Page 99 - Clinical Pearls in Cardiology

Auscultation of the Precordium 87

In most clinical scenarios, the wide spilt is either due
to a premature A2 component due to early left ventricular
emptying (as in severe MR) or delayed P2 component
due to late right ventricular emptying (as in severe PS)
and the split is mobile. Wide and fixed (nonmobile)
splitting is the hallmark of ASD, and is often the first
clinical clue towards the diagnosis of this condition in
an asymptomatic adult. It should be remembered that
during sustained arrhythmias like atrial fibrillation,
proper clinical evaluation of respiratory variation of
A2–P2 split is difficult.
5. What is the reason for the wide and fixed splitting of
S2 in atrial septal defect?
Atrial septal defect or ASD is associated with increased
pulmonary blood flow due to the left-to-right shunt.
This causes dilatation and increased distensibility of the
pulmonary arteries. So there is a greater decrease in the
pulmonary vascular resistance, and so the pulmonary
hangout interval is prolonged. This is responsible for the
wide A2–P2 split in ASD. In addition to being wide, the
A2–P2 split in ASD is also fixed. Two important factors
are responsible for the fixed A2–P2 split in those with
ASD and they are the following:
1. Because of the gross dilatation of the pulmonary
arteries, there is only a negligible decrease in the
pulmonary artery resistance with inspiration and so
the already delayed pulmonary hangout interval is
not prolonged more during inspiration.
2. The phasic changes in the systemic venous return
during inspiration and expiration are associated with
reciprocal changes in the volume of the left-to-right