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Cardiovascular Renal Disease
Source: Disturbances Of The Heart
With the strennousness of this era, this disease or condition, which
may be regarded as one of the accompaniments of normal old age, has
become of grave importance, and nowadays frequently develops in
early middle life. If it is diagnosed in its incipiency, and the
patient follows the advice given him, the progress of the disease
will generally be inhibited, and a premature old age postponed.
In the beginning the symptoms and signs of this disease are
generally those of hypertension, and the treatment and management is
that advised in hypertension. If the kidneys show irritation, as
manifested by the presence of albumini and casts in the urine, or if
they show insufficiency in the twenty-four-hour excretion of one or
more salts or other excretory product, the diet and life must be
more carefully regulated than advised in hypertension, and the
treatment becomes practically that of chronic interstitial
Sooner or later, in most instances of this disease, whether
hypertension, chronic endarteritis or interstitial nephritis or any
combination of these conditions is most in evidence, the heart will
hypertrophy. As long as the circulation in the heart itself is good
and not impaired by coronary sclerosis, and as long as this slowly
developing chronic myocarditis has not advanced far, cardiac
symptoms will not be in evidence; but if these conditions occur, or
if the blood pressure is so greatly increased as to damage the
aortic valve or strain and dilate the left ventricle, symptoms
rapidly appear, and the heart must be carefully watched.
Subsequently, as the disease advances, if the patient does not die
of angina pectoris, apoplexy or uremia, the symptoms of cardiac
decompensation will develop. As the heart begins to fail, a
dilatation of the right ventricle causes passive congestion of the
kidneys, and the chronic interstitial nephritis may progress more
rapidly. It is often difficult to decide which is more in evidence,
heart insufficiency or kidney insufficiency. The more the heart
fails, the more albumin will generally appear in the urine, and the
lower the blood pressure, especially the diastolic. The more
insufficient the kidneys, the higher the blood pressure, especially
the diastolic. The location of the edema will aid in deciding which
condition is most in evidence. If the edema is pendent in feet, legs
and perhaps genitals when the patient is up, with its disappearance
at night, and more or less backache and pitting of the back in the
morning, it is the heart that is most rapidly failing. If there is
more general edema, the hands and face puffing, and there are
considerable nausea and vomiting, headache and drowsiness, and
perhaps muscular twitchings, with neuralgic pains, the most serious
trouble at that particular time lies in the kidney insufficiency.
Kisch [Footnote: Kisch: Med. Klin., Feb. 27, 1916.] sums up the
procedural symptoms and signs of cerebral hemorrhage. The heart is
generally enlarged and hypertrophied. The patient is likely to be
overweight or adding weight, and to suffer from intestinal
indigestions. Signs of sclerosis of the blood vessels of the brain
are evidenced by transient dizziness; headaches; impaired sleep;
loss of memory, especially for names and words; slight disturbances
of speech, momentary perhaps, and more or less temporary localized
numbness of the hands or feet, or arms or legs, with perhaps
flushing of some part of the body, or little localized spasms of
vessels of other parts of the body, causing chilliness.
There is also a marked hereditary tendency to apoplexy.
Cadwalader, [Footnote: Cadwalader, W. R.: A Comparison of the Onset
and Character of the Apoplexy Caused by Cerebral Hemorrhage and by
Vascular Occlusion, The Journal A. M. A., May 2, 1914, p. 1385.]
after considerable investigation, has come to the conclusion that
large hemorrhages into the brain are the rule in apoplexy, and that
small hemorrhages are rare, and he is inclined to think that even
small, as well as large hemorrhages, are more frequently fatal than
supposed. In other words, he thinks that many of the nonfatal
hemiplegias are caused by vascular obstruction and softening and not
by hemorrhage. He finds that sudden death, or death within a few
minutes, does not occur from hemorrhage, even if the hemorrhage is
large, though a rapidly developing and persistent coma usually
indicates a hemorrhage. If the coma is not profound and is slow in
its onset, with symptoms noticed by the patient, and cerebral
disturbance, he believes it to be caused generally by softening of
the cerebral center, due to some obstruction of the blood flow, and
not to hemorrhage. While occasionally a slowly increasing loss of
consciousness may be due to hemorrhage, he thinks it is doubtful if
real hemorrhage ever occurs without loss of consciousness, while
softening of some part of the cerebrum may occur without
unconsciousness. He thinks that the size of the hemorrhage is of
more importance than its situation in causing the profoundness of
the symptoms, but he repeats that nonfatal cases of hemiplegia are
generally caused by vascular occlusion and subsequent softening, and
not by hemorrhage.
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