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Pathologic Physiology





Category: Uncategorized
Source: 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 general 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.





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