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sions of the pericardium produce an increase in the area of præcordial dulness.* Nothing, however, can be more repugnant to facts, or more calculated to mislead than an unqualified statement of this kind. Observations at the bedside, confirmed by careful examinations in the deadhouse, prove conclusively that adhesions of the pericardium do not even give rise necessarily to enlargement of the heart; and that, although universal, they may, by absorption, become so thin as not appreciably to thicken the walls of the heart. Common sense revolts at the idea of such adhesions producing any extension of the area of dulness; and, in truth, the statement that pericardial adhesions occasion extension of præcordial dulness will only hold good in respect to cases in which pericarditis has recently occurred, and in which, although the fluid exudation has been absorbed, a thick coating of plastic lymph remains, and has not yet undergone complete solidification. When extension of dulness upwards is observed years after an attack of pericarditis, it may be referable to thickening caused by coexistent pleurisy, or to hypertrophy and dilatation of the heart, or to the fact of the heart having become adherent to the anterior parietes of the chest by lymph effused in the anterior mediastinum, but assuredly not to lymph effused years before into the pericardium. In certain instances of oldstanding and universal pericardial adhesions, which had led to atrophy of the heart, I have even noted a decrease in the normal area of præcordial dulness.
Endocarditis has no appreciable effect on the præcordial dulness, nor has valvular disease, except in virtue of the hypertrophy and dilatation to which after a time it ordinarily gives rise.
The causes which produce a diminution in the area of præcordial dulness are far less numerous and of much less importance than those which lead to its increase. Pneumothorax, and emphysema of the lungs -especially of the left lung—are the only causes, external to the heart and the pericardium, which operate in bringing about this result, and when emphysema is accompanied by bronchitis, the effect is seen most strikingly developed. Not only is the heart displaced by the dilated lung, but the lung pressing in front of it causes a diminution in the area of dulness, and a great decrease in the sense of resistance.
The only cause which can operate within the pericardium in producing a diminution of the præcordial dulness, is the presence of air or
* Walshe, loc. cit., p. 202.
gas in the pericardial sac, consequent on traumatic injury to the organ. Cases such as these are extremely rare, and practically are of little importance.
The only cause of diminished præcordial dulness existing in the heart itself is atrophy of its substance. A decrease in the bulk of the heart, by admitting a closer approximation of the anterior margins of the right and left lungs, diminishes the extent of surface over which the organ remains uncovered by pulmonary tissue, and thus lessens the area of dulness and the sense of resistance to the finger.
When the ear is applied to the surface of the chest in the præcordial region, two sounds, referable to the action of the heart, are distinctly audible. These sounds follow each other in quick succession, and are separated by intervals of silence. The first or systolic sound is synchronous with the systole or contraction of the ventricles, with the stroke of the heart against the chest walls, with the pulsation of the arteries near the heart, and nearly so with the pulse of the radial artery ; the second or diastolic sound is synchronous with the diastole or filling of the ventricles, with the recedence of the heart from the chest-walls, and with the systole or pulseless condition of the large arteries. The noiseless interval between the first and the second sounds is termed the first interval of silence; that which succeeds the second sound is styled the second interval of silence.
These sounds and intervals of silence are of different duration, and succeed each other in a certain order of succession, which is termed the “rhythm” of the heart. The first sound is long, the first silence extremely short; the second sound is short, and the second silence long. Both sounds and both intervals of silence are comprised within the period of time between two successive arterial pulsations, and, therefore, if we suppose the heart to be beating at the rate of 60 in a minute, they together occupy exactly a second of time. This being the case it will be readily understood that it is difficult, if not impossible, to determine accurately the true relative duration of each sound and each interval of silence, but it may be stated roughly that if the whole period between two pulsations be divided into twenty equal parts, about seven of these will be occupied by the first sound, one by the first interval of silence, four by the second sound, and eight by the second interval of silence. * Practically, when the pulse is over 80, the first interval of silence is scarcely appreciable by the ear, so that the first sound appears to be followed immediately by the second; whereas, on the other hand, when the pulse is slow and does not exceed 50 or 60 the first interval of silence is very perceptible.
The two sounds of the heart are unlike one another in intensity, pitch, quality, and duration. The first, as heard over the left apex of heart, is apparently deep-seated, of a dull, low-pitched, booming character, at once louder and more prolonged than the second sound, which is clear, short, and flapping, and comparatively superficial. The two syllables tubb, dúp, if clearly articulated, convey a tolerable idea of the sounds." But there are other differences which require special consideration. The two sounds not only differ from one another, but each varies in its character at different portions of the surface of the chest. Thus at the right apex the first sound is less dull and less prolonged than at the left, and the second sound is clearer and more abrupt; whilst at the base of the heart, or rather just above the origin of the large vessels, the first sound on both sides resembles that heard at the right apex, and the second sound is louder, clearer, and more flapping than at the apex. The first sound is heard loudest at the apex, and becomes gradually weaker as it is traced upwards towards the base of the heart; the second sound is heard loudest and clearest at midsternum opposite the third cartilage, and loses in intensity as it is traced upwards or downwards.
* Laennec estimated the time occupied by the two sounds and the first interval of silence at rather more than three times the period of the second silence, whilst Volkmann, who endeavoured to measure their duration by the aid of vibrating pendulums, declares that the two sounds and the first interval of silence do not together occupy more time than the second interval of silence. Few observers would be found to bear out Laennec's estimate ; but my own conviction is equally opposed to that of Volkmann, and I believe that the proportions given in the text represent very closely the relative duration of the sounds and intervals of silence when the pulse is about 76 in a minute. When the heart is pulsating very slowly Volkmann's statement may be more correct.
+ Dr. C. J. B. Williams, to whom the profession are so much indebted for his contributions towards the elucidation of all auscultatory phenomena, was the first, I believe, to suggest this mode of imitating the sounds of the heart.
The extent to which both first and second sounds are propagated in the chest varies greatly; the variation being dependent in part on the intensity of the sounds themselves, but even more so on the condition of the surrounding pulmonary tissue. Emphysema, by impairing the conducting power of the lung, has the effect of preventing their transmission, and consolidation of the lung has the contrary effect. Under ordinary conditions they are more readily propagated to the left than to the right, and are often audible on the left side posteriorly when they are quite inaudible on the right.
But the sounds sometimes pass beyond the boundaries of the chest and are transmitted far along the track of the larger vessels. The conditions which conduce to this result are:—First, activity of the circulation; secondly, thickness and elasticity of the vessel ; thirdly, nervous excitement. Under these circumstances both sounds are usually to be heard in the carotid and axillary arteries, and they may be audible even in the femoral. They gradually decrease in force in proportion as the vessels are further and further removed from the centre of circulation, until at length the second sound ceases to be audible, and at a still greater distance from the heart both sounds become inaudible.
It has been maintained by Dr. Walshe and other writers that the sound heard in the arteries is not conducted from the heart, but is generated in the vessels themselves by the “impulsion and friction of the blood,” “ the vibration of their walls,” and “the current-like motion given to their column of blood by the form of the vessels.” “It is not conceivable,” says Dr. Walshe,* “that sound audible in the popliteal or radial artery is the mere result of conduction from the heart.” A few experiments on the conduction of sound through fluid contained in elastic tubes will satisfy any one that this conclusion is incorrect, and that sonorous vibrations are transmitted along the arteries as readily as the vibrations which, in certain forms of cardiac disease, take their origin in the heart, but convey a sensation of thrill to every artery in the body. That the sounds are not generated in the vessels under ordinary circumstances, is obvious from the fact that they are rarely to be heard in the radial and popliteal arteries except under the conditions above referred to, as augmenting the sounds of the heart and favouring their transmission; whereas if they took their origin from the vessels or their contents, they ought to be invariably present. The only condition under which a sound is generated in the arteries is where their internal
* Loc. cit., p. 270.
coats are roughened by disease, and then the sound assumes the character of a murmur.
With a view to a clear comprehension of the cause of these cardiac sounds, it will be desirable to analyse a complete action of the heart, and to consider what is going on at the time of their occurrence.
A complete action of the heart comprises the following events, which take place as set forth below. Rhythm. / Duration. , Occurrences which take place at different periods of
the heart's action. Systolic, or First
The ventricles contract to expel the blood from Sound
their cavities; the mitral and tricuspid valves, which are closed partly by the action of the elastic tissue which enters into their composition,* and partly by the action of the blood in the ventricles, are rendered tense by the impulsion of the blood against their ven. tricular surface and by the contraction of the columnæ carneæ; the blood is driven through the aorta and pulmonary artery; the valves at the orifices of those vessels are forced back against the arterial walls by the onward current of the blood ; the vessels themselves are dilated; the impulse of the heart against the chest walls takes place; the auricles become relaxed, and permit blood to flow into them from the vena cava and pulmonary veins, and the fluid contents of the ventricles are in a state of molecular collision.
First interval of
en This is the moment which elapses after the com.
plete systole of the ventricles before the elastic tissue which enters into the composition of the semilunar valves has effected their closure, and the aorta and pulmonary artery have contracted on the blood within them sufficiently to produce the forcible recoil of the blood on the semilunar valves which produces their sudden tension.
The auricles continue to receive blood from the large systemic veins; the muscular contraction of the ventricles ceases; the pressure of the blood on the ventricular surface of the auriculo-ventricular valves being removed, a certain amount of blood begins to pass through them from the auricles, and occasions passive dilatation of the ventricles; the aorta and pulmonary artery contract on the blood within them, and by forcing it against the upper surface of the
semilunar valves throw them into a state of tension. * See · Med.-Chir. Trans.,' vol. xliv, p. 43.