and we know that the vibrations of the voice, cough, or glottic breathing, are audible at the thoracic parietes: to suppose, then, that the bronchial sound should not be audible there, would involve a suspension of physical laws.

Dr. Sanderson's theory is in part built on the supposition that the lung may be divided into an extensible and an inextensible portion; that the air-cells are elastic and the air-tubes not. Now I am sure this is not true: I do not mean to say that the air-cells are not greatly more extensible than the tubes, though how much we do not know; but it is impossible to examine the smaller tubes minutely without seeing that they are in a high degree elastic and extensible. And remembering their constitution, we should antecedently conclude that they would be so, for their walls are largely endowed with yellow elastic fibres; indeed, the elastic coat is, with the exception of the epithelial, the only one that is continued down to the very extremities of the bronchial ramifications; so that the smallest tubes may be said to consist entirely of elastic tissue with a lining of a single layer of epithelium, and surrounded with the smallest possible quantity of connective. Again, it is impossible to imagine the air-cells dilating without the bronchial tubes dilating too. What is it that surrounds the bronchial tubes? The parenchyma of the lung-air-cells. If we make a section of a small bronchial tube, we shall find it imbedded among air-cells, which are in contact, but not communicating, with its outer wall, just as the branches of the portal vein course their way among the lobules of the liver. Now, is it possible to imagine that these air-cells can dilate without the channel that they surround dilating also? Let A (Fig. 4) be a small bronchial tube seen in section, and B, B, B, air-cells in contact with its outer wall; the expansion of these air-cells is manifestly impossible without increasing the calibre of the cylindrical channel which they bound, unless we suppose them to expand in one direction only-that is, in a radiating direction, and not laterally, which would be gratuitous and unreasonable.

Or perhaps this may be more clear thus. Let a (Fig. 5) be a circle formed by twelve circles, b b b, each of them three-quarters of an inch

But

in diameter. The circumference of the circle will be nine inches. if the smaller circles undergo an expansion of one-third of their diameter, so that instead of three-quarters of an inch, the diameter of each is an inch, the diameter of the whole circle which they form will have increased from nine inches to twelve. So that it is impossible for the air-cells to expand without the tubes which are everywhere surrounded with them expanding too, unless we suppose a vacuum to be formed; for the thin areolar web surrounding each tube, although capable of extension in any one direction, is incapable of occupying any additional space. It seems to me impossible to help believing that the air-tubes do in this passive manner expand, the smaller ones considerably, at each inspiration.

But above all, in proof that the calibre of the bronchial tubes is increased at inspiration and diminished at expiration, we have the capital fact a fact that I have adverted to in my work on asthmathat one constantly finds dry musical sounds at expiration which are inaudible at inspiration; in fact, that dry sounds are expiration sounds, and that it is the common thing to find them confined to expiration. Now, how it is possible to explain this, except by supposing that the air-tubes undergo a diminution of calibre at each expiration, I cannot imagine. On this supposition it is quite intelligible. For suppose, which is often the case, the source of the sound is a plug of tenacious mucus sticking to the side of the tube. At inspiration, when the tube is expanded in common with the other tissues of the lung, the plug of mucus does not sufficiently obstruct the air to throw it into musical vibrations; but at expiration the elastic tube, no longer expanded, is left to its own natural disposition to contract, and the plug of mucus which in the patulous state of the tube was not equal to the production of any considerable narrowing, is now sufficient to produce a very narrow strait, perhaps almost a complete occlusion, and musical sounds are immediately generated. The mucus plug is a constant, it cannot vary at each inspiration and expiration, and yet the conditions for the generation of the sound do vary, for the sound varies; and this variation can only be produced, as I conceive, by variations in the calibre of the tube-contraction at expiration-so that what was a relatively small becomes a relatively great narrowing. If my explanation is not correct I should be glad to hear some other offered; of the fact there can be no doubt. If my explanation is correct, it is a proof that the tubes do undergo expansion and contraction at each respiration, like the cellular structure of the lungs.

There is another fact that in my opinion tends strongly to show that the bronchial sound furnishes a good deal of the material of the respiratory murmur-it is the inaudibleness of the murmur at expiration. If Dr. Sanderson's view were correct, the respiratory murmur ought to be as loud at expiration as inspiration: the same amount of air rushing out of the same orifice, close to the surface, in the same time, or even less time, ought surely to make as much sound as when it rushed in. If, however, we imagine the staple of the sound to be furnished from a distance, convexion comes into operation, and its

audibleness will depend on the "set" of the air-current. If a bell is rung close to the ear, it makes no difference which way the wind blows, but if it is rung at a distance, we shall hear it plainly if the wind blows towards us, while when the wind blows away it may be quite inaudible. So, the fact that the direction the air is taking in the bronchial tubes determines the audibleness or inaudibleness of the respiratory murmur, shows that the sound is influencible by convexion -in other words, has a distant source, and is not generated at the superficies.

I cannot therefore subscribe to Dr. Sanderson's views:

Because the air-rush, which Dr. Sanderson admits to be the cause of the sound, is at its minimum at the very part which he claims as the seat of the respiratory murmur:

Because it is impossible to conceive but that the sound generated in the entire system of air-passages must be conducted to the surface by the air in the bronchial ramifications:

Because the alternate audibleness and inaudibleness of the respiratory murmur shows it to have such a seat that its conveyance to the ear is influenced by the direction the air is taking in the bronchial tubes.

I pass now to the consideration of another set of views-those of Spittal and Beau-who transfer the seat of the respiratory murmur to the very opposite end of the air-passages, M. Beau believing that it depends on the rush of air through the pharynx, and Dr. Spittal that the chink of the glottis is its seat.

Now, with regard to the pharyngeal and glottic breath sounds, I believe that any one may, in his own person, satisfy himself of two things:

1st. That there really are such sounds.

2ndly. That they have nothing to do with the production of the ordinary respiratory murmur.

With regard to the so-called pharyngeal sound, I must premise that I do not believe it is produced in the pharynx at all, but at the isthmus faucium, by dropping the soft palate upon the root of the tongue, and so producing a narrow horizontal chink; through this the air rushes and generates the sound in question; it is of a thick, faucial, guttural character, and is the sound that marks the first heavy breathing of sleep before snoring comes on. The glottic sound is produced by the voluntary partial closure of the glottis, so narrowing the chink that the air rushes through it; it is the laryngeal element of whispering, and we hear it well in the breathing of chronic laryngitis. Each of these sounds may be produced at pleasure; we know when we are making them and when we are not; and if we listen to the chest of any one who is thus voluntarily making and unmaking them, we can tell in a moment, as I have already stated, when they are being produced and when remitted. With regard to the faucial sound, I may remark that it can never be made with the mouth shut -the glottic sound can; the opening or closure of the mouth makes no difference to it.

How, then, can these sounds have anything to do with the respiratory murmur? We cannot make and unmake it; we cannot vary it at will; we cannot affect it by anything except by the length and strength of the respiratory acts.

Dr. Walshe and Dr. Herbert Davies have attributed the excess of the inspiratory over the expiratory sound to a greater resistance offered to the air by the lung tissues in inspiration than expiration. I must confess I am quite at a loss to comprehend the possibility of such an increased resistance. It is in consequence of the increased capacity of the air chambers and channels of the lung that the tension of the intra-thoracic air is diminished, and the inspiratory current generated. The atmospheric pressure, balanced during a state of respiratory rest by the resistance of the walls of the air-tubes and cells, is no longer balanced; the pressure of the walls is temporarily taken off the air by their dilatation, and a state of minus tension is produced. It seems to me, then, that there must not only be not more, but less resistance to the air at inspiration than at expiration, and that this lessened resistance is the very cause of inspiration.

Dr. Herbert Davies specifies that it is the elastic contractility of the lung that offers greater resistance to the inspired air than the expired. This seems to me to imply the idea that the contractility of the lung is overcome by the distending force of the inspired air, instead of the air being drawn in in consequence of the contractile tendency of the lung being overcome by the expanding parieties of the chest. If the contractility of the lung were not, for the time, overcome, and more than overcome, no air could be drawn in. We may regard, then, the contractility of the lung at inspiration as potentially nil. It is to the parieties of the thoracic cavity, and to them alone, that the elasticity of the lung offers any antagonism during inspiration; and it is at expiration only, when the muscular distension of the chest ceases, that the elastic resiliency of the lung is allowed to reassert itself, and the elastic lung-tissues react upon the intra-thoracic air. The resistance, therefore, offered to the air by the elasticity of the lung is an expiration and not an inspiration resistance.

In the opinion of Dr. Herbert Davies the inequalities of the internal surface, produced by the cartilaginous rings of the windpipe and bronchi, tend to throw the air into vibrations, and contribute to the respiratory murmur. I think it has yet to be shown that the rings of the windpipe and bronchi do produce any inequalities of surface. For my part I have never been able to see it; it has always appeared to me that the cylindrical smoothness of the internal surface is not in the slightest degree broken or interfered with by them. Indeed, to suppose that it would be, would be to suppose that Nature had been clumsy, and that she had thrown unnecessary obstruction in the way of that free flow of air into and out of the lungs, which is the essential condition of healthy breathing, and which all the other arrangements of respiration conspire to favour.

55-XXVIII.

13

ART. II.

A Statistical Account of Four Hundred Cases of Acute Rheumatism admitted into the Wards of the Middlesex Hospital during the Years 1853-59. By GEORGE WILLIAM FLEETWOOD BURY, Esq., Fellow of the Royal College of Surgeons, late Registrar to the Hospital.

FOUR hundred and seventy-six cases of acute fibrous rheumatism were admitted into the wards of the Middlesex Hospital during the six years commencing from 1853.

The following table exhibits the number of cases admitted, and the nature of the complication which occurred among them:

It is here necessary to state that under the different heads of heart complication are included only those instances of cardiac mischief which were considered either to have originated with the present rheumatic attack, or those in which, during the present attack, new cardiac disease had been grafted on old structural and rheumatic changes. No example, therefore, of simply old heart disease-the result of previous rheumatic attacks-has been entered as a complication.

From the tables we find that more than one half, or about 53.7 per cent. of those attacked with the disease suffered from heart complication of one kind or another, and that women suffered in a much greater proportion than men. In the latter, the per-centage was 45.3; in the former, 62.2.

Endocarditis has been by far the most common form of heart complication, and its combination with pericarditis stands next in order of frequency. Pericarditis without endocarditis was present in only thirty-five cases, whilst nine cases alone are recorded of endo- or peri