Second interval of silence

8

20

The ventricles are still relaxed, and blood continues to pass into them from the auricles and into the auricles from the large vessels, until at length the auricles contract, and, by forcing their contents through the auriculo-ventricular opening, complete the dilatation of the ventricles and distend their cavities.

Throughout the whole period of the action of the heart, the two surfaces of the pericardium glide over each other to a greater or less

extent.

It will be obvious, by reference to the above statement, that there are many conceivable causes of sound both during the systole and diastole of the heart, and they require careful consideration before a satisfactory conclusion can be arrived at respecting the causation of the sounds of the heart. Those which are in operation during the first sound of the heart must take precedence of the others, and may be briefly stated as follows:

1st. The muscular contraction of the ventricles.-The doctrine taught by many physiologists attributes to muscular contraction the principal share in the production of the first sound of the heart. Hope, Williams, Stokes, Walshe, Davies, and other physicians in this country, and many others of the leading authorities abroad, have contended for the predominance of this cause of sound, and in proof of their position have cited the fact that sound is produced by the violent or spasmodic contraction of voluntary muscles. But, although the violent contraction of voluntary muscle is to some extent soniferous, its ordinary quiet contraction is not so; and careful experiment has proved that when the heart is acting quietly, the contraction of its muscular fibres is almost if not quite unproductive of sound.* In short, it may

* Dr. Halford's admirably conceived experiments, at which I had the privilege of being present, proved this beyond dispute. When the ingress of blood into the heart was prevented, the first sound wholly ceased, although the ventricle continued to contract forcibly and rhythmically. Dr. Markham has raised an objection to any inference from this experiment, on the ground that as there was no blood for the heart to contract upon, the heart's contractions must have been abortive. But they were forcible enough to jolt the head placed on a stethoscope applied to the heart, and the eye could detect little difference between the force of their contraction when the blood was admitted into the heart, and when it was excluded. Therefore if they are to be considered abortive, the contraction of voluntary muscle which, in like manner, takes place without any substance for the muscle to contract upon, must also be regarded as abortive, and, therefore, ought not to be soniferous. Again, if the contraction of a small muscle like the ventricle of a human fœtus is productive of sound, it is difficult

be stated that during the ordinary tranquil action of the heart, muscular contraction does not contribute to the production of the first sound, but that under certain conditions of excitement, when the heart is irritable, and is acting violently, this source of sound comes into operation. In proof of which I would refer to the peculiar dull, muffled noise which is super-added to and confuses the first sound of the heart in certain instances in which the heart is acting violently—a sound which subsides as soon as the heart resumes its ordinary mode of action.

--

2ndly. The sudden and forcible closure of the mitral and tricuspid valves. — The authorities already mentioned have dwelt but little on this source of sound, but Dr. Billing and other physiologists in this country and abroad, including Rouanet, Bouillard, Bryan, Brakyn, Valentin, and Kiwish, have insisted on this sudden tension of the auriculo-ventricular valves as the sole cause of the first sound. Dr. Billing was the first to propound this view, which of late has found an able advocate and expositor in Dr. Halford; and although I consider it somewhat too exclusive if applied to all diseased conditions of the heart, Dr. Halford's recent experiments have led me to believe that in a healthy state of the circulatory apparatus, the forcible tension of the mitral and tricuspid valves is the principal source of the first sound, and, under ordinary circumstances, the sole cause of the sound as it reaches the ear applied to the chest walls. Indeed, the loudness and clearness of the first sound of the heart, when the ventricles are thin, and the impulse by no means forcible, and its weakness when the walls of the ventricles are thick and their contraction strong, are quite in keeping with the valvular origin of the sound, and utterly inconsistent with its muscular origin; so also is the fact that when the ventricles are much hypertrophied, and the auriculo-ventricular valves rigid, the first sound is scarcely audible at the apex.*

to understand why the contractions of much larger muscles, such as exist in the auricle of an adult, and still more so in the auricle of a horse or an ox, should not be attended by sound, and yet experience proves conclusively that they are not so. Further, there is no reason for believing that the ordinary contraction of the muscular tissue of the heart would be more productive of sound than the ordinary contraction of voluntary muscle, and in the latter case sound is usually absent-sound being excited only when the muscle is contracting violently.

*It is sometimes asserted that in these cases the weakness of the sound at the apex is attributable to the fact that in hypertrophy the muscular contraction is more or less imperfect. But no assertion can be more gratuitous or unfounded. So forcible are the muscular contractions in hypertrophy, that the whole chest sometimes heaves under their influence, and as the sound emitted by the contraction of the voluntary

3rdly. The rush of blood over the surface of the ventricles, and through the aorta and pulmonary artery, and the throwing back of the semilunar valves against the sides of the vessels, the dilatation of the vessels themselves, and the molecular collision of the blood.-The endocardium, the semilunar valves, and the internal coat of the arteries are so exquisitely smooth that the friction of the blood against them is reduced to a minimum; and as observation and experiment have proved conclusively that in a healthy condition of the arteries no appreciable sound is produced in them by the current of blood, nay, more, as it is admitted that no sound is excited by the rush of blood and the collision of its particles during the systole of the auricles, when the blood comes in contact with the irregular surface of the walls of the ventricles, it is highly improbable that any sound would arise from the current of blood or the collision of its particles during its passage from the ventricles through the exquisitely smooth ventricular opening, and equally smooth arteries, the more so as not the slightest vacuum occurs at any period of the heart's action; and, therefore, there can be no dashing of blood, and no violent collision of the blood globules amongst themselves. As well might we expect to elicit sound by succussing a patient with fluid in the pleura, as to expect sound to be produced by the motion of the blood in the cavities of the heart. Therefore I would maintain that when the circulatory apparatus is healthy, and the heart is acting tranquilly, these sources of sound do not contribute to the production of the first sound of the heart as heard through the walls of the chest. When the heart and great vessels are diseased, and more especially when under such circumstances they are acting violently and irregularly, the phenomena included in this paragraph may become distinctly soniferous and not only serve to alter the character of the first sound, but to produce a murmur.

It is maintained by some observers that the causes under discussion contribute largely to the production of the first sound as heard at the base of the heart; and Skoda and his followers speak of an arterial first sound as distinct from the cardiac first sound. The arguments, however, by which they attempt to support their position appear to me to be utterly fallacious. In the first place it is stated that the first sound may be heard in all the large arteries of the body, however distant from the centre of

muscles is never so loud as when the muscles are hypertrophied, as in the case of the pectoral muscles of the "navvy," and of the deltoid muscles of the blacksmith, so there is no reason for doubting that the same holds good in regard to the muscular structure of the heart.

circulation, and that this fact is incompatible with its transmission from the heart. But there is no valid foundation for this assertion. Indeed it is directly negatived by experiment. If a long, thin elastic Indiarubber tube be filled with water, and a stethoscope be applied to one end whilst sonorous vibration is excited at the other, it will be manifest to the merest tyro in auscultation that the transmission of the first sound of the heart along the larger arteries is not only possible, but extremely probable.

Again, the fact that the first sound is sometimes heard as loud or even louder in the carotid artery than over the aortic orifice is adduced in proof of the same position; but what can be more probable than that in certain instances in which the chest walls are thick, or a portion of emphysematous lung or some other imperfect conducting medium intervenes between the aorta and the ear, the first sound in a vessel like the carotid which is not far removed from the centre of circulation, and lies quite superficially, should be heard louder than over the distant aorta.

Again, it is stated that the first and second sounds differ in character, tone, and duration, and that on that account, if the second sound is referable to the forcible closure of the valves, the first sound cannot be so. But this objection will not bear discussion. Not only are the auriculo-ventricular valves larger and thicker than the semilunar valves, but their free borders, unlike those of the semilunar valves, are attached to the heart by the tendinous cords and carneæ columnæ which are necessarily thrown into vibration by the forcible tension of the valves, and complicate the mere valvular flapping sound which would otherwise result from the closure of the valves. Further, the walls through which the sound of their tension is conducted to the ear are thicker and less vibratile than the walls to which the semilunar valves are attached. So far from being an argument against the valvular origin of the first sound, the fact alluded to is a powerful argument in its favour, for if the first sound were not more prolonged, and of a different character and tone from the second sound, assuredly it could not arise from the closure of the auriculo-ventricular valves.

Again, it is stated that in certain cases of regurgitant disease of the mitral valve, where the first sound at the left apex is replaced by a murmur, the first sound at the base of the heart is almost normal in character. This statement, if correct, would be deserving of attention, but I cannot admit that it is so. Frequently, indeed, when a mur

mur masks the first sound at the left apex, the first sound is heard comparatively clear at the base, but so it is also at the right apex-the normal sound in both instances being referable to actions going on in the right as well as in the left chambers of the heart. In short, the clear sound of valvular flapping overpowers the murmur at the base, just as the murmur overpowers and masks the sound at the left apex, though not at the right; the slight transmission of the murmur being referable to the lowness of its pitch as compared with the sound produced by the sudden tension of the valves. The correctness of this view is proved by the fact that when the mitral valve is connected with a rigid bony ring, and is unable to flap, so that the first sound at the apex is really replaced, not merely masked, by a murmur, the murmur, though slight, is heard over the base of the heart, and, indeed, entirely replaces the normal sound. This fact, which I have not seen noticed in any work on auscultation, has enabled me on more than one occasion to diagnose the condition of the valves here referred to, and to predict that it would be found after death.

4thly. The impulse of the heart against the walls of the chest.—Whilst witnessing Dr. Halford's experiments, I satisfied myself that the socalled impulse of the heart bears no sort of resemblance to a blow, but is simply the result of pressure exerted by the walls of the heart as they assume a globular form during contraction; and further, that whilst the heart is acting quietly, the ear is not conscious of any sound produced by its impulse. Therefore I cannot doubt that under ordinary circumstances the so-called impulse of the heart does not contribute to the production of the first sound.

The possible causes of sound which are in operation during the period of the second sound may be briefly stated as follows:

1st. The auricles continue to receive blood from the large systemic veins, the auriculo-ventricular valves are forced back against the walls of the ventricles, and a certain amount of blood passes from the auricles through the auriculo-ventricular openings into the ventricles. In the normal state the blood enters the auricles, and passes from the auricles into the ventricles in a steady current, and, as there is no roughness or other cause of friction in the lining membrane of either auricles or ventricles, and no vacuum to admit of splashing, it is highly improbable that any sound should be thereby produced capable of transmission to the surface of the chest. So also the falling back of the auriculoventricular valves must be unproductive of sound.