hypothermia hyperthermia

basal metabolic rate

determines the rate of metabolism of nutrients and rate of skeletal muscle contraction

how heat can be absorbed from surroundings

• conduction -direct contact

• convection - normal heat transfer

• radiation- absorption of infrared energy

Heat retention mechanisms

• piloerection (hairs trap heat)

• vasoconstriction- prevents loss from convection)

• behavioural - huddling, nesting

• shivering

cooling mechanisms

• decreasing metabolic rate

• heat in tissues is transferred to skin

• Evaporation- sweating in horses, panting in dogs

• Vasodilation- of skin vessels to enhance loss of heat from body surface

• behavioural - decreased activity, seeking shade

dog ,cat normal temp

38.5 +- 0.5

Cattle normal temp

8.5 +- 0.5

Equine normal temp

38.0+- 0.5

Fever fatal temp

43 and above

hypothermia fatal temp

28

Fever

aka pyrexia, physiological hyperthermia

fever in dogs and cats

>39.1 but can allow up to 39.4 if stressed or hot outside

Treatment options for fever

1. treat underlying problem

2. non steroidal anti inflammatories

3. passive cooling (fan, cool towels, fluids)

Pathological Hyperthermia

occurs when

1. excessive heat generation

2. cannot cool off fast enough

intrinsic risk for hyperthermia

• obesity'

• long coat

• dehydration

• respiratory problems

• genetic predisposition to drugs

• exercise

extrinsic risk for hyperthermia

• environmental temp reaches body temp

• >80% humidity

• overcrowding, poor ventilation, shipping transport, capture stress

• water deprivation

Heat stress

mild hyperthermia or heat exhaustion

Heat stress

often subclinical, or mild clinical symptoms

prognosis is good if does not progress to heat stroke

• 39.1-41.5

• lethargy, sweating, pating

• decreased athletic performance

• decreased production

• changes in electrolytes

Heat stress treatment and prevention

• passive surface cooling

• shade

• ventilation

• fans,misting

• water

heat stroke

severe hyperthermia

• core body temp exceeds 41.5 for a sustained period of time

• any body temp above 43 is critial

Treating heat stroke

goal is to decrease to 39.5 within 30-45 min

1. cool

2. cardiovascular support - supports blood flow, minimizes shock

3. proactive/supportive - gi protectants, plasma transfusion

heat stroke cooling methods

• passive surface cooling - cool room, shade

• active surface cooling - if <43 apply cold packs

• active core cooling - critical heat stroke - chilled fluids, cool enemas

MU Agonist induced hyperthermia in cats

• cats administered mu-opioids may develop hyperthermia

• morphine, hydromorphone, fentanyl

• during anesthetic temp increases gradually

• intervein at 41(usually 30-90min after drug is given)

• treat by reversing the opioid

• buprenorphine, butorphanol, naloxone

• can be fatal if not caught

Malignant hyperthermia

• fatal hyperthermia triggered by exposure to inhaled general anesthetics (isoflurane and sevoflurane)

• can happen in all species- most common in pigs

• inherited defect in skeletal muscle metabolism, no effect unless triggered by gas anesthetic

• once triggered temp will rise 1-2 every 5 min will rapidly exceed 43

cause of malignant hyperthermia

• mutation causes excessive Ca relase by sarcoplasmic reticlum only when exposed to anesthetic

• excessive Ca causes muscles to contract and stay contracted

• muscle generate heat

• muscles also switch to anaerobic metabolism and this leads to metabolic acidosis

treatment for Malignant hyperthermia

• stop anesthetic

• start aggressive cooling

• muscle relaxants

• aggressive CV support

hypothermia

• pathological decrese in body temp

• due to

  1. increased heat loss

  2. lack of heat production

hypothermia due to increased heat loss (primary)

• usually related to environmental conditions

• cold temps

• wet

• low BSC

• neonates (cant regulate temp)

• small animals (decreased surface area)

hypothermia due to lack of heat production (secondary)

• can occur with severe illness like shock

• brain trauma

• effect of general anesthetic

• all general anesthetic agents cause vasodilation( blood vessels dilate and encourage cooling)

mild hypothermia

• 34-37 C

• clinical signs - lethargy, depression, shivering, loss of suckle reflex

Moderate hypothermia

• 28-33C

• Clinical signs- uncoordinated to unconscious,

• pathological changes- decreased metabolism, loss of thermoregulation (shivering, vasoconstriction, decreased muscle function)

• loss of heat generating mechanisms

Severe hypothermia

• <28C

• clinical signs uncloncuois, coma, death

• pathological changes, organ dysfunction, DIC, CNS shutdown

Treatment of hypothermia

1. maintain heat using surface methods

2. support vital functions- O2, antiarrhythmic drugs, warm Iv fluids

3. active arming methods- Warm IV fluids, enerms, inguinal, axilla, neck warming

   stop warming at 37C rectal

Rewarming methods

1. passive surface warming

2. active surface warming

3. active core warming

passive surface warming

• Always do first

• goal- maintain heat and prevent more loss

• how to- get out of cold and wet, transfer to warm shelter, dry off, blanket, foil wrap, bubble wrap

Active surface warming

• Goal- provide mild heat to the body surface, body transfers heat to core

• how to- warm bottles to axilla, inguinal, neck, to warm the blood as it flows.,forced air blankets

• warning- if to hot will make things worse, aim for normal body temp range at skin surface

Active core warming

• Goal- provide large amounts of heat to body core

• breathe in warmed air, warm IV fluids, warm enema

• Monitor every 15 min

after drop phenomenon

• occurs if the patient reaches 37C, but active heating sources not removed

• patient becomes to warm in the core- to cool down again, blood from the periphery(which is always cooler) will move to teh core, and cause sudden decrease in the coretemp despite all your efforts

• sudden decrease in core temp can precipitate heart and CNS dysfunction

Rewarming shock

• occurs if there is external warming without core warming at the same time

• causes sudden vasodilation, of blood vessels in the skin, blood moves to skin’s surface to fill blood vessel space, this draws blood away from the vital organs and the patient can go into shock

• note- this is different from simply causing the body to lose even more heat

Frost bite

• frozen tissue (usually skin but can include underlying subcutaneous tissue and muscle after cold exposure)

Frostbite risk factors

• cold, wet, windchill

• neonates <48hr of age

• really old or really ill

• if there is already poor perfusion of extremities (cows that lay in show and body weight compress blood vessels in muscle, vascular disease in diabetics)

Frostbite pathology

• ice crystals and expansion of frozen water cause permanent tissue damage

• lack of blood flow means increased risk of tissue necrosis

• increased risk of bacterial infection upon thawing due to damage to protective skin layer, lack of movement of immune cells into are, certain bacteria like to colonize necrotic tissue

frostbite clinical signs

• skin is hard, cold, pale, loss of sensation or pain

• soind solid “knocking sound” when tapped

frostbite treatment

1. take out of cold

2. slow passive surface rewarming

   never rub, more as little as possible, never immerse in hot water

3. protect damaged area

4. support core organs (iv fluids)

5. anti inflammatories, pain control, antibiotics

6. NEVER THAW AND REFREEZE, BETTER TO LEAVE FROZEN

Frostbite prognosis

• only know after tissue thaws

• when skin thaw will be red, swollen, painful

• if skin is to damages, will become necrotic

• necrotic tissue has very high risk of bacterial infection

• may regain full function or require amputation/ euth