History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: June, 1941 Vancouver Medical Association Jun 30, 1941

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of the
JUNE, 1941
No. 9-
With Which Is Incorporated
Transactions of the
Victoria Medical Society
Vancouver General Hospital
iSt. Paul's Hospital
In This Issue:
SUMMER SCHOOL PROGRAMME^— ;^^^^^^^::     ___. jgjj 250
NEWS AND gjgjii^l^^B^^^B^B^^B JIB ^B  252
ARTERY HEART DISEASE—Dr. G. F. Strong. _^ ;;jjfr;      .-fll§ 267
REVIEW OF SPINAL ANALGESIA—-Drw G. Stonehouse  WSf\-- 280
SUMMER SCHOOlJJUNE 17th to 20th inclusive, 1941 ii
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combine* d draehm«, In wafr.
Dose: One or two
nf exces9 aoa
■*«m"*?^rtaSw* to strong^^ DUaxol
the stomach, ye^ 3Ufpl     aad. T^ o{ the
stimulate the ^""^     on the acid cpncenu   ukened to
«erts i ¥£3£££* ££&££££oeu;
stomach. This ^    •" fc,^ while v^*™.*.  &,. normal
the buffer action of the b      ^ interfere ^^n
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digestive process, g d l3 excreicu
of pregnancy.
Dtool is palatable and protective. _^
Ci is also supplied in Powder form.
Published Monthly under the Auspices of the Vancouver Medical Association
in the interests of the Medical Profession.
Offices: 203 Medical- Dental Building, Georgia Street, Vancouver, B. C.
Dr. J. H. MacDermot
Dr. G. A. Davidson Dr. D. E. H. Cleveland
All communications to be addressed to the Editor at the above address.
June, 1941
No. 9
OFFICERS, 1940-1941
Dr. W. M. Paton Dr. C. McDiabmid Dr. D. F. Busteed
President Vice-President Past President
Dr. W. T. Lockhart Dr. R. A. Palmer
Hon. Treasurer Hon. Secretary
Additional Members of Executive: Dr. Gordon Burke, Dr. Frank Turnbull
Dr. F. Brodie Dr. J. A. Gillespie Dr. G. H. Clement
Auditors: Messrs. Plommer, Whiting & Co.
Clinical Section
Db. Karl Haig Chairman Dr. Ross Davidson Secretary
Eye, Ear, Nose and Throat
Db. J. A McLean Chairman Dr. A. R. Anthony Secretary
Pediatric Section
Db. R. P. Kinsman Chairman Dr. G. O. Matthews Secretary
Db. F. J. Bulleb, Db. D. E. H. Cleveland, Db. J. R. Davtes,
Db. A. Bagnall, Db. A. B. Manson, Dr. B. J. Harrison
Dr. J. H. MacDermot, Dr. D. E. H. Cleveland, Dr. G. A. Davidson.
Summer School:
Db. H. H. Caple, Db. W. W. Simpson, Db. Kabl Haig, Db. J. E. Habbison,
Db. H. H. Hatfield, Db. Howard Spohn.
Db. A. W. Hunter, Db. W. L. Pedlow, Db. A. T. Henby
V. O. N. Advisory Board:
Db. W. C. Walsh, Db. R. E. MoKechnie II., Db. L. W. McNutt.
Metropolitan Health Board Advisory Committee:
Db. W. D. Patton, Dr. W. D. Kennedy, Db. G. A. Lamont.
Greater Vancouver Health League Representatives:
Dr. R. A. Wilson, Dr. Wallace Cobubn.
Representative to B. C. Medical Association: Db. D. F. Busteed.
Sickness and Benevolent Fund: The Pbesident—The Tbustees.
#«* ill*'
If fan
The New, Dry
Micro Test for Urine Sugar
One drop of urine on a little Galatest powder gives an immediate
positive or negative reaction. No test tubes or bunsen burner required.
Co/or chart and full particulars on request
THE DENVER CHEMICAL MFG. CO., 153 Lagauchetiere St. W.# Montreal {Vancouver   health   department
Total population—estimated —     272,352
Japanese population—estimated  8,769
Chinese population—estimated   8,558
Hindu population—estimated   360
Rate per 1,000
Total deaths i 292
Japanese deaths  „ 2
Chinese deaths .  20
Deaths—residents only  249
Male,  251;   Female,  245    496
INFANTILE MORTALITY: April, 1941 April, 1940
Deaths under one year of age      10 13
Death rate—per 1,000 births—      20.2 31.9
Stillbirths (not included in above)      11 10
99 9
March, 1941
Cases   Deaths
April, 1941
Cases   Deaths
May 1-15,1941
Cases   Deaths
Scarlet Fever  12
Diphtheria —'it —  0
Chicken Pox  84
Measles  — 1437
Rubella  303
Mumps :  7
Whooping Cough  13
Typhoid Fever	
Undulant Fever	
Erysipelas .	
Meningococcus Meningitis
Paratyphoid Fever	
West North
Burnaby  Vancr.  Richmond   Vancr.
Vane.  Hospitals &
Clinic  Private Drs.  Totals
V. D. figures not received from Victoria.
Another Product of the Bioglan Laboratories, Hertford, England
Stanley N. Bayne, Representative
Descriptive Literature on Request
Vancouver, B. C.
Page 249 J---:, IS;
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A valuable nutritive aid, presented in palatable liquid form especially suitable for
oral administration to infants and children. "Thironex" combines iron in its most
readily absorbable form, with copper as a catalyst, and all the known factors of the
Vitamin B Complex.
Each Fluid Ferrous Chloride (Citrated)      -      13.3 grains (Fe: 4 grains)
Ounce   Contains'   Copper Sulphate       - 0.1 grain (Cu: 0.04 grain)
Extract of Liver as derived from 7 grams of fresh calves' liver
Supplemented by:   Vitamin Bi 275 International Units
Riboflavin- 100 gamma
Nicotinic Acid -----      -----5 mg.
® Vitamin B6, Filtrate and Haematopoietic Factors
are supplied in the liver extract content.
Available in 16 oz. bottles—literature and professional specimens on request
AYERST, McKENNA & HARRISON LIMITED • Biological and Pharmaceutical Chemists • MONTREAL, CANADA
Hotel Vancouver, June 17 to 20, 1941
Tuesday, June 17th
9:00 a.m.—Dr. Struthers: "Artificial Feeding of Infants."
10:00 a.m.—Dr. Janes: "The Diagnosis and Management of Carcinoma of the Breast."
11:00 a.m.—Dr. Osgood: "Therapeutic Thinking."
12:30 p.m.—LUNCHEON, Mayfair Room, Hotel Vancouver.
Speaker: Dr. Perrin H. Long.
3:00 p.m.—CLINIC.
8:00 p.m.—Dr. Long: "Modern Nutrition—Pills or Food?"
9:00 p.m.—Dr. Gibbons: "Rickettsial Diseases in Man."
Wednesday, June 18 th
9:00 ajn.—Dr.  Struthers:   "Cerebrospinal Meningitis,  with Particular. Attention  to
10:00 a.m.—Dr.  Osgood:   "The  Treatment  of  Subacute  Bacterial  Endocarditis   and
Staphylococcic Bacteriaemias with Neoarsphenamine and Sulphathiazole."
11:00 a.m.—Dr. Long: "Modern Methods in the Control of Infections."
2:30 p.m.—CLINIC.
8:00 p.m.—Dr. Fluhmann: Gynecologic Factors in the Investigation of Sterility."
9:00 p.m.—Dr. Janes: "Tumours of the Parotid Gland."
Thursday, June 19 th
9:00 a.m.—Dr. Fluhmann: "The Gonadotropic Hormones."
10:00 a.m.—Dr. Janes: "Carcinoma of the Bronchus (Lung)."
11:00 a.m.—Dr. Struthers: "Chronic Non-tuberculous Pulmonary Disease, with Particular Attention to Chronic Basal Bronchitis and Bronchiectasis."
8:00 p.m. | —Panel Discussion on Chemotherapy:
9:00 p.m. j     Dr. Osgood; Dr. Long; Dr. Fluhmann; Dr. Struthers.
Friday, June 20 th
9:00 a.m.—Dr. Long: "The Clinical Use of Sulphanilamide and its Derivatives in the
Treatment of Bacterial Infections."
10:00 a.m.—Dr. Fluhmann: "The Clinical Use of Estrogenic Hormones."
11:00 a.m.—Dr. Janes: Lung Abscess."
2:30 p.m.—CLINIC.
8:00 p.m.—Dr. Osgood: "The Recognition of Cardiac Arrhythmias without the Use
of an Electrocardiogram."
9:00 p.m.—Dr. Struthers: "Rheumatism in Childhood—Manifestation and Treatment."
DR. PERRIN H. LONG, Professor of Preventive Medicine, Johns Hopkins University
School of Medicine, Baltimore, Md.
DR. R. M. JANILS,Department of Surgery, University of Toronto.
DR. E. E. OSGOOD, Assoc. Professor of Medicine, University of Oregon Medical School,
Portland, Ore.
DR. C. FREDERIC FLUHMANN, Assoc. Professor of Obstetrics and Gynecology,
Stanford University School of Medicine, San Francisco, Calif.
DR. R. R. STRUTHERS, Professor in Pcediatrics, McGill University, Faculty of Medicine, Montreal, Que.
DR. R. J. GIBBONS, Laboratory of Hygiene, Dept. of Pensions and National Health.
Page 250
!f i ': if $?$<$£
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Synthetic Vitamin Bi Hydrochloride)—Available in solution for parenteral administration and in Tablet and Micro-
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RIBOFLAVIN SQUIBB—Available in 1 mg. capsules for oral
PYRIDOXINE HYDROCHLORIDE SQUIBB—Pyridoxine Hydrochloride Squibb is supplied in Microcaps for oral administration and in Solution for parenteral use.
NICOTINIC ACID SQUIBB—Tablets Nicotinic Acid Squibb,
25, 50 and 100 milligrams each—for oral administration.
NICOTINAMIDE (Nicotinic Acid Amide) SQUIBB—Avail
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B-Complex Capsules Squibb
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For Literature Write 36 Caledonia Road, Toronto.
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lk3 FACTOR The last number of the Bulletin, judging by the record number of requests for
extra copies, was of considerable interest to our readers, chiefly on account of the report
of the Cancer Meeting, which drew very favourable comment. It is also the largest
number we have ever had—both in reading matter and in advertising material. It is
therefore the greater pity that certain very serious mistakes should have occurred in the
makeup of the issue—and it is with sincere regret that we tender our apologies to certain people who have a genuine grievance against us.
In the first place, in the Report of the meeting, the name of Dr. H. H. Murphy,
of Victoria, was omitted as the author of the very scholarly paper on Cancer Research:
which was one of the three main papers, and was distinctly one of the highlights of the
meeting. Dr. Murphy's name was on the manuscript as sent to the printer, and we do
not understand how it came, alone of all those who spoke, to be omitted. Victoria contributed a great deal to this meeting—Dr. Murphy's paper being followed by a thoughtful discussion by Dr. T. McPherson of that city. We have written; to Dr. Murphy,
personally expressing our regret, but we take this opportunity of saying publicly that
we are very sorry.
Then, nearer home, a very bad mistake was made. The Vancouver General Hospital Publications Committee furnished three excellent short papers on Parenteral
Administration of Fluids in Children and generally. These three were all marked to
go together in the Vancouver General Hospital Section, and in some mysterious way got
separated, so that the whole effect is spoiled, and the coherence of the three into a
unit destroyed. Again we are very sorry—and have written to that effect to the Publications Committee of the Hospital.
The Annual Meeting of the Medical Services Association will be held on Friday,
July 4th, at 8 p.m., in the Medical-Dental Auditorium, and we urge all our members
who can possibly manage to attend it, to do so. The M-S-A., as it is called, is now an
actively functioning organisation, and we think it is on the high road to success. It has
been carefully thought out by the B. C. Medical Association—has been certified as
actuarially sound by competent actuaries, and provides for excellent medical service at
moderate cost on terms which are fair to all concerned.
But we do not think that the medical profession as a whole is quite conversant with
all the facts about the M-S-A that it should know. We should not be content merely
to accept the M-S-A, even to agree to work for it—we should be enthusiastic, even
aggressive, supporters of it—selling it to our patients, urging them to organise and join
it. We should first know what its advantages are—just why we should support it. We
should be familiar with the working of it, the cost of it, the benefits to be derived from
it by the public—and we are confident that if we knew all these things, we should be
very actively working for its progress and success. Details, any facts you may want to
know, can be readily obtained from the office of the M-S-A in the Medical-Dental
Bldg. We believe, too, that a visit to the Annual Meeting will repay anyone who can
possibly go.
This organisation started its work at the worst possible time—but also, in one sense,
at the best possible time. For it is badly needed—and it is our answer, as a profession,
to the charges that have been made against us so often—that we have no constructive
plan of our own, but merely obstruct and oppose those who would suggest and bring
forward a plan. Well, we have here a constructive plan of our own, equitable from our
point of view, and beneficial to us, it is true—but also equitable and fair and very
beneficial to those who become subscribers to it.    We must make this succeed—for it
Page 251
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provides a real working scheme of Health Insurance, along the lines, and based on the
principles, that we have so often drawn and enunciated. It has become a success in
Ontario—let us see to it that we make it a success here. It is vitally important that
this organisation should live and thrive, not only as a source of great benefit and service
to the public, but from our own selfish point of view. It may, it should, turn out to
be a bulwark of considerable value and efficacy against certain dangers that threaten us
as a profession. In the meantime, it is a source of considerable monetary gain and satisfaction to all of us who have had anything to do with it.
Dr. and Mrs. A. N. Dobry are receiving congratulations on the birth of a
son on
May 5th.
Congratulations are being received by Dr. and Mrs. Gordon Stonehouse on the birth
on May 8 th of a daughter.
Lieut. C. C Covernton, son of Dr. and Mrs. C. F. Covernton, and Miss Betty Bingay
were married on May 17th.
Dr. R. E. McKechnie II has been in the wilds of British Columbia, and during his
peregrinations visited Gun Lake where he saw Mrs. Vanderburgh, well known as formerly
Miss J. M. Choate, our Librarian. Doctor McKechnie brought greetings from Mrs.
Vanderburgh and told us that they have a very delightful place which gives promise of
being a popular fishing resort.
Dr. and Mrs. A. C. Frost and Dr. and Mrs. J. W. Arbuckle travelled to Montreal to
attend the graduation exercises of their sons from McGill University.
Dr. and Mrs. W. A. Whitelaw are visiting in Montreal.
Colonel Lavell H. Leeson was at the coast during May.
•^ *i* •«■ »5*
Dr. C. G. G. Maclean is now with the R.C.A.M.C.
Dr. J. E. Walker has entered the R.C.A.M.C.
Major S. G. Baldwin has been appointed to command No. 12 Field Ambulance. This
means promotion to the rank of Lieut.-Colonel. Major Baldwin has been next Senior
Officer with Lieut.-Colonel Roy Mustard of 13 th Field Ambulance. Capt. M. R. Caver-
hill, an officer in the 13 th Ambulance will be transferred to the 12th and assist Major
Baldwin in the mobilization of that Unit.
Dr. Ethlyn Trapp will present a paper, "The Radiation Treatment of Carcinoma of
the Uterus," to the Victoria Medical Society at the June meeting.
Word has been received from Capt. H. R. L. Davis, Lieut.-Col. F. J. Haszard, Lieut.-
Col. H. A. DesBrisay, Major Andrew Turnbull, Capt. J. A. Ireland and Capt. Henry
Scott, all of whom are serving with the Canadian Army Overseas.
Doctors E. F. Chapman, W. H. Fahrni and C. S. Rennie of the Interne Staff of the
Vancouver General Hospital are now serving with the R.C.A.M.C.
Page 252 fl
Dr. J. McDiarmid of New Westminster is now with the R.C.A.M.C.
Capt. H. R. L. Davis in a letter told of having seen Major W. L. Boulter. Apparently
iey were in the same camp" and they were going to attend a meeting on that afternoon
k the office of the A.D.M.S.
Major Andrew Turnbull, Radiologist at No. 1 Canadian General Hospital asked to be
jemembered to his medical friends in British Columbia.
Lieut.-Col. G. C. Kenning, D.M.O., M.D. No. 11, is a frequent visitor in Vancouver.
Dr. P. L. Straith of Courtenay visited the office this month.
Dr. Ross Stone of Vanderhoof has returned after a lengthy visit at the coast.
Capt. F. H. Stringer was in Vancouver for a short visit.
The following members from British Columbia will contribute to the programme
of the Annual Meeting of the Canadian Medical Association in Winnipeg: Dr. G. F.
Amyot of Victoria, Provincial Health Officer; Dr. Earle R. Hall of Vancouver; Dr. A.
B. Nash of Victoria; Dr. Ethlyn Trapp; Dr. S. E. C. Turvey and Dr. Wallace Wilson
of Vancouver.
Doctors W. A. Clarke of New Westminster and J. R. Naden of Vancouver have
been asked to participate in Conferences on Economics and Fractures, respectively.
Dr. T. C. Holmes of Burns Lake has left to do post-graduate study. During his
absence Dr. Robert MacKenzie of Grantham's Landing is carrying on the practice.
Dr. H. N. Watson of Duncan called at the office while last in Vancouver.
Dr. N. E. Morrison of Nelson visited the office.   He spent two weeks on the Coast.
Dr. G. W. Ross has moved to Vanguard, Sask.
Dr. and Mrs. H. F. Inglis of Pennant, Sask., are receiving congratulations on the
birth of a daughter, April 15th.
Dr. J. L. Coltart, who is now associated with Dr. R. W. Irving at Kamloops, took an
X-Ray course at Toronto General Hospital during March and April. The course was
conducted by Dr. G. E. Richards and staff. While the course was primarily for military medical men, Doctor Coltart reports that it was very well organized. He also
took some special work at the Sick Children's Hospital.
Dr. W. H. White of Penticton attended the Annual Meeting of the Spokane Medical
Dr. and Mrs. L. F. Brogden of Penticton have been visiting at the coast.
*V *^ *** *s*
We are glad to report that Dr. Osborne Morris of Vernon is much improved in
Dr. R. B. White of Penticton is reported to be enjoying life with a new car and,
also, a new dog,—the latter was a present from his old friend, Doctor Osborne Morris.
Page 253
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Dr. and Mrs. H. V. Gale of Copper Mountain are receiving congratulations on the
birth of a daughter.
Dr. J. S. Daly of Trail has returned from a post-graduate course in Boston.
#       *       *       *
Dr. G. F. Young has left Salmo, and Dr. W. McK. McCallum is taking over the
practice at that point.
Capt. F. E. Coy is at present in the West Kootenay conducting medical boards.
Dr. A. S. Underhill of Kelowna is reported to have joined the R.C.A.F. Medical
Service and stationed at Jericho. Doctor Underhill served with the Royal Flying Corps
in the last war.
Dr. R. W. Patten of Chilliwack has left to serve with the R.C.A.M.C.
The Chilliwack Medical Society elected officers as follows: President, Dr. J. D.
Moore; Vice-President, Dr. A. R. Wilson; Secretary-Treasurer, Dr. G. A. C. Roberts.
Dr. and Mrs. A. R. Wilson of Chilliwack are to be congratulated on the birth of
Dr. E. Therrien of West Vancouver is motoring in the Interior of British Columbia.
The North Shore Medical Society held a special meeting devoted to Cancer when
all Cancer cases for 1940 in the North Vancouver General Hospital were reviewed.
Dr. J. M. English of Surf Inlet takes his patients by plane to Prince Rupert.
Dr. R. Geddes Large of Prince Rupert is taking his new fifty-foot cruiser on a trial
Dr. L. W. Kergin of Prince Rupert enjoys a good car and has just treated himself to
a new Buick.
Prince Rupert has a fine new hospital. The old hospital building has been demolished
and plans are already under way for an annex. This will be known as the Military
The sympathy of the profession is extended to Dr. William A. Wilson of Vancouver
in the loss of his wife by death.
Dr. and Mrs. C. E. McRae of Williams Lake are receiving congratulations on thi
birth of a son.
Doctors John Christie, D. E. H. Cleveland, H. A. MacKechnie, C. G. G. Maclean,
W. L. Lockhart and D. H. Williams attended the Spring Semi-annual Meeting of the
Pacific Northwest Dermatological Association in Tacoma, on May 8 th. This Association,
composed of dermatologists practising in British Columbia, Washington and Oregon, is
the only international dermatological society on the continent.
Doctors G. A. Bird and G. B. Bigelow of Victoria have"closed their offices and joined
up with the R.C.A.M.C.
Page 254 . :.
Dr. H. V. Hughes, until recently at St. Joseph's Hospital, has taken an office in the
Campbell Building, Victoria, and set out in general practice.
Dr. John D. Stenstrom, formerly of Vancouver, has opened offices in the Pemberton
Building in Victoria.
Doctors Lyall Hodgins of Vancouver, W. T. Barrett, M. J. Keys and J. W. Lennox
of Victoria, spent a very enjoyable 24th of May at Qualicum Beach. Dr. Keys cleaned
up on the game, as usual.
Dr. George T. Wilson of New Westminster has been rusticating during the past
few weeks. He visited the Cowichan Lake on Vancouver Island and fished in the Cowi-
chan River. He also cast a wicked fly at some of the Rainbows in the Kamloops Lakes.
He tells us he caught some big fish and plenty of them—but we're from Missouri.
Dr. S. Cameron MacEwen of New Westminster, and his son Bruce, made an extended tour by automobile through the Interior, finally arriving at Nelson, and returning
over Rossland Mountain. It was interesting to note that he was allowed forty-eight
hours in the United States and was able to return via Seattle.
Dr. and Mrs. John McCaffrey of Agassiz are receiving congratulations on the birth
on May 27th of a daughter.
Congratulations are being received by Dr. and Mrs. R. W. Garner of Port Alberni
on the birth of a son.
Dermatologic Therapy in General Practice, 1940, by Marion B. Sulzberger and Jack Wolf.
Surgical Clinics of North America—Symposium on Traumatic Surgery, April, 1941.
Transactions of the American Association for the Study of Goitre, 1940.
Medical Clinics of North America—Symposium on New Methods  in Diagnosis and
Treatment, May, 1941.
The Pharmacological Basis of Therapeutics, by Louis Goodman and Alfred Gilman, 1941.
Multiple Human Births, 1940, by Horatio Hackett Newman.
The Library is collecting data on Industrial Medicine, and now has certain material
available. The Department of Pensions and National Health at Ottawa, and the American Medical Association have both been approached by the Library Committee and on
their advice the purchase of relevant publications is under consideration.
Pamphlets on the following subjects have so far been received from Ottawa:
A Memorandum on Occupational Hazards in the Aeroplane Industry.
Occupational Hazards in the Munitions Industry.
Benzol Poisoning—Information for Employers and Employees.
T.N.T. Poisoning—Information for Employers and Employees.
Nitrous Fume Poisoning—Information for Employers and Employees.
A bibliography of current literature is being compiled, and following are some of
the subjects listed:
Study of Asbestosis in the Asbestosis Industry.
Chronic Benzene Poisoning.
Page 255 S?T
The Relative Toxicity of Lead and some of its Compounds.
Toxicity and Potential Danger of Carbon Monoxide.
Prevention and Treatment of Affections Occurring in the Magnesium Industry.
In addition to the above, the Library already has the following books:
Occupational Affections of the Skin, 1928, by R. Prosser White.
Occupational Diseases of the Skin, 1939, by Louis Schwartz and Louis Tulipan.
Industrial Toxicology, 1934, by Alice Hamilton.
Symposium on Legal and Industrial Medicine—Medical Clinics of N®rth America,
March,  1914.
Three other books are on order but have not been received in the Library yet.   The
titles are listed below:
Spray Painting Hazards, 1939, by Jakob Jakobsen.
Industrial Hygiene, 1940, by A. J. Lanza and Jacob A. Goldberg.
Toxicity of Industrial Solvents—Summaries of published works, compiled by
Ethel Browning, 1937.
: <«
The profession mourns the passing of a member who served in this province during
many years and in that time made a very fine contribution to medical practice and the
welfare of the people.
The late Dr. Whillans died suddenly on April 20th while doing locum tenens for
Dr. McKenzie Morrison at Stewart. He had practised at Hedley and Princeton before
settling in Victoria in 1910. He served during the last War with No. 5 General Hospital. After the War Dr. Whillans returned to Victoria and then went to Stewart,
where he practised during ten years.
Dr. Whillans had retired from active practice but became a real sheet-anchor of the
College office as he served in all parts of the province very willingly and acceptably. He
could be depended upon to relieve on short notice in any.emergency.
Born in Ottawa sixty-nine years ago, he graduated from McGill and was registered
in British Columbia in 1899. He was a member of the Masonic Order and had shewn
interest in public affairs.
Mrs. Whillans and her daughter have the sincere sympathy of the profession and an
assurance that the late Dr. Whillans was held in high esteem by his colleagues.
In the Cancer Meeting reported in the May issue of the Bulletin, the importance
of a Biopsy Service for the Province was stressed, and the Bulletin heartily endorses
this suggestion. Every medical man should be seized of the necessity for such a service,
and the value it would have. Each of us should have three things constantly in mind.
First, the advisability of biopsy at the earliest possible moment. Secondly, the right and
proper method of obtaining such a specimen, by punch or otherwise (many specimens
are useless because badly taken, and there are risks to avoid as well), and thirdly, the
proper way of sending such biopsies to a laboratory (the medium used is of vital
importance, 5 per cent formalin being easily the best). Any competent pathologist wu
gladly give his advice in these matters. Meantime, as far as is in our power, we should
continue to urge a provincial service. It may be suggested that there is no money available for this. We do not know, of course, much about this—but if even one or two
biopsies a month are the means of early, accurate diagnosis and of saving a life, it is very
cheap at any price—and if the government realizes that such a service will be use
and used properly, it will be more ready to institute it.
Page 256
For many years, there has been a friendly international conflict raging between ourselves in British Columbia, and our medical confreres in Washington, to the south of us,
especially centred around Vancouver and Seattle. It is a war of divots and of mashie
niblicks, of long grasses and low grosses, and, towards the close of day, of tall stories
and tall glasses, of limericks and some of the more curious variations of biological history.
The war has made some difference in the methods of warfare, in the location of the
battlefields, and so on, but it has not wholly put an end to these periods of entertainment
and good fellowship: and this year we had our annual tournament, the Capilanrj Golf
Club being the scene of battle. From all sides our guests descended on us. Seattle sent
52 stalwarts, Victoria 8, New Westminster 2, one came from Cloverdale, and Vancouver
rolled up 65 strong. The weather was fine, everyone was out to enjoy himself, and most
men took the day off and played the full 36 holes. Seattle, we must admit, played a
very strong game, and on balance, must be regarded as the winners, though no definite
announcement is forthcoming. A Seattle man, Dr. Lamson, was the winner of low net
with a 66, while the low gross of 77 went to Dr. Bigelow of Victoria: both scores, over
the long Capilano course, are highly creditable. Dr. Stromberg of Seattle won the prize
for being closest to the pin on a selected hole, while another Seattle man, Dr. Dorland,
won the highly dubious honour of having 'tlie high gross—no figures have been made
available, and perhaps it is just as well. Dr.- Neilson of Vancouver got the longest drive,
and thereby did much to retrieve our losses.
Then Dinner, in the sumptuously-appointed Club House, where Dr. P. A. McLennan
acted as Toastmaster, and spoke in witty vein. Others who spoke, and their names are
known to us all as brilliant exponents of post-prandial oratory (especially after a golf
tournament) were Drs. Perry, Houston, and Woodward of Seattle. In all, 135 men sat
down to dinner, and work in Vancouver the next day was very quiet, and restricted to
absolute necessities.
And so to the boats for Victoria and Seattle, to which we convoyed our guests at
the last possible minute, tired, replete, and we hope, sharing with us the memory of
a very good time. 	
The Bulletin, beginning with this issue, is making an appeal to all medical men in
British Columbia which we believe will meet with a ready and generous response. We
are establishing a fund to be known as "The Bulletin Fund" for the relief of British
medical men and their families in Great Britain, where, as a result of the war, there is
urgent need for help. It will be a branch of the War Relief Fund of the British Medical
Association, and will be remitted to Great Britain as opportunity arises. We are calling
for subscriptions, and are publishing the names of a few who have already subscribed.
We shall publish monthly names of all others who come in to the scheme. The smallest
or the largest amount will be gladly received.
There is no need for any words of ours to impress upon all who may read this, the
vital, urgent need for help. Many of our colleagues in Britain, men like ourselves, are in
very dire necessity today. They have lost absolutely everything — practice, homes,
money, and nothing we can ever do can possibly be adequate to meet this need. We
live here in ease, many of us in comparative affluence, and we owe a great debt to those
men over there. Time is of the essence of the contract, the urgency is immediate and
overwhelming, and we urge all who can to make as large and generous a contribution as-
they possibly can. We have taxes to pay, war funds to aid, charitable organizations to
support—all these things are true—but our duty here is a plain one, too, and as long as we
have any money at all to spare we must do what we can. So do not delay—get out
your cheque book, and give as much as you possibly can. Send money to the office of the
British Columbia or Vancouver Medical Association, earmarked "Bulletin Fund for
Relief of British Medical Men and Their Families." We are in communication with
Ottawa, where this scheme must first be submitted and approved.   Until it is approved,
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your money will be held.  Remember—"He gives twice who gives quickly."
Nor should we forget that today in British Columbia we have as honoured guests
some of these same victims of the ruthlessness of the Hun. We should be thinking of
them, too, and perhaps in an organized way, doing what we can to help. The British
Columbia Medical Association executive could perhaps organize this effort, and we throw
out the suggestion to them. Probably they have already taken this under advisement and
will have something to suggest. They can, we feel sure, count on the help and support
of all of us.
The following list represents a number of men who subscribed within 24 hours of
the inception of this scheme. Many others, we know, would have subscribed with equal
alacrity, but it was not possible, in the limited time, to get into touch with them—so
we would ask them to send their names in themselves.
Please send your name, with the amount you wish to subscribe, to "The Bulletin
of the Vancouver Medical Association," 203 Medical-Dental Bldg. The details of
how to make out your cheque, etc., will be sent you as soon as possible.
This is, of course, open to all British Columbia medical men, and we will very gladly
accept contributions from any part of the Province.
Dr. A. M. Agnew $50.00
Dr.  L. H. Appleby  50.00
Dr. J. W. Arbuckle  50.00
Dr. T. D. Bain  5.00
Dr. P. W. Barker  10.00
Dr. Murray Blair  25.00
Dr. H. H. Boucher  50.00
Dr. R. B. Boucher  50.00
Dr. Harold Caple   10.00
Dr. D.   B.   Cleveland... 40.00
Dr. Maurice Fox  50.00
Dr.  D. D. Freeze  10.00
Dr. G. E. Gillies  50.00
Dr. Colin Graham  50.00
Dr. Wilfred Graham.... 5.00
Dr. B. J. Harrison  10.00
Dr. J. E. Harrison  50.00
Dr. Lyall Hodgins  50.00
Dr. A.  W.  Hunter   25.00
Dr. R.  P.  Kinsman  25.00
Dr. Oliver S. Large  10.00
Dr. T. H. Lennie  25.00
Dr. Arthur L. Lynch.. 50.00
Dr. J. H. MacDermot.. 50.00
Dr. Colin McDiarmid .. 10.00
Dr. H. H. Mcintosh  50.00
Dr. R. E. McKechnie II 10.00
Dr. P. A. McLennan ... 25.00
Dr. A. Y. McNair  15.00
Dr. Neil McNeill   10.00
Dr.  F. H. Mayhood     5.00
Dr. G. A. Minorgan     5.00
Dr. W. L. C. Middleton  25.00
Dr. H. H. Milburn  20.00
Dr. Wm. Morris  10.00
Dr. W.  M. Paton  50.00
Dr.  R. A. Palmer  25.00
Dr. A. B. Schinboin.... 50.00
Dr. J.  W.  Shier  25.00
Dr. K. Shimo-Taka-
hara    20.00
Dr. R. A. Simpson  10.00
Dr. G.   F.   Strong  50.00
Dr. M. W.  Thomas    5.0
Dr. J. W. Thomson...
Dr. C. H. Vrooman...
Dr. W. A. Whitelaw.
Dr. D. H. Williams.
Dr. Wallace Wilson .... 50.00
British  Columbia  Medical  Association
(Canadian Medical Association, British Columbia Division)
President .Dr. Murray Blair, Vancouver
First Vice-President Dr. C. H. Hankinson, Prince Rupert
Second Vice-President JDr. A. H. Spohn, Vancouver
Etonorary Secretary-Treasurer Dr. Walter M. Paton, Vancouver
Immediate Past President . Dr. F. M. Auld, Nelson
Executive Secretary Dr. M. W. Thomas, Vancouver
Annual Meeting — Royal Alexandra Hotel
Winnipeg — June 23, 24, 25, 26, 27, 1941
General Council will meet on Monday and Tuesday.
Round-Table Conferences, instituted so successfully two years ago, will be continued
this year on the mornings of Wednesday, Thursday and Friday, from 9 to 10 o'clock.
General Sessions will be held on Wednesday, Thursday and Friday mornings froi
10:15 o'clock until 12:00 noon.
The various sections will hold their meetings on the afternoons of Wednesday, Thurs
day and Friday.
Thursday night has been given over to a dinner meeting under the auspices of th
Committee on Medical Economics, of which Dr. Wallace Wilson of Vancouver is
Golf on Tuesday.
Railway Fares—Vancouver to Winnipeg
CONVENTION RATE RETURN—Fare and one third, plus  10%
tax, bought on certificate (30-day limit) $ 68.42
SPECIAL EXCURSION RATE—30-day limit—plus tax $ 60.67
Date of purchase:—JUNE 6th, 7th, 8th ONLY.
Please Note—This ticket, although purchased early is good during
•i Convention dates.
SLEEPER—Lower $ 13.20
Section    18.50
Compartment — 1    33.00
2—    37.40
Drawing Room — 1 .    39.60
2    46.20
REGULAR RETURN FARE—Plus tax (3 months limit) $ 74.36
PLEASE NOTE: The cheap Excursion Tickets must be purchased on
JUNE 6th- 7th or 8 th.
Extract from letter from Dr. T. C. Routley, General Secretary,
Canadian Medical Association.
Three Hundred and Fifty Canadian Doctors Required
During the Next Year for Military Service
The Association is authorized by the military authorities in Ottawa to say that
medical officers for the Canadian Navy, Army and Air Force are needed now, and it is
anticipated that 350 will be required during the coming year. So far, and without any
direct appeal having been made, the medical profession of Canada has responded well
in that approximately one-tenth of its number, namely, more than 1,200 Doctors, are
already in active military service.
It is appreciated that essential Dominion, Provincial, Municipal and civilian requirements must, as far as possible, not be embarrassed. However' the needs of the military
services must be met and these may be classified for the next year's requirements into
the following groups:
(1) For service in Canada—These may be in medical category "A", "B" or "C'\
and in this class can be considered those over 40 years of age. Approximately
140 additional of these will be required.
(2) For overseas service—These should be in category "A" and preferably under
40 years of age. About 210 of such will be required.
No promise can be held out to any officer of definite appointment to overseas service, nor must there be any strings attached to the offer of service, although we are
assured by the military authorities that every effort will be made to see that proper
recognition is made of every man's qualifications and that he is used to the best advantage. It must be recognized that care is necessary with regard to the selection of specialists according to the requirements of the services at any one given time.
All medical men who are desirous of offering their services should immediately contact one of the senior medical officers of the Services in the District in which they reside.
Page 259
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|       for the NAVY, ARMY and AIR FORCE   |
NAVY—Senior Medical Officer:
Surg.-Commander D. W. Johnstone,
Senior Medical Officer,
Esquimalt, B. C.
ARMY—Royal Canadian Army Medical Corps,    *
District Medical Officer:
Lieut.-Col. G. C. Kenning,
D.M.O., M.D. No. 11,
Victoria, B. C.
AIR FORCE—Medical Services:
Principal Medical Officer:
Wing Commander E. E. Day
Principal Medical Officer,
Western Air Command,
Belmont Building,
Victoria, B. C.
Communications to any of these three Senior Officers should be directed to
the addresses given above.
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The Annual Dinner and Golf Tournament of the Fraser Valley Medical Society was
held at the Vancouver Golf Club on May 17th, 1941. Owing to the rain, the golf was
not a marked success.
A very fine dinner was served, following the liquid refreshments. The members of
the Society turned out in force, and in addition there were several guests present. The
Armed Forces were represented by Capt. Ira White, Capt. Begg, Lieut. Rennie and Lieut.
McDiarmid. Dr. M. W. Thomas, Executive Secretary of the British Columbia Medical
Association, was present. The lay guests were Mr. Jack Boothe, Mr. Rick Foote, and
Mr. Davies.
Following the dinner, a presentation was made to Lieut. J. M. McDiarmid- who, in
turn, thanked the Society.
Dr. Thomas gave a short but interesting talk on the medical man in relation to the
present conflict, and the position of the profession in B. C.
Immediately after the dinner, the regular meeting, and election of officers, was held.
The following officers were elected for 1941-42: Dr. A. W. Bowles, President; Dr. F. D.
Sinclair, Vice-President; Dr. R. E. Mitchell, Secretary-Treasurer. .
Following the election of officers, the Society was entertained by Mr. Boothe, who
drew cartoons of several of the members. Mr. Davies performed some of his well known
tricks. Mr. Foote performed, with his usual brilliance, on the piano. Dr. J. T. Lawson, the
singer of the Society, was absent owing to illness. At a late hour, the meeting adjourned.
Page 260
We are reproducing below a very significant letter and circular: the former
from Dr. C. T. Routley, General Secretary of the Canadian Medical Association; while
the latter speaks for itself. There is a very profound significance in these two things.
A very brief summary of the situation is necessary to make clear the importance of
this episode to medical men everywhere.
Peterborough, Ont., is an industrial town, and one of its larger industries is the
Canadian General Electric Co.: whose employees have for years had a health insurance
scheme of their own, which provided for house and office calls, but not for surgery or
specialties. A trifling deduction, somewhere in the neighbourhood of fifteen cents a
month, provided this: and two medical men did the work. The Company's personnel has
grown very greatly, and more medical help was necessary. The Benefit Assopiation
wrote to all medical men, suggesting that they send in their names to form a list. From
this list certain men would be chosen to do this work—still at the pittance mentioned.
This led to a crisis in Peterborough, and Dr. Routley's advice was asked. He came
to Peterborough, and consulted first the mdical men: advised them to refuse to do the
work, which they did. Immediately a storm arose, and the medical profession was
accused by the leaders of the men's Association of every crime in the calendar, and considerable newspaper publicity of an adverse sort was engaged in. Dr. Routley went and
saw the men's executive, and arranged a meeting between doctors and men: where, after
discussion, terms were reached. The letter from the Benefit Association was one result,
and to read it makes one rub one's eyes. But the important things are—first, the proof
of the necessity for, and the value of medical organisation—the real benefits that we
derive, and can in increasing measure derive, from a strong national medical association:
second, the proof that we can, by mutual discussion, arrive at agreements that will benefit both sides: third, the proof that our conception of medical service, namely, free choice
of doctor, maintenance of our standards of practice, and payment by schedule of fees,
is a practical one, and will appeal to the public, as it does to us. We must continue to
stick to our carefully thought out policies and principles—this Peterborough episode is
much more than a local success——it is another laboratory experiment that has a great
deal to teach us. —Editor.
Doctor Wallace Wilson, 184 College Street, Toronto 2,
203 Medical-Dental Building, May 3rd, 1941.
Vancouver, B. C.
Dear Doctor Wilson:
This letter is to bring you up to date on the Peterborough situation. In reviewing
the file I observe that I have already sent you a copy of the original contract offered by
the employees to the Doctors of Peterborough, also the comments of the employees when
they learned that there was medical opposition to their plan. Since then I have had a
number of conferences with the Peterborough Doctors and representatives of the employees including their adviser, and spent two days in Peterborough last week trying to
bring the matter to a head.
I think you will observe from the enclosed that the medical profession of Peterborough has made fine progress in the negotiations. In fact I am quite proud of their
achievements. It was a lot of fun last Friday addressing a mass meeting of Doctors and
employees and I must say I felt at the conclusion of the meeting that they were going
to get together. A committee of six was recommended, three Doctors and three employees, to carry out an experiment for say six months on a fee service basis, with the
profession gambling to take a loss on their business for this trial period if the amount
of money provided by the employees is not sufficient to meet the costs in full.
It would seem to me that the new arrangement offers a real opportunity for a plan
to be developed in Peterborough of great benefit to both sides. Further, this new plan
replaces the iniquitous 15c medicine which was in existence for six or seven years.
Page 261 •;;;*
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It strikes me that the enclosed memorandum is worthy of a place in our publications
in whole or in part.  Don't you think their rules are splendid?
With kindest regards, I am,
Yours sincerely,
T. C. Routley, General Secretary.
Canadian General Electric Company Limited
Peterborough Works
To all Members and Employees of Peterborough Works:
Commencing May 1, 1941, employes who are members of the Benefit Association
and who are paying for the physician's services, will be entitled to medical services from
their own physician. An arrangement has been made with the Peterborough Medical
Association which will be in effect during the next six months on an experimental basis.
We would ask all members to realize that this is an experimental effort and we will be
glad to hear any ideas you may have to offer.
In presenting this plan of medical service, we have in mind that there should be one
standard of service—the best—and that to guard the employees' health, the service must
be adequate. The local Medical Association members have pledged themselves to give
us this service and when we determine what the cost for such services should be, the fees
will be adjusted.   There will be a new contract made at the end of this six-month period.
Members are asked to keep a record of the service received and the number and dates
of calls made at the physician's office and the number of visits your physician makes to
you at your home. You are asked to do this so that, if necessary, we can check up at
the end of each month with the doctors to see that the accounts rendered are correct.
If it is necessary to check an account, we want you to have the record.
The Medical Association has advised us that there are some people who change from
one physician to another during the same month. While there is nothing to stop anyone
from changing his physician at anytime when there is just cause or lack of confidence,
we would advise you that such practice will be discouraged and you are expected to
choose your own physician who you are confident can look after your health.
Briefly, here are the rules you must follow in order that we may operate the plan
with the minimum of attention:
(1) If you go to the physician's office or have him come to your home, tell him you
are a member of "General Electric Employees Medical Services" and give him
your Clock No. and Name. If you don't do this the account would be sent to
you for payment instead of the Society.
(2) Call your physician at any hour if there is an emergency.
(3) If no emergency exists, call him at proper hours.
(4) Try to see him at his regular office hours.   This will accommodate both of you.
(5) When possible, leave orders for visits in the early part of the day.
(6) Do not demand his time when he is at meals.
(7) Unless necessary, do not make demands of his hours allotted to sleep. Do not
nurse your ailments all day and then call him after he has gone to bed.
(8) Allow him all rest possible on Sunday. Remember you like at least one day off
in seven.
(9) Physicians are made of the same material as their patients and so require rest,
food, sleep and time for study and proper recreation. The rested physician will
give you better advice than one who is overworked.
We feel that this is a great forward step in the history of our Association and we
hope you may derive greater benefits from the services provided.
May 1, 1941.
Page 262
Employees' Mutual Benefit Association.
A. Day, President. College of Physicians and Surgeons
President i Dr. Wallace Wilson, Vancouver
Vice-President ;—Dr. W. A. Clarke, New Westminster
Treasurer Dr. F. M. Bryant, Victoria
Members of Council—Dr. F. M. Auld, Nelson; Dr. F. M. Bryant, Victoria; Dr. W. A.
Clarke, New Westminster; Dr. Thomas McPherson, Victoria; Dr. H. H. Milburn,
Vancouver; Dr. Osborne Morris, Vernon; Dr. Wallace Wilson, Vancouver.
Registrar Dr. A. J. McLachlan, Vancouver
Executive Secretary Dr. M. W. Thomas, Vancouver
The First Annual General Meeting of the Medical Services Association will be held
at 8 p.m. on Friday, July 4th, 1941, in the Auditorium of the Medical-Dental Building,
Vancouver, B.C.   It is requested that as many Professional Members as possible attend.
The main business of the Meeting will be to receive the Report of the Directors with
the Balance Sheet and Financial Statement for the seven months of operations, from
Incorporation to May 31st, 1941, Reports of Officers, election of Directors and appointment of Auditors for the ensuing year.
Election of Directors
Each Member present in person shall be entitled to vote, provided that when electing
the Directors, each member shall vote only for the Director representing the class of
members to which he belongs. The Provisional Directors retire from office, and of the
four Directors to be elected, two shall be elected by the Employee Members and one by
the Professional Members and one by the Employer Members. Nomination of candidates for the Director representing the Professional Members has been referred to the
Committee on Economics of the College.
Professional Members
The following list of Professional Members has been taken from the records of the
Medical Services Association as of May 31st, 1941. A few doctors have overlooked
sending applications for membership. Any doctor whose name does not appear can
become a Professional Member by completing the application card, mailed to him by the
Executive Secretary of the College.
Why You Should Be a Member
It is important that all doctors become Professional Members and give their support
to this Organization, which has been set up to provide a means whereby groups may
budget for the cost of medical care under terms and conditions in keeping with the
normal practice of medicine.
Professional Members, M-S-A.
Prince Rupert and District:
Dr. C. A. Armstrong Ocean Falls
Dr. W. E.  Austin Hazelton
Dr. John P. Cade Prince Rupert
Dr. George E. Darby Bella Bella
Dr. J. M. English Surf Inlet
Dr. C. H. Hankinson Prince Rupert
Dr. L. W. Kergin Prince Rupert
Dr. R. G. Large _■ Prince Rupert
Dr. Duncan T. R. McColl
Queen Charlotte City
Dr. S. G. Mills Terrace
Prince Rupert and District:
Dr. J. H. Rivers Bella Coola
Dr. G. D. Sax ton Ocean Falls
Dr. J. E. Whiting Port Simpton
Prince George and District:
Dr. Gerald R. Baker Quesnel
Dr. Donald Beach : McBride
Dr. J. H. Black Wells
Dr. R. B. Brummitt Smithers
Dr. C. Ewert Prince George
Dr. Stanley P. Findlay Fraser Lake
Dr. L. M. Greene Smithers
Page 263
m 4 ft
Prince George and District:
Dr. T. C. Holmes Burns Lake
Dr. J. C. Kovach ' Quesnel
Dr.    E. J. Lyon ..Prince' George
Dr. J. G. MacArthur Prince George
Dr. C. E. McRae , Williams Lake
Dr. F. A. Olacke Wells
Dr. W. R.  Stone Vanderhoof
No. 4 District:
Dr. H. J. Alexander Vernon
Dr. W. F. Anderson Kelowna
Dr. F. W. Andrew Summerland
Dr. M.  G.  Archibald , Kamloops
Dr. N. J. Ball Oliver
Dr. Alan Beech Salmon Arm
Dr. D. M. Black ! Kelowna
Dr. B. de F. Boyce - —. . Kelowna
Dr. L. F. Brogden Penticton
Dr. J. M. Burnett Greenwood
Dr. H. L. Burris Kamloops
Dr. J. S. Burris .Kamloops
Dr. A. D. Callbeck - Penticton
Dr. H.  I. Campbell-Brown Vernon
Dr. J. L. Coltart Kamloops
Dr. W. A. Drummond Salmon Arm
Dr. John P. Ellis Lytton
Dr. A. F. Gillis — Merritt
Dr. J. E. Harvey Vernon
Dr. R. Haugen Armstrong
Dr. J. Stanley Henderson Kelowna
Dr. Robert  W.  Irving Kamloops
Dr. D. M. King Bralorne
Dr. C. M. Kingston ^ Grand Forks
Dr. William J. Knox Kelowna
Dr. J. H. Kope Enderby
Dr. D. McCaffrey Princeton
Dr. H. McGregor Penticton
Dr. H. B. McGregor Penticton
Dr. W. K. Massey '. Ashcroft
Dr. Wm. J. S. Millar ! Blue River
Dr. Osborne Morris Vernon
Dr. L. A. C. Panton Kelowna
Dr. J. R. Parmley Penticton
Dr. F. E. Pettman Vernon
Dr. J.  C Poole Revelstoke
Dr. W. Scat chard Chase
Dr. N. W. Strong Vernon
Dr. W. Truax Grand  Forks
Dr. A.  S.  Underhill Kelowna
Dr. Alfred W. Vanderburgh
West Summerland
Dr. G. L. Watson Revelstoke
Dr. W. H. White Penticton
Dr. C. J. M. Willoughby Kamloops
Dr. Gordon Edward Wride Hedley
Dr. A. J. Wright ' Vernon
Kootenay District:
Dr. F. M. Auld Nelson
Dr. D. J. Barclay Golden
Dr. L. E. Borden Nelson
Dr. G.  R. Barrett Nelson
Dr. M. R. Basted   Trail
Dr. H. R. Christie . Rossland
Dr. W. A. Coghlin  Trail
Dr. C.  E. Cook Michel
Dr. F. E. Coy     Invermere
Dr. D. J. M. Crawford   Trail
Dr. J.   S.   Daly ...  Trail
Dr. B. Dunham   . Nelson
Dr. W.  J.  Endicott    Trail
Page 264
Kootenay DistrictT
Dr. Arnold Francis New Denver
Dr. R. R. M. Glasgow \ Michel
*■  Dr. V. B. Gpresky.^3_ __Castlegar
Dr. F. W. Green __*_: Cranbrook
Dr. W. O. Green 1 Cranbrook
Dr. E.  S.  Hoare —Trail
Dr. W.   S.  Huckvale__ Kimberley
Dr. M. E. Krause j: j I Trail
Dr. Wilfrid Laishley  Nelson
Dr. William Leonard . .Trail
Dr. N. E. Morrison   Nelson
Dr. J. Vernon Murray Creston
Dr. R. B. Shaw _._ Nelson
Dr. M. J. Swartz Cranbrook
Dr. J.  B.  Thorn : Trail
Dr. W. M. Toone Nelson
Dr. E.  E. Topliff _ Rossland
Dr. F.   L.  Wilson Trail
Dr. Wm. Workman _ Coal Creek
Dr. Leonard B. Wrmch Rossland
Dr. G. F. Young Salmo
Fraser Valley District:
Dr. R. N. Anderson Ladner
Dr. A.   N.  Beattie . j loco
Dr. A. W. Bowles New Westminster
Dr. Lawrence Broe .Hammond
Dr. B. Cannon New Westminster
Dr. H. E. Cannon I Abbotsford
Dr. L.  S. Chipperfield |i—-Port Coquitlam
Dr. D. A. Clark New Westminster
Dr. W. A. Clarke New Westminster
Dr. H: - W. Epp _..____... _.!_. Sardis
Dr. Einar H. Erickson j Mission
Dr. Wm. E.  Henderson Chilliwack
Dr. Earl K. Hough New Westminster
Dr. Alfred A. King Ladner
Dr. J. T. Lawson ._ New Westminster
Dr. C. R.  Learn | New Westminster
Dr. A.  McBurney Langley
Dr. J. A. McCaffrey Agassiz
Dr. P. S. McCaffrey Agassiz
Dr. R.  McCaffrey Chilliwack
Dr. J. M. McDiarmid _ New Westminster
Dr. E. H. McEwen New Westminster
Dr. S. C. MacEwen New Westminster
Dr. W.  H. Mclntyre  Mission
Dr. G. H. Manchester J New Westminster
Dr. J. Margulius New Westminster
Dr. Joseph D.  Moore Chilliwack
Dr. D. G. Morse Haney
Dr. R. W. Patten Chilliwack
Dr. V. W. Pepper New Westminster
Dr. G. S. Purvis . New Westminster
Dr. G. A. C. Roberts  Chilliwack
Dr. J. G. Robertson New Westminster
Dr. Wm. A. Robertson New Westminster
Dr. Arthur O. Rose Langley Prairie
Dr. A.  C.  Ross New Westminster
Dr. J. F. Sparling ; Haney
Dr. O. Van Etter  New Westminster
Dr. Andrew R. Wilson Chilliwack
Dr. George T. Wilson New Westminster
Dr. E. W. Wylde New Westminster
North Shore District:
Dr. H. Dyer  North Vancouver
Dr. H. Carson Graham North Vancouver
Dr. T.  Alexander Johnston ...West Vancouver
Dr. J.   W.   Lang I West Vancouver
Dr. R. V. McCarley North Vancouver North Shore District:
Dr. G. A. McLaughlin—
Dr. E. A. Martin	
Dr. D. J. Millar _
North Vancouver
North Vancouver
North Vancouver
North Shore District:
Dr. A. C. Nash West Vancouver
Dr. Claire M. R. Onhauser West Vancouver
Dr. E.   Therrien West Vancouver
Vancouver and District:
Alex M. Agnew
A. G. Elvin
Thomas K. McAlpim
T. H. Agnew
R. J. Elvin
R. H. McCutcheon
W. E. Ainley
W. T. Ewing
J. H. MacDermot
A. R. Anthony
J. C. Farish
Colin A. McDiarmid
Thomas B. Anthony
Ernest P.  Fewster
J. McKay Macdonalc
L. H. Appleby
J. Fitz Osborne
Frank McEown
J. W. Arbuckle
M. Fox
S. A. McFetridge
T. F. H. Armitage
G. H. Francis
H. A. McKechnie
J. R. Arthur
D. D. Freeze
R. E. McKechnie
I. A. Balmer
Anson C. Frost
R. E. McKechnie II
A. W. Bagnall
E. H. Funk
W. C. McKechnie
P. W. Barker
R. Gilchrist
C. S. McKee
S. A. Bell
J. A. Gillespie
W. Boyd McKee
Murray Blair
B. D. Gillies
G. E. McKenzie
S. Blumberger
G. E. Gillies
W. J. MacKenzie
E, Bolton
Charles Gould
A. J. MacLachlan
H. H. Boucher
Wilfrid L. Graham
T. K. MacLean
R. B. Boucher
J. H. B. Grant
D. McLellan
Frederic Brodie
A. A. Gray
R. A. McLeod
A. O. Brown
E. J. Gray
Hugh Macmillan
Clarence E. Brown
A. B. Greenberg
Lachlan Macmillan
W. Harold Brown
L. O. Griffin
J. A. McNab
R. K. Brynildsen
J. C. Grimson
Allan Y. McNair
A. L. Buell
K. P. Groves
Neil McNeill
F J. Buller
E. Gung
J. McNichol
G. L. Burke
W. G. Gunn
L. W. McNutt
Gordon Burke
Karl J. Haig
M. M. MacPherson
W. Keith Burwell
Earle R. Hall
C. G. G. Maclean
D. F. Busteed
M. Halperin
W. T. Maguire
Harold H. Caple
J. E. Harrison
A. B. Manson
R. S. P. Carruthers
W. E. Harrison
G. O. Matthews
John Christie
B. Harry
D. M. Meekison
Fred Chu
R. de L. Harwood
H. H .Milburn
G. H. Clement
W. H. Hatfield
Robert D. Millar
D. E. H. Cleveland
Frank J. Hebb
Dorothy Miller
Wallace A. Coburn
A. Taylor Henry
J. W. Millar
F. W. Brydone-Jack
F. S. Hobbs
Donald W. Moffatt
E. Harvey Cooke
Lyall Hodgins
W. A. Moffatt
C. F. Covernton
J. A. Houston
Wm. Morris
K. L. Craig
A. L. Hunt
W. G. Morris
E. Johnston Curtis
A. W. Hunter
B. B. Moscovich
T. Dalrymple
E. S. James
J. Moscovich
G. A. Davidson
E. A. Johnson
R. P. Mulholland
J. Ross Davidson
Gordon C. Johnston
D. S. Munroe
C. E. Davies
W. D. Keith
A. Murdoch
John R. Davies
W. D. Kennedy
J. R. Naden
Isabel Day
W. W. Kennedy
J. R. Neilson
F. Day-Smith
Geo. E. Kidd
R. E. Page
O. DeMuth
Alexander King
W. M. Paton
C E. Derkson
R. P. Kinsman
W. D. Patton
R. N. Dick
G. W. Knipe
W. L. Pedlow
A. N. Dobry
E. H. Kuwabara
S. B. Peele
W. A. Dobson
J. J. A. Labrecque
Dallas G. Perry
W. J. Dorrance
B. E. Lang
Florence E. Perry
Victor Drach
W. H. Lang
Hugh H. Perry
Gordon C. Draeseke
Oliver S. Large
G. A. Petrie
Hubert Dumont
P. L. Lavers
E. K. Pinkerton
D. A. Dunbar
R. Grant Lawrence
John Piters
F. C. Dunlop
G. H. Lee
H. H. Planche
Gerald P. Dunne
T. H. Lennie
H. Powell
E. O. DuVernet
D. M. Lineham
P. Ragona
Watson Dykes
William T. Lockhart
E. F. Raynor
C. M. Eaton
A. Lowrie
M. M. Resnik
R. Elder
A. L. Lynch
F. N. Robertson
B. S. Elliott
E. E. Rogers
H. M. Ross
H. R. Ross
Frederick E. Saunders
Gustav Schilder
A. B. Schinbein
G. E. Seldon
W. F. Shaw
J. W. Shier
S. Sievenpiper
W. W. Simpson
F. L. Skinner
Bruce S. Smith
J. A. Smith
Lee Smith
J. E. Spankie
Howard Spohn
Robert A. Stanley
D. A. Steele
R. G. Stevenson
Neil A. Stewart
W. H. S. Stockton
J. B. Story
G. F. Strong
G. A. Sutherland
J. A. Sutherland
W. H. Sutherland
Ivan C. C. Tchaperoff
Douglas Telford
J. Lyle Telford
J. C. Thomas
J. W. Thomson
D. A. Tompsett
Ethlyn Trapp
A. E. Trites
F. H. Trousdale
E. B. Trowbridge
F. A. Turnbull
H. L. Turnbull
S. E. C. Turvey
M. Uchida
G. A. Upham
C. H. Vrooman
H. Wackenroder
John E. Walker
Jas. T. Wall
W. C. Walsh
L. H. Webster
R. C. Weldon
John A. West
T. R. Whaley
W. E. Wilks
Donald H. Williams
Howard Willis
R. A. Wilson
Wallace Wilson
W. A. Wilson
L. G. Wood
K. G. Yip
R. E. Ziegler
C. A. Graves
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H 4
It ? Mm
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,4 k| 1;;
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If ti
I. H
!  ;. i
It J
Dr. D. E. Alcorn
Dr. V. L. Annett
Dr. G. F. Aylward
Dr. D. M. Baillie
Dr. L. W. Bassett
Dr. A. D. Bechtel
Dr. W. W. Bell
Dr. D. Berman
Dr. G. B. Bigelow
Dr. G.  A. Bird
Dr. E. W. Boak
Dr. John Brown
(Sooke Harbour)
Dr. F. M. Bryant
Dr. G. B. B. Buffam
Dr. Norman C. Cook
Dr. P. A. C. Cousland
Dr. C. W. Duck
Dr. W. E. J. Ekins
Dr. H. W. Elkington
Dr. J. M. Fowler
Dr. D. W. Graham
Dr. T. W. A. Gray
Upper Island District:
Victoria and District:
Dr. George Hall
Dr. A. N. Hanson (Sidney)
Dr. C. M. Henry
Dr. A. Herstein
Dr. C. D. Holmes
Dr. Irene B. Hudson
Dr. R. A. Hunter
Dr. Samuel Janowsky
Dr. Stuart G. Kenning
Dr. M. J. Keys
Dr. F. B. Leeder
Dr. J. W. Lennox
Dr. O. C. Lucas
Dr. D. S. McHaffie (Duncan)
Dr. M. D. McKichan
Dr. J. M. MacKinnon
Dr. A. E. McMicking '
Dr. E. L. McNiven
Dr. T. McPherson
Dr. J. H. Moore
Dr. W. H. Moore
Dr. George More
Dr. Arthur B. Nash
Dr. R. D. Nasmyth
Dr. R. C. Newby
Dr. L. L. Ptak
Dr. H. E. Ridewood
Dr. W. H. B. Roberts
Dr. Hermann M. Robertson
Dr. R. B. Robertson
Dr. W. E. Scott-Moncrieff
Dr. Glenn Simpson
Dr. A. C. Sinclair
Dr. F. T. Stanier
(Cobble Hill)
Dr. J. D. Stenstrom
Dr. J. A. Stewart
Dr. J. P. Vye
Dr. W. P. Walker
Dr. H. J. Wasson
Dr. H. N. Watson
T. J. Agnew Courtenay
T. A. Briggs j Courtenay
E. N. East . Qualicum
Robert Elliott Parksville
E. D. Emery Nanaimo
Richard W. Garner Port Alberni
Alan B.  Hall : Nanaimo
N. B. Hall I Campbell River
G. B. Helem Port Alberni
C. T. Hilton Port Alberni
E. R.  Hicks r Cumberland
N. H. Jones Port Alberni
V.   E.   Latimer Port Alberni
Josiah McKee _. Courtenay
P.  M.  McLean  Chemainus
G. K. McNaughton Cumberland
B T. H. Marteinsson Port Alberni
A. H. Meneely Nanaimo
A. P.  Miller Port Alberni
H. A. L. Mooney  Courtenay
W. C.  Pitts . Alberni
W. A. Richardson ... Campbell River
P. L. Straith  Courtenay
S. L. Williams Nanaimo
Other Districts:
Dr. W. E. Bavis . Port Renfrew
Dr. H. A. W. Brown Fort St. John
Dr. Ella Cristall .= Tofino
Dr. Sidney E.  Evans Tofino
Dr. J. J. Gibson Tulsequah
. Dr. W. R. S. Groves Port Renfrew
Dr. H. S. Hamilton Alert Bay
Dr. A. W. Holm Sechelt
Dr. J.  R.  Ireland Port Alice
Dr. Gordon  James Britannia Beach
Dr. E. Lewison Zeballos
Dr. Ormond O. Lyons Powell River
Dr. William N. McKee Dawson Creek
Dr. Robert   McKenzie Grantham's  Landing
Dr. H.  A. McLean  Ceepeecee
Dr. G. W. Meyer Telegraph Creek
Dr. M. MacKenzie Morrison T„Stewart
Dr. R. H. O'Callaghan  Ganges
Dr. R. D. Rush_ 1 .. Ganges
Dr. N. J. Paul Squamish
Dr. T. E. Roberts Mayne Island
Dr. D. B. Ryall Alert Bay
Dr. J. A. Street Woodfibre
Dr. J. B. Swinden  Ucluelet
Dr. M. W. Thomas, Executive Secretary.
Doctors doing City Relief Work are requested to fill in the card number of
the patient correctly and legibly on their prescriptions.
Failure in this respect causes much annoyance and trouble for the Social
Service Department and the pharmacists.
G. F. Strong, M.D.
Vancouver, B. C.
Delivered before the Vancouver Medical Association, March 12th, 1941.
The rising mortality from heart disease is due to the increasing incidence of those
forms of heart trouble due to arterio-sclerotic changes in the coronary arteries. The
growth of our knowledge regarding these conditions during the last two decades has been
tremendous. To present these observations on the subject of coronary artery heart
disease it would seem desirable to first give a brief historical sketch; then describe the
views prevailing twenty to twenty-five years ago; next enumerate the important
advances made in the last two decades, with mention of those men chiefly responsible for
such advances; and finally discuss the present state of our knowledge of this subject.
Medical thought has travelled far from the days of Hippocrates, who taught that the
heart as the ruler of all organs was itself invulnerable, and was not attacked by disease.
Without attempting any detailed history of the development of our knowledge of heart
disease as a whole, but confining ourselves only to the growth of our ideas regarding the
blood supply to the heart, it is worth noting that among the earliest observers were
Vieussens and Thebesius1. The former in 1706 described the coronary arteries and also
mentioned vascular channels connecting these arteries with the lumen of the heart.
Thebesius two years later, 1708, made an injection of the coronary veins and found that
these vessels also communicated with the heart cavity, and since then all these small
vessels, whether arterial or venous, that are connected with the lumen of the heart have
been called Thebesian veins. Coronary sclerosis was described about this same time by
Drelincourt and Bellini. Lancisi was the first to note the fact that coronary sclerosis
could cause cardiac enlargement. Morgagni in 1760 was first to connect coronary
changes with the clinical symptoms similar to angina, and cardiac infarction. Great
credit must go to the outstanding English clinician, Heberden, who in 1768 gave us
the first accurate clinical description of angina pectoris. Little has been added to the
picture that he presented nearly two hundred years ago, and he is rightly regarded as the
pioneer clinician of coronary artery disease. Fourteen years after his first report he
presented in 1782 a series of one hundred cases of angina. His contributions were distinctly clinical, and were typical of the school that included Fothergill, Jenner, and
Parry. Jenner is credited with the definite suggestion that in angina pectoris, coronary
sclerosis was the essential lesion. This suggestion was made in a letter to Parry in which
Jenner pointed out the fact that he did not wish to make his views public out of deference to his friend John Hunter, who suffered from angina. After Hunter's death in
1793, the story was released along with the post mortem findings in Hunter's case. It
is an interesting fact that Hunter suffered his first attack in 1773, an attack which was
undoubtedly a cardiac infarction. Thereafter he suffered angina and was as he himself
described it "at the mercy of any fool who chose to make him angry." He died twenty
year later in 1793, suddenly, of another coronary thrombosis which developed during a
fit of anger occurring at a hospital board meeting. The subject of the discussion was
not disclosed.
With the turn of the nineteenth century there developed the first evidences of the
controvery that was to long continue regarding the basis of angina pectoris. Early
adherents of the coronary basis for the production of the pain in angina were Jenner
and Parry, the latter of whom had a clear conception of the importance of the role of
myocardial ischemia. Later there was to appear the aortic concept of angina in which
the pain was attributed to tension on or distension of the first part of a diseased aorta.
So bitter and voluminous did this argument become that the more important issues were
lost to sight.   Burns in 1809 confirmed the coronary idea by experiments on a ligatured
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limb. Laennec, to be followed by Hope in England and Stokes in Ireland, offered the
theory that angina was not to be attributed to an abnormality of the vessels or of the
muscle, but rather to a nervous disturbance.
At about this time medical thought along these lines was deflected by sudden great
emphasis on physical diagnosis, and increase in the study of heart disease became mostly
a matter of the consideration of physical signs. Virchow in 1850, with his emphasis on
cellular pathology, brought a good deal of attention to bear on the condition of the
heart muscle as to degeneration, fatty change, fibrosis, and the like, and Cohnheim on
the basis of experiments on dogs taught that coronary arteries were end arteries, sudden
occlusion of which was always fatal. The eminence of Cohnheim and his whole school
was such that we find his ideas dominating clinical thinking until after the turn of the
twentieth century. During this period angina pectoris received a great deal of attention,
and many autopsy protocols revealed cardiac infarcts which were almost without exception considered to be terminal events. Dock of St. Louis in 1896 wrote a good paper
calling attention to the occurrence of pericarditis in cases of coronary thrombosis with
myocardial infarction, and lamenting the fact that the profession was so slow in taking
up the study of this disease. Broadbent in 1906 wrote that there were no characteristic
physical signs or symptoms by which thrombosis of a coronary artery could be diagnosed
Osier's part in the changing knowledge of heart disease is of great interest. As one
of the leading teachers of medicine and clinicians of the end of the nineteenth and beginning of the twentieth century, and one always interested in heart disease, we naturally
are concerned with his views. Angina always interested him, as shown by his frequent
writings and lectures on that subject. In his lectures at Johns Hopkins Hospital in
18962 he noted the rarity of angina in his experience, and pointed out that in the ten
years in Montreal he did not see a case of the disease, either in private practice or at the
Hospital, and after leaving Montreal he had records of sixty cases, forty of which he
considered true angina. How different his case records would be today! At the time
of the Lumleian Lectures delivered before the Royal College of Physicians in 19103, his
series had grown to 268—an increase of only 200 cases in fourteen years in the practice
of one of the leading, if not the leading medical consultant of his day. The tremendous
increase in incidence of angina is illustrated by the fact that Paul White, a consultant
of comparable standing, has recently reported4 as many as one hundred new cases of
true angina in eight months. Osier reported many autopsies showing coronary obstruction, but influenced by Cohnheim's teachings, regarded these usually as terminal,
although he distinctly comments on the occurrence of pericarditis as an evidence of
cardiac infarction.
Sir James McKenzie has also made most valuable contributions to our knowledge of
heart diseases, and has an admirable text book on angina0 in which many cases of the
severest type, so-called status anginosus, are described. Autopsy protocols of these
patients reveal definite coronary occlusion with resulting myocardial infarction, but the
fact remains that the ante-mortem diagnosis of coronary occlusion was not made, and
treatment was never directed along the lines that would have seemed indicated if the
presence of an infarction had been considered.
We come, therefore, to the early decades of the present century with our concepts
of heart disease somewhat confused. As to angina, there still waged the conflict between
the coronary and the aortic theory. Adherents of the former by now included Osier
and McKenzie, while chief proponents of the latter were Allbutt, Wenckebach, and
Vaquez. Views of other aspects of heart disease were not so well defined as at present.
Valvular disease was apt to be considered as an entity, and a patient was treated for a
murmur without realizing, for example, that the significance of an aortic diastolic murmur due to rheumatic heart disease was quite different from such a murmur associated
with luetic aortitis. The emphasis was on structure rather than on function and etiology,
which were apt to be overlooked. The knowledge of the arrhythmias was most fragmentary, and as a result treatment was inadequate.   Acute cardiac dilatation was a com-
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iPK mon diagnosis, though we know now that it rarely if ever occurs, and that the condition
called acute dilatation in those days was probably paroxysmal tachycardia. Acute indigestion was a common clinical diagnosis, and was the misnomer given as the cause of
many a sudden death due to acute coronary occlusion. Status anginosus was another
name applied to a condition that we now all recognize as acute cardiac inf arctidrjd * Much
was said and written regarding the various degenerative changes affecting the myocardium, such as chronic myocarditis, myocardial degeneration, fatty degeneration, myocardial necrois, myocardial fibrosis, both local and general, without an entirely clear
conception of the underlying vascular conditions that usually produce these heart muscle
The English deserve special mention for great clarification of our ideas at that time.
McKenzie with his polygraph took the first step toward our understanding of the arrhythmias. With his emphasis on the importance of heart function and the significance
of the symptoms of dyspnoea and pain as evidences of heart failure, he helped to get the
profession away from regarding heart disease only as a matter of structural change. By
way of an aside, it is interesting to note that in those days the term heart failure was
loosely used to cover any one of several conditions affecting the heart, and a patient was
certified as dying of heart failure because his heart ultimately stopped, without any
thought as to the cause of the heart trouble or the form that it had taken. This became
so much a handicap to scientific thought that even registrars of vital statistics were concerned, and the designation of heart failure as a cause of death became inacceptable. In
the course of the last few years, we have come to use the term again as an improvement
on cardiac decompensation, and we find now that as a descriptive term congestive heart
failure serves a very useful purpose. Sir Thomas Lewis followed on McKenzie's work
and further clarified our ideas of cardiac physiology particularly in regard to the arrhythmias, in the study of which he was first to make free use of the new method, electrocardiography. Much honour for the great progress made in our knowledge of heart
disease should therefore go to these two men.
The credit for first making the ante-mortem diagnosis of coronary thrombosis a
subject of general knowledge must go to that grand old man of American medicine,
James B. Herrick of Chicago. He published his first paper6 on this subject in the
Journal of the American Medical Association in 1912, a report of six cases with one
autopsy, in the discussion of which he dared to dispute the word of the mighty Cohnheim
and refute the idea that coronary arteries are end-arteries, the sudden occlusion of which
must always be immediately fatal. He mentions the evidence brought forward by
Spaltholtz that coronary arteries show a rich anastomosis even in vessels of considerable
calibre. He quotes West in Transactions of Pathological Society of London in 1882 as
citing several cases in which there was complete obstruction of one coronary, yet the
patient had long survived. He points out the fact that the clinical picture may closely
resemble that of an acute abdomen. He mentions the importance of the Thebesian
vessels and makes the point that gradual obliteration of the coronary circulation give;
time for compensatory adjustments.
This paper received little if any attention, and in 1919 Herrick published a second
report' including two more autopsied cases, and a note regarding the experimental work
by Smith at the Presbyterian Hospital in which cardiograms were obtained after ligating.
one of the coronary arteries of a dog. This was the first suggestion regarding the possibility of diagnosis of coronary thrombosis from the electrocardiogram, or of localizing
the infarct. From this time on the interest in coronary disease has never lagged, anc
there has gradually accumulated an imposing literature on the subject. In 1930 R. W.
Scott said that the medical history of the future doubtless will record as one of the
important contributions to medicine of the past twenty years the general recognition
of coronary thrombosis. The electrocardiograph which was regarded as a research instrument during the first two decades of this century, has gradually come into its propev
place.    With the widespread use of this instrument and with the appearance of the
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portable and foolproof models, the method has become avaialble to practically all who
need it.
Herrick therefore deserves all credit for his important part in the advance of our
knowledge of this condition. He has since then been a consistent contributor to the
literature of this subject, and has recently sounded the important note of warning that
there is danger of the pendulum swinging too far so that every condition causing pain
in the chest and under the sternum or in the epigastrium may be wrongly diagnosed as
coronary occlusion.
Since the acceptance of Herrick's views depended on a revamping of our ideas regarding the anatomy and pathology of the coronary vessels, the work of our Canadian Louis
Gross8, must not be overlooked. As already indicated, Cohnheim had taught that coronary arteries were end-arteries, sudden obstruction of which would prove immediately
fatal. Spalteholtz showed that this was not true, but Gross succeeded in making this
graphically clear. By an ingenious technique meticulously followed, he was able to show
the normal coronary circulation more clearly than it had previously been shown, and
also to demonstrate the changes that were natural with advancing years. He found
evidence of rich anastomoses between the coronary arteries and the arteries of the adjacent and attached organs and epicardial fat. He showed that in the seventh decade the
vascular architecture of the heart is well prepared to receive the brunt of the obliteration
of even a main coronary artery, not only on account of the existence of abundant and
free anastomoses, but also by the non-negligible factor of the development of a dense
network of arteriae telae adiposae which can compensate and supply considerable blood
to the subjacent muscle. These fat vessels occur regardless of pathology, but with
gradually developing coronary occlusion they also show a compensatory increase.
As already indicated, great honour is due Doctor Herrick for being the first to
emphasize that it was possible to make the ante-mortem diagnosis of coronary thrombosis. The next clinician to contribute greatly to our knowledge of this condition was
Dr. Samuel A. Levine of Boston. While it is not generally known, Levine's first paper
on this subject was written in 1916, when he was unaware of Herrick's contribution of
1912. It is not, however, the question of priority that is so important to the advance of
our knowledge, as Levine's greatest contribution, his monograph published in 1929
which was, and still is an authoritative summary of the whole problem. In this paper he
reports 145 cases collected from hospital and private practice in the preceding thirteen
or fourteen years. Levine was first to call attention to the leucocytosis and fever occurring in cases of cardiac infarction, and also pointed out the resemblance to acute abdominal conditions.
The next important contribution was in 1920 by Pardee 10, in which he described the
high and low take-off of the R-T segment, and the sharply inverted or coronary T wave.
His work received such general recognition that the wave was often called the Pardee
T wave. The significance of Pardee's findings lay in the fact that it made possible the
diagnosis of coronary occlusion from the electrocardiogram.
The next step in the advance of our knowledge came with the introduction of the
fourth or precordial lead, a lead taken with one electrode on the left leg, and the other
at or just inside the apex beat. It was found that in a small number of cases the three
standard leads failed to reveal the electrocardiographic abnormalities from which the
diagnosis of a cardiac infarct could be made, whereas the precordial lead did indicate
such change. In the majority of instances the evidence is apparent in the three standard
leads as well. The credit for emphasizing the value of the fourth lead must go to Dr.
Frank N. Wilson of Michigan. He first predicted the information one could get from a
purely mathematical formula, then obtained such tracings from experimental animals,
and finally confirmed these observations on clinical cases of coronary thrombosis1
While many others, notably Wolferth and Wood of Philadelphia12 have added to our
understanding of the precordial lead, Wilson must have credit for starting that study.
The fourth lead has also been of great value in the localization of the infarction, for
while this may be done from the three standard leads, the evidence of the precordial lead
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. t,; is always helpful. There is an interesting observation to be made in relation to this fourth
lead. In the early work on this continent this precordial lead was often taken in such a
way (the electrodes were so applied) as to cause waves of a positive nature to have a
downward deflection and vice versa. This was the opposite of the situation regarding the
standard leads, and as reports began to appear in the medical literature of the English
speaking world, the greatest confusion arose. To overcome this a simple expedient was
adopted; a joint committee was set up by the American Heart Association, and the
Cardiac Society of Great Britain and Ireland, and by an interchange of views agreement
was reached in 1938 that all should follow the more logical method by which all positive
waves were indicated by an upward deflection.
Among the early contributors to our knowledge of coronary disease was Dr. Robert
L. Benson, at that time head of the pathological department of the University of Oregon.
He submitted some of the most valuable observations on the pathology of coronary
disease, one of his most notable contributions being the report in 1933 of forty cases
of rupture of the heart13. Earlier contributions during 1925 and 192614,15 did much
to focus attention on the whole subject of coronary sclerosis and occlusion, and the
attendant complications.
The English school from Heberden to McKenzie and Lewis had contributed enormously to the sum total of our knowledge of heart disease in general, and angina pectoris
in particular, but the fact remains that they were slow to take up the diagnosis of
cardiac infarction. Considering the wealth of their contributions to the diagnosis, prognosis and treatment of angina, and it is to be pointed out that little has been added to
their clinical concepts, it is amazing that nothing appeared in the English literature
regarding the ante-mortem diagnosis of cardiac infarction for some years after the
subject had been generally accepted on this continent. Papers by Gibson16 and McNee17
in 1925 were the first to appear, but it was not until 1928 that Parkinson and Bedford18
presented their excellent cardiographic study of the successive changes after cardiac
infarction. This article emphasized the reciprocal relationship of the changes in the first
and third lead and is one of the most widely quoted on the subject. In the same year
there was a good review of diseases of the coronary arteries by Allan19.
Continued progress in the study of coronary artery diseases has come mostly from the
United States, where among others Fred M. Smith deserves credit for his consistent
efforts. He was associated with Dr. Herrick in early experimental work on changes in
the cardiogram following ligation of a coronary artery7 and he has contributed studies
of the normal coronary circulation20 and has also observed changes occurring in sclerosis
and thrombosis, as well as the effect of certain drugs21. Wolferth and Wood and their
associates have, as already indicated, contributed much to our understanding of the precordial lead12' 22, and have also made a study of methods of localizing the infarct23, 24.
The question of the localization of the infarct is one of more than academic interest since
it seems generally agreed that anterior infarcts carry a definitely poorer prognosis. J.
T. Wearn was one of the first25 to write about coronary thrombosis following Herrick's
introduction of the subject, and he has since given us valuable studies of the coronary
circulation, particularly in relation to the role of the Thebesian vessels1, 26. He has also
made some important observations regarding the coronary circulation, and the relation
between muscle fibre and blood supply in normal and and hypertrophied hearts2'' 28, 20.
In the last decade notable contributions have come from New York, where Levy and
his associates, and Master and others have made important additions to the sum total of
our knowledge. Levy edited the excellent summary of diseases of the coronary artery
in 193930a and has done much to correlate the clinical findings and structural changes
found at autopsy31. From Chicago the contributions of Katz32, Saphir33 and others
have added much to our original concepts. More recent studies have emphasized the
importance of coronary insufficiency and made it clear that infarction is a serious event
in coronary artery disease, and that it may occur as a result of plugging of a coronary
artery or as an evidence of acute coronary insufficiency, conversely obstruction of a large
branch may occur without an infarction.    Schlesinger34 has devised a new method of
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the post-mortem study of coronary artery heart disease by injection of the coronary
arteries with multi-colored radiopaque media, a new technique for cutting or unrolling
the heart, ^plus. x-ray study followed by minute dissection of the coronary vessels.
Blumgart and his associates35,63 have presented excellent clinical pathological studies
which have shown considerable light on the relationship between angina pectoris, coronary insufficiency or failure, and myocardial infarction.
In our consideration of present day views on this subject, it is well to remember
that coronary artery heart disease is the commonest form of acquired organic heart
trouble. It presents itself to us clinically in the form of angina pectoris, coronary insufficiency, cardiac infarction' or the congestive failure resulting from long-standing,
coronary sclerosis. If,in addition to the hardening of the coronary arteries there is also
a hypertension, as there frequently is, an added physiological burden is thrown on the
heart muscle. The cardiac manifestations may occur suddenly or may be extremely
insidious in their onset.
Angina pectoris is now generally believed to be due to an acute temporary relative
coronary insufficiency with.^resulting myocardial iscjwemia. This may mean transient
spasm or only that the coronary arteries are unable to dilate to increase the coronary
blood flow as required during exercise, a condition that would naturally be accentuated
by any factors which increased the demands on the heart or decreased the effectiveness of
the coronary circulation. Thus in hypertension or hyperthyroidism there are increased
demands on the myocardium, and in anaemia the nutritive value of the circulating blood
is diminished. In any of these conditions an angina might be brought out that would
not otherwise appear, and, conversely, the correction of any of these will at times cure
the angina. With enlargement of the heart, as in hypertension, for example, there is
increase in the size of the individual muscle fibre but no increase in capillary supply or
in the amount of blood flowing through tne coronary arteries; in fact the calibre of the
arteries may be actually reduced. The importance of this relative coronary insufficiency
cannot be denied. It has been emphasized by many observers, and is geographically illustrated in the camera lucida drawings by Gross and Spark37 in which the relation between
muscle fibre and capillary supply in a normal heart (300 gram) and hypertrophied heart
(750 gram) is well shown. As Wearn29 pointed out, the usual relationship of one capillary per fibre is maintained, but the tremendous increase in the size of the muscle fibre-
as shown by the cross-section, results in a relative diminution in blood supply even
without gross coronary damage which is usually also present.
The reaction of any patient to pain is directly affected by the stimulus producing the
pain and the sensitivity of the patient. In a hypersensitive person considerable distress
may arise from comparatively slight coronary insufficincy. In a hyposensitive person,
on the other hand, the degree of coronary insufficiency may progress to a considerable
extent before attacks of pain are experienced. In some instances, instead of pain, the
patient suffers from anginal equivalents such as paroxysmal dyspnoea, so-called cardiac
asthma, usually nocturnal, paroxysmal arrhythmias, or only recurring weak spells.
Coronary insufficiency, therefore, has become the crux of this whole problem of
coronary artery heart disease. As already indicated, angina pectoris represents a transient,
often relative inadequacy of coronary blood flow, whereas cardiac infarction, at the
other end of the scale, results from a complete localized coronary insufficiency of sufficient extent extent and duration to cause necrosis of the myocardium. Between these
two conditions there are found instances of what have been called acute coronary insufficiency or acute coronary failure in which the attacks are more severe than those of
angina. Cardiac infarction can result from occlusion of a coronary artery or from a
severe grade of acute coronary insufficiency38. Sudden death which is most commonly
due to heart disease, and usually coronary artery heart disease, is most often a result of
acute coronary insufficiency occurring with or without actual coronary occlusion
To put this in another way, sudden death is not only the result of coronary occlusion,
whether that be due to arteriosclerotic plugging or intravascular thrombosis, but is often
the result of acute coronary insufficiency alone.   Acute coronary insufficiency may be
Page 272 provoked in a patient with coronary sclerosis by anything producing profound shock,
with lowering of the blood pressure, as postoperative shock, acute haemorrhage, tachycardia, pulmonary embolism, or by extreme grades of aortic stenosis. In such instances,
therefore, it is possible to find infarction of the myocardium without evidence of a
definite obstruction of the artery supplying that area.
The present day emphasis on pain in coronary artery heart disease is apt to make us
lose sight of the fact that in many instances of coronary sclerosis pain1 either in the
form of angina pectoris or cardiac infarction, may never occur. Certain patients develop
evidence of congestive heart failure as a result of the myocardial degeneration that occurs
following insufficient coronary blood supply. Occasionally this degenerative process
may actually destroy the nerve endings in the myocardium, but more commonly the
gradual development of coronary sclerosis encourages the establishment of a collateral
supply of sufficient degree to prevent that grade of coronary insufficiency necessary to
cause pain in that particular individual. The congestive failure due to coronary sclerosis
presents only the problem of failure or decompensation common to any form, of heart
disease, with the added note that in this type of failure sudden death from coronary
occlusion or acute coronary insufficiency is always a greater possibility.
Angina Pectoris.—There seems no necessity to review the whole subject -of angina
pectoris. While it is true that the name denotes a symptom, there can be no doubt that
it also connotes a fairly definite group of patients who suffer from cardiac effort pain
or distress. This pain, usually substernal, may radiate to the neck, shoulders, or arms.
It is more common down the left arm, but may occur in the right or both. The outstanding characteristic of the pain of angina is that it is brought on by exertion or
excitement, more particularly after a meal or in cold weather, and that it is relieved by
rest. It is important to remember that the pain of angina may occur only at a point
some distance from the heart, as in the neck, jaw, shoulder* elbow, or wrist, and these
patients may show little or none of the usual substernal pain.
Another outstanding characteristic of angina is its uncertainty; one case may go on
for years with little if any change, whereas another of similar age and clinical findings
may die suddenly, usually of acute coronary insufficiency. Some few cases of angina
recover, so too hopeless an outlook must be avoided. While syphilis never causes a diffuse
sclerosis of the coronary arteries, it may by the aortitis it produces cause such narrowing
of the coronary orifices as to seriously reduce the coronary circulation, and so cause a
degree of coronary insufficiency sufficient to produce angina. This is especially true after
aortic regurgitation has developed.
It is important to remember that the diagnosis of angina may have to be made on
the basis of the symptoms alone, for there are cases in which all objective evidence, both
physical signs and laboratory findings, is normal. This is not the rule, and it is more
common to find hypertension or a history of it, evidences of increased peripheral or
retinal arteriosclerosis, cardiac enlargement, or such abnormalities as gallop rhythm or
pulsus alternans. The laboratory findings usually confirm these observations, and the
x-ray shows enlargement of the heart, usually of the left ventricle, and often widening,
elongation, or increased density of the aorta, while the electrocardiogram shows most
often some evidence of myocardial involvement which we have come to associate with
coronary sclerosis.
While it is true and important that we cannot make clinical or pathological diagnoses
from the cardiogram, it is equally true that in a middle-aged person suffering from heart
symptoms suggestive of angina, the changes in the cardiogram are not likely to be due
to the half dozen other things besides coronary sclerosis that can so distort the normal
tracing. The normal cardiogram presents a very definite picture, and alterations of
that pattern have acquired certain importance. The common electrocardiographic
changes found in angina are deviation, usually depression of the R~T or S-T segment
away from the iso-electric base line and significant T wave inversion39. Deviation of
the R- or S-T segment must be greater than 1 mm., or in other words this part of the
tracing must be more than 1 mm. above or below the iso-electric line before this devia-
Page 273
S m
\ u
W lit
* WW
ii ri
3il! *:
tion is of significance. This alteration which causes a high or low take-off is to be dis-
tinguished from the more marked deviation of this segment found in acute infarction.
The T waves are normally upright, though it is within normal limits for T3 to be flat
or inverted, but this normal inversion of T3 is of a different form from the so-called
coronary type of T wave. Of particular significance is inversion Ti and 2' T^ and 4,
or of T2 and 3.
The changes found in angina may be permanent, and then are taken as indicative of
the myocardial changes resulting from long-continued myocardial ischaemia due to
coronary insufficiency, either relative or absolute, or the changes may be temporary as
those brought on by exertion sufficient to produce an attack or by induced anoxaemia.
The latter procedure has been advocated as a clinical test for coronary insufficiency40,41.
The points that distinguish the changes in the electrocardiogram occurring in angina
from those seen in cardiac infarction will be discussed later.
As already indicated, angina may continue unchanged for years, or it may be complicated by the occurrence of a fatal or non-fatal cardiac infarction, or it may slowly
improve and even disappear. In some instances angina has its onset after acute cardiac
infarction while in other cases such a cardiac accident may terminate the attacks of
substernal effort pain, another example of the extreme uncertainty of this condition.
Every case of angina pectoris must be distinguished from cardiac infarction. There
is still far too great laxity of thought in this regard. In angina there is a relative coronary insufficiency of such degree as to produce a temporary myocardial ischaemia with
resulting pain. When the pain subsides there is ordinarily no permanent gross change
in or damage to the heart muscle. In infarction, on the other hand, there is very definite
and serious permanent damage. If the infarct is large and comprises the whole thickness of the heart muscle the after effects are most serious, and treatment must include
a period of absolute bed-rest sufficient to permit complete healing of this area. The
severity of the pain is not a safe criterion by which to distinguish between angina and
infarction. For while in the main it is true that the pain of infarction is much more
severe and prolonged than in angina, it is possible to have severe angina that produces
more distress than a mild infarction. The degree of sensitiveness of the patient is also a
factor to be considered.
In addition to making the distinction between angina pectoris and cardiac infarction
it is now necessary that we try to differentiate the clinical picture of acute coronary
insufficiency or coronary failure. This may cause an infarction or it may only produce
a more severe anginal attack. The typical pain of angina is transitory and is relieved by
rest or nitroglycerine. Coronary insufficiency may produce pain of longer duration,
yet not of such degree as that met in typical cardiac infarction, and in coronary insufficiency there may be none of the signs of myocardial weakness; as tachycardia and
hypotension, or of myocardial necrosis' as fever, leucocytosis and increased sedimentation
rate. The distinction is most important, and has been recently stressed by Master
and Blumgart 35, 36.
Cardiac Infarction.—Herrick in 1912 and again in 1919 drew attention to the fact
that it was possible to diagnose coronary thrombosis before death, and that this vascular
accident that resulted in cardiac infarction was not always fatal. These contributions
of his brought the whole subject of coronary artery disease into sharp focus, and led to
the great advance in our knowledge of these conditions in the past two decades. Further
reasons for increased study and knowledge of myocardial infarction are to be found in
the sudden widespread use of the electrocardiograph in clinical medicine, and the increasing incidence of postmortem examinations.
It was soon found, for example, that all instances of sudden obstruction of the
lumen of a coronary artery were not due to intravascular thrombosis, but might result
from the intimal changes of the arteriosclerotic process itself. It has also been generally
agreed that thrombosis or occlusion never occurs in a normal coronary artery. The
coronary sclerosis that is the important underlying pathological finding is of the type
Page 274
if*. affecting medium-sized arteries and may be part of a general arteriosclerosis or may
occur as a localized manifestation of this degenerative process.
The changes that occur are mainly intimal and consist first in the appearance of
plaques due to infiltration of connective tissue; as the plaque increases in size, evidences
of nutritive capillaries are found, and with further increase central degeneration occurs
and calcium is deposited. The resulting intimal roughening is an important factor in
the production of the intravascular thrombosis. Occlusion is more obten, however,
produced by the arteriosclerotic process itself43, either by actual plugging of the lumen
by the plaque or more frequently by intramural haemorrhage. The presence of these
haemorrhages has led to a considerable discussion. Some believe them to be a result of
sudden increase in intravascular pressure, and others regard them as inevitable manifestations of the arteriosclerotic process.
The infarct presents the typical picture of anaemic necrosis with acute myocardial
degeneration and softening' followed by a leucocytic infiltration, and later connective-
tissue replacement. The time relationships have recently been studied44 and it was found
that the rate of healing depends on the size and location of the infarct, small infarcts
healing in about five weeks, and large ones in two months. Rupture may occur at any
time in the first two weeks, most commonly around the end of the first week. Localized pericardial and endocardial reactions may occus, and on the latter a mural thrombus
may be formed. From this thrombus a fragment may be disloged to cause an embolism,
always a serious complication following cardiac infarction.. The occurrence of an
infarct depends on the state of the collateral circulation, for if sufficient vascularity
exists sudden complete obstruction of even a large coronary artery might fail to produce an infarct. A further recent development35 has been the finding that an infarct
might develop at some distance from the site of the obstruction to the lumen of the
artery, indeed so far distant that obstruction of the left coronary might cause infarction
of that area of the heart muscle supplied by the right coronary artery or vice versa.
The symptoms of the typical attack are so well known as to require but brief mention here. Severe subsetrnal pain, especially in a patient with known hypertension or
effort angina, similar in location and radiation to the pain of angina, but much more
severe and prolonged, and not relieved by rest or nitrites, is characteristic of acute
cardiac infarction. The pain is only relieved by opiates and even then may last for
hours, pain of longer duration adding to the gravity of the outlook. As in angina' the
pain may be epigastric and so simulate an acute surgical abdomen; the pain may also in
rare instances occur at some distance from the heart. Shock is the next important
symptom of infarction, and is always present in some degree, the extent of the shock
probably varying directly with the size of the infarct. Nausea and vomiting may occur
and mayadd tor the^difficuky of distinguishing infarction from a surgical emergency.
The patient is usually immobilized by the pain, but in other instances extreme restlessness occurs. The pulse rises and the blood1 pressure drops, though the time relationship
of these changes is not always the same. The tachycardia may be prominent from the
first but the drop in blood pressure may be deferred for twelve hours or more after the
onset of the pain. Physical examination often reveals a typical facies, and the usual
finding on examining the heart is a change in the character of the heart sounds with
softening or muffling of the first sound at the apex. Within six to eight hours the
temperature begins to rise, and while usually not high, remains elevated for three or
four days. With the fever a leucocytosis occurs, and the sedimentation rate is soon
increased. The return of this latter finding to normal serves as a useful indication of
the healing of the infarct. A pericardial rub is heard in only about twenty percent of
cases, and even then may be most transient, lasting only a few hours; when it is
detected it may help to settle an otherwise difficult diagnosis.
In the typical case the pain is usually controlled within the first twelve, certainly
within the first twenty-four hours, and the patient may after a few days feel perfectly
well.   This is where difficulty often arises, as it is imperative for the patient to stay in
Page 275 Jl ¥
bed long enough to permit complete cicatrization of the infarct, a matter of six to
eight weeks, with a similar period of convalescence.
The typical- case offers no diagnostic difficulty as is evidenced by the fact that it is
readily recognized by our summer internes, fourth year medical students. It is the
atypical, and particularly the mild case, that offers great difficulties and is a constant
challenge to our diagnostic acumen. Mistakes can of course be made both ways. A
cardiac infarct can be missed and the patient may collapse and die within a few hours
or days of leaving our office. In another instance a patient may be forced to keep to
his bed for six to eight weeks for a condition other than an actual infarct* The commonest error would seem to be the confusing of angina with true infarction, although
there are always to be considered all the other causes of chest, substernal, and epigastric
pain when considering the doubtful case. The pain may be slight or absent in the hypo-
sensitive individual. In such a case the diagnosis may be possible only by proper interpretation of the sudden onset of shock, sudden change in cardiac rhythm, sudden appearance of dyspnoea, particularly the paroxysmal nocturnal dyspnoea, or cardiac asthma,
which has come to be accepted as an anginal equivalent. It is in these cases that the
cardiogram or, better, serial cardiograms have come to have such importance. The
diagnosis of cardiac infarction may in a few* instances be delayed until the occurrence
of embolism causes a careful investigation into the patient's recent health.
The prognosis of cardiac infarction is notably uncertain. There can be no better
rule to follow than to emphasize this to the family at the first and every opportunity.
In spite of every care and possible attention a patient with infarction may die suddenly
without warning. Statistics as to prognosis have little value because we can never
determine how often this condition occurs in a community. We know that the majority of sudden deaths are due to acute coronary insufficiency, some of which may occur
so suddenly that no cardiac infarct has time to develop. In other instances death occurs
suddenly after the infarct has occurred. For the patients that survive the first hours
of the attack the next critical period is the first three days, the next most uncertain
time is at the end of the first week when the softening of the infarct has reached its
maximum, as it is then that spontaneous cardiac rupture may occur; there then follows
the period of danger from embolization.
The uncertainty of the prognosis should not lead us to adopt a hopeless attitude. It
is possible for the patient to make a complete recovery from cardiac infarction and
indeed instances are at hand of recovery from more than one attack. The extent of the
recovery of function is of course variable, and while in a few patients total and permanent disability results, there are more of those who survive the first few weeks that
go on to complete recovery. In the first ten years after the general acceptance of
Herrick's views the profession took a very serious view of cardiac infarction, and many
a case was classified as a total disability. With increased knowledge and with better
diagnosis of the milder cases, that view has been altered until it is now recognized that
many of these patients make a complete recovery and are able to return to their ordinary
The Electrocardiogram in Cardiac Infarction.
It is here that this method has achieved its greatest usefulness, for while a cardiogram is not essential in making the diagnosis in a typical case, it is always a desirable
graphic record of the extent of the myocardial damage. In the atypical case it is indispensable, and frequently the diagnosis can only be made after the study of not one but
several serial cardiograms. Just when these should be taken and the interval between
tracings depends on circumstance. It is needless to add that the fourth lead will on
occasion enable us to diagnose cardiac infarction which cannot be detected in the limb
The important alterations in the cardiogram in myocardial infarction are shown in
the Q-R-S, the RS-T segment, and in the T waves.   The reciprocal relationship of some
of these changes is extremely important18.   In the Q-R-S widening and notching indicative of intraventricular delay or bundle branch block is one of the changes that may I
Page 276 found. An increase in the amplitude of Q3, or Q2 and Q3 may indicate a posterior
infa*ctV-ind":m"*Similar way the absence of R4 may point to an anterior lesion. Changes
in the RS-T segment are usually an important indication of acute infarction. In the
anterior infarct this segment is early elevated in the first and fourth, depressed in the
third lead, and as healing occurs these deviations tend to return to the base line. In
posterior lesions the reverse is apt to be true, and the RS-T segment is depressed in the
first and fourth, and elevated in the third lead. The RS-T segment is certainly the
most important portion of the tracing from which to estimate the age of the infarct.
HZ      1    33C
FIG.X Abaptej) from   Bohning-KATZ ^3Z )-H3S.
Fig. 1.    A schematic representation of the usual changes in anterior and in posterior
infarction as shown in the first, third, and fourth leads.
Page 277
• HI
" *
-> 1
lif fj*i
?1 W,J
The T wave changes are also important. In anterior lesions the T waves are inverted
in the first and fourth leads, whereas T2 and 3 are upright. In posterior infarction Ti
is upright, T2 and 3 inverted, and T4 upright and often exaggerated. Fig. I is a
schematic representation of the usual changes in anterior and in posterior infarction as
shown in the first, third and fourth leads. The second lead is omitted since it usually
follows the third lead changes.
The time relationship of these changes is important and often of value when we
attempt to make a diagnosis from the cardiogram. Evans46 has pointed out that in
anterior infarction R4 usually disappears immediately and remains absent, there is early
elevation of the RS-T segment which returns to normal in several weeks, and the T4
inversion occurs in three or four days and is permanent in about half the cases. In
posterior lesions the depression of R-T4 occurs within the first few days in about two-
thirds of the patients and returns to normal in several weeks; T4 is upright and usually
of increased amplitude, reaching its peak in two or three weeks. A recent suggestion24
indicates the possibility of localizing infarcts on the lateral walls of the left ventricle.
If all these changes occurred in a textbook fashion to fit our convenience and the case
the role of the electrocardiographer would be a happier one. The variations in these
findings are infinite, but no more infinite than the variations in the size, shape, location
and number of infarcts in the myocardium. The most disconcerting finding is a normal
tracing in the face of apparently positive clinical evidence of cardiac infarction but
this will seldom occur if the clinical diagnosis is based on sound conclusions and if
serial cardiograms are obtained. Always it must be remembered that the electrocardiograph is only a laboratory instrument of precision, to be used in conjunction with all
the other means at our disposal to make a diagnosis and direct effective treatment.
Emphasis on the electrocardiographic alterations in angina and infarction should not
lead us to overlook the- changes that may occur in coronary sclerosis without* pain. In
such cases presenting congestive heart failure the cardiogram is rarely normal and the
changes that occur are, like those in angina and infarction, alterations in the ventricular
portion of the complex, the Q-R-S, the RS-T segment, and the T waves. Painless
infarction may of course account for some of these changes but many are the result of
gradual coronary narrowing. Anything that reduces coronary blood flow may also lead
to such alterations, as, for example, aortic valvular lesions, either regurgitation or
stenosis, or luetic aortitis with narrowing of the coronary orifices. These changes may
also result from long-standing coronary insufficiency such as occurs in hypertrophy
where the size of the muscle fibre increases but the blood supply remains unchanged or
is diminished by the accompanying coronary sclerosis.
Coronary artery heart disease is the commonest form of organic heart trouble and
is the cause of the increasing incidence of death from heart disease. It presents itself
in the form of angina pectoris, coronary insufficiency, cardiac infarction' and congestive
heart failure. The basis of all these is coronary insufficiency, relative or absolute, localized or general, of a degree sufficient to produce an effect in the patient concerned. The
electrocardiogram offers the best and ofiten the only means of establishing the proper
diagnosis so essential to the effective handling of the presenting symptoms, the complications, and the after-care of the patient suffering from coronary artery heart disease.
1. Wearn, J. T., Mettber, S. R., Klumpp, T. G., and Zschiesche, L. J.: The Nature of the Vascular
Communications Between the Coronary Arteries and the Chambers of the Heart. Am. Heart }.,
1933, 9:143.
2. Osler, "W.: Angina Pectoris and Allied States.   Lectures Johns Hopkins Hospital.   MacMillan.   1897.
3. Osler, W.: Angina Pectoris.   Lumleian Lectures.   Lancet, 1910, 1: 697, 839, 973.
4. White, Paul D.: Heart Disease.   MacMillan, N.Y.   1931.   p. 609.
5. McKenzie, J.: Angina Pectoris.   Oxford Medical Publications, London, 1923.
6. Herrick, J. B.: Clinical Peatures of Sudden Obstruction of the Coronary Arteries: J.A.M.A., 1912,
7. Herrick, J. B.: Thrombosis of the Coronary Arteries.   J.A.M.A., 1919, 72:387.
8. Gross, L.: The Blood Supply to the Heart.   Hoeber, N.YY., 1921.
9. Levine, S. A.: Coronary Thrombosis, Various Clinical Features.   Medicine, 1929, 8:245.
Page 278 10.
Pardee, H. E. B.: An Electrocardiographic Sign of Coronary Artery Obstruction. Arch. Int. Med.,
1920, 26:244.
(a) Wilson,  F.  N.:  The  Distribution  of  the  Potential  Differences  Produced  by  the   Heart   Beat
Within the Body and at Its Surface.   Am. Heart J., 1930, 5:599.
(b) Wilson, F. N., MacLeod, A. S., and Barker, P. S.: The Order of Ventricular Excitation in
Human Bundle-branch Block.   Am. Heart J., 1932, 7:305.
(c) WrLSON, F.  N.:  Chapter  on  Electrocardiography.   Diseases  of Coronary  Arteries  and  Cardiac
Pain.   MacMillan, N.Y., 1939.
Wolferth, C.  C, and Wood,  F.  C:   The  Electrocardiographic  Diagnosis  of Cardiac  Infarction.
Modern Concepts of Cardiovascular Disease, May and June, 1935, 4: nos. 5 and 6.
Benson, R. L., Hunter, W. C, and Manlove, C. H.: Spontaneous Rupture of the Heart.   Am. J.
Path., 1933, 9:295.
Benson, R. L.: The Present Status of Coronary Arterial Disease.   Arch. Path, and Lab. Med.,  1926,
Benson, R. L., and Hunter, W. C: The Pathology of Coronary Arterial Disease.   Northwest Med.,
1925, 24:606.
Gkbson, A. G.: The Clinical Aspects of Ischemic Necrosis of the Heart Muscle.   Lancet, 1925, 2:1270.
Mcnee, J. W.: The Clinical Syndrome of Thrombosis of  the Coronary  Arteries.   Quart.  J.  Med.,
1925, 19:44.
Parkinson, J., and Bedford,  D.  E.:  Successive  Changes  in  the  Electrocardiogram  after  Cardiac
Infarction  (Coronary Thrombosis).   Heart,  1928,  14:195.
Allan, G. A.: Diseases of the Coronary Arteries.   Brit. M. /., 1928, 2:232.
Smith, F. M.: Concerning the Anatomy of the Coronary Arteries. Am. J. M. Sc, 1918,  156:706.
Smith, F. M.: Coronary Circulation.   Arch. Int. Med., 1927, 40:281.
Wolferth, C. C, and Wood, F. C: Acute Cardiac Infarction.   Arch. Int. Med., 1935, 56:77.
Wood, F. C, Bellet, S., McMillan, T. M., and Wolferth, C.C: Electrocardiographic Study of
Coronary Occlusion.   Arch. Int. Med., 1933, 52:752.
Wood, F. G, Wolferth, C. C, and Bellet, S.: Infarction of the Lateral Wall Left Ventricle.
Am. Heart /., 1938, 16:3 87.
Wearn, J. T.: Thrombosis of the Coronary Arteries with Infarction of the Heart.   Ant. J. M. Sc,
1923, 165:250.
Wearn, J. T.: Role of Thebesian Vessels on Circulation of the Heart.   /. Exper. Med., 1928, 47:293.
Wearn, J. T.: The Extent of the Capillary Bed of the Heart.   /. Exper. Med., 1928, 47:273.
Shd?ley, R. A, Shd?ley, L. J., and  Wearn, J.  T.:  Capillary  Supply  in  Hypertrophied  Hearts.
/. Exper. Med., 1937, 65:29.
Wearn, J. T.: Vascular Changes and Their Effect on the Efficiency of the Human Heart.   Tr. A.
Am. Physicians, 1938, 53:88.
(a) Levy, R. L.: Diseases of the Coronary Arteries and Cardiac Pain.   MacMillan, N.Y., 1939.
(b) Levy, R. L., and Bruenn, H. G.: Acute Fatal Coronary Insufficiency. /.A.M.A., 1936, 106:1080.
Bruenn, H. G., Turner, K. B., and Levy, R. L.: Notes on Cardiac Pain and Coronary Disease.
Am. Heart J., 1936, 11:34.
Bohning, A., and Katz, L. N.: Four Lead Electrocardiogram in Cases of Recent Coronary Occlusion.  Arch. Int. Med., 1938, 61:241.
Saphir, O., Priest, W. S., Hamburger, W. W., and Katz, L. N.: Coronary Arteriosclerosis Coronary
Thrombosis, and Resulting Myocardial Changes.   Am. Heart J., 1935, 10:567.
Schlesinger, M. J.: An Injection Plus Dissection Study of Coronary Artery Occlusions and Anastomoses.  Am. Heart J., 1938, 15:528.
Blumgart, H. L., Schlesinger, M. J., and Davis, D.: Studies on the Relation of the Clinical
Manifestations of Angina Pectoris, Coronary Thrombosis, and Myocardial Infarction to the Pathological Findings.   Am. Heart J., 1940, 19:1.
Blumgart, H. L., Schlesinger, M. J., and Zoll, P. M.: Angina Pectoris, Coronary Failure, and
Acute Myocardial Infarction.   J.A.M.A., 1941, 116:91.
Gross, H., and Spark, C: Coronary and Extra-coronary Factors in Hypertensive Heart Failure.
Am. Heart J., 1937.   14:160.
Frhedberg, C. K., and Horn, H.: Acute Myocardial Infarction not due to Coronary Artery Occlusion.  /.A.M.A., 1939, 112:1675.
Bourne, G, and Evans, C: The Four Lead Electrocardiogram in Angina of Effort. Lancet, 1938,
Levy, R. L., Bruenn, H. G., and Russell, N. G., Jr.: The Use of the Electrocardiographic Changes
Caused by Induced Anoxaemia as a Test for Coronary Insufficiency. Am. J. M. Sc, 1939, 197:241.
Riseman, J. E. F., Waller, J. V., and Brown, M. G.: The Electrocardiogram during Attacks of
Angina Pectoris; its Characteristics and Diagnostic Significance. Am. Heart J., 1940, 19:683.
Master, A. M., Dack, S., and Jaffe, H. L.: Activities Associated with Onset of Acute Coronary
Artery Occlusion.   Am. Heart J., 1939, 18:34.
Horn, H., and Finkelstein, L. E.: Arteriosclerosis of the Coronary Arteries and the Mechanism of
their Occlusion.   Am. Heart J., 1940,  19:655.
Mallory, G. K., White, P. D., and Salcedo-Salgar, J.: The Speed of Healing of Myocardial Infarction.   Am. Heart J., 1939, 18:647.
Levine, H. D., and Levine, S. A.: An Electrocardiographic Study of Lead iv with Special Reference
to Angina Pectoris.   Am. J. M. Sc, 1936, 191:98.
Evans, C: Changes in the Chest Lead Electrocardiogram in Corontory ThromboA. Brit. Heart J.,
1939, 1:161.
Page 279
m H
M P'
By G. Stonehouse, M.D.
This review covers 500 cases of spinal analgesia in the Vancouver General Hospital
over the eight months previous to December, 1940. In 80% or 397 cases, pontocaine
hydrochloride was used; in 20%, or 103 cases, novocaine was used. In solution these two
drugs have a specific gravity approximating that of spinal fluid, in contrast to nuper-
caine, which is lighter than spinal fluid.
Three deaths occurred as a direct result of spinal analgesia. One was a genito-urinary
case which went into extreme shock soon after the drug was given, and died on the
table. This patient was extremely sick before the operation and any anaesthetic would
have been very dangerous. Post-mortem examination disclosed "myocardial degeneration,
liver degeneration, horseshoe kidney/* The second patient was also a genito-urinary
case in which severe shock occurred during the operation, and he died three days later.
No post-mortem examination was performed. The third patient was a poor risk as he
had an intestinal obstruction. Shock occurred early, and not responding to stimulants
he died six hours after operation.  No post-mortem examination was done.
Success of Spinal Analgesia
In 94% of the patients, analgesia was complete, and no further supplementary
anaesthesia was needed.   In 6%, or 30 cases, it was incomplete.   Of these, eight cases^
were given morphia or nothing due to the mildness of the discomfort or shortness of
the operation.  The remaining 22 were supplemented as follows:
1. Gas: Eleven cases.
Eight, uneventful post-operative course.
One, bronchopneumonia (Dagenan).
One, nausea for one day.
One, headache on the second day.
2. Ethyl Chloride and Ether: Five cases.
Nausea, post-operatively.
3. Sodium Pentothal: Four cases.
Two, headache.
One, backache.
One, perspiration one to four days.
4. Second Spinal: One case.
Course uneventful.
5. Local: One case.
Course uneventful.
The failure of the analgesia appeared to be due to one or more of the following
1. Too low analgesia. This appeared to be the chief cause, rather than insufficient
dose of the drug, because 80% of the failures had a full dose (20 mgm.) of
2. Injection of the drug with the tip of the needle partially through or outside the
dura matter, so that part or all of the drug may be injected into the soft tissues
of the back.
3. The drug may become "pocketed" among the network of the Cauda equina and
hence not reach the desired height.
4. Loss of potency of some ampoules of the drug, as occurred with novocaine.
Page 280 Age of the Patient
The age of the patient in this series varies from thirteen to eighty-three, with an
average of forty-five years.
13 -20
70- 80
Table I.
Complications During Analgesia
This paper has been prepared from the surgeon's viewpoint, but it would be well to
discuss briefly the complications during spinal analgesia. These views are expressed in
Current Researches in Anesthesia and Analgesia (September-October, 1939), and I
quote from an article by Apgar:
1. "Nausea and Vomiting may be due to several factors:
(a) Oxygen want from respiratory depression.
(b) Reflex stimulation of the atonomic nervous system by visceral traction,
especially on the common bile duct.
(c) Manipulation of a full stomach.
(d) Toxicity of pontocaine and novocaine.
2. "Respiratory Depression forms one of the chief hazards in spinal anaesthesia. Unrecognized and untreated respiratory repression probably forms the cause of most spinal
anaesthesia fatalities. It is the result of high spinal producing intercostal paralysis and
varying degrees of phrenic paralysis. Deaths from this cause are preventable by artificial
respiration and adequate oxygen until the anaesthetic has worn off. Carbon dioxide is
definitely contra-indicated because it dilates the peripheral circulation, lowering the blood
pressure still further."
In our series we had no cases of respiratory depression.
3. Blood Pressure (Quotation from the work of Co Tui in Current Researches in
Anesthesia and Analgesia, March-April, 1938).
"In experiments on dogs a triphasic blood pressure curve was demonstrated during
spinal anaesthesia. The first phase was the fall in blood pressure occurring before the
spinal injection was complete. This is a result of and accompanied by a rise in the
volume and temperature of the lower extremities due to paralysis of the sympathetic
vaso- nerves with subsequent flooding of the lower vascular tree. This fall is very transient, and followed by the second phase or compensatory rise in blood pressure brought
about reflexly through the aortic nerves and carotid sinus."
These two phases probably occur also in man as well, for patients will often voluntarily state they feel a flooding of heat through their legs even before the spinal injection
is complete.
"Then as the drug spreads upwards paralyzing one spinal nerve after another fewer
and fewer unaffected segments remain to maintain this compensation, and we see the
third phase—a gradual and perhaps prolonged pressure fall. In this phase another factor
may play a part—namely, intercostal paralysis leading to anoxia and accumulation of
carbon dioxide, which further adds to the fall. Artificial respiration, or administration
of oxygen by washing out the carbon dioxide, will raise the pressure to that extent to
which carbon dioxide contributed to the fall."
A factor ontributing to this proclonged fall as shown by other investigators is, and
I quote, "Paralysis of the adrenalin secretion through paralysis of the sympathetic system.
This may be of great importance clinically. It may handicap mobilization of blood sugar
as well as mobilization of fibrinogen, and thus lengthen the clotting time. These theoretical possibilities require experimental confirmation." However, workers have shown
that   spinal anaesthetized dogs die more readily from haemorrhage than normal ones."
Page 281
:i 1*1>1
"i-ii «H\\
•J i I
Sugar in the form of five per cent glucose intravenous and adrenalin injection are very
effective in the prophylaxis and treatment of spinal shock.
In our series we divided spinal shock into three stages:
First Stage: Here the patient was comfortable with or without pre-medication of
blood pressure stimulants, and with or without stimulants during the analgesic.
Second Stage: Here the patient became uncomfortable within the first twenty minutes or half hour of the analgesia but regained complete feeling of well-being after blood
pressure stimulants were given.
Third Stage: Here the patient went into more profound shock during the analgesia
and in spite of treatment the patient's comfort was not completely restored.
You will note that the criterion chosen for the patient's shock was the patient's
comfort rather than the blood pressure. This has been the practice of our staff, and if
the patient says he feels well and looks well, his condition usually is excellent. Furthermore, in a spinal analgesia the patient's feeling of well-being is of primary concern.
Note: Here I owe you some explanation for classifying a comfortable patient in the
first stage of shock. As mentioned above, this is not the accepted form of classification.
However, even these so-called "comfortable" patients have some early mild drop in
blood pressure and this is classified as "mild shock."
Most patients in our series felt quite comfortable with a drop in blood pressure of
twenty to thirty points. Below this level the patient may complain of one or more of
the following symptoms:
(1) A feeling of heat with perspiration.
(2) Nausea and vomiting.
(3) Shortness of breath (rarely).
Many workers consider shortness of breath with partial or complete respiratory
paralysis a very important and not uncommon phenomenon. In this series, shortness of
breath was a rare finding and we had no cases of respiratory paralysis. If treatment is
given early for these symptoms, the subjective and objective symptoms will probably
not occur, and the patient will remain comfortable throughout. With the early appearance of these symptoms the following treatment may be instituted:
(1) Ephedrine Hydrochloride is best given half an hour pre-operatively. It may also
be given for a falling blood pressure, but with variable effect.
(2) Adrenalin Hydrochloride, given intramuscularly, will prevent any further drop
in blood pressure and will usually raise the blood pressure somewhat.
(3) 5% Glucose intravenously is probably the most effective in shock cases where
a prompt rise in blood pressure and a prolonged effect is desired. It is particularly suitable for elderly patients with arterio-sclerosis and cardiac degeneration
where vasomotor and heart stimulants may be harmful or contra-indicated.
Other stimulants used less frequently are coramine and caffeine.
Success of Treatment During Operation
Seventy-five per cent of our series were comfortable throughout operation. Of th«s
percentage, 39, or 8%, were given treatment. Twenty-three were given intravenous
five per cent glucose; 12 were given ephedrine, and 4 adrenalin. Sixty-seven per cent of
the series were comfortable without treatment.
One hundred and fifteen were given stimulants for second stage shock to good effect.
Ten, or 2%, went into third stage shock and responded poorly to treatment, seven
Distribution of Cases
Table II.
r Shock i
Region                                              Cases              First Second Third      Incomplete     Fatal
Abdominal           65                    33 24 (37%) 7
Leg   and   Hip j      107                    92 12 (11%) 1                  2
Perineal   |f|  71 63 8 (11%)
Kidney, Bladder, Prostate, Hernia—    257                 218 27 (11%) 5                 4
Page 282 Pre-Medication
Table III.
Cases Shock %
Nembutal     231 34 14
Nembutal  and Morphia 1       28 9 32
Morphia 125 34 27
Nil S : 116 15 15
This would seem to indicate that no pre-medication was almost as effective in preventing shock as nembutal. However, those cases without pre-medication were often
short and given low spinal analgesia, such as for cystoscopy, whereas those given nembutal required longer analgesia, such as orthopaedic cases. We think the nembutal makes
the patient less alert, mjore comfortable during the operation, and often he will doze
during most of the operation.
Morphine and morphine with nembutal show a higher percentage of spinal shock
and do not seem to give as much protection as nembutal itself.
Post-Operative Complications
Seventy-one per cent were free of post-operative complications due to spinal analgesia.   One hundred and forty-six cases, or 29%, had complications in the following
order of frequency:
Cases %
Headache  52 10.4
Nausea and Vomiting  . _ 36 7.2
Perspiration  28 5.6
Backache  16 3.2
Mental Disturbances  7 1.4
Gas  5 1.0
Hiccough - 4 0.8
Headache may be due to
(1) Gradual seepage of cerebro-spinal fluid through puncture hole in the dura for
some time post-operatively with lowering of the cerebro-spinal fluid pressure
and dilatation of the cerebral veins.
(2) Toxic action of the drug on the vital centres similar to general anaesthesia
and alcohol.
(3) Habitual headache tendency.
Headache usually begins on the second day post-operatively, lasting one to three
days, moderately severe in character, but may persist up to a week. It responds well to
a mild sedative such as aspirin with codeine.
Nausea and Vomiting are probably due to the toxic effect of the drug. This percentage is extremely low in contrast to general anaesthesia.
Perspiration is probably due to a temporary upset in the autonomic nervous system.
Backache may be due to
(1) Injury to spinal nerves by the spinal needle.
(2) Injury to spinal tissue outside the canal.
(3) Stretching of ligaments and muscles through changing the curvature of the
lumbar spine due to relaxation of the parts.
Mental Disturbances: Of the seven cases, five were genito-urinary cases over seventy-
five years of age. They were quite comfortable during the operation, but post-operatively developed such symptoms as confusion, irritability, and disorientation. The sixth
case, a man of seventy-seven, went into third degree shock during the leg operation and
was confused for two days post-operatively. The seventh case, a man of fifty-four, was
comfortable throughout the operation, but was also confused for one day post-operatively.
Bronchopneumonia and Pneumonitis: It was impossible from the charts to get data
on this post-operative complication. The literature mentions that post-operative pneumonia and pneumonitis after spinal analgesia are no more frequent than after general
Hiccough: Of the four cases mentioned, two had hiccough pre-operatively.
Page 283
J    A
J   IT   I
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ifttti i
Unusual Cases
An unusual case that occasionally occurs is the one that goes into sudden coll|
immediately after spinal injection has been completed.  In one of our patients, the shoe
was so severe that the patient thought he was going to die.   He was extremely pale
the pulse was soft and slow as in an extreme case of spinal shock.   One ampoule
coramine  was given intravenously, followed in  a  few minutes  with five minims?
adrenalin intravenously.   The patient was then taken into the operating room from
anaesthetic room and intravenous fluids given.  He recovered in ten minutes.  This pati
was a young man, aged thirty-eight, and appeared healthy before the spinal analgl
was given.   On questioning he gave a history of habitual fainting spells.   On one ocd
sion while on the ward in bed he fainted on seeing intravenous fluids given to a neai
Another case of typical anginal attack occurred in a middle-aged man having
transurethral resection performed.   About three-quarters of the way through the o
tion he suddenly complained of a vise-like pain in the left chest with accompany!
shock.   A quarter grain of morphia was given, followed by intravenous fluids,
patient died in bed about two hours later.
The only absolute contra-indications are:
(1) Infection in the spinal canal.
(2) Infection of the soft tissues of the back.
The border-line between absolute and relative contra-indications is a wide one
Age: The very old and the very young are usually poorer risks for spinal analges
and yet prostatic resection recently done on a man aged ninety-two was successful.
Hypertension: The hyperpiesic patient is a better risk for spinal analgesia than
"toxic" or "symptomatic" hypertensive patient.   Generally speaking, the elderly patia
with hypertension, who have prostatic resection, do well.   In the "toxic" variety, othl
organs are necessarily involved, and hence a general anaesthetic is indicated.
"Nervous" Patient is only relatively a contra-indication, for  a sedative such ;
nembutal usually suffices to calm him.
Spinal Injuries would appear to be a contra-indication, and yet we have given spina
analgesia in this group successfully.
Cord Lesions: We used to think that in this type of pathology the spinal drug would
not be absorbed. We have given a number in the hospital with no untoward results and
excellent analgesia.
Obesity is a contra-indication only insofar as the technical difficulties of adminia
tration of the drug.
Toxicity: The very "toxic" patient is a poor risk for any anaesthetic, but it is felt
that an anaesthetic where the patient is better controlled, such as general anaesthesia, i
a safer method.
1. Five hundred cases of spinal analgesia are reviewed with three fatalities.
2. Ninety-four per cent of the spinal analgesia were complete and needed no supplementary anaesthesia.
3. Seventy-five per cent of the patients were comfortable throughout the operatii
To eight per cent of these some form of treatment was given for shock.   The relatiij
values of stimulants are reviewed.
4. Distribution of  cases  is  given  graphically  along  with merits  of  various ptj
5. The rarity of post-operative complications is particularly noted.
Owing to improvements in the drugs for spinal analgesia, and to adequate prepafi
tion of the patients, and to skilled anaesthetists, spinal analgesia has probably become one
of the safest and most useful methods at our disposal.
(To Dr. Freeze for his helpful criticism, and to the Record Office for their invarc
able assistance, I wish to express my indebtedness and gratitude.)
Page 284


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