1987 年 28 巻 2 号 p. 143-156
Considerations of the physical basis of cardiac contraction and sound generation explain the mechanism of the first sound. Older theories examining this sound as the result of valve closure or stiffening are refuted. It has been demonstrated that the normal first sound originates in the left ventricle alone and that accelerations and decelerations, "timed" by mitral and aortic valves events, are its cause. Three components have been recognized in the first sound: a occurs when the left ventricular wall and septum have reached a certain tension; b when the aortic valve opens; c when the peak of the aortic pulse has been reached. The ventricular septum is an integral and essential part of the left ventricle. In left bundle branch block, abnormal activation of the septum transforms this into a passive structure resulting in a slower rise of left ventricular pressure and a longer isovolumic period. This causes a small and delayed first sound, whose components, however, are still separated by normal intervals. In right bundle branch block, the first sound has a normal amplitude and its components are separated by normal intervals. If there is a larger late component, it is a c component, similar to that of normal elderly subjects. A larger c component may also be found in atrial septal defect. The cannon sound of AV block is caused by more rapid deceleration due to higher atrial pressure at the onset of ventricular contraction resulting in intense vibrations. The first sound of arrhythmias varies in the different conditions and even in different subjects, due to the effect of several variable factors. Elevated left atrial pressure, stiffening of the mitral valve in mitral stenosis, causes a slow onset and a more rapid rise of LV pressure. This results in a delayed, but larger, first sound. The action of catecholamines on the myocardium dramatically increases the first sound. The latter can be considered as an index of contractility and may be of great interest during stress tests.
