Abnormalities of Splitting of the Second Heart Sound

Normal physiologic splitting of S2 was discussed in the section The Cardiac Cycle. This section deals with abnormalities of splitting.

Any condition that delays right ventricular systole, either electrically or mechanically, delays P2 and produces a widened splitting of S2. Right ventricular emptying is delayed by a right bundle branch block or pulmonic stenosis. The pulmonic component of S2 is delayed during both inspiration and expiration, and wide splitting of S2 occurs.

Any condition that shortens left ventricular systole allows A2 to occur earlier than normal, and wide splitting likewise occurs. Conditions such as mitral regurgitation, ventricular septal defect, and PDA shorten left ventricular systole, and the S1-A2 interval is shorter than normal. In these conditions, there is a ''double outlet'' to the left ventricle, and systole therefore is shorter. In a ventricular septal defect, with a left-to-right shunt, not only is left ventricular systole shorter but also right ventricular systole is prolonged. Both factors are crucial in producing the wide splitting of S2.

Any condition, either electrical or mechanical, that delays left ventricular emptying produces paradoxical splitting of S2. Left bundle branch block or aortic stenosis delays left ventricular emptying. These conditions delay the closure of the aortic valve after right ventricular systole and P2 have occurred. The normal sequence of A2-P2 is reversed. During inspiration, P2 moves normally away from S1 toward A2. The split is said to be narrowed. With expiration, P2 moves normally and approaches S1; the P2-A2 split widens. This widening during expiration is paradoxical. Other conditions, such as left ventricular failure and severe hypertension, delay left ventricular ejection and cause paradoxical splitting of S2.

Fixed splitting of S2 is the auscultatory hallmark of an atrial septal defect. In this situation, the split is wide and does not change with respiration. This is because inspiratory increases in venous return to the right atrium normally raise its pressure. During expiration, the right atrial pressure is lower, but the left-to-right atrial shunt keeps the volume in the right atrium constant during respiration; therefore, normal splitting does not occur.

Normal physiologic splitting of the second heart sound and abnormalities of splitting are illustrated in Figure 14-35.

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