Luisada A A
Jpn Heart J. 1987 Mar;28(2):143-56. doi: 10.1536/ihj.28.143.
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.
对心脏收缩的物理基础和声音产生的考量解释了第一心音的机制。将此声音视为瓣膜关闭或硬化结果的旧理论被驳斥。已证明正常的第一心音仅起源于左心室,二尖瓣和主动脉瓣事件“定时”的加速和减速是其成因。第一心音已被识别出有三个成分:a成分在左心室壁和室间隔达到一定张力时出现;b成分在主动脉瓣打开时出现;c成分在主动脉脉搏峰值达到时出现。室间隔是左心室不可或缺的重要组成部分。在左束支传导阻滞时,室间隔的异常激活使其转变为被动结构,导致左心室压力上升较慢且等容期延长。这会导致第一心音微弱且延迟,但其成分之间的间隔仍正常。在右束支传导阻滞时,第一心音振幅正常,其成分之间的间隔也正常。如果有较大的晚期成分,则为c成分,类似于正常老年受试者的情况。在房间隔缺损时也可能发现较大的c成分。房室传导阻滞时的大炮音是由于心室收缩开始时心房压力较高导致更快速的减速,从而产生强烈振动所致。心律失常时的第一心音在不同情况下甚至在不同个体中都会有所不同,这是由于多种可变因素的影响。左心房压力升高,二尖瓣狭窄时二尖瓣硬化,会导致左心室压力起始缓慢且上升更快。这会导致第一心音延迟但更大。儿茶酚胺对心肌的作用会显著增加第一心音。后者可被视为收缩力的指标,在压力测试期间可能具有重要意义。