CHAP, iv.] THE VASCULAR MECHANISM. 271 



148. In an anacrotic pulse the first rise is not the highest, 

 but a second rise B, Fig. 50, which follows and is separated from it 

 by a notch is higher than or at least as high as itself. Such an 

 anacrotic wave, though it may sometimes be produced temporarily 

 iii healthy persons, is generally associated with diseased conditions, 

 usually such in which the arteries are abnormally rigid. In de- 

 scribing the ventricular systole we spoke of the pressure within the 

 ventricle as reaching its maximum just before the opening of the 

 semilunar valves ; and this is apparently the normal event ; but 

 there are curves which seem to shew that after the first sudden 

 rise of pressure which opens the valves, followed by a brief 

 lessening of pressure, which appears on the curve as a notch, 

 the pressure may again rise and that to a point higher than 

 before. And a similar curve is sometimes described by the front- 

 to-back diameter of the ventricle. The systole opens the valves as 

 it were with a burst ; this is followed by a slight relapse, and then . 

 the systole, strengthening again, discharges the whole of the 

 ventricular contents into the aorta and so brings about a tardy 

 maximum expansion. And what is thus started in the aorta 

 travels onward over the arterial system. It is difficult to see how 

 these anacrotic events can be produced except by a certain 

 irregularity in the ventricular systole, and indeed the anacrotic 

 pulse is frequently associated with some disease or defect of the 

 ventricle. 



149. Venous Pulse. Under certain circumstances the pulse 

 may be carried on from the arteries through the capillaries into the 

 veins. Thus, as we shall see later on, when the salivary gland is 

 actively secreting, the blood may issue from the gland through the 

 veins in a rapid pulsating stream. The nervous events which give 

 rise to the secretion of saliva, lead at the same time, by the agency 

 of vaso-motor nerves, of which we shall presently speak, to a dilata- 

 tion of the small arteries of the gland. When the gland is at rest, 

 the minute arteries are, as we shall see, somewhat constricted and 

 narrowed, and thus contribute largely to the peripheral resistance 

 in the part; this peripheral resistance throws into action the 

 elastic properties of the small arteries leading to the gland, and 

 the remnant of the pulse reaching these arteries is, as we before 

 explained, finally destroyed. When the minute arteries are dilated, 

 their widened channels allow the blood to flow more easily through 

 them and with less friction ; the peripheral resistance which they 

 normally offer is thus lessened. In consequence of this the elasti- 

 city of the walls of the small arteries is brought into play to a 

 less extent than before, and these small arteries cease to do their 

 share in destroying the pulse which comes down to them from the 

 larger arteries. As in the case of the artificial model, where the 

 f peripheral ' tubing is kept open, not enough elasticity is brought 

 into play to convert the intermittent arterial flow into a con- 

 tinuous one, and the pulse which reaches the arteries of the gland 



