Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Distinguish haemodynamically important atrial septal defects from a usually incidental PFO and route closure decisions through specialist congenital or stroke services.
ASD presentation ranges from an incidental murmur to exertional limitation, atrial arrhythmia, right-heart failure or pulmonary hypertension. Primum, sinus venosus and coronary-sinus defects need careful anatomical definition and usually surgical rather than device treatment.
PFO closure is a secondary-stroke-prevention decision, not treatment for an incidental bubble-study finding. Neurology and interventional cardiology should agree that the infarct is embolic and no more likely cause is present.
Incomplete formation of septum secundum or excessive resorption of septum primum leaves a true tissue deficiency at the fossa ovalis and permits persistent interatrial flow.
Primum, sinus venosus and coronary-sinus defects reflect different embryological abnormalities and often coexist with AV-valve or anomalous pulmonary-venous anatomy, affecting whether surgery rather than device closure is needed.
A PFO results when septum primum and septum secundum fail to fuse after birth. It is a flap-like potential channel, not missing septal tissue, and is commonly incidental.
Because left-atrial pressure usually exceeds right-atrial pressure, blood crosses a true ASD into the right heart. Shunt size depends on defect anatomy and ventricular compliance.
Chronic excess flow dilates the right atrium and ventricle and increases pulmonary blood flow, producing the pulmonary flow murmur and relatively fixed splitting of the second heart sound.
In a susceptible minority, a large longstanding shunt can remodel pulmonary arterioles and raise pulmonary vascular resistance. Advanced disease may reverse or make the shunt bidirectional, causing cyanosis and potentially making closure unsafe.
Atrial dilatation and remodelling promote flutter or AF. Transient right-to-left flow across an ASD can also permit venous thrombus to bypass the lungs and enter systemic arteries.
A PFO does not usually cause haemodynamically important resting volume loading. Transiently raised right-atrial pressure, or favourable anatomical streaming in selected patients, can direct blood through the flap and permit paradoxical embolism or positional hypoxaemia.
Right-ventricular heave, ejection systolic murmur at the upper left sternal edge and a wide fixed split S2 reflect increased pulmonary flow.
Exertional dyspnoea, reduced exercise capacity, atrial flutter/fibrillation, right-heart failure or pulmonary hypertension may appear in adulthood.
A cortical embolic infarct plus a large right-to-left shunt, atrial septal aneurysm or temporally related venous thrombosis raises causal likelihood only after other sources are excluded.
Dyspnoea and desaturation when upright that improve supine can occur with positional right-to-left shunting through a PFO.
Cyanosis, clubbing and advanced pulmonary hypertension suggest right-to-left shunting and make routine closure dangerous.
A PFO has a flap tunnel, usually no haemodynamically important resting left-to-right shunt and no chronic RV volume overload. TOE defines septal anatomy, while contrast imaging demonstrates right-to-left passage.
This also permits right-to-left passage. Bubbles typically appear in the left heart later than with an intracardiac shunt, but timing alone is imperfect; pulmonary-vein observation and chest imaging can localise the connection.
Anomalous venous return can cause unexplained RV volume overload and commonly accompanies sinus venosus ASD. TOE, CT or CMR maps pulmonary-vein connections missed on routine TTE.
Both may cause an upper-left sternal ejection murmur, but pulmonary stenosis has an outflow gradient and innocent murmurs lack fixed S2 splitting and RV volume overload.
AF, carotid or intracranial arterial disease and small-vessel disease may better explain an infarct than an incidental PFO. Stroke pattern and comprehensive vascular and rhythm assessment discriminate.
A significant ASD chronically overloads the RV and can eventually cause dilatation, functional tricuspid regurgitation, reduced exercise capacity and systemic venous congestion. A PFO alone does not cause this volume load.
In a minority with a large longstanding ASD, high pulmonary flow can contribute to irreversible pulmonary vascular disease, bidirectional or reversed shunting and cyanosis. Closing the defect when pulmonary vascular disease is advanced may precipitate right-heart failure.
Atrial dilatation and remodelling create arrhythmic substrate, to which surgical scar may contribute after repair. Arrhythmia may first reveal an adult ASD and can persist or appear even after late repair.
A venous clot can cross an ASD or PFO during right-to-left flow and cause stroke or systemic infarction. Positional shunting can rarely produce platypnoea-orthodeoxia.
Chronic RV volume loading blunts respiratory variation in pulmonary valve closure, producing the classic fixed split S2.
Right-ventricular volume overload and pulmonary vascular state drive ASD closure decisions more than a single measured diameter.
A probe-patent flap may allow transient right-to-left passage without the chronic volume load of an ASD.
An intracardiac shunt generally opacifies the left atrium early; delayed appearance should raise intrapulmonary shunting.
In advanced pulmonary vascular disease an ASD may decompress the right heart; closing it can precipitate failure.
Calling an incidental PFO the cause of stroke before excluding AF and arterial disease.
Offering PFO closure for primary prevention in an asymptomatic person.
Using defect diameter alone to judge ASD significance.
Closing an interatrial shunt without assessing pulmonary vascular resistance when PH is suspected.
Discharging an adult after childhood ASD repair with no plan for arrhythmia or residual-lesion review.
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On examination of an otherwise stable adult, which auscultatory finding most strongly suggests a haemodynamically significant secundum ASD?
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes