ASD Flashcards

1
Q

Presentation

A
  • Lesions not recognised in childhood tend to present in 3rd and 4th decade
  • Dyspnoea (pulmonary HTN or AF)
  • Palpitations (atrial rhythm disturbances)
  • TIA/Stroke - paradoxical emboli, AF
  • right heart failure
  • unexplained respiratory tract infections
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2
Q

Signs

A
  • features of associated syndromes eg marfans syndrome (low set ears, flat nasal bridge, prominent epicanthic folds, glossoptosis, simian palmar crease)
  • signs of stroke
  • pulse could be irregular die I AF
  • normal, elevated due to HF or TR due to RV overload
  • thrust over RV if overloaded
  • On Auscultation:
  • S1 normally normal but could be pronounced as TV leaflets opened vigourously by volume overloaded RA then shut vigourously by overloaded and hyperdynamic RV
  • soft ejection systolic murmur due to exaggerated flow through normal PV for same reason as above
  • PSM 2ry to TR if caused by RV overload
  • S2 is fixed and widely split. P2 occurs later due to increased PV flow. Communication between atria prevent the normal variations in pressure between both during respiration
  • P2 May be louder due to pulmonary HTN
  • rarely soft low-pitch diastolic murmur in large ASD due to increased blood flow over an effectively narrowed TV
  • signs of right heart failure
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3
Q

Severity

A

Large ASD indicated by:

  • evidence of RV overload
  • pulmonary HTN
  • soft low-pithed diastolic murmur
  • AF (due to LA enlargement 2ry increased pulmonary venous return)

Less severe

  • absence of the above
  • soft pulmonary systolic murmur
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4
Q

Types

A

Primum ASD
- more correctly AV separation defect. Often associated with VSD and other defects. Abnormality in development of endocardial cushions so defect is in ostium premum (related to Down’s syndrome)

Secondum ASD
- defect in fossa ovalis due to incomplete development of septum secondum or excessive resorption of septum primum during development. This does not include patent foramen ovale

Sinus venosus ASD - abnormal folding of septum causing IVC also emptying into LA and also commonly pulmonary veins emptying into RA.

Coronary sinus ASD
- defect in wall between LA and coronary sinus

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5
Q

Investigations

A
  • ECG: AF, abnormal p-waves 1st HB, partial RBBB, LAD in primum, RAD in secendum
  • CXR - cardiomegaly, atrial enlargement, pulmonary artery dilatation
  • TTE, bubble contrast may be necessary
  • TOE to further assess defectsamd suitability for closure. Need to see sinus venosus defect
  • R+L cardiac catheterisation. Can be useful for measuring pressures if Echo inconclusive. Can also assess reversibility of pulmonary HTN. If >40 then needed preoperarively anyway
  • cardiac MRI - detailed anatomy definition and function and shunt assessment
  • lung biopsy if right heart catheter with vasodilator test unclear in reversibility of pulmonary HTN
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6
Q

Management

A

No intervention required in most.
Offer surgery if:
- paradoxical embolism
- symptomatic
- significant shunt (ratio pulmonary to systemic flow >1.5)
- significant pulmonary HTN (>2/3 systemic) AND shown to have reversibility with right heart catheter dilation and the shunt fraction is at least 1.5

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7
Q

Lutembacher syndrom

A

Coexistence of secondum ASD and rheumatic MS. Can also be acquired by atrial septal puncture for PBMV to treat rheumatic MS

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