Aortic Insufficiency Aortic Regurgitation
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Disturbances Of The Heart
This lesion, though not so common as the mitral lesion, is of not
infrequent occurrence in children and young adults as a sequence of
acute rheumatic endocarditis. If it occurs later in life it
generally is associated with aortic narrowing, and is a part of the
general endarteritis and perhaps atheroma of the aorta. Sometimes it
is caused by strenuous exertion apparently rupturing the valve.
This form of
alvular disease frequently ends in sudden death. On
the other hand, it is astonishing how active a person may be with
this really terrible cardiac defect. This lesion, from the frequent
overdistention of the left ventricle, is one which often causes
pain. While the left ventricle enlarges enormously to overcome the
extra distention due to the blood entering the ventricle from both
directions, the muscle sooner or later becomes degenerated from poor
coronary circulation. Unless the left ventricle can do its work well
enough to maintain an adequate pressure of blood in the aorta, the
coronary circulation is insufficient, and chronic myocarditis is the
result. If the left ventricle has maintained this pressure for a
long time, edemas are not common unless the cardiac weakness is
serious and generally permanently serious: that is, slight weakness,
in this lesion, does not give edemas as does slight loss of
compensation in mitral disease, and unless the weakness of the
ventricle is serious, the lungs are not much affected.
The physical sign of this lesion is the diastolic murmur, which is
loudest of the base of the heart, is accentuated over the aortic
orifice, and is transmitted up into the neck and the subclavians,
and down over the heart and down the sternum with marked pulsation,
of the arteries (Corrigan pulse) and often of some of the peripheral
veins, notably of the arms and throat.
If the left ventricle becomes dilated the mitral valve may become
insufficient, when the usual lung symptoms occur, with hypertrophy
of the right ventricle; and if it fails, the usual venous symptoms
of loss of compensation follow. This lesion not infrequently causes
epistaxis, hemoptysis and hematemesis.
Digitalis is always of value in these cases, but it should not be
pushed. If a heart is slowed too much, the regurgitation into the
left ventricle is increased. Therefore such hearts should not be
slowed to less than eighty beats per minute, or sudden anemia of the
brain and sudden death may occur. These patients must not do hard
work.