Harvard Psychological Studies, Volume 2

by Unknown

These curves are constructed in this way. The lines AB represent the time of the interval of one heart-beat. The straight line EB represents the decreasing volume of the artery and the curves on AB represent the elastic movement of the arterial wall. Both are synchronous movements, and a line perpendicular to AB gives the corresponding points. The points of the resulting movement are found by arithmetical addition of the two ordinates. The results of these constructions prove that the curves show the dicrotic elevation only if the elastic force is great enough to make a vibratory movement possible. Aperiodic movements do not produce this elevation. The friction is always great for the movement of the walls of an artery, and there are only the two possibilities, of a vibratory movement which dies out quickly, and of an aperiodic movement. This accounts for the fact that the dicrotic elevation may be missing sometimes, and that in other cases several secondary elevations may be seen, the number of which, however, is always limited, and their relative height rapidly diminishing. It may be remarked that the length of the lines AB seems essential to the form of the resulting curve. Curves I and III differ very much in the length of the lines AB, while the lines AE are equal and the vibratory movements are only slightly different. The resultants, nevertheless, seem to differ very much. It is easy to see that a different speed of the recording drum will have an effect on the tracings which is similar to that of a change in the length of the lines AB in the constructions. This is one more reason why mere inspection of the curves cannot give a satisfactory result.

These constructions show that the sphygmographic curves must show great variations, since the amount of blood pumped into the system, the elasticity of the arteries and friction of the surrounding tissues are subjected very likely not only to individual but also to local and temporal variations. But under given conditions only a certain form of the pulse wave is possible, and this form does not change so long as these conditions do not change. The sphygmograms in Fig. 6 show some of the typical forms of the pulse curve.

Fig. 6

No. I shows the influence of high arterial tension, and No. II of low tension. The first corresponds to No. II in Fig. 5, the second to Nos. I and III. Nos. IV and V of Fig. 5 show the effect of great friction and small elasticity. The constructions differ in the form of the elastic movement; the position of equilibrium is reached with different velocity in both cases. The resulting movements differ slightly in the form of the catacrotic phase. Both forms may be seen in No. III of Fig. 6. This sphygmogram was taken from an artery with low tension, and this form of the sphygmographic curve is well known as characteristic of the "soft" pulse. If the artery has lost to a large extent the qualities of an elastic body, and if the outflow is very rapid, the pulse curve shows nothing but the slight elevation of the travelling wave; No. IV in Fig. 6 shows a curve of this character.

This theory explains many surprising facts which resisted every attempt at explanation. The anacrotic part shows a steep ascent, because it is due to the sudden arrival of the blood wave. It seems that an interruption in the descent may be seen only in abnormal cases. The sphygmograms of twelve normal individuals were observed regularly by me during more than a year without once discovering an anacrotic elevation.

The hemautographic curve of Landois is produced in this way. The form of this curve depends on the velocity of the escaping jet of blood. The velocity of the blood flow depends on the resistance of the arterial system in the sense that the velocity decreases when the resistance increases. When the arterial wall is in the negative phase of vibration the lumen of the artery is smaller, and, therefore, the velocity smaller. This is confirmed by the actual tracings of the velocity of the circulation by Marey.

It is also obvious that the dicrotic elevation never can arrive before the primary wave, because the arterial wall cannot perform elastic vibrations before it is expanded by the impulse of the arriving blood wave. Neither is it surprising that the "dicrotic wave" seems to travel in the same direction and with a velocity equal or almost equal to the velocity of the pulse wave. Such a difference can be produced only by a difference in the time of the vibrations of the arteries at different points of the body. The time of one vibration is necessarily very short, and the length of this interval depends on the circumstances which determine the elasticity of the arterial wall and the friction. These conditions may be subjected to local variations. If, therefore, the time-interval between the primary and the secondary elevation is measured at two different points (e. g., at the carotid and at the radialis) a difference of time may be found. Starting from the supposition that the dicrotic elevation is due to a wave travelling in the blood, one could attribute this difference of time to a velocity of the "dicrotic wave" which is slightly different from the velocity of the primary wave. The fact that the dicrotic elevation appears later in places farther from the heart was interpreted as a proof that the wave travelled out from the heart. No theory which assumes that the dicrotic elevation is due to a wave travelling in the blood can give a reason why two waves of the same form and origin should travel through the same liquid at different velocities.

At this point a theory must be mentioned, which was brought forward recently, because it is based on measurements of the velocity of propagation of the dicrotic wave. This theory is connected with Krehl's theory of the function of the valves. The blood, according to Krehl, enters the aorta through a small opening, and expanding in a large space it produces fluctuations and eddies, which would close the valves if they were not kept open by the blood which streams through under high pressure. They must, therefore, close at the moment when the aortic pressure is equal to the intraventricular pressure. This occurs shortly after the moment indicated by the beginning of the decline of the intraventricular pressure curve. Now the second sound of the heart is heard somewhere in the descending part of the cardiogram[71] and the measurements of Huerthle[72] have shown that the second sound is heard 0.02" after the beginning of the descent of the cardiogram. This seems to indicate that the second sound of the heart is in a temporal relation to the closure of the valves. Many theories of the origin of the sounds of the heart agree on this one point that the second sound is due to a noise in the muscles. It therefore may be supposed that the second sound is due to the tension of the valves when they close or shortly afterwards. The problem now would seem to be to find an elevation in the descending branch of the curve of intraventricular pressure, or in the tracings of the apex beat, which could be attributed to the closure of the valves. It was taken for granted that the curves of intraventricular pressure and those of the apex beat were identical. In many of these tracings an elevation was found which may be called "the wave f." This elevation is not found in all the tracings, and its position seems to be rather variable. Edgren[73] remarks that the wave f was always found near the abscissa no matter whether the preceding decline of the curve was great or small. In some of Chauveau's tracings the wave f is missing or indistinct,[74] in others it is very well marked and approximately in the middle of the descending branch of the curve.[75]