The factors that are responsible for the intensity of S1 are as follows:
The rate of rise of ventricular pressure
The condition of the valve
The position of the valve
The faster the rate of rise of left ventricular pressure is, the louder the mitral component of S1 is. Increased contractility increases the intensity of S1. Decreased contractility softens S1.
When the atrioventricular valve stiffens as a result of fibrosis or calcification, its closure is louder. The pathologically deformed valve of mitral stenosis produces an accentuated or louder S1. After many years, as the valve becomes increasingly calcified, it becomes unable to move, causing S1 to soften.
The position of the valve at the time of ventricular contraction affects the intensity of S1. The arc of coaptation is the angle through which the valve closes. If the valve is in a midposition, it travels less than when it closes from a widely opened position. The more it is opened, the wider the arc of coaptation, and the louder is S1. This situation is directly related to the pressure in the left atrium at the moment that the left ventricular pressure exceeds it and closes the valve. This can occur in conditions in which there is a shortened PR interval on the electrocardiogram. The mitral valve is opened normally during diastole for ventricular filling. The P wave of the electrocardiogram corresponds to atrial contraction, which elevates left atrial pressure (the "a" wave of the left atrial tracing), further opening the mitral valve in late diastole. If the PR interval is short, ventricular contraction occurs so quickly after atrial contraction that the atrial pressure is still high when the left ventricular pressure exceeds it. The mitral valve stays open longer and closes later than normal, during the rapid rate of rise of pressure of the ventricle, which accentuates S1.
In general, the longer the PR interval, the softer the S1. Lengthening of the PR intervals, as is seen in Wenckebach's phenomenon,* produces an S1 that softens until the dropped beat occurs.
Whenever the heart is farther from the chest wall, the S1 is softer than normal. In patients who are very obese or who have chronic obstructive lung disease, the intensity of the S1 is softer than normal. In patients with a large pericardial effusion, the S1 is likewise soft.
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