Tyler Wynn
The second heart sound (S2) is a short burst of auditory vibrations that can provide valuable clues about the heart. It is produced by the closure of the aortic and pulmonic valves, with the aortic valve (A2) closing first, followed by the pulmonic valve (P2). S2 is normally split during inspiration and single during expiration, with the interval between A2 and P2 increasing on inspiration and disappearing on expiration. The intensity of P2 is determined relative to A2, and an elevated P2 intensity can indicate pulmonary hypertension or an atrial septal defect. S2 can exhibit persistent (widened) splitting, fixed splitting, paradoxical (reversed) splitting, or the absence of splitting, with each type providing insights into cardiac function and potential abnormalities.
| Characteristics | Values |
|---|---|
| Sound produced by | Closure of the aortic and pulmonic valves |
| Aortic valve closure sound | A2 |
| Pulmonic valve closure sound | P2 |
| A2 sound | Louder than P2 |
| A2 sound | Heard all over the chest |
| P2 sound | Soft and heard only at the pulmonic region |
| P2 sound | Heard at left parasternal, intercostal space 2 |
| P2 intensity | Elevated if louder than A2 at the pulmonic region |
| Wide splitting | Detected by presence of splitting during expiration, wider during inspiration |
| Paradoxical splitting | Reverse of normal physiology, splitting during expiration, singular during inspiration |
| Fixed splitting | Same amount of splitting throughout the entire respiratory cycle |
| Persistent (widened) splitting | Both A2 and P2 are audible during the entire respiratory cycle |
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What You'll Learn
- The second heart sound (S2) is produced by the closure of the aortic and pulmonic valves
- A2 occurs just before P2, and the combination of these sounds make up S2
- A physiologic split S2 occurs when A2 precedes P2 by a distance that allows both sounds to be heard separately
- A paradoxical split S2 occurs when the splitting is heard during expiration and disappears during inspiration
- Diagnoses like pulmonary hypertension, severe aortic stenosis, and atrial septal defect can be suspected with close attention to S2
The second heart sound (S2) is produced by the closure of the aortic and pulmonic valves
A2 is normally much louder than P2 due to higher pressures on the left side of the heart. This means that A2 radiates to all cardiac listening posts and is the main component of S2. P2 is usually only heard at the left upper sternal border. During inspiration, the pulmonary artery is able to tolerate more blood volume before the pressure above the valve. This results in a physiologic split S2, where the A2 sound precedes P2 by a great enough distance to allow both sounds to be heard separately. This occurs during inspiration when increased venous return to the right side of the heart delays the closure of the pulmonic valve and decreased return to the left side of the heart hastens the closure of the aortic valve. During expiration, the distance narrows, and the split S2 is no longer audible.
A paradoxical split S2 heart sound occurs when the splitting is heard during expiration and disappears during inspiration, the opposite of the physiologic split S2. This occurs in any setting that delays the closure of the aortic valve, including severe aortic stenosis and hypertrophic obstructive cardiomyopathy, or in the presence of a left bundle branch block. A fixed split S2 is caused by an atrial septal defect, resulting in altered cardiac hemodynamics that cause a fixed delay in PV closure. Persistent (widened) splitting occurs when both A2 and P2 are audible during the entire respiratory cycle, and the splitting becomes greater with inspiration and less prominent with expiration.
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A2 occurs just before P2, and the combination of these sounds make up S2
The second heart sound (S2) is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2, and the sound produced by the closure of the pulmonic valve is termed P2. Normally, A2 occurs just before P2, and the combination of these sounds makes up S2. A2 is normally much louder than P2 due to higher pressures in the left side of the heart. A2 can be heard widely all over the chest, while P2 is usually only heard at the left upper sternal border. Therefore, A2 is the main component of S2.
A physiologic split S2 occurs when the A2 sound precedes P2 by a significant distance, allowing both sounds to be heard separately. This happens during inspiration when increased venous return to the right side of the heart delays the closure of the pulmonic valve, and decreased return to the left side of the heart hastens the closure of the aortic valve, further separating A2 and P2. During expiration, the distance narrows, and the split S2 is no longer audible. A physiologic split S2 normally occurs during inhalation because the decrease in intrathoracic pressure increases the time needed for pulmonary pressure to exceed that of the right ventricular pressure.
A paradoxical split S2 heart sound occurs when the splitting is heard during expiration and disappears during inspiration, the opposite of the physiologic split S2. A paradoxical split S2 occurs in any setting that delays the closure of the aortic valve, including severe aortic stenosis and hypertrophic obstructive cardiomyopathy, or in the presence of a left bundle branch block.
A fixed split S2 is a rare finding on a cardiac exam. When found, it almost always indicates the presence of an atrial septal defect. A fixed split S2 occurs when there is always a delay in the closure of the pulmonic valve, and there is no further delay with inspiration. A fixed split S2 occurs in patients with altered cardiac hemodynamics, resulting in a fixed delay in pulmonic valve closure. During inspiration, there is an increase in venous return to the right side of the heart, and thus increased flow through the pulmonic valve, delaying its closure.
A persistent (widened) split S2 occurs when both A2 and P2 are audible during the entire respiratory cycle, and the splitting becomes greater with inspiration and less prominent with expiration. A persistent split S2 would occur in the setting of a right bundle branch block, pulmonary hypertension, or pulmonic stenosis (delayed P2) or severe mitral regurgitation/ventricular septal defect (early A2 closure).
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A physiologic split S2 occurs when A2 precedes P2 by a distance that allows both sounds to be heard separately
The second heart sound (S2) is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2, and the sound produced by the closure of the pulmonic valve is termed P2. Normally, A2 occurs just before P2, and the combination of these sounds makes up S2.
During expiration, the distance narrows, and the split S2 is no longer audible. A2 is normally much louder than P2 due to higher pressures on the left side of the heart. Thus, A2 radiates to all cardiac listening posts and is the main component of S2. P2 is usually only heard at the left upper sternal border.
A paradoxical split S2 heart sound occurs when the splitting is heard during expiration and disappears during inspiration, the opposite of the physiologic split S2. A paradoxical split S2 occurs in any setting that delays the closure of the aortic valve, including severe aortic stenosis and hypertrophic obstructive cardiomyopathy, or in the presence of a left bundle branch block.
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A paradoxical split S2 occurs when the splitting is heard during expiration and disappears during inspiration
The second heart sound (S2) is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2, and the sound produced by the closure of the pulmonic valve is termed P2. Normally, A2 occurs just before P2, and the combination of these sounds makes up S2. A physiologic split S2 occurs when the A2 sound precedes P2 by a great enough distance to allow both sounds to be heard separately. This happens during inspiration when increased venous return to the right side of the heart delays the closure of the pulmonic valve, and decreased return to the left side of the heart hastens the closure of the aortic valve, thereby further separating A2 and P2. During expiration, the distance narrows, and the split S2 is no longer audible.
A paradoxical split S2 heart sound occurs when the splitting is heard during expiration and disappears during inspiration — the opposite of the physiologic split S2. Paradoxical splitting is the reverse of normal physiology, with the second heart sound splitting during expiration and occurring singularly during inspiration. A paradoxical split S2 occurs in any setting that delays the closure of the aortic valve, including severe aortic stenosis and hypertrophic obstructive cardiomyopathy, or in the presence of a left bundle branch block.
The paradoxical splitting of S2 indicates pathology due to a delay in the aortic valve closing. Aortic stenosis, hypertrophic cardiomyopathy, left bundle branch block, and a ventricular pacemaker could all cause a reverse splitting of the second heart sound. The respiratory variation of the second heart sound can be categorised as normal (physiologic) splitting, persistent (audible expiratory) splitting, persistent splitting without respiratory variation (fixed splitting), and reversed (paradoxical) splitting.
During inspiration, the chest wall expands and causes the intrathoracic pressure to become more negative (akin to a vacuum). There is an increase in blood volume in the right ventricle during inspiration, so the pulmonary valve (P2 component of S2) stays open longer during ventricular systole due to an increase in ventricular emptying time. The aortic valve (A2 component of S2) closes slightly earlier due to a reduction in left ventricular volume and ventricular emptying time. Thus, the P2 component of S2 is delayed relative to that of the A2 component. This delay in P2 versus A2 is heard as a slight broadening or even "splitting" of the second heart sound.
During expiration, the chest wall collapses and decreases the negative intrathoracic pressure. The pulmonary valve (P2) closes before the aortic valve (A2), and splitting is maximal on expiration and minimal or absent on inspiration. The identification of the reversed order of valve closure may be possible by judging the intensity and transmission of each component of the second sound.
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Diagnoses like pulmonary hypertension, severe aortic stenosis, and atrial septal defect can be suspected with close attention to S2
The second heart sound (S2) is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is called A2, and the sound produced by the closure of the pulmonic valve is called P2. A2 is normally louder than P2 due to higher pressures on the left side of the heart. A2 can be heard all over the chest, while P2 is usually only audible at the left upper sternal border.
S2 can exhibit different types of splitting, including persistent (widened) splitting, fixed splitting, paradoxical (reversed) splitting, and the absence of splitting. Persistent splitting occurs when both A2 and P2 are audible during the entire respiratory cycle, with the split becoming greater during inspiration due to increased venous return and less prominent during expiration. Fixed splitting, on the other hand, exhibits the same amount of splitting throughout the respiratory cycle. Any condition that causes a non-fixed delay in the closure of the pulmonic valve or early closure of the aortic valve will result in a wide split S2. For example, a right bundle branch block (RBBB) causes a delay in the closure of the pulmonic valve, resulting in a delayed P2 without affecting A2. In contrast, severe mitral regurgitation or a ventricular septal defect leads to early A2 closure.
Diagnoses like pulmonary hypertension, severe aortic stenosis, and atrial septal defect (ASD) can be suspected or confirmed by paying close attention to the characteristics of S2. For instance, in the case of pulmonary hypertension, there is often a delay in the closure of the pulmonic valve, resulting in a wide split S2. Paradoxical splitting, where the second heart sounds split during expiration and remain singular during inspiration, can be indicative of aortic stenosis. Additionally, a fixed split S2, where the degree of splitting remains constant throughout the respiratory cycle, is pathognomonic for the presence of an atrial septal defect. This is due to the continuous blood flow from the left side to the right side of the heart, resulting in a lengthened cardiac cycle on the right side.
It is important to note that the presence or absence of certain splitting patterns in S2 does not always indicate a specific diagnosis. Other cardiac sounds and clinical findings must also be considered to make a comprehensive assessment. Additionally, in patients with obesity, emphysema, or pericardial fluid, P2 may be difficult to hear, resulting in a single audible A2 heart sound.
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Frequently asked questions
The second heart sound (S2) is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2, and the sound produced by the closure of the pulmonic valve is termed P2.
A2 is normally much louder than P2 due to higher pressures in the left side of the heart. A2 can be heard widely all over the chest, whereas P2 is normally soft and only heard at the pulmonic region (left parasternal, intercostal space 2).
Splitting in S2 refers to the separation of A2 and P2 sounds. Normally, A2 occurs just before P2, but in some cases, they can be separated enough to be heard individually. This is known as a physiologic split S2.
A paradoxical split S2 occurs when the splitting is heard during expiration and disappears during inspiration, which is the opposite of a physiologic split S2. It can be caused by severe aortic stenosis, hypertrophic obstructive cardiomyopathy, or a left bundle branch block.
