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Conditions Causing Change In Blood Pressure





Category: Uncategorized
Source: Disturbances Of The Heart

Woolley [Footnote: Woolley, P. G.: Factors Governing Vascular
Dilatation and Slowing of the Blood Stream in Inflammation, THE
JOURNAL A. M. A., Dec. 26, 1914, p. 2279.] quotes Starling as
finding that the blood vessels dilate from physical and chemical
changes in the musculature, and that this dilatation is caused by
deficient oxidation and accumulation of the products of metabolism,
including carbon dioxid. This dilatation ordinarily is transient and
not associated with exudation, but in inflammation the dilatation is
persistent and there is exudation. The carbon dioxid increase during
exercise stimulates a greater circulation of oxygen in the tissues
which later counteracts the normal increase in acid products. In
inflammatory processes, however, the acid accumulates too rapidly to
allow of saturation. In this case the circulation becomes slowed and
the cells become affected.

Besides these charges in the blood vessels of the muscles, the
general blood pressure becomes raised on exercise, the heart more
rapid and the temperature somewhat elevated, and the breathing is
increased. This increased heart rate does not stop immediately on
cessation of the exercise, but persists for a longer or shorter
time. The better trained the individual, the sooner the speed of the
heart becomes normal.

Benedict and Cathcart [Footnote: Benedict and Cathcart: Pub. 77,
Carnegie Institute of Washington.] have found that the increased
absorption of oxygen, showing increased metabolism, persists after
exercise as long as the heart action is increased.

Newburgh and Lawrence [Footnote: Newburgh, L. H., and Lawrence C.
H.: The Effect of Heat on Blood Pressure, Arch. Int. Med., February,
1914, p. 287.] have found that increased temperature in animals,
equal to that occurring in persons suffering with infection, reduces
the blood pressure, causing a hypotension. This shows that high
temperature alone in an individual sooner or later causes
hypotension.

Although prolonged pain may cause a fall of blood pressure from
shock, the first acute pain may cause a rise in blood pressure, and
Curschmann [Footnote: Curschmann: Munchen. med. Wehnschr., Oct. 15,
1907.] found that the blood pressure was high in the gastro-
intestinal crises of tabes and in colic, and that the application of
faradic electricity to the thigh could raise the blood pressure from
8 to 10 mm. in normal individuals.

The positive effect of decomposition products in the intestine, more
especially such as come from meat proteins, is well recognized; but
the importance, in high pressure cases, of the absorption of toxins
derived from imperfectly digested food remaining in the bowels over
night is not sufficiently recognized. Patients with high blood
pressure should not eat a heavy evening meal, and especially should
they not eat meat. Willson [Footnote: Willson, R. N.: The
Decomposition Food Products as Cardiovascular Products, THE JOURNAL
A. M. A., Sept. 25, 1915, p. 1077.] well describes the condition
caused by the absorption of these toxins. If the heart muscle is
intact, he finds such absorption in high pressure cases will show
diastolic as well as systolic increase:

The vessels pulsate and throb; the skin is pale; the head aches;
the tongue is coated; the breath is foul; vertigo is often
distressing; and not infrequently the hands and feet feel distended
and swollen. A thorough house-cleaning of the gastro-intestinal
canal causes the expulsion of the offending substances and the
expulsion of gas, whereupon the blood pressure often resumes its
normal level and the symptoms disappear.

Wilson suggests that not only the meat proteins, but also the
oxyphenylethylamin in overripe cheese may often cause this
poisoning; and cheese is frequently eaten by these people at
bedtime. Of course if any particular fruit or article of food causes
intestinal upset in a given individual, they should be avoided.

When the heart is hypertrophied in disease, the cavities of the
ventricles are probably also generally enlarged, and therefore they
propel more blood at each contraction than in normal persons and
thus increase the blood pressure.

The blood pressure is raised not only by intestinal toxemia and
uremia, but also by lead poisoning and the conditions generally
present in gout.

It has been pointed out by Daland [Footnote: Daland: Pennsylvania
Med. Jour., July, 1913.] that nervous exhaustion may raise the blood
pressure in those who are neurotic, and he finds that this
hypertension may exist for months in some cases. On the other hand,
in neurasthenics the blood pressure is generally lowered. As he
points out, there is often a very great increase in the systolic
blood pressure at the menopause, while the diastolic pressure may
not be high. This makes a very large pressure pulse. This suggests
the possibility of disturbances of the glands of internal secretion.
This hypertension is generally improved under proper treatment.

Schwarzmann [Footnote: Schwarzmann: Zentralbl. f. inn. Med., Aug. 1,
1914.] studied the blood pressure in eighty cases of acute
infection, and found that a high diastolic blood pressure during
such illness indicates a tendency to paralysis of the abdominal
vessels, and hence a sluggish circulation in the vessels of the
abdomen. He found that in seriously ill patients this high diastolic
pressure is of bad prognosis. He also found that a lower systolic
pressure with a lower diastolic pressure is not a sign that the
heart is weakening, but only that the visceral tone is growing less.
On the other hand, when the diastolic pressure rises while the
systolic falls, this is a sign of failing heart.

Newburgh and Minot [Footnote: Newburgh, L. H. and Minot, G. II: The
Blood Pressure in Pneumonia, Arch. Int. Med., July, 1914, p. 48.]
find that the blood pressure course in pneumonia does not suggest
that there is a failure of the vasomotor center. They found that
"low systolic pressures are not invariably of evil omen." They also
found that the systolic pressure in fatal cases is often higher than
in those in which the patients recovered, and they found that the
rate of the pulse is more important in determining the treatment
than the blood pressure measurements.

The work which has been described under this section is of interest
as indicating the newer experimental work on the physiology of blood
pressure. Much of it is new, however, and it is difficult to draw
absolute therapeutic conclusions from the evidence offered.





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