The heart produces a characteristic rhythm of sounds as it pumps blood, often described as “lub-dub.” This rhythmic pattern is generated by the closing of the heart’s four valves. The first sound, S1, is the “lub,” and the second sound, S2, is the distinct “dub.” S2 marks the end of ventricular contraction (systole) and signifies the beginning of the heart’s resting and filling phase (diastole). Analyzing the S2 sound, particularly its timing and quality, offers specific clues about the health of the heart’s major outflow valves and the pressures within the great vessels. Variations in S2 are often the first audible signs of underlying cardiovascular conditions, making it a valuable diagnostic tool.
The Origin and Components of the S2 Sound
The S2 heart sound consists of two distinct acoustic components generated by the closure of the semilunar valves: the aortic and the pulmonary valves. These valves are located at the exits of the left and right ventricles. The first component is the aortic sound (A2), resulting from the closure of the aortic valve after the left ventricle ejects blood into the high-pressure systemic circulation. The second component is the pulmonic sound (P2), caused by the closure of the pulmonary valve after the right ventricle ejects blood into the lower-pressure pulmonary circulation.
A2 usually occurs a few milliseconds before P2 because the higher pressure in the aorta causes the aortic valve to close earlier. This higher closing pressure also makes the A2 sound louder and widely transmitted across the chest. The sound itself is not produced by the physical contact of the valve leaflets. Instead, it results from the abrupt deceleration of the blood column, which causes the valve structures and vessel walls to vibrate immediately after the valves snap shut. During most of the respiratory cycle, the interval between A2 and P2 is so brief that the two sounds fuse, and the listener perceives only a single “dub” sound.
Understanding Normal Physiologic Splitting
Normal physiologic splitting occurs when the two components of S2 separate audibly during inspiration but fuse during expiration. This temporary separation is a healthy variation caused by the interplay between respiration and blood flow dynamics. When a person inhales, the negative pressure in the chest cavity draws more blood into the right side of the heart. This increased volume prolongs the right ventricle’s ejection time, delaying the closure of the pulmonary valve (P2).
Simultaneously, the negative intrathoracic pressure slightly impedes blood return from the lungs into the left atrium, causing a temporary decrease in left ventricular volume. The left ventricle finishes its ejection sooner, causing the aortic valve (A2) to close marginally earlier. The combination of an earlier A2 and a delayed P2 widens the interval, making the split audible during inspiration.
When the person exhales, the flow dynamics reverse. Right ventricular volume returns to baseline, and P2 moves closer to A2. This causes the two components to fuse back together, and S2 is heard as a single sound. The ability of S2 to split during inspiration and fuse during expiration is the standard for a healthy, responsive cardiovascular system.
Pathologic Variations and Clinical Significance
Variations from the normal respiratory pattern of S2 splitting signal abnormalities in the heart’s pressure, volume, or electrical conduction systems.
Fixed Splitting
Fixed splitting occurs when the A2 and P2 components are audibly separated throughout both inspiration and expiration, with no change in the interval. This is a hallmark feature of an atrial septal defect (ASD), a congenital condition involving a hole between the upper chambers of the heart. The defect causes a constant, excessive volume of blood to flow into the right atrium. This permanently overloads the right ventricle and delays P2 closure, regardless of the respiratory cycle.
Paradoxical Splitting
Paradoxical, or reversed, splitting is a deviation where the S2 sound is single during inspiration but splits during expiration. This happens when a condition delays the closure of the aortic valve (A2) so significantly that it closes after the pulmonic valve (P2). Common causes include severe obstruction of the left ventricular outflow tract, such as aortic stenosis, or a disruption in the electrical conduction system, like a left bundle branch block, which delays left ventricular contraction.
Single S2
An S2 that remains consistently single, even during deep inspiration, may also indicate underlying pathology. This can occur if one of the semilunar valves is structurally unable to produce a sound, such as in severe calcification associated with aortic or pulmonary stenosis. A single S2 can also happen if one valve is missing (atresia), or if pressures are severely altered, making the split too narrow to detect.
Intensity Changes
The intensity of the S2 components holds diagnostic value, separate from the timing of the split. A loud or accentuated P2 suggests elevated pressure in the pulmonary circulation, most commonly seen in pulmonary hypertension. The high pressure in the pulmonary artery forces the pulmonary valve shut with greater force, increasing the sound’s loudness. Conversely, a diminished or soft A2 may be heard when the aortic valve is severely stenotic (narrowed) and stiff, preventing it from closing with its usual force. These acoustic variations provide crucial insights into the heart’s mechanical and hemodynamic state.