thrill and murmur, or murmur only, the diagnosis of mitral narrowing should be made with very great caution.

The two lesions sometimes coexist, but since the auscultatory phenomena of mitral stenosis, so far as the presystolic murmur is concerned, may be exactly simulated (see p. 203) by those of aortic incompetence, it is, under the circumstances mentioned above, often extremely difficult and occasionally impossible to decide positively whether the latter affection is or is not complicated by the former.

The differential diagnosis must be based on a general consideration of the whole of the symptoms and physical signs, assisted by the cardiographic and sphygmographic evidence.

If the presystolic murmur is wanting, as is the case in the final stage of the disease, the short, sharp first sound of mitral stenosis may be mistaken for that of dilatation of the heart. The absence of the second sound at and to the left of the apex would, however establish the diagnosis of mitral stenosis.

A rumbling presystolic murmur is sometimes heard in the mitral area after an attack of pericarditis or in association with pericardial adhesions in the case of children. The murmur heard under these circumstances has not the peculiar vibratory character of the bruit audible in cases of mitral narrowing, nor does it terminate abruptly in the first sound. Furthermore, the first sound does not present the characteristic modification observed in mitral stenosis.

The association of regurgitation through the mitral opening with narrowing of the orifice sometimes leads to difficulty in the detection of the latter affection in the absence of the presystolic murmur.

The diagnosis, in this event, turns largely on the characters of the first sound at the apex, since the effect of regurgitation is to obscure and destroy it, whereas the effect of stenosis is to shorten and exaggerate it. If therefore the first sound at the apex is short and loud, and is followed and not obscured by a systolic bruit, which is neither well conducted into the left axilla, nor audible at the angle of the left scapula, the presence of mitral stenosis may reasonably be suspected. The absence of the second sound at and to the left of the apex would be further evidence in favour of the existence of mitral narrowing.

Moreover, if the symptoms and physical signs of pulmonary congestion and enlargement of the right ventricle, associated with an apical systolic murmur, are more marked than the amount of regurgitation through the mitral orifice, estimated on other grounds, would account for, the possibility of such a complication as mitral stenosis must be taken into consideration.

It appears also that regurgitation through the mitral orifice would occur much more commonly in association with mitral stenosis were it not that the high pressure in the left auricle during the ventricular systole is sufficient to prevent any reflux through the imperfectly closed auriculo-ventricular aperture (Samways).

ESTIMATION OF THE DEGREE OF NARROWING IN MITRAL STENOSIS

The extent of the lesion is determined by a consideration of the following data:-

1. The pulse. So long as the pulse is regular in force and frequency and the artery is of medium size, the amount of mitral narrowing cannot be very great.

Great reduction in the size of the artery and a small, weak, and extremely irregular pulse are among the indications of severe obstruction.

2. The degree of enlargement of the left auricle.-The increase of dulness in the third and fourth intercostal spaces, immediately to the left of the sternum, will indicate roughly the size of the left auricle.

3. The degree of enlargement of the right ventricle.-The size of this chamber and the force of the ventricular contraction furnish the most reliable evidence of the extent of the mitral narrowing, since it is on this side of the heart and on the left auricle that the stress of the lesion falls.

4. The presence or absence of the aortic second sound at and to the left of the apex.-If the second sound is audible at and to the left of the apex the degree of stenosis is probaby slight, for the reasons which have already been given.

The absence of the second sound in this situation is an indication that the narrowing of the orifice is considerable.

5. The amount of accentuation of the pulmonic second sound.— In the absence of pulmonary complications and provided the tricuspid valve is competent, the degree of pronunciation of the pulmonic second sound affords a means of gauging the blood pressure in the lungs, and hence of estimating the degree of obstruction to which the lesion has given rise.

6. The severity of the arterial anæmia and venous engorgement. So long as there are no complications, and provided the compensatory changes are well developed, the presence of marked arterial anæmia and venous engorgement is significant of serious obstruction.

In order to facilitate the estimation of the extent of the lesion, and to serve as a guide to the prognosis in mitral stenosis, Sir W.

Broadbent has divided the progress of the disease into three stages, which are as follows:

1. The first stage which is characterised by

(a) A presystolic murmur

(b) The gradual development of a short and sharp first sound at the apex

(c) Accentuation and reduplication of the pulmonic second sound.

2. The second stage which is characterized by

(a) The disappearance of the second sound at and to the left of the apex

(b) A short, sharp first sound

(c) A variable diastolic murmur

3. The third stage which is characterized by

(a) The disappearance of the presystolic murmur

(b) A short and sharp first sound

(c) A tricuspid systolic murmur

In the light of what has already been said with regard to the estimation of the degree of obstruction at the mitral opening, a further explanation of these stages is unnecessary.

It may, however, be pointed out that under this classification, which is based on auscultatory signs, the second and third stages are interchangeable. Thus a case which has reached the third stage may, under favourable conditions and by means of suitable treatment, be restored to the second, a feature that does not obtain with respect to the first two stages.

CHAPTER XIII

AORTIC INCOMPETENCE

Pathogenesis--Morbid Anatomy-Effects on the Heart and Circulation -Compensation-Sudden Death-Symptoms-Complications-Physical Signs -Diagnosis-Estimation of the Amount of Regurgitation.

ETIOLOGICAL PATHOLOGY

THE chief causes of aortic incompetence are: (1) Acute, sub-acute, or chronic valvulitis of rheumatic, and probably, in some instances, of syphilitic origin; (2) chronic valvulitis (sclerosis) due to prolonged muscular strain; and (3) atheroma, which may attack the valve primarily, or as the result of the extension of the morbid process from the root of the aorta.

Syphilis and chronic alcoholism frequently co-operate with mechanical strain in the production of aortic valvular disease; they are also important factors in the causation of atheroma.

It is often impossible to distinguish between the effects of strain and atheroma, since they are both the result, for the most part, of a common cause, viz. increased arterial tension.

As the result of the operation of one or other of the morbid processes above mentioned, the free margins of the aortic cusps become thickened, rigid, and retracted, or otherwise deformed, so that their proper adaptation is rendered impossible.

The sclerosed tissue is often the seat of ulcerative changes, which may lead to perforation, laceration, or rupture of a flap, and thus. to incompetence of the valve. It is also not uncommon to find the thickened segments infiltrated with calcareous salts.

In some instances the proper adaptation of the cusps of the valve is prevented by a growth of vegetations.

Rupture of a segment of a healthy aortic valve is occasionally due to sudden and violent strain. External violence-to wit, a blow on

the outside of the chest-has in a few cases been the cause of the rupture af an aortic cusp.

In rare instances aortic incompetence occurs as a congenital lesion.

Dilatation of the root of the aorta may involve the orifice of the vessel, and by this means may give rise to relative incompetence of the valve. The lesion is, however, of rare occurrence.

The valvular changes which lead to aortic incompetence are frequently, indeed usually, accompanied by some induration of the fibrous ring surrounding the orifice of the vessel. The subsequent contraction of the cicatricial tissue leads to more or less constriction of the opening, with the result that valvular incompetence is commonly combined with a variable degree of narrowing of the aortic aperture.

PATHOLOGICAL RESULTS

Effects on the Heart and Circulation

In consequence of the valvular incompetence, a certain quantity of blood flows backwards from the aorta into the left ventricle during its diastole. The ventricle is, therefore, now supplied from two sources, and at the end of diastole its contents exceed the normal by the amount which has returned from the aorta. The accommodation of this additional quantity of blood necessitates an increase in the capacity of the chamber, which can be effected only by the stretching of its elastic walls. This process, if continued, becomes dilatation; hence the earliest effect of aortic incompetence is to produce dilatation of the left ventricle from overfilling. The increased work involved in the propulsion of a larger amount of blood than normal leads to hypertrophy of the ventricular walls, provided, of course, the myocardium enjoys sufficient nutrition.

There is, however, a further and more important cause of dilatation and hypertrophy of the left ventricle in aortic insufficiency, inasmuch as the ventricle has to withstand, during its diastole, the distending effects of the regurgitant stream under the pressure of the arterial recoil.

The strain imposed on the walls of the ventricle by this means will vary with the extent of the lesion and the state of arterial tension. It is probably considerable in all cases, and constitutes the chief source of overwork which has to be performed by the ventricle.

Dilatation would quickly get the upper hand of hypertrophy at the outset were it not that the ventricle falls back on its reserve power, which temporarily staves off the distending effects of the lesion. The subsequent occurrence of hypertrophy restores and maintains the tone of the ventricle, and prevents more dilatation of the chamber than is necessary to accommodate the amount of blood by which it is overcharged.

If hypertrophy did not occur, the reserve power of the heart