Synonyms.—Mitral Regurgitation; Mitral Insufficiency.
Definition.—Mitral incompetency is an imperfect closure of the auriculo-ventricular opening, permitting a regurgitation of blood during the contraction of the left ventricle, and due to an abnormal condition of the leaflets or to an enlarged opening.
Etiology.—The most frequent cause leading to change in the mitral valves, whereby the leaflets become adherent, thickened, or curled, is rheumatic endocarditis, though these same changes may occur from endocarditis due to other causes. Disease of the chordae tendineae, whereby they are forcibly contracted, or become weakened, permitting them to dip into the orifice, may give rise to insufficiency.
Alcohol and syphilis are not to be overlooked as factors producing sclerotic changes in the mitral valve. Aortic valvular changes may give rise to mitral insufficiency, through increased tension of the blood in the left ventricle.
Dilatation of the left ventricle may give rise to enlargement of the mitral orifice, the leaflets remaining whole; the insufficiency here being relative. Incompetency also may be due to ulcerative endocarditis from the infectious fevers, in which case there may be perforation of the leaflets.
Degeneration of the muscular walls of the ventricle, either by causing such extensive dilatation as to prevent a closure of the orifice, or to so affect the muscular substance as to prevent a proper coaptation of the leaflets during the systole, will give rise to muscular incompetency. Long continued, severe physical training or extraordinary physical exertion may give rise to it.
Pathology.—The changes that are found in this, the most frequent of all valvular lesions, are varied. There will be thickening in some cases, with curling of the leaflets, while in others there will be adhesions of the segments; in another, nodulation or perforation may be seen. In some there is a change in the chordae tendinese, such as undue contraction; or the opposite condition prevails, and there is relaxation. In rare cases there is a rupture of the chordae tendineae.
Adhesions of one or both segments to the wall of the ventricle have also been found. As a result of the inability of the mitral "valves to effectually close the mitral opening following the auricular systole, there is a regurgitation of blood into the left auricle, which meets the stream coming from the pulmonary veins; as a result, there is an increased amount of blood in the auricle, which causes its dilatation. In order to expel this abnormal amount, increased work is thrown upon it, which causes hypertrophy as well. This increased volume of blood in the auricle impairs the pulmonary circulation, and the lungs become engorged.
With each contraction of the left auricle an increased quantity of blood is emptied into the left ventricle, causing dilatation and hypertrophy of the same. As a result of the pulmonary congestion, the right ventricle is not able to completely empty its contents: hence dilatation, followed in turn by hypertrophy of the right heart, takes place. Finally the right auricle passes through the same compensatory changes of dilatation and hypertrophy.
These compensatory changes take place so gradually that the patient may enjoy good health for years; for the hypertrophied heart throws the normal amount of blood into the aorta and general circulation. Finally, however, the incompetency becomes extreme, or compensation fails, and the left ventricle is unable to properly empty itself, and, as a result, the auricle becomes greatly distended, the pulmonary circulation engorged, the right heart embarrassed, and the systemic veins congested. The result of this pulmonary engorgement causes dilatation of both arteries, and degeneration and atheromatous deposits are not uncommon.
After all this disturbance, the right ventricle heroically does its increased work, and the patient may live for months with embarrassed respiration, cough, and evidences of respiratory lesions; but ultimately the right ventricle is unequal to the task, there is aggravated insufficiency of the tricuspid valves, and general systemic congestion.
The portal circulation is affected, cerebral engorgement follows, cyanosis becomes marked, and the extremities become edematous. Cyanotic induration of liver, spleen, and other viscera takes place.
Symptoms.—Nature comes to the patient's rescue, and, by gradual and progressive changes, so fortifies the cardiac structure that a patient may live for years without the knowledge of a valvular lesion. As long as the hypertrophied ventricles are able to meet the demands made upon them, the patient suffers no inconvenience, save an embarrassed respiration after active exertion, such as going up stairs, climbing a hill, running for a car, or the many seeming necessities of every-day life.
Finally the earlier and minor symptoms develop, even while compensation remains good, and are prophetic of later changes. The face becomes slightly flushed, the lips and ears become blue, and the veins of the cheeks become slightly enlarged. Slight exertion now gives rise to dyspnea and cough, the expectoration often being tinged with blood; palpitation of the heart, with pre-cordial pain, is also often present. The disturbed respiration, the cough, the bloody, frothy sputum, may deceive both patient and physician unless a physical examination be made.
As the disease progresses, there finally comes a period when compensation is disturbed and more pronounced symptoms appear. Venous engorgement is the first evidence of this disturbed condition, and is shown in the increased cyanosis. The skin is not only cyanotic, but also jaundiced, induced by engorgement of the liver.
The dyspnea now becomes marked, owing to pulmonary congestion, and the patient's distress is apparent. This is especially so when the patient attempts to sleep, as he suddenly awakens with a sense of suffocation and a feeling as though the heart was going to stop its work. Cough is now a prominent symptom, and the patient expectorates a frothy, bloody serum. Dropsical effusion begins first in the feet, gradually extending up the limbs, finally resulting in general anasarca.
The position of the patient is now upright, and he occupies his chair day and night. The liver and spleen become engorged; there is often gastric irritation, with catarrh of the stomach and intestines. The urine is very scanty, highly colored, albuminous, and contains tube casts; sometimes but four or six ounces of chalky, bloody urine is passed in twenty-four hours.
The patient does not often suffer acute pain, the distress mostly arising from dyspnea and his inability to lie down and obtain a good night's rest. Sudden death is a rare termination of this form of heart disease.
Physical Signs.—Inspection.—The apex beat is seen to be displaced downward and to the left, depending upon the extent of enlargement of the left ventricle. It may be seen as low as the sixth interspace near the axillary line. In children the precordia is prominent, even bulging, the area of the apex beat is enlarged, and, in the latter stages, is diffuse and waving.
After the right ventricle becomes dilated, we often notice epigastric pulsation. Wavy pulsations in the cervical veins also follow extreme dilatation of the right heart. As compensation fails, the lips and ears become dark and general cyanosis appears.
Palpation.—By placing the hand flat over the precordium, a systolic thrill may be felt over the apex, though this is by no means constant. It is synchronous with the first sound. The apex beat is displaced downwards and to the left, and is full and strong during the period of compensation, but: with its disturbance becomes irregular, and, later, waving and feeble.
By placing the hand over the epigastrium, after extreme dilatation of the right ventricle, epigastric pulsation is observed. The pulse is but little, if any, changed during the period of compensation, though exertion may give rise to some irregularity. When compensation fails, it loses its impulse and becomes irregular.
Percussion.—Owing to hypertrophy of both left and right ventricles, there is a greater area of dullness in a transverse direction in mitral lesions than in any other valvular disease. It may extend from an inch or more, to the right anterior axillary line. A slight increase in dullness upward along the border of the sternum is due to hypertrophy of the left auricle.
Auscultation.—The most constant and characteristic sign of regurgitation heard on auscultation is the mitral or systolic murmur, which is heard over the apex and partly, or entirely, replaces the first sound. It is of a blowing character, sometimes terminating in a musical tone, and is transmitted to the axilla, and may be heard at the angle of the scapula; in fact, if the contraction be strong, it may be heard all over the chest.
If the contraction be weak, the murmur may be heard over the base of the heart when inaudible elsewhere. Sometimes, by changing from the erect to the recumbent position, the murmur may be heard. At times there may be heard a soft, blowing, presystolic murmur.
Another very important sign is due to hypertrophy of the right ventricle, which causes an increased tension in the pulmonary vessels, that gives rise to the accentuated pulmonic second sound, and is heard over the third left costal cartilage.
Where there is extreme dilatation, and especially if dropsy be present, there can be heard a soft, low-pitched, systolic murmur at the ensiform cartilage and at the lower sternal region, and is due to tricuspid insufficiency. Combined murmurs may be heard of a rough or harsh character, though they are not constant.
Diagnosis.—The diagnosis of mitral insufficiency is generally comparatively easy, if we bear in mind the three characteristic signs:
First, a systolic murmur obliterating the first sound. It is of a blowing character, terminating in a musical note and heard with maximum intensity over the apex, but also transmitted to the axilla and back.
Second, accentuation of the pulmonary second sound, heard over the third costal cartilage.
Third, the increased transverse dullness extending from an inch or more to the right of the sternum to the left axillary line.
Add to these, blueness of the ears, nose, and lips, dyspnea, and more or less cough, and the picture is complete.
There are two other forms of valvular disease that may be mistaken for mitral insufficiency, since each is accompanied by a systolic murmur—aortic stenosis and tricuspid incompetency. In aortic stenosis the sound is harsh, and heard best over the base of the heart, while in mitral insufficiency it is heard at the apex.
In aortic stenosis, the area of dullness is but little increased, and that to the left, while the area of dullness in mitral insufficiency is more extensive than any other lesion. The tricuspid systolic murmur is soft and low, and heard with greatest intensity at the base of the ensiform cartilage.