JP SMILES
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Core temp < 35 °C
Research limited to either mild hypothermia
in healthy subjects or case reports
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Heat loss occurs through
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Radiation
Conduction
Convection
Evaporation
Hypothermia results in derangement of
multiple organ systems
Shivering – increases metabolic rate but only
while glycogen stores last and down to temps
of 30 °C
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Initial tachycardia and peripheral
vasoconstriction
Subsequent bradycardia (refractory to
atropine), hypotension and fall in cardiac
output
Osborn J waves appear < 32 °C
Anti-arrythmic drugs and
inotropes/vasopressors are generally
ineffective at temperatures < 30 °C
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Loss of fine motors skills and co-ordination
then loss of gross motor skills
Progressive decrease in GCS
Cerebrovascular auto regulation is lost at 24
°C
20 °C EEG is flat and patient appears dead as
cerebral metabolism falls
Temperatures at which shivering is lost varies
widely 24 °C - 35 °C
Temp < 28 °C = rigidity, mydriasis, and
areflexia
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Initially rise in resp rate followed by depression
and basal metabolic rate slows
CO2 retention and resp acidosis can occur
Significant fall in O2 consumption and CO2
production (50% at 30 °C)
Apnoea can develop
Initial left shift of the oxygen dissociation curve
◦ Impaired O2 delivery and tissue hypoxia
◦ Lactic acidosis
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If acidosis becomes severe the curve shifts back
R again
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Cold induced diuresis
GFR falls as CO and renal blood flow fall
ARF in 40% of patients who require ICU
Initial hypokalaemia due to shift of
extracellular potassium into cells
Hyperkalaemia can occur with acidosis
secondary to cell death
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Intestinal motility decreases below 34 °C
Ileus < 28 °C
Oral medication is not appropriate
Hepatic impairment can occur due to reduced
CO (Raised lactate and therefore Hartmans is
a bad idea)
Pancreatitis and Mesenteric Venous
Thrombosis are both common
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Increased blood viscosity fibrinogen and
haematocrit
Coagulopathy may develop
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Mild (35 °C - 32 °C)
Moderate (32 °C - 28 °C)
Severe (<28 °C)
Temperature measurement
Accurate low reading digital of mercury
thermometer
Placed 15 cm rectally of oesophageally (better
as cold faeces can effect rectal temperatures)
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UEC
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Glucose
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CK
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FBC
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COAG
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LFT
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LIPASE
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VBG
◦ Hypo or hyperkalaemia/ARF/low HCO3◦ Hypo/Hyperglycaemia
◦ May be elevated
◦ Increased haematocrit due to cold induced diuresis and hypovolaemia
◦ Thrombocytopaenia
◦ Coagulopathy and DIC is common
◦ Transaminitis
◦ Pancreatitis
◦ Initial respiratory alkalosis
◦ Secondary respiratory and metabolic acidosis
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ECG
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Bradycardia
PR/QRS/QT prolongation
Variable ST and T wave changes
Osborn J waves
Arrythmias
 AF/VT/VF/1st, 2nd, 3rd Degree HB
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These waves were definitively described in
1953 by JJ Osborn
Also called J waves
Delayed depolarisation
Represented as ST elevation
at the QRS – ST junction
< 32 °C
Proportional to the degree of hypothermia
Not pathognomonic
◦ SAH/Cerebral injuries/Myocardial ischaemia
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ABC
Remove wet clothing and insulate
Gentle handling – rough handling and
invasive procedures have historically been
thought to increase risk of cardiac arrythmias
Now thought these risks have been
overemphasised
Consider co-existent pathology
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Intubation as necessary
IV Access (drugs IV only. IM SC poor absorption)
Urinary catheter
NGT
Temperature and cardiac monitoring
Fluid resuscitation
◦ Dehydration is often present
◦ Warmed fluids
◦ Dextrose is good
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Avoid drugs until core temp 30 °C – ineffective
and may accumulate until released
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Rewarming – mild hypothermia
Endogenous rewarming
◦ Exercise if possible
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Passive external warming
◦ Warm dry environment
◦ Cover with warm blankets
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Rewarming – moderate hypothermia
Active external rewarming
Warm blankets
Radiant heat source
Bair hugger
2°C per hour
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Rewarming – severe hypothermia
Includes cardiopulmonary arrest
Warmed humidified inhaled oxygen
Warmed IV fluids
Warmed left pleural lavage
Warmed Peritoneal lavage
Cardiopulmonary bypass
Most other methods are ineffective
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Arrythmias
VF may occur spontaneously in < 29 °C
Sinus brady and AF with slow ventricular
response are common and can be considered
physiological with hypothermia
AF usually reverts spontaneously on
rewarming
Drugs and electricity are unlikely to work
until temp is > 30 °C
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ETT – Warmed humidified air 42 °C - 46 °C
Aggressive active core warming
◦ Warmed saline/peritoneal lavage/pleural lavage/bypass
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VF/VT – Single defibrillation appropriate and
initial drug therapy. If no response defer further
attempts or drug doses until core rises above 30
°C
PEA/Asystole – Again wait till core temp above
30°C (atropine not likely to be effective)
Many anecdotal reports of unexpected survival
Not dead till they are warm and dead!!!!
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Heat stroke
Heat exhaustion
Heat cramps
These may occur as a continuum
Bhut Jolokia pepper
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Core body temp > 40 °C
Hot dry skin
CNS abnormalities (delirium/coma)
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Classical – Occurs due to exposure to a high
environmental temperature
Exertional – Occurs in the setting of
strenuous exercise
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Oxidative phosphorylation stops at
temperatures > 42 °C
Cell damage
Loss of thermoregulatory compensatory
mechanisms
Hypoxia, increased metabolic demands,
circulatory failure, coagulopathies and
inflammatory response
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Tachyarrythmias and hypotension
Two types exist with exertional heat stroke
◦ Hyperdynamic group – high cardiac output and
tachycardia
◦ Hypodynamic group – Low cardiac output, increase
peripheral vascular resistance
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Cardinal features of heat stroke
Delirium, lethargy, coma and seizures
Can be permanent (up to 33%)
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Injured cells leak phosphate and calcium
Hypercalcaemia and Hyperphosphataemia
Hypokalaemia is seen early
◦ Secondary to heat induce hyperventilation leading
to respiratory alkalosis
◦ Sweat and renal losses
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Hyperkalaemia is seen later
◦ Potassium losses from damaged cells and renal
failure
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Hyperuricaemia develops secondary to the
release of purines from injured muscle
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ARF in approx 30%
◦ Direct thermal injury to kidneys
◦ Pre-renal insult of volume depletion and renal
hypoperfusion
◦ Rhabdomyolysis
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Exertional heat stroke is associated with
haemorrhagic complications
Petechial haemorrhages or eccyhmosis
secondary to direct thermal injury or DIC
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Similar to sepsis
The actions of inflammatory mediators
account for the multi organ dysfunction
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Consider in patients with altered mental state
and exposure to heat
Classic triad of hyperthermia, neurological
abnormalities and dry skin
Measure temp with rectal/oesophageal probe
Sweating can still be present
Hypotension and shock 25%
◦ Hypovolaemia, peripheral vasodilatation and cardiac
dysfunction
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Sinus tachy
Hyperventilation – a universal finding in heat
stroke
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UEC
◦ Hypokalaemia
◦ Hyperphosphataemia and hypercalcaemia
◦ Hyperkalaemia and hypocalcaemia may be present
if rhabdomyolysis has occurred
◦ Renal impairment
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Urate – is frequently high and may play a role
in the development of acute renal failure
Glucose – elevated in up to 70%
LFT
Almost always seen in exertional heat stroke
(AST and LDH most commonly elevated)
CK – 10000 to 1000000 in rhabdomyolysis
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FBC – WCC as high as 30 -40,000
Coag – routinely abnormal and DIC may occur
Acid Base:
◦ Lactic acidosis
◦ Compensatory respiratory alkalosis
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Myoglobin – serum or urine myoglobin may
be elevated
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ECG
◦ Rhythm disturbances (sinus tachy, SVT + AF)
◦ Conduction defects (RBBB and intraventricular
conduction defects)
◦ QT prolongation (most common secondary to low
K+ , Ca 2+ and Mg 2+)
◦ ST changes (secondary to myocardial ischaemia)
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CXR:
◦ ARDS
◦ Aspiration
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If prompt effective treatment not undertaken
mortality approaches 80%
A
– ETT if needed
◦ Consider early
◦ Avoid suxamaethonium
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B
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C
◦ Monitor Resp Rate and O2 sats
◦ Look for evidence of aspiration if GCS decreased
◦ Check for ARDS and ventilate as per lung injury protocol
◦ May be a large fluid deficit
◦ N saline is probably best (CSL – lactate and avoid K+
containing fluids)
◦ Monitor heart rate, BP, CVP and urine output
◦ Picco/Swan-Ganz pulmonary artery catheter may be
indicated
◦ Pressors may be needed but avoid adrenergic agents as
they can impair heat dissipation by causing peripheral
vasoconstriction (dopamine)
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D – Intubate if needed
E – Temperature should be measured by
oesophageal or rectal probe
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Mainstay of therapy and must be initiated
from the onset
Use prehospital may be lifesaving
Initially remove patient from heat source and
remove all clothing
Evaporative cooling – tepid water on the skin
with fans
Ice water immersion – most effective method
but practically difficult and cant use
monitors/equipment and uncomfortable for
the patient
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Ice packs to axilla, groin and neck
Cooling blankets and wet towels
Peritoneal lavage and cardiopulmonary bypass
can be considered in severe resistant cases
Shivering may occur in rapid cooling – this will
increase oxygen consumption and heat
production
◦ Sedate
◦ paralyse
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Paracetamol and aspirin are ineffective and
should not be used
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Mortality should be less than 10% with
prompt treatment
Most recover without sequalae
Residual neurological defects are reported
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Heat exhaustion – mild heat stroke
Same physiological process
Patients can still have the capacity to
dissipate heat and the CNS is not impaired
Volume depletion is still a problem
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Painful involuntary spasms of major muscles
Usually in heavily exercised muscle groups
Dehydration and salt loss also thought to plat
a role
Rest rehydrate and replace salts