no single articulate symbol can be devised, applicable to the heart's sounds in more than one point. The subjoined series is offered for the four points of prominent clinical interest. The acute accent-mark is used to show where the accent falls (twice, when it falls very strongly ;) the marks of long and short where one or other character is prominent.

The eye gathers from these symbols the tendency to equalization in length of the sounds observable at the bases, as well as the transference of the accent from the first to the second sound at the apices and bases respectively.

The extent to which the heart's sounds are audible in health, is not subject to any fixed rule. One great mistake,† commonly committed by authors who attempted to define it, is not considering separately the first and second sounds. From this omission, the ordinary starting proposition, that "the heart's sounds are heard at their maximum in the præcordial region," becomes an error: the second sound is, in truth, heard in nine people out of ten, more clearly at mid-sternum, on the level of the second interspace, than at any point of the præcordial region,even limiting that region to the space in which the heart is uncovered by lung during tranquil breathing. The thickness of the soft parts, the form of the chest, and many other physical conditions, perfectly independent of disease of any of the thoracic organs, modify the extent of propagation so variously, that there can be no practical utility in laying down rules subject to perpetual exceptions. But the lines of propagation of the two sounds severally agree in most healthy persons, whatever be their absolute intensity at their seat of production; changes in these lines point positively to some modifying cause, and hence their establishment is clinically valuable. Now the first sound passes slantingly upwards to the left acromial angle, growing weaker and weaker on the way; it loses much more on the way to, and at, the right acromial angle: its propagation backwards

* The left and right second interspaces close to the edge of the sternum. † Some authors speak of the sound being audible in healthy male adults, of moderate stoutness, even at the right side posteriorly; others hold that the space over which they are heard seldom exceeds two square inches!

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is clearest and fullest to the left, so that while audible at the left back, it may be inaudible at the right. The second sound, with the base-region as its centre, radiates to the right and left acromial angles, with greater clearness to the left than the right; posteriorly it reaches the surface at the right side less clearly than at the left.

The difficulty of unravelling the mechanism of the healthy sounds of the heart is emphatically proved by the fact that, from the time of Laennec to the present day, at least twentynine theories have been proposed in its explanation. It would be a tiresome, and indeed useless, task to review these theories seriatim: the better plan seems to be to state with as much brevity as possible the rationale of the sounds, supported by the greatest amount of clinical and experimental evidence.

The occurrences which are possible sources of sound, and with which the first sound is coincident, appear to be,—at its commencement, the impulsion of the blood in the ventricles against the auricular valves; the sudden tension of these, and the sharp collision of a portion of their surfaces; the attrition of the bloodelements inter se within the ventricles, or their impulsion against their walls; the projection of blood from the ventricles against the orifices of the pulmonary artery and aorta, and the columns of blood contained within them; the shock of the heart's apex against the side, or against lung-substance, if this be interposed; and the attrition of the pericardial surfaces near the apex;towards its close, when their contained blood has been expelled, the collision of the surfaces of the ventricles;-and, throughout its entire duration, the sustained muscular contraction of the walls of the ventricles, with, at a period varying with the condition of the heart's substance, the perfect tension of the muscular fibres. Now, if we except pericardial attrition (inasmuch as the healthy first sound has no shade of friction-quality in it,*) and,

* This is, in my mind, a much more conclusive reason for its rejection than the fact that the first sound continued, not obviously changed, after the pericardium had been removed in living animals. Such continuance would merely prove that pericardial attrition took no prominent part in generating the sound. But in exceptional cases (and where there is no reason to believe the pericardium diseased,) the first sound has a distinct, though slightlymarked, attrition quality. This was evident, for instance, in a woman (Roberts, U. C. H., Oct. 10, 1850,) with general moderate dilated hypertrophy, in whom the knock of the heart against the side was occasionally distinctly sonorous, and accompanied with a sensation of faint rubbing, palpable to the hand: all three signs disappeared under rest and appropriate treatment.

probably, collision of the blood-elements among themselves within the ventricles (inasmuch as experiments seem to show that such collision is, at the least, rarely sonorous,) all these phenomena are more or less constant, and more or less powerful causes of the sound. That the sound derives its dull, booming prolongation from muscular contraction, seems unquestionable, not only because it retains these characters when the heart contracts after separation from the body, and the action of the auricular valves is prevented, but because it may in these characters be pretty closely imitated by the contraction of voluntary muscles." Nor can there be any doubt that the tension and surface-collision of the auricular valves, and sharp shock of the blood against their ventricular surfaces, give the comparative sharpness to the first sound,-a character which may be detected by attention at its outset, and which, in certain states of altered contractility of the muscular fibres, almost covers or rivals in strength the sound generated by these: the elements of sonorousness exist in these conditions; and when they are experimentally interfered with, a corresponding change follows in the character of the first sound. The projection of the ventricular blood against the orifices of the large vessels, the flattened valves, and the bases of the columns of blood they contain, combined with the sudden extension of the arterial coats beyond, have strong clinical and experimental claims to a share in the first sound. A sound is audible in the arteries synchronous with the heart's systole, under circumstances in which the idea of mere conduction from the heart is quite inadmissible: such sound may be heard in the femoral and even popliteal arteries sometimes, where no disease of these vessels or of the aorta exists. Again, in certain cases of mitral regurgitant disease, where the systolic sound at the left apex is completely deficient (a murmur only existing there,) the first sound may be discovered with the quality of health at the aortic base. There is a want of clear evidence that the collision of the surfaces of the ventricles contributes to the production of the sound at its close; but it seems, at the least, probable that such

* In a remarkable case (which I saw with Mr. Hardwicke) of hypertrophy of the recti abdominis, with contractions (partly reflex, partly voluntary,) of their tissue, the variation in intensity of the sound, according as the contractions were slow or quick and abrupt, was very remarkable: in the latter case, the sound had a very distinct resemblance to the first sound of the heart.

is the fact, and that the clicking character of the sound, after profuse hemorrhage, may, in part, be due to this cause. Lastly, the heart's shock against the side, especially when the posture of the individual, the period of the respiratory act, or other conditions, allow the surface of the organ to play fully against the parietes, indubitably increases the first sound, and gives it in particular cases a knocking character.*

The essential causes of the first sound, then, seem to be muscular action (walls of ventricles,) valvular tension (auricular valves,) and forcible shock of fluids against resisting membranes (orifices of large vessels;) while various subsidiary causes act occasionally, especially impulsion of solids against solids (heart's apex against the chest walls.)

The phenomena synchronous with the second sound are: the diastole of the ventricles and rush of blood into their cavities; the sudden recedence of the heart's apex from the chest walls; the abrupt fall of the auriculo-ventricular valves to the sides of the ventricles; the sudden tension of the sygmoid valves, and impulsive fall of the columns of blood against them during the arterial systole; the arterial systole itself.

Now, of all these causes, the most effectual is (as originally taught from clinical observation by Dr. Carswellf) the tension of the sygmoid valves: the absolute disappearance of the natural second sound at the aortic orifice, and its persistence at the pulmonary orifice, in cases of insufficiency of the aortic valves, is a sufficient proof of the fact. The quality of the sound, and the site of its maximum force, as already described, depose, too, in favour of its membranous origin, and of its localization at the orifices of the great vessels. The fall of

* Where a thick layer of emphysematous lung intervenes, and sometimes even without this, I think there is reason to believe the first sound may be given an intermittently murmurish character at the apex, independently of any disease in the mitral valve, simply by the apex-point of the heart impinging against the lung, and moving some of its contained air. I have observed the phenomenon (during suspension of the respiration) where this seemed its sole plausible explanation.

† See Archives Gén. de Méd., t. xxvi., 1831.

The experiments made on large animals leave the mechanism of the second (and, à fortiori, that of the first) sound far from satisfactorily established: the matter really rests on clinical evidence. Thus, in Hope's records of experiments in which both pulmonary and aortic valves were hooked up, the simple statement is made, that the "natural second sound entirely ceased, and was replaced by a prolonged hissing." (Dis. of Heart. Ed. 3, p. 35.) We are left in the dark as to whether the second sound was thus ascertained to have become inaudible at the base only of the heart, or over

the columns of blood on the surface of the valves, (though not so sonorous as if the valves, instead of being opened out by the receding blood, as they are, were first expanded, and then received the shock of the fluid from above, as is affirmed to be actually the case by M. Hamernik,) must intensify the sound of valvular tension. Whether the arterial systole itself plays any part in its production, is yet open to inquiry.

Whatever be the force of the arguments in favour of the active character of the diastole of the ventricles, it seems certain, as matter of experiment, that the phenomenon is soundless. Skoda argues, that as exceptional cases occur in which the second sound is weak at the base, and loud and clear at the apex (while there is no diastolic impulse against the chest wall,) it must originate in part in the ventricular region; and suggests that it may be produced either, " perhaps, sometimes," by the stroke of the blood against the ventricular walls during the diastole of the heart; or by separation of the heart's apex from the surface, against which it had been pressed during the systole; or by separation from the parietes of the portion of the pericardium which had been driven against these during the systole. I am disposed to believe that there may be more truth in this notion than there seems on surface-consideration of it: if the chest be percussed with the point of a finger, while the ear is applied to a solid stethoscope in a neighbouring spot, two sounds are heard for each blow; the first strong, corresponding, of course, to the direct impulse; the second, very weak, to the removal of the finger from the point percussed. Now the recedence of the heart's point from the side is here imitated. Further, in the normal state, the blood enters the ventricles from the auricles, with a current so calm as to render it singularly unlikely that audible sound can be the result. But in cases of highly marked aortic regurgitation, blood falls with notable force into the left ventricle, and may conceivably generate sound. I have unquestionably heard, at the left apex, a distinct sound in more than one such case, while at the aortic base the ordinary regurgitant murmur alone existed: such cases would probably be more frequently met with, were it not for its entire surface. From several passages in the context, the former seems the more likely; and hence the records at least of these experiments leave it still an open question, whether or not the natural second sound is in any small degree ventricular in site, or capable of becoming so, when aortic regurgitation exists.