Which factors are responsible for the loudness of S1?
In addition to shape and thickness of the chest wall, three major factors play a role:
1. The rate of rise in left ventricular pressure: This is a function of ventricular contractility, with stronger contractions causing a faster rise in left ventricular pressure and thus brisker and more forceful A-V closure. Hence, a loud S1 is typical of the hyperkinetic heart syndrome, whereas a soft (muffled) S1 is instead common in congestive heart failure, whose failing ventricles can only generate a slow rise in systolic pressure.
2. The separation between atrioventricular leaflets at the onset of ventricular systole: The closer the leaflets, the softer S1 is; conversely, the wider apart the leaflets, the louder S1 is. This mechanism feeds into two other important variables:
The duration of the P-R interval: A short P-R forces the ventricles to contract while the leaflets are still widely separated, so that their closure occurs on a steeper part of the left ventricular pressure curve. This, in turn, means a more forceful and louder closure. Conversely, a long PR provides enough time for the leaflets to come close to each other, thus softening S1. A muffled S1 used to be quite common in rheumatic fever with first- degree A-V block. The progressive PR lengthening of the Wenckebach phenomenon may also gradually (and increasingly) soften S1.
The atrioventricular pressure gradient: A large A-V pressure gradient keeps the leaflets widely separated until ventricular pressure rises high enough to shut them close. Since the closure takes place on a steeper part of the left ventricular pressure curve, it will be forceful and loud. Hence, the longer the ventricle has to contract in order to close the A-V valve, the louder S1 will be. This is quite common in mitral stenosis,
where it contributes to the loudness of S1.
3. The thickness of the atrioventricular leaflet: The thicker the leaflets, the louder S1 is (banging hardbacks against each other generates more noise than banging paperbacks). Still, a soft S1 may indicate leaflets that are too rigid. Hence, a thickened and stenotic mitral valve may generate a booming S1 early on in the disease, but a softer (or absent) S1 when the leaflets get eventually calcified and fixed.
In addition to shape and thickness of the chest wall, three major factors play a role:
1. The rate of rise in left ventricular pressure: This is a function of ventricular contractility, with stronger contractions causing a faster rise in left ventricular pressure and thus brisker and more forceful A-V closure. Hence, a loud S1 is typical of the hyperkinetic heart syndrome, whereas a soft (muffled) S1 is instead common in congestive heart failure, whose failing ventricles can only generate a slow rise in systolic pressure.
2. The separation between atrioventricular leaflets at the onset of ventricular systole: The closer the leaflets, the softer S1 is; conversely, the wider apart the leaflets, the louder S1 is. This mechanism feeds into two other important variables:
The duration of the P-R interval: A short P-R forces the ventricles to contract while the leaflets are still widely separated, so that their closure occurs on a steeper part of the left ventricular pressure curve. This, in turn, means a more forceful and louder closure. Conversely, a long PR provides enough time for the leaflets to come close to each other, thus softening S1. A muffled S1 used to be quite common in rheumatic fever with first- degree A-V block. The progressive PR lengthening of the Wenckebach phenomenon may also gradually (and increasingly) soften S1.
The atrioventricular pressure gradient: A large A-V pressure gradient keeps the leaflets widely separated until ventricular pressure rises high enough to shut them close. Since the closure takes place on a steeper part of the left ventricular pressure curve, it will be forceful and loud. Hence, the longer the ventricle has to contract in order to close the A-V valve, the louder S1 will be. This is quite common in mitral stenosis,
where it contributes to the loudness of S1.
3. The thickness of the atrioventricular leaflet: The thicker the leaflets, the louder S1 is (banging hardbacks against each other generates more noise than banging paperbacks). Still, a soft S1 may indicate leaflets that are too rigid. Hence, a thickened and stenotic mitral valve may generate a booming S1 early on in the disease, but a softer (or absent) S1 when the leaflets get eventually calcified and fixed.