Table Of ContentSHOCK
PATHOGENESIS AND THERAPY
AN INTERNATIONAL SYMPOSIUM
STOCKHOLM, 27th-30th JUNE, 1961
SPONSORED BY CIBA
CHAIRMAN
u.s.
VON EULER
STOCKHOLM
EDITED BY
K.D.BOCK
BASLE
WITH 120 FIGURES
SPRINGER-VERLAG
BERLIN HEIDELBERG GMBH 1962
This book bas also been published in German under the title
SCHOCK
Pathogenese und Therapie
Ein internationales Symposion
ISBN 978-3-662-28249-6 ISBN 978-3-662-29767-4 (eBook)
DOI 10.1007/978-3-662-29767-4
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Springer-Verlag Berlin Heidelberg GmbH.
© by Springer·Verlag Berlin Heidelberg 1962
Originally published bySpringer-Verlag OHG Berlin· Găttingen-Heidelberg 1962
Softcover reprint of the hardcover 1st edition 1962
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Contents
Opening remarks (U. S. VON EuLER). . . . • . . . . . . . . . . . VII
Definition and classification of various forms of shock. (R. F. RusHMER,
R. L. VAN CrTTERS, and D. F~tANKLIN) . . . . . . . . . . . . 1
Discussion: voN EULER, GREGERSEN, KRoG, NICKERSON, RusHMER. 23
Comparison of various forms of experimental shock (J. FINE) . . . . 25
Possible role of endotoxin in the perpetuation of shock (R. P. GILBERT) 40
Discussion: FINE, GELIN, GRoss, HALPERN, HowARD, SPINK 45
Hemodynamic factors in shock (D. E. GREGG). . . . . . . 50
Nervous adjustments of the vascular bed with special reference to patterns
of vasoconstrictor fibre discharge (B. FoLKOW). . . . . . . . . . . 61
Discussion: BACQ, FOLKOW, GREGG, KRAMER, NICKERSON, RUSHMER,
STitOM . . . . . . . . . . . . . 73
Metabolic aspects of shock (L. MIGONE). . . . . . . . . . . . . . . 76
Discussion: BACQ, KRAMER, MIGONE . . . . . . . . . . . . . . . 95
Microscopic observations of the mesenteric circulation in rabbits subjected to
reversible and irreversible haemorrhagic shock (S. BELLMAN, P. B.
LAMBERT, and J. FINE) • . . . . . . . . . . . . . . . . . . 96
Discussion: BErN, BELLMAN, FINE, GELIN, GRoss, HALPERN, IMHOF,
MIGONE, NrcKEitSON, SPINK . . . . . . . . . . . . . . . . . . 99
The nature of irreversible shock: its relationship to intestinal changes
(R. C. LrLLEHEI, J. K. LoNGERBEAM, and J. C. RoSENBEitG) 106
Discussion: BACQ, BErN, GILBERT, GREGERSEN, LILLEHEI, MmoNE,
NICKERSON, RUSHMER . . . . . . . . . . . . . . . . . . . . 130
Renal faihtre in shock (K. KRAMER) ............... 134
Renal blood flow and renal clearances during hemorrhage and hemorrhagic
shock (E. E. SELKURT) . . . . . . . . . . . . . . . . . . . . 145
The participation of the adrenal glands in endotoxin shock. (B. HoKFELT,
S. BYGDEMAN, and J. SEKKENES) . . . . . . . . . . . . . . . 151
Aldosterone and alterations in circulatory reactivity following endotoxins
(H. J. BErN) . . . . . . . . . . . . . . . . . . . . . . . . . 162
Discussion: ADAMs-RAY, BErN, HALPERN, HoKFELT, HowARD, NICKER·
soN, SPINK, UvN.As . . . . . . . . . . . . . . . . . . . . . 169
Reflex mechanisms and the central nervous system (E. NEIL). . . . . . 17'!.
The effects of emotional stress on the circulation through voluntary muscles
(A. D. M. GREENFIELD) .................... 177
Discussion: BACQ, BErN, FINE, FOLKOW, GREENFIELD, GREGERSEN,
KRAMER, NEIL, NICKERSON, RusHMER, STROM, UvN.As . . . . . . 180
Hemorrhagic and post-hemorrhagic shock (J. M. HowARD) ...... 186
The effect of hypovolaemic (stagnant) and arterial hypoxia on the distri
bution of cardiac output in dogs and rats (L. TAKACS) . . . . . . . 195
IV Contents
Observations on haemo-respiratory effects of acute haemorrhage (H. BJuR
STEDT and J. C. G. CoLERIDGE) . . . . . . . . . . . . . . . . 200
Discussion: ALLGOWER, BACQ, BING, BocK, BoHR, BREWIN, BULL, VON
EuLER, FINE, GELIN, GILBERT, GREGERSEN, GRoss, HoKFELT, How
ARD, KRAMER, LILLEHEI, MIGONE, NICKERSON, 8ELKURT, SPINK,
TAKACS. . . . . . . . . . . . . . . . . . 205
Clinical aspects of traumatic shock (J.P. BULL) . . . . . . . . . . . 216
Discussion: BULL, FINE, GREGERSEN, NICKERSON ........ 222
Pathogenesis and therapy of shock due to infection: experimental and
clinical studies (W. W. SPINK) ................. 225
Toxic factors in shock (with special reference to burns) (M. ALLGOWER). 240
On the pathogenetic therapy of shock (B. K. OssiPOV) . . . . . . . . 248
Myocardial shock (K. MATTHES) ................. 253
Discussion: BAcQ, BioRcK, BuLL, voN EuLER, FINE, GRoss, HALPERN,
LILLEHEI, MATTHES, NICKERSON, RUSHMER, SELKURT, SENNING,
SPINK, TROELL. . . . . . . . . 267
Allergic shock (B.-N. HALPERN). . . 276
Discussion: HALPERN, SPINK, UvN.As 291
Radiation shock (Z. M. BAcQ). . . . 293
Discussion: BAcQ, BEIN, FrNF., GREGERSEN 300
Shock and extracorporeal circulation (A. SENNING). 304
Discussion: HALPERN, KRAMER, LILLEHEI, NICKERSON, SENNING 311
Humoral and myogenic factors in shock: evaluated by means of isolated
arteriolar smooth muscle response (D. F. BoHR and P. L. GoULET) .. 314
Hypothermia in shock (E. G. BREWIN) ...•........... 319
Discussion: ADAMS-RAY, BACQ, BREWIN, FINE, GREGERSEN, HALPERN,
IMHOF, KROG, MIGONE, NEIL, SENNING . . . . . . 327
Fluid substitution in shock (L.-E. GELIN). . . . . . . . . . . . . . 332
Further aspects of fluid substitution (M. I. GREGERSEN). . 348
Discussion: ALLGOWER, BACQ, BuLL, FoLKOW, GELIN, GREGERSEN,
KRAMER, NEIL, NICKERSON, SELKURT ... 351
Drug therapy of shock (M. NICKERSON). . . . . . . 356
Some aspects of treatment in shock (G. STROM) . . . 371
Discussion: GILBERT, LILLEHEI, NICKERSON, SPINK. 375
Closing remarks (U. S. VON EuLER) . 377
List of authors . 380
Subject index . . . . . . . . . . 381
Participants in the Symposium on "SHOCK"
Stockholm, 27th-30th June, 1961
ADAMS-RAY, J., Kirurgiska Avd., Karolinska Sjukhuset, Stockholm (Sweden)
ALLGOWER, M., Chirurgische Abteilung, Ratisches Kantons- und Regional
spital, Chur (Switzerla11d)
BAcQ, Z. M., Laboratoire de Pathologic et Therapeutique Generales, Uni-
versite de Liege, Liege (Belgium)
BErN, H. J., CIBA Research Laboratories, Basle (Switzerland)
BELLMAN, S., Serafimerlasarettet, Stockholm (Sweden)
BING, J., Universitetets Institut for Eksperimentel Medicin, Kobenhavn
(Danmark)
BroRcK, G., Serafimerlasarettet, Stockholm (Sweden)
BJURSTEDT, H., Flyg- och Navalmedicinska Avd., Karolinska Institutet,
Stockholm (Sweden)
BocK, K. D., CIBA Research Laboratories, Basle (Switzerland)
BoHR, D. F., Physiology Department, University of Michigan, Ann Arbor
(U.S.A.)
BREwrN, E. G., Surgical Unit, St. Thomas's Hospital Medical School,
London (Great Britain)
BuLL, J. P., Industrial Injuries and Burns Research Unit, Birmingham
Accident Hospital, Birmingham (Great Britain)
VON EULER, U. S., Fysiologiska Institutionen, Karolinska Institutet, Stock
holm (Sweden)
FINE, J., Department of Surgery, Harvard Medical School, Boston, Mass.
(U.S.A.)
FoLKOW, B., Fysiologiska Institutionen, Goteborgs Universitet, Goteborg
(Sweden)
GELIN, L.-E., Sahlgrenska Sjukhuset, Kir. Klin. II, GOteborgs Universitet,
Goteborg (Sweden)
GILBERT, R. P., Department of Education and Research, Evanston Hospital
Association, Evanston, Ill. (U.S.A.)
GREENFIELD, A. D. M., Department of Physiology, The Queen's University
of Belfast, Belfast (Northern Ireland)
GREGERSEN, M. I., Department of Physiology, College of Physicians and
Surgeons, Columbia University, New York, N.Y. (U.S.A.)
GREGG, D. E., Department of Cardiorespiratory Diseases, Walter Reed
Army Medical Center, Washington, D. C. (U.S.A.)
GRoss, F., CIBA Research Laboratories, Basle (Switzerland)
HALPERN, B.-N., Centre de Recherches Allergiques et Immunologiques,
Hopital Broussais, Paris (France)
HoKFELT, B., Endokrinologiska Avd., Karolinska Sjukhuset, Stockholm
(Sweden)
HowARD, J. M., Department of Surgery, Hahnemann Medical College,
Philadelphia, Pa. (U.S.A.)
IMHOF, P., Lory-Abteilung, Inselspital, Bern (Switzerland)
KRAMER, K., Physiologisches Institut der Universitat, Gottingen (Germany)
VI Participants in the Symposium "SHOCK"
KRoG, J., Institutt for Eksperimentell Medisinsk Forskning, Universitetet i
Oslo, Oslo (Norway)
LILLEHEI, R. C., Department of Surgery, The Medical School, University of
Minnesota, Minneapolis (U.S.A.)
MATTHES, K., Medizinische Universitatsklinik, Heidelberg (Germany)
MmoNE, L., Istituto di Patologia Speciale Medica e Metodologia Clinica,
Universita di Parma, Parma (Italy)
NEIL, E., Department of Physiology, Middlesex Hospital Medical School,
London (Great Britain)
NICKERSON, M., Department of Pharmacology and Therapeutics, Faculty
of Medicine, University of Manitoba, Winnipeg (Canada)
0SSIPOV, B. K., Department of Clinical Surgery, Central Institute for
Postgraduate Study, Moscow (U.S.S.R.)
RusHMER, R. F., Department of Physiology and Biophysics, University of
Washington School of Medicine, Seattle (U.S.A.)
SELKURT, E. E., Department of Physiology, School of Medicine, Indiana
University Medical Center, Indianapolis (U.S.A.)
SENNING, A., Chirurgische Universitatsklinik A, Kantonsspital, Ziirich
(Switzerland)
w.
SPINK, vV., Department of Medicine, The Medical School, University of
Minnesota, Minneapolis (U.S.A.)
STROM, G., Klin.-Fysiol. Avd., Akademiska Sjukhuset, Uppsala (Sweden)
TAKACS, L., A Budapesti Orvostudomanyi Egyetem, II. Sz. Belklinikaja,
Budapest (Hungary)
TROELL, L., Marinledningen, Fack, Stockholm (Sweden)
UvN.As, B., Farmakologiska Institutionen, Karolinska Institutet, Stockholm
(Sweden)
Opening remarks
By
u. s.
VON EULER
I should like to begin by saying how extremely pleased we are
that so many of you have been able to attend this symposium.
Yesterday I heard some rather favourable comments on the choice
of participants at this meeting. I can only say that Dr. GRoss and
I have simply picked the best men we knew. This is not precisely a
conventional shock symposium, as you may have noticed. In the
usual type of symposium on shock, those participating consist
almost exclusively of experts on this particular problem. I am very
happy that in this instance we have been able to have participants
from several adjacent fields, particularly as I think everybody must
now admit that the problem of shock has to be solved by joint
efforts from many sources. We know that, in addition to surgery
and clinical medicine, much information from the fields of physi
ology, pharmacology, endocrinology, clinical physiology, pathology,
and allergy will be needed - not to mention biochemistry and bio
physics; and I feel that it is only by uniting our efforts and pooling
our knowledge that we may have some hope of arriving at a closer
understanding of the pathogenesis and nature of shock. One of the
advantages of a small meeting of this kind is that we do not need to
give very lengthy accounts of our ideas or of the results on which
they are based. Everybody here is a distinguished scientist, and I
think this makes for free and frank discussion and brief presen
tations. On the other hand, I believe that many of us will be grateful
for a little more detail as regards technical problems. We cannot
each of us be versed in all the details of the technical questions dealt
with, and therefore it is always very good to have a few explanatory
comments on the techniques used. At least, speaking for myself, I
have frequently found that ideas and concepts can be grasped
quite quickly, but that one often requires further information on
the underlying techniques.
Definition and classification of various forms of shock
By
R. F. RusHMER, R. L. vAN CITTERS, and D. FRANKLIN
A scientific term is useful when it conveys precise meaning to
serve as a reliable tool for communication. The term "shock" is
widely used in many different contexts to convey many different
meanings and has no universally accepted definition. From the
clinical point of view, the term is most commonly used in referring
to patients with acute systemic arterial hypotension accompanied
by other signs and symptoms. The clinical manifestations vary
widely but often include pallor, weakness, sweating, and rapid
thready pulse. However, the essential characteristic is a markedly
depressed systemic arterial pressure. Thus, the causes of shock must
be sought among the factors which determine the pressure in the
svstemic arteries.
• Factors determining systemic arterial pressure. The mean pres
sure maintained within the systemic arterial system is determined
by the balance between the inflow into the system (cardiac output)
and the total peripheral resistance. Some of the prominent mech
anisms which determine cardiac output and total peripheral
resistance are illustrated schematically in Fig. I.
The cardiac output is the product of the stroke volume and the
heart rate. Since the left ventricle may be neither completely
filled during diastole nor completely emptied during systole, the
stroke volume must be considered as the difference between the
diastolic and systolic volumes. The diastolic volume is determined,
among other things, by the effective ventricular filling pressure
and the resistance to distension offered by the ventricular walls
(distensibility). This statement is an oversimplification because the
distensibility or compliance of the ventricular walls varies during
the various phases of filling and also depends somewhat upon the
rate of distension. Control of distensibility by neural or humoral
mechanisms, as suggested in Fig. 1, remains controversial but may
occur during changes in posture (1).
The effective ventricular filling pressure is determined by the
pressure difference inside and outside the ventricle at the end of the
diastolic period. The extracardiac pressure as measured either from
Shock Symposium 1
2 R. F. RusHMER, R. L. VAN CrTTERS, and D. FRANKLIN:
the pericardial or pleural spaces can be influenced by respiratory
activity and by pathological conditions affecting either the peri
cardium or the lungs. Hemorrhage into the pericardium produces
tamponade, which in turn increases extracardiac pressure, restricts
ventricular distensibility and leads to marked reduction in systemic
Factors determining S!!slemic Cat1ses of sgslemic Classili'calion
arterial presst1re arlerial 17!/po/ension of "Shock"
Exs an qvi na/ion
l?!lpo"lension
I
/Jeh!ldrolion
hf!polension
Sef!lleslra/ion
!Jgpolension
1/enlricvlar compression
17!/po/ension
Coronarg insvflicienc!l
hgpolension
Avlonomic imbak!nce
h,qpolension
/7iscero/ atrerenl
!Jqpolension
Stiinalic afferent
llf!polension
Sp/andmic dt!alion
ligpolension
Readif/e !Jgperemia
hgpolension
Allergic
h!lporension
Fig. 1. The reduced systemic arterial pressure is characteristically common to all the various
symptom complexes associated with the term "shock". The causes of shock can be classified
in terms of the various mechanisms which can influence the level of the systemic arterial
pressure. Note that the term "shock" has been used to designate arterial hypotension from
virtually every possible cause of systemic arterial hypotension. Each of the causes of arterial
hypotension should be assigned a concise name which is clearly defined and established
experimentally. If such a list of terms were employed consistently, the term "shock" could
be completely abandoned
arterial pressure. The intraventricular pressure is related to central
venous pressure, which is largely a reflection of the relationship
between the total blood volume and the capacity of the venous
system. The total blood volume can be diminished by either blood
loss or loss of body fluids. Severe systemic arterial hypotension can
be produced by any mechanism which causes sufficient reduction
in total blood volume (e.g. internal or external hemorrhage, burns
or cholera). As an extreme example, CLARKSON et al. (2) recently
described a patient who developed cyclical edema and "shock"
