History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: August, 1935 Vancouver Medical Association Aug 31, 1935

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ASSOCI ATldJif- -193s
Vol. XI.
AUGUST, 1935
In This Issue:
Radiation Ointment
Obtainable at:
or any
Western Wholesale Drug Co.
(1928) Limited
Titblfthgti nfttonthly under the zAuspiccs of the Vancouver Siledical ^Association in the
Interests of the ^Medical "Profession.
203 Medical Dental Building, Georgia Street, Vancouver, B. C.
Editorial Board:
Dr. J. H. MacDermot
Dr. M. McC. Baird Dr. D. E. H. Cleveland
All communications to be addressed to the Editor at the above address
Vol. XI. AUGUST, 193 5    No. 11
OFFICERS   193 5-193 6
Dr. C. H. Vrooman Dr. \\". T. Ewing Dr. A. C. Frost
President Vice-President Past President
Dr. G. H. Clement Dr. W. T. Lockhart
Hon. Secretary Hon. Treasurer
Additional Members of Executive—Dr. T. R. B. Nelles, Dr. F. N. Robertson
Dr. W. D. Brydone-Jack Dr. J. A. Gillespie Dr. F. Brodie
Auditors: Messrs. Shaw, Salter & Plommer
Clinical Section
Dr. J. R. Neilson     Chairman
Dr. Roy Huggard      Secretary
Eye, Ear, Nose and Throat
Dr. E. E. Day      Chairman
Dr. H. R. Mustard   —- ._..  Secretary
Paediatric Section
Dr. G. A. Lamont   — ~ — —-  Chairman
Dr. J. R. Davies   Secretary
Cancer Section
Dr. J. W. Thomson    —-  Chairman
Dr. Roy Huggard _   ; Secretary
Library Summer School
Dr. G. E. Kidd Dinner Dr- H- A- DesBrisay
Dr. \V. K. Burwell _    r ' Dr. H. R. Mustard
„     „   ,   „ Dr. Lavell Leeson t^     ,  W7 -r . „„„
Dr.C A. Ryan „     T „ TT Dr. 1. W. Thomson
„    .,,. _  T, L>r. J. h. Harrison t\    r- r  p„„„„.r
Dr. \V. D. Keith _    •'   T Dr. C h. T>ro\vn
t.      TT    ,    ~ UR. A. LOWRIE t^      t   t?   W7   ..,
Dr. H. A. Rawlings Dr. J. E. Walker
Dr. A. W. Bagnall Dr. J. W. Arbuckle
Publications Credentials
Dr. J. H. MacDermot Dr. H. A. Spohn
Dr. Murray Baird Dr. J. W. Thomson
Dr. D. E. H. Cleveland Dr. W. L. Graham
V. O. N. Advisory Board
Dr. I. T. Day
Reb. to B. C. Medical Assn.
Dr. W. H. Hatfield
Dr. W. C. Walsh
Dr. A. B. Schinbein
Sickness and Benevolent Fund —
- The President — The Trustees PUBLIC HEALTH
Diphtheria Antitoxin
Diphtheria Toxin for Schick Test
Diphtheria Toxoid   (Anatoxine-Ramon)
Scarlet Fever Antitoxin
Scarlet Fever Toxin for Dick Test
Scarlet Fever Toxin
Tetanus Antitoxin
Anti-Meningitis Serum
Anti-Pneumococcic Serum   (Type 1)
Anti-Anthrax Serum
Normal Horse Serum
Smallpox Vaccine
Typhoid Vaccine
Typhoid-Paratyphoid Vaccine
Pertussis Vaccine
Rabies Vaccine   (Semple Method)
Price List Upon Request
Connaught Laboratories
University of Toronto
Depot for British Columbia
Macdonald's Prescriptions Limited
Medical-Dental Building, Vancouver, B. C. VANCOUVER HEALTH DEPARTMENT
Total Population  (Estimated)       244,329
Japanese  Population   (Estimated)           8,037
Chinese Population   (Estimated)        7,803
Hindu Population  (Estimated)     276
Rate per 1,000
Total Deaths  	
Japanese Deaths 	
Chinese  Deaths _ 	
Deaths—Residents  only 	
Birth Registrations—
Male, 159; Female, 176
Deaths under one year of age	
Death rate—per  1,000 births 	
Stillbirths   (not included in above).
June 1st
to 15th, 1935
Cases     Deaths
Scarlet   Fever   	
Diphtheria   -... 	
Chicken Pox   	
Measles      237
Rubella              3
Mumps              26
Whooping-cough       61
Typhoid Fever.. 	
Undulant Fever 	
Meningitis   (Epidemic).
Encephalitis Lethargica
June, 193 5
Cases     Deaths
"The most effective therapy available."
Indications:   Hyperpiesia  (essential hypertension), paroxysmal high
blood pressure,  early arterio-sclerosis  (not due to renal disease).
Formula:   Each 1 cc. Ampoule contains
Pancreas—25 grammes of the fresh hypotensive principle;
Anterior Lobe Pituitary—2 grammes of fresh substance;
rrammes of fresh substance.
Biological and Research
Ponsbourcie Manor, Hertford, England.
Rep., S. N. BAYNE
1432 Medical Dental Building        Phone Sey. 4239
Vancouver, B. C.
Ask the Doctor who has used it."
Page 232 il 111
\ liJll
lb I sill
Pl ft ill
For the rest of your natural life
I sentence you to the hypodermic needle I
THIS is the verdict feared by every diabetic. It is the sentence which the
physician should avoid wherever possible.
For proper indications and in emergencies, there is of course no complete
substitute for insulin. But many diabetics thrive on oral treatment with
Pancrepatine, which contains the hormone of pancreas and liver ACTIVE
Pancrepatine spares insulin and never causes hypoglycemic shock. It spares
the patient the discomfort of the hypodermic needle. It reduces urinary
sugar—frequently clears it up entirely. Also controls polydipsia and polyuria.
Prescribe 2 to 4 globules of Pancrepatine t.i.d. Supplied in bottles of 100
hormone-active globules protected against ferment action.
Obtainable  from B.  C.  Drugs   Limited,  Vancouver;  Georgia   Pharmacy,  Vancouver: McGill &  Omie, Victoria.
Past, Present and Future
The Editor in Chief of these pages is now disporting himself by the wild
sea waves, and, we hope, building up his vitamin reserves against the fogs
and strenuous days ahead. We hope, too, that he is protecting the calvarium
from an overdose of actinic rays while practising putting on the sands, and
we warn his usual golfing cronies to watch out for dirty work at the crossroads when he returns. In his absence it devolves upon a more halting pen to
trace some rough characters across his usual page. This duty we undertake
with diffidence, spurred on, it is true, by the not unpleasant stings of a well-
known voice from the Library. As so often happens, our big opportunity to
become loudly vocal finds us with a confusion of ideas on the current
medical scene, a good deal of emotional colour, a paucity of words, and, for
political reasons, a variety of inhibitions.
Seated here, then, in temporary occupation of the editorial chair which
stands at a window of the Medical-Dental Building, let us by contemplation
compose our scattered thoughts. Outside, the new Pontiac vies with the
shining 193 5 Model Ford at the street corners. There seem to be more cars,
newer and shinier cars, more people and better-dressed people on the streets
than at any time since the late lamented decline and fall of the stock market
gave the doctors a fresh interest in medicine. We wonder idly how many of
our bills are unpaid because their owners are paying instalments on these
whizzing new models, but immediately check such a mercenary thought.
We feel guilty of an old-fashioned individualistic acquisitiveness in what we
had always thought was a competitive world, but realise that this attitude
is now so antiquated as to be almost revolutionary. Turning round hastily,
we admire the flowers so tastefully arranged by nurse, our furniture, our
carpet (now, alas, becoming worn in spots), the favorite old print, our
papers, books, the tools of our trade. We conclude that this is really quite a
presentable place in which to interview a client, and we go on to think of
all the other pleasant offices gathered together under what might be called
this large expensive Overhead.
We ask ourselves, what is the point of this loose grouping together of
medical men, all paying high rents, with expensive furniture, equipment and
assistance? Are we really any better able to do our. job in these suroundings
than the old-time doctor who had an office in his house, read the books he
bought himself, and drove his horse and buggy furiously at fifteen miles an
hour? Have we really made any progress, or have we merely become more
mechanical and complicated in our methods?
Various facts seem to emerge in answer to these questions. The chief
equipment of our predecessors were clinical acumen, sound judgment and
experience, which still remain the basis of all good medical work. Modern
methods of investigation, used in conjunction with the foregoing, and
properly interpreted, will undoubtedly in many cases lead to earlier and
more accurate diagnosis, but may be entirely misleading if unskillf ully used.
There is no doubt at all that modern clinical medicine, with the aid of adequate laboratory, x-ray, pharmaceutical and nursing services, can perform
prodigies that were undreamed of even twenty-five years ago. The centralisation of these services, which could not possibly be acquired, nor indeed
intelligently used, by each individual doctor, furnish one reason for the
development of professional office buildings.
Page 233
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Again, it is true that the great body of medical information, both in
diagnosis and treatment, has enlarged so enormously of late that no one
man could possibly be an expert along all its divergent lines. Most general
practitioners (except those with an inferiority complex!) will admit that
they cannot always do the best that can be done for all their patients. It is
the fashion nowadays to criticise "specialists," but it has to be remembered
that specialists are created by special aptitude, special training, and public
demand. For this reason they have existed since the days when one man
could make a better arrow-head than his neighbour, and will continue to
exist until all men become robots. To our way of thinking, the patient receives the best service when he is in charge of one man, who can obtain for
him expert assistance in diagnosis or treatment when required. Enlightened
patients appreciate and frequently demand this type of service, especially
in obscure or difficult cases. The efficiency and convenience of grouping
together men of different aptitudes under one roof is the second reason for
the existence of medical office buildings.
Finally, we admit that a good brand of medicine could be practised in
a shack on the head-waters of the Fraser River, but its scope would be
decidedly limited. The retailer has shown that an attractive shop on the
busiest street corner will produce the best results, and the same rule would
seem to apply to the retailing of medical services. There is nothing intrinsically bad in a "good stand," an attractive office, recent issues of the best
magazines and a pleasant nurse. On the contrary, all these things are good
in a doctor's office as elsewhere, and we feel that to do away with them
would be a retrograde step.
It has to be admitted that this concentration of our forces in a few
buildings is expensive. The estimated average overhead of a centrally located
doctor in Vancouver is about two hundred dollars per month, a fact which
the laity, and even professional economists, have been known to forget. It
would be possible largely to eliminate this expense if all doctors were to go
back to practising in their homes and walking to work as their grandfathers
did. We ask you to visualise such a scheme in operation. We admit that
much good work could still be done, with loss of time, convenience and
efficiency. Such a scheme would be cheaper, but we think that it would lead
to less efficient medical service and so inevitably to the detriment of the
The business side of medicine follows the same rules that apply to other
businesses. In commerce, as well as in the moral and spiritual world, it is
roughly true that we get just about what we pay for. Real bargains are not
nearly so common as the public is sometimes led to believe. The bargain
counter article may look pretty for a time, but is inclined to lack the quality
of endurance. Today, apparently by public demand, the business world is
being flooded by cheap trash. We should like to remind our friends of the
laity that they have always obtained, in the way of medical services also, just
about what they have been willing to pay for, or perhaps a bit more; but in
this, as in other things, if they are unwilling to pay for quality, they will
inevitably receive trash. We should like to remind our colleagues that they
may be able for a short time to supply an article worth one dollar at a price
of twenty-five cents, but that eventually the price must go up or the quality
go down. We consider that the quality of medical services obtainable in
Vancouver at the present time, as in the rest of British Columbia, compares
very favourably with any similarly situated part of the civilized world, and
Page 234 we urge our colleagues to stand together with, united voice to resist any extension of the all-pervasive cheapening influence to our profession, a process
which must lead inevitably to the deterioration of our powers, to the lasting
detriment of those who entrust their lives to our care. —M. B.
Dr. E. T. W. Nash has accepted an appointment at Mayo in the Yukon
Territory and left for the north on July 13 th. On the morning of that day
he was married to Miss Truda Harvey, whose mother resides at Mission,
B. C. Mrs. Everard Nash is a former graduate of St. Paul's Training School
for Nurses.
Another medical man to take the plunge was Dr. Frederick Sidney
Hobbs, formerly of Calgary. On July 13 th he was married to Miss
Catherine Bridgman, also of Calgary. Dr. Hobbs is in charge of Dr. Harold
Caple's practice while he is away in Europe.
Still another medical marriage was that of Dr. Emile Therrien, who has
taken over Dr. Bayfield's practice in West Vancouver. Dr. Therrien's bride
was Miss Berni^e McCartney of Langley Prairie. They were married on
July 24th at Langley.
Dr. H. S. B. Qalbraith, who has been surgeon on the Empress of Asia
for the past two or three years, has obtained leave of absence and left on
July 15 th for Europe. After visiting in Banff and Chicago, Dr. Galbraith
plans to go on to Edinburgh to take up Eye, Ear, Nose and Throat work.
From Edinburgh he will go to Vienna and expects to be awav for a considerable time. Eventually he intends to come back and practise in Vancouver.
It is with very deep regret that we have to chronicle the death of Dr.
Douglas Corsan, of Fernie, who passed away very suddenly on Saturday,
July 13 th. Dr. Corsan represented District No. 5 on the Council of the
College of Physicians and Surgeons, having been elected in 1929 and reelected on two occasions since then. At the Annual meeting of the Council
on May 6th, 193 5, Dr. Corsan reminded his fellow members that he was
that day celebrating the 50th anniversary of his graduation in medicine
from McGill University.
We have been asked to draw attention once more to the procedure to be
followed when notifying the Vancouver Medical Association of maternity
relief cases. Only cas-*s which are to be confined in the home come under
the arrangement between the Vancouver Medical Association and the
authorities and particulars of these cases should be sent in immediately the
doctor is retained to attend the case. The doctor must give the patient's
name, address, relief number and expected date of confinement and must
definitely state on his notification that the patient will be confined at home.
The Vancouver Medical Association immediately notifies the City Relief
Department and if everything is in order the patient obtains the extra relief
for the last four months of pregnancy. Immediately the patient is confined
Page 23 J Gentle
the doctor must notify the Vancouver Medical Association, putting on his
notification the words "confined at home." All information sent in must
be in writing on the doctor's stationery and signed by him. No information
will be accepted by telephone. It is pointed out that until the Association has
received the doctor's letter stating he has been retained to attend a case the
patient cannot obtain the extra relief, as such relief is only granted by the
Relief Department on receipt of the form sent in to them by the Association.
The Committee on Medical Relief reports as follows: As instructed by the
special meeting of the Vancouver Medical Association on the 2 5 th ultimo, the following letter was sent to the City Council:
Vancouver, B.  C,
June 27th, 193 5.
During the year 1934 an arrangement was made between your honorable body
and the Vancouver Medical Association by which the latter undertook to provide
medical care for those citizens of Vancouver who are receiving civic relief, the
Society to receive $3000.00 per month as remuneration in full for this service.
This was understood to be a temporary arrangement in order to accumulate data
upon which to base a scheme which would be equitable both to the community and
to the medical profession.
At the end of the year the Medical Relief Committee met your Relief Committee,
with whom were sitting the Chairman of the Finance Committee and the City
Comptroller. The accounts for eleven months were available for consideration, and
it was shown that medical practitioners were receiving approximately one-quarter
of the minimum fees ordinarily charged for similar work. Our Committee pointed
out the inadequacy of this remuneration, which would scarcely cover overhead
expenses, and asked that the amount be doubled so as to provide an approximate
half of the usual fees.
The City Relief Committee, while expressing sympathy with the request of the
Medical Relief Committee, considered that they could not make promises in December which would have to be implemented by the new Council shortly to be elected.
They, therefore, proposed an extension of the existing arrangement to cover the first
quarter of 193 5. During that three months the Committee of the new Council would
have an opportunity to familiarize themselves with the whole question and be prepared to enter into further arrangements with the medical profession.
This proposal was agreed to by the Medical Relief Committee and the agreement
subsequently ratified by the Vancouver Medical Association.
Since then, in March, 193 5, and again in June, the Medical Relief Committee has
attended at the Council meetings at which this question has been brought up, but
no action has been taken by the Council. Meanwhile medical care has been provided
to all persons requiring it who are on city relief.
In view of the above I have been directed by the Vancouver Medical Association
to make the definite proposal that medical services, to citizens on city relief, shall be
remunerated by the City in the sum of $6000.00 per month, but if at the end of the
year such sum is found to be in excess of one-half the minimum fees, such excess
shall be returned to the City.
am further instructed to state that this concession of one-half their ordinary
recompense made to the City in consideration of the very difficult conditions obtaining in the community at the present time is not to be regarded as a precedent binding
upon the medical profession except for a definite period to be agreed upon.
I am further instructed to request that a reply be made to this communication
within two weeks from July 1st, prox.
Yours faithfully,
H. R. Mustard, M.D., Secretary,
Relief Administration Committee, Vancouver Medical Association.
There was no reply except an acknowledgment of its receipt by the Mayor.
On the 15th inst. a second letter was sent as follows:
Gentlemen: July 15th, 1935.
We have received no reply to our letter of the 27th ultimo, except an acknowledgment from the Mayor. We propose to notify all members of the medical profession practising in the City
that our agreement with the City Council providing for the medical treatment of
citizens on relief now terminates after being in abeyance for four months. We will
expect our associates to continue to care for these people until the end of July,
following which they will be referred to the Relief Committee of the City Council.
Our members will continue to respond to any emergency calls where life may be
endangered by delay, whether they receive any recompense or not. Such has been the
attitudfe of the medical profession for all time and we trust it will never change.
The profession reaffirms its willingness to attend these relief cases on the basis
of the offer made last February, namely, fifty per cent of the regular minimum fees
for office and house attendance.
Yours faithfully,
H. R. Mustard, M.D., Secretary.
Relief Administration Committee.
A telephone message was received on the 22nd inst. requesting the Committee
to meet the Mayor in his office on the following day.
Your Committee duly attended but were given no opportunity to state their
case. The only contribution apart from the Mayor's views was made by Alderman
Smith, who said that the Council would be prepared to increase the monthly
remuneration by $1000.00, or $4000.00 in all. This amount would provide approximately for 3 5 % of the accounts.
Members of the medical profession in Vancouver will be circularized advising
them of our failure to obtain even half remuneration for relief work and requesting them to refer relief patients to the civic relief office, except such emergency
cases as may require immediate attntion, which should always be seen whether payment is accepted or not.
So far as your Committee is aware the foregoing has no application to the
maternity relief, which continues as before.
With Special Reference to the Cardiovascular System.
Address by Dr. Charles Hunter, of Winnipeg, at the Summer School
of the Vancouver Medical Association, June, 193 5.
There is no need for me to stress the importance of Essential Hypertension, which the general practitioner and specialist alike encounter every
day. Fahr indeed claims that 23% of all deaths in persons over 50 are due
to Essential Hypertension.
Recording Blood Pressure: A word may be said in regard to the
method of recording the blood pressure. With the patient comfortably
seated or lying, the cuff of the manometer is applied to the arm, the brachial
artery is located by palpation at the bend of the-elbow; the cuff is inflated
till the pulse is obliterated, the stethoscope is applied over the brachial artery
and the pressure in the cuff allowed to fall slightly till rhythmical thumping
sounds are heard. The point on the manometer at which these rhythmical
sounds are first regularly heard, is the systolic blood pressure, which is
usually 5 to 10 millimeters of mercury higher than that obtained by palpation. As the pressure is allowed to drop further, the sounds rapidly disappear
and reappear later as clear, sometimes bell-like, sounds, which with further
drop become dull and muffled and rapidly disappear. The diastolic blood
pressure is usually taken at the lowest point where the clear sound is present
and not when the sound disappears entirely. There is a varying difference of
5 to 10 millimeters between the point at which the clear sound is present
and that at which all the sounds disappear.
The Auscultatory Gap: In a small number of cases, a mistake may be
made in estimating the systolic blood pressure; the rhythmical thumping
sounds heard after the pulse has been obliterated and the pressure allowed
Page 237 i ul
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slowly to fall, disappear but reappear possibly 20 or 40 millimeters of mercury lower down, again vanishing till the usual diastolic clear sounds are
heard. Thus, if the systolic pressure be estimated by slowly raising the
pressure in the cuff till the sounds reappear, the lower "interjected" phase
may be mistaken for the systolic blood pressure, a mistake guarded easily
against by controlling the auscultatory method by palpation at the wrist
and by always initially raising the pressure till the pulse is obliterated.
What Constitutes Hypertension? A systolic blood pressure over
150 and a diastolic over 95 (some claim 140 and 90 as the limits) may be
regarded as abnormal at all ages; in young adults, the upper limit of normal
may be placed at 140 while the lower normal limit of systolic blood pressure
may be put at 100. In old age, there is a marked tendency for the systolic
blood pressure to rise with much less change in the diastolic, giving rise to
an increased pulse pressure; this is due to the loss of elasticity from arteriosclerosis of the aorta and large blood vessels with more blood immediately
passing into the peripheral arteries. The systolic blood pressure is subject to
great temporary variations, as every practitioner knows. A nervous person
may, at the beginning of the examination, give a blood pressure reading 20
millimeters or more above that recorded at the same sitting when he is
reassured; around the menopause, temporary rises of blood pressure are not
at all uncommon, while even the diastolic blood pressure, which is far more
stable, yet presents minor variations. It must be particularly emphasized that
Essential Hypertension should not be diagnosed from a rise in the systolic
blood pressure alone. A constant rise of the diastolic to 95 or 100 is essential
for the diagnosis. Thus a high systolic and low diastolic blood pressure,
e.g., 160/80, is found in exophthalmic goitre, in aortic regurgitation, in
heart block, in emotional states and often in arteriosclerosis of the larger
arteries. It may be pointed out, however, that a formerly high blood pressure may become lowered to normal or subnormal values from coronary
occlusion and its consequences. On the other hand, in failing heart, the
systolic blood pressure may be maintained by accompanying constriction of
the peripheral stream.
Etiology: The etiology of essential hypertension is still unknown.
Hereditary and constitutional factors, associated with advancing years, are
certainly at play. It is quite uncommon under 40 and admittedly some 80%
of cases occur between 40 and 69 years. A tendency to cerebral haemorrhage,
to angina pectoris, to myocardial disease, and to essential hypertension is
marked among immediate relations of persons suffering from essential hypertension. Today,, I saw a man of 5 0 with beginning definite essential hypertension; two sisters in middle age have blood pressures over 200 and a brother
died at 50 of angina pectoris. Thus O'Hare, Walker and Vickers elicited a
family history of vascular disease in 68% of 300 hypertensive patients. A
very large number have a strong build with heavy bony framework and
good muscles, along with a tendency to obesity, but there are many exceptions to this type; there is an inherited nervous and vascular make-up as the
background for secondary exciting factors. Thus emotional and mental
strains play an accessory role, precipitating and aggravating the increase in
blood pressure, in those individuals who have the inherited constitutional
predisposition. It has been proved that essential hypertension is not due to
excess of adrenalin or of vasopressin (posterior pituitary secretion) circulating in the blood. Yet the endocrine system is a factor in many cases.
Tumours of the adrenal medulla cause a paroxysmal hypertension which
disappears on successful operation; some tumours of the adrenal cortex are
Page 23S
— associated with a permanent hypertension identical with essential hypertension, and in other cases, diffuse hyperplasia and circumscribed adenoma
formation are found in the ccrtex, but, after all, such findings are exceptional.
Cushing has roused interest by his picture of basophilic adenomata of
the pituitary in which essential hypertension is present; an increase of
basophilic cells extending backwards through the pars nervosa has been
found in many other cases of essential hypertension and Cushing suggests
that this basophilic hyperplasia in some way activates the posterior pituitary
gland to extra production of vasopressin. This generalization is as yet quite
Only exceptionally in hyperthyroidism is there a true essential hypertension; in exophthalmic goitre there is a marked increase in the systolic
and usually some lowering of the diastolic blood pressure, but in some cases
of long standing and towards middle age, true hypertension is found with
permanent heightening of the diastolic pressure. There is sometimes an
increase in the basal metabolic rate in essential hypertension, but this seems
to be the result of the cardiovascular condition rather than the cause.
Up to the age of 40, the blood pressure of diabetics and normal healthy
individuals runs approximately parallel; after 40, the incidence of hypertension among the diabetics is twice that found in non-diabetics of corresponding age.
Though around the menopause women are peculiarly liable to hypertension, this is in many cases fluctuating and temporary in character and
the great majority of women exhibit no such change—temporary or permanent.
One may summarize the evidence by saying that the average case of
essential hypertension shows no clinical or post mortem evidence of disease
of the endocrine system.
(The speaker laid great stress on the fact that at the outset essential
hypertension is functional and not organic; and that this phase persists for
a considerable time.  This is of immense importance as regards treatment.)
The role of the nervous system in the causation of essential hypertension
underlying the disease, is a functional, and later an organic constriction of
the arterioles; the sympathetic nervous system with its vasomotor centre in
the medulla maintains and may increase the tone of the arterioles, thus increasing the resistance, and this is balanced in health by the parasympathetic
vasomotor nervous system, particularly through the carotid sinus and the
aortic depressor reflexes. (The carotid sinus is the ampulla-like dilatation
at the division of the external and internal carotids.) A decreased function
of the depressor (parasympathetic) reflexes or an increased function of the
sympathetic will elevate the blood pressure. Experimentally, destmction of
the aortic and carotid sinus nerves is followed by definite and persistent
hypertension along with tachycardia, and it has been suggested that
atheromatous changes about the carotid sinus may diminish the sensitivity
of these nerves so that their usual inhibitory action is diminished. There is,
however, no post mortem proof of marked atheromatous changes about the
carotid sinus or that stimulation of the sinus by direct pressure with the
finger fails in ordinary cases of essential hypertension to give the usual
response—a lowering of blood pressure and slowing of the heart. It would
seem in essential hypertension there is an irritability of the sympathetic
nervous system—an increased pressor nervous mechanism, but how this
comes about—apart from what we vaguely term the constitutional inherited
Page 23 9 r*.
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factor—we do not know. Medullary arteriosclerosis, local circulatory disturbances from pressure caused by medullary tumours or from asphyxia,
are quite exceptional! so, too, the hypertension present in anterior poliomyelitis with bulbar involvement.
""Much research has been done on the presence of vasoconstricting substances in the blood. Excess of adrenalin and excess of vasopressin from the
posterior pituitary have each been urged to explain essential hypertension;
retention of Guanidine bases has been championed by Major; an increase of
the serum cholesterol has been incriminated; an increased ratio of the potassium over the calcium salts in the blood has been found by Kylin and others.
Other investigators have suggested a possible deficiency of depressor bodies
in the blood and have incriminated Histamine, Adenosin, Acetyl-choline
and Kallicrein. But all this work on the presence of vasoconstricting, and
the deficiency of normal depressing bodies in the blood has been quite
The kidney function is normal throughout in all but some 5 to 10% of
the cases of essential hypertension. The rise in blood pressure accompanying
actual glomerulonephritis is not due, as used to be thought, to the increased
local vascular resistance, for this can be readily compensated for by corresponding dilatation of the arterioles elsewhere, but by stimulation of the
vasomotor centres with resulting general vasoconstriction.
The influence of age. Condition is quite rare under 40—most cases are
from 40 to 60. There is probably a progressive accumulation of intercellular
cement substances and loss of elasticity of tissues, changes which result in a
shrinkage of the lumen of the small arterial vessels and in a secondary progressive rise in blood pressure. Tobacco and alcohol per se do not apparently
promote essential hypertension; there is no evidence that an excess of protein
in the diet causes essential hypertension; over-eating, especially of fats, may
be a factor in increasing both weight and, apparently, blood pressure.
Pathology: In the early stages, there is no structural change, as confirmed occasionally by accidental death or by cerebral haemorrhage occurring
soon after the discovery of essential hypertension. Von Bergmann indeed
states that many years may pass with considerable rise in blood pressure
without the most careful post mortem disclosing any changes in the walls
of the blood vessels. Wallgren found in 31 of 12 8 cases of high blood pressure, no more changes than in any individual of the same age; Fishberg
records 3 cases of essential hypertension with no vascular change.
Later, however, in the great majority of cases, microscopic changes are
present in the arterioles, particularly in those of the kidney, spleen, pancreas,
liver and brain. In the kidneys, the arterioles—the afferent vessels to the
glomeruli—show hyaline deposits in their intimal coats narrowing the
arterioles and ultimately occluding them with resulting atrophy and disappearance of the glomerulus affected, while in the renal arteries next in
size to these arterioles (the interlobular arteries) there is hyperplasia of the
internal elastic membrane, which later undergoes progressive fatty and
hyaline change and connective tissue proliferation. The muscular layer of
the involved arterioles atrophies gradually with replacement fibrosis; muscular hypertrophy in the media of the larger arteries is common enough; in
the aorta, well marked arteriosclerosis is frequent with moderate or severe
arteriosclerosis of the coronary arteries, especially of the branches supplying
the left ventricle, which bears the initial strain in hypertension. The question of cerebral arteriosclerosis and its consequences will be taken up later.
It is very important to note that the pathological findings in the arterioles.
40 are not universal and are particularly lacking in the arterioles of the skin,
the muscles and the viscera, though investigators at the Mayo Clinic have
found the arterioles of the voluntary muscles frequently show marked hypertrophy of the muscular layer of the media.
The persistently raised blood pressure, diastolic as well as systolic, leads
to hypertrophy and dilatation of the cardiac muscle. The rate at which such
hypertrophy occurs seems to vary greatly and so good observers as Lewis and
Christian emphasize that unknown factors are involved, in addition to the
obvious increased resistance to the cardiac outflow.
Cardiac hypertrophy is due almost exclusively to increase in the thickness of the individual muscle cells and not to increase in their number. It is
admittedly impossible, in many cases, to say post mortem why the hypertrophied heart muscle has played out; sometimes the muscle cells show signs
~f degeneration, and in most cases there is more or less marked interstitial
fibrosis, due often to coronary artery disease.
From the clinical standpoint, essential hypertension may be arbitrarily
divided into three staees:
1. First, with no symptoms;
2. Second, with symptoms and comparatively few physical signs;
3. Third, with marked physical signs.
1. Stage without symptoms: These cases are discovered accidentally
during ordinary routine or life insurance examination; the systolic blood
pressure is found permanently raised above 150 (or in young people, 140)
and the diastolic at least 90 to 95 millimetres of mercury; little if any
enlargement of the heart will be detected at this stage; the second aortic
sound may be somewhat loud; in the fundus the arteries may be narrow in
calibre and obviously tense, denting the veins as they pass.
In such a case, the physician should proceed with great circumspection.
The fear of blood pressure in the laity must be considered, and every precaution taken lest harm rather than good to the patient result from the
early discovery of hypertension. If the individual be of normal weight, if
his habits and manner of life are correct, if his philosophy of life seems adequate, if his worries are reasonably faced, there would seem to be no indication for treatment. But a thorough knowledge of the patient's circumstances and of the hereditary influences is advisable and an accurate sizing-up
of the man himself is very desirable. When speaking of the etiology of
essential hypertension, one recognized the hereditary, constitutional and
aging factors as the dominant background—little to be influenced by treatment. But the prevention and elimination of the secondary precipitating
factors should be our therapeutic goal. So often, much can be accomplished
in this line should the patient's habits of life be bad. So many patients work
too hard, relax too little, eat too much and worry over things great and
small. One has to regulate the patient's whole life, if possible; hard work,
mental or physical, in itself does not apparently heighten blood pressure.
Worry or tension does, and a saner philosophy is so often urgently necessary.
Worry is associated with a prolonged stimulation of the sympathetic nervous
system—-a stimulation which in animals is life saving but temporary.
One has to strike the mean between alarming the patient unduly about
his condition and not taking the situation sufficiently seriously. The hours
of work, of recreation, of sleep, must be considered, and in play, relaxation
rather than high efficiency should be aimed at, for often a man seems to
worry almost as much over his golf score as over his business. A woman, too,
often finds her social and club activities trying and these may have to be
Page 241 curtailed or at least taken less seriously. Longer hours in bed may be necessary; the week-ends, and how they are spent, should be considered, and often
extra rest at that period insisted on. Obesity, especially combined with
sedentary habits, is associated in a high percentage of cases with increased
blood pressure; a gradual loss of weight results sometimes in a considerable
fall of blood pressure, but in any case the person's efficiency is increased and
his tendency to breathlessness diminished by the disappearance of extra fat,
while the strain on the heart, always threatened in hypertension, is diminished. There is ordinarily no objection to the usual amount of protein in the
diet in high blood pressure.
Many years (5 to 10) of high blood pressure often elapse before any
symptoms appear, indeed a decade may pass without hypertension doing any
discernible harm and the patient may ultimately die of some intercurrent
disorder; the high blood pressure is more fluctuating than later in the disease, and is influenced favourably by the measures described. Agreeing with
this clinical finding is the absence pathologically of any structural change in
the arterioles—the disease is still a functional one and capable, theoretically
at least, of recession.
2. We pass now to the second stage—the stage with symptoms but comparatively few physical signs. The actual symptoms vary in character;
sometimes the patient is aware of an uncomfortable thumping, at times
extra systoles are present in runs, at times a slight precordial discomfort
especially on sleeping on the left side, or a vague ache in the left chest is
experienced. More often, breathlessness on exertion is the first symptom.
The patient finds that some wonted exercise—walking at his usual pace,
possibly climbing stairs in a hurry—produces unusual breathlessness. A
heavy meal and a walk afterwards may particularly make him aware of the
change. A stout, physically lazy individual may have very little cardiac
reserve without knowing it, and even a comparatively slight, but for him
unusual, exertion may to his surprise make him breathless. Less often, a
little cedema about the ankles may attract attention, but it must be remembered many middle-aged or elderly people who stand much on their feet
and who get little other exercise have a dependent oedema about which thev
become alarmed but which has no serious significance.
At other times, a passing infection, influenza, e.g., may leave the patient
weak and, when he resumes work, more breathless than before, or the
inception of an abnormal rhythm such as auricular fibrillation, or especially
mild anginal symptoms may appear. Angina pectoris, indeed, in mild or
severe form, is frequently the symptom which brings the patient to the
physician. Sometimes cardiac asthma with sudden paroxysmal dyspnoea and
orthopncea at night appears early, though usually the patient has had some
warning in breathlessness on exertion or palpitation previously; the air-hunger may be extreme in the attack, associated with a rapid "gallop rhythm"
heart; the left ventricle is weakening with a still powerful right heart so that
the pulmonary circuti is over-filled with cedema of the lungs while there is
complete absence of venous stasis.
The early symptoms of essential hypertension are frequently unconnected with the heart; migraine in early life is not uncommon; cold clammy
hands in nervous, irritable youngish people are sometimes seen, in my experience, as the earliest symptom; headaches, especially on waking, and vague
rheumatic pains, lack of energy, fatigue, depression, giddiness and irritabil$|8
may appear early; one may get a hint when an otherwise healthy individual
complains of being very uncomfortable in a hot bath or on a hot, moist day;
■42 normally, the blood pressure falls under these conditions, but in some cases
of essential hypertension, an inverse reaction occurs and the blood pressure
rises. For diagnostic purposes, this inverse blood vessel reaction is sometimes
useful—dipping a hand or foot in hot water may lead to pallor instead of
reddening, or after removal of the blood pressure apparatus, instead of the
normal reactive hyperaemia, one finds an anaemia of the capillaries lasting for
many minutes and due to a strong arterial contraction from the pressure of
the sphygmomanometer.
With such symptoms, the patient now presents definite physical signs—
the firm pulse, difficult to obliterate at the wrist or above the elbow, attracts
attention; the blood pressure varies enormously in individual cases from 160
or 170 to 220, usually, and from 95 to 120 in diastolic pressure. The heart
is now definitely enlarged, the apex is more than four inches from the mid-
sternum, and the apex beat is heaving, lifting the palpating finger with
abnormally great force, while the second aortic is unusually loud. Even at
rest, such a patient may breathe rapidly, 30 or more respirations a minute,
with no bronchitis or other complication to account for it, and this unusual
respiratory frequency should at once make one suspicious of an associated
hypertension, for with such breathlessness due to simple cardiac failure, the
evidence of venous stasis would be much more marked. The veins in the
neck, too, should be inspected carefully, for, as Lewis emphasized, the first
signs of circulatory breakdown are to be found there. The height to which
the veins fill when standing or lying down, the height in the neck to which
the venous pulse in the deeper veins reaches when standing and lying, wi
assist in determining the amount of back pressure present. In the fundus,
contraction and tortuosity of arteries, with the swollen veins indented; the
arteries are often marked by a bright central reflex—the "silver-wire"
Treatment in the Second Stages In all these cases, where physical signs
are beginning to appear, where to the original functional contraction of the
arterioles, pathological and irreversible changes in the arterioles are setting
in, the treatment suggested in the first stage is still applicable, but with some
modifications. It is often very advisable to get the patient to take a complete
rest for a month or six weeks or, if circumstances allow it, still longer. Even
complete rest in bed for a week or two, with mild hypnotics to secure sleep,
may be advantageous. Such rest helps in two ways: rest in bed often of itself
allows a drop of blood pressure of varying degree; it also helps the heart by
diminishing its work, and if this is combined with'a suitable diet considering
the nutrition of the patient (in plethoric individuals, Karrell's diet for a few
days, possibly combined with blue pill and saline occasionally), if the mental
attitude of the patient be studied and modified as far as possible, if sufficient
sleep (in which a drop of blood pressure of 20 to 40 millimetres may occur)
be secured by luminal or possibly the combination of sodium bromide and
chloral hydrate, very marked improvement can be secured in many cases.
It is obvious that the patient with commencing cardiac symptoms must
consider his whole life, his general outlook, his work and play, his holidays,
his diet,-his tobacco and liquor, all in the bearing on his blood pressure and
its beginning influence on his heart. Especially, the doctrine of relaxation—
of acceptance of inevitable worries and troubles with resignation, of forswearing the old habits of anticipating troubles which never come—must
be preached and steadily maintained before the patient's eyes as a practica
ideal. We as physicians do not take our responsibility in these cases suffr
ciently seriously; much more good can be effected at this stage by a dis
P-ivc 24. I  »
i Ii
P» nil
criminating regime than we can obtain in the later stage of actual heart
failure. It is usually reckoned that after symptoms develop in essential
hypertension, 5 to 10 years or longer will elapse, bar accidents, before the
fatal issue; skillful management will prolong in very many cases the earlier
stages, during which the patient pulls his full weight in the community and
may in fact fill with success the highest positions in the country. In passing,
one may note that essential hypertension patients in this stage stand operations very well—the blood pressure often improving during the enforced
The third and final stage of essential hypertension—with marked physical
signs: It is not implied that every case progresses slowly; sometimes the first
indication of essential hypertension in an energetic middle-aged man who
counts himself in perfect health is a serious or fatal cerebral haemorrhage or
angina pectoris. But, as indicated, long before marked physical signs appear,"
many warning signals have usually been given though possibly entirely
ignored. The physical signs to be expected may be readily surmised when
we remember that one gets a clue to the relative frequency of symptoms and
physical signs in the third stage of essential hypertension by analyzing the
causes of death: 44% die of myocardial insufficiency following hypertrophy
and dilatation, 16c/0 of coronary disease, 20% of cerebral haemorrhage and
thrombosis, 12% of accident and intercurrent disease and 8% of renal
insufficiency (Bell & Clawson—420 patients). .
It is thus to the heart that we must usually look in advancing cases of
essential hypertension. The hypertrophied cardiac muscle seems to bear
within itself the seeds of future insufficiency, in many cases at least, because
of associated arteriosclerosis of the coronary arteries with attending reduction of the blood supply. The symptoms and physical signs of cardiac failure
develop generally slowly and insidiously, though at times, even in the absence '
of any anginal pain, they may show up rapidly without obvious reason.
Breathlessness on very slight exertion or at rest appears; the veins in the
neck are full and pulsation rises higher even when in the erect position; the
heart enlarges further to the left, the loud aortic second sound weakens, and
as the left ventricle gives way, the strain is thrown more and more on the
right ventricle with increasing accentuation of the pulmonic second sound,
beginning backward pressure showing in rales at the bases of the lungs,
enlargement of the liver and cedema of the legs.
The muscular chest with subcutaneous fat often masks largely the
cardiac enlargement; weak and distant sounds are present, often with systolic murmurs at apex or base, but such sounds may be heard in obese individuals with no myocardial weakness; the rate of the heart may be normal
at rest though rising rapidly on very slight exertion; a constantly rapid
heart should suggest associated hyperthyroidism or abnormal rhythm. Frequent extra systoles or auricular fibrillation may be present; alternation of
the pulse—an ominous sign—may be sometimes detected by noting that
after the pulse is entirely obliterated by the sphygmomanometer only the
stronger alternate beats reach the wrist as the air is allowed slowly to escape
from the cuff on the upper arm with commencing return of the pulsations
below. The blood pressure may not fall even with advanced myocardial
weakness, as peripheral constriction may fully compensate. Cardiac asthma
as already described is common, disappearing, however, as the right ventricle
gives way; Cheyne-Stokes' breathing, in sleep especially, is very common
and is often overlooked.
Palpitation and precordial oppression are often present, but in possibly
Page 244 16% of cases, definite angina pectoris or cardiac infarction occurs. Women
are much less subject to these complications of high blood pressure than
men, because their diastolic pressures are generally lower and there is less
tendency to coronary arteriosclerosis (the reason for this is unknown; the
fact, however, is admitted by all). Angina pectoris may indeed be the
symptom which first drives the patient to the physician; Lewis says that
one-third of all anginal cases have high blood pressure, while more than
one-half of the patients with cardiac infarction have essential hypertension
with coronary arteriosclerosis.
Nearly always following cardiac infarction, the blood pressure drops,
sometimes to normal and even subnormal levels, and if the patient is first
seen at this time, the preceding condition of hypertension may be overlooked, though the changes in the arteries in the fundus, a careful general
examination and history should usually prevent such a mistake. The drop
in blood pressure following cardiac infarction is due to the associated
peripheral shock in this condition, preventing the vasoconstriction of arterioles which would otherwise mask the cardiac weakness by maintaining a
normal blood pressure. In patients who survive, the blood pressure usually
rises considerably, though rarely reaching its former level; in a number
(and these, I think, with worse prognosis) the blood pressure rises very little.
Christian states that the development of auricular fibrillation, following
cardiac infarction, is a favourable sign. Apart from cardiac infarction, the
blood pressure may remain high, even with advanced myocardial insufficiency, till just before death.
Diagnosis: In the diagnosis of essential hypertension, difficulties sometimes arise. A constantly raised diastolic as well as systolic blood pressur
is essential for this diagnosis—but one must remember the fall already
noted to be often present after cardiac infarction, also in moribund patients
and in some cases of malnutrition. The heightened diastolic pressure
excludes the arteriosclerosis of elderly people. A still more frequent source
of error is the presence of albumen in the urine and a few hyaline and possibly granular casts. But most cases of essential hypertension can concentrate the urine satisfactorily: a specific gravity of 1023 to 102 5 in itself,
generally obtainable if fluids are restricted for 24 hours, will exclude chronic
glomerulonephritis even if the phenolsulphonphthalein test shows reduced
function, as is often the case when the heart is failing. It is true that patients
in the late fifties or sixties may show only a specific gravity of 1015 but the
volume of urine is then usually sufficient to prevent retention and the blood
urea estimation, occasionally necessary in cases of doubt, is little if at all
raised. It must be remembered that in some 7% of cases true renal insufficiency develops on a preceding essential hypertension, and this is especially
the case in relatively young sufferers (3 5-45 years of age), in whom a
malignant type of hypertension may progress rapidly with severe headache,
neuro-retinitis, often haematuria, and uraemia.
Prognosis : The height of the diastolic pressure, which is the measure of
the steady strain on the cardiovascular system, is far more important than
the systolic and when a steady diastolic of 130 or more millimetres of mercury is obtained, over 50% live less than two years. Two to five years may
be put as the average duration of life after manifest evidence of congestive
heart failure or angina appears. In general, the younger the patient with
essential hypertension, the more serious the prognosis. Women have a much
better outlook than men, as has been emphasized by all writers. Hypertensive neuro-retinitis is ominous, death occurring within two year in 90' { ; i ii
ill Ik
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W it
the younger physician should cultivate acquaintance writh the ophthalmoscope much more than he does.
The electrocardiographic changes may be of considerable assistance.
Taken by and large, the electrocardiogram is of more importance to life
insurance companies than to the general practitioner. The changes shown
have an average significance which is very helpful for the life insurance companies in determining prognosis of large numbers, especially as they can not
rely on obtaining a frank and honest personal history in many cases. But
in general practice and for the individual case, the cardiogram is only one
of many factors which have to be considered, and much harm has been done
by a prognosis based on electrocardiographic findings alone. The general
sizing up of the patient, the careful history, the development of symptoms
and the ordinary physical examination will, in most cases, supply the general
practitioner with all the information in regard to prognosis and treatment
he requires. It may be readily granted that in well-to-do middle-aged and
elderly patients, a cardiogram is highly desirable in every case, and that, even
in poor patients, a cardiogram is sometimes essential to make the diagnosis,
for by it alone, at times, can a definite diagnosis of serious heart trouble be
made. The cardiogram is of especial value in doubtful cases of cardiac
infarction, especially when the differential diagnosis from an abdominal
catastrophe has to be made; occasionally, too, help is needed in analysing
the exact form of arrhythmia present. But it must be strongly urged that
the general diagnosis of myocardial disease must and should rest with the
practitioner, who bases his diagnosis and prognosis on the ordinary examination of the patient. The younger practitioner, however, should familiarize
himself with cardiographic findings, which are only exceptionally, I think,
difficult to interpret.
Similarly, an x-ray is at times very valuable, but here again, in most
cases, the attentive consideration of the chest by the ordinary methods will
give one all the information necessary. No doubt, a thick chest wall with
overlying fat, or the presence of emphysema, may make it impossible to
determine accurately the size of the heart; sometimes the apex beat cannot
be felt, sometimes the heart sounds are so feeble that it is difficult to say
even on auscultation where the apex beat lies; the reaction of the patient to
exercise, or in more advanced cases his breathlessness at rest, together with
the signs of beginning cardiac failure in the veins, in the enlarged liver, in
the concentrated urine, will usually give one a sufficiently accurate picture.
Here, too, the financial circumstances of the patient should be taken into
consideration and a well-to-do individual may well have the additional
advantage of an x-ray.
Treatment: The treatment in the earlier stages of commencing heart
failure has been already outlined and the necessity for sufficient rest has
been emphasized. Exercise temporarily raises the blood pressure, systolic and
diastolic (especially systolic)—part of the response to increased need for
oxygen during muscular work plus increased minute discharge from the
ventricle effected by accelerated heart rate and augmented systolic discharge
—there is dilatation of capillaries of muscles and possibly constriction of
visceral arterioles. In the later stages, with cedema commencing at the
extremities and working upwards, with some enlargement of the liver, with
distension of the belly from gas through non-absorption of gases by the blood
in the presence of stasis, complete rest in bed is obviously indicated. A Gatz
bed is particularly useful, when obtainable; otherwise, the usual arrange-
Page 246 ment of pillows to support the head and upper part of the body and corresponding pillows under the knees.
As regards tobacco and liquor, the physician must use discretion in cutting these down. Tobacco and liquor, as stated above, do not per se cause
essential hypertension; they add greatly to the comfort and sense of well-
being so important to ensure calm and peace of mind—and while they must
be supervised, this supervision must be intelligently exercised.
Diet: There is nothing gained by restricting the proteins in essential
hypertension, and even in chronic nephritis, so long as the blood urea is not
raised, nothing is gained by such restriction. This point should be particularly emphasized, because, even now, it is common to find marked restriction in proteins, leading to increased anaemia and weakness of the patient.
Easily digested proteins in the form of fish, chicken and even red meat, may
be given in usual amounts; highly seasoned things and condiments should
be interdicted and the use of extra salt discouraged. Should oedema be present,
the restriction of salt should be still further curtailed. No salty foods
should be provided, and even the meat and vegetables should be boiled and
the water run off so as to reduce the salt contained, while saltless butter
should be provided. The lighter vegetables such as asparagus, spinach, squash,
vegetable marrow and tomatoes, the lighter fruits such as oranges, grapefruit, stewed prunes; melba toast, with saltless butter, and a limited amount
of milk puddings or jelly may be allowed. Undernourishment with sufficient
protein in stout patients.
When a case is first seen, with considerable cedema, breathlessness and
cardiac distress, it is frequently wise to give only a tumbler of milk three
times a day with possibly a little orange quice, and this diet may, with advantage, be continued for three or four days, combined with salines to gently
purge the patient. In failing heart, sleeplessness, which is common, must be
combatted. Morphine, grain 1/6, hyoodermically, in acute cases is very
serviceable. 1 J4 grains of luminal at night is often very useful both in
securing a eood night's rest and, by relieving the restlessness and nervousness, in actually lowering the blood pressure; this drug, in fact, may often,
in the early stages of hypertension, be used with advantage, say l/z grain
three times a day after meals and at night, for its general soothing effect.
In other cases, sodium bromide and chloral hydrate, in 20-grain doses each,
at night, may be useful.
Vasodilators, in the form of nitrites, have little place in the treatment
of essential hypertension per se, though in paroxysmal dyspnoea and in waves
of vaso-constriction, which may occur, they may be of temporary value.
The use of drugs to directly lower the blood pressure has not proved of much
value; sodium thiocyanate 1 to 5 grains, three times a day, has been given
over long periods and is endorsed by Rudolph, of Toronto, and others. Pure
potassium sulphocyanate, ^4 to 1 grain, three times a day after meals for a
week, then twice a day for the second week and once daily for the third week,
has been strongly endorsed by Gager. I have seldom used the cyanates and
have seen, in Winnipeg, more harm than value from their use.
Potassium iodide, in doses of 5 to 10 grains, three times a day, is an old
standby of doubtful value. In anginal cases, and in those with a previous
history of coronary thrombosis, euphyllin, 1 l/z grains, three times a day,
seems, sometimes, definitely of value, apparently by improving the coronary
circulation. In cases of edema, theocin, 5 to 10 grains, three times a day, for
a few days; diuretin, 10 grains, three times a day, and, above all, the use of
ammonium nitrate, l/z drachm, four times a day, over long periods, com-
P.iV 24'
|i i
*■ H't in
bined with the use of salyrgan, 1 cc.—occasionally 2 cc.—intramuscularly
or intravenously, twice a week, is the best diuretic we possess for removing
chronic cedema.
So far, nothing has been said in regard to the use of the drug paramount
in all failing heart cases—digitalis. It was long believed that digitalis was
rather contraindicated in high blood pressure, as tending to raise the blood
pressure still more. That has proved a fallacy, and digitalis is used just as
freely in the failing heart of hypertension as in the failing heart of valvular
disease. In the early stages, before definite symptoms of myocardial insufficiency set in, when the patient is only a little short of breath on somewhat
unwonted exertion, many good observers, including Christian and Mosen-
thal, and long before them, George Balfour of Edinburgh, believe that small
doses, say 10 minims of the tincture, three times a day over long periods,
are of definite value, combined with the usual other measures in preventing
cardiac breakdown. But when definite signs of venous engorgment appear,
digitalis is our sheet-anchor and has to be used in the usual way.
The Cerebral Lesions of Essential Hypertension: I have arbitrarily postponed consideration of the cerebral lesions of essential hypertension, as much new work has been done in this field.
Symptoms: Even in the early stages, many complain of pressure in the
head, fatigue, dizziness, irritability and insomnia. Migraine may be present
in early life or the headache, appearing later, may recur, as Janeway pointed
out, in the early morning hours. These functional "nervous" complaints
require closer attention than they frequently receive—indeed, the underlying hypertension is often overlooked. Later, headache may be more insistent; failing memory and inability to concentrate may occur; transient weakness of a limb, passing inability to articulate or to find the right word, numbness in an arm or leg—these complaints may last only a few minutes to an
hour or two, but may recur after weeks or months—especially when the
patient is fatigued. Cerebral arteriosclerosis is common in essential hypertension, bvit probably a passing spasm in a hypertonic cerebral artery is all
the pathology present in many of the lighter cases. In all too many patients,
however, such mild "angio-spastic insults," as Kauffman calls them, are
followed sooner or later by a hemiplegia or aphasia, involving the same area
of the brain as that first affected in the transient spell of weakness.
The old view has been that cerebral haemorrhage occurred, in cases with
high blood pressure, from the rupture of an arteriosclerotic artery or from
the bursting of a miliary aneurysm, as described by Charcot. The condition
has been regarded as a purely mechanical one; high blood pressure, weakened
artery, rupture of the wall at one spot and a greater or lesser haemorrhage
ploughing the substance of the brain. It is now known that such a mechanical conception does not represent the truth. It has been shown experimentally that a pressure of 1,000 m.m. of mercury or more is required to
rupture the average arteriosclerotic artery in the brain, and such a pressure
is, of course, at least three times as much as is met with clinically. Schwartz,
in the course of eight years, has investigated 400 cases of apoplexy of all
types, in his service at Frankfurt, and has never been able to find any evidence of primary rupture of an intracerebral artery in cases of hypertension.
Studying intensively the smaller haemorrhages in hypertension and the edges
of massive haemorrhages, he has proved conclusively that these are due to
the coalescence of multiple tiny haemorrhages around the terminal twigs,
the capillaries and venules of the vascular area involved; that though no
loss of continuity in the vessels is present, the smaller artery or arteries in-
Page 24 S
■M volved may show longitudinal or nodular thickenings, due to infiltration of
the adventitious coats with blood. Such nodular infiltrations, indeed, are
shown to correspond the old Charcot's miliary aneurysms, formerly supposed
to be a source of cerebral haemorrhage.
All recent investigation goes to show that even massive haemorrhages
are due initially to such multiple tiny haemorrhages coalesci
with the interference to the circulation produced and the resulting rapid
necrosis of vessels, extravasation of blood may occur through such secondarily weakened walls and add to the haemorrhage already existing.
Schwartz has shown that, in cerebral embolism and cerebral thrombosis, in many cases an exactly similar picture is present—the terminal area
of the vessel involved in the embolism or thrombosis becomes the site of a
haemorrhage, due not to any rupture of vessel but again to perivascular
haemorrhages of the terminal twigs, capillaries and venules, while the vessel
involved may itself show haemorrhagic thickening of its adventitia. The
arterial tree at the base of the brain, supplying the basal ganglia, is particularly susceptible in all forms of cerebral apoplexy—the collateral circulation
there is much less free than in the arteries supplying the cerebral cortex.
Schwartz emphasizes that extensive haemorrhages occur in cases of essential hypertension in which there are no traces of any arteriosclerotic change
in the vascular area involved; that symmetrical haemorrhages of the same
date frequently occur, or, in some cases, multiple haemorrhages at distant
While these facts are beginning to receive general acceptance, there is
still considerable doubt as to the origin of the multiple tiny haemorrhages
and the perivascular sleeves. The experimental work of Bicker seems to offer
the best explanation. Forbes and Wolff, in America, have demonstrated that
the pial vessels in the cat possess an efficient vasomotor control and their
results were corroborated by Stohr microscopically, while Penfield has shown
that the intracerebral arteries also possess nerve fibres—thus disposing of
the view long championed, in England especially, that the cerebral vessels
are not under vasomotor control.
In essential hypertension, variations in blood pressure occur, as we know
clinically, far more readily, and individual arteries are more liable to undergo
variations of diameter from local stimulation than in the normal state. Thus,
after the pulse has been obliterated at the wrist by the sphygmomanometer,
one finds in many cases of hypertension, instead of the usual reactive hyperaemia, anaemia of the capillaries which may last many minutes, due to stron
vasoconstriction following the stimulus of the constricting
Now Bicker has shown experimentally that (l) weak stimulation of a
small artery by mechanical, chemical or thermal means causes dilatation and
increased rate of blood flow; (2) moderate stimulation causes the artery to
contract with dilatation of the terminal capillaries, thus slowing the blood
stream; while (3) still stronger stimulation causes contraction of the small
artery or arteriole, up to complete closure, while the flow in the capillaries
and veins becomes increasingly sluggish till complete stasis occurs. (The
more peripheral the artery or vascular twig, the more susceptible it is to
stimulation—from stimulation, first dilatation from stimulation of the
vasodilators occurs, then contraction from stimulation of the vasoconstrictors, and lastly, increased dilatation from continued action of the vasodilators
after complete paralysis of the vasoconstrictors. Thus the capillaries and
possibly the supplying arteriols may be dilated from paralysis of the con-
Pa^ 249 •. V
•III .■ <• •kilr'li I
trictors while the higher segment of the artery is still contracted from vasoconstriction) .
The most common and important condition is that in which the arteriole
or artery immediately proximal to the arteriole becomes narrowed by vasoconstrictor stimulation while the dependent capillaries and venules are
dilated beyond; during the inevitable slowing of the blood stream distal to
the constriction, there may escape by diapedesis from the unruptured capillaries and venules, plasma, leucocytes and finally red blood cells into the
surrounding tissue, and even by diaresis, red blood cells may pass through
the dilated and loosened arterioles, while a similar exudate takes place from
the capillaries of the adventitious coat of the smaller vessels, forming a
vascular collar or sleeve. With complete stasis, all movement from the
vessels ceases; should the constriction of the arteriole or smaller artery
rapidly pass to complete closure, the stasis results before any exudate occurs,
and thus we have, in place of haemorrhage, an anaemic infarction such as of
old we associated with cerebral thrombosis and not with hypertension. In
both cases, however, the functional disturbance of the circulation is the
central fact—the presence or absence of haemorrhage in the resulting lesion
is purely incidental. All stages may occur from a transient constriction of a
cerebral vessel leaving no residual trace (a purely functional state) to a
massive haemorrhage, made up of innumerable perivascular haemorrhages,
aided, perhaps, by secondary necrosis of vessel walls from the lack of oxygen
and resulting leakage through the necrosing arterial wall.
It should be noted that a similar picture occurs in cerebral embolism and
in cerebral thrombosis to that seen in the vascular lesions of hypertension.
In cerebral embolism, obviously the primary cause is the sudden occlusion
by the embolus of the arterial trunk; here, too, actual rupture of a vessel is
but rarely seen and the resulting functional disturbance of the circulation,
as described above by Bicker, gives rise to the local lesion, which may be
haemorrhagic or anaemic; the strength of the heart, the initial gradual or
immediate closure of the artery involved, seem to be factors determining
the haemorrhagic or anaemic quality of the infarct, as well as the state of
the collateral circulation around.
In the lesion of hypertension, there seems no doubt that a sudden rise of
blood pressure in hypertonic arteries (always unduly sensitive to stimuli)
reaches a critical stage where, at the most vulnerable points of the artery,
such powerful stimulation occurs as to lead to marked constriction or actual
closure of the small vessel with resulting dilatation of the dependent capillaries and venules; there results the exudate of lymph, leucocytes or red cells,
as described by Bicker, who holds that the stimulation is conducted along
the vascular channels up and down by nervous paths in the wall, and thus
that distant vascular channels may be simultaneously involved; others consider that it is not necessary to assume nervous conduction, that the sudden
impact of the rising blood pressure is transmitted to the end capillaries, with
the above described functional disturbance of the local circulation.
Some Notes from the Address by Dr. Wm. Dock.
The speaker began by reminding his audience that it is as well to be
cautious in the use of quinidine, which has come so widely into use of late
years. Medical opinion on this drug is somewhat divided, and there are many
who fear to use it.
Page 250 There are two problems in connection with drugs, the first of which
concerns the clinician. He has to decide whether a given drug is useful, and
how to use it.
The other problem is that of the pharmacologist, who usually follows
in the wake of the clinician.
Most drugs are discovered by the patient. This, at least, is the history of
the majority of drugs. The medical profession has learned empirically of
the value and use of drugs from their use by patients. The pharmacologist's
business is to dig us the reason for the use of the drug, and tell the clinician
of its properties, its dangers, its action on the tissues of the body—the
dangers connected with its use, and so on.
Perhaps to no drug is this more applicable than to digitalis, whose properties were first
discovered by the people who used it for heart trouble, were next made use of empirically
by the doctor, and now for a long time have been the subject of exhaustive investigation
by the pharmacologist.
Quinidine. This drug is only of value in the treatment of cardiac cases when the
rhythm is out of order. Thus it is of value in treating the arrhythmias, extra-systoles, etc.
It is of no value in heart failure, or anginas, unless the mechanism of the heart is out
of order.
It may be used, too, as a prophylactic where abnormal rhythm is likely to appear, e.g.,
after an attack of coronary thrombosis.
Quinidine has some disadvantages. It is likely to cause dizziness, tinnitus, and gastrointestinal symptoms, urticaria, even collapse. Idiosyncrasy to the drug, as to quinine, is far
from rare—in fact the toxic symptoms are those of cinchonism. These untoward effects
may follow even a small dose, and we must be on the lookout for them.
Quinidine in excessive dosage will cause cardiac irregularity—ventricular, tachycardia,
and fibrillation; in fact, the same irregularities that in normal doses it is used to correct.
The toxic dose, apart from idiosyncrasy, is much bigger than the physiological dose,
as is the case with most other drugs.
Digitalis. This is of greatest value where there is a rapid ventricular rate, e.g., in
auricular fibrillation. It does not affect the auricle, but slows down the ventricular rate.
These properties of digitalis and quinidine are easily demonstrated. Digitalis may be
useful in reverting cardiac irregularity, e.g., in flutter, where it may restore the heart to
regular action.
It is occasionally used in warding off attacks of paroxysmal tachycardia, although these
are best treated after onset by quinidine. They may be averted, however, by full doses of
digitalis. In patients where there is heart failure without any irregularity, the value of
digitalis is hard to establish. It is usually thought that there must be irregularity, and Sir
James McKenzie felt that he had established this as an axiom.
Where heart failure is accompanied by a regular rhythm, digitalis will only work in
certain cases. Vandenback and Christian got results in a certain number of cases, but in
every one of these cases, the patient was put to bed, under rigid dietary conditions.
There is a control period in these cases, where great improvement comes from the use
of digitalis in good-sized doses.
A great many such cases will get better with rest alone, and we must beware of
excessive enthusiasm; but there is no doubt that in certain of these cases the results are
spectacular, the urinary output increases considerably, and the patient is very much relieved. Results are best in valvular disease, worst where there is a rheumatic factor present.
Tabulating results, we find results as follows:
Auricular fibrillation with valvular trouble, where the pulse rate is over 120, we get very
marked benefit in 8 5% from the use of digitalis;
Non-valvular heart disease with auricular fibrillation—60%;
Rheumatic heart disease with auricular fibrillation—5 5%;
Where there is regular rhvthm, in the non-valvular cases we get 51% of good results, while
in rheumatic heart disease only 31% are benefited.
But Dr. Dock feels that even ii three out of four fail, still we should give the drug a
thorough trial; we should not be influenced by statistics. If there is a chance for improvement, we must not neglect this chance.
Digitalis, like quinidine, is of no value in anginal states, where there is shock (e.g.,
after coronary thrombosis) or fever or in nervous or hyperthyroid tachycardia, though it
has been used for the latter.
Digitalis like quinidine causes auricular fibrillation  in  certain cases;  it  causes extra-
Page 251
H w
systoles to a greater degree than quinidine, and it causes a nausea, which is like seasickness.
The outstanding characteristic of this nausea is the prostration that accompanies it.
How These Drugs Work
They have a very marked effect on cardiac irritability.
They depress myocardial irritability. Irritability in the heart varies with the stage of
the heart cycle. It disappears in systole, and returns in diastole.
Auricular muscle irritability is much greater than ventricular. These drugs affect the
rate at which muscular irritability is recovered, and by depressing the irritability, they slow
up the rate of its recovery.
By recovery wc mean a recovery to the point where the beat returns, and can be propagated through heart muscle. This is the crucial point of cardiac irritability: not a mere
response to stimuli. There must be actual recovery to a definite point.
Normally, this recovery occurs very rapidly, within a fraction of a second.
If the vagus is stimulated, recovery is less rapid, while atropine, by removing the vagus
influence, shortens recovery time.
Digitalis in the maximum safe dose causes marked slowing of recovery.
Quinidine in maximum tolerable dose causes even more marked slowing.
Digitalis causes arrhythmia sooner than quinidine.
Conductivity varies with the irritability; they are different phases of the same process.
Quinidine depresses auricular conductivity more than ventricular; the effects disappear
in about six hours—hence dose must be repeated in not longer than six hours.
In their action on cardiac irritability, digitalis and quinidine vary according to vagus
tone; while they diminish irritability, this would not in itself account for the ectopic beat
irregularities that are caused. These originate in zones of lessened irritability set up by the
use of these drugs in the cardiac muscle, digitalis having a more marked effect than quinidine.
[At this point in his address, Dr. Dock became highly technical, and as he depended
largely on the use of slides, a rather intricate explanation, we feel that it would be unfair
to him to try to report this part.
He went on, however,, to consider several important points in connection with the
action and use of digitalis.]
I I I I 1 I 1 1 I 1 I 1 I I I I I 1 I I I I I 1 I 1 1 I I 1 1 I I I I I I 1 I I I I I I I I 1 I I I
Equal to the |
I Famous Spas of Europe
Many physicians, after visiting leading spas in Europe, find
the waters at Harrison Hot Springs are more highly mineralized. Bad Nauheim is particularly comparable "with Harrison,
as to location and elevation. For heart, nervous and rheumatic cases, the treatments at Harrison are found particularly beneficial. Specific information will be gladly
Relax and Revitalize
at thi
Page 252 (1) Digitalis does not raise blood pressure, as we used to be told it did. As a matter
of fact it lowers it.
(2) Digitalis does not goad on the heart, or drive it; it "lubricates" its action, and
allows it to work more efficiently and easily, and to do more work.
(3) In treating cases with these drugs, we must know how to use them—parenteral
administration is very unsatisfactory; best given by mouth, or by rectum.
(4) The effect of digitalis lasts for many days, and we must gauge our dosage accordingly; quinidine, as stated above, wears off in about 6 hours, when given in full doses.
(5) Quinidine is the better in treating auricular fibrillation persisting after thyroidectomy—also in venereal disease.
Enlarged hearts and mitral stenosis do better with digitalis—the post-coronary thrombosis perhaps better with quinidine. The auricular fibrillation goes on, but the ventricular
rate improves.
With aortic insufficiency, hearts rarely fibrillate, and quinidine is the best drug here.
Where we have mitral stenosis, the presence of auricular fibrillation is an advantage,
while it is a grave disability in aortic insufficiency.
Experience, said the speaker finally, is of course necessary in the use of these drugs,
but we must not let the risk of using quinidine frighten us too much.
In the cases where it is indicated it should be used. The prognosis is bad in any case,
and we may well take our courage in our hands and "putt for the hole."
SITUATION WANTED—General qualifications for doctor's
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Your patients will cooperate willingly
when delightfully palatable Petrolagar is
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Petrolagar is a mechanical emulsion of
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Samples free on request
Petrolagar Laboratories of Canada, Ltd.
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that really are nicer
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Page 2 5
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Complete  bibliography  and  detailed  literature upon request to  the
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Phone Seymour 698
73 0 Richards St., Vancouver, B. C. Results from
Lack of Pasteurization
in Great Britain
DR. A. C. BAXTER, Assistant Director of the Illinois State
Department of Public Health, states, in an address before
a group of dairymen at the University of Illinois:
"Striking evidence of the influence of pasteurization is found
by comparing the mortality from tuberculosis in Great Britain with
that in the United States and Illinois.
"Pasteurization is not a general practice in Great Britain.
Neither has tuberculosis been eliminated from the dairy herds in
that country to any substantial extent.
"On the other hand, the public health organizations of Great
Britain are much more extensive and have been active for a much
longer period than in the United States. A comparison of specific
death rates is therefore all the more significant when some factor
such as the pasteurization of milk is involved.
"In 1929 the death rate from all forms of tuberculosis in
England and Wales was 96 per 100,000 population. In the same
year the rate was 76 in the United States and 70 in Illinois.
"For 1930 the rate was 90 in England and Wales, 72 in the
United States and 63 in Illinois.
"For a closer analysis of these data it is necessary to take the
1928 statistics, the most recent available in detail from Great
Britain. In that year the general death rate from tuberculosis in
England and Wales was 93 per 100,000 population and in the
United States 79.
"For pulmonary tuberculosis, however, the rate in England
and Wales was only 76 against 70 in the United States, not a great
"For non-pulmonary tuberculosis, the types most frequently
due to bovine infection, the rate in England and Wales was 17
against 9 in the United States. In other words, the death rate from
those forms of tuberculosis most frequently of bovine origin in
England and Wales, 'where pasteurization is not a general practice
and where cattle are highly infected with tuberculosis, was nearly
twice that which prevailed in the United States."
Because they have to do with distant lands, these statistics
probably will not receive much consideration in the United
States. However, in Canada, where the ties with Great Britain
are closer, they should be considered thoughtfully.
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One of the disadvantages of the ordinary wet
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Under the influence of an Antiphlogistine
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Antiphlogistine is an antiseptic dressing of just
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Made in Canada AND    THE
New knowledge has brought new viewpoints regarding dietary constituents—particularly the vitamins. Primitive provender was vastly
different from the food of today. Moreover, the methods of cooking
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full dietary requirements have been met. Among other things we
know that vitamins A and D are indispensable to normal growth,
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to furnish an adequate amount of these vitamin factors in a palatable
form, unobjectionable to the most finicky of patients. Years of intensive research on nutritional problems have led to the development of
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For many years Parke,
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Parhj-Djtts Hjliver Oil with Viosterol is supplied in 5-cc.   and 50-cc.   amber
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Dispensing Opticians
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A Medical Institution for the restoration of health, situated eighteen
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Modern facilities for the treatment of all classes of patients with the
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Vitamin A-.
Vitamin B(B.)
Vitamin C	
Vitamin D	
Vitamin E	
Vitamin G	
Calories per oz.
— to +
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+ +
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+ to + +
+ +
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Pablum is rich in
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Pablum consists of wheat-
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Supplies vitamins A, B, E,
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* **The daily use of specific vehicles for vitamins C and D (e. g.» orange juice for C and cod liver oil or
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PABLUM (Mead's Cereal thoroughly pre-cooked by aj
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Having a fiber content of only 0.9%, Pablum can be re<
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Westminster 288


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