Chapter XLVI: Part 46

A diastolic murmur heard at or below the level of the aortic valves, chiefly {664} audible in the line of the sternum, indicates considerable aortic incompetence. If a diastolic murmur is inaudible in the carotids, it is usually preceded by a systolic murmur, which has its maximum intensity at the aortic valves or in the so-called aortic area: such a murmur indicates comparatively trifling incompetence with considerable obstruction, probably produced by calcified semi-lunar valves.

If a diastolic murmur is distinctly audible in the carotid arteries, it is invariably preceded by a loud systolic murmur in them, the systolic portion of the murmur not being very plainly audible in the aortic nor in any part of the cardiac area: this indicates very considerable incompetence with comparatively trifling obstruction.

DIFFERENTIAL DIAGNOSIS.--The diagnosis of aortic regurgitation is generally not difficult, as it rests almost exclusively upon the existence or nonexistence of a diastolic murmur. It may, however, be mistaken for aortic stenosis, for mitral obstruction, for pericarditis localized over the aorta, for aneurism of the aorta, for aneurism of the aorta immediately above the valves, patency of the ductus arteriosus, for insufficiency of the pulmonic semi-lunar valves, and, occasionally, for a rough and inelastic condition of the ascending aorta.

1st. Mitral obstruction gives a presystolic murmur, while aortic reflux produces a diastolic murmur. Mitral stenosis is accompanied by no hypertrophy or dilatation of the left ventricle, whereas these conditions are always present with aortic reflux. The quality of a presystolic mitral murmur is harsh and rough, and it has a churning, blubbering, or grinding character, while aortic reflux has a murmur of low pitch and of a soft, blowing, or musical character. Mitral stenosis is accompanied by a purring thrill which is absent in aortic regurgitation. The murmur of mitral stenosis is the longest of all the cardiac murmurs. The murmur of mitral stenosis is never heard behind, whereas that of aortic regurgitation is often heard at the sides of the chest and along the spinal column. Finally, mitral stenosis is attended by well-marked pulmonary symptoms during active physical exertion, which are rarely present in aortic insufficiency.

2d. A pericardial friction sound over the aorta has its maximum intensity over the seat of its production, and is usually audible during both the cardiac systole and diastole. In aortic regurgitation the character of the pulse, the existence of hypertrophy and dilatation of the left ventricle, and the carotid pulsation will establish the diagnosis.

3d. An aneurism at the sinuses of Valsalva is diagnosticated by the history of the case, the presence of the murmur over the pulmonary artery, the evidences of arterial degeneration, the absence of left ventricular dilatation and hypertrophy, and the peculiar jerking pulse. An aneurismal murmur is circumscribed, has a booming quality, and is usually systolic in rhythm and never transmitted to the apex of the heart.

4th. Patency of the ductus arteriosus is a rare condition: in a case where this was diagnosticated[15] the murmur was audible at the left of the sternum, was not everywhere continuous with the second sound, was only transmitted very feebly to the left, and had a wavy character, sufficient of itself to distinguish it from an aortic regurgitant murmur.

[Footnote 15: _Guy's Hosp. Rep._, Ser. 3, vol. xviii., 1872-73.]

5th. Insufficiency of the pulmonic semi-lunar valves is the rarest of all valvular lesions: the murmur should be diastolic, having its maximum intensity in the second intercostal space of the left side; it should be transmitted only downward and toward the right apex; and should not be attended by arterial pulsation, a jerking pulse, or by left ventricular hypertrophy and dilatation.

6th. A diastolic murmur in the ascending arch, due to roughening, rigidity, {665} and dilatation of the artery, is also rare, while the condition which some say can produce it is very common.

Two cases are recorded in which the diagnosis rested upon the character of the pulse, throbbing of the arteries, and the absence of hypertrophy and dilatation of the left ventricle.[16]

[Footnote 16: Bellingham _Dis. of Heart_, 1857, p. 152; also _Trans. Path. Society_, vol. iii., March, 1868, p. 3, article by Prof. Law.]

Mitral Stenosis.

Stenosis, or obstruction of the auriculo-ventricular opening of the left heart, is due partially to constriction at the base of the mitral valves, and partially to adhesions of the valve-tips or chordæ tendineæ. It usually occurs as a consequence of rheumatic endocarditis, rarely of atheromatous degeneration, and is most likely to occur in endocarditis affecting young persons.

Mitral disease is present in one-half the cases of valvular diseases of the heart. Usually, insufficiency and stenosis of the mitral orifice occur together, and stenosis probably never occurs without some insufficiency.

MORBID ANATOMY.--As a result of acute exudative or interstitial endocarditis, the valves are rendered shorter and narrower, as well as thicker and more cartilaginous, than normal. These rigid valvular projections not only obstruct the flow of blood from the auricle to the ventricle, but allow of its regurgitation from the ventricle into the auricle. In mitral stenosis there is not only thickening and contraction of the valves, but the valve-tips or the chordæ tendineæ become adherent, and sometimes each papillary muscle gives rise to a corrugated, cylindrical mass pierced with one or more slits, indicating the chordæ of which it was originally made up. The wall of the valve, especially toward its free edge, is greatly thickened, and these thickened portions are so dense that they have a distinctly cartilaginous feel. On the valvular flaps that have undergone this sclerotic change calcareous masses are very frequently developed, and are especially liable to form when a gouty diathesis exists.

When the chordæ tendineæ and papillary muscles have become adherent, the edges of the valves are drawn down toward the apex of the heart; and since the flaps are adherent for a greater or less distance upward from their bases, the valve presents a funnel-shaped appearance with its base looking toward the auricle and its apex toward the ventricle, whose smaller opening, rarely circular, usually resembles a slit with its axis in the line which unites the original segments of the valve. This button-hole slit may scarcely admit the tip of the little finger, while the normal mitral orifice permits the easy introduction of three fingers.

Annular (ring-like) stenosis is far more common at the mitral than at the aortic orifice. Hard, wart-like vegetations frequently develop on the puckered and seamed flaps, which increase the already existing obstruction. Sometimes the funnel-shaped appearance is wanting, and the flaps are stretched horizontally across, with a small opening in the centre, like a diaphragm: looked at it from the auricle, this slit is often crescentic in shape.

In cases of long standing the vegetations may become calcified. If the new tissue in the diseased valves undergoes fatty change and softens, ulcerative processes are set up and the chordæ tendineæ may rupture. On the floor of such ulcers calcareous masses and débris are frequently found.

Hayden thinks that "all funnel-shaped mitral stenosis is the result of primary acute inflammation and thickening of the valve-segments, with cohesion of their adjacent edges." Out of 62 cases of mitral stenosis, 59 assumed the button-hole form, and 3 only the funnel-shape (Fagge and Hayden).

{666} In rare instances the tendons will adhere to the wall of the heart as well as become matted together. Adjacent to the valves the endocardium will usually be found slightly thickened.

The following changes are developed in the heart and vessels as the result of mitral stenosis: The left ventricle becomes smaller, and sometimes its walls are thinner than normal. The aorta is also small and thin-walled. An almost necessary result of mitral stenosis is dilatation, with subsequent hypertrophy of the left auricle. Sometimes the auricular cavity is enormously dilated--so much so that fifty years ago Thurman described it as true aneurism of the left auricle.[17] Not infrequently the left auricular walls are from one-eighth to one-fourth of an inch in thickness. Its appendix is elongated, assuming a peculiar curved form, the aperture between it and the auricle becoming wider than normal. Moxon records a case of extensive mitral stenosis where the appendix was two and three-quarter inches long.

[Footnote 17: _Med.-Chir. Trans._, vol. iii., Ser. 2, p. 244.]

As soon as the auricular hypertrophy ceases to be compensatory and dilatation begins, the pulmonary circulation becomes obstructed, causing increased tension in and distension of the pulmonary vessels. The walls of the pulmonary vessels, especially those of the main trunk, are thickened and hypertrophied; in rare cases they have been found twice the thickness of those of the aorta.

Although mitral stenosis is a disease of youth, and atheroma one of old age, yet it not infrequently happens that even before the age of puberty atheromatous degeneration occurs in the pulmonary vessels, especially in the small branches, as a result of the increased blood-tension in the pulmonary system.[18]

[Footnote 18: _Trans. Path. Society_, vol. xvii. p. 90.]

The passive pulmonary hyperæmia which results from the obstructed pulmonary circulation may lead to those changes which collectively constitute brown induration of the lung. Another occasional occurrence, directly due to extensive mitral stenosis, is nodular hemorrhagic infarction. Hemorrhagic infarction of the lungs is in nearly every case preceded by thrombosis of the right side of the heart.

In some instances the enormously dilated left auricle may, by pressing on a bronchus, reduce its calibre one-half, and thus interfere with the functional activity of the left lung. When the pulmonary hyperæmia is extensive violent physical exertion or violent coughing may cause a rupture of one of the larger pulmonary vessels, and true pulmonary apoplexy result.

Bronchorrhoeal expectoration of large quantities of glairy mucus is a very frequent result of the intense hyperæmia of the mucous membrane of the bronchial tubes which sometimes occurs in mitral stenosis. The secretion is increased with every increase in the passive hyperæmia. The lungs are at all times so liable to congestion and oedema that any sudden or violent exercise may lead to a rapidly fatal result. Again, when the conditions enumerated have existed for some time, mitral stenosis may lead to hypertrophy of the right heart. In some rare cases the tricuspid orifice has become slightly insufficient.

ETIOLOGY.--Mitral disease is especially met with in the young, and in the child it is almost invariably a stenosis. The average age is about thirty-one; it is very rare to find it occurring after the fiftieth year of life. It seems from statistics that it is nearly twice as frequent in females as in males.

It is not infrequently of congenital origin. Acute rheumatic endocarditis is its most frequent cause. The mitral valves are more frequently affected in chorea than the aortic. In some few instances stenosis results from extension of the inflammatory process from the aortic semi-lunar valves, or prolonged aortic regurgitation and stenosis may lead mechanically to mitral disease, but not to stenosis. Niemeyer regards atheroma as an exceptional cause of mitral stenosis. No other authority regards it as a possible cause.

{667} It is a question whether scarlatina or diphtheria tends to produce in children a valvular endocarditis which is followed by mitral stenosis. It seems plausible, since in many young children it is certain that mitral stenosis has not resulted from either rheumatism or chorea. Finally, with the exception of atheroma, all the causes enumerated in the etiology of aortic stenosis may be the cause of mitral stenosis.

SYMPTOMS.--Rational Signs.--The subjective cardiac symptoms of mitral stenosis are few. There may be no such symptoms. Usually, after violent exercise there is more or less cardiac palpitation, but this will cease as soon as the auricle can relieve itself, which is readily accomplished by the patient's assuming a recumbent position on the right side with the head slightly elevated. This class of patients as a rule are pale and anæmic. There is a sharp pain frequently felt in the region of the apex, which is always suggestive of mitral stenosis. The pulse is regular and normal in character so long as the auricular hypertrophy compensates for the auricular dilatation.

When the ventricle is unable to receive and discharge its normal quantity of blood with normal regularity, the pulse becomes small in volume, feeble in force, rapid and irregular in rhythm. The sphygmograph exhibits a tracing, frequently called the mitral pulse; the sphygmograph tracing is the same as when the ventricle throws a greatly diminished blood-current into the aorta (Fig. 44). This is asystolism, and the pulse is a clear indication of the condition.

Balfour differs from other authorities in the statement that among the most remarkable subsidiary phenomena of mitral stenosis is irregularity of cardiac rhythm, which, always present in a greater or less degree, is sometimes a diagnostic phenomenon. The auricular systole commences earlier than normal on account of its hypertrophy. This premature contraction of the auricle, stimulating ventricular contraction, is indicated by a second ventricular systole which is much less forcible than the first.

The passive pulmonary hyperæmia attending the advanced stages of this form of cardiac disease causes habitual dyspnoea, which is exaggerated by physical exertion and is attended by a dry, hacking, teasing cough which resembles the so-called nervous cough.

After violent or prolonged exertion there may be bronchorrhoea, a pint of glairy, watery mucus often being expectorated in a few moments. Not infrequently severe exercise induces attacks of profuse, watery, blood-stained expectoration, indicative of pulmonary congestion and oedema. Sometimes the exertion of walking rapidly against a strong wind will induce such intense congestion and oedema of the lungs in one with extensive mitral stenosis as to cause sudden death.

Hæmoptysis is not infrequent, small quantities of pure florid blood being expectorated.

Orthopnoea is not a frequent symptom of mitral stenosis, for even in extensive and long-standing cases the pulmonary congestion is not constant, as the auricle is able ordinarily to empty itself, and only becomes engorged during active physical exertion or great mental excitement.

It should be mentioned here that the old idea, that "mitral stenosis sometimes produces hypertrophy of the left ventricle," is fallacious. In no instance can it be attributable to mitral stenosis.

{668} Physical Signs.--Inspection.--As the left ventricle does not receive its normal quantity of blood, the cardiac impulse is feeble. Sometimes it has a visible undulating movement.

Palpation.--On palpation, although the apex-beat is less forcible than normal, a distinct purring thrill will be communicated to the hand: this thrill is a constant attendant of mitral stenosis, and may be regarded as its diagnostic sign. It should be remembered, however, that a purring thrill does not always indicate mitral stenosis. It is most distinct at the apex-beat, although it may be diffused over the whole præcordial space. It either continues through the entire diastole or is only present just before the systole. It is sometimes called a presystolic thrill. It ceases with the apex-beat. The only conditions besides mitral stenosis which will cause a purring thrill at the cardiac apex are mitral regurgitation, with extensive dilatation of the left ventricle, and left ventricular aneurism; in both instances the thrill will not be presystolic, but systolic.

Percussion.--The increased size of the left auricle may cause an increase in the area of cardiac dulness upward and to the left at the inner part of the second left interspace. This increased area of dulness will only be recognized on careful percussion during expiration.

Auscultation.--Mitral stenosis is characterized by a loud churning, grinding, or blubbering presystolic murmur; this murmur is of longer duration than any other cardiac murmur, on account of the time required for the blood to pass through the narrowed and obstructed orifice. It ends with the commencement of the first sound and the apex-beat, being synchronous with the purring thrill. The murmur is heard with its maximum intensity a little above the apex-beat.

Cryan records a case where the murmur was absent, but the diagnosis of mitral stenosis was made from the other symptoms. At the autopsy the orifice would barely admit the tip of the little finger, and the absence of the murmur was accounted for by the smallness of the aperture.[19]

[Footnote 19: _Trans. Path. Society_, Dublin, Part 2, vol. iv., 1870.]

As a rule, mitral stenosis is accompanied by the loudest as well as the longest cardiac murmur. The murmur is always louder when the patient is erect than when in the recumbent posture. For a few days before death, and at any time when there is great constitutional debility, the murmur may be held in abeyance. A presystolic murmur is never present when auriculo-ventricular narrowing does not exist. When this lesion does exist it is never permanently, and very seldom temporarily, absent. A prolonged murmur and a sharp first sound indicate a funnel-shaped stenosis. A murmur immediately following the second sound, and running through the apex-beat, indicates great contraction of the orifice--diaphragmatic contraction. The murmur of mitral stenosis is very rarely, if ever, conveyed to the left of the apex-beat, and it is rarely heard more than two inches to the right of the apex. The second sound of the heart is intensified over the pulmonary valves. When mitral reflux and mitral obstruction coexist, the two murmurs run into each other, constituting a single murmur that may be mistaken for a systolic murmur. The harsh character of the presystolic element of the murmur can always be recognized.

A mitral obstructive murmur is never soft or musical, but there is a rare form of presystolic mitral which is so short as to resemble a tone. A mitral stenotic murmur does not often merge into the first sound of the heart, but is usually separated from it by a short interval. Sometimes a stenotic murmur only becomes audible when the patient sits up. In about one-third of all cases of stenosis of the mitral orifice the second sound is reduplicated. It is best heard at the apex and when the heart's action is slow. The reduplication may be temporarily absent. Pulmonary congestion efficiently accounts for {669} this reduplication. Geigel ascribes it to "non-coincidence in the closure of the valves." Guttman regards it as originating at the stenotic orifice itself. Balfour thinks that thrill and reduplication of the second sound are sufficient to make a diagnosis in the absence of murmur. Some regard the length of the pause between the murmur and the first sound as a measure of the stenosis--the shorter the pause, the greater the stenosis.

DIFFERENTIAL DIAGNOSIS.--The diagnosis of mitral stenosis is not difficult; it mainly depends upon the existence of two physical signs--the purring thrill and a loud, long, blubbering presystolic murmur.

Mitral obstruction may be mistaken for the murmur of aortic regurgitation (see page 657), for a pericardial friction located over the apex, for a prolonged systolic murmur replacing the first sound at the apex, and for a prediastolic basic murmur transmitted to the apex.

1. To diagnosticate between local pericarditis and mitral stenosis, the same methods are employed and the same rules are to be observed as were mentioned in the diagnosis between aortic reflux and local pericarditis (p. 664).

2. A prolonged systolic apexial murmur, enduring as it does for the period of the first sound, that of the short pause, and reaching the second sound, is often accompanied by a muffled second sound readily mistaken for the first. The diagnosis of this murmur rests upon its soft and blowing character, the synchronism of the murmur with the systolic impulse and carotid pulsation, and the fact that there is no murmur with the second sound at the base.

A prediastolic murmur is distinguished from a mitral stenotic murmur by its progressively diminishing intensity from the base to the apex, by its being accompanied by hypertrophy of the left ventricle, and by a jerking, irregular pulse. The preceding tracings explain themselves.

Mitral Regurgitation.

Regurgitation at the mitral orifice is due to a condition of the mitral valves which allows the blood to flow back from the left ventricle into the left auricle. The backward effects of mitral reflux are more varied than those of any other valvular lesion.

It is a common form of valvular disease, and in the majority of cases is the result of acute exudative or interstitial endocarditis.

MORBID ANATOMY.--The most common lesions which give rise to mitral regurgitation are thickening, induration, and shortening of the mitral valves. In rare instances it may occur independent of valvular disease from displacement of one or more of the segments of the valve, the result of changes in the papillary muscles, chordæ tendineæ, or the ventricular walls. It may also occur in extreme anæmia, or from relaxation of the papillary muscles and dilatation of the left ventricle, without a corresponding elongation of the papillary muscles, and from rupture of the chordæ tendineæ. In most instances, however, the valves are shortened, thickened, and indurated.

In some instances lime salts and large masses of chalky matter are found {670} imbedded in the indurated valves. In such cases the surface and edges of the valves are so rough and jagged that more or less obstruction accompanies the regurgitation.

All these changes, except calcification, may also occur in the chordæ tendineæ and columnæ carneæ. The valves may also become adherent to the walls of the ventricles, or as a result of the shrinking and shortening of the chordæ tendineæ the valve-flaps may not pass back to the plane of the orifice.

Again, the valves or the chordæ tendineæ may be ruptured, so that the valves are pressed during the cardiac systole back into the auricle. If the chordæ tendineæ which are inserted nearest the centre of the valve become lengthened, that part of the flap will be bent upon itself, having evidently yielded to the blood-pressure, and this allows of regurgitation. Sometimes, when the valves appear perfectly healthy, by the application of the water test they will be found to be insufficient.

The first effect of mitral regurgitation is dilatation of the left auricle, due to the pressure of the two blood-currents during its diastole--one from the lungs, and the other from the left ventricle. This dilatation leads to thickening and hypertrophy of the left auricular walls. Following this, the pulmonary circulation is impeded, the pulmonary vessels enlarge, and they may undergo degeneration as a result of the continued regurgitant pressure.

Passive congestion of the lungs with brown or pigment induration is an early pathological sequel of mitral regurgitation. The constant interference with the return circulation from the lungs obstructs more or less the outward current of blood to the lungs from the right ventricle. As the obstruction is a gradual one, the right ventricle becomes so hypertrophied as to overcome it. Consequently, the hypertrophied right ventricle compensates at first for the mitral regurgitation, and as long as the right ventricle is able to fully overcome the abnormal pressure of the blood in the lungs from the mitral regurgitation, so long the patients are comfortable. Sooner or later, however, the compensatory hypertrophy of the right ventricle ceases, and a secondary dilatation occurs which admits of no compensation.

This final dilatation of the right ventricle is favored by the myocardial degeneration, which occurs as a result of defective nutrition of the heart-walls; when this condition is reached the veins throughout the body are placed in a similar condition to those in the lungs.

This general venous congestion is indicated by passive hyperæmia of the abdominal viscera and by cyanosis of the surface during active physical exercise.

The liver is the organ first affected, on account of its great vascularity and from the fact that the hepatic veins do not collapse readily and possess no valves. Thus the liver becomes enlarged and stony (the nutmeg liver) as a result of the obstruction to the emptying of the hepatic vein, and when there is coexistent obstruction of the bile-ducts jaundice will be present.

This portal obstruction induces passive hyperæmia of the intestines and stomach, enlargement of the spleen, and large and painful hemorrhoidal tumors. The impediment to the return of blood from the brain causes cerebral congestion; from the kidney, renal congestion; and, finally, the obstruction to the systemic venous return leads to the accumulation of fluid in the areolar tissue and in the cavities. This dropsy generally begins in the feet and extends upward. In females the obstruction in the vena cava inferior induces derangements of the menstrual functions. Ascites, hydrothorax, hydro-pericardium, and pulmonary oedema may subsequently develop.

In addition to these changes, the dilated and hypertrophied left auricle throws an abnormal quantity of blood with abnormal force into the left ventricle during its diastole, which leads to dilatation of its cavity and necessitates a compensatory hypertrophy of the left ventricular walls. This {671} hypertrophy of the left ventricle increases the force of the reflux current, so that during excitement and active physical exertion pulmonary congestion, oedema, and cerebral apoplexy are liable to occur. In many cases of mitral regurgitation, when the venous engorgement is excessive, general dropsy is favored by the anæmia produced by the obstruction of the thoracic duct.

Friedreich maintains that the augmented tension in the venous system causes an increased resistance in the systemic arteries, which leads to left ventricular hypertrophy.

ETIOLOGY.--Mitral regurgitation may occur at any age; it is especially liable to follow rheumatic endocarditis in the young.

Acute exudative and interstitial endocarditis of rheumatic origin is the primary cause of most of the changes which lead to mitral insufficiency. These changes cause the extensive retractions and thickenings which are present in most cases.

It may occur in conditions of extreme anæmia or where there is degeneration of the walls of the left ventricle.

It is not infrequently secondary to changes at the aortic orifice, produced either by an extension of endocarditis from the aortic to the mitral valves and their appendages, or by the secondary mitral valvulitis excited by regurgitant blood-currents from the aorta.

Mitral insufficiency may also be the result of the enlargement of the left auriculo-ventricular orifice which accompanies excessive dilatation of the left ventricle.

Disease of the columnæ carneæ and chordæ tendineæ, when their structures are so weakened as to allow the flaps of the valve to pass back of the plane of the orifice, will also cause mitral insufficiency.

Ulcerative endocarditis may cause it, either by perforation and rupture of the valves or by rupture of the chordæ tendineæ.

SYMPTOMS.--During the early stage of mitral insufficiency, when the hypertrophy of the right ventricle compensates for the regurgitation, there are no rational symptoms which would lead one to suspect its existence; but when the right ventricle is unable to overcome the obstruction to the pulmonary circulation caused by the regurgitant blood-current, there will be more or less dyspnoea, accompanied by a short, hacking cough, with an abundant expectoration of frothy serum. Sometimes the watery expectoration is blood-stained.

Frequently, the blood-stained expectoration is accompanied by free hæmoptysis, although it should be remembered that profuse hæmoptysis is far more frequent with stenosis than with regurgitation at the mitral orifice. But a cough and watery expectoration with occasional dark blood-stains are usually present as an advanced symptom of mitral regurgitation. Active physical exertion increases the dyspnoea and causes cardiac palpitation.

In advanced cases the extremities, face, and lips become blue, the result of the interference with the capillary circulation, and the liver becomes enlarged and hardened--conditions easily recognized by palpation and percussion.

The patient will complain of a sense of weight and fulness in the right hypochondrium, and there will be anorexia, nausea, and a sense of oppression in the epigastrium. Sometimes the hepatic circulation becomes so obstructed that the biliary secretion is interfered with, and jaundice will be added to the cyanotic discoloration, which gives to the surface a peculiar greenish hue.

Following the hepatic derangement are frequent attacks of gastric and intestinal catarrh and evidences of embarrassed renal circulation.

The urine is diminished in quantity, high-colored, and loaded with lithates. Sometimes albumen and fibrinous or blood casts are found in it.

{672} Headache, dizziness, vertigo, stupor, somnolence, and sometimes a peculiar form of delirium of short duration, result from the passive cerebral hyperæmia induced by obstruction in the superior vena cava.

A late symptom of mitral regurgitation is dropsy, which results both from impaired general nutrition and the abnormal blood-pressure in the venous system, both together causing an exudation of the watery portion of the blood through the walls of the vessels. Dropsy, from mechanical causes having their seat in the heart, first appears in the lower extremities, the ankles becoming oedematous, and thence may extend over the whole body. For this condition to be reached it may require several years or only a few months, depending upon the general condition of the patient and the amount of the reflux. With the general anasarca the dyspnoea becomes extreme; the serous cavities of the body as well as the lungs become oedematous; erythema may occur in the region of the groins, the skin exhibiting a tendency to diffuse gangrene.

Late in the disease pulmonary hemorrhagic infarction may occur as a result of metastasis, and this, in the vast majority of cases, lights up a rapidly fatal pneumonia.

All these changes, however grave and urgent they may be, are gradual in their development, so that the condition of the patient is not so insufferable as its description would lead one to suppose.

The pulse of mitral regurgitation is at first in no respect characteristic. It remains regular in force and rhythm, but later it becomes somewhat diminished in force and volume, irregular in its rhythm, and increased in frequency, but never jerking in character. This tracing illustrates my meaning. While it remains full it is feeble and always compressible. When the heart's action is excited, it has a certain tremulousness: these last-named characteristics are to be regarded more as the result of the failure of the left ventricle than of changes in the valvular insufficiency. If a mitral regurgitant pulse has any distinctive peculiarity, it is its diminution in volume.

Coincident mitral or aortic stenosis may render the pulse regular even in extensive mitral regurgitation.

Physical Signs.--Inspection.--The area of visible cardiac impulse extends over an abnormal space, and is more or less distinct according as the right ventricular hypertrophy is moderate or extensive. Sometimes the thoracic wall is seen to rise and fall with each cardiac cycle, and not infrequently the epigastrium exhibits slight pulsation corresponding in rhythm with the heart-beats.

The epigastric pulsation is due to the right ventricular hypertrophy always found with extensive mitral regurgitation.

Skoda, Bamberger, and Leyden record a few instances in which inspection revealed a double impulse accompanying, with more or less regularity, each cardiac systole. This double impulse only occurs in aggravated cases of {673} mitral insufficiency, and arises from non-coincidence of contraction of the two ventricles.

The jugular veins appear swollen, and this is always most conspicuous when the patient is lying down.

Palpation.--The apex-beat is displaced to the left. When hypertrophy predominates over dilatation, the apex-beat is felt lower than normal. When the dilatation exceeds the hypertrophy, the apex-beat is carried outward and often slightly upward. The impulse is diffused and more or less forcible according as the right or left ventricular hypertrophy predominates. This systolic frémissement is most noticeable when the base of the heart lies close to the chest-wall from retraction of the margin of the left lung.

Purring tremor, systolic in rhythm, felt most intensely at the apex and becoming feebler the farther the hand is removed from that part, either to the right or upward, is invariably due to mitral reflux.

Hayden says that it is exceptional to have a purring thrill with simple mitral reflux. I have never found it except in those cases where left ventricular dilatation greatly exceeded the hypertrophy.

Percussion.--Percussion reveals an increase in the area of cardiac dulness, especially laterally; it extends both to the left and right of the normal line, as well as downward. The area of superficial as well as deep-seated dulness will be increased laterally and downward.

Auscultation.--Mitral insufficiency is attended by a systolic murmur which either completely or partially replaces the first sound of the heart. The quality of the murmur is variable, and not in itself as distinctive as that of mitral stenosis. It is usually a soft and blowing bellows murmur; sometimes, toward its end, the murmur will assume a distinctly musical character.

While the first sound of the heart may be heard distinctly in the early stages of mitral reflux, later the murmur in nearly all cases takes the place of the heart-sounds. Hence many English writers rightly denominate this murmur as post-systolic rather than systolic in its nascent stages. It is heard with its maximum intensity at the apex-beat. Its area of diffusion is to the left on a line corresponding to the apex-beat. It is audible at or near the inferior angle of the left scapula. It can be heard between the lower border of the fifth and the upper border of the eighth vertebra, at the left of the spine, with nearly the same intensity as at the apex. The murmur may be absent from the latter situation until cardiac hypertrophy is developed.

The second sound of the heart over the pulmonary valves is accentuated, while below the junction of the third rib with the sternum on the left side both heart-sounds are feeble. Skoda first drew attention to exaggeration of the second pulmonary arterial sound as a positive and unerring indication of mitral regurgitation.

An intensified pulmonary second sound requires a strong right ventricle and an intact tricuspid valve, and is not always present. In general terms, the area of diffusion of a mitral regurgitant murmur is toward the left of the apex-beat. Whatever may be its character, the murmur is generally loudest at its commencement. A loud systolic murmur at the apex, and not heard at the back, is probably not produced by mitral reflux.

As at the aortic orifice, so at the mitral, stenosis and regurgitation are apt to occur in the same individual, giving rise to a combined presystolic and systolic murmur, which is a continuous murmur that begins shortly after the second sound of the heart and often continues until the second sound commences. The two sounds, although mingling to form one murmur, can, in the majority of cases, be readily distinguished from each other, for the point of maximum intensity and the very limited area of diffusion of a presystolic murmur readily distinguish it from a mitral systolic which is audible in the left scapular region. It is important to recognize the existence of both these {674} murmurs in estimating the prognosis in any case. Guttman mentions a case where five distinct murmurs were combined and yet clearly distinguishable.

DIFFERENTIAL DIAGNOSIS.--It is usually not difficult to recognize mitral regurgitation. The seat and rhythm of the murmur and its area of diffusion are sufficient to distinguish it from other cardiac murmurs. The character of the pulse, the symptoms referable to the right heart, and the pulmonary complications will also assist in its diagnosis.

It may, however, be mistaken for aortic obstruction, since both give rise to a systolic murmur, for tricuspid regurgitation, for fibroid disease of the heart, and for roughening of the ventricular surface of the mitral valve or of the ventricular wall near the aortic orifice.

The diagnosis between mitral regurgitation and aortic stenosis has already been given (see page 657).

Mitral and tricuspid insufficiency both produce a systolic murmur, but a mitral regurgitant murmur has its maximum of intensity at the apex, and is conveyed toward the left axillary and scapular regions, while the maximum intensity of a tricuspid regurgitant murmur is to the right of the base of the xiphoid cartilage, and it is transmitted upward and to the right: the area of transmission establishes the diagnosis.

Pulmonary symptoms are prominent in mitral reflux, and absent in tricuspid regurgitation. The pulmonary second sound is markedly enfeebled in tricuspid regurgitation, and markedly intensified in mitral regurgitation.

Fibroid disease of the heart may produce a systolic apex murmur, but it is an exceedingly rare disease, a pathological curiosity.[20]

[Footnote 20: In the _Pathological Transactions_ (1874, vol. xxv. p. 64) Fagge records a few cases, and mentions that perhaps one positive indication of fibroid disease of the heart, rather than of a valvular lesion, may be found in its resisting treatment with greater obstinacy.]

Roughening of the ventricular wall gives rise to a murmur which has its maximum intensity at the base of the heart, and is transmitted along the aortic arch and into the vessels which spring from it in the thorax.

The vibration of an irregular chordæ tendineæ stretched across the aortic orifice, its extremities being inserted into opposite walls of the ventricle, may produce a systolic musical murmur, but the line of its transmission will correspond to that of an aortic obstruction. A systolic mitral murmur due to the sudden rupture of one or a number of the valve-flaps, of the papillary muscles or tendons, is accompanied by a loud systolic blowing murmur, which is immediately accompanied by all the urgent symptoms of acute pulmonary congestion.

Pulmonary Obstruction.

On account of the infrequency of disease of the pulmonic valves very little is known of the phenomena to which such diseases may give rise. In fact, they are so rare that there is no written history of their subjective symptoms; their diagnosis is only arrived at by exclusion, and they cannot be recognized except by the physical signs which attend them.

As has been already stated, endocarditis in the right heart is rare, except in intra-uterine life, and the various conditions of the aorta, atheroma, aortitis, etc., which I have mentioned in the etiology of aortic valvular disease have no analogues in the pulmonary vessels.

Usually, valvular disease of the right heart is the sequela of lesions in the left. It must be remembered, however, that the pulmonary artery may become atheromatous. I have already shown (see p. 666) how certain valvular diseases of the left heart may induce such a pathological condition. But even under such conditions disease of the pulmonary valves is rare. Balfour {675} believes that constriction of the pulmonary artery may occur at various periods of intra-uterine life. As a rule, the pulmonary valves are subject to no lesions except congenital malformation.

MORBID ANATOMY.--Bertin records an instance of pulmonary obstruction where the valves, distorted and adherent, formed a horizontal septum across the orifice, it being barely one-fourth of an inch.

A rigid tricuspid valve has been found to be the cause of obstruction at the pulmonary orifice, the pulmonary valves themselves being normal. A few autopsies have revealed obstructions at the pulmonary artery, caused not so much by valvular defect as by aneurisms, tumors of the pericardium or of the anterior mediastinum, enlarged bronchial glands, or pressure of a solidified lung.

The pulmonary artery may be occluded just beyond the valves by a cancerous tumor, and there are examples where a phthisical process in the left lung has induced it.

A murmur indicative of pulmonary obstruction may be produced by a cardiac thrombosis.

I have placed these statements under the head of its morbid anatomy for the reason that they cannot be appreciated and their pathological significance realized during life.

Reasoning from analogy, obstruction at the pulmonary orifice ought to be followed by compensatory hypertrophy of the right ventricle and accompanied by tricuspid regurgitation and dilatation of the right auricle.

Ormerod records 3 cases[21] where pulmonary obstruction was diagnosticated during life, and where the post-mortem proved the accuracy of the diagnosis: 2 of these cases occurred in men under twenty-eight, and the other in a woman of twenty-one. In 2 of these cases all the other cardiac valves were healthy. The pulmonic orifice would barely admit the introduction of a goosequill. Warburton Bigbie mentions a case (man æt. eighteen) where reflux and stenosis at the pulmonary orifice coexisted. There were four valves, and these were incompetent. All the other valves were normal.

[Footnote 21: _Edin. Med. and Surg. Journ._]

Congenital stenosis of the infundibulum of the right ventricle is the probable result of foetal myocarditis or of syphilis.

I have never met but two pulmonic obstructive murmurs where subsequent autopsies were obtained. In both cases it was found that the murmur had been produced by mediastinal tumors pressing on the pulmonic artery so as to diminish the calibre.

ETIOLOGY.--Pulmonary stenosis is rarely the result of endocarditis or of degenerative changes in the pulmonary artery. Bertin states that when abnormal communication between the two sides of the heart has existed, the arterial blood has excited endocarditis in the right heart.

Syphilis has been advanced as a possible cause of degenerations at the pulmonic orifice.

SYMPTOMS.--The only rational symptoms that have been noted in the few recorded cases of pulmonic disease admit of manifold explanations, and no one is either constant or diagnostic. In some cases anæmia existed, in others there were cardiac palpitation, dyspnoea, cyanosis, and dropsy; but none of these belong exclusively to a pulmonic lesion nor do they necessarily depend upon it.

Physical Signs.--Inspection, palpation, and percussion give negative rather than positive results. In a few instances palpation may give a systolic thrill confined to the second left intercostal articulation. Such a frémissement results both from roughness and contraction of the pulmonic orifice.

Auscultation.--A systolic murmur is heard with its maximum intensity directly over the pulmonic valves; it is very superficial, and consequently {676} very distinct, and it is limited in its diffusion. It is never heard at the xiphoid cartilage nor along the course of the aorta. If it has an area of diffusion, it is toward the left shoulder. The murmur is loud and soft in character, sometimes bellows. It is not audible in the vessels of the neck nor is it attended by arterial pulsation.

When phthisical consolidation partially occludes the pulmonary artery, a loud but soft systolic murmur is heard, which is sometimes high-pitched and musical, and often entirely suspended during a full inspiration. In some few instances there is a bruit de diable in the jugular veins.

DIFFERENTIAL DIAGNOSIS.--It is possible to confound a pulmonic obstructive murmur with a mitral regurgitation which is propagated upward into the left auricular appendix. But the area of a mitral regurgitant is also backward, and by this it could be distinguished from a pulmonic obstruction. Besides, in mitral disease the pulse is very different from the pulse of pulmonary stenosis.

Aortic stenosis can hardly be mistaken for pulmonary obstruction, for the arterial pulsation, the peculiar pulse, and the transmission of the murmur into the arteries of the neck will suffice to discriminate between them.

An aneurism at the sinus of Valsalva may produce a systolic pulmonary murmur by the pressure which it produces upon the pulmonary artery. It would be impossible to distinguish it from a pulmonic stenosis.

The diagnosis of pulmonary obstruction is usually reached only by exclusion.

Pulmonary Regurgitation.

This form of valvular lesion is exceedingly rare; indeed, many doubt its occurrence. The lesion seldom occurs except as the result of injury or congenital defect, and there are but few well-authenticated cases in medical literature.[22]

[Footnote 22: _Path. Trans._, vol. xvi. p. 74.]

The statement[23] that the pulmonary valves exhibit a cribriform condition nearly as often as the aortic is not sustained in this country by the results of post-mortems. In one of the cases to which I have referred (p. 675) as an example of pulmonary stenosis the valves were likewise found insufficient. In Bigbie's case (referred to on p. 675), where there were four flaps to the valve (producing obstruction), there was marked insufficiency coexisting.

[Footnote 23: _Dis. of the Heart_, Bellingham.]

The morbid anatomy, etiology, and rational symptoms do not require a separate consideration. The anatomical appearances are the same as those found in similar conditions of the aortic valves, and the etiology and rational symptoms are the same as those of pulmonic stenosis.

Physical Signs.--Theoretically, pulmonic regurgitation should be accompanied by a diastolic murmur having its maximum intensity over the pulmonic valves, and its area of diffusion should be downward and toward the xiphoid cartilage. It should be soft and blowing in character. This murmur is rarely heard alone: it is usually associated with obstruction at the same orifice or with some murmur whose origin is on the left side of the heart.

Niemeyer states that dyspnoea, hemorrhagic infarction, and consumption of the lungs have followed insufficiency at the pulmonary orifice. No other authority mentions any such symptoms, while the assignment of valvular disease as a cause of phthisis is not based upon clinical facts.

With a pulmonic regurgitant murmur there should be on palpation and percussion physical evidences of hypertrophy and dilatation of the right heart, the rationale of whose production would be identical with that which was considered in aortic regurgitation. I have never heard a regurgitant pulmonic murmur.

{677} DIFFERENTIAL DIAGNOSIS.--The murmur of pulmonary regurgitation may be mistaken for that of aortic regurgitation. The points in connection with their differentiation are fully discussed on p. 664.

The PROGNOSIS and TREATMENT are identical with those of the former lesion.

Tricuspid Stenosis.

This valvular lesion is so rare that there are no established rules for its diagnosis.

Its MORBID APPEARANCES and ETIOLOGY are the same as those of pulmonic stenosis.

The SYMPTOMS of tricuspid stenosis would be those due to obstruction to the entire venous circulation. The right auricle would be dilated, and there would be visceral enlargements in the abdomen, cyanosis of the face and extremities, scanty and albuminous urine, hemorrhoidal tumors, headache, dizziness and vertigo due to passive cerebral hyperæmia, and finally general anasarca. The few recorded cases were associated with mitral stenosis with one exception, a case of Bertin's.[24]

[Footnote 24: _Traité des Maladies du Coeur_, Obs. 17.]

In a case exhibited by Quain the tricuspid flaps, thick and opaque, were united for one-third of their extent. In the other cases the valve-flaps formed a diaphragm whose central opening varied in size, admitting only the point of one finger. In every condition of tricuspid stenosis the heart was enlarged.

Tricuspid stenosis (as in pulmonic stenosis) may be the result of pressure of tumors.

In all well-authenticated cases the chief symptoms seem to be extreme lividity, palpitation, and dyspnoea.

Physical Signs.--Inspection reveals general cyanosis. The jugulars are turgescent and exhibit presystolic pulsation. This pulsation is sometimes the only inconvenience the patient suffers.

Palpation may discover a venous thrill at the base of the neck.

Percussion may show the right auricle to be greatly enlarged, and cardiac dulness will be increased laterally and toward the right.

Auscultation.--Tricuspid stenosis should be attended by a presystolic murmur whose maximum intensity would be at the lower portion of the sternum just above the xiphoid cartilage. This murmur may be propagated faintly toward the base, but never toward the apex of the heart. It is sometimes accompanied by fremitus.

Hayden offers the following diagnostic point: The murmur of mitral stenosis (without which tricuspid stenosis never occurs) is limited to the apex region; a murmur of the same rhythm is produced at the sternum by tricuspid stenosis, "and between these two localities there is a point where no murmur can be heard."

It is unnecessary to consider its differential diagnosis.

The lesion would be diagnosticated (if at all) by exclusion, and prognosis and treatment would depend on the gravity and sequelæ of the accompanying condition--viz. Mitral Stenosis (q. v.), for the rule is, that stenosis of the tricuspid never occurs unless there is extensive mitral obstruction, and the latter condition is always the predominant one.

Tricuspid Regurgitation.

Regurgitation at the tricuspid orifice is generally secondary to mitral stenosis or regurgitation; primary disease of the tricuspid valves, however, is not infrequent.

{678} MORBID ANATOMY.--The valvular lesions which lead to tricuspid insufficiency are similar to those which produce mitral insufficiency. The valves are thickened, shrunken, and opaque, the papillary muscles are shortened, thickened, and the chordæ tendineæ undergo similar changes and are sometimes adherent.

The valves or the chordæ tendineæ and columnæ carneæ may rupture; in either case acute and extensive insufficiency results, as has been stated. Acute endocarditis of the right heart is rare in adult life, but when it occurs the tricuspid valves are its primary and principal seat.

The reason for this is found in their anatomical structure and in the tension to which they are subject in diseases of the mitral valves. They are rarely the seat of rheumatic endocarditis or calcareous degenerations.

Ulcerative endocarditis is seldom met with in the right heart. In a case recorded by Charcot and Vulpian one of the tricuspid valves was softened and perforated, presenting numerous vegetations. Scattered abscesses in the lungs were found in this case.

Any infection through emboli from the tricuspid flaps will produce secondary effects within the thoracic cavity. The first effect of tricuspid regurgitation is dilatation of the right auricle; following this there will be more or less hypertrophy of its walls. As soon as the valves in the subclavian and jugular veins are no longer able to resist the regurgitant current jugular pulsation follows. But before this occurs the tributaries of the inferior cava and the organs to which they are distributed will become greatly engorged, for they have no valves to resist the regurgitant current, as are found in the veins coming from the upper part of the body. The inferior cava and the hepatic veins sometimes become enormously distended under these circumstances, and the liver will show the peculiar section that has gained for it the name of nutmeg liver.

Following the hepatic changes, the skin assumes a dingy yellow hue. When this is combined with cyanosis it produces a peculiar greenish tint which is only met with in heart disease. The spleen enlarges and hardens; the mucous membrane of the stomach is congested, ecchymotic, and often presents numerous hemorrhagic erosions. Intestinal catarrh is subsequently developed, and the general venous congestion within the abdominal cavity is exhibited by hemorrhoids and ascites. The kidneys become congested and stony, and thrombi may form in the femoral vein and induce subsequent pulmonary infarctions.

The stasis in the veins below the diaphragm is accompanied by transudation of serum--first in the ankles, and thence the dropsy progresses upward until the patient may finally reach a condition of general anasarca. The obstruction to the general systemic circulation which results may subject the left ventricle to so much extra labor that it hypertrophies, and then we have the infrequent occurrence of disease of the left heart following that of the right.

Since tricuspid reflux has mitral disease for its principal cause in abnormal cases, the heart becomes greatly enlarged and a condition of extreme cardiac dilatation and hypertrophy is reached.

ETIOLOGY.--As has been stated, the most frequent cause of tricuspid regurgitation is mitral disease, either stenosis or regurgitation. Any condition of the lungs which will produce hypertrophy and dilatation of the right ventricle will lead to it; it is met with in extensive pulmonary emphysema, in cirrhosis of the lung, and in extensive chronic bronchitis. Balfour regards chronic bronchitis as its most frequent cause after mitral stenosis.

It is possible for any valvular disease in the left heart, when of long duration, to lead to tricuspid regurgitation. From all these causes the rationale is {679} the same: the abnormal amount of blood in the right ventricle presses with undue force against a valve, which physiologists regard as normally slightly insufficient; the stress upon the valve-flaps and the valvular attachments is such that endocardial inflammation is excited at the part subject to the greatest strain, and valvular insufficiency is the result.

It is possible for disease of the tricuspid valves to result from any of the causes which have been enumerated on p. 666 as etiological factors in valvular diseases.

SYMPTOMS.--Tricuspid regurgitation being in the majority of cases secondary to some other valvular disease or some chronic pulmonary affection, its symptoms during the early stages are vague and masked by those of the primary disease. But as soon as the valves become so insufficient that the venous return is markedly impeded, a train of symptoms is developed which has its origin in the visceral derangements already referred to.

In addition to these symptoms there may be, with extensive tricuspid regurgitation, cardiac palpitation, cardiac dyspnoea, and marked irregularity in the force and rhythm of the heart. The liver and spleen are enlarged, the skin becomes dingy, and there is obstinate constipation with hemorrhoids. The liver is likewise rendered very liable under such circumstances to attacks of interstitial hepatitis. Venous stasis is evinced by dyspepsia, nausea, vomiting, and hæmatemesis. The secretion of the kidneys is scanty, dark-colored, of high specific gravity, often containing albumen and casts.

Passive cerebral hyperæmia is marked by headache, dizziness, vertigo, and muscæ volitantes, and there is a peculiar mental disturbance which is not met with in any other form of heart disease.

Late in the disease, if the patient is placed in a horizontal position, the face becomes turgid and blue, and if he remain long in the recumbent position stupor and coma may supervene. Jugular and epigastric pulsation are characteristic physical signs.

A very late symptom is dropsy, which begins at the ankles and extends upward until there is general anasarca. It is a point to be noticed that in the dropsy from tricuspid reflux the genital organs suffer slightly if at all.

Physical Signs.--Inspection.--In extensive tricuspid disease the area of the cardiac impulse is increased more than in any other valvular lesion. This area sometimes extends from the nipple to the xiphoid cartilage, and it may reach as high as the second right intercostal space. There is a visible impulse in the jugular veins, more apparent in the right than in the left. Sometimes the veins in the face, arms, and hands, or even the thyroid and mammary veins, are seen to pulsate.