Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise residual or unrepaired VSD and PDA in adults, identify closure indications and avoid intervention after irreversible pulmonary vascular disease.
VSDs vary by site and haemodynamic effect. Perimembranous defects can distort the aortic valve; muscular defects may be multiple. Adult intervention is uncommon and needs an ACHD team because anatomy, pulmonary resistance and associated lesions determine risk.
A PDA joins the descending aorta to the pulmonary artery. Persistent pulmonary overcirculation can dilate the left heart; advanced pulmonary vascular disease can reverse ductal flow and cause differential cyanosis.
Incomplete formation or alignment of the interventricular septum leaves a perimembranous, muscular or outlet communication. Location influences spontaneous closure, valve distortion and procedural planning.
Failure of the fetal connection between the descending aorta and pulmonary artery to close after birth leaves a continuous systemic-to-pulmonary communication.
A defect may persist after earlier surgery or occur with other congenital lesions. Operative history and current anatomy are therefore essential before attributing adult symptoms to one shunt.
After pulmonary vascular resistance falls, a VSD usually carries oxygenated blood from the left to the right ventricle, mainly during systole. A PDA carries blood from the aorta to the pulmonary artery during systole and diastole while aortic pressure remains higher.
Excess pulmonary flow returns to the left atrium and ventricle, causing volume loading and dilatation when the communication is haemodynamically important.
A small restrictive VSD maintains a large pressure gradient and loud high-velocity systolic jet, whereas a large non-restrictive VSD may sound quieter as ventricular pressures equalise. A PDA instead produces continuous flow and, when the shunt is substantial, bounding pulses and a wide pulse pressure.
In a large unrepaired VSD or PDA, persistent high pulmonary flow and pressure can cause pulmonary arteriolar remodelling, raising pulmonary vascular resistance and reducing the original left-to-right gradient.
When pulmonary vascular resistance becomes sufficiently high, a VSD can reverse and cause central cyanosis. Reversed PDA flow enters the descending aorta distal to the left subclavian artery, so lower-limb cyanosis may exceed upper-limb cyanosis.
Harsh pansystolic murmur at the lower left sternal edge, often with a palpable thrill; symptoms may be absent.
Exertional dyspnoea, recurrent respiratory symptoms, displaced apex and signs of left-heart volume overload suggest haemodynamic significance.
Continuous machinery-like murmur below the left clavicle with bounding pulse and wide pulse pressure; the murmur may disappear after shunt reversal.
A new early diastolic murmur in a perimembranous or outlet VSD suggests developing aortic regurgitation.
Cyanosis, clubbing, erythrocytosis, haemoptysis or syncope signals advanced pulmonary vascular disease and makes closure hazardous.
Both can cause a pansystolic murmur, but mitral regurgitation is maximal at the apex and often radiates to the axilla rather than producing a lower-sternal thrill.
A lower-sternal pansystolic murmur that strengthens on inspiration, with prominent jugular v waves or a pulsatile liver, favours tricuspid regurgitation over VSD.
A benign continuous cervical murmur changes with posture or gentle venous compression. A PDA murmur persists beneath the left clavicle and may accompany bounding pulses.
An arteriovenous fistula or another aortopulmonary communication can generate continuous flow. Cross-sectional or Doppler imaging demonstrates the connection rather than relying on auscultation alone.
Pulmonary hypertension without a congenital communication lacks the earlier left-to-right volume-load pattern. Congenital imaging, clinical history and invasive haemodynamics help determine whether a shunt caused the vascular disease.
A substantial left-to-right shunt chronically enlarges the left atrium and ventricle, eventually causing exertional breathlessness, reduced ventricular function and overt heart failure.
Irreversible pulmonary vascular remodelling can raise pulmonary arterial pressure and resistance enough to reverse the shunt, producing cyanosis. Routine closure is then dangerous because it can precipitate right-heart failure.
A high-velocity jet through a perimembranous or outlet VSD can draw an adjacent aortic cusp into the defect, progressively impairing leaflet coaptation.
Turbulent shunt jets can damage endocardial or ductal surfaces and support infection. Valve involvement, embolisation or abscess formation may then complicate the congenital lesion.
Right-to-left flow permits paradoxical embolism, while chronic hypoxaemia causes erythrocytosis and haemostatic disturbance. Haemoptysis, stroke or other embolic events may result.
A restrictive VSD produces a high-velocity turbulent jet and may be louder than a large non-restrictive defect.
As pulmonary vascular resistance rises, the pressure gradient and classic murmur may diminish while disease worsens.
With reversed PDA flow entering distal to the left subclavian artery, toes may be more cyanosed than fingers.
Perimembranous and outlet VSDs can draw an aortic cusp into the defect, causing progressive regurgitation.
A visible communication is not itself an indication; ventricular volume load and pulmonary vascular resistance determine benefit and safety.
Equating a loud VSD murmur with a large defect.
Reassuring after a murmur becomes quieter without reassessing pulmonary pressure.
Closing a shunt before invasive haemodynamic assessment when significant PH is suspected.
Missing aortic regurgitation in a perimembranous or outlet VSD.
Giving routine dental antibiotic prophylaxis contrary to NICE CG64.
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An adult has bounding pulses, a wide pulse pressure and a continuous murmur below the left clavicle. Which lesion is most likely?
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.
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