the more serious cases of heart disease which we meet with in older
subjects--excluding of course chronic valvular disease originating
remotely in endocarditis. But I ought to repeat here what I have
already mentioned, that syphilis as a cause of cardio-vascular
lesions is very often associated with other morbific influences,
particularly strain and alcohol. Of its position as the principal
cause of grave disease of the valves as distinguished from the walls
of the heart, originating in middle life, there can be no question.
No fewer than nine out of 28 cases, of which I have private notes,
were the subjects of double aortic disease; practically all the
others had a loud ringing second sound over the aorta, significant
of degeneration; pain of anginal type in half the cases was the
prominent complaint; and two-thirds of the subjects had sclerosis
of the radial artery. When we consider that syphilis does also
affect the myocardium primarily; that fibroid disease, chronic
aneurysm and fatty degeneration of the heart are all traceable to
specific disease of the coronaries in many instances; and, finally,
that many of the subjects of syphilitic cardio-vascular disease
have perished before 40, the magnitude of this cause can be fully
realised. I believe that the profession in general have not yet
woke up, if I may say so, to the gravity of this subject. How
seldom we inquire for a history of specific disease in patients
coming to us with cardiac disease in middle life! To no one, as
far as my reading goes, are we so much indebted for the truth on
this subject as to my friend and colleague Dr. Mott. Thirteen
years ago he published a paper on 21 cases of sudden death from
cardio-vascular disease, and in nine of these there was a history of
either actual or probable syphilis. What was of greater interest,
however, at that early date, he drew attention to the association
of syphilitic cardio-vascular lesions with Bright's disease in the
broad acceptation of the term. Dr. Mott's work in the interval on
syphilitic lesions of the arterial system of the brain has been so
brilliant, and is so generally known, that it requires nothing more
than this appreciative mention by me, and it saves me the trouble of
an excursion into the subjects of cerebral hæmorrhage and thrombosis
in connection with these lectures.
NERVOUS STRAIN.
I confess that it is difficult to say much that is of real
diagnostic value on the clinical aspect of cardio-vascular disorders
and disease from nervous strain. As I remarked in discussing this
subject from the etiological point of view, several factors come
into play besides nervous excitement followed by exhaustion and
their effects on the heart, great vessels and cerebral arteries;
and the cases, therefore, are found to present a puzzling variety
of features. Certain clinical characters are, however, common to
the majority. Arterial tension is high; the radial artery is thick,
sometimes markedly so; the heart enlarges; and in about one-half of
the cases a systolic murmur is to be heard either in the aortic or
in the mitral area, significant of chronic endocardial lesions--all
readily intelligible results of cerebral strain in the light of
our knowledge of the innervation of the cardio-vascular system. I
have already pointed out that in some of these patients polyuria
and temporary albuminuria occur along with the high tension and
the increased action of the heart; but the heart may fail later
on. The direct cardiac symptoms of which they complain are of the
ordinary character, palpitation with accelerated cardiac frequency
and pain (not angina) being the most common at first, feelings of
indescribable discomfort and suffocation in the more advanced stage.
A great deal that I might have had to say on the very interesting
subjects of pseudo-angina, and the climacteric and pre-climacteric
disturbances of the circulation in women, I am reluctantly compelled
to omit from want of time.
* * * * *
After having reviewed, as I have attempted to do, the principal
clinical characters of the disorders and diseases of middle and
advanced life under their several causes, it may appear for a
moment strange that the most important of all the clinical types of
cardio-vascular degeneration has been mentioned only incidentally.
This is chronic Bright's disease, which, from its complex
pathological relations, its widespread effects on the heart and
circulation and the organs that they supply, and the far greater
gravity of these than those of any of the other causes which we have
studied (unless it be syphilis), is a subject of endless interest to
us all. Fortunately for me my immediate predecessor in this chair on
the medical side, our distinguished Fellow, Dr. Samuel West, took
for his subject the "Clinical Aspects of Granular Kidney," and thus
relieved me of a task which he was so much better able to discharge
than I. Emphysema must also be passed over with the single remark
that it is a very common accompaniment both of vascular and cardiac
degenerations.
I trust you do not conclude that the description which I have just
given you of the clinical characters of these various disorders and
diseases of the heart is in any sense complete. It only relates to
the most prominent symptoms and signs as they present themselves to
us in what might be called the every-day life of the patient, at a
period in the history of his case precedent to failure. In all of
them there may occur occasional attacks of acute embarrassment of
the heart and lungs from one or more of a variety of causes, such
as indigestion, excitement or over-exertion. Sooner or later, also,
there occurs either cardiac dropsy--insidiously developed after
increasing local distress, growing dyspnœa and "bad nights"; or
Bright's disease; or cerebral thrombosis or hæmorrhage, or acute
myocardial failure with angina: or the patient dies from failure of
the heart in the course of some acute disease such as bronchitis or
pneumonia. Neither have I considered it necessary in this lecture to
dwell on some of the rarer phenomena occasionally met with, such as
tachycardia and bradycardia. I may have occasion to refer to them
next time in connection with prognosis.
LECTURE III.
MR. VICE-PRESIDENT AND GENTLEMEN,--In this, the concluding lecture
of the series, I will attempt to deal with the applications of
the facts and considerations which I submitted to you on the two
previous occasions when I had the honour to address you. I trust
that what I then laid before you proved to be of some interest.
Let us see now whether it is practically useful. However much the
etiology and pathology of the diseases and disorders of the heart
and arteries in middle and advanced life may deserve study as
matters of natural history, we should be disappointed if they could
not be turned to account in prognosis and treatment. These are the
subjects I propose to discuss this evening.
Now, prognosis and treatment, to be rational and useful, have to be
based on as full and as correct a diagnosis as knowledge permits.
The present disposition is to fall short of this; to rest content
with an incomplete diagnosis. We say that the patient's "heart
is dilated," that he has "arterial degeneration," that there is
"fatty degeneration." But you will remember that we have found that
cardiac dilatation may be present in every kind of cardio-vascular
degeneration; that the arteries are naturally enlarged and thickened
after middle life, and that we refused to call these changes morbid.
Clearly, therefore, a purely anatomical diagnosis of this sort
is insufficient. If you are asked what the prognosis is of fatty
degeneration of the heart, you answer that you must first be told
whether syphilitic or gouty disease of the coronary arteries, or
strain, or alcoholism, or phosphorus-poisoning or anæmia is the
cause of it. When you are planning the treatment of dilatation of
the heart you first determine whether the dilatation is a result
of the stretching of a sound heart by overfilling during muscular
effort, or of the insufficient emptying of failing chambers with
degenerated and feeble walls. Obviously what we ought to determine
in these instances and in every instance is the origin of the
disease. The ultimate diagnosis to be reached for practical purposes
is the etiological diagnosis.
Is this possible? Does our knowledge of the nature, characters and
course of these cardio-vascular affections enable us to say, after
investigating a case, what the kind of the pathological change is
that constitutes the disease, or in what respect the physiological
mechanisms are disordered? Can the cause of these degenerations of
the heart and arteries be determined in each instance? How is the
practitioner to proceed to do so? What method might be followed with
advantage in making a complete diagnosis of heart disease in older
subjects?
A man of 60 consults us about his heart. He says that it has caused
him a good deal of concern lately. More specifically he describes
a sense of oppression behind the sternum as often as he exerts
himself, and palpitation with consciousness of irregular cardiac
action when he goes to bed. We inquire for other familiar cardiac
symptoms, such as pain, angina, fluttering, faintness, giddiness,
and a sense of impending death. We find that one or more are present
occasionally, and that they have increased in number and degree
during the last few months or years. Perhaps cough, nocturnal
orthopnœa and dropsy may be beginning to give trouble. The next
part of the inquiry relates to the patient's previous history
from childhood upwards. Which of the acute diseases has he had?
Acute rheumatism, chorea, scarlet fever, typhoid, diphtheria and
influenza must be mentioned individually, and in women the nature
of any puerperal disease from which they may have suffered. Gout,
irregular gout, gravel, eczema, sick headache, asthma must be
inquired after with the same minuteness, and so must syphilis. We
next hear an account of any accident which the patient may have met
with, such as a blow, or a fall from a horse or a carriage. This
brings us naturally to question him about his occupation and modes
of relaxation and amusements--whether active or sedentary, regular
or irregular, their characters otherwise, and their direct effects,
including strain. More difficult to elicit is a correct account of
the patient's habits--in respect of food, stimulants and tobacco,
and his manner of life generally. As I said in my first lecture,
this is an inquiry which the family practitioner has an opportunity
to carry out much more successfully than the hospital physician
or consultant. The family practitioner has known for years of his
cardiac patient's work and worries; it may be of his large eating,
of his secret drinking, of the history of syphilis in earlier years.
It is always well also to inquire after a family history of gout,
rheumatism and heart disease. A list of questions like this sounds
far more formidable than it is in reality. A few minutes suffice to
arrive at the truth. We already have a pretty fair notion what we
have to deal with, whether strain, gout, syphilis, tobacco, an old
rheumatic lesion, or a combination of two or more of these.
We next proceed to physical examination, beginning with the pulse
and arteries, and passing on to the heart and associated structures.
The characters of the præcordial impulse--particularly the seat
of the apex-beat and the strength of the impulse--are closely (I
might almost say laboriously) investigated. We must never yield to
the temptation to disregard weakness or absence of the impulse.
Like many other negative signs it is apt to be overlooked. Then the
præcordial dulness is mapped out by means of light percussion.
Finally, auscultation reveals to us the presence or absence of
murmurs and the characters of the sounds--in the standing and
recumbent postures, and, if necessary, after a little exertion. The
relative loudness of the first and second sounds over the different
parts of the præcordia is particularly worthy of note.
Now let us suppose that we have found a mitral systolic murmur. We
ask ourselves whether it is structural or whether it is functional,
that is, due to relaxation and dilatation of the ventricular walls.
If structural, with which (if any) of the diseases elicited in the
man's previous history would it correspond? Most probably with
gout or glycosuria. Thus we attempt to connect the lesion with
its cause, and the cause with its effects, and have reached the
ultimate diagnosis. So with other valvular murmurs: for example,
an aortic diastolic murmur proves to be related to syphilis. If
there be no murmur audible, we naturally think of dilatation with
failure, or of enlargement from strain, from Bright's disease, from
arterial sclerosis, from emphysema, from an insufficient or impure
blood-supply in the coronary arteries, from disordered innervation,
or from some rarer cause, such as adherent pericardium; and then,
with these associations in our minds, we review once more the
patient's history, and generally succeed in our diagnosis.
Here let me recount the significance of the principal signs and
symptoms which I detailed to you in my last lecture, considered in
the reverse order on this occasion, some of which are of real value
in differentiating the causes of cardio-vascular degeneration. To
begin with negative facts: a mitral pre-systolic murmur is never
significant of a degenerative lesion. Secondly, when we meet with
an aortic diastolic murmur, whether alone or along with an aortic
systolic murmur, we may safely conclude that we have to deal with
something more than atheroma produced by regular or irregular gout
and associated metabolic disturbance, cardio-vascular disease of
nervous origin and alcoholic or tobacco heart, even if there be
evidence of the presence of one or more of these in the case.
Aortic incompetence developed in later life is the result of
syphilis, or of acute or chronic valvular strain; but, of course,
many instances of this lesion met with after the age of 40 can
be traced to juvenile endocarditis of rheumatic or other origin.
Always a serious lesion, aortic incompetence due to syphilis, or to
syphilis and strain, is particularly grave, as being so frequently
associated with coronary disease and consequent myocardial
degeneration--fatty or fibroid, acute softening, and sudden fatal
failure. A fully-developed basic systolic murmur, audible over the
aortic area and manubrium and along the course of the carotid,
is a very common sign of atheroma of the aortic arch and valves
and great vessels in association with regular or irregular gout,
diabetes, corpulence and allied disorders of nutrition. It is also
one of the physical signs of syphilitic and traumatic affections of
the aorta and aortic valves and of remote endocarditis. Further,
these lesions are so often accompanied by similar degenerations in
the coronary arteries and consequent myocardial degeneration, that
the basic systolic murmur ought at least to raise the suspicion
of this in the observer's mind. An ill-developed basic systolic
murmur is not uncommon in alcoholism, chronic Bright's disease and
nervous strain, but it is difficult to dissociate from anæmia. A
fully-developed systolic murmur audible in the mitral area, I mean
independently of ventriculo-auricular leakage in cardiac failure,
is usually traceable to early endocarditis of rheumatic or other
origin, rarely to injury, including ordinary juvenile strain of the
valves or walls, or to Graves's disease. But in some instances it
is unquestionably due to valvular atheroma and attendant sclerosis,
caused by gout or other disturbances of metabolism, including the
effects of free living; and in these instances the observer must
not overlook the possible association of coronary disease and fatty
degeneration. If a systolic mitral murmur prove to be somewhat
indefinite and affected by posture, cubitus and effort, to vary
under observation from day to day, and to disappear under treatment,
it is of no more value to us in differential diagnosis than that
it signifies relaxation and weakness, or disorderly action, of the
left ventricle, consequent on any one of the recognised causes of
failure or disturbance of the heart, including the different cardiac
poisons, overwork, anæmia, acute disease, poverty and the like, and
this whether in a heart previously sound or previously enlarged or
previously the seat of valvular disease. An accentuated ringing
second sound in the aortic area, or more extensively, is of great
value in the diagnosis of arterial tension and of aortic atheroma or
of both, but it is associated with far too many different causes to
be of much use in differential diagnosis. It should suggest a most
careful search for Bright's disease. Slight reduplication of the
first sound is common over the heart strained in youth and the heart
degenerated by alcoholism and metabolic disorders, but everyone
knows that it is not unusual in a variety of other conditions,
healthy and morbid. On the other hand, the _bruit de galop_, or
cantering rhythm of cardiac sounds--definite doubling of the first
sound followed by loud, accentuated, ringing second sound--is
practically pathognomonic of Bright's disease, and is one of the
most valuable, because one of the most ominous, of physical signs in
connection with the cardio-vascular system. A normally-sized heart
with irregularity, increased frequency, and a variable systolic
murmur in the mitral area, is characteristic of tobacco poisoning. A
heart enlarged on both sides, and acting irregularly without murmur,
is (apart from cardiac failure) suggestive of strain in early life.
Cardiac symptoms taken individually are of less diagnostic value
than signs. No symptom is pathognomonic. Palpitation is a nearly
universal phenomenon of cardiac disease and disorder. Faintness and
actual faints are not uncommon in cases of early cardiac strain,
gouty heart, and nervous disturbances. Angina we meet with, you
will remember, in regular and irregular gout, tobacco heart, strain
(especially strain after 40), and in syphilis and alcoholism,
whilst pseudo-angina is extremely common in nervous women: thus
angina is of less diagnostic value than might have been expected.
A high-tension pulse I have found most often in Bright's disease,
in juvenile strain, and in cardio-vascular affections of nervous
origin; a low tension pulse in connection with alcoholic and tobacco
poisoning, and with senile strain.
When we review these facts, I think we are entitled to conclude that
the physical signs and symptoms carefully determined by clinical
investigation may be confidently employed, along with the patient's
previous personal history, and the history of his present illness,
to differentiate from each other the causes of cardio-vascular
degeneration in individual cases. And, further, that they inform
us of the seat of at least some of the lesions, valvular, parietal
and vascular. A little trouble, patience and attentive observation
are all that are required to reach a complete or working diagnosis.
Now we may approach the great practical subjects of prognosis and
treatment with some confidence.
PROGNOSIS.
Beginning with the simplest kind of cardio-vascular disorder, let us
see what the prognosis is in tobacco heart. You will have gathered
from what I had to say on this subject in my last lecture, and
indeed you know as men of observation and experience, that it is
comparatively favourable. All the cases I have had an opportunity to
watch did well, provided the cause of their distress was avoided and
the heart and vessels were otherwise healthy. Further, improvement
begins early, and it may be rapid and recovery complete; but you
will remember that one patient, whose case I detailed to you,
continued to have alarming angina for six months after giving up
tobacco. Recurrence attends resumption of the habit, but some of
its votaries contrive to continue to smoke just short of inducing
serious discomfort. Unless a successful effort at reform be made,
cardiac trouble may continue indefinitely. But even then I cannot
say that I have seen serious damage done by tobacco alone in
sound hearts, nor arterial sclerosis, as has been stated by some
authorities.
An entirely different and most unfavourable estimate is to be formed
of the prospect of life in the alcoholic heart. Naturally, a certain
proportion of cases recover if the disease be of recent development,
the condition uncomplicated, and treatment faithfully carried
out. Unfortunately, as a rule, we have to deal with alcoholism in
which all these conditions of success are wanting. The habit is
established, other organs besides the heart are involved, other
diseases than alcoholism are present, and the patient has neither
the inclination nor the power to follow our advice. Cirrhosis,
neuritis, dementia complicate the cardiac degeneration, or, more
correctly, it complicates one or all of these. Chronic Bright's
disease is made to account for a number of deaths in the mortality
returns that strictly belong to alcoholism. Occasionally the end
comes suddenly from fatty degeneration, or in the course of some
acute disease; otherwise, as we have seen, by slow cardiac failure
and dropsy.
Prognosis in gouty heart, including the heart of the man with
goutiness, glycosuria and other irregular forms of the disease, is
a subject of considerable practical difficulty. In my last lecture
I read to you a short account of the case of a friend of my own
who had had occasional attacks of gouty angina for 40 years. And
certainly a large proportion of the old ladies of 60 or 70, whom
you all have had as patients for years on end with weak heart
and systolic murmur in the aortic area, owe their disablement
to gout, if my observations are correct. The lesion proper of
the aorta and aortic valves in these cases is atheroma, but the
damage is accompanied with repair in the form of sclerosis, which,
by increasing the loudness of the bruit, adds unreasonably to
our anxiety about the case. Equally certain it is that patients
belonging to this class improve under treatment. Still, the
condition of arrest cannot go on indefinitely. In addition to
extrinsic dangers, particularly those of Bright's disease, cerebral
thrombosis and hæmorrhage, and bronchitis, failure of the heart
is liable to supervene and prove fatal from the gravest of all
intrinsic causes, namely, coronary degeneration. As this increases,
the myocardium is steadily more and more impoverished; its
contractile vigour declines, and residual dilatation of the chambers
sets in with mechanical congestion of the viscera. Complaints of
"the heart" increase, the breathing becomes oppressed, the face
assumes more and more the characteristic "cardiac" appearance, and
dropsy creeps up the lower limbs. Even then the prognosis is not
hopeless, for undoubtedly a certain proportion of cases of dropsy in
old persons with degenerated heart and vessels are still amenable to
rational treatment. But the case has occasionally a more dramatic
termination. As I was able to illustrate after my second lecture by
a specimen from the Museum of Charing Cross Hospital, a branch of
one of the coronary arteries that has been narrowed by atheroma for
an indefinite length of time, with consequent cardiac weakness and
discomfort, may any moment become thrombosed rapidly, apparently
in consequence of some passing depression or other unfavourable
influence, just as in thrombosis of degenerated cerebral vessels.
Fatal angina is the result. This is a point of great practical
importance--that sudden death will occur in old gouty subjects not
from the lesion of which a basic or an apical systolic murmur is the
evidence and which causes us concern, but from associated coronary
atheroma, which we probably never suspect; indeed, that it may occur
in those subjects with no murmur whatsoever to attract our attention
and excite our fears.
Still more unfavourable must be the forecast in syphilitic lesions
of the heart and vessels. Of 18 of my cases in which the result was
known, only one-half improved under treatment, and 20 per cent. of
them died within a few years (some indeed within a few weeks) of the
discovery of their disease. Cardiac failure accounts for most of the
deaths, whether developed gradually with dropsy, which proves to be
intractable; or progressing rapidly with great cardiac distress,
including angina; or occurring suddenly, as it often does. Aneurysm
makes its appearance in other instances, of which the patient dies,
or he is carried off by general paralysis or Bright's disease.