Chapter XLV: Part 45

A mitral murmur alone occurs in about 50 per cent. of cases of rheumatic endocarditis. It is usually developed early, and before it becomes distinct it is preceded by prolongation of the first sound. This is a transition sound between a normal heart-sound and a murmur. It is a feeble, wavering sound, extending over the slight interval which normally exists between the first and second sounds.

Other changes that are not murmurs, but which frequently precede them, are loud, ringing normal sounds, muffled first sound, feeble first and {649} intensified second sound, doubling of the first sound, roughness of the first sound, and a humming over the right heart.

Complete absence of the heart-sounds is a rare but possible antecedent of an endocardial murmur. A mitral murmur in acute endocarditis is usually audible over a limited area. It is the exception to hear it both in front and at the back. Very frequently it is heard most distinctly over the stomach.

When the blood becomes dammed back into the lungs, there is an extra strain upon the pulmonary semi-lunar valves, and then the second sound will be accentuated over these valves on account of the sharp shock which they sustain during diastole. With this accentuation of the second sound over the pulmonary orifice, the first pulmonic sound may be feeble or absent. A subdued or absent first sound shows tension of the artery.

Reduplication of the second sound in a mitral endocarditis is probably due to the difference in time occupied by the ventricles in emptying themselves. A tricuspid murmur occurs in 50 per cent. of the cases of acute mitral endocarditis--a pulmonic in about one-third of the cases. They are superficial and scratchy in character, and indicate a relaxed condition of the vessels and a thin condition of the blood. These murmurs are never permanent. Mitral endocarditis is accompanied by aortic murmurs in about 16 per cent. of cases. Acute mitral endocarditis occurring with chorea is as apt to become interstitial as when it is of rheumatic origin.

Aortic murmurs are usually soft and blowing, but they may be musical, whistling, or twangy. In aortic endocarditis the second sound is usually lost over the carotids. Incompetency of the aortic valves is met with only in the interstitial form of endocarditis.

In about 12 per cent. of the cases of exudative endocarditis arising from rheumatism a regurgitant murmur will be heard at the tricuspid orifice, but such murmurs are not the result of endocarditis of the right heart.

Tricuspid murmurs are present in 50 per cent. of all cases of recent mitral murmurs, in about 40 per cent. of recent aortic murmurs, and in about one-fourth of mitro-aortic murmurs. Such tricuspid murmurs are due to an increase in the slight normal insufficiency existing at the tricuspid orifice. They are of short duration, and are heard over the body of the heart over the right ventricle. Sometimes they are vibrating in character.

In children aortic endocarditis is rare; at this period obstruction at and regurgitation through the mitral orifice commonly occur together.

The physical signs of interstitial endocarditis are such as are due to those changes in the valves which will be considered under the head of Cardiac Murmurs, and their Relations to Valvular Diseases.

DIFFERENTIAL DIAGNOSIS.--Acute exudative endocarditis may be mistaken for pericarditis, and its murmur may be mistaken for the murmur produced by aortitis and for those that develop during the course of fevers.

The friction sounds of pericarditis are superficial in character, and are limited to the præcordial space, while the murmurs of endocarditis are distant, and each murmur will have its area of diffusion beyond the præcordial space. A pericardial sound is distinctly a friction, creaking, or rubbing sound; it has a to-and-fro character, while the murmur of endocarditis is soft and blowing.

Endocardial murmurs accompany the heart-sounds, while pericardial friction sounds are not always rhythmical with the heart-sounds.

The intensity of a pericardial friction is increased when the patient bends forward at the end of a full inspiration or when the stethoscope is pressed firmly over the præcordial region; and in the last-named case it becomes distinctly grazing and rubbing in character. In endocarditis these methods produce no difference in either the intensity or the character of the murmur. There is an endocardial thrill in endocarditis not present in pericarditis.

{650} As soon as effusion occurs in pericarditis the absence of pain, the alteration in the character of the pulse, the great increase in dulness, and the disappearance of the adventitious sounds will decide the diagnosis.

Aortitis has most of the symptoms of endocarditis, but in addition the pulse is more rapid, the respirations are more hurried, and pain which shoots down the spine and is increased by motion is present in the præcordial region. Not infrequently aortitis is accompanied by cutaneous hyperæsthesia.

Acute inflammation of the aorta is exceedingly rare, and in the few cases observed has been complicated by very grave diseases. Indeed, Powell, Lebert, and Rindfleisch doubt its existence.

In the _Medico-Chirurgical Transactions_ (vol. xlvii. p. 129) Moore gives a case where rigors, fever, intense and painful throbbing of the aorta, and embolic infarction of distant organs occurred, with symptoms so resembling those of endocarditis that few would venture to favor a diagnosis of aortitis during life.

The functional cardiac murmurs which occur in fevers are usually heard only at the base of the heart, while those of endocarditis are most frequent and distinct at the apex. There are no symptoms of obstruction present with febrile murmurs, while they are frequently present in endocarditis.

It is often difficult to determine whether an endocardial murmur is of old or recent origin: if during an attack of acute rheumatism an endocardial murmur is developed under daily examination, it is a certain index of acute exudative endocarditis. If a murmur exists at the first examination which is systolic, soft, and blowing in character, and not accompanied by the evidences of cardiac hypertrophy, there is good reason to believe that it is produced by an acute endocardial inflammation.

If, on the other hand, the murmur is rough in quality, diastolic, and cardiac hypertrophy exists, it cannot be regarded as a sign of acute endocarditis.

The rules for distinguishing murmurs due to interstitial endocarditis from functional murmurs will be given under the head of Cardiac Murmurs.

PROGNOSIS.--Exudative endocarditis is rarely a direct cause of death, but it seldom results in complete recovery. Acute mitral endocarditis terminates in permanent valvular disease in over 25 per cent. of the cases. The elements that will render the prognosis immediately unfavorable in any case are the symptoms of embolism or of metastasis. Sudden splenic enlargement, with tenderness over its site, albuminuria or hemiplegia, when accompanied by the physical signs of acute insufficiency or perforation of a valve with cyanosis, dyspnoea, and disturbance of the heart-rhythm, will render the prognosis exceedingly unfavorable. All these symptoms are diagnostic of acute ulcerative endocarditis, and therefore when the signs of endocarditis appear during the course of pyæmia, diphtheria, or other septic condition, the liability to these conditions must be considered.

When even exudative endocarditis is accompanied or followed by typhoid symptoms its prognosis is unfavorable. In children bronchial complications, catarrhal pneumonia, and intercurrent diarrhoea may lead to a fatal issue. Death may result from acute insufficiency of the heart or from complications.

The prognosis in interstitial endocarditis will depend upon the seat and extent of the valvular lesions which it produces. It will be more fully considered under the head of Valvular Diseases.

In cardiac aneurism death may result from rupture of the aneurismal sac, from apoplexy, or from secondary diseases in other organs.

TREATMENT.--Acute exudative endocarditis is rarely, if ever, idiopathic. It is so constantly associated with certain infectious diseases, and especially with acute articular rheumatism, that its treatment must be determined by the condition under which it occurs.

{651} In every case the patient must have absolute rest in bed in a room whose temperature should never be below 70° or 75° F. The præcordial region should be covered with flannel, and care exercised not to expose the surface when physical examination of the heart is made. Some authorities claim that an ice-bag applied to the præcordial space during the active period of an acute endocarditis will arrest and limit the inflammatory process. My own experience does not sustain the results claimed for this plan of treatment.

In rheumatic endocarditis antirheumatic remedies are indicated, the joints must be kept absolutely at rest, and such local treatment should be resorted to as will relieve pain and give the greatest comfort to the patient.

If the blood is kept alkaline, as indicated by the urine, the liability to endocarditis is diminished.

To ensure rest small doses of opium are often required; but opium cannot be administered as freely in endocarditis as in pericarditis.

During the whole course of acute endocarditis the strength of the patient must be maintained by the judicious use of concentrated nutriment, with some preparation of iron.

When endocarditis occurs with septic diseases and is attended by typhoid symptoms, or when it assumes the ulcerative form, alcoholic stimulants, quinine, and iron must be freely administered.

In endocarditis complicating Bright's disease the rapid elimination of the urea must be established. The severe pain over the præcordial space may be relieved in many subjects by the application of a few leeches to the region.

Experience proved that the employment of mercury (internally) and blue ointment (externally) to lessen the plasticity of the blood, and the internal use of iodide of potassium (for the absorption of fibrinous exudation), were harmful, before it was demonstrated that the theory on which their use was based had no foundation.

Cardiac Murmurs, and their Relations to Valvular Diseases of the Heart.

DEFINITION.--A cardiac murmur is an adventitious or abnormal sound produced within the heart or blood-vessels, either by obstruction to the blood-current, an abnormal direction of the blood-current, or by a change in the blood-constituents.

HISTORY.--The systematic study of cardiac murmurs and valvular diseases dates from the discovery of auscultation by Laennec. Previous to his discovery there are a few recorded cases where observers during the seventeenth and eighteenth centuries described forms of valvular diseases. One of the first to describe a valvular lesion of the heart was Vieussens in 1716. At the close of the seventeenth century Willis and Riverius published cases of valvular disease. In all these instances it was the aortic valves that were diseased, and the discovery of their condition was undoubtedly due to the peculiarity of the radial pulse which is so marked and striking in aortic disease.

In Friedreich's article in Virchow's _Handbuch_, "Krankheiten des Herzens," Meckel's essay of 1756 is given as the first paper on endocardial disease.

John Hunter[2] in 1794 gives a lengthened account of a most interesting case of aortic valvular disease. Senac[3] gives an account of disease of the auriculo-ventricular valves; and Allan Burns, whose work was published in 1809, describes aortic regurgitation and obstruction, and supposes that "a reflux current can produce a hissing noise, something like what is described as audible palpitation in some diseases of the heart."[4]

[Footnote 2: _Treatise on the Blood_, etc.]

[Footnote 3: _Treatise on the Heart_, 1783.]

[Footnote 4: _Obs. on some of the most Frequent and Important Dis. of the Heart_, Allan Burns, Edinburgh, 1809.]

{652} The subject of vegetations upon the valves was very fully considered by Corvisart in 1806. Corvisart was the first to mention the importance of what is now called the purring thrill. He stated that "it probably came from a difficulty experienced by the blood in going through an orifice disproportionate to the amount of fluid." Laennec regarded murmurs or bruits as the result of spasmodic contraction of the heart or arteries. Corrigan in 1829 defined murmurs as "the result of the development of currents and the intrinsic collision of the moving liquid."

In 1842, Gendrin gave cardiac murmurs as bruits de frottement endocardiaques, and established the friction theory. He also called attention to the fact that alteration in the constituents of the blood will produce murmurs which are heard in arteries of medium calibre.

Bouillaud describes a murmur as an exaggeration of the normal bruit caused by blood-friction against the segments of the heart, and he says that according to the size or condition of the orifice the murmur will be rasping, sawing, or blowing.

Chauveau states that bruit de souffle is produced by the vibration of a nei e fluide, always formed when blood rushes through a part of the circulatory system actually or relatively dilated.

This nei e fluide has its best development in anæmia, when it is termed the bruit du diable, for the jugular veins do not collapse and the volume of blood in anæmia is diminished. Chauveau's theory is applicable to anæmic murmurs, but not to all cardiac murmurs.

Hope states that "valve murmurs are produced by collision of the blood-particles against one another, or that either the liquid alone or the liquids and solids conjointly may develop murmurs."

There are many who have advocated the tension theory--viz. that an increase in tension and force can so exaggerate a normal sound as to produce a murmur. This theory has no clinical foundation. Often, however, valve-lesions may exist, and the blood-current be so weak, the propulsive force so feeble, that no murmurs are audible.

Some observers are of the opinion that spasm of the papillary muscles and chordæ tendineæ and weakening of these structures through fatty degeneration can cause temporary murmurs.

The conditions that determine the character of a cardiac murmur, its pitch, quality, and intensity, are subject to the same physical laws as govern the formation and quality of sound elsewhere. They are the rapidity and force of the moving body, the obstructions which it meets, and the physical properties of the media of conveyance. The same vibration that produces a murmur may produce an endocardial thrill, called sometimes purring thrill.

Far more important, however, than loudness, pitch, or quality of a murmur are its rhythm, its point of maximum intensity, and the area of its diffusion, all of which can best be considered in connection with the physical signs of each valvular lesion.

During a cardiac diastole the heart-cavities are all filling; just before the commencement of the cardiac systole the blood is forced from the lungs and the cavæ through the auricles into the ventricles, while the mitral and tricuspid valves are pressed against the walls of the ventricles, and no obstruction is offered to the blood-current. If, as the result of disease, any obstruction exists at either one of the auriculo-ventricular orifices, the blood as it passes through the opening will impinge on such obstruction and cause a presystolic murmur.

During a cardiac systole the filled ventricles contract; blood is thrown through the semi-lunar openings, the flaps of whose valves are pressed against the walls of the vessels, so that no obstruction is offered to the outgoing {653} current. At the same instant the auriculo-ventricular valves close their orifices, so that blood may not be forced back into the auricles.

If, as a result of disease, the semi-lunar valves should obstruct the outgoing current, or the mitral or tricuspid valves should not wholly close the auriculo-ventricular orifices, then in the one case the direct blood-current, as it passes over the obstruction at the semi-lunar orifices, would produce a systolic murmur, and in the other the backward current through the abnormal opening at the auriculo-ventricular orifice would also produce a systolic murmur.

Again, if the lungs and the aortic system (when filled at the systole) have, back of them, a semi-lunar valve that does not completely close that end of the circuit, the blood will regurgitate into the ventricles during the period of cardiac rest, so that semi-lunar incompetence will cause a diastolic murmur.

ENDOCARDIAL MURMURS.

Rhythm. Situation. Orifice. Nature.
Systolic 1 Basic, Aortic, Obstructive.
" 2 " Pulmonary, "
" 3 Apical, Mitral, Regurgitant.
" 4 " Tricuspid, "
Diastolic 1 Basic, Aortic, "
Presystolic 1 Apical, Mitral, Obstructive.[5]

[Footnote 5: Pulmonary regurgitant murmur (diastolic) and tricuspid obstructive murmur (presystolic) are so rarely met with that, clinically, they may be disregarded.]

The following is the order of relative frequency of cardiac murmurs: 1. Mitral regurgitation; 2. Aortic obstruction; 3. Aortic regurgitation; 4. Mitral obstruction; 5. Tricuspid regurgitation; 6. Tricuspid obstruction; 7. Pulmonary obstruction; 8. Pulmonary regurgitation. The most frequent combinations of murmurs are--1. Aortic obstruction and regurgitation; 2. Mitral obstruction and regurgitation; 3. Mitral obstruction and tricuspid regurgitation; 4. Aortic obstruction and mitral regurgitation; 5. Double valvular disease at aortic and mitral orifices (four murmurs).

It is often difficult, after having satisfied ourselves of its existence, to determine the rhythm of an endocardial murmur. To resolve this difficulty it is necessary to determine which is the first and which the second sound of the heart.

The first sound of the heart is synchronous with the carotid pulse, the radial pulse, and the apex-beat. It may be wholly replaced by a systolic murmur, but the second sound is always heard following the apex-beat, for the pulmonic and the aortic valves are never diseased at the same time.

Having determined the existence of a murmur, its rhythm, pitch, intensity, and quality, we next determine its point of maximum intensity. These points of maximum intensity for murmurs at the four valvular orifices of the heart may be briefly summarized as follows: Murmurs arising at the mitral valve are loudest at the apex of the heart or immediately above it; tricuspid murmurs are loudest over the lower part of the sternum; pulmonary murmurs, in the second left intercostal space close to the sternum; and aortic murmurs, in the second right intercostal space at the edge of the sternum and over the whole length of the body of that bone.

Valvular diseases which cause murmurs result either in a condition of the valves that allows regurgitation, or one that obstructs the onward blood-current. Valvular insufficiency arises when extensive retraction, perforation, or partial detachment of the valves prevents them from completely closing their respective orifices. And when the chordæ tendineæ have been ruptured, or when calcareous degeneration has made the valves or the parts in the immediate vicinity abnormally rigid, the regurgitant current through the aperture thus left gives rise to a regurgitant murmur.

{654} When the valves are thickened, retracted, adherent, hypertrophied, or degenerated, so that their edges are prevented from being accurately applied to the walls of the ventricles or vessels, they obstruct the current of blood, and the impinging of the blood-current against the obstruction gives rise to obstructive murmurs. These conditions--stenosis and insufficiency--are often found coexisting, but rarely in equal degree, one usually predominating sufficiently over the other as to give a dominant character to the murmur.

The lesions which produce these conditions may be temporary or permanent--temporary when they occur during the course of acute endocarditis, and permanent when they consist of a new growth either of connective, fibroid, calcareous, or atheromatous tissue, which alters the form of the valves and impairs their function. Acute and chronic valvular disease may produce the same murmurs. The effect of the valvular deformity depends entirely upon its seat.

In the study of the relations of valvular lesions to cardiac murmurs physical signs are the important factors in their diagnosis, and it is necessary always to bear in mind the normal physiological conditions which constitute a complete cardiac pulsation.

The apex of the normal heart is felt between the fifth and sixth ribs on the left side, about two inches below the nipple and one inch to its sternal side. The base of the heart is on a level with the third costal cartilages. The tricuspid valve lies behind the middle of the sternum, on a line with the articulations of the cartilages of the fourth ribs with the sternum. The mitral valve lies behind the cartilage of the fourth left rib, near the edge of the sternum. The aortic valves lie behind the sternum, a little below the junction of the cartilages of the third ribs with the sternum, near its left edge. The pulmonary valves lie behind the junction of the third left rib with the sternum.

Let it be remembered that the tricuspid orifice is the most superficial, then the pulmonary, next the aortic, and, deepest of all, the mitral orifice. Ranged from above downward, the pulmonary orifice comes first, then the aortic, then the mitral, and lastly the tricuspid.

Aortic Obstruction, or Stenosis.

Stenosis at the aortic orifice is a common cardiac lesion, and one that is always accompanied by more or less hypertrophy of the left ventricular walls.

MORBID ANATOMY.--In aortic obstruction the cardiac valves will be found to present some or all of the changes which have been described as taking place in the course of acute and interstitial endocarditis, together with degenerative changes due to atheromatous, calcareous, fibroid, fatty, or connective-tissue metamorphosis.

Sometimes the valves may be covered with thick, warty, irregular excrescences that cause loud murmurs, and yet do not seriously interfere with the outgoing blood-current. At other times stenosis of the aortic orifice may be so extensive as to almost obliterate it. When such is the case, the extent of the lesion will be measured much more by the consequent hypertrophy and its effects on the systemic circulation than by the loudness or harshness of the murmur which it produces.

Very frequently the valves are so rigid that they cannot be pressed back against the wall of the aorta, and these unyielding prominences are greater obstacles to the outgoing current of blood than vegetations on the surface of the valves.

In a few rare cases the outlet may be diminished by constriction of the {655} aorta at the point of insertion of the valves. Adhesion of the aortic valves begins at their bases and extends along their free edges to their tips; sometimes they become fused together into a mass, so that they project into the blood-stream in the form of a funnel irregular in shape and studded with calcareous nodules. The line of attachment of the valves to the aorta frequently becomes entirely obliterated.

In some instances the contraction of the valves between their points of attachment causes them to form a deep pocket or pouch, and their points of attachment may be a quarter of an inch apart.

Obstructions at the aortic orifice are frequently accompanied by atheromatous changes in the aorta, the result of chronic inflammation of its tunics--arteritis deformans.

As a result of aortic stenosis the wall of the left ventricle becomes hypertrophied. This change is a gradual one, and is called compensatory hypertrophy: it is due to the increased force required to propel the blood through the constricted orifice.

After a time insufficiency of the mitral valves is apt to occur, caused either by the extension of endocardial inflammation from the aortic valves or by the forcible pressure of blood upon the ventricular surface of the valves.

A slight thickening or roughening of the aortic valves may cause slight obstruction to the outgoing blood-current, which will interfere but little with the emptying of the ventricular cavity, and which rarely leads to hypertrophy of their walls.

ETIOLOGY.--Aortic obstruction is most frequently met with in early and advanced life, the mean age being forty-seven years. It is not uncommon in children; valvular lesions have been found in children under two years of age. It may be induced where the aorta is defectively developed, and some think that imperfect development of the trachea may lead to imperfect expansion of the chest, and thus induce disease of the aortic valve.[6]

[Footnote 6: Barlow in _Guy's Hospital Reports_, S. 1, vol. vi. p. 235.]

Its most frequent cause is acute exudative and interstitial rheumatic endocarditis. The origin of nearly all valvular disease may be traced back to an attack of rheumatic fever. Next to acute rheumatism, chorea is its most frequent cause. Bright's disease and pyæmia may cause it, and atheroma or arteritis deformans extending to the valves will give rise to valvular lesions which cause obstruction.

Any of the conditions that cause acute exudative and interstitial endocarditis may effect changes in the valves, and the tissue thus developed, undergoing atheromatous, fatty, fibroid, calcareous, or connective-tissue change, will cause obstruction.

Increased tension of the aorta may be the result of chronic spinal deformity, and may be regarded as the indirect cause of aortic stenosis.

The connection between cancer and cardiac valvular disease is to be noticed, if not as cause and effect, at least as a remarkable and noteworthy coincidence.

Women are far less subject to aortic obstruction after rheumatism than men. In men the aortic valves are subject to more pressure and strain than in women, and hence non-rheumatic disease of these valves is very common, while in women it is very rare.

Aortic disease especially occurs in men whose occupations involve repeated, sudden, and great muscular effort.

In old age the walls of the aorta are weakened, and when aortic disease is met with in young subjects it must be regarded as the result of a premature senile condition of the vessels. Allbutt says that in Leeds quite young men have aortic valvular disease, and Peacock mentions several cases where the {656} disease has occurred in young girls who have been placed at service before they were fully developed.

Sometimes the valves are found to be studded with vegetations, apparently of syphilitic origin. Corvisart and Virchow both admit the possibility of such an origin for valvular disease of the heart, but no unquestionable case has as yet been advanced in proof of it. It has been claimed that this is the reason why soldiers so frequently suffer from heart disease; but sailors are notoriously more subject to syphilis than soldiers, and heart disease is rare among them.

The reason is evidently to be found in their mode of dress: sailors wear loose clothes, soldiers have the tightest possible fitting garments. More force is required to pump the blood through the constricted vessels, hence arises more strain on the aorta and more strain on the valves.

Single, sudden muscular efforts have in a limited number of cases produced disease at the aortic orifice.

Aortic valvular disease more frequently than mitral is of non-rheumatic origin; it is slower in its development, and is more commonly met with in advanced life.

SYMPTOMS.--The subjective symptoms of obstruction at the aortic orifice are not usually well marked. Extensive aortic stenosis is not incompatible with a state of comparative good health. As the obstruction to the outflow of blood from the ventricle increases, compensatory ventricular hypertrophy enables the heart to fill the arterial system and relieve the pulmonary pressure. As soon as the ventricular hypertrophy no longer compensates for the obstruction, the arteries are inadequately filled; the left auricle cannot empty itself into the left ventricle, and hence the pulmonary vessels are abnormally full, as is also the entire venous system. The scanty arterial supply gives the pallor to the face which so frequently accompanies this condition, and syncope is liable to occur as a result of partial cerebral anæmia.

These are late effects, and in many cases do not make their appearance until the mitral valve is secondarily involved. The pulse in aortic stenosis is normal in frequency, diminished in volume and power, usually regular in rhythm, though it may be intermittent, and is compressible and jerky in character.

As a general rule, in aortic stenosis signs of arterial anæmia precede evidences of venous engorgement. The obstruction to the exit of blood is shown in the sphygmographic tracing by a slanting or oblique up-stroke, as seen in the accompanying tracing, or, as Mahomed says, "the influence of percussion is lost." Tracings of the pulse in aortic stenosis sometimes show considerable separation between the percussion and the tidal waves. In some rare instances the pulse is slowed. There may be slight palpitation, and pain in the chest may sometimes occur in paroxysms; but pain in the chest is far more common in regurgitation than in obstruction. Aortic obstruction is more frequently connected with cerebral embolism than any other valvular lesion.

The left middle cerebral artery is the most common seat of aortic cardiac emboli. The left lower limb is more subject to embolism from aortic valvular disease than the right. The splenic and renal vessels are also the frequent seat of such emboli. Sometimes embolism is due to small auricular or ventricular {657} clots that form behind the obstruction. Such clots have occluded the aortic orifice and caused sudden death.[7]

[Footnote 7: _Pathological Transactions_, vol. ix. p. 91.]

PHYSICAL SIGNS.--The physical signs of aortic obstruction are generally distinctive and easily appreciated.

Inspection.--The visible area of the cardiac impulse is abnormally increased. Very extensive increase in the area of impulse is frequently accompanied by a lifting of the chest-wall over the heart.

Palpation.--The impulse is felt to be forcible, and is sometimes accompanied by a heaving or lifting motion. The apex is displaced toward the left and slightly downward. A sensation will sometimes be imparted to the hand during systole similar to that produced on the sense of hearing by the whizzing of a missile by the ear. This is often nothing more than an intensified endocardial thrill. This systolic frémissement radiates to the ensiform process of the sternum, being most intense in the second right intercostal space.

Percussion.--The area of cardiac dulness will be increased in proportion to the displacement of the apex-beat to the left. The increase in dulness measures the amount of left ventricular hypertrophy.

Auscultation.--Aortic stenosis produces a systolic murmur which more frequently accompanies than replaces the first sound of the heart. The maximum intensity of this murmur is usually at the second sterno-costal articulation of the right side, but it may be heard with equal intensity over the whole upper part of the sternum, and followed up the aorta and along the carotids; again, it may be loudest at the xiphoid cartilage, or it may be heard with greatest intensity at the junction of the left third rib with the sternum. In most cases the first sound is heard with the murmur, but the murmur may entirely replace or obscure it. This murmur is usually loud and harsh in character, and is loudest at the beginning of the systole. Harshness is one of its distinguishing characteristics.

In pure aortic stenosis the aortic second sound may be inaudible, and is always feeble, but the pulmonic second sound will always be audible. The area of diffusion of this murmur follows the law that a murmur is propagated in the direction of the blood-current. It is conveyed along the aorta into the carotids, and one of its characteristics is that it is heard in the great vessels of the neck. It may sometimes be heard in the thoracic and abdominal aorta.

When an aortic obstructive murmur is heard at the apex its intensity is diminished, and when heard behind it is most distinct at the left of the third and fourth vertebræ near their spines, and frequently extends downward along the spine in the course of the aorta, but with diminished intensity. It is to be noted here that a systolic murmur, audible at the base, and traceable along the ascending arch toward the end of the right clavicle, is by no means limited to cases of aortic stenosis, although aortic stenosis always produces a murmur with these characteristics.

Arterial murmurs, synchronous with the cardiac systole, are far more frequent than diastolic murmurs. When the mitral or tricuspid valves are thickened or incompetent, or when the myocardium is the seat of extensive fatty degeneration, the murmur of aortic obstruction will entirely replace the first sound of the heart.

DIFFERENTIAL DIAGNOSIS.--Aortic obstruction may be mistaken for mitral regurgitation, tricuspid regurgitation; an anæmic bruit, for the murmur of a thoracic aneurism and for a murmur produced by a scabrous condition of the ascending arch of the aorta.

1. Both mitral and tricuspid regurgitation, as well as aortic stenosis, are recognized by a systolic murmur. The murmur of aortic obstruction is heard with its maximum intensity at the second right sterno-costal articulation, and {658} diminishes in intensity toward the apex. The murmur of mitral regurgitation is heard with greatest intensity at the apex-beat. The murmur of aortic obstruction is conveyed into the vessels of the neck; that of mitral regurgitation to the left, in the direction of the apex-beat, and is heard behind, between the fifth and eighth dorsal vertebræ, at the left of the spine, with very nearly the same intensity as at the apex. The pulse in aortic stenosis is hard, firm, and wiry in character, but regular, while in mitral regurgitation the pulse is irregular in rhythm as well as in force, is never incompressible, and is easily increased in frequency. Gastric, intestinal, renal, hepatic, and bronchial symptoms are present in mitral regurgitation, while the subjective symptoms of aortic obstruction are cerebral in character. The pulmonic second sound is generally feeble in aortic stenosis, while in mitral regurgitation it is intensified. The murmur of aortic stenosis is harsh; the murmur of mitral regurgitation is soft, and frequently musical in character.

2. Tricuspid regurgitation is also accompanied by a systolic murmur. But while the murmur of aortic stenosis has its maximum intensity at the right second sterno-costal articulation, the murmur of tricuspid regurgitation is very rarely heard above the third rib: this is an important diagnostic sign. Tricuspid regurgitation is accompanied by jugular pulsation, while the murmur of aortic obstruction is heard in the arterial trunks of the neck. To distinguish between intrinsic pulsation of the jugular vein and throbbing of the carotid arteries press lightly on the vessel above the clavicle; this arrests pulsation when due to tricuspid disease, while if due to aortic stenosis the result is negative. Moreover, respiration influences jugular pulsation, while it has no influence over carotid throbbing. The area of transmission of tricuspid regurgitant murmurs is not more than two inches from the point of their maximum intensity; whereas the aortic obstructive murmurs are conveyed along the sternum into the vessels of the neck. There is nothing peculiar or abnormal about the pulse of tricuspid regurgitation, while the hard and wiry pulse of aortic obstruction is quite characteristic.

3. An anæmic bruit may be mistaken for aortic stenosis, since the rhythm and seat of the bruit are often identical with those of the stenosis. Anæmia, however, produces a murmur that is heard loudest in the carotids, and is accompanied by a venous hum, the bruit du diable, which is continuous, and heard best on the right side of the neck. Thus in anæmia there are three murmurs, arterial, cardiac, and venous. In aortic disease the murmur has its maximum intensity at the second sterno-costal articulation of the right side, and is not accompanied by a venous hum. There is always more or less cardiac hypertrophy in stenosis, and an increase in the force of the apex-beat, while anæmia is attended by a feeble cardiac impulse. The murmur is soft and blowing in anæmia and harsh and rasping in aortic obstruction. The pulse is characteristic in aortic stenosis; in anæmia it may have a thrill, but is never hard and wiry. Lastly, the subjective signs of anæmia will render the diagnosis comparatively easy, especially when the hum in the veins coexists.

Aortic disease usually occurs in those who have passed middle life as a rule, and in men, while young females are the chief subjects of anæmic murmurs.

4. Thoracic aneurism may produce murmurs resembling those of aortic stenosis. The dilating impulse on palpation, the normal force of the heart-beat, the single or double bruit, the pain,--all these symptoms of thoracic aneurism are absent when aortic stenosis alone is present. Moreover, the history of the case will greatly aid in the diagnosis; and, lastly, aneurismal murmurs have their maximum intensity at the seat of the tumor, and not at the base of the heart.

5. A murmur from a scabrous state of the arch of the aorta is exceedingly {659} rare. It is located higher up than that of aortic stenosis, is not transmitted into the cervical vessels, and has its maximum intensity over the transverse portion of the arch.

Aortic Insufficiency, or Regurgitation.

Aortic insufficiency is an abnormal condition of the aortic valves which prevents their complete closure and allows a backward current of blood to flow from the aorta into the left ventricle during the diastole. This lesion is rarely found unassociated with aortic stenosis, and together they constitute one of the most important and frequent valvular lesions. It is sometimes called aortic incompetence, aortic inadequacy, and aortic reflux.

MORBID ANATOMY.--In a normal heart at diastole the aortic semi-lunar valves are firmly closed, so as to completely fill the orifice between the left ventricle and the aorta. In aortic insufficiency the valves are prevented from performing their normal function, on account of the following anatomical changes. As a result of interstitial endocarditis the valves may have been thickened, puckered, and shortened, so that they do not meet when brought into the plane of the orifice.

When the central portion of the segment is indurated, the whole valve subsequently curls up, either toward the orifice or back against the wall of the aorta, and in either case there is insufficiency of the valves. In the first case there is insufficiency with great obstruction; in the second, with but very slight obstruction.

These processes of thickening and shortening are usually the result of the train of changes which attend and follow endocardial inflammation, but they may also come as the result of an atheromatous process extending from the aorta to the valves; and it may be mentioned here that the atheromatous changes, by impairing the elasticity of the aortic walls, become a source of imperfect coronary circulation, and hence prepare the heart for that dilatation whose other causes will subsequently be described.

Regurgitation may result not so much from shortening as from adhesion of the valve-tips to the walls of the aorta. There may be depression of the valves which comes from over-extension, and then extreme insufficiency will be the result. When this pathological lesion occurs, usually only one segment is involved. Complete retroversion of the valves is a questionable lesion; still, it may occur. Again, one or more segments may be more or less detached from their points of insertion, or from the same causes a valvular aneurism or a diseased valve may be torn or ruptured, and then perforation allows a free opening for the regurgitant passage of the blood.

After extensive obstruction has existed for a long time little tunnels may form by the side of the valves and permit a regurgitant current from the aorta to the ventricle. The aortic valves are more liable to laceration than any other valves. Not infrequently the ragged edge of a lacerated or displaced aortic valve is found covered with fibrinous efflorescences of larger or smaller size.

During a cardiac diastole, normally, the blood is passing from the auricle into an empty ventricle; when, however, regurgitation has persisted for a considerable time, there will be added to the primary stream (which of itself is capable of filling the cavity of the ventricle) a regurgitant stream from the aorta, and by this combination of two streams the left ventricle becomes over-distended and permanently dilated. This dilatation occurs all the more readily since during the diastole the ventricular walls are relaxed and less capable of resisting the increased blood-pressure. Thus, permanent dilatation of the left ventricle occurs in a comparatively short time; and to overcome {660} the dilatation and the obstruction to the cardiac circulation the left ventricular walls hypertrophy. The hypertrophy goes on increasing until it compensates for the dilatation; but before this point is reached the ventricular cavity sometimes becomes very much dilated and the left heart reaches an immense size.

This dilatation and hypertrophy may be so extensive that the organ often weighs twenty or thirty ounces, a case being recorded where the enormous weight of forty-eight ounces was reached.[8] The heart is then frequently called the cor bovinum. In such cases the organ has a peculiar pointed form, the right ventricle appearing like a mere appendix. The left ventricle is thus capable of containing so much blood, and such an abnormally large amount is thrown into the aorta at each cardiac cycle, that the arterial system is largely over-filled. Hence the arteries are elongated during their pulsations more than in health, and often become distinctly flexuous with each cardiac pulsation.

[Footnote 8: See Hilton Fagge, _Diseases of the Valves of the Heart_.]

The increase in the ventricular power and in the amount of blood contained in the ventricles and thrown against the aortic walls leads to endarteritis and subsequent atheromatous degeneration of the arterial walls, and the arteries become so brittle that during excitement they may suddenly rupture and cerebral apoplexy result; aneurism is also liable to be developed under such conditions.

In the normal heart the aortic recoil is the force which propels the blood into the coronary arteries. When the aortic valves are insufficient, and furnish little or no resistance to the return blood-current, the coronary blood-supply is consequently diminished. When perfect compensation has existed for some time, it begins to fail, and dilatation again commences at the expense of the walls of the heart. This dilatation is aided, first, by the condition of the coronary arteries above referred to, and, secondly, by the fact that aortic recoil is now expended as much in driving a regurgitant current into the ventricle as in forcing blood through the coronary vessels.

In some cases atrophy of the papillary muscles allows the mitral flaps to swing back into the left auricle when increased pressure is exerted upon them. When from any one of these causes mitral incompetence becomes secondary to, and coexistent with, aortic insufficiency, all the signs of impeded venous circulation will be present. These changes will be considered under the head of Mitral Disease.

When over-distension of the left ventricle causes incomplete emptying of the left auricle, a greater or less amount of passive hyperæmia of the lungs may be present without mitral insufficiency.

ETIOLOGY.--The etiology of aortic insufficiency is similar to that of aortic stenosis. Rheumatic endocarditis is undoubtedly its most frequent cause, but it may also have its origin in sudden and violent muscular effort, atheroma of the aorta, endarteritis, congenital malformation, and enlargement of the aortic orifice. Congenital malformation or congenital non-development is, according to Virchow, a frequent cause in chlorotic females.

In many cases the atheroma that causes the incompetence is of gouty origin, especially when gouty kidneys coexist or when alcoholismus is associated with a gouty diathesis.

Sometimes aortic incompetence is the result of imperfect development of the aortic valves. A rare case is recorded in the _Pathological Transactions_ (vol. xvi. p. 77), where a young man fell from a height upon his side and tore off an entire flap of the semi-lunar valve: there was no external mark of injury, and the rupture was plainly due to the transmission of rapid vibrations from the jarred surface. Valvular inadequacy sometimes results from dilatation of the aorta at its origin.

{661} There can be little doubt but that the interstitial inflammation which gives rise to the valvular changes which allow aortic regurgitation is often excited by the violence with which the aortic valves are closed by the backward rush of blood on the aortic recoil during prolonged and violent physical exertion.

Thus, although rheumatism plays a very important part in its development, it is so far from being its sole cause that C. Hilton Fagge says that in at least half the cases of this form of valvular disease met with in London hospitals one fails to elicit a rheumatic history.

SYMPTOMS.--Rational Signs.--So long as hypertrophy of the left ventricle compensates for its dilatation, the individual will suffer little or no inconvenience, even though the regurgitation is extensive. When the regurgitant stream is a very small one there will also be little or no disturbance of the general health.

But the compensation is only maintained for a short time. When the equilibrium is lost the eccentric hypertrophy induces excessive heart-action during mental excitement or violent muscular effort. The action of the heart then becomes labored, and the patient becomes anxious, nervous, and fretful. Sufferers from aortic regurgitation are generally aware that exercise will augment all their uncomfortable symptoms. Their respirations are accelerated by moderate exercise, and are accompanied by cardiac palpitation. As the insufficiency increases attacks of headache and vertigo become more and more prolonged and severe; the patient complains of muscæ volitantes, dyspnoea, giddiness, and is compelled to sleep with his head elevated. Palpitation is now a constant symptom, and a visible carotid impulse is persistently present.

A comparatively frequent symptom of aortic regurgitation is a distinctly paroxysmal shooting or stabbing pain over the heart, in the left shoulder, or extending down the left arm. Sometimes this pain is accompanied by numbness and a peculiar whiteness of the skin along the line of the pain. In other cases the pain passes from the middle of the sternum to the right arm. This pain is increased by mental excitement and muscular exertion, and sometimes by over-distension of the stomach. In a few cases patients will complain of a sickening fluttering of the heart.

When the nutrition of the hypertrophied ventricular walls becomes markedly interfered with, or when insufficiency of the mitral valves occurs, the veins of the systemic circulation become overloaded, as is evidenced by cyanosis and dropsy; the dropsy appears first as oedema of the feet, and gradually extends upward until a condition of general anasarca is reached. The cyanosis is increased after slight exertion, and is accompanied by dyspnoea, carotid pulsation, and puffiness of the face.

In the advanced stages of the disease there is orthopnoea, sudden starting in sleep, angina pectoris, and in some cases albuminuria and enlargement and tenderness of the liver. Attacks of syncope at first occur only after active muscular exercise, but later they occur independently of it, and are extremely distressing. These patients are in danger of death at any moment, either during a state of the utmost calm or the most intense excitement; the danger is greater, however, during exertion.

The pulse is the most characteristic subjective symptom of this form of valvular lesion. It was first accurately described by Sir Dominick Corrigan,[9] and it is frequently called Corrigan's pulse. He especially said that the disease was indicated by visible pulsation of the vessels of the head, neck, and upper extremities. On account of the elongation of the arteries during their pulsation, and their becoming distinctly flexuous, the pulse is frequently called the locomotive pulse. It is large and distinct, rapidly projected against the finger, and just as quickly the arterial tension sinks to its minimum and the {662} impulse vanishes. It is sometimes accompanied by a vibrating jar, on account of which it is called the water-hammer, jerking, splashing, or collapsing pulse. Its characteristics are more apparent when the arm is raised above the head. Although slightly infrequent, quick, and jerking, it is always regular in rhythm; the radial impulse is felt a little after the apex-beat. Thus the pulse-wave of aortic regurgitation travels slowly along the arteries. This delay in the pulse is constant.

[Footnote 9: _Edin. Med. and Surq. Journ._, April, 1832.]

As soon as the systemic circulation is overloaded from insufficiency of the heart or from secondary mitral insufficiency, the pulse becomes feeble and irregular upon the slightest exertion, and may intermit, but it is still of the same peculiar jerking character. The sphygmographic tracings of this pulse show a high upstroke and absence of the dicrotic wave.

This vibrating pulse or pulse of unfilled arteries is usually possessed of fulness of volume, but when obstruction coexists it may be small and flickering unless the arteries are calcified or atheromatous. The pulse of aortic insufficiency taken by the sphygmograph resembles strongly the pouls des vieillards, but the senile pulse gives a rounded instead of a pointed summit. Still, in old age the two tracings may be indistinguishable.[10] The peculiar crochet or beak is noticeable in graphic tracings of the pulse of aortic inadequacy.

[Footnote 10: Marey, _Phys. Méd. de Circ. du Sang_, Paris, 1863.]

Stokes has described, under the designation of steel-hammer pulse, a peculiar and characteristic pulsation of the arteries which occurs in cases of acute rheumatic arthritis supervening upon chronic inadequacy of the aortic valves. The pulse is abrupt and energetic, as the rebound of a smith's hammer from the anvil; it is exhibited, however, only in the arteries adjacent to the affected joints.[11]

[Footnote 11: _Continued Fever_, 1874, p. 244.]

PHYSICAL SIGNS.--Inspection.--There is an increase in the area of the apex-beat, which is plainly more forcible and is visible over a wider area than in aortic obstruction. After compensation has ceased to balance the forces in the heart the apex-beat becomes more and more feeble and diffused. One of the most important points obtained by inspection is pulsation of the carotids and the vessels of the upper extremities. Becker and Quincke have observed pulsation of the retinal vessels in cases of extensive aortic regurgitation.[12]

[Footnote 12: _London Ophth. Hosp. Rep._, Feb., 1873.]

Palpation.--On placing the hand over the præcordial region a heaving, lifting impulse will be perceived, which is transmitted over a large portion of the thoracic walls. The apex-beat is displaced downward and toward the left, sometimes as far as the eighth rib and two and a half inches to the left of the left nipple. Occasionally a continuous diastolic thrill, equally intense during the whole of the diastole, is felt over the sternum, most distinctly at the site of the aortic valves. In some cases there is a slight pulsation in the scrobiculus cordis.

{663} Percussion.--The area of percussion dulness corresponds to the extent of the cardiac enlargement. Deep dulness is elicited below and to the left of the normal area, and its outline has more of an oval contour than in health. So soon as the cardiac dilatation exceeds the hypertrophy, the area of dulness will extend horizontally rather than vertically, and it may be carried slightly upward, the apex beating in the axillary space. The area of dulness may extend six and a half inches from right to left, and from the upper edge of the third rib to the line of the liver dulness. The superficial area of dulness is likewise increased horizontally and toward the left.

Auscultation.--Aortic regurgitation is characterized by a diastolic murmur, which may take the place of, or immediately follow, the second sound of the heart. It is very distinct at any point over the base of the heart, but usually has its maximum intensity either at the sternal end of the second right costal cartilage, in the second right intercostal space, or at the sternal junction of the third rib on the left side. It is transmitted over the sternum, and sometimes will be loudest at the xiphoid cartilage, and is thence transmitted in the direction of the apex. Its area of diffusion is greater than that of any other cardiac murmur: it is not only conducted down the sternum to the xiphoid cartilage and to the apex, but it may be heard at the sides of the chest along the spinal column, and sometimes faintly in the ascending and transverse portions of the arch, in the carotids, and in rare instances as far as the radial arteries. The murmur of aortic reflux is accompanying rather than substitutive, for the pulmonic second sound is audible at the right base.

Foster[13] regards incompetency of the posterior segment of the valve as producing a murmur which is conducted to the apex, whereas inadequacy of either or both of the anterior segments is accompanied by a murmur which is conducted to the ensiform cartilage. This point has a practical bearing on account of the relationship of the anterior segments of the valve to the coronary arteries. If the murmur indicates a lesion of the posterior flap of the valve, the prognosis will be better. When the second sound of the heart is distinct the murmur immediately follows it. Many English writers call the murmur a post-diastolic aortic murmur.

[Footnote 13: _Med. Times and Gaz._, 1873, vol. ii. p. 658 _et seq._]

Although having the greatest area of diffusion, aortic reflux has not the loudest murmur; it is soft, blowing, sometimes rough, and frequently musical. It is loudest at the beginning of diastole, gradually decreasing in intensity, although it may preserve its rushing, blowing character during all the diastole.

An aortic regurgitant murmur may temporarily disappear if a plug of fibrin closes the orifice, or if the walls of the left ventricle are the seat of extensive fatty degeneration, the aorta being rigid and inelastic.[14] When aortic stenosis coexists there will be a double murmur, audible over a very large space, having its maximum intensity at the right edge of the sternum in the second interspace.

[Footnote 14: _Brit. Med. Journ._, 30th March, 1882.]

Systolic and diastolic murmurs, though sometimes separated by a well-defined pause, may run into each other. If mitral regurgitation occurs with aortic regurgitation, each murmur retains its own location of maximum intensity. In rare instances, when two segments of the valve are healthy, a clear aortic second sound is heard, which is preceded by a faint reflux murmur. Such a murmur is said to be prediastolic in rhythm. Aortic reflux murmurs are often very indistinct, and can only be heard when the patient is in the recumbent posture. There is no necessary connection between the amount of reflux and the loudness of the murmur.