The S2 heart sound is produced by the closure of the two semilunar valves: the aortic valve and the pulmonic valve. These valves snap shut at the end of each heartbeat’s pumping phase, creating the characteristic “dub” in the familiar “lub-dub” rhythm. S2 actually has two components, one from each valve, that normally occur so close together they sound like a single beat.
The Two Components of S2
S2 is really two sounds layered on top of each other. The first component, called A2, comes from the aortic valve closing. The second, called P2, comes from the pulmonic valve closing a fraction of a second later. The two must be separated by at least 20 milliseconds for the human ear to distinguish them as separate sounds. Most of the time, they’re close enough together that you hear one crisp sound.
A2 is the louder of the two. It radiates widely across the chest and can be heard with a stethoscope almost anywhere over the heart. P2 is softer and confined to a small area near the upper left side of the breastbone. When a clinician listens at the lower left chest (the mitral area) and hears S2, they’re essentially hearing only the aortic component.
Where S2 Falls in the Cardiac Cycle
S2 marks the boundary between systole (when the ventricles contract and push blood out) and diastole (when the ventricles relax and refill). During systole, the left ventricle pumps blood through the open aortic valve into the aorta, and the right ventricle pumps blood through the open pulmonic valve into the pulmonary artery. As the ventricles finish contracting, pressure inside them drops below the pressure in those large arteries. Blood briefly tries to flow backward, catching the valve leaflets and forcing them shut. That closure creates S2.
The right ventricle starts ejecting blood slightly before the left ventricle, and it also takes a little longer to finish. Because of this longer ejection time, the pulmonic valve closes after the aortic valve, which is why P2 consistently follows A2.
Why S2 Splits When You Breathe In
One of the most distinctive features of S2 is that it can split into two audible beats during normal breathing. When you inhale, your chest expands and creates negative pressure that draws extra blood into the right side of the heart. The right ventricle now has more blood to pump, so it takes slightly longer to finish ejecting. This delays pulmonic valve closure. At the same time, the pulmonary artery’s low resistance allows it to absorb more blood before pressure builds up enough to shut the valve.
The result: during inspiration, A2 and P2 separate by about 0.02 to 0.08 seconds (averaging 0.03 to 0.04 seconds). That’s just enough for a trained listener to hear two distinct sounds instead of one. When you breathe out, the gap narrows and the two components merge back into a single sound. This is called physiological splitting, and it’s completely normal.
Splitting is best heard at the second or third intercostal space on the left side of the breastbone. That’s the one spot on the chest where the softer P2 is audible enough to be distinguished from A2.
Where to Listen for S2
To hear the aortic component clearly, a stethoscope is placed at the second intercostal space to the right of the breastbone. For the pulmonic component, the stethoscope moves to the second intercostal space on the left. In practice, the aortic component is so much louder that it dominates S2 at almost every listening position. Picking up the pulmonic component, and therefore hearing the split, requires focusing on that upper left parasternal area.
Abnormal Splitting Patterns
Changes in S2 splitting can signal underlying heart or lung problems. There are three main abnormal patterns, each pointing to a different set of causes.
Wide Splitting
When the gap between A2 and P2 is wider than normal, it usually means the right ventricle is taking too long to finish pumping. The most common cause is right bundle branch block, a delay in the electrical signal that triggers right ventricular contraction. Pulmonic valve stenosis (a narrowed pulmonic valve) also produces wide splitting, and the width of the split correlates with the severity of the narrowing. In patients with high blood pressure in the lungs, S2 is typically heard as a single sound because the normal delay disappears. A wide S2 in those patients suggests severe right ventricular dysfunction, often from long-standing disease or a massive blood clot in the lungs.
Fixed Splitting
Normally the split widens with inspiration and narrows with expiration. When it stays the same width regardless of breathing, it’s called fixed splitting. The classic cause is an atrial septal defect, a hole between the heart’s two upper chambers. The hole creates a shared chamber that disrupts the normal respiratory variation in blood flow to the right ventricle. Blood also shunts from left to right through the defect, overloading the right ventricle with extra volume and prolonging its ejection time. This keeps the split wide and constant through each breath cycle.
Paradoxical (Reversed) Splitting
In paradoxical splitting, the normal order flips: the pulmonic valve closes first, and the aortic valve closes second. Because the aortic closure is now delayed, inspiration (which pushes P2 later) actually brings the two sounds closer together instead of pulling them apart. You hear two sounds on expiration and one sound on inspiration, the opposite of normal. This pattern occurs when the left ventricle’s ejection is significantly delayed, as in severe aortic valve stenosis, left bundle branch block, or certain abnormal electrical pathways in the heart.
What Changes S2 Loudness
The intensity of S2 depends largely on the pressure in the arteries when the valves close. Higher pressure slams the valve leaflets shut more forcefully, producing a louder sound. A loud A2 can reflect high systemic blood pressure, while a loud P2 can indicate pulmonary hypertension (high pressure in the lung arteries). Normally P2 is soft because pulmonary artery pressure is much lower than aortic pressure. When P2 becomes as loud as or louder than A2, it’s a notable finding.
Conversely, a diminished S2 can result from stiff, calcified valve leaflets that no longer snap shut crisply. This is common in older adults with calcific aortic stenosis, where the valve leaflets have thickened and lost flexibility over years. The valve still closes, but the sound it generates is muffled.