CHAP, iv.] THE VASCULAR MECHANISM. 283 



wave. Careful measurements shew that the distance between 

 the primary and dicrotic crests is either the same or certainly not 

 less in the smaller or more distant arteries than in the larger or 

 nearer ones. This feature indeed proves that the dicrotic wave 

 cannot be due to reflection at the periphery or indeed in any way 

 a retrograde wave. Besides the multitudinous peripheral division 

 would probably render one large peripherically reflected wave im- 

 possible. Again, the more rapidly the primary wave is obliterated 

 or at least diminished on its way to the periphery the less 

 conspicuous should be the dicrotic wave. Hence increased ex- 

 tensibility and increased elastic reaction of the arterial walls 

 which tend to use up rapidly the primary wave, should also lessen 

 the dicrotic wave. But as a matter of fact these conditions, as we 

 have said, are favourable to the prominence of the dicrotic wave. 



We may conclude then that the dicrotic wave like the primary 

 wave begins at the heart, and travels thence towards the periphery. 

 But even if this be admitted observers are not agreed as to the 

 mechanism of its production. As we stated ( 134) there seemed 

 to be evidence that the ventricle discharged its contents so 

 rapidly that during the latter part of the systole it remained 

 contracted though empty. In accordance with this view the 

 following explanation of the development of the dicrotic wave has 

 been given. 



When a rapid flow of fluid through a tube is suddenly stopped 

 a negative pressure makes its appearance behind the column of 

 fluid ; owing to its momentum the fluid tends to move onward, 

 though there is now no following fluid to take its place. The 

 sudden cessation of the flow from the ventricle, due to the ventricle 

 being suddenly emptied, must, it is argued, lead to a similar 

 negative pressure ; and indeed, as we have said, the negative 

 pressure which may be observed in the ventricle has, by some, 

 been referred to this cause. In a rigid tube such a negative 

 pressure simply leads to a reflux of fluid ; when the tap of a 

 running water supply is suddenly turned off, the click which is 

 heard is caused by the fluid being thus brought back against the 

 tap. In a thin collapsible tube again such a negative pressure 

 simply leads to a collapse of the tube near the tap. But in an 

 elastic tube like the aorta the effects of such a negative pressure 

 are complicated by those of the elastic action and the inertia of 

 the walls of the tube. Upon the sudden cessation of the flow 

 from the ventricle, the expansion of the aorta ceases, the vessel 

 begins to shrink. This shrinking is in part due to the elastic 

 reaction of the walls of the aorta, but is increased by the 

 "suction" action of the negative pressure. In thus shrinking 

 however under these combined causes, the aorta, through the 

 inertia of its walls, and of the contained blood is carried too far, 

 it shrinks too much, and in consequence, the negative pressure 

 moreover having by this time passed away, begins to expand again. 



