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Pathologic Physiology

Categories: Uncategorized
Sources: Disturbances Of The Heart

The development of permanent injury to one or more valves of the

heart may have been watched by the physician who cares for a patient

with acute endocarditis, or it may have been noted early during the

progress of arteriosclerosis or other conditions of hypertension. On

the other hand, many instances of valvular lesions may be found

during a life-insurance examination, or are discovered by the

physician making a genera
physical examination for an indefinable

general disturbance or for local symptoms. without the patient ever

having known that he had a damaged heart. The previous history of

such a patient will generally disclose the pathologic cause or the

physical excuse.

As soon as a valve has become injured the heart muscle hypertrophies

to force the blood through a narrowed orifice or to evacuate the

blood coming into a compartment of the heart from two directions

instead of one, as occurs in regurgitation or insufficiency of a

valve. The heart muscle becomes hypertrophied, like any other muscle

which is compelled to do extra work. Which part or parts of the

heart will become most enlarged depends on the particular valvular

lesion. In some instances this enlargement is enormous, increasing a

heart which normally weighs from 10 to 12 ounces to a weight of 20

or even 25 ounces, and extreme weights of from 40 to 50 ounces and

even more are recorded.

As long as the heart remains in this hypertrophied condition, which

may be called normal hypertrophy since it is needed for the work

which has to be done in overcoming the defect in the valve, there

are no symptoms, the pulmonary and systemic circulation is

sufficient, and the patient does not know that he is incapacitated.

Sooner or later, however, the nutrition of the heart, especially in

atheromatous conditions, becomes impaired, and the lack of a proper

blood supply to the heart muscle causes myocardial disturbance,

either a chronic myocarditis or fatty degeneration. If there is no

atheromatous condition of the coronary arteries, and arterial

disease is not a cause of the valvular lesion, compensation may be

broken by some sudden extra strain put on the heart, either muscular

or by some acute sickness or a necessary anesthetic and operation.

From any of these causes the muscle again becomes impaired, and the

heart, especially the part which is the weakest and has the most

work to do relatively to its strength, becomes dilated, compensation

is broken, and all of the various circulatory disturbances resulting

from an insufficient heart strength develop.