STRESS OF

FLUID AND TEMPERATURE

 Deficit
Fluid
Excess
Stress of
Hypothermia
Temperature
Hyperthermia
 FLUID
DEFICIT AND
EXCESS
FLUIDS

• 50-60% of the human body is water

(decreases with age)
• Body fluids are classified according to
their location with most of the body’s
fluids found within the cell
–Intracellular
–Extracellular (mainly responsible for
transport of nutrients and wastes)
 FLUIDS

• Fluid compartments are separated

by selectively permeable
membranes that control movement
of water and solutes
• The process of homeostasis involves
delivery of oxygen and nutrients to
the cells and removal of waste
 HEMOSTASIS OF FLUID

• Homeostasis means keeping everything normal

• Necessary for organs to perform work
• Transport nutrients, e-lytes, and O2 to the cells
– Excretion of wastes
– Regulates body temp
– Lubricates joints and membranes
– Medium for food digestion
 ECF shifts between the intravascular space (blood
vessels) and the interstitial space (tissue) to maintain
the fluid balance within the ECF compartment
TRANSPORT OF
WATER AND FLUIDS
• Osmolality: concentration of a solution
determined by the number of dissolved
particles per kilogram of water. Osmolality
controls water movement and distribution
in body fluid compartments
• Diffusion: the random movement of
particles in all directions through a solution
• Active transport: movement of solutes
across membranes; requires expenditure of
energy
 TRANSPORT OF WATER AND FLUIDS

• Filtration: transfer of water and solutes

through a membrane from a region of
high pressure to a region of low pressure

• Osmosis: movement of water across a

membrane from a less concentrated
solution to a more concentrated solution
ASSESSMENT FOR FLUID BALANCE
• History of potential factors which place
patient at risk
• Vital signs
• Input and output
• Body weight
• Skin
• Mucus membranes
• Vascular system
 FLUID VOLUME DEFICITE
Hypovolemiai: Dehydration:
Isotonic extracellular fluid Hypertonic extracellular fluid
deficit deficit
• Deficiency of both • Deficiency of water
water & electrolytes • Caused by water loss
• Caused by decreased related to high blood
intake, increased lost glucose, inadequate
(bleeding, vomiting, ADH production, high
diarrhea), fluid shift fever, excess sweating
 ASSESSMENT OF FLUID DEFICIT

• Hypotension
• Weak rapid pulse
• Temperature decreased if hypovolemic, and
increased in dehydration
• Weight loss
• Skin turgor poor in dehydration and possible
edema in hypovolemic
• Concentrated urine and blood
 TREATMENT OF DEFICIT

• Correct cause
• IV fluids
• Input and output
 FLUID VOLUME EXCESS

Extracellular: Intracellular:
Isotonic fluid excess Water excess

• Excess of both water • Excess of body water

and electrolytes without excess
electrolytes
• Caused by retention
of water and • Caused by over-
hydration in the
electrolytes related presence of renal
to kidney disease; failure;
overload with administration of
isotonic IV fluids D5W
ASSESSMENT OF FLUID VOLUME EXCESS

Isotonic Hypotonic
– Hypertension – Systolic B/P
– Bounding pulse – Decreased pulse
– Crackles, dyspnea – Increased
– Weight gain respirations
– Edema in – Weight gain
extremities – Cerebral edema
– JVP – Irritable, confused
– Irritable, confused
TREATMENT OF FLUID VOLUME EXCESS

Isotonic Hypotonic

– Correct cause – Correct cause

– Restrict H2O and – Restrict H2O
Na intake
– Diuretics – IV fluids with E-
– Digitalis lytes
– Possible dialysis
HYPOTHERMIA
 Definition Core temp: < 35 °C

Mild: 32-35C

Classification Moderate: 28-32C

Hypothermia

Severe: < 28C

Accurate low reading digital

of mercury thermometer

Measurement Placed 15 cm rectally of

oesophageally (better as cold
faeces can effect rectal
temperatures)
 98-95 oF Shivering begins

Mild
Violent shivering, loss of
95-90 oF
coordination

Symptoms & Shivering stops, muscles stiffen,

Signs 90-86 oF skin is blue or puffy, patient
incoherent

Pupils dilate, breathing & pulse

Severe 86-80 oF
slow, impaired responsiveness

Unresponsive & rigid, pulse

unobtainable, breathing very
<80 oF
slow (not dead until warm and
dead)
 HEAT PRODUCTION PHYSIOLOGY

Basal
Anterior Thyroid /
metabolism
hypothalamus Sympathetic
(Metabolic rate)

Preshivering Shivering Posterior

muscle tone
(2-5x) hypothalamus
(2x)
HEAT PRODUCTION PHYSIOLOGY
Above 32C:
Vasoconstriction
Shivering
Basal metabolic rate

Below 32C:
No shivering

Below 24C:
No basal metabolic rate
 PATHOPHYSIOLOGY

Radiation (55-65%): gradient

between environment and
exposed body area
HEAT LOSS Conduction (2-3%): direct
contact with cold substance
Convection (10-15%): wind
Evaporation (20-35%)
 PATHOPHYSIOLOGY

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
 CVS

CNS

RESPIRATORY
System Related
Hypothermia RENAL

GI

HAEMATOLOGY
 CVS EFFECTS
• 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
 CNS EFFECTS
• 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
 RESPIRATORY EFFECTS
• 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
• If acidosis becomes severe the curve shifts back R
again
 RENAL EFFECTS

• 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
 GI EFFECTS

• 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
 HAEMATOLOGY EFFECTS

• Increased blood viscosity

fibrinogen and haematocrit
• Coagulopathy may develop
 INVESTIGATIONS
• Electrolyte • COAG
– Hypo or – Coagulopathy and DIC is
hyperkalaemia/ARF/low HCO3- common
• Glucose • LFT
– Hypo/Hyperglycaemia – Transaminitis
• CK • LIPASE
– May be elevated – Pancreatitis
• FBC • VBG
– Increased haematocrit due to – Initial respiratory alkalosis
cold induced diuresis and – Secondary respiratory and
hypovolaemia metabolic acidosis
– Thrombocytopaenia
 INVESTIGATIONS

• ECG
–Bradycardia
–PR/QRS/QT prolongation
–Variable ST and T wave changes
–Osborn J waves
–Arrythmias
• AF/VT/VF/1st, 2nd, 3rd Degree AV
BLOCK
 OSBORN WAVES
• 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
• When T< 33C
• Amplitude proportional to the degree of hypothermia
• Not pathognomonic
– SAH/Cerebral injuries/Myocardial ischaemia
• 25%-30% of patients
• Positive-negative deflection
• Usually V3-V6
Osborn Waves
 MANAGEMENT
• 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
 MANAGEMENT
• 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
• Avoid drugs until core temp 30 °C – ineffective and
may accumulate until released
 MANAGEMENT
MILD HYPOTHERMIA

• Endogenous rewarming
–Exercise if possible
• Passive external warming
–Warm dry environment
–Cover with warm blankets
 MANAGEMENT
MODERATE HYPOTHERMIA

• Active external rewarming

• Warm blankets
• Radiant heat source
• Bair hugger
• 2°C per hour
 MANAGEMENT
SEVERE HYPOTHERMIA

• Includes cardiopulmonary resuscitation

• Warmed humidified inhaled oxygen
• Warmed IV fluids
• Warmed left pleural lavage
• Warmed Peritoneal lavage
• Cardiopulmonary bypass
• Most other methods are ineffective
 MANAGEMENT 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
 MODIFICATION OF ACLS FOR
HYPOTHERMIA
• ETT – Warmed humidified air 42 °C - 46 °C
• Aggressive active core warming
– Warmed saline/peritoneal lavage/pleural
lavage/bypass
• 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!!!!
HYPERTHERMIA
 DEFINITION

• Elevation of core body temperature above

the normal diurnal range of 36ºC to 37.5ºC
due to failure of thermoregulation
• Hyperthermia is not synonymous with the
more common sign of fever, which is induced
by cytokine activation during inflammation,
and regulated at the level of the
hypothalamus
 PREDISPOSING FACTORS
• Age of the patient: less • Medications: i.e. diuretics
tolerable in peds and (dehydration), beta
geriatric. blockers (vasodilation),
• Health of the patient: psychotropic‘s (CNS
regulation)
i.e. diabetics can
become hyperthermic • Level of acclimation:
adjusting to environment
more easily because of change
the damage DM inflicts • Length of exposure
on their autonomic
nervous system • Intensity of exposure
(thermoregulatory • Environmental factors
input, vasodilation, such as humidity and
perspiration) wind
 PHYSIOLOGY
• Body temperature is maintained within a
narrow range by balancing heat load with heat
dissipation.
• Body's heat load results from both metabolic
processes and absorption of heat from the
environment
• As core temperature rises, the preoptic
nucleus of the anterior hypothalamus
stimulates efferent fibers of the ANS to
produce sweating and cutaneous vasodilation.
 PHYSIOLOGY
• Evaporation is the principal mechanism of heat loss in
a hot environment, but this becomes ineffective
above a relative humidity of 75%
• Other methods of heat dissipation
– Radiation- emission of infrared electromagnetic
energy
– Conduction- direct transfer of heat to an adjacent,
cooler object
– Convection-direct transfer of heat to convective air
currents
• These methods cannot efficiently transfer heat when
environmental temperature exceeds skin
temperature.
 PHYSIOLOGY
• Temperature elevation  ↑ O2 consumption
and metabolic rate  hyperpnea and
tachycardia
• Above 42ºC (108ºF), oxidative phosphorylation
becomes uncoupled, and a variety of enzymes
cease to function
• Hepatocytes, vascular endothelium, and neural
tissue are most sensitive to these effects, but all
organs may be involved
• Risk of multiorgan system failure
 HEAT RELATED ILLNESS

• Heat stroke: Critical organ damage, significant

mortality, markedly elevated body
temperature, usually > 105’
• Heat exhaustion: Serious but no organ
damage, mild hyperpyrexia
• Heat cramps: Painful, easily treated,
acclimation occurs
• These may occur as a continuum
ORGAN SYSTEMS RESPONSIBLE
FOR HEAT LOSS

• Skin: vasodilatation and perspiration

• Cardiovascular: increased cardiac output
to compensate for peripheral
vasodilatation with increased volumes of
blood to periphery
• Respiratory: some degree of evaporation
 HEAT STROKE
• Heatstroke results when the body’s
thermoregulatory mechanisms are
overwhelmed by the heat stress.
• The body’s temperature rises markedly with
eventual multisystem organ failure.
• Core body temp > 40 °C
• Hot dry skin
• CNS abnormalities (delirium/coma)
 Classical
HEAT
STROKE
Exertional
 HEAT STROKE CLASSICAL
• Occurs due to exposure to a high
environmental temperature
• Older or debilitated exposed passively to
significant thermal stress over hours or
days.
• Ability to respond is compromised by CV
disease, drugs, alcohol.
• Usually perspiring for significant time and
profoundly dehydrated
 HEAT STROKE EXERTIONAL

• Occurs in the setting of strenuous

exercise
• younger, physically fit with normal
thermoregulatory system
• Frequently not dehydrated and may
be wet with perspiration
• Significantly elevated body
temperature
 PATHOPHYSIOLOGY
• Oxidative phosphorylation stops at
temperatures > 42 °C
• Cell damage
• Loss of thermoregulatory compensatory
mechanisms
• Hypoxia, increased metabolic demands,
circulatory failure, coagulopathies and
inflammatory response
 CVS

NEUROLOGICAL

MUSCULOSCELETAL
System Related Heat
Stroke
RENAL

HAEMATOLOGICAL

IMMUNOLOGICAL
 CVS EFFECTS

• 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
 NEUROLOGICAL EFFECTS

• Cardinal features of heat stroke

• Altered mental status always
• Delirium, lethargy, coma and
seizures
• Can be permanent (up to 33%)
 RHABDOMYOLYSIS
• 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
• Hyperkalaemia is seen later
– Potassium losses from damaged cells and renal failure
• Hyperuricaemia develops secondary to the release
of purines from injured muscle
 HEPATIC

•Central lobular necrosis

•Elevated liver function tests
 RENAL EFFECTS

• ARF in approx 30%

–Direct thermal injury to kidneys
–Pre-renal insult of volume
depletion and renal hypoperfusion
–Rhabdomyolysis
 HAEMATOLOGICAL

• Exertional heat stroke is

associated with haemorrhagic
complications
• Petechial haemorrhages or
eccyhmosis secondary to direct
thermal injury or DIC
 IMMUNOLOGICAL

• Similar to sepsis
• The actions of inflammatory
mediators account for the
multi organ dysfunction
 ASSESSMENT
• 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
 ASSESSMENT
• Hypotension and shock 25%
–Hypovolaemia, peripheral
vasodilatation and cardiac dysfunction
• Sinus tachy
• Hyperventilation – a universal finding in
heat stroke
INVESTIGATION

• Hypokalaemia
• Hyperphosphataemia and
hypercalcaemia
• Hyperkalaemia and hypocalcaemia
may be present if rhabdomyolysis
has occurred
• Renal impairment
 INVESTIGATION

• 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
 INVESTIGATION

• FBC – WCC as high as 30 -40,000

• Coag – routinely abnormal and DIC may occur
• Acid Base:
– Lactic acidosis
– Compensatory respiratory alkalosis
• Myoglobin – serum or urine myoglobin may
be elevated
 INVESTIGATION

• 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)
 INVESTIGATION

• CXR:
–ARDS
–Aspiration
MANAGEMENT OF HEAT STROKE

If prompt effective treatment

not undertaken mortality
approaches 80%

ABC FIRST !!
 MANAGEMENT OF HEAT STROKE

• A
– ETT if needed
– Consider early
– Avoid suxamaethonium
•B
– Monitor Resp Rate and O2 sats
– Look for evidence of aspiration if GCS decreased
– Check for ARDS and ventilate as per lung injury
protocol
 MANAGEMENT OF HEAT STROKE

•C
– 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)
MANAGEMENT OF HEAT STROKE

• D – Intubate if needed
• E – Temperature should be
measured by oesophageal or
rectal probe
 COOLING METHODS
• 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
 COOLING METHODS
• 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
• Paracetamol and aspirin are ineffective and should
not be used
 OUTCOME

• Mortality should be less than

10% with prompt treatment
• Most recover without sequalae
• Residual neurological defects are
reported
 HEAT EXHAUSTION
• 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
 HEAT EXHAUSTION
• Salt or water depletion in the face of heat
stress
• Mild hyperpyrexia, nausea, vomiting,
lightheadedness, dehydration with only
minimal altered mental status
• Leads rapidly to heatstroke if not rapidly
reversed
• Treated with cooling measures, also IV Normal
Saline, further electrolyte replacement guided
by serum electrolyte levels
 HEAT CRAMPS
• Painful involuntary spasms of major
muscles
• Usually in heavily exercised muscle
groups
• No changes in mental status or fever
• Dehydration and salt loss also thought
to plat a role
 HEAT CRAMPS

• Usually caused by replacement of water

without adequate salt resulting in a low
sodium state in the muscles
• Rest rehydrate and replace salts
• Treated with cooling measures, fluid and
electrolyte replacement via IV.
QUESTION