The first heart sound (S1) results from the closing of the mitral and tricuspid valves. The sound produced by the closure of the mitral valve is termed M1, and the sound produced by closure of the tricuspid valve is termed T1. The M1 sound is much louder than the T1 sound due to higher pressures in the left side of the heart; thus, M1 radiates to all cardiac listening posts (loudest at the apex), and T1 is usually only heard at the left lower sternal border. This makes the M1 sound the main component of S1.
CLINICAL PEARL: A split S1 heart sound is best heard at the tricuspid listening post, as T1 is much softer than M1.
The M1 sound occurs slightly before T1. Because the mitral and tricuspid valves normally close almost simultaneously, only a single heart sound is usually heard. However, in about 40% to 70% of normal individuals — as well as in certain cardiac conditions — a “split S1” sound can be appreciated. This occurs when the mitral valve closes significantly before the tricuspid valve, allowing each valve to make a separate audible sound. Inspiration delays the closure of the tricuspid valve in a normal person, due to increased venous return, thereby enhancing the splitting of the S1 sound.
A split S1 sound is common in the setting of a right bundle branch block or ventricular tachycardia/premature ventricular contractions, or PVCs, with a right bundle branch block morphology. A RBBB causes the electrical impulse to reach the left ventricle before the right ventricle. Dyssynchrony then occurs, resulting in the left ventricle contracting before the right ventricle, thus the pressures in the LV rise before that of the right ventricle.
This delays the closure of the tricuspid valve, resulting in a split S1 sound. A left bundle branch block has the opposite effect on S1. In this setting, the electrical impulse reaches the RV before the LV, thus the pressure in the RV rises before that of the LV. This forces the tricuspid valve closed earlier, resulting in complete overlap of M1 and T1, and thus no audible split S1 sound.
CLINICAL PEARL: A RBBB results in a widened split S1, whereas a LBBB results in the absence of a split S1.
Four factors affect the intensity of the first heart sound. Because the M1 portion of S1 is much louder than T1, it is only important to discuss what affects the intensity of M1.
- Chest wall thickness: The first factor is the thickness of the chest wall. Individuals with obesity will have a soft S1, whereas thinner people will have a more intense S1. The greater the distance separating the leaflets of the mitral valve at the beginning of systole, the louder the S1; this is affected by the duration of the PR interval on the ECG.
- Length of PR interval: Remember that the PR interval represents part of diastole, meaning a longer PR interval would result in a longer diastolic filling time. As the LV fills, the pressure gradually increases. This gradual increase in pressure causes the mitral valve leaflets to slowly drift together. Therefore, when ventricular systole occurs in the setting of a long PR interval, the leaflets will be separated by a smaller distance, and the S1 sound will be softer. The converse is also true. A short PR interval results in an accentuated S1, as the mitral valve leaflets will be further apart at the onset of ventricular systole.
CLINICAL PEARL: A short PR interval results in an accentuated S1, whereas a long PR interval results in a soft S1.
- Valve leaflet mobility: The mobility of the valve leaflets is another factor influencing the intensity of M1. In mild to moderate mitral stenosis, the increased left atrial pressure causes the mobile portions of the mitral valve leaflets to be more widely separated, resulting in an accentuated M1 sound. In severe to critical mitral stenosis, the valve leaflets are so calcified and immobile that the M1 sound is diminished or absent.
CLINICAL PEARL: Mild to moderate mitral stenosis results in a loud S1, whereas severe to critical mitral stenosis results in a soft S1.
- Ventricular contraction rate: The rate of ventricular contraction also affects the intensity of S1. The faster the heart rate and the faster the rise in ventricular pressure, the louder the S1. Thus, high flow states such as anemia, thyrotoxicosis or sepsis would result in an accentuated S1. Also, during exercise or any other setting of tachycardia, the S1 will be accentuated.