valve occurs, a typhoid state rapidly supervenes. The patient is forced
to assume the sitting position on account of the intensity of the
dyspnoea, cyanosis is sudden and extreme, and the symptoms of multiple
embolism make their appearance. The febrile symptoms are marked; the
temperature may reach 106-107° F.; the patient becomes jaundiced; and
there are frequent rigors, which, with the paroxysmal febrile attacks,
simulate the icteric form of malarial fever. The spleen becomes
enlarged and tender, the urine becomes scanty, dark-colored,
albuminous, and of high specific gravity, and in severe cases delirium
and coma occur.
Some cases of endocarditis putrida (as some German pathologists call
it) are attended with nausea, vomiting, and diarrhoea. The frequency
with which this form of endocarditis is associated with pneumonia
certainly suggests a blood-poison of great intensity. Although it is
rarely met with except in septic conditions, it may occur late in
severe forms of rheumatic and traumatic endocarditis or when there has
been pre-existing suppurative disease of the bones.
The symptoms which attend embolism from detachment of the fibrinous
efflorescences upon the valves are due to the arrest of such a plug in
an artery whose calibre is too small to admit of its passage. Beyond
the obstruction the circulation is arrested; hence results either an
infarction or necrosis of the part whose blood-supply is thus shut off.
The organ most liable to be the seat of such emboli is the spleen, and
after this the kidney and the brain. Hence the occurrence of hemiplegia
with aphasia or marked cerebral symptoms in the course of acute
endocarditis is indicative of cerebral embolism.
There are no positive subjective symptoms of interstitial endocarditis.
There may be palpitation and a sense of uneasiness, sometimes amounting
to {648} pain at the præcordial region, with irregularity in the action
of the heart, but all of these, when taken together, are not sufficient
for a diagnosis. This can be made only from changes in the heart-sounds
produced by changes in the valves and valvular orifices.
PHYSICAL SIGNS of exudative endocarditis.--Inspection.--Upon inspection
it will sometimes be noticed that the area of the cardiac impulse
exceeds the normal--that it is irregular and often tumultuous. As the
disease advances, the apex-beat and the impulse grow more indistinct,
but never to the same extent or so suddenly as in pericarditis. In
children the vessels of the neck exhibit venous stasis far more
frequently than in adults.
Palpation.--At the onset of an endocarditis the cardiac impulse is more
forceful than normal, and the heart-action is frequently irregular. In
some instances the heart thumps violently against the chest-walls. The
force of the cardiac impulse varies from day to day. The impulse is
stronger when pain is present over the præcordial space. If during the
entire course of the disease there is no decrease in the force of the
apex-beat, it may be inferred that there is no deficiency in the
muscular power of the heart. When acute endocarditis supervenes upon
long-standing valvular disease, there will be an alternate increase and
diminution in the area and force of the impulse. When the walls of the
heart become weakened by subsequent myocarditis, or when the
endocardial inflammation is itself very extensive, the force of the
apex-beat is diminished. An endocardial thrill is frequently present in
acute exudative endocarditis.
Percussion.--The area of cardiac dulness in endocarditis is normal,
unless changes at the valvular orifice retard the outflow of blood from
the lungs, and then the right-heart cavities become engorged and the
area of dulness will extend beyond the normal limits. But it is to be
remembered that the increase is always slight, except in those few
cases where the heart-cavities are both suddenly and extensively
distended with blood or masses of fibrin. Extensive myo- or endocardial
inflammation may so weaken the heart-walls that they will dilate, and
then percussion will reveal an enlargement in the area of cardiac
dulness.
Auscultation.--On auscultation a murmur or murmurs can be heard over
the various cardiac orifices. The fact that valvular disease may have
previously existed makes it important, at the first visit to a patient
who is suffering from acute articular rheumatism, chorea, Bright's
disease, etc., to carefully examine the heart. When cardiac hypertrophy
exists and valvular disease has pre-existed, it is difficult, if not
impossible, to recognize acute exudative endocarditis or to determine
the time of its advent if it exist. The most important and constant
sign of endocarditis is a systolic murmur, its greatest intensity being
over the apex; but this murmur, which is soft and blowing in character,
the so-called bellows murmur, may be either ventricular or valvular. In
all cases it is due to roughening or thickening of the endocardium. It
often changes its point of maximum intensity during the acute period of
the disease. It is developed at the onset of the disease, and when one
is on the lookout for endocarditis, this will be the first evidence of
its occurrence. And yet in some instances no murmur may be present
during the entire course of an endocarditis.
A mitral murmur alone occurs in about 50 per cent. of cases of
rheumatic endocarditis. It is usually developed early, and before it
becomes distinct it is preceded by prolongation of the first sound.
This is a transition sound between a normal heart-sound and a murmur.
It is a feeble, wavering sound, extending over the slight interval
which normally exists between the first and second sounds.
Other changes that are not murmurs, but which frequently precede them,
are loud, ringing normal sounds, muffled first sound, feeble first and
{649} intensified second sound, doubling of the first sound, roughness
of the first sound, and a humming over the right heart.
Complete absence of the heart-sounds is a rare but possible antecedent
of an endocardial murmur. A mitral murmur in acute endocarditis is
usually audible over a limited area. It is the exception to hear it
both in front and at the back. Very frequently it is heard most
distinctly over the stomach.
When the blood becomes dammed back into the lungs, there is an extra
strain upon the pulmonary semi-lunar valves, and then the second sound
will be accentuated over these valves on account of the sharp shock
which they sustain during diastole. With this accentuation of the
second sound over the pulmonary orifice, the first pulmonic sound may
be feeble or absent. A subdued or absent first sound shows tension of
the artery.
Reduplication of the second sound in a mitral endocarditis is probably
due to the difference in time occupied by the ventricles in emptying
themselves. A tricuspid murmur occurs in 50 per cent. of the cases of
acute mitral endocarditis--a pulmonic in about one-third of the cases.
They are superficial and scratchy in character, and indicate a relaxed
condition of the vessels and a thin condition of the blood. These
murmurs are never permanent. Mitral endocarditis is accompanied by
aortic murmurs in about 16 per cent. of cases. Acute mitral
endocarditis occurring with chorea is as apt to become interstitial as
when it is of rheumatic origin.
Aortic murmurs are usually soft and blowing, but they may be musical,
whistling, or twangy. In aortic endocarditis the second sound is
usually lost over the carotids. Incompetency of the aortic valves is
met with only in the interstitial form of endocarditis.
In about 12 per cent. of the cases of exudative endocarditis arising
from rheumatism a regurgitant murmur will be heard at the tricuspid
orifice, but such murmurs are not the result of endocarditis of the
right heart.
Tricuspid murmurs are present in 50 per cent. of all cases of recent
mitral murmurs, in about 40 per cent. of recent aortic murmurs, and in
about one-fourth of mitro-aortic murmurs. Such tricuspid murmurs are
due to an increase in the slight normal insufficiency existing at the
tricuspid orifice. They are of short duration, and are heard over the
body of the heart over the right ventricle. Sometimes they are
vibrating in character.
In children aortic endocarditis is rare; at this period obstruction at
and regurgitation through the mitral orifice commonly occur together.
The physical signs of interstitial endocarditis are such as are due to
those changes in the valves which will be considered under the head of
Cardiac Murmurs, and their Relations to Valvular Diseases.
DIFFERENTIAL DIAGNOSIS.--Acute exudative endocarditis may be mistaken
for pericarditis, and its murmur may be mistaken for the murmur
produced by aortitis and for those that develop during the course of
fevers.
The friction sounds of pericarditis are superficial in character, and
are limited to the præcordial space, while the murmurs of endocarditis
are distant, and each murmur will have its area of diffusion beyond the
præcordial space. A pericardial sound is distinctly a friction,
creaking, or rubbing sound; it has a to-and-fro character, while the
murmur of endocarditis is soft and blowing.
Endocardial murmurs accompany the heart-sounds, while pericardial
friction sounds are not always rhythmical with the heart-sounds.
The intensity of a pericardial friction is increased when the patient
bends forward at the end of a full inspiration or when the stethoscope
is pressed firmly over the præcordial region; and in the last-named
case it becomes distinctly grazing and rubbing in character. In
endocarditis these methods produce no difference in either the
intensity or the character of the murmur. There is an endocardial
thrill in endocarditis not present in pericarditis.
{650} As soon as effusion occurs in pericarditis the absence of pain,
the alteration in the character of the pulse, the great increase in
dulness, and the disappearance of the adventitious sounds will decide
the diagnosis.
Aortitis has most of the symptoms of endocarditis, but in addition the
pulse is more rapid, the respirations are more hurried, and pain which
shoots down the spine and is increased by motion is present in the
præcordial region. Not infrequently aortitis is accompanied by
cutaneous hyperæsthesia.
Acute inflammation of the aorta is exceedingly rare, and in the few
cases observed has been complicated by very grave diseases. Indeed,
Powell, Lebert, and Rindfleisch doubt its existence.
In the _Medico-Chirurgical Transactions_ (vol. xlvii. p. 129) Moore
gives a case where rigors, fever, intense and painful throbbing of the
aorta, and embolic infarction of distant organs occurred, with symptoms
so resembling those of endocarditis that few would venture to favor a
diagnosis of aortitis during life.
The functional cardiac murmurs which occur in fevers are usually heard
only at the base of the heart, while those of endocarditis are most
frequent and distinct at the apex. There are no symptoms of obstruction
present with febrile murmurs, while they are frequently present in
endocarditis.
It is often difficult to determine whether an endocardial murmur is of
old or recent origin: if during an attack of acute rheumatism an
endocardial murmur is developed under daily examination, it is a
certain index of acute exudative endocarditis. If a murmur exists at
the first examination which is systolic, soft, and blowing in
character, and not accompanied by the evidences of cardiac hypertrophy,
there is good reason to believe that it is produced by an acute
endocardial inflammation.
If, on the other hand, the murmur is rough in quality, diastolic, and
cardiac hypertrophy exists, it cannot be regarded as a sign of acute
endocarditis.
The rules for distinguishing murmurs due to interstitial endocarditis
from functional murmurs will be given under the head of Cardiac
Murmurs.
PROGNOSIS.--Exudative endocarditis is rarely a direct cause of death,
but it seldom results in complete recovery. Acute mitral endocarditis
terminates in permanent valvular disease in over 25 per cent. of the
cases. The elements that will render the prognosis immediately
unfavorable in any case are the symptoms of embolism or of metastasis.
Sudden splenic enlargement, with tenderness over its site, albuminuria
or hemiplegia, when accompanied by the physical signs of acute
insufficiency or perforation of a valve with cyanosis, dyspnoea, and
disturbance of the heart-rhythm, will render the prognosis exceedingly
unfavorable. All these symptoms are diagnostic of acute ulcerative
endocarditis, and therefore when the signs of endocarditis appear
during the course of pyæmia, diphtheria, or other septic condition, the
liability to these conditions must be considered.
When even exudative endocarditis is accompanied or followed by typhoid
symptoms its prognosis is unfavorable. In children bronchial
complications, catarrhal pneumonia, and intercurrent diarrhoea may lead
to a fatal issue. Death may result from acute insufficiency of the
heart or from complications.
The prognosis in interstitial endocarditis will depend upon the seat
and extent of the valvular lesions which it produces. It will be more
fully considered under the head of Valvular Diseases.
In cardiac aneurism death may result from rupture of the aneurismal
sac, from apoplexy, or from secondary diseases in other organs.
TREATMENT.--Acute exudative endocarditis is rarely, if ever,
idiopathic. It is so constantly associated with certain infectious
diseases, and especially with acute articular rheumatism, that its
treatment must be determined by the condition under which it occurs.
{651} In every case the patient must have absolute rest in bed in a
room whose temperature should never be below 70° or 75° F. The
præcordial region should be covered with flannel, and care exercised
not to expose the surface when physical examination of the heart is
made. Some authorities claim that an ice-bag applied to the præcordial
space during the active period of an acute endocarditis will arrest and
limit the inflammatory process. My own experience does not sustain the
results claimed for this plan of treatment.
In rheumatic endocarditis antirheumatic remedies are indicated, the
joints must be kept absolutely at rest, and such local treatment should
be resorted to as will relieve pain and give the greatest comfort to
the patient.
If the blood is kept alkaline, as indicated by the urine, the liability
to endocarditis is diminished.
To ensure rest small doses of opium are often required; but opium
cannot be administered as freely in endocarditis as in pericarditis.
During the whole course of acute endocarditis the strength of the
patient must be maintained by the judicious use of concentrated
nutriment, with some preparation of iron.
When endocarditis occurs with septic diseases and is attended by
typhoid symptoms, or when it assumes the ulcerative form, alcoholic
stimulants, quinine, and iron must be freely administered.
In endocarditis complicating Bright's disease the rapid elimination of
the urea must be established. The severe pain over the præcordial space
may be relieved in many subjects by the application of a few leeches to
the region.
Experience proved that the employment of mercury (internally) and blue
ointment (externally) to lessen the plasticity of the blood, and the
internal use of iodide of potassium (for the absorption of fibrinous
exudation), were harmful, before it was demonstrated that the theory on
which their use was based had no foundation.
Cardiac Murmurs, and their Relations to Valvular Diseases of the Heart.
DEFINITION.--A cardiac murmur is an adventitious or abnormal sound
produced within the heart or blood-vessels, either by obstruction to
the blood-current, an abnormal direction of the blood-current, or by a
change in the blood-constituents.
HISTORY.--The systematic study of cardiac murmurs and valvular diseases
dates from the discovery of auscultation by Laennec. Previous to his
discovery there are a few recorded cases where observers during the
seventeenth and eighteenth centuries described forms of valvular
diseases. One of the first to describe a valvular lesion of the heart
was Vieussens in 1716. At the close of the seventeenth century Willis
and Riverius published cases of valvular disease. In all these
instances it was the aortic valves that were diseased, and the
discovery of their condition was undoubtedly due to the peculiarity of
the radial pulse which is so marked and striking in aortic disease.
In Friedreich's article in Virchow's _Handbuch_, "Krankheiten des
Herzens," Meckel's essay of 1756 is given as the first paper on
endocardial disease.
John Hunter[2] in 1794 gives a lengthened account of a most interesting
case of aortic valvular disease. Senac[3] gives an account of disease
of the auriculo-ventricular valves; and Allan Burns, whose work was
published in 1809, describes aortic regurgitation and obstruction, and
supposes that "a reflux current can produce a hissing noise, something
like what is described as audible palpitation in some diseases of the
heart."[4]
[Footnote 2: _Treatise on the Blood_, etc.]
[Footnote 3: _Treatise on the Heart_, 1783.]
[Footnote 4: _Obs. on some of the most Frequent and Important Dis. of
the Heart_, Allan Burns, Edinburgh, 1809.]
{652} The subject of vegetations upon the valves was very fully
considered by Corvisart in 1806. Corvisart was the first to mention the
importance of what is now called the purring thrill. He stated that "it
probably came from a difficulty experienced by the blood in going
through an orifice disproportionate to the amount of fluid." Laennec
regarded murmurs or bruits as the result of spasmodic contraction of
the heart or arteries. Corrigan in 1829 defined murmurs as "the result
of the development of currents and the intrinsic collision of the
moving liquid."
In 1842, Gendrin gave cardiac murmurs as bruits de frottement
endocardiaques, and established the friction theory. He also called
attention to the fact that alteration in the constituents of the blood
will produce murmurs which are heard in arteries of medium calibre.
Bouillaud describes a murmur as an exaggeration of the normal bruit
caused by blood-friction against the segments of the heart, and he says
that according to the size or condition of the orifice the murmur will
be rasping, sawing, or blowing.
Chauveau states that bruit de souffle is produced by the vibration of a
nei e fluide, always formed when blood rushes through a part of the
circulatory system actually or relatively dilated.
This nei e fluide has its best development in anæmia, when it is termed
the bruit du diable, for the jugular veins do not collapse and the
volume of blood in anæmia is diminished. Chauveau's theory is
applicable to anæmic murmurs, but not to all cardiac murmurs.
Hope states that "valve murmurs are produced by collision of the
blood-particles against one another, or that either the liquid alone or
the liquids and solids conjointly may develop murmurs."
There are many who have advocated the tension theory--viz. that an
increase in tension and force can so exaggerate a normal sound as to
produce a murmur. This theory has no clinical foundation. Often,
however, valve-lesions may exist, and the blood-current be so weak, the
propulsive force so feeble, that no murmurs are audible.
Some observers are of the opinion that spasm of the papillary muscles
and chordæ tendineæ and weakening of these structures through fatty
degeneration can cause temporary murmurs.
The conditions that determine the character of a cardiac murmur, its
pitch, quality, and intensity, are subject to the same physical laws as
govern the formation and quality of sound elsewhere. They are the
rapidity and force of the moving body, the obstructions which it meets,
and the physical properties of the media of conveyance. The same
vibration that produces a murmur may produce an endocardial thrill,
called sometimes purring thrill.
Far more important, however, than loudness, pitch, or quality of a
murmur are its rhythm, its point of maximum intensity, and the area of
its diffusion, all of which can best be considered in connection with
the physical signs of each valvular lesion.
During a cardiac diastole the heart-cavities are all filling; just
before the commencement of the cardiac systole the blood is forced from
the lungs and the cavæ through the auricles into the ventricles, while
the mitral and tricuspid valves are pressed against the walls of the
ventricles, and no obstruction is offered to the blood-current. If, as
the result of disease, any obstruction exists at either one of the
auriculo-ventricular orifices, the blood as it passes through the
opening will impinge on such obstruction and cause a presystolic
murmur.
During a cardiac systole the filled ventricles contract; blood is
thrown through the semi-lunar openings, the flaps of whose valves are
pressed against the walls of the vessels, so that no obstruction is
offered to the outgoing {653} current. At the same instant the
auriculo-ventricular valves close their orifices, so that blood may not
be forced back into the auricles.
If, as a result of disease, the semi-lunar valves should obstruct the
outgoing current, or the mitral or tricuspid valves should not wholly
close the auriculo-ventricular orifices, then in the one case the
direct blood-current, as it passes over the obstruction at the
semi-lunar orifices, would produce a systolic murmur, and in the other
the backward current through the abnormal opening at the
auriculo-ventricular orifice would also produce a systolic murmur.
Again, if the lungs and the aortic system (when filled at the systole)
have, back of them, a semi-lunar valve that does not completely close
that end of the circuit, the blood will regurgitate into the ventricles
during the period of cardiac rest, so that semi-lunar incompetence will
cause a diastolic murmur.
ENDOCARDIAL MURMURS.
Rhythm. Situation. Orifice. Nature.
Systolic 1 Basic, Aortic, Obstructive.
" 2 " Pulmonary, "
" 3 Apical, Mitral, Regurgitant.
" 4 " Tricuspid, "
Diastolic 1 Basic, Aortic, "
Presystolic 1 Apical, Mitral, Obstructive.[5]
[Footnote 5: Pulmonary regurgitant murmur (diastolic) and tricuspid
obstructive murmur (presystolic) are so rarely met with that,
clinically, they may be disregarded.]
The following is the order of relative frequency of cardiac murmurs: 1.
Mitral regurgitation; 2. Aortic obstruction; 3. Aortic regurgitation;
4. Mitral obstruction; 5. Tricuspid regurgitation; 6. Tricuspid
obstruction; 7. Pulmonary obstruction; 8. Pulmonary regurgitation. The
most frequent combinations of murmurs are--1. Aortic obstruction and
regurgitation; 2. Mitral obstruction and regurgitation; 3. Mitral
obstruction and tricuspid regurgitation; 4. Aortic obstruction and
mitral regurgitation; 5. Double valvular disease at aortic and mitral
orifices (four murmurs).
It is often difficult, after having satisfied ourselves of its
existence, to determine the rhythm of an endocardial murmur. To resolve
this difficulty it is necessary to determine which is the first and
which the second sound of the heart.
The first sound of the heart is synchronous with the carotid pulse, the
radial pulse, and the apex-beat. It may be wholly replaced by a
systolic murmur, but the second sound is always heard following the
apex-beat, for the pulmonic and the aortic valves are never diseased at
the same time.
Having determined the existence of a murmur, its rhythm, pitch,
intensity, and quality, we next determine its point of maximum
intensity. These points of maximum intensity for murmurs at the four
valvular orifices of the heart may be briefly summarized as follows:
Murmurs arising at the mitral valve are loudest at the apex of the
heart or immediately above it; tricuspid murmurs are loudest over the
lower part of the sternum; pulmonary murmurs, in the second left
intercostal space close to the sternum; and aortic murmurs, in the
second right intercostal space at the edge of the sternum and over the
whole length of the body of that bone.