THOUGHTS ON BROKEN WIND. 
61 
Medical Gazette for Nov. 21 has come accidentally into my 
hands; and in it I find a clinical lecture on cases of bronchitis 
and emphysema by R. B. Todd, M.D. F.R.S., Physician to 
King’s College Hospital, which bears so much on my entire 
subject, that I would, had I room, gladly insert the whole 
of it. I extract what follows. 
“Such are the changes and physical signs which we find in 
the early attacks of bronchitis. But when there have been 
repeated attacks of this disease—and especially when these 
acute attacks have supervened upon a continuous chronic bron¬ 
chitic state (if I may be allowed to coin such an adjective), the 
lungs undergo very serious changes which interfere very greatly 
with their functional integrity and activity. These changes are 
of various kinds: sometimes one or more bronchial tubes are 
obliterated (as first, I believe, pointed out by Dr. Stokes), and 
the pulmonary lobule or lobules to which they lead collapse 
from the absence of their usual distending medium, the air, and 
become more or less wasted. The adjacent tubes and their 
corresponding air-cells dilate to receive more air, just as the 
tubes of one lung would if the other were compressed by fluid, 
but probably to a much greater degree; and thus we may have 
in the same lung, at parts, a collapse and an atrophy of portions 
of the lung, and at other points expansion and permanent dila¬ 
tation of the air-tubes and air-cells. 
“But there are other and more important causes in operation 
to produce the dilatation of the air-cells and tubes; these are, the 
disturbed state of breathing caused by the bronchial irritation, 
and more especially the difficulty of expiration and the mischief 
done to the tissues of the bronchial apparatus by the repeated 
attacks of inflammation. Thus the bronchial irritation gives 
rise to a more or less asthmatic state, in which the act of in¬ 
spiration is performed with considerable force, and that in a 
state of lung which is ill suited to resist the pressure of the in- 
rushing air. The muscular fibres of the bronchial tubes must, 
by the repeated attacks of inflammation of the mucous mem¬ 
brane, be more or less weakened. Now, the most probable 
office of these fibres is to regulate the admission of air into the 
lungs, and thereby to protect its delicate tissues against undue 
pressure, just as the muscular fibres of the arteries regulate the 
flow of blood into them, and to a certain extent antagonise the 
heart’s force. Hence, in an enfeebled state of this muscular 
apparatus, the bronchial tubes will yield under the force of the 
inspired air, aud become more or less dilated; and an undue 
quantity of air will rush in most abundantly at those parts 
where the muscles are weakest, and therefore afford least re¬ 
sistance. 
