298 THE MECHANICS OF THE HEART 



venous compartments, in consequence of which the blood within them 

 is placed under a lower pressure than it would be otherwise. The 

 veins outside the thorax, on the other hand, are exposed to the atmos- 

 pheric pressure. Obviously, therefore, this negative pressure in the 

 central part of the circulatory system must disappear immediately 

 upon opening the chest, because the ensuing collapse of the lungs 

 nulUfies their elastic pull upon the blood-vessels. The opposite effect 

 may be produced under normal conditions by raising the intrathoracic 

 pressure, as may be done by holding the breath or by making forced 

 expiratory movements. A far-reaching venous engorgement and 

 arterial deficiency may thus be incited, which are indicated, on the one 

 hand, by the swelUng of the superficial veins and, on the other, by the 

 lessened ampHtude of the arterial pulse. Obviously, this rise in the 

 venous pressure must be associated with a lessened filling power of 

 the auricles, because the relaxation of these parts is then greatly 

 hindered by the pressure resting upon their outer surfaces. 



If a continuous record is made of the changes in the intra-auricular 

 pressure with the help of an elastic manometer, the curve so obtained 



'.?T*/ rj^-^<»f 



Fig. 153. — The Curve of Intra-auricular Pressure. 

 ABy systole; BD, diastole; DA, pause; C, second summit; E, third summit. 



presents the details indicated in Fig. 153. The systolic period of the 

 auricle occurs between A and B, and the diastolic between B and D. 

 Between this point and the beginning of the next cardiac cycle {DA) the 

 auricle is said to be at rest. The wave as a whole exhibits three eleva- 

 tions, namely, one each at 5, C and D. The first, no doubt, is due to the 

 contraction of the auricle, and indicates the point of maximal intra- 

 auricular pressure. The second summit (C), interrupts the steady fall 

 in pressure accompanying the relaxation of the auricular muscula- 

 ture {BD). Its cause is to be sought in the slight upward displace- 

 ment of the auriculoventricular septum occasioned by the contraction 

 of the ventricles. The size of the aiu-icular cavity is somewhat dimi- 

 nished thereby, causing the pressure to rise. The third elevation (E) 

 is dependent upon the quick inrush of venous blood which results as 

 soon as the auricular wall becomes passive. This rather abrupt initial 

 rise soon gives way to a more gradual one, as the auricles become filled. 

 The auriculoventricular valves are forced open at E. A certain quan- 

 tity of blood then escapes into the now diastohc ventricles. This 



