When cardiac involvement occurs it may be evidenced by an increased rapidity
and an irregularity of heart action, dyspnoea, augmented restlessness and fever.
Cardiac pain is rare; palpitation is frequent. The febrile movement is not
markedâ€” 101Â° to 102Â° F. (38.4Â° to 38.9Â° C).
The physical signs are not characteristic but it is usually upon these that the
diagnosis is based. In the earlier attacks the size of the heart is not increased,
the apex impulse being usually in the normal site (fifth left interspace,
3 J inches from the mid-sternal line), murmurs due to the valvular lesions
(see p. 563) may be present but do not in every case signify an involvement
of the endocardium; a ventriculo-systolic bruit at the apex often being the
result of a myocarditis; basic murmurs of functional character should not be
mistaken for true organic sounds.
An increasing roughness in the first sound at the apex changing to
a distinct murmur may be an evidence of endocarditis, and accentuation and
reduplication of the pulmonic second sound are not infrequent. Endocar-
dial murmurs are often inconstant.
The symptoms of malignant endocarditis are also indefinite but in most in-
stances the irregular fever, chills and sweats of sepsis, cerebral symptoms and
prostration are present. Particularly should we suspect this condition when
these symptoms appear with pneumonia, in the puerperium, etc., and the
heart should be carefully examined for physical signs. Symptoms of embo-
lism throw much light upon the diagnosis; with cerebral embolism paralyses,
delirium or coma may be observed; increase in the size of the spleen with
sudden pain referred to this organ, pain in the lumbar region with bloody
urine, the occurrence of metastatic abscesses, impaired sight from retinal
embolism, are characteristic manifestations. The temperature may be
remittent or continuous, fever is, however, a constant symptom; haemorrhagic
and erythematous rashes are not rare. Cardiac symptoms such as dyspnoea,
palpitation and opression are inconstant, but the pulse and respiration are
increased in rate. Jaundice may be present, and albuminuria with casts is
the rule. Clinically the affection may be considered as occurring in three types:
a. The septic or pycemic type which is usually associated with wounds,
puerperal or other sepsis, and gonorrhoeal infection. Here the symptoms
are characteristic of septicaemia, and the chills, sweats and irregular fever may
whoUy mask any cardiac manifestations unless embolism occurs. The tem-
ACUTE ENDOCARDITIS. 559
perature may resemble that of quotidian or double tertian malaria. The
leucocytes are increased and pathogenic micro-organisms may be cultivated
from the blood.
b. The typhoid type is characterized by a gradual onset, a temperature
curve resembling that of enteric fever, sweats, a rash not unlike that of typhoid,
prostration, drowsiness, tympanites and abdominal tenderness, diarrhoea,
the typhoid tongue and often no cardiac symptoms. This is the most common
c. The cerebral type is evidenced by delirium or coma and other symptoms
resembling those of a basilar or cerebrospinal meningitis.
The physical signs are atypical. Murmurs may or may not exist and when
detected may be inconstant and difl&cult to locate and time with accuracy;
co-existent pericarditis and primary chronic endocarditis may still further
The diagnosis is often difficult; in all fevers of septic type daily and most
careful examination of the heart should be .performed. The occm-rence of
embolism renders the diagnosis much more simple. From enteric fever
the condition may be separated by its less enlarged and more tender spleen,
by the presence of leucocytosis and by the absence of the Widal reaction;
the writer recollects a case seen several years ago which came to autopsy
with a diagnosis of enteric fever in which typical valvular vegetations were
found and in which the Widal reaction was negative. It must not be forgotten
that infarction may rarely occur in enteric fever. Malaria may be excluded
by blood examination. Cultural blood tests in endocarditis usually reveal
the presence of pathogenic micro-organisms.
The prognosis in simple acute endocarditis is good as to recovery but seldom
is the heart left undamaged; rarely, however, this may occur. The fact that
the murmur has disappeared is by no means an assurance that the valves are
intact and it is not to be forgotten that successive attacks are not infrequent.
In malignant myocarditis the outcome is invariably fatal although the
course of the disease may be prolonged for months; this may take place when
the infection is superadded to a chronic valvular defect; the symptoms are a
persistent temperature with progressive emaciation and weakness, until at
the last embolic manifestations may occur. The usual case terminates within
one month to two weeks. One case fatal in two days has been reported.
Treatment. 0/ acute simple endocarditis. Unfortunately we possess no
therapeutic measure whereby we can cause a return of the diseased valve to
its normal condition, consequently we should endeavor to prevent in so far
as possible the occurrence of the endocardial lesion. Rheumatism, being the
most frequent cause, we should advise all individuals of rheumatic tendency
to avoid exposrure, to wear proper clothing and to maintain as high a standard
of bodily nutrition as possible. Rheumatism being present, while it is by no
560 DISEASES OF THE HEART AND BLOOD-VESSELS.
means certain that in the salicylates we have a means of preventing the inci-
dence of endocardial inflammation, it should receive early and thorough
treatment by the salicylates and alkalies (see p. 108). Where cardiac involve-
ment is present or there is any likelihood that it will occur, absolute rest in
bed should be insisted upon; it is as important to keep an inflamed valve
as nearly at rest as possible as it is to immobilize an inflamed joint. The
confinement to bed should be prolonged for several months if necessary.
Blisters over the heart are of doubtful value but if the action of the organ
is too^rapid or violent our best means of inducing quiet is by the application
of the Leiter coil or the ice bag, preferably the former as it is more comfort-
ably borne by the patient. If the circulation becomes depressed hot com-
presses should be substituted for the cold. The drug of most use as a heart
tonic and which should be administered as soon as signs of weakness are
evident, is strychnine. It may be given in doses of -g^^ to Jq of a grain
(o.ooi to 0.003) 3 times a day. Aconite has been recommended as useful
in conditions of over-action but is depressant and altogether less advantageous
than the application of cold. Dyspnoea may be reheved by the administra-
tion of opium or morphine which act as heart tonics in addition. Pain is
not a common symptom but may be combated if necessary by these drugs
also, the coal tar analgesics possessing too depressing an action. Fever
seldom requires special treatment but may be relieved by cool sponging.
Restlessness and sleeplessness may be controlled by the bromides or sulphon-
The administration of the iodides is advocated in the hope that these may
influence the tendency to the production of permanent connective tissue
changes in the valves and it is possible that they may prove beneficial. Pref-
erably we should give a drachm (4.0) of the syrup of hydriodic acid three times
daily, one-half an hour before meals in a wine glass of water, but potassium
iodide may also be employed in doses of 10 grains (0.66) three times a day. This
treatment should be continued for a long time if it is to accomplish any result.
Throughout the disease the bowels and kidneys should be kept active and
much benefit will accrue if the action of the liver is stimulated from time to
time by a few fractional doses of calomel followed by a saline.
The diet should be nourishing, easily digestible and above all such as not to
cause tympanitic distention of the stomach and intestines which will greatly
interfere with the heart's action. Broths, meat juices, eggs, milk and the
like may be allowed. Frequent small meals are much to be preferred to fewer
and larger ones.
The treatment of malignant endocarditis consists first in the removal of
the cause by surgical means when this is apparent and operation is practicable.
The septic uterus should be cleaned out, foci of bone necrosis excised, etc.;
rheumatism, if the causal factor, should receive proper treatment; metas-
CHRONIC ENDOCARDITIS. 56 1
tatic abscesses when they occur shoiild be opened and drained if in such
location as to render this possible. The general management of this type of
acute endocarditis is in other respects similar to that of the simple form; anti-
streptococcus serum shoiild be administered, for, while the results up to this
time obtained by the employment of this agent have not been markedly
encouraging, in some few instances benefit has been conferred, and at any
rate no harm can be done. The ordinary daily dose is about 5 drachms (20.0)
given hypodermatically. When the infection is the result of the presence of
pneumococci, gonococci or any pathogenic bacteria save those of suppuration,
it is not to be expected that this treatment wiU do good.
Beer yeast has accomplished encouraging results in septic infections of
' various types and its use has been suggested in septic endocarditis. It may
be given by mouth, rectum or under the skin. The antiseptic action of the
colloidal silver salts should benefit the septic condition obtaining in this affec-
tion, consequently we may employ generous inunctions of Crede's ointment.
Synonym. Chronic Valvular Disease of the Heart.
Definition. A permanent sclerotic change in the cardiac valves character-
ized by thickening, shrinkage, adhesions and calcification of the flaps and
their chordae tendinese and resulting in obstruction or insufiSciency of the cardiac
.Etiology. Chronic endocarditis is rarely a primary affection; in most
instances the condition is secondary to acute endocarditis of rheumatic or
other origin. Other causes are chronic alcoholism, gout, syphilis, plumbism,
prolonged muscular over-exertion and rheumatism and other acute infections.
The sclerotic change which occurs in all connective tissue structures as a
result of senility renders old age a predisposing factor. Men are more prone
to the disease than women.
Pathology. The initial change is a thickening of the valve which begins
at the edges of the cusps and is due to an increase in the normal connective
tissue at this situation; while this change is of slight degree the function of
the valve may be undisturbed but the process continues to advance until the
entire cusp is thickened and stiffened. Later the newly produced tissue
shrinks which causes the valve flap to retract and to become partly immo-
bilized. This shrinkage may involve the chordae tendineae as well as the
valve proper in which case the retraction is more marked and perfect closure of
the valve becomes impossible. Adhesions between the cusps now form, still
further interfering with their action; particularly in the mitral valve is this
likely to be a serious condit ion since it may reduce the mitral opening to hardly
more than a slit. Further changes are the deposition of lime salts which
may result in stiffening of the valves or in the formation of hard nodules pro-
562 DISEASES OF THE HEART AND BLOOD-VESSELS.
jecting from their margins; in extreme degrees the fibrous ring of the valve
becomes infiltrated with the calcareous substance and as a consequence is
rigid and almost bony. Fatty degeneration is evidenced by yellow areas
upon the valvular surfaces or margins. Fibrous changes may involve the
apices of the papillary muscles and there may be sclerotic patches in the
endocardial lining of the walls of the heart. With the changes of chronic
endocarditis the vegetations of an acute process may also be present.
Congenital valvular defects may be due to malformations or to inflamma-
tory^processes occurring in the foetus. Such lesions most frequently affect
the right side of the heart; rarely they may be observed in the left side.
The different valves are affected in the following order of frequency: (i)
The mitral; (2) the aortic; (3) the tricuspid; (4) the pulmonary. Lesions of
more than one valve often co-exist.
This is the most common valvular lesion. The incompetent valve allows
the blood to regurgitate from the left ventricle into the left auricle during the
heart's systole; the endeavor of the auricle to prevent this back flow results in
hypertrophy, and ultimately in dilatation and the backward rush of blood
to the lungs results in congestion of these organs. Further changes now
take place in the right side of the heart, hypertrophy of the right ventricle is
induced by its effort to overcome the pulmonary congestion; this it is able
to do for a time and during this period the right ventricle is able to pump
an excessive quantity of blood through the lungs to the left ventricle and
compensation is furthered by a hypertrophy of the walls of this structure which
now ensues. At length, however, the strain becomes too great for the right
ventricle, it dilates, producing a relative insuflSciency of the tricuspid valve,
regurgitation into the right auricle follows with further backing up of the blood
current into the great veins of the neck and finally a general systemic venous
congestion takes place.
By the term "relative insufficiency" employed above is meant a condition
of valvular incompetency, due to no pathological lesion of the valve, but
occurring as the result of the dilatation of a heart cavity and consequently
of its orificies which the normal-sized valves become of insufficient size to
close. This form of leakage is observed most often in the auriculo-ventric-
ular valves and may not be detected during life since physical signs may be
-Etiology. Mitral insufficiency is the result of changes in the cusps of the
valve, whereby they are retracted and shrunken, with associated sclerosis
of the chordae tendineae or of dilatation of the ventricular wall in which latter
case the insufficiency is of the relative type. The initial cause of the valvular
incompetency is an acute or chronic endocarditis.
Symptoms. While compensation is suflacient to overcome the effects
of the regurgitation of blood through the leaking valve these are often wholly-
absent, unless there is a sudden ruptvure of a cusp due to ulceration. While
compensation is still good the patient may complain of slight palpitation
and dyspnoea on exertion and facial congestion and clubbing of the fingers
may be present. The initial symptoms of failing compensation are increasing
dyspnoea and accompanying palpitation with irregularity. Symptoms due
to the congestion are now present; these are cough with mucoid and perhaps
bloody sputum; attacks of bronchitis are frequent, to which the pulmonary
engorgement predisposes. Congestion of the alimentary tract results in
digestive disorders with nausea and perhaps vomiting, congestion of the
liver causes enlargement and sometimes jaundice, tenderness, pulsation, and
secondary increase in the size of the spleen; to congestion of the kidneys is
due albuminuria, with hyaline casts and in some instances red blood cells; the
urine is usually diminished in quantity. (Edema, usually first involving the feet
and ankles, now appears and spreads to the subcutaneous tissue of other parts
of the body and into the serous cavities, especially the peritonaeum and pleura.
Physical Signs. Inspection reveals an apex impulse displaced downward
and to the left, it is usually more forcible than under normal conditions and
if dilatation is in excess of hypertrophy it is diffuse and undulatory . In emaciated
and young subjects the precordium may bulge and an impulse due to the
systole of the right ventricle may be visible below the ribs in the left para-
sternal line; pulsation in the veins of the neck may be present. â€¢
Palpation confirms the signs disclosed by inspection; the apical impulse
is increased in force; a ventriculo-systolic thrill may be detected at the apex
in very rare instances.
Percussion reveals an area of cardiac dulness increased to the left, and
when the right ventricle is enlarged, beyond the right border of the sternum.
Auscultation. The characteristic murmur of mitral insufficiency is a
ventriculo-systolic murmur, soft and blowing, and heard with greatest intensity
at the apex; it is transmitted toward the axilla and often is audible in this
At xiphoid cartilage
At xiphoid cartilage
At 2d right cartilage (aortic area)
At 2d left Interspace (pul-
At aortic area
At pulmonic area
Table of heart murmurs giving the time at which the murmur occurs, the place at which
it is heard with maximum intensity and the lesion causing the murmur.
564 DISEASES OF THE HEART AND BLOOD-VESSELS.
situation and posteriorly at the level of the apex and between the scapula
and the vertebral column; when very loud it may be heard over the entire
chest; it may wholly or partly obliterate the first sound at the apex. If com-
pensation has failed and dilatation has taken place the murmur may disappear
and be replaced by atypical valvular sounds. It may not be present in all
cases of mitral insuflEiciency but it may be rendered audible, in many instances
where it is apparently absent, by muscular exertion. A ventriculo-systolic
thrilj is very rare.
An important sign is an accentuation of the pulmonic second sound heard in
the second left space close to the sternum; this is due to the increased tension
in the pulmonary artery. If there is marked left ventricular hypertrophy
the aortic second sound will also be increased in intensity.
The pulse is practically normal in the stage of full compensation; upon
the onset of failure of compensation it becomes irregular in force and fre-
quency; the irregularity may continue after the re-establishment of com-
The diagnosis. A ventriculo-systolic murmur, loudest at the apex, and
transmitted into the axilla, accompanied by other signs of cardiac dilata-
tion and hypertrophy and an accentuated pulmonic second sound, is charac-
teristic of mitral insufl&ciency; unfortunately there are murmurs similar in
character and transmission which are of doubtful origin but are certainly
not the result of valvular defect; these may be functional or are caused by some
little understood ventricular condition. They are not associated with dila-
tation or hypertrophy or an increased pulmonic second sound. The ventriculo-
systolic murmur of aortic obstruction may be loudest at the apex but is not
transmitted to the left nor accompanied by an accentuated pulmonic second
sound. The ventriculo-systohc murmur of tricuspid insufl&ciency is heard
with greatest intensity at the xiphoid cartilage. An associated rumbling
auriciilo-systolic murmur of mitral obstruction is more likely to be present
in true than in relative insufl&ciency.
Obstruction of the mitral orifice is in almost if not quite all instances accom-
panied by mitral insufl&ciency. Obstruction to the free passage of blood
through the valve is the result of thickening and shrinkage of the mitral ring,
of the cusps and of their chordae tendineae. The blood prevented from
freely passing into the left ventricle distends the left auricle, which becomes
hypertrophied, and is backed into the pulmonary circulation, the right ventricle
and finally the general venous circulation. Hypertrophy of the left ventricle
is conspicuously absent. Compensation may prevent the appearance of
symptoms for a long period of time but ultimately relative tricuspid insuffi-
MITRAL OBSTRUCTION. 565
ciency and systemic congestion occur. In the milder degrees of mitral obstruc-
tion the orifice may allow the passage of a finger while in the more extreme
instances it may be almost wholly obliterated or reduced to a mere slit â€” the
button-hole stenosis of Corrigan. In the shghtest grades of obstruction where
the edges of the flaps are adherent to one another the orifice is funnel-shaped.
The chordae tendineae may be so shrunken that the papillary muscles seem
to be inserted directly into the flaps. The heart is seldom more than slightly
enlarged, the increase in size affecting chiefly the left auricle and right ventricle.
.etiology. Mitral obstruction is more commonly seen in young persons,
especially females. The condition may rarely be congenital but is usually
the result of an acute or chronic endocarditis. Certain apparently idio-
pathic instances may be the result of whooping cough or of some other acute
Symptoms. While compensation is present these are absent; after it has
failed they are practically identical with those of mitral insufficiency.
Physical Signs. The lesion may exist for a long time without physical
signs, the typical murmur of this condition being a notoriously inconstant one.
Upon inspection the apex impulse, left ventricular hypertrophy being absent,
is seldom found displaced. If hypertrophy of the right ventricle is present
the apex beat may be slightly to the left of and below its normal position and
pulsation may be noticed just below the ensiform cartilage. The hypertro-
phied left auricle may produce an impulse, auriculo-systolic in time, in the
second left interspace close to the sternum. After the failure of compen-
sation a jugular pulsation may be visible due to a relative tricuspid insufifi-
ciency, and with this, hepatic pulsation may be observed. Bulging of the lower
part of the sternum and of the fifth and sixth left costal cartilages, due to en-
largement of the right ventricle, may occur in poorly nourished children.
Palpation reveals the absence of increased force in the apex impulse, and
if compensation is disturbed, this may be weaker than normal, a palpable
impidse may be present just below the ensiform cartilage and to its left as a
result of right ventricular hypertrophy. A very typical sign is a distinct
auriculo-systolic thrill which is often to be felt at the apex or just to the inside
of this point. It is localized, rough in quality and often stops, with a sudden
shock, with the occurrence of the apical impulse. This thrill is not constant
but is pathognomonic of mitral obstruction.
Percussion shows an enlargement of the area of cardiac dulness toward
the right due to increase in the size of the right ventricle and to the left as a
result of the hypertrophy of the left auricle. The cardiac enlargement
is seldom very marked.
Auscultation. The characteristic murmur of simple mitral obstruction (see
p. 563) is an auriculo-systolic murmur, usually rather sharply localized at
the cardiac apex and slightly to its inner side; rarely it may be transmitted
566 DISEASES OF THE HEART AND BLOOD-VESSELS.
upward or heard posteriorly. In quality it is rumbling, rough, or purring,
and its loudness increases until it terminates suddenly with the apical first
sound; it is synchronous with the thrill spoken of above. The pulmonic second
sound is accentuated as a result of the h^'pertrophy of the right ventricle; no
left ventricular hypertrophy being present, the aortic second sound is not inten-
sified but there maybe duplication of the second sound at the base due to a syn-
chronous closing of the pulmonic and aortic valves.
The pulse in extreme mitral obstruction is characteristically small; in the
slight^er grades of the lesion it may be unchanged. With the onset of failing
compensation the apical murmiir and thrill may disappear but the forcible
first sound may persist. The heart action becomes irregular and the gallop
rhythm may occur; there may be more apex beats than palpable radial pulsa-
tions, the so-called pulsus bigeminus, here the sphygmographic tracing may
show a small ascent between two higher ones.
The diagnosis of uncomplicated mitral obstruction, with the character-
istic auriculo-systolic thrill and rumbling murmur which stops abruptly
with the impact of the apex against the chest wall, and with an accen-