Sympathetic activity under cold stress is investigated. Predominantly vagal cardio-depressive reflexes are discussed besides currently known mechanisms of sudden death after water immersion. Pronounced circulatory centralization in diving animals as well as following exposure in cold water indicates additional sympathetic activity. In cold water baths of 15 C, measurements indicate an increase in plasma catecholamine levels by more than 300 percent. This may lead to cardiac arrhythmias by the following mechanisms: cold water essentially induces sinus bradycardia; brady-and tachycardiarrhythmias may supervene as secondary complications; sinusbradycardia may be enhanced by sympathetic hypertonus. Furthermore, ectopic dysrhythmias are liable to be induced by the strictly sympathetic innervation of the ventricle. Myocardial ischemia following a rise in peripheral blood pressure constitutes another arrhythmogenic factor. Some of these reactions are enhanced by alcohol intoxication

Buhring, M.

Spies, H. F.

English

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t
G
PATHOGENESIS 7F SUDDEN DEATH FOLLOWING
WATER IPMIER: ION (IM11ERSION SYNDROME)
M. Bdhring and H. F. Spies
Translation of "Syrapatho-adrenal AktivitAt bei akutem Kaltestress.
zum Mechanismus pl6tzlicher TodesfAlle im 4olasser", Zeitschrift
fdr Rechtsmedezin, Vol. 83, 1979, pp 121-127.
(NASA-T,1- 7u i42) PATHCGENESIS Ut SUDDEN
DEATH FOLLOWING WATEd IMdERSICN (IMMEar;IUN
SYNUiiUME) (Natiociai A e LOUautiCS acrd S^dCt=
Administration)	 1,4 p dC A02 /MF Au1 CSCL Ooh
N81-zJ723
UaclaS
GJ/52 4161)0
Rte "i CD
NASA S71 FACUT1
^`.	 ACCESS DEPT,
NATIONAL AERONAUTICS AND SPACE ADMINISTRATION
WASHINGTON, D. C.
	
MARCH 1981
ik
STANDARD TITLE PAGE
NASA rt N	 76542	 2. Government Accession Me. 2.	 Recipient's Catalog No.
d. Title .nd Subtitle . PATHOGENESIS OF SUDDEN S. Rowe Dote March 1981
DEATH FOLLOWING WATER IMMERSION
e. Performing Organi lotion Code(IMMERSION SYNDROME)
7.	 AutAoAsl
M. B^hring and H. F. Spies 1. Performing Orgonief ion Rope„ Me.
10. wait Unit No.
11.	 Contract or Grant No.
e . Performing Orgeniaarion Name and Address
Leo Kanner Associates 13.	 Typo of Report and Period Covered
Redwood City, California 94063 Translation
12.	 Sponsoring Agency Name and Address
National Aeronautics and Space Admin. 1d	 Sponsee ing Agency Cede
Washington, D. C. 20546
	 e
15.
	 Supplementery Notes
Translation of "Sympatho-adrenal AktivitAt bei akutew
KAltestress.	 Zum Mechanisrus pldtzlicher TodesfAlle im
Wasser", Zeitschrift fdr Rechtsmedezin, Vol. 83, 1979,
pj. 121-127.
1e. Abstract	 Predominantly vagal cardio-depressive reflexes discussed besides
currently known mechanisms of sudden death after water.immersion. Pro-
nounced circulatory centralization in diving animals as well as following
exposure in cold water indicates additional sympathetic activity.
	 In col
water baths of 15 0C authors' measurements indicate increase in plasma ca-
techolamine levels by more than 300%. 	 This may lead to cardiac arrhyth-
mias by the following mechanism:
	 Cold water essentially induces sinus
bradyeardia.	 Brady- and tachycardiarrhythmias may supervene as secondary
complications.
	 Sinusbradycardia may be enhanced by sympathetic hyperton-
us.	 Furthermore, ectopic dysrhythmias are liable to be induced by the
strictly sympathetic innervation of the ventricle. 	 Myocardial ischemia
following a rise in peripheral blood pressure constitutes another
arrhythmogenic factor. 	 Some of these reactions are enhanced by alcohol
intoxication.
17.	 Key words (Soloetetl by Author(a1) 13. Dmsrl bu tlon Statement
rcwning, sudden death follow-
ing water immersion,
irimniersion syndrome Unclassified - Unlimited
19.	 Security Clessil. (of this report) 20.	 Sacwrity Clessil. (of this pye) 21. No. of Pegs s 22.	 Price
Unclassified Unclassified 12
NASA-MO
PATHOGENESIS OF SUDDEN DEATH FOLLOWING
WATER IMMERSION (IMMERSION SYNDROME)
1
M. BOhring and H. F. Spies
Primary submersion [37), water stroke [19], the "immersion 	 122*
syndrome" [24) or hydrocution 1231 present a special type of
death by drowning. In typical cases the swimmer, after being in
the water for only a few moments, suddenly disappears from the
view of the astonished observer and drowns. In some cases drowning
is preceded by a brief struggle.
This sort of death is relatively frequent 11, 17, 20, 21, 25,
33, 371; for the assessor it is often hard to decide, whether the
case is one that entitles to compensation in the sense of general
accident insurance conditions [1, 10, 12, 20, 21, 25, 31, 33, 38,
43).
It happens repeatedly, that for many such subjects death in-
tervenes when they are under the influence of alcohol, often only
to a slight degree [13, 16, 18, 20, 24, 30, 32, 33, 36), so that
the amount of intoxication is not an adequate explanation for an
crdinary drowning through impairment of coordination.
It is usually assumed, that in such cases death involves a re-
flex event. In addition to anaphylactic cold reaction, immersion,
Goltz and vestibular reflexes, the discussion centers especially a-
round vagomediated cardiodepressive reactions. These are assumed
to be released by sensitive structures in the laryngeal area follow-
ing aspiration of water and of abnormally created anxiety with the
possibility of psychogenic unconsciousness [38); in the end anxiety
Numbers in the margin indicate pagination in the foreign text.
1
K ..4
and bodily exertion are assumed to result in stress respiration,
which in syncotropic types 181 induces abnormal decrease in BP or
impaired rhythm.
In most clarification experiments there is a unilateral assess
-ment only of the part played by vague reaction processes. They a-
rose as the result of the well known cold bradycardia and in part
of impressive immersion bradycardia found in vertebrates that live
in water and breathe with their lungs [3, 4, 11, 261 and in humans
[28, 34].
However, with bradycardia there was also the development of a
significant centralization of circulation. In this context air o-
riented animals show a minimal lifespan for attaining longer and
longer submersion periods. In humans this centralization may be
the reason for a surprisingly longer survival of children who have
been submerged 12, 22, 401. Recently this phenomenon occasioned a
large number of revival experiments with people wno had remained be-
low water for as long as 38 (!) minutes [27].
In addition to the familiar transformations in the direction of
vagotonia, these observations already indicate simultaneous sympa-
thetic activation of autonomic regulation. Thus, at least for hu-
mans, water temperature appears to be significant: the observa-
tions referred to above were made exclusively in a cold water con-
text. Nemiroff [27] gives 216C as the critical temperature for an
adult.
We wondered, whether sympathetic activity could be demonstrated
under cold stress. This would produce new points of view for the
genesis of primary submersion. We thought it would be a good idea
2
to determine the plasma catecholamine level .
Test Procedure
The test subjects were 20 healthy males aged 22-37 (x a 27.3).
Following an hour's preliminary rest on a lift platform they were
2
lowered with it into 15°C water, which a circulation system kept in
constant movement. Following 10 min of this, the water temperature
was uniformly raised 1.5°/min until it was one degree below actual
rectal temperature (Fig. 1).
3i •c
bddbft
k
C mN^^
u°c	 16 ^w Mam.m^..^ d
is
48
n
e
6	 !6	 !0	 70	 10	 !9
Fig. 1. Circulation values, body tem-
perature and plasma catecholamine le-
vel during 10 min immersion in 15°C
water. Preliminary rest and subse-
quent warming of water to within 1°C
of actual rectal temperature. Range
of mean error shown by brackets.
Key: a. pulse rate
b. blood pressure
c. water temperature
d. under rectal temperature
e. prerest in minutes
crease in the pulse rate.
At the start of prerest
insertion of a venous cathe-
ter, blood sampling shortly
before start of immersion
and at minutes 5, 10, 40, 70
of immersion. Adrenaline
and norepinephrine measured
by Passon and Peuler method
(29). Continuous recording
of pulse rate and rectal tem-
perature, auscultatory BP
measurement.
Results (see Fig. 1)
After 10 min immersion
the noradrenaline levels are
340% of the initial values.
Only with central cooling of
the organism do the adrena-
lin levels rise considerably
(up to 250% in immersion mi-
nute 70).
During the cold water
phase the rectal temperature
drops considerably and the
elevated catecholamine lev-
els are not expressed by the
moderate and short term in-
Ptmin
is 0
In to
w
^o
3
SINUSRNYTHMUS
a
	
14 	kMput	 KALTREIt
CMa^nst►M^n ^^ NenRrmaa►
4ti% C	 InAkanal i
b.
rMOt SINUSRRAOYCARDIE f
^	 ^	 h k:Rnycaroc
NEU RHYTHMUSSIORUNG	 HER MYTHMUSSTORUNG
:, M. SA • Mack SinufknaNn-	 L M, u*w oW anlrikuWs
funkOW20tl►anq	 Tachyarft 0~ 11i
I Zunahma 9N EKTOPIE PO
Fig. 2. Vagal (white arrow) and sym-
pathetic (black arrow) reactions in
cold stress may induce bradycardiac
and tachycardiac rhythm disturbances
in several ways. Some reaction pro-
cesses are intensified by alcohol
(wavy arrow). Details in the text.
Key: a. cold stimulation
b. vascular constriction
c. heightened resistance
d. attendant increased car-
diac effort leading to
e. ischemia
f. reflex sinus bradycardia
g. bradycardiac disturbance
of heart rhythm, e.g. SA
block, disturbances of
sinus node functioning
h. tachycardiac disturbance
of heart rhythm, e.g. su-
pra or ventricular tachy-
cardia, ventricular fib-
rillation (increase of
ectopy)
Using balanced catecho-
lamine measurements from the
urine, Wennmalm 1411 made a
plausible point for the
first time in regard to hu-
mans of a sympathetic acti-
vation in cold water. Now
that increased adrenaline
and norepinephrine in the
plasma have been demonstra-
ted, one must rethink the
genesis of cases of sudden
death in water. They in-
volve pathological reflex
processes affecting the
heart with fatal rhythm
impairment under certain
conditions (Fig. 2).
A first danger is al-
ready to be founC in reflex
sinus bradycardia itself,
which yields numerous possi-
bilities for bradycardiac
and tachycardiac rhythm
disturbances. How the bra-
dycardia comes to be cannot
yet be stated with certain-
ty. Is it released direct-
ly by cutaneous thermorecep-
tion and vagal reflex, or	 124
is it to be regarded only
as the result of a cardio-
4
depressor reflex following primary hypertonia? Simultaneous sympa-
thetic stimulation takes hold at different places:
1. The heightened peripheral resistance occasioned by norepi-
nephrine results, via baroreceptors, in reinforced bradycardia. La-
tent disturbances in the functioning of the sinuatrial circuit and
in the buildup of stimulation in the sinus nodes may appear with ad-
ditional vigor.
2. Increased resistance in the arterial system induces cardiac
overload in the form of increased afterload. In cases of hemodyna- 125
mically effective coronary heart disease there is danger of tachy-
cardiac, usually ventricular, rhythm impairment.
3. A third possible complication is associated with the spe-
cial manner in which the heart reacts to autonomic stimuli. Within
*he His-Purkinje system only the sinus node and the AV node show a
sensitive reaction to stimulation by the vagus as well as the beta-
sympathetic system. The ventricular myocardium has exclusively sym-
pathetic innervation and with stimulation there is a lowering of the
fibrillation threshold. then at the same time there is retarded sti-
mulation following the ordinary pathway from the cranial, there is
particularly great danger of a tachycardiac ventricular rhythm dis-
turbance.
The initial situation when alcohol is in the picture is that of
an enlarged periphery, even if intoxication is moderate. The norepi-
nephrine encounters a wider open vessel, instant resistance increase
in some cases is greater and along with it a reflex type sinusbrady-
cardia. Another possibility would be increased flow of catecholamine
to produce the required vasoconstriction. Here however there is the
danger of ectopy in the form of the abovementioned selective sympa-
thetic innervation in the ventricular area.
We consider this concept significant for the following reason: 1126
numerous descriptions have been given of rhythm disturbances in ca-
ses of sudden cold effect [5, 26, 28, 34, 35, 44). Cases of sudden
5
death were noted by Lartique (23] only for temperatures below 180C.
In other authors there is little data about water temperature. It
is likewise true that the statistics cited above for the survival
of drowned children and adults count only for cold water.
In regard to cold sensitivity it is to be noted that cold re-
ception is possible only in the range of 18-340C 1141: colder tem-
peratures take the pain receptor path. It may be that the colder
temperatures are treated by the CNS in a completely different way.
In immersion bradycardia the specific cold sensitivity of the
face is important 15, 9, 12). We ourselves have shown the fact of
increased sensitivity of the upper body when compared with the low-
er [6]. Thus, where there is question of certifying cases of sud-
den death in water, we consider it imperative that the water temp-
erature and the topography of the cold effect be considered.
Footnotes
1. M. BOhring, Department of Physicodietetic Therapy and H. F. Spies,
Cardiology Department, both at the Center for Internal Medicine,
Clinic of the Johann-Wolfgang-Goethe University, Theodore-Stern-
Kai 7, D-6000 Frankfut/M., West Germany.
2. We followed a suggestion from the Pharmacology Center in the Cli-
nic of the Johann-Wolfgang-Goethe University. We are grateful to
Prof. D. Palm, M. D. and Mrs. E. Appel, Ph.D. for sharing their
findings with us.
6
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10


Pathogenesis of sudden death following water immersion (immersion syndrome)

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