The Cause of Death after Rescue E. L. Lloyd Department of Anaesthetics, Princess Margaret Rose Hospital, Fairmilehead, Edinburgh, Scotland
Abstract E. L. Lloyd, The Cause of Death after Rescue.
IntJSportsMed,Vol 13,Suppl l,S196—S199, 1992 It is recognized that some people die from hypothermia even though they are alive and uninjured when rescued. The traditional explanation is that this is due to ventricular fibrillation resulting from the afterdrop of core
occur through an imbalance between the active vascular ca-
pacity and the circulating fluid volume i.e. relative hypovolaemia or fluid overload. The actual mechanism in any individual case depends both on the history of the cooling and the method of rewarming used. Some deaths will how-
ever occur due to continued cooling of the body or to ventricular fibrillation precipitated by rough handling.
temperature. This hypothesis was based on inadequate measurement and failure to consider the physiology of
Key words
cold. It should now be discarded. Most deaths after rescue
overload, ventricular fibrillation
Introduction
Cold, hypothermia, hypovolaemia, fluid
Traditional_Explanation
It has long been known (10), though still not al-
During the Dachau experiments (1), the Nazis
ways appreciated, that some people die from hypothermia
noticed that, after the person had been removed from cold water, the rectal temperature continued to drop for a while before rising. Because death often occurred at about the time
even though they are alive and uninjured when rescued. lnt.J.SportsMed. 13(t992)S196—S199 GeorgThieme Verlag StuttgartNew York
this 'afterdrop' was at its lowest, it was assumed that the after-
Downloaded by: East Carolina University. Copyrighted material.
S196 Intl Sports Med. 13(1992,)
The Cause Cause of of Death Deathafter afterRescue Rescue
Int.J.SportsMed. 13 (1992) S197
drop caused the death and, even though there was no ECG
value priorto tocooling cooling[25 [25]), depending on on the the potential potential volume volume value prior 3), depending
monitoring, it was postulated that death was due to ventricular fibrillation (VF) caused by the continued cooling.
of fluid available, which in turn is related to the duration of
However, However, it is difficult to accept that a tempera-
The fluid status of any liypothermic hypothermic individual will depend on the relative importance of these responses.
vasoconstriction there is unlikely to be a large volume of blood sequestered in the periphery. The afterdrop is less at the heart
than in the rectum (8, 12, 16, 19), and though the peripheral temperatures start to rise immediately on removal from the cold (8, 12, 16, 19), there is no increase in limb or extremity flow during the afterdrop even during surface rewarming (28). There is therefore no evidence of a peripheral pool of blood. The afterdrop is therefore the result of the normal physical laws of heat flow and reflects the re-establishment of the normal body temperature gradients (9, 10,1 6, 30). The ogre of the afterdrop should now be relegated to history.
Other Mechanisms As the heart cools it becomes more susceptible to developing arrhythmias, and mechanical irritation as mild as the heart having its position changed by rolling a patient for bedmaking (15) may trigger VF. However, if left undisturbed,
In very prolonged exposure to mild to moderate cold, vasoconstriction, vasoconstriction, and and therefore therefore fluid fluid loss loss from fromcold cold induced diuresis, will be minimal. The loss of fluid from the
vascular space caused by the fluid shifts will have been replaced by fluid intake, and any rapid return of fluid to the intravascular space during rewarming may result in fluid overload and pulmonary oedema.
3. Vascular responses When a subject is in the cold, there is a continuous stream of impulses from the cold receptors in the skin reinforcing vasoconstriction. But when the cold stress on the skin is removed, the cutaneous cold impulses are reduced, the vaso-
constrictor tone is therefore also reduced, and the active volume of the vascular bed is increased. If there is insufficient
available fluid e.g. through dehydration due to diuresis, and/or fluid shifts, the Central Venous Pressure (CVP) will fall and then the Blood Pressure (BP) i.e. collapse due to relative hypovolaemia.
the cooling heart usually stops in asystole (13, 23). VF may also be triggered by hypoxia, by rapid changes in pH or electrolytes
Experimental Findings
in the blood, or in temperature gradients within the heart muscle (16, 18).
There are three relevant effects effects of of exposure exposure to to cold.
1. Energy reserves The body responds to cold by increasing heat output and therefore the energy reserves are utilised. With rapid cooling, e.g. in cold water, the energy reserves are relatively undepleted and, once removed from the cold, the person will rewarm. With less severe severe cold, cold, the the body body temperature temperature will willonly only
fall when the energy reserves are exhausted. With their reduced heat generating capacity these people may continue to cool, and die, even in a mildly cold environment.
2. Fluid balance in the cold
Cold induced vasoconstriction shunts blood into the deep capacitance vessels, and the relative excess of volume is removed by a diuresis (2—4, 11, 13, 16). Respiratory moisture loss is increased by exercise especially in cold dry air e.g. in the polar regions and at high altitude (16). Also cold air is dry, evaporation is rapid and even 1 —2 litres/day sweat loss may be unnoticed (11). However, even with total body dehy-
dration, exercise causes an increase in the intravascular fluid volume (29), thus increasing the cold diuresis and worsening any dehydration. During exposure to cold, fluid also shifts from the intravascular into the extravascular and then intracellular (3,4,21,25). space (3, 4, 21, 25).During Duringrewarming rewarmingthese these fluid fluid shifts shifts reverse and the circulating blood volume increases (up to 130% of the
In a study with sheep, cardiovascular parameters were measured and some unexpected changes were recorded corded (Fig. (Fig. 1) 1) (16, (16, 20). 20). Because Because of of small small numbers, numbers, not not all all the the changes reached statistical significance but the changes were very similar to those found in a human experiment (12) and during the clinical treatment of patients (16) which suggests that they are valid.
During spontaneous rewarming there was a drop in peripheral resistance resistance reflecting reflecting relaxation relaxation of of vasoconvasoconstrictor tone (Fig. I). 1). The The CVP CVP and and BP BP both both fell. fell. The The fall fall in in BP BP with spontaneous rewarming is a well recognized clinical phenomenon (3), and many patients admitted to hospital with a reasonable BP develop a variable degree of hypotension after admission, during a time they are beginning to rewarm spontaneously (7, 16, 26). The bradycardia (Fig. 1) is also seen clinically (3).
In the hot bath, the positive warmth on the skin should lead to a greater relaxation of vasoconstriction. There was a fall in peripheral resistance but surprisingly the CVP and BP BP rose (Fig. 1), suggesting an influx of fluid. The The superficial superficial tissues have had the longest exposure to cold stress, and therefore experienced the greatest fluid shifts. During hot bath rewarming they are also the ones exposed to the greatest heat input, and this rapidly and completely reverses the fluid shifts.
This probably explains why climbers, who were pulseless when brought off the hill, were successfully revived in a hot bath (5). The rise of CVP slowed during rewarming to normothermia, as the deeper tissues with less fluid were rewarmed.
Downloaded by: East Carolina University. Copyrighted material.
ture reached at the nadir of the afterdrop is more dangerous than a similar temperature recorded during continued cooling. Also the original explanation for the afterdrop was the return of cold blood from the periphery, but due to peripheral
cold exposure (3, 13).
S198 mt. J. Sports Med. 13(1992) 10
40 o
MEAN PRESSURE MEAN ARTERIAL ARtERIAL PRESSURE
mmHg
E. L. Lloyd
tnt/min/ Kg tnt/mm/Kg
3D 30
07 4Ti.
—10
B
SH
Discussion
CARDIACOUTPUT CARDIAC OUTPUt
I
N
—"I
2 CENTRAL VENOUS PRESSURE _,r
N
SH
cms H20
PERIPHERAL RESISTANCE UNITS
0
Consideration of fluid and vascular status explains most post-rescue phenomena. For example, collapse during rewarming is almost unknown during rewarming from immersion hypothermia whereas it is relatively common in exhaustion hypothermia (22), the highest mortality occurring if
victims are rewarmed naked in a warm room (14). Collapse and death sometimes occur during rescue from water (10), probably through a profound drop in blood pressure from gravitational pooling of blood in the periphery due to removal of the hydrostatic squeeze and a vertical position e.g. using a single strop helicopter hoist or climbing a ship's ladder (10).
—1
SH
I
Patients hypothermic through malnutrition
20 HEART RATE beats/mm
oe
20 STROKE StROKE VOLUME VOLUME 10
N
20 20
PULMONARY PRESSURE PULMONARY PRESSURE
mmHg
15
10
- -i:
mt/bent mt/beat
— — —*
—
SH
TEMPERAtURE TEMPERATURE SH I PULMONARY RES1STANCE PULMONARY RESST4NCE
-2 -2m-
4-—
Conclusion
Death following rescue is usually the result of an an imbalance imbalance between between the the active active vascular vascular capacity capacity and and the the efefvoiume. Some deaths may be due to fective circulating fluid volume. handling.
_4I '•*-6
I
SH
N
-4
of -5L B
16).
continued cooling or to VF, usually precipitated by rough
N
r UNItS
hypothermia where too rapid rewarming (even if spontaneous) produces cerebral and/or pulmonary oedema (2,
N
S
5n 8
(27), and elderly hypothermic patients (6) have been exposed to a relatively mild degree of cold for a long period, and are similar to patients rewarming following prolonged induced
I
-6 SH
H
B
I
Fig. 1
Cardivascular changes during cooling and rewarming sheep — — aa comparison comparison of of three three methods. methods. B B == Base Base line line readings readings before before cooling cooling by by immersion. immersion. Each sheep was considered to have a reading of zero and changes are recorded as changes from the base line. SN = SN = StabEe Stable hypothermia after been reStabEehypothermia hypothermiaafter afterthe theanimal animal had had been been re-
moved from the cold water and after the afterdrop had occurred. = Intermediate temperature during rewarming — a rise of about one degree centigrade.
N = Normothermia.
•—— —. changes changes during during cooling. •———I x— — —x changes during rewarming in a hot bath.
changes during spontaneous rewarming. •—— — —. —. changes changesduringairwaywarming. during airwaywarming. — —. changes Standard errors are indicated.
References Alexander L.: The treatment of shock from prolonged exposure to cold, especially in water. Combined Intelligence Objective Subcommfttee,1945, committee, 1945,Item ItemNo No 24, 24, File FileNo No26—37. 26—3 7. 2 committee, Bloch M.: Re-warming following prolonged hypothermia in man. M. D. Thesis. Thesis. University of London. 1965. M.D. Burton Burton A. A. C., C., Edholm Edholm 0. 0. G.: G.: Man Man in in aa cold cold environment. environment. London, London, Edward Edward Arnold Ltd., 1955.
Danzl D. F.: Accidental hypothermia. In Rosen P., Baker F. J., Braen G. R., Dailey R. R. I-I., H., Levy Levy R. R. C. C. (eds), Emergency Medicine, Concepts and Clinical Practice, Vol 2: Trauma, Boston, Mosby, I 983,pp477—496. l983,pp477—496. 6 Davies L. W.: Treatment of hypothermia. Lancet ii: 656, 1975. Duguid H., Simpson R. G., Stowers J. M.: Accidental hypotherDuguid mia.Lancetii: 1213—1221,1961. CunnfngA. A.J., J., Bardlian Bardhan K. K. D., Triger D. R.: Severe hyFell R. I-I., H., Cunning pothermia pothermia as as aa result result of of barbiturate barbiturate overdose overdose complicated complicated by by carcardiac arrest. Lanceti:392—394, 392—394,1968. diacarrest.Lanceti: 1968. 8 Golden F StC.: Why rewarm? In Matter P., Braun P., deQuervain
M., Good W. (eds) Skifahren und Sicherheit III. Davos, BuchdruckereiDavosAG, druckerei DavosAG, 1979, l979,pp pp163—167. 163—167.
During Airway Warming (AW) (Fig. 1) there is the same reduction in input from the cold sensors in the skin as during spontaneous rewarming, and any warming of the central thermostat should further aggravate the situation. The ab-
sence of an initial drop, and the later rise, in peripheral peripheral reresistance with AW may reflect the return of cerebral control of vasomotor tone. The BP rose early while the CVP showed a delayed rise coinciding with the inclusion of peripheral, fluid containing tissues in the expanding warm core. The tachycartachycar. dia associated with AW has also been noted during core rewarming with peritoneal dialysis (24). These findings are reflected in clinical cases (15—17).
Golden F. StC., StC., 1-lervey Hervey G. G. R.: R.: The The "after-drop" and death death after after Flyrescue from immersion in cold water. In Adams J. S. (ed) Hypothermia Ashore and Afloat. Aberdeen, Aberdeen University 10
' 12
Press, 198 l,pp37—56. l,pp37—56. Golden Golden F. StC., Hervey G. R., Tipton M. J.: Circum-rescue collapse: Collapse, sometimes fatal; associated with rescue of immersion victunis. Nay Med Serv77: 77:139 139—149, victums. fRay JRoyNavMedServ —149, 1991. 1991. Hamlet M. P.: Fluid shifts in hypothermia. In Pozos R. S., Wittmers L. E. (eds), The Nature and Treatment of Hypothermia, London, Croom Helm, 1983,pp 94—99. don,CroomHelm, l983,pp94—99. Hayward Hayward J. S., Eckerson J. D., Kemna D.: Thermal and car-
diovascular changes during three methods of resuscitation from 13
II: 21—33, 1984. mild hypothermia. Resuscitation 11:21—33, Keatinge W. R.: Survival in Cold Water. Edinburgh, Blackwell Scientific Publications, 1969.
Downloaded by: East Carolina University. Copyrighted material.
2 28
mt. J. Sports Med. 13(1992) S199
The Cause of Death after Rescue
17 18
1986.
Lloyd E. L.: Airway warming in the treatment of accidental hypothermia: a review. J Wilderness Med 1: 65— 78, 1990. Lloyd E. L., Mitchell B.: Factors affecting the onset of ventricular
fibrillation in hypothermia: a hypothesis. Lancet ii: 1294—1296, 19
20
21 22 23 24
1974.
Lloyd E. L., Mitchell B., Williams J. T.: Rewarming from immersion hypothermia. A comparison of three methods. Resuscitation 5:518,1976. Lloyd E. L., Mitchell B., Williams J. T.: The cardiovascular effects of three methods of rewarming from immersion hypothermia. Resuscitation 5:229—233, 1976. Maclean D., Emslie-Smith D.: Accidental Hypothermia. Edinburgh, Blackwell Scientific Publications, 1977. Marcus P.: The treatment of acute accidental hypothermia. Aviat SpaceEnvironMed60: 834—843,1979. Niazi S. A., Lewis F. J.: Profound hypothermia in man; report of a case.AnnSurgl47:254—266, 1958. Patton J. F., Doolittle W. M.: Core rewarming by peritoneal dialy-
sis following induced hypothermia in the dog. J Appi Physiol 33: 800—804,1972.
25
Popovic V., Popovic P.: Hypothermia in Biology and Medicine.
London, Academic Press, 1974. Pugh L. G. C. E.: Cold stress and muscular exercise with special reference to accidental hypothermia. BrMedJii: 333—337, 1967. 27 Sadikali F., Owor R.: Hypothermia in the tropics. A review of 24 cases. Trop GeogMed26: 265—270, 1974. 28 Savard G. K., Cooper K. E., Veale W. L.: Possible mechanisms for the after-drop of core temperature upon rewarming from mild hypothermia. Presentation at Sixth International Symposium on Circumpolar Health. May 13—18, 1984. Anchorage, Alaska. 1984. Abstracts p77. 29 Tappan D. V., Jacey M. J., Heyder E., Gray P. H.: Blood volume 26
responses in partially dehydrated subjects working in the cold. 30
Aviat Space Environ Med55:296—30l, 1984. Webb P.: Afterdrop of body temperature during rewarming: an alternative explanation. JAppiPhysiol 60: 385—390, 1986.
E. L. lloyd Department of Anaesthetics Princess Margaret Rose Hospital Fairmilehead Edinburgh, EH1O 7ED Scotland
Downloaded by: East Carolina University. Copyrighted material.
16
Lilja G. P.: Emergency treatment of hypothermia. In Pozos R. S., Wittmers L. E. (eds), The Nature and Treatment of Hypothermia, London,CroomHelm, l983,pp 143—151. Lloyd E. L.: Accidental hypothermia treated by central rewarming viathe airway. BrJAnaesth 45:41—48, 1973. Lloyd E. L.: Hypothermia and Cold Stress. London, Croom Helm,
Abstract E. L. Lloyd, The Cause of Death after Rescue.
IntJSportsMed,Vol 13,Suppl l,S196—S199, 1992 It is recognized that some people die from hypothermia even though they are alive and uninjured when rescued. The traditional explanation is that this is due to ventricular fibrillation resulting from the afterdrop of core
occur through an imbalance between the active vascular ca-
pacity and the circulating fluid volume i.e. relative hypovolaemia or fluid overload. The actual mechanism in any individual case depends both on the history of the cooling and the method of rewarming used. Some deaths will how-
ever occur due to continued cooling of the body or to ventricular fibrillation precipitated by rough handling.
temperature. This hypothesis was based on inadequate measurement and failure to consider the physiology of
Key words
cold. It should now be discarded. Most deaths after rescue
overload, ventricular fibrillation
Introduction
Cold, hypothermia, hypovolaemia, fluid
Traditional_Explanation
It has long been known (10), though still not al-
During the Dachau experiments (1), the Nazis
ways appreciated, that some people die from hypothermia
noticed that, after the person had been removed from cold water, the rectal temperature continued to drop for a while before rising. Because death often occurred at about the time
even though they are alive and uninjured when rescued. lnt.J.SportsMed. 13(t992)S196—S199 GeorgThieme Verlag StuttgartNew York
this 'afterdrop' was at its lowest, it was assumed that the after-
Downloaded by: East Carolina University. Copyrighted material.
S196 Intl Sports Med. 13(1992,)
The Cause Cause of of Death Deathafter afterRescue Rescue
Int.J.SportsMed. 13 (1992) S197
drop caused the death and, even though there was no ECG
value priorto tocooling cooling[25 [25]), depending on on the the potential potential volume volume value prior 3), depending
monitoring, it was postulated that death was due to ventricular fibrillation (VF) caused by the continued cooling.
of fluid available, which in turn is related to the duration of
However, However, it is difficult to accept that a tempera-
The fluid status of any liypothermic hypothermic individual will depend on the relative importance of these responses.
vasoconstriction there is unlikely to be a large volume of blood sequestered in the periphery. The afterdrop is less at the heart
than in the rectum (8, 12, 16, 19), and though the peripheral temperatures start to rise immediately on removal from the cold (8, 12, 16, 19), there is no increase in limb or extremity flow during the afterdrop even during surface rewarming (28). There is therefore no evidence of a peripheral pool of blood. The afterdrop is therefore the result of the normal physical laws of heat flow and reflects the re-establishment of the normal body temperature gradients (9, 10,1 6, 30). The ogre of the afterdrop should now be relegated to history.
Other Mechanisms As the heart cools it becomes more susceptible to developing arrhythmias, and mechanical irritation as mild as the heart having its position changed by rolling a patient for bedmaking (15) may trigger VF. However, if left undisturbed,
In very prolonged exposure to mild to moderate cold, vasoconstriction, vasoconstriction, and and therefore therefore fluid fluid loss loss from fromcold cold induced diuresis, will be minimal. The loss of fluid from the
vascular space caused by the fluid shifts will have been replaced by fluid intake, and any rapid return of fluid to the intravascular space during rewarming may result in fluid overload and pulmonary oedema.
3. Vascular responses When a subject is in the cold, there is a continuous stream of impulses from the cold receptors in the skin reinforcing vasoconstriction. But when the cold stress on the skin is removed, the cutaneous cold impulses are reduced, the vaso-
constrictor tone is therefore also reduced, and the active volume of the vascular bed is increased. If there is insufficient
available fluid e.g. through dehydration due to diuresis, and/or fluid shifts, the Central Venous Pressure (CVP) will fall and then the Blood Pressure (BP) i.e. collapse due to relative hypovolaemia.
the cooling heart usually stops in asystole (13, 23). VF may also be triggered by hypoxia, by rapid changes in pH or electrolytes
Experimental Findings
in the blood, or in temperature gradients within the heart muscle (16, 18).
There are three relevant effects effects of of exposure exposure to to cold.
1. Energy reserves The body responds to cold by increasing heat output and therefore the energy reserves are utilised. With rapid cooling, e.g. in cold water, the energy reserves are relatively undepleted and, once removed from the cold, the person will rewarm. With less severe severe cold, cold, the the body body temperature temperature will willonly only
fall when the energy reserves are exhausted. With their reduced heat generating capacity these people may continue to cool, and die, even in a mildly cold environment.
2. Fluid balance in the cold
Cold induced vasoconstriction shunts blood into the deep capacitance vessels, and the relative excess of volume is removed by a diuresis (2—4, 11, 13, 16). Respiratory moisture loss is increased by exercise especially in cold dry air e.g. in the polar regions and at high altitude (16). Also cold air is dry, evaporation is rapid and even 1 —2 litres/day sweat loss may be unnoticed (11). However, even with total body dehy-
dration, exercise causes an increase in the intravascular fluid volume (29), thus increasing the cold diuresis and worsening any dehydration. During exposure to cold, fluid also shifts from the intravascular into the extravascular and then intracellular (3,4,21,25). space (3, 4, 21, 25).During Duringrewarming rewarmingthese these fluid fluid shifts shifts reverse and the circulating blood volume increases (up to 130% of the
In a study with sheep, cardiovascular parameters were measured and some unexpected changes were recorded corded (Fig. (Fig. 1) 1) (16, (16, 20). 20). Because Because of of small small numbers, numbers, not not all all the the changes reached statistical significance but the changes were very similar to those found in a human experiment (12) and during the clinical treatment of patients (16) which suggests that they are valid.
During spontaneous rewarming there was a drop in peripheral resistance resistance reflecting reflecting relaxation relaxation of of vasoconvasoconstrictor tone (Fig. I). 1). The The CVP CVP and and BP BP both both fell. fell. The The fall fall in in BP BP with spontaneous rewarming is a well recognized clinical phenomenon (3), and many patients admitted to hospital with a reasonable BP develop a variable degree of hypotension after admission, during a time they are beginning to rewarm spontaneously (7, 16, 26). The bradycardia (Fig. 1) is also seen clinically (3).
In the hot bath, the positive warmth on the skin should lead to a greater relaxation of vasoconstriction. There was a fall in peripheral resistance but surprisingly the CVP and BP BP rose (Fig. 1), suggesting an influx of fluid. The The superficial superficial tissues have had the longest exposure to cold stress, and therefore experienced the greatest fluid shifts. During hot bath rewarming they are also the ones exposed to the greatest heat input, and this rapidly and completely reverses the fluid shifts.
This probably explains why climbers, who were pulseless when brought off the hill, were successfully revived in a hot bath (5). The rise of CVP slowed during rewarming to normothermia, as the deeper tissues with less fluid were rewarmed.
Downloaded by: East Carolina University. Copyrighted material.
ture reached at the nadir of the afterdrop is more dangerous than a similar temperature recorded during continued cooling. Also the original explanation for the afterdrop was the return of cold blood from the periphery, but due to peripheral
cold exposure (3, 13).
S198 mt. J. Sports Med. 13(1992) 10
40 o
MEAN PRESSURE MEAN ARTERIAL ARtERIAL PRESSURE
mmHg
E. L. Lloyd
tnt/min/ Kg tnt/mm/Kg
3D 30
07 4Ti.
—10
B
SH
Discussion
CARDIACOUTPUT CARDIAC OUTPUt
I
N
—"I
2 CENTRAL VENOUS PRESSURE _,r
N
SH
cms H20
PERIPHERAL RESISTANCE UNITS
0
Consideration of fluid and vascular status explains most post-rescue phenomena. For example, collapse during rewarming is almost unknown during rewarming from immersion hypothermia whereas it is relatively common in exhaustion hypothermia (22), the highest mortality occurring if
victims are rewarmed naked in a warm room (14). Collapse and death sometimes occur during rescue from water (10), probably through a profound drop in blood pressure from gravitational pooling of blood in the periphery due to removal of the hydrostatic squeeze and a vertical position e.g. using a single strop helicopter hoist or climbing a ship's ladder (10).
—1
SH
I
Patients hypothermic through malnutrition
20 HEART RATE beats/mm
oe
20 STROKE StROKE VOLUME VOLUME 10
N
20 20
PULMONARY PRESSURE PULMONARY PRESSURE
mmHg
15
10
- -i:
mt/bent mt/beat
— — —*
—
SH
TEMPERAtURE TEMPERATURE SH I PULMONARY RES1STANCE PULMONARY RESST4NCE
-2 -2m-
4-—
Conclusion
Death following rescue is usually the result of an an imbalance imbalance between between the the active active vascular vascular capacity capacity and and the the efefvoiume. Some deaths may be due to fective circulating fluid volume. handling.
_4I '•*-6
I
SH
N
-4
of -5L B
16).
continued cooling or to VF, usually precipitated by rough
N
r UNItS
hypothermia where too rapid rewarming (even if spontaneous) produces cerebral and/or pulmonary oedema (2,
N
S
5n 8
(27), and elderly hypothermic patients (6) have been exposed to a relatively mild degree of cold for a long period, and are similar to patients rewarming following prolonged induced
I
-6 SH
H
B
I
Fig. 1
Cardivascular changes during cooling and rewarming sheep — — aa comparison comparison of of three three methods. methods. B B == Base Base line line readings readings before before cooling cooling by by immersion. immersion. Each sheep was considered to have a reading of zero and changes are recorded as changes from the base line. SN = SN = StabEe Stable hypothermia after been reStabEehypothermia hypothermiaafter afterthe theanimal animal had had been been re-
moved from the cold water and after the afterdrop had occurred. = Intermediate temperature during rewarming — a rise of about one degree centigrade.
N = Normothermia.
•—— —. changes changes during during cooling. •———I x— — —x changes during rewarming in a hot bath.
changes during spontaneous rewarming. •—— — —. —. changes changesduringairwaywarming. during airwaywarming. — —. changes Standard errors are indicated.
References Alexander L.: The treatment of shock from prolonged exposure to cold, especially in water. Combined Intelligence Objective Subcommfttee,1945, committee, 1945,Item ItemNo No 24, 24, File FileNo No26—37. 26—3 7. 2 committee, Bloch M.: Re-warming following prolonged hypothermia in man. M. D. Thesis. Thesis. University of London. 1965. M.D. Burton Burton A. A. C., C., Edholm Edholm 0. 0. G.: G.: Man Man in in aa cold cold environment. environment. London, London, Edward Edward Arnold Ltd., 1955.
Danzl D. F.: Accidental hypothermia. In Rosen P., Baker F. J., Braen G. R., Dailey R. R. I-I., H., Levy Levy R. R. C. C. (eds), Emergency Medicine, Concepts and Clinical Practice, Vol 2: Trauma, Boston, Mosby, I 983,pp477—496. l983,pp477—496. 6 Davies L. W.: Treatment of hypothermia. Lancet ii: 656, 1975. Duguid H., Simpson R. G., Stowers J. M.: Accidental hypotherDuguid mia.Lancetii: 1213—1221,1961. CunnfngA. A.J., J., Bardlian Bardhan K. K. D., Triger D. R.: Severe hyFell R. I-I., H., Cunning pothermia pothermia as as aa result result of of barbiturate barbiturate overdose overdose complicated complicated by by carcardiac arrest. Lanceti:392—394, 392—394,1968. diacarrest.Lanceti: 1968. 8 Golden F StC.: Why rewarm? In Matter P., Braun P., deQuervain
M., Good W. (eds) Skifahren und Sicherheit III. Davos, BuchdruckereiDavosAG, druckerei DavosAG, 1979, l979,pp pp163—167. 163—167.
During Airway Warming (AW) (Fig. 1) there is the same reduction in input from the cold sensors in the skin as during spontaneous rewarming, and any warming of the central thermostat should further aggravate the situation. The ab-
sence of an initial drop, and the later rise, in peripheral peripheral reresistance with AW may reflect the return of cerebral control of vasomotor tone. The BP rose early while the CVP showed a delayed rise coinciding with the inclusion of peripheral, fluid containing tissues in the expanding warm core. The tachycartachycar. dia associated with AW has also been noted during core rewarming with peritoneal dialysis (24). These findings are reflected in clinical cases (15—17).
Golden F. StC., StC., 1-lervey Hervey G. G. R.: R.: The The "after-drop" and death death after after Flyrescue from immersion in cold water. In Adams J. S. (ed) Hypothermia Ashore and Afloat. Aberdeen, Aberdeen University 10
' 12
Press, 198 l,pp37—56. l,pp37—56. Golden Golden F. StC., Hervey G. R., Tipton M. J.: Circum-rescue collapse: Collapse, sometimes fatal; associated with rescue of immersion victunis. Nay Med Serv77: 77:139 139—149, victums. fRay JRoyNavMedServ —149, 1991. 1991. Hamlet M. P.: Fluid shifts in hypothermia. In Pozos R. S., Wittmers L. E. (eds), The Nature and Treatment of Hypothermia, London, Croom Helm, 1983,pp 94—99. don,CroomHelm, l983,pp94—99. Hayward Hayward J. S., Eckerson J. D., Kemna D.: Thermal and car-
diovascular changes during three methods of resuscitation from 13
II: 21—33, 1984. mild hypothermia. Resuscitation 11:21—33, Keatinge W. R.: Survival in Cold Water. Edinburgh, Blackwell Scientific Publications, 1969.
Downloaded by: East Carolina University. Copyrighted material.
2 28
mt. J. Sports Med. 13(1992) S199
The Cause of Death after Rescue
17 18
1986.
Lloyd E. L.: Airway warming in the treatment of accidental hypothermia: a review. J Wilderness Med 1: 65— 78, 1990. Lloyd E. L., Mitchell B.: Factors affecting the onset of ventricular
fibrillation in hypothermia: a hypothesis. Lancet ii: 1294—1296, 19
20
21 22 23 24
1974.
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London, Academic Press, 1974. Pugh L. G. C. E.: Cold stress and muscular exercise with special reference to accidental hypothermia. BrMedJii: 333—337, 1967. 27 Sadikali F., Owor R.: Hypothermia in the tropics. A review of 24 cases. Trop GeogMed26: 265—270, 1974. 28 Savard G. K., Cooper K. E., Veale W. L.: Possible mechanisms for the after-drop of core temperature upon rewarming from mild hypothermia. Presentation at Sixth International Symposium on Circumpolar Health. May 13—18, 1984. Anchorage, Alaska. 1984. Abstracts p77. 29 Tappan D. V., Jacey M. J., Heyder E., Gray P. H.: Blood volume 26
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E. L. lloyd Department of Anaesthetics Princess Margaret Rose Hospital Fairmilehead Edinburgh, EH1O 7ED Scotland
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