160 THE VASCULAR MECHANISM. 



the valves together ; and, in the opinion of some, is the real cause of the 

 closure of the valves ; others, however, as we shall see later on, maintain 

 that subsequent to this reflux due to mere negative pressure a somewhat later 

 reflux, in which the elastic reaction of the arterial walls is concerned, more 

 completely fills and renders tense the pockets, causing their free margins to 

 come into close and firm contact, and thus entirely blocks the way. The 

 corpora Arantii meet in the centre, and the thin membranous festoons or 

 lunulse are brought into exact apposition. As in the tricuspid valves, so 

 here, while the pressure of the blood is borne by the tougher bodies of the 

 several valves, each two thin adjacent lunulse, pressed together by the blood 

 acting on both sides of them, are kept in complete contact, without any 

 strain being put upon fhem ; in this way the orifice is closed in a most 

 efficient manner. 



The ventricular systole now passes off, the muscular walls relax, the 

 ventricle returns to its previous form and position, and the cycle is once 

 more ended. 



What thus takes place in the right side takes place in the left side also. 

 There is the same sudden sharp auricular systole beginning at the roots of 

 the pulmonary veins, the same systole of the ventricle, but, as we shall see, 

 one much more powerful and exerting much more force ; the mitral valve 

 with its two flaps acts exactly like the tricuspid valve, and the action of the 

 semilunar valves of the aorta simply repeats that of the valves of the 

 pulmonary artery. 



We may now proceed to study some of the cardiac events in detail. 



117. The change of form. The exact determination of the changes in 

 form and position of the heart, especially of the ventricles, during a cardiac 

 cycle is attended with difficulties 



The ventricles, for instance, are continually changing their form : they 

 change while their cavities are being filled from the auricles, they change 

 while the contraction of their walls is getting up the pressure on their con- 

 tents, they change while under the influence of that pressure, their contents 

 being discharged into the arteries, and they change when, their cavities 

 having been emptied, their muscular walls relax. 



We may take it for granted that the internal cavities are obliterated by 

 the systole, for it is probable that practically the whole contents are driven 

 out at. each stroke, and probably also each cavity is emptied from its apex 

 toward the mouth of the artery. 



With regard to changes in external form, there seems no doubt that the 

 side-to-side diameter is much lessened. It seems also clear that the front-to 

 back diameter is greater during the whole time of the systole than during 

 the diastole, the increase taking place during the first part of the systole. If 

 a light lever be placed on the surface of the heart of a mammal, the chest 

 having been opened and artificial respiration being kept up, some such curve 

 as that represented in Fig. 52 is obtained. The rise of the lever in describing 

 such a curve is due to the elevation of the part of the front surface of the 

 heart on which the lever is resting. Such an elevation might be caused, 

 especially if the lever were placed near the apex, by the heart being " tilted " 

 upward during the systole, but only a small portion at most of the rise can 

 be attributed to this 'cause; the rise is perhaps best seen when the lever is 

 placed in the middle portion of the ventricle, and must be chiefly due to an 

 increase in the front-to-back diameter of the ventricle during the beat. We 

 shall discuss this curve later on in connection with other curves and may 

 here simply say that the part of the curve from b' to d probably corresponds 

 to the actual systole of the ventricle, that is, to the time during which the 

 fibres of the ventricle are undergoing contraction, the sudden fall from d 



