Harvard Psychological Studies, Volume 2

by Unknown

Edgren made experiments on the temporal relation of the wave f and of the dicrotic wave, which to avoid misunderstandings he calls the "wave f´." His experiments were made as follows. A sphygmogram from the carotid and a cardiogram were taken simultaneously, the points of the writing-levers being in the same vertical line. The wave f´ appeared a little after the wave f. The length of this interval could be calculated by measuring the distance between these waves, as the speed of the drum was known. From this was subtracted the time of propagation of the dicrotic from the heart to the point where the instrument was fixed. In this way it was found that the time between the appearance of the wave f and of the wave f´ was equal to the time of propagation of the dicrotic wave from the heart. Edgren concluded that the dicrotic wave is in close temporal relation to the closure of the valves.[76] To this comes the supposition that the wave f´ is due to a change of pressure proceeding from the heart. The wave f´, therefore, could be attributed to the tension of the valves.[77] Edgren and Tigerstedt are the chief exponents of this theory.

In so far as this theory assumes that the dicrotic elevation is due to a wave travelling from the heart to the periphery,[78] it is open to all the arguments against a theory of the central origin of the dicrotic wave. Against the more special assertion that the dicrotic elevation is in connection with the closure of the valves, the following facts must be mentioned. We grant that the tracings of the apex beat may be directly substituted for the curves of intraventricular pressure, although this is by no means obvious, since one tracing gives the form of the pressure changes and the other the effect of the shock of the heart against the wall of the chest. It is, furthermore, not proved that the wave f is due to the closure of the valves and that the waves f and f´ correspond to each other so closely as Edgren's experiments seem to indicate. His measurements of the length of lines were made with an exactitude of 0.1 mm., but his computations were carried to the third decimal place of a second. The third decimal is generally inexact and the second in a large number of cases. Experimental evidence, furthermore, directly contradicts the statement that the dicrotic elevation corresponds to the wave f. Fredericq[79] traced pressure curves in the ventricle and in the aorta, and determined the points of equal pressure in both curves. He thus found that a point near the beginning of the descent of the curve of intraventricular pressure corresponds to the dicrotic. His experiments are rather conclusive against the theory in question, since the wave f is very well marked in these tracings of Fredericq. The following facts, however, are fatal for the theory that the closure of the valves causes the dicrotic elevation: The dicrotic wave disappears in diseases like atheroma and arteriosclerosis which do not impair the function of the valves, but affect the elasticity of the arterial wall, and it is not affected by valvular insufficiency. The independence of the dicrotic from the function of the valves is conclusively proved by v. Kries, who found the dicrotic elevation in the femoral artery of an animal whose heart was replaced by a valveless bag.

All these facts, on the contrary, can be understood easily in the light of the theory that the sphygmographic curve gives the movements of the arterial wall, which movement is conditioned by the decreasing amount of blood in the artery, and the elastic vibrations of the wall around a variable position of equilibrium. In some cases the conditions of the problem are rather simple, and admit an analytic treatment, the results of which fit closely to the experimental facts. This part of the theory, however, has merely physiological interest, and therefore is discussed in a separate paper. It may be mentioned at this point that this theory of normal dicrotism is essentially identical with the theory of abnormal dicrotism as stated by Galen. He believed that the second beat of the pulsus bis feriens was due to an elastic vibration of the arterial wall. "Ex eodem genere sunt dicroti; nam arteria in occursu quasi repellitur, moxque redit.... Neque enim tum arteria contrahitur, sed quasi concuteretur, occidit; cuius delapsum a primae distentionis termino nulla dirimit manifesta quies, ut animadvertitur in contractione: sed simulatque attolli destitit, recidit atque ita paulisper vibrata, mox occurrit iterum."[80] Galen, however, is mistaken in his view, and in his observation that sometimes three or more pulse-beats may be felt with the finger. No form of the pulse is known where three or more beats may be felt for every heart-beat, and the actual tracings exclude the possibility of this observation for the pulsus bis feriens. The pulsus bis feriens is due to an increase of the frequency of the heart-beats. If the new pulse wave arrives before the vibrations of the arterial wall have had time to subside, the new wave and the already existing vibration may interfere in such a way as to produce this abnormal pulse form.

The form of a single wave of the sphygmographic curve may be influenced by changes in the following conditions:

(1) The pulse wave may have an initial form which cannot be represented by the schematic curve in Fig. 1. This may be due to an irregularity of the function of the ventricle. The action of the heart has an influence on the length of the waves, which length is determined by the rapidity of the heart-beats. This influence has been mentioned before. A change in the rapidity of the heart-beats has no great influence on the form of the catacrotic part of the curve so long as the impact of the new pulse wave does not arrive before the vibrations of the arterial wall have had time to subside.

(2) Differences of the elasticity of the arterial wall affect materially the form of the catacrotic part of the sphygmographic curve. It has also some influence on the height of the curves, because the amplitude of elastic vibrations depends on the elastic force for a given force of the shock. The degree of elasticity of the arterial wall is subjected to individual variations, and it depends in a given subject on the state of innervation of the wall.

(3) The surrounding tissues have a certain influence, since their resistance determines the friction opposing the vibration. This accounts for the fact that merely local conditions, such as a change of the position of the arm or the adjustment of the instrument, may change the form of the pulse curve. For instance, if the sphygmogram is taken from the a. radialis the instrument is placed between the styloid process of the radius and the tendon of the flexor carpi radialis. In the neighborhood of this place are two venae comites and a superficial branch of the median or radial vein. A change in the position of the arm will have a certain influence on the circulation in the veins, and influence the turgor of these vessels. Increased turgor increases the friction, and thus produces the different forms of the tracings.

(4) The changes of the turgor of the artery, moreover, cause a general rise or lowering of the curve. This symptom is essentially ambiguous for the turgor of the artery may be changed as well by an increase or decrease of the amount of blood pumped into the arterial system as by a decrease or increase of the amount of blood which passes through the capillaries.

The influences mentioned under (1) may be seen in tracings taken from cases of cardiac insufficiency, and have merely pathological interest. All the other influences, however, can be observed in the curves which are traced for psychological purposes. The changes in the general rise or fall of the curves are not so very hard to observe,[81] and for the observation of the rapidity of the heart-beats it is only necessary to trace a time-curve and count the number of beats or measure the length of every single beat. Also the changes of the height of the waves can easily be measured. This has been done conscientiously by several observers. It is by far harder to see the changes in the form of the catacrotic branch, and only a few keen observers have seen them. These changes of the pulse curve under the influence of feelings were proved as facts by experiments, but their interpretation was doubtful. With the exception of the rapidity of the heart-beats, which could easily be observed in some other way, all the symptoms of the influence of feelings on circulation are ambiguous. A difference in height of the single waves may be due to a change in the amount of blood which is pumped into the artery, but it also may be due to a change in the amplitude of the vibrations of the artery. The form of the catacrotic part of the sphygmographic curve may be changed by a different state of innervation of the arterial wall, but it also may be due to an increase or decrease of the friction of the surrounding tissues. The general rise or fall of the curve may indicate a change in the amount of blood which leaves the left ventricle, but it also may indicate a change in the amount of the capillary outflow.