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Definition.—An inflammation of the pericardium or serous covering of
the heart.
Varieties.—Acute, Plastic or Fibrinous, Subacute or Sero-fibrinous,
which includes the Purulent and Hemorrhagic; Adhesive or Chronic
Synonyms.—Fibrinous Pericarditis ; Dry Pericarditis.
Etiology.—This form of pericarditis occurs more frequently in the
young and middle-aged than at any other period of life, and occurs in
males far more frequently than in females. It may be divided into
primary and secondary forms.
The primary form occurs very rarely, though bruises or injuries of
various kinds may result in so great an irritation and determination of
blood as to give rise to inflammation. The old idea, once so prevalent,
that cold was the exciting cause, is rapidly giving way before more
careful observation and experimentation, and nearly all writers are now
agreed that pericarditis is a secondary affection. Metchnikoff goes so far
as to declare that there can be no such a condition as idiopathic
First in importance as a causal factor may be classed rheumatism;
Bouillard declaring that in every case of rheumatism there will be some
lesion of the heart; and while we regard this as a very extravagant
statement, we may be quite conservative and yet place rheumatism as
the cause in at least fifty per cent of all cases of pericarditis.
Chronic nephritis and tuberculosis may give rise to the acute form, but
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is more common in the subacute variety. Toxins from the infectious
diseases seem to influence the pericardium quite early, resulting in
inflammation. Scarlet fever, measles, diphtheria, influenza, and tvphoid
fever in particular, give rise to it, though any infectious fever may have
its influence in the same direction.
The extension of the inflammatory condition from neighboring organs,
especially pleurisy and pneumonia, is a frequent cause, more of this
form than of the other varieties. Carcinoma by poisoning the blood and
encroaching upon neighboring tissues may give rise to this form.
Pathology.—The changes that occur may be general or local, usually
the latter, and are similar to those which occur in pleurisy and
peritonitis. At first the membrane is red, smooth, injected, and swollen,
but soon becomes rough and thickened by the deposit of a fibrinous
exudate. As a result of the friction of the surfaces, the membrane
becomes roughened or wrinkled, resembling tripe in appearance, and
when the exudate is thick, this friction results in giving the membrane a
jagged-looking surface, giving rise to the shaggy or hairy heart of the
older writers.
In this variety there is but little serous fluid, the natural secretion being
arrested or greatly diminished. The myocardium may also be affected; in
fact, there can scarcely ever be a severe pericarditis without involving
more or less tlie heart itself. Where the disease has continued for some
time, the heart is apt to be flabby and dilated, with more or less fatty
If adhesions of the two surfaces have taken place, there is apt to be
hypertrophy of the heart. At other times the nutrition of the heart is so
impaired as to give rise to atrophy.
Symptoms.—Primary Form.—If the disease is primary, which is very
rare, and if the patient be a young subject, there will be a chill, followed
by a febrile reaction, a dry skin, scanty secretion of urine, constipation,
and the general symptoms of an inflammation.
There is pain in the precordial region that varies from a dull, aching
sensation to one of an intense, sharp, lancinating character, which
extends from the nipple to the back and down the left arm. There is a
sense of great anxiety, and though there may be but little pain. the
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patient has an anxious expression that can not be disguised. The pulse
varies from one hundred to one hundred and thirty per minute, and in
the early stage is full and strong.
If the pleura is involved, there will be embarrassed respiration.
Secondary Form.—Since the very large per cent of cases of pericarditis is
preceded by some other disease, the symptoms relating to the heart are
more or less obscured, and often the disease is entirely overlooked and
the discovery made post-mortem. In confirmation of this is a statement
made by an ex-intern of our city hospital, that of five post-mortems that
came under his observation where pericarditis was found, not a single
case had been diagnosed during life.
If the inflammation be very acute, pain of greater or less intensity will
be felt in the precordial region, extending to the left arm, with more or
less constriction in the precordial -region. Dyspnea is often present, but
not a constant feature. The pulse is increased in frequency, and, though
full and bounding in the early stage, becomes more feeble in long
protracted cases. The fever that attends is rarely severe in character, the
temperature not often exceeding 102°.
Physical Signs.—Inspection, if the patient be spare, may reveal
increased force of the apex-beat. In severe cases the veins of the neck
are swollen, and tlie pulsation of tlie jugulars are visible.
Palpation.—Palpation may reveal friction fremitus, which is due to the
rubbing of the changed pericardial surfaces one upon the other, and is
most intense to the left of the sternum. During the early and later
stages it is more readily detected, there being but little effusion at these
Percussion.—But little, if any, information is gained by percussion.
Auscultation.—The most positive information, and we might say
pathognomonic signs, are obtained by auscultation. The pericardial
friction rub is due partly to the exudate and partly to the dry condition
of the membrane. This sound is usually double, and corresponds to both
diastole and systole, though it may be triple and sometimes quadruple.
The sound is generally more pronounced than endocardial murmurs,
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and is harsh or creaking, resembling the sound of bending new leather,
the sounds becoming more smooth and diffuse as the effusion increases.
The maximum sound is heard between the fourth and fifth interspace
near the sternum. The sound is intensified bv changing the pressure of
the stethoscope, moderately firm pressure giving the maximum sound,
while very firm pressure causes it to entirely disappear.
The intensity of the sound is also influenced by the respiration, being
usually louder on inspiration, though occasionally louder on expiration.
Change of position will also influence and modify the sounds; thus the
sitting position gives greater intensity to the sounds than when the
patient is lying down.
Diagnosis.—In some cases the diagnosis is very readily made, while in
others it is quite difficult, and in some cases impossible. The most
positive sign is the characteristic friction rub, and to the skilled and
practiced ear, the harsh rubbing or creaking sound near the ear is
readily distinguished from the blowing and more distant sound of
We would recognize it from valvular lesions by the more constant and
long-continued adventitious sounds of the latter, and also by the fact
that change of position from the sitting position to that of lying down
does not effect so marked a change in the latter as in the former disease;
also, the modified sounds, by changing the degree of pressure of the
Pleural sounds are magnified during respiration; in fact, are suspended
if the patient be requested to hold his breath; while in pericarditis the
suspension of respiration does not necessarily impair the sounds.
Prognosis.—The prognosis is favorable, so far as life is concerned, the
disease rarely terminating fatally; however, there is great danger of
more or less adhesions, that leave the heart subject to more serious
wrongs in later years. At times it assumes the chronic form.
In rare cases resolution is complete, the disease lasting but a few weeks.
Where death occurs, it is usually the result of an intense primary
disease, such as a severe croupous pneumonia, or severe chronic
nephritis, or severe valvular disease.
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Treatment.—The patient should be made acquainted with his true
condition in order that he may the more readily acquiesce in the
quietude which he will be compelled to assume to get the best results
from treatment. He should occupy the recumbent position the greater
part of the time, and should refrain from all conversation or reading
that would tend to undue excitement.
The diet should be light, one that is readily appropriated, and given in
concentrated form. Very little fluid should be allowed, no more than is
absolutely necessary, and hot drinks should be entirely prohibited.
During the acute stage, to control the fever, we use the special
sedatives. Aconite for the small frequent pulse, five drops to a half a
glass of water, of which a teaspoonful will be given every hour.
Occasionally we find excessive heart power in the early stage with a full
bounding pulse; in this case veratrum ten to thirty drops to a half a
glass of water, and a teaspoonful every one, two, or three hours.
Where there is a sense of weight and oppression, not due to effusion,
give lobelia a half dram to a half a glass of water, teaspoonful every
Bryonia.—Where there is pain of a sharp, lancinating character,
bryonia is a remedy of great merit; being an anti-rheumatic and at the
same time an agent whose specific action is upon serous membranes, it
is doubly indicated.
Asclepias combines nicely with bryonia, especially if the skin be dry and
Macrotys will be the better remedy where there is muscular soreness; a
dram to a half glass of water will give better results than the small dose.
The early Eclectics accomplished better results from a decoction of the
fresh root, but this is not readily obtained by the majority of physicians,
and we will have to depend upon the less efficient tincture.
After the more active symptoms subside, to establish secretion from the
kidneys and promote absorption of the exudate, potassium acetate, well
diluted, will be a good treatment.
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Digitalis, strychnia, and nitroglycerin must not be used too early, or we
will overstimulate and exhaust the power of the heart, and only when
the soft pulse indicates the failing power of the heart are they
permissible. Cactus and crataegus, however, may be used at any stage.
When he have the history of rheumatism, the anti-rheumatics, given
according to their indicated use, will prove beneficial. If uric acid be
present, potassium acetate, or lithiate, should be given till it disappears.
Where the patient is able to travel, change of air and climate will often
prove highly beneficial, though a very high altitude should be avoided.
Synonyms.—Sero-fibrinous Pericarditis; Hemorrhagic Pericarditis;
Purulent Pericarditis.
Etiology.—This form is frequently preceded by the acute form just
described, or, like the former, it follows or is accompanied by
rheumatism. Bright's disease is not an infrequent forerunner of it.
Tuberculosis is also a common cause, especially of the purulent and
hemorrhagic variety. Septicemia and the eruptive fevers are also
diseases that should be considered in the purulent and hemorrhagic
In children, the disease may come on so insidiously that quite a
pericardial effusion may have taken place before the physician discovers
it. In such cases there is generally a tubercular taint.
Pathology.—This variety is frequently, if not always, preceded for a
few days by plastic pericarditis, and is attended by the same anatomic
changes; namely, a smooth, swollen, and injected membrane, in the
early stage, followed soon after by a plastic exudate, usually more
pronounced than in the acute form.
The pericardial layers being covered with a sticky exudate, gives the
membrane a roughened appearance. This is soon followed, however, by
an effusion of variable character and quantity, serum largely
If the result of rheumatism, the effusion will be serous in character; but
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if caused by Bright's disease, tuberculosis, cancer, the eruptive fevers,
septicemia, or pyemia, the effusion will be of a lower grade, pus largely
predominating, or there will be a mixture of pus and blood.
The quantity varies from a few ounces to two or three pints. With the
absorption of the more fluid portion of the exudate, the lymph becomes
organized, and adhesions take place, sometimes so firmly as to almost, if
not entirely, obliterate the peri-cardial sac.
If the exudate is composed largely of pus, the myocardium presents a
roughened and eroded appearance, and, being softened by the presence
of pus, degeneration of its walls takes place, or there will be dilatation
and thinning of its walls. Endocarditis is also a frequent result.
Symptoms.—If a primary lesion, a rare case, the symptoms common to
all inflammations are present; namely, the chill, followed by fever,
accompanied by a dry tongue, arrest of the secretions, increased
temperature, and increased frequency of the pulse. There is nausea and
sometimes vomiting. Pain of a dull, aching character is felt in the
precordial region, or, if the pleura is involved, it will be of a sharp,
lancinating character, extending to the back and down the left arm.
As soon as effusion takes place, dyspnea becomes the most distressing
feature. If large in quantity, the left lung is burdened by pressure, and
the breathing is quite labored. The right ventricle is also pressed upon,
obstructing the cardio-pulmonary circulation. Although the pulse may
be full and strong during the early stage, it is now small and weak,
owing to pressure by the effused material.
When the disease is secondary, the primary lesion may so overshadow it
that it will be entirely overlooked, especially if it follow pleurisy or
pneumonia, and often the disease is not recognized till the dyspnea
becomes marked, or there is effacement of the intercostal spaces; even
then the disease has been overlooked and pronounced pleurisy.
In tubercular children, the disease may come on insidiously, the child
growing anemic; he is of a waxy or transparent color, with a gradually
increasing dyspnea, till the pericardium becomes distended with the
effused fluid.
Physical Signs.—Inspection.—The skin and mucous surfaces are pale
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and cyanotic in appearance, and the veins in the neck are usually more
distended and prominent than in health.
In the young, there will be, if much effusion, effacement, or even
bulging of the intercostal spaces.
The breathing will be labored, and the patient will have an anxious
expression peculiar to heart affections. The position, if lying, will be
dorsal, though some will experience greater relief by lying upon the left
side, thus giving greater relief to the right heart.
As the exudation increases, the upright position is assumed, with the
head and shoulders thrown forward.
In the early stage, the apical beat is increased and is quite perceptible,
but disappears with the presence of the effusion.
Palpation.—During the early stage, the apical beat is increased and felt
in the normal position, but as the exudate appears, it becomes more
feeble and is felt at a higher point and to the left, finally disappearing
with the increase of the effused material.
Oppolzer taught that the apical beat changed with the position of the
patient; thus if the beat had disappeared, changing the patient to the
left side, or bending the body forward, would cause its return. Gerhardt,
however, well says that this is not peculiar to pericarditis, as the apex
beat is changed even in health by. change of position.
If myocarditis accompanies the disease, the systole is greatly enfeebled,
and the apex beat disappears quite early. In case of hypertrophy, or
where there are old adhesions, the apex beat may be retained
throughout, notwithstanding the presence of a large quantity of effused
Percussion.—The increase in dullness depends upon the amount of
effusion, the dullness assuming a triangle, the base being dependent.
The dullness may extend, in extreme cases, from a half inch to the right
of the sternum, to the right nipple line, and as far to the left as the
axillary line, and as high as the second, or, in extreme cases, to the first
interspace to the left of the sternum.
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Should there be old pleural adhesions confining the lungs to the
anterior chest-wall, the pericardium, with its fluid, will be carried
backward, and percussion in this case would give resonance, the area of
dullness being diminished rather than increased.
Auscultation.—The friction sound, already described, is heard during
the initial stage, but disappears with the presence of the effusion, to
return again with its absorption. The heart-beat, at first strong, becomes
gradually weaker as the disease progresses, and is not due, as has
generally been regarded, to the increased distance from the chest-wall
by the intervening fluid, but to the weakened condition of the muscular
walls of the heart, due to more or less disease of the myocardium as a
complication. This view is held by Shrotter, who gives, as proof, that the
fetal heart-sounds are heard through a much larger quantity of
amniotic fluid than ever occurs in pericarditis.
Where the fluid is small in quantity, we mav hear the murmurs due to
endocarditis, when this complication exists.
Diagnosis.—This disease is often overlooked, owing to the primary
lesion; but if a careful examination is made, it can be recognized by the
characteristic friction rub in the early stage, and the triangular area of
dullness, extending in severe cases to the first interspace.
The pericardial sound is a rough, grating noise near the ear. The
endocardial sound is blowing, and distant from the ear.
We recognize it from pleurisy by the absence of the sharp, lancinating,
stablike pain characteristic of pleurisy, and also by the cessation of the
friction sound during a momentary suspension of respiration, the
friction sound continuing in pericarditis without regard to respiration;
from cardiac dilatation, by the history of rheumatism, of the former, also
septic or infectious diseases, and the presence of pain in the cardiac
region. In cardiac dilatation there will be a history of heart disease, an
absence of fever and pain, and there will be no friction sound in the
Prognosis.—The prognosis in this form must be guarded; for while
some cases are so mild as to pass unnoticed, others are so severe as to
prove fatal in a few days. In mild cases, the disease may terminate
favorably within a week or two, all evidence of inflammation
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disappearing, and the effusion of serous material be entirely absorbed
in the course of two or three weeks. When the disease is the result of
scurvy or pyemia, death may occur in forty-eight or seventy-two hours.
The condition of the heart must also be taken into consideration in the
prognosis. If the heart be in good condition—that is, if there be no
structural change—the prognosis will be favorable, but just in
proportion as degenerative changes take place' will the outcome be
If endocarditis complicate the disease, valvular lesions are almost sure to
exist, and this always renders the disease more grave, as does dilatation
of the heart.
The cause giving rise to the disease must also be taken into
consideration in making a prognosis; thus septicemia, scurvy, Bright's
disease, and the infectious fevers give rise to a more grave form than
The character of the effusion also determines to a great extent the
gravity of the ca'se. Thus, if serum alone is the product, the case may be
hopeful; but if it be purulent or hemorrhagic, the outlook will be
Treatment.—In the early stage the treatment will be the same as for
the plastic form; namely, absolute quiet, and the avoidance of
everything that would irritate or excite the patient. The indicated
sedative, and bryonia, asclepias, macrotys, or lobelia will be given, as
the case may require. Spigelia will be useful during this stage, where
there is a sharp, stabbing pain, accompanied by great oppression and
undue anxiety. As the disease progresses and the effusion becomes more
pronounced, we rely upon such remedies as give tone to the
overburdened heart and stimulate the absorbents to carry off the
accumulated fluid. Strophanthus influences the heart favorably when
given in the small dose, and at the same time excites the kidneys to
greater secretion. To a half glass of water add ten or twenty drops. of the
tincture, and give a teaspoonful every one, two, or three hours.
Apocynum.—Of the many remedies recommended for cardiac troubles,
however, I know of no remedy in the materia medica equal to that of
apocynum, especially with effusion in the pericardium. The action is
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Document Outline

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      • Treatment of Valvular Lesions.
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      • FIGURE 23.
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      • FIGURE; 24.
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