To hear both components of S₂, listen carefully with the diaphragm of the stethoscope over the pulmonic area. Listen for S₂ just after the T wave in the patient’s electrocardiogram (ECG).

The splitting of S₂ into the A₂ and P₂ components is heard best during inspiration over Erb’s point.

Remember, inspiration causes an increase in the venous return to the right side of the heart. This increased venous return prolongs the right ventricular ejection time. Inspiration also reduces pressure in the pulmonary artery, resulting in a delayed P₂ or closure of the pulmonic valve. A decrease in blood flow to the left side of the heart occurs simultaneously, resulting in a shorter left ventricular ejection time.

Therefore, A₂ is heard earlier than P₂. (♦Sound 6) This means that a normal S₂ split is heard during inspiration, and the A₂ and P₂ components fuse during expiration.

While listening to S₂, you must determine the intensity of the A₂ and P₂ components and note the duration of the A₂-P₂ interval as well as its relationship to the respiratory cycle. (♦Sound 6) You should also document the S₂ split, noting whether the A₂-P₂ interval increases or decreases during inspiration and expiration.

The intensity of A₂ and P₂ changes proportionally with the difference in pressure gradients across the closed aortic and pulmonic valves. For example, P₂ may be louder than normal in conditions associated with elevated pulmonary artery diastolic pressure, as occurs in some patients with heart failure, mitral stenosis, Eisenmenger’s syndrome, or other congenital heart diseases. When P₂ increases in intensity, it’s sometimes heard over the mitral area and along the left sternal border. (♦Sound 7)

A₂ intensity increases when diastolic pressure in the aorta increases. (♦Sound 8) This commonly happens during exercise; during states of excitement such as extreme fear; in hyperkinetic conditions, such as thyrotoxicosis, fever, and pregnancy; and in systemic hypertension. However, if the patient has left ventricular decompensation, ventricular relaxation is slower, and the pressure gradients may not be great enough to produce an accentuated A₂.

Conversely, A₂ intensity may be diminished in conditions that alter the development of diastolic pressure gradients, such as aortic regurgitation and hypotension. (♦Sound 9) A₂ intensity also decreases when ventricular dysfunction is present, such as after an acute myocardial infarction. With this condition, P₂ may become louder if the pulmonary artery pressure rises and systemic pressure falls. A₂ is also softer or absent when aortic valve motion is restricted, as in severe aortic stenosis.

Abnormal splitting is related to valvular dysfunction to alterations in blood flow to or from the ventricles, or to both. These changes may cause the normal S₂ split to be absent during both phases of the respiratory cycle. Thus, only a single S₂ is heard over Erb’s point. In another case, the split sounds may persist through inspiration and expiration with little or no respiratory variation. (♦Sound 10) The split sounds may also be heard paradoxically on expiration. The A₂-P₂ intervals vary, as does the intensity of A₂ and P₂ during the respiratory cycle. (♦Sound 11) Changes in S₂ splits are usually most noticeable at the beginning of inspiration and expiration. (See PCG and ECG showing abnormal S₂ split with no respiratory variation in a patient with elevated pulmonary artery diastolic pressure and PCG and ECG showing abnormal S₂ split during respiratory cycle, page 32.)