofed coronary sinus defects, as well as secundum defects with inadequate rims: surgical patch closure
Antiplatelet therapy for about 6 months after device closure while the device endothelializes: aspirin, with a short initial course of clopidogrel added in some centers
Second-line / adjunct
Symptom-directed management of atrial arrhythmias (rate or rhythm control, anticoagulation per CHA2DS2-VASc)
PFO closure in patients <60 with cryptogenic stroke and high-risk features (atrial septal aneurysm or large shunt) — supported by RESPECT, CLOSE, REDUCE trials
Diuretics and pulmonary vasodilators (sildenafil, bosentan) for ASDs with Eisenmenger physiology
Endocarditis prophylaxis NOT routinely required for isolated ASD per AHA guidelines (only for first 6 months after device closure or repair, or if a residual defect remains adjacent to prosthetic material)
Platypnea-orthodeoxia syndrome: dyspnea and hypoxemia upright that improves supine, due to positional right-to-left shunting
PANCE pearls
Wide and fixed split S2 is the auscultatory hallmark — does NOT vary with respiration.
Primum ASDs (associated with Down syndrome and AV canal defects) classically have LEFT axis deviation on ECG, while secundum ASDs cause RIGHT axis deviation.
PFO closure for cryptogenic stroke is supported in patients <60 with high-risk features (large shunt or atrial septal aneurysm). Closure is not routinely indicated for migraine alone.
ASD frequently presents in middle-aged women with new-onset atrial fibrillation or unexplained right heart enlargement — keep on the differential.
References
ACC/AHA 2025 — 2025 ACC/AHA/HRS/ISACHD/SCAI Guideline for the Management of Adults With Congenital Heart Disease (Gurvitz et al., J Am Coll Cardiol 2026;87:822-976)
RESPECT Trial — Long-Term Outcomes of Patent Foramen Ovale Closure or Medical Therapy after Stroke (Saver et al., NEJM 2017)
CLOSE Trial — PFO Closure or Anticoagulants versus Antiplatelet Therapy after Stroke (Mas et al., NEJM 2017)
REDUCE Trial — PFO Closure or Antiplatelet Therapy for Cryptogenic Stroke (Søndergaard et al., NEJM 2017)
Practice Cardiovascular questions on FirstPassPA
Turn this outline into retention. 7,700+ board-style questions with an AI tutor that explains every answer — free to start, no card required.
Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.