2ndly. The dilatation of the ventricles.—Whilst witnessing Dr. Halford's experiments I satisfied myself that this action is unproductive of sound.

Skoda has suggested that during the dilatation of the ventricles the heart recedes from the walls of the chest, and in so doing may occasion sound; and in corroboration of his theory he has cited the fact that in exceptional cases the second sound, though weak at the base, is clear at the apex of the heart, and therefore must be partly of ventricular origin. My own opinion is adverse to his theory and to the conclusion he draws from the fact cited in support of it. Direct experiment, which shows that the second sound is heard clear, loud, and unaltered in character, when the heart does not come in contact with the ribs, proves that the cause assigned by Skoda contributes little if at all to its production, and the fact cited in support of his view is more readily explicable by supposing that in the cases referred to the transmission of the sound at the base of the heart, was stopped by the intervention of fat or a portion of emphysematous lung-a condition which I have found existing in two cases precisely resembling those alluded to by Skoda. The fact, however, which is most fatal to his theory is that the recedence of the heart from the chest walls is a physical impossibility, unless it be supposed that at each diastole, the lung pushes between the heart and the chest walls-which observation clearly proves that it does not do.

3rdly. The contraction of the aorta and pulmonary artery on the blood within them, and the impulsion of the blood against the semilunar valves.— Theoretical considerations and experimental observations alike favour the belief that, under ordinary circumstances, the contraction of the vessels is noiseless; and inasmuch as there is nowhere any vacuum in the heart or great vessels, and consequently there can be no dashing of blood, but only a greater or less degree of pressure, it is difficult to conceive how the impulsion of the blood against the semilunar valves can be productive of sound.

4. The sudden closure of the semilunar valves.-This unquestionably is the principal and, as I believe, the sole cause of the second sound of the heart. Direct experiment and clinical observation alike attest this fact. As soon as the entrance of blood into the heart is stopped, and the valves therefore cease to set, the second sound ceases also. Readmit the blood and the sound instantly recommences.* Again, insert

* This I can testify from personal observation. For full details see Dr. Halford's experiments, as detailed in his pamphlet On the Action and Sounds of the Heart.'

the nozzle of a pair of bellows into the aorta, and cause the valves to close suddenly by air instead of blood, and a sound closely resembling the second sound is produced.* Again, hook back one or more of the semilunar valves so as to prevent them from closing the orifice of the vessel, as in the experiment detailed by Dr. Williams, and the second sound ceases, and is replaced by a murmur. Additional proof is also furnished by regurgitant disease of the aortic valves. When these

valves are so damaged as not to close the orifice of the vessel, but to admit of regurgitation, the natural second sound disappears at the aortic orifice, though it continues as before at the pulmonary orifice. More decided proof can hardly be conceived.

Thus, then, to sum up the conclusions I have formed respecting the sounds of the heart in health, I would state

1st. That both sides of the heart contribute to the production of the two sounds.

2ndly. That the synchroniety of the causes which give rise to the first and second sounds respectively on the two sides of the heart lead to a blending of the sounds generated on the two sides, so that two sounds only are heard accompanying the heart's action instead of four.

3rdly. That the first sound as heard on the chest walls is produced wholly by the sudden tension of the auriculo-ventricular valves, but is modified under certain conditions by the violent contraction of the muscular structure of the heart.

4thly. That the second sound is referable to the sudden tension of the semilunar valves.

5thly. That the differences of character observable between the first and second sounds are due to differences in the structure, position, and attachments of the auriculo-ventricular and semilunar valves respectively, the former being deep-seated and connected with tendons and muscles which, equally with themselves, are thrown into vibration by the tension to which they are subjected, whereas the latter are free from muscular and tendinous attachments, and have not the thick muscular walls of the heart interposed between them and the ear of the observer.t

* See experiments by Mr. Brakyn, reported in 'Lancet' for 1851.

† Skoda speaks of a ventricular first sound and an arterial first sound; of a ventricular second sound and an arterial second sound, and makes a distinction between the causes of the sound in the several instances. I am satisfied that the distinction has no foundation in fact, and that the first sound when normal is of ventricular, and

Thus, then, it will be obvious that circumstances which affect the action of the heart and arteries must lead to modifications in the intensity of the two sounds, and not unfrequently to alteration in their quality, pitch, and rhythm. And this holds good when the heart is healthy, as well as when it is structurally diseased.*

The first sound will be loudest in those cases in which the supply of blood is moderate and regular, the nervous influence in full force, the muscular structure of the heart thin but powerfully contractile, and the cavities of the ventricles and the auriculo-ventricular valves relatively large-conditions under which the ventricles contract forcibly, the tension and vibration of the auriculo-ventricular valves is very great, and the extent of sound-generating surface is at its maximum. Under the same conditions, the second sound will be the loudest when the current of blood is forcible, and the elasticity of the arteries great; for these are circumstances which lead to an unusually strong recoil of the blood on the semilunar valves, and to their more than usually forcible closure and vibration. Thus, in children in whom these conditions exist, the sounds are more intense than in adults, in whom the structures have lost some of their elasticity, and in whom the walls of the heart and chest are thicker, and therefore less favourable to the transmission of sound. But under no circumstances is increased intensity of the sounds observed more strikingly than when the patient is under the influence of nervous excitement. In this case the sounds are remarkably increased, the first sound more especially so, and to such a degree may this increase proceed, that the pulsation of the heart may be audible even by bye-standers. Flatulence and acrid secretions in the stomach and bowels may have a similar effect, and certain morbid the second of arterial origin. The extraordinary readiness with which sound is propagated through fluid would hardly be credited by those who have not tested it experimentally, and in itself it affords a sufficient explanation of the propagation of the first or ventricular sound along the arteries, and of the second sound downwards into the ventricle. The rare cases which are cited as evidence that "the origin of the second sound is to be found in the ventricle," admit of another explanation, as see ante, pp. 30-2.

* Causes external to the heart itself may influence the transmission of the sounds to the ear, and thus may modify their intensity as heard on the chest walls; but even admitting, for the sake of argument, that the patient's posture is the same, that the structures which intervene between the heart and the chest walls are in precisely the same condition, and, in like manner, that the walls of the chest are of uniform thickness and texture, and, therefore, are possessed of the same conducting power-admitting these facts, the sounds will be found to var according to the circumstances above stated.

poisons in the blood may exercise a similar influence, whilst all depressing and enervating diseases which weaken the heart, impair the nervous force, or render the blood less stimulating in its character, diminish the intensity of the sounds-of the first sound, by lessening the force of the ventricular contraction, and consequently, of the tension and vibration of the auriculo-ventricular valves; of the second, by diminishing the force with which the blood is driven into the arteries, and with which the artery contracts, and, therefore, by proportionably lessening the force with which the blood recoils on the semilunar valves.

But there is yet another circumstance, irrespective of disease in the heart itself, to which special reference should be made, in regard to its bearing on the intensity of the sound; I refer to the freedom with which the blood circulates through the heart. When the quantity of blood is large, or any impediment exists to the cardiac circulation, so that an excessive quantity of blood accumulates in the heart, the ventricle contracts forcibly but fruitlessly, to propel it, and a dull confused sound results from the violent, yet imperfect muscular contraction. The character of the ventricular sound is modified accordingly, and the sound is obscured and no longer clear. When, on the contrary, the quantity of blood is small, and no impediment exists to its circulation, the ventricles contract naturally, and the first sound is heard clear and distinct. This is often exemplified by the result of venesection and profuse hæmorrhage. Under the same circumstances the contractility of the artery is more than ordinarily excited, and the second sound is heard clearer than usual, and of higher pitch.

In disease of the heart these modifications of the sounds are met with in every variety. In dilatation of the heart, with moderate hypertrophy of its walls, the conditions necessary for the production of an intensely loud, though not a particularly clear first sound, are developed to the greatest degree; the heart is more extensively in contact with the anterior walls of the chest than usual; the ventricles are capacious; the valves are developed to a corresponding extent; and the muscular structure is strong enough to contract forcibly on the contained blood, and yet not thick enough to prove a serious impediment to the transmission of sound to the ear. In regard to the second sound, the same causes are in operation. The enlargement of the ventricles leads to a corresponding increase in the size of the arterial orifices, and of the valves which close them, whilst the force of their contraction leads to an unusually forcible propulsion of the blood, and to a corresponding

increase in the force of its recoil on the semilunar valves, with a consequent increase of vibration and sound. In simple dilatation, when not accompanied by such an amount of fatty degeneration of the muscular structure of the heart as to impair the contractile power of the ventricles, the conditions exist which are favourable to the production of a loud and unusually clear first sound. The heart is more than ordinarily in contact with the chest walls, the cavities of the ventricles are large, the valves consequently large; the contractile power of the ventricles is considerable, and their walls are thin, and in no way calculated to impede the transmission of sound to the ear. Therefore, as might have been expected, the sound is not only louder, but clearer and more abrupt--more distinctly valvular than in health. The second sound ist also loud, in consequence of the size of the semilunar valves, and of the column of blood which reacts upon them.

In simple hypertrophy without dilatation, the walls of the heart are abnormally thick, and the cavities of the ventricles, therefore, relatively contracted; the play of the valves is unusually small, and the quantity of the blood to act upon them is also small, whilst the density of the muscular structure deadens the vibrations and prevents their transmission to the ear. Therefore at the apex, where, if it were due to muscular contraction, the first sound should be loudest, it is often inaudible; whilst it is audible over the aorta and pulmonary artery in consequence of its being transmitted along the current of the blood.* Even then, however, the sound is comparatively weak. In like manner, the smallness of the current of blood ejected from the ventricles at each systole of the heart leads to a comparatively weak recoil on the semilunar valves, and so to a diminution in the intensity of the vibration, and of the loudness and clearness of the second sound. In atrophy of the heart, when the heart is small and the walls are thin and weak, the first sound is clear, but short and feeble, in consequence of the small size of the auriculo-ventricular valves, and of the diminution of force with which the vibration consequent on their closure takes place. The same holds good in respect to fatty degeneration and softening, fibrous or other infiltration, and whatever tends to impair the muscular power of the heart or lessen the extent of surface or the play of the valves, without at the same time increasing the thickness of the cardiac walls. Nevertheless in all these cases the first sound is loudest at the apex.

* See notes, pp. 28-9.