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LONDON:

M'GOWAN & DANKS, STEAM PRINTERS,

GREAT WINDMILL STREET,

HAYMARKET.

Being the Incorporation of the Journals hitherto known as “The Medical Press”

WEDNESDAY, DECEMBER 23, 1868.

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This Manual embraces the treatment of every variety of Deformity,
Debility and Deficiency of the Human Body.

By HEATHER BIGG, Assoc. Inst. C.E., Mechanician to the
Princess of Wales.

London: John Churchill and Sons; and of the Author, 56, Wimpole

street, W.

Now ready, Third Edition, revised and enlarged, 8vo, cloth, 68.

ON the Immediate Treatment of Stricture of the

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Surgeon to the Royal Orthopedic and Great Northern

Hospitals, &c.

Club-foot: its Causes, Pathology, and Treatment.

Being the Jacksonian Prize Essay for 1864. With 100 Engravings.

8vo, cloth, 128.

The Spine, Lateral and other Forms of Curvature:
their Pathology and Treatment. With 5 Plates, and 60 Wood En-
gravings. 8vo, cloth, 108. 6d.

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London: Longman and Co: Dublin: Fannin and Co.

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tates into the ventricle during the period of diastole,
hence, one reason for a direct diminution of the coronary
wave; but more than this, the abnormal egress opened to
the passage of the blood by the chink of the insufficiency,

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The heart receives the blood destined for its nutrition,
from the coronary arteries, but, by an unique exception,
they do not receive their maximum repletion at the
moment of the ventricular systole. When the blood is
propelled into the aorta by the contraction of the ven-
tricle, it passes in a direction directly perpendicular to the
orifices of these vessels, consequently, without entering them,
and it would be with difficulty only that the nutritive
arteries received a small portion of the systolic wave.
This condition (a general one) is further aided in a large
proportion of subjects by the relative position of the
coronary arteries and sigmoid valves. Frequently, in-
deed, the orifices open so close to the mitral zone of the
aorta that when the valves open during systole, they fall
back towards the orifices and close them, in which case, it
is certain that the nutritive arteries can receive no blood
at the moment of the ventricular systole. During the
diastole, on the contrary, everything conspires to secure
abundant irrigation of the heart. The valves are closed,
and the column of blood assumes a retrograde direction;
checked by the closed valves, it finds no egress but by the
orifices of the coronary arteries largely open to admit it;
a portion of blood enters, and the repletion of the arteries
is complete. In fine, the injection of blood into the tissue
of the heart occurs, principally (I do not say entirely) at
the moment of the ventricular diastole, and the pressure
of the retrograde column is the most powerful agent in
the occurrence.

Such being the mode in which the normal nutrition of
the heart is effected, it is easy to see the great distur-
bance that would accrue from imperfect closure of the aortic
valves. A portion of the aortic column of blood regurgi-

column upon the patent orifices of the coronary arteries,
and this pressure affording the vis a tergo for the move-
ment of the blood in the coronary arteries, imparts, finally,
to aortic insufficiency the two following effects: diminution
of the amount of blood supplied to the coronary arteries, and
diminution of the pressure causing this blood to circulate; in
other words, the heart receives less blood, and that, under less
than normal pressure. The nutrition of the heart is thus
fundamentally modified and rendered less active. But this
is not all. The diminished volume and tension of the blood
in the coronary arteries necessarily, induces a retardation
of its course in the corresponding veins. This, again, pro-
duces in the venous radicles and in the intermediate capil-
lary network, interstitial stasis, augmenting, uselessly, the
volume of the heart, and restricting that free interchange
of elements which constitutes the supreme act of nutrition.

To such source of disorder, another, acting in a similar
manner, may be superadded, viz.: the abnormal pressure
exercised upon the cardiac capillaries during the period of
diastole by the surplus blood which fills, to a maximum,
the left ventricle.

Thus, shackled, in the initial act which prepares it-ad-
mission of the nutrient blood-shackled in the final act
which constitutes it--interchange of the materiel-the
nutrition of the heart is fatally defective, and its tissue
degenerates.

While investigating the nature of the muscular tissue
generally, Billroth has shown that it tends to degenerate
into connective tissue whenever its nutrition is com-
promised, and certain researches of Traube have confirmed
these results in reference to the heart. The change then,
is not simply into fat, as Stokes and Paget supposed, but
rather one of a fibro-fatty description. The development
of this degeneration is frequently hastened by myocar-
ditis, contemporaneously existing with the endocarditis
which caused the valvular disease."

The intra-cardiac papillary muscles naturally participate
in these disorders, and end in atrophy, thus directly com-
promising the action of the mitral valve. My learned
friend, Professor Bamberger, of Würzburg, affirms that the
papillary muscles are always hypertrophied in cases of aortic
insufficiency. Traube, on the contrary, describes them as

In the case of our female patient, the rupture of compensation has obviously been the united effect of two exciting causes, over-exertion and obstinate bronchitis. We have seen the beneficial results of repose and appropriate treatment in the case. Nevertheless, I do not believe that this patient can be restored to the state of health she enjoyed prior to her admission into the hospital; she is 69 years old, and has always lived under bad hygienic conditions; her disease dates, at least, 15 years; dilatation of the ventricle has induced secondary mitral insufficiency; the aorta is dilated and atheromatous, and from the existence of these conditions, I am persuaded that the nutrition of the cardiac tissue has been compromised for a long period, and, that the occurrence of asystolie, has been but slightly hastened by those extrinsic influences we have alluded to. I do not believe that compensation can be completely reestablished. She has been in the hospital four weeks, and during three weeks, at least, the alarming symptoms she first suffered from, have ceased: so long as she remains at rest in bed, all seems well, but, the moment she rises, dyspnoea supervenes, the face acquires a cyanotic tint, and the legs begin to swell; the heart can only perform its proper function while she remains in the horizontal position, consequently, I regard her condition as hopeless. She would, assuredly, very speedily sink, if she were compelled to keep the erect position during the day. Repose may, for a time, prolong existence; this is the only possible hope in her case.

I cannot quit this subject, without pointing out to you the frequency of sudden death in cases of aortic insufficiency. No disease of the heart is exempt from this sudden termination, but it is never more to be dreaded than in cases of this description, and I would particularly recommend to your perusal the work that my friend, and colleague, Dr. Mauriac, has devoted to this point of pathology. Bear well in mind this fact, every patient suffering from aortic insufficiency may die suddenly, whenever the compensation is not perfectly exact. The mechanism of this accident is easily apprehended. Remember that the left ventricle is both dilated and enfeebled; under the influence of exertion, emotion, or any other cause influencing the innervation of the heart, either in a direct or reflex manner, the action of the ventricle is suddenly arrested, and it ceases to contract; the double column of blood from the auricle and the aorta enters and distends its cavity; the degenerated muscular walls have no reactive power, the pause of a second- becomes a definite paralysis, and the faintness,-a mortal syncope.

being in such cases, always elongated, flattened and atrophied. It seems to me, that these contradictory opinions are quite reconcilable, all depending upon the time the examination is made. At the commencement of compensation, the papillary muscles become hypertrophous in common with the left ventricle; subsequently, when the disease has produced the changes I have described, these muscles, also, participate in the change and atrophize. It is, now, that secondary mitral insufficiency results, assuredly one of the most curious points in the history of the affection. So long as the hypertrophy of the ventricle and papillary muscles keeps pace with the dilatation, the respective dimensions of the mitral orfice and its valves remain unchanged, and the closure of the orifice is complete. But, when the hypertrophy halts and yields to the abnormal state of nutrition, when the muscles of the valves, submitted to an abnormal elongation, begin to waste, when, in a word, dilatation acquires the ascendency, the diameter of the mitral orifice aguments in the same proportion, the zone enlarges, and as the valves preserve their original dimensions, there arises a defect of relation between the curtains of the valves and the aperture they ought to close; the closure is now imperfect, and mitral insufficiency results. Whenever, in the case of a patient known to be suffering from aortic insufficiency, without mitral disease, a murmur, during the first period, is heard at the apex of the heart without anteceding acute disease, we may feel assured of the existence of mitral insufficiency originated by exaggerated dilatation of the left ventricle. This accident is of ill-omen, inasmuch as it denotes a disorder of compensation, though not one of immediate peril. Often, on the contrary, during the first phase of this second period, a favourable change in the state of the circulation and, consequently, in the condition of the patient, is observed; indeed, the mitral incompetence opens out a way of escape for the blood which over-distends the ventricle, and acts as an auxiliary by diminishing the sum total of its work. The ventricle empties itself more easily, the auricles dilate in their turn, and this new phase in compensation may retard for a period more or less long, the accidents of confirmed asystolie. In consequence of the considerable degree of dilatation of the heart in the case of our patient, I fancy, that the mitral incompetence, which we have detected, is a secondary lesion precisely of this description. Whenever the compensation of a cardiac affection is compromised the prognosis becomes serious-this is a general fact; but the gravity of the affection is, nevertheless, not always of the same amount, and, in order to form an accurate judgment, the conditions under which the The cases of Williams, Elliotson, Hope, and many equilibrium is disturbed, must be carefully borne in mind. others, demonstrate the fact and the explanation I have Permit me to explain myself. If the disturbance can be offered of it. Occasionally, even, the cessation of the referred to some positive exciting cause-exertion, for heart's action occurs without any obvious exciting cause. example, unusual fatigue, bronchitis, or other affection The ventricle, for an instant, forgets its functions as it capable of inducing momentary disorder of the circulation were, and taken by surprise by the blood which over disalready compromised-the prognosis is, under such circum-tends it, loses all power of action, ceases to contract, and stances, less serious, the derangement of compensation is the patient dies. but an accident and not the result of the natural increase The statistics of Aran enables us to appreciate approxiof the cardiac disease, and we may fairly hope that, as mately, the comparative frequency of this termination in soon as the superadded cause disappears, matters will re- aortic insufficiency. This acute observer found that in 113 vert to their original condition. This confidence is well-instances of sudden death from disease of the heart, 25 grounded when the compensating equilibrium is destroyed for the first time. But, when the disorder results without any appreciable exciting cause, the prognosis acquires an absolute gravity, and, I would add, becomes at once unfavourable. The asystolie is, then, the immediate result of changes occurring in the cardiac structure, and the mechanism is no longer susceptible of repair because the direct agents of compensation are destroyed. Two conclusions are deducible from these facts. In a case of complete or incomplete asystolie, the practitioner should most carefully endeavour to discover the possibly exciting causes of the disturbance, and he should, moreover, scrupulously investigate those cases in which disease is compensated, with especial regard to the disastrous consequences of overfatigue of every description, dietetic errors, and particularly those following exposure to cold.

cases occurred in isolated disease of the aortic valves, and in 9 other cases, simultaneous disease of these valves existed. Thus, 34 deaths out of 113, were to be imputed

to disease of the aortic orifice.

This special danger inherent in cases of aortic insufficiency, is of great practical importance. It imposes upon the practitioner a paramont obligation. Under such circumstances he should forewarn the relatives of the patient of the possible danger which threatens life. No other resource remains to lessen beforehand our share of responsibility.

Three months subsequently our patient died, and the autopsy, made by my friend Dr. Pierreson, who discharged temporarily, the duties of chef de clinique, confirmed the diagnosis in every particular. The heart was hypertrophied

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