648 SPECIAL PHYSIOLOGY. 



and the entrance of the blood into the great arteries. At this period 

 the auricles are beginning to dilate. Moreover, the first sound is 

 speedily followed by the pulse, that in the facial artery occurring 

 about g^th of a second, and that in the radial artery at the wrist |th 

 of a second, afterwards. The second sound coincides with the closure 

 of the semilunar valves, and the opening of the auriculo-ventricular 

 valves; whilst, at this period, the ventricles begin to dilate, and the 

 auricles continue their already commenced diastole. The pause of 

 silence, which succeeds to the second sound, coincides with the full 

 dilatation, and the subsequent contraction, of the auricle, and also 

 with the completed dilatation of the ventricles; during this pause, the 

 semilunar valves are closed, and the auriculo-ventricular valves are 

 open. . yt- 



The causes of the heart's sounds have been very closely investi- 

 gated, owing to the changes which they undergo in disease, and to the 

 peculiarity of the sounds which are then developed. The first sound 

 is usually referred to the closure of the auriculo-ventricular valves, 

 either directly and solely, as being dependent on the sudden tension 

 of their segments, or partially and indirectly, as due also to the mus- 

 cular sound of the contracting ventricular walls, the sudden passage 

 of the blood into the great arterial trunks, and the impulse of the 

 heart itsef against the side of the chest. Unless these valves were 

 closed, the walls of the ventricles would not act so forcibly as they 

 do ; neither would the blood rush into the great arteries, nor would 

 the impulse of the heart be so decided. Whilst, therefore, as is com- 

 monly believed, the tension and vibration of the tissue of the closed 

 auriculo-ventricular valves may be really the chief cause of this sound, 

 yet the three other accessory causes, viz., the muscular sound of the 

 ventricles, the sound of the moving blood, and its friction against the 

 orifices of the arteries, and, lastly, the impulse of the heart against 

 the chest, may contribute to the production of the sound as actually 

 heard. But the importance of these causes has probably been over- 

 rated. That the muscular sound is not essential, is shown by the 

 fact, ascertained experimentally, that the sounds are not heard, if the 

 great veins be compressed, so that no blood enters the heart, although 

 its contractions may continue; the production of any sound by the 

 internal movement of the blood, or its rushing through the arterial 

 openings, is doubtful; and ordinary muscular contraction does not 

 give rise to any loud or sudden sound. The cause of the second sound 

 appears to be better determined; it is attributed almost entirely to 

 the tension of the suddenly closed semilunar valves, across the orifices 

 of the aorta and pulmonary artery. The tension of the membranous 

 substance of the valves is sufficient to cause a loud sound; but, by 

 many authorities, the collision of the columns of blood in the great 

 arteries, against themselves, and against the valves, so as to produce 

 that tension, is regarded as a conjoint cause of the actual sound heard 

 in the heart. When, in living animals, one segment of each of these 

 valves is held back by a hooked needle, so that it cannot close, the 

 second sound of the heart ceases. This sound has also been imi- 

 tated in dead animals, by injecting fluid into the aorta, against the 



