Hypothermia - Extreme Physiology

Cold air is a worse stressor than heat.

It can lead to:

1. Peripheral cooling - incapacitation or cold injury

2. Deep body cooling - hypothermia

Hypothermia - when body temperature reaches below 35 degrees

Unresponsive

Decrease in minute ventilation rate

Temperature regulation impaired

Tachycardia or bradycardia

Amnesia

Below 32 degrees shivering stops

Eventually coma and death

1. Mild - early onset, easy to recover from

2. Moderate - significant

3. Severe - death zone, losing reflexes and responses

Increased heat production (shivering, non-shivering thermogenesis)

Decreased heat loss (peripheral vasoconstriction)

Behavioural responses (clothing, shelter and huddling)

Low ambient temperature

High wind speed

Rain

Fatigue/exhaustion

Immersion

Inadequate clothing

Shock following traumatic injury

Body size and composition

Age - particular old and young

Starvation

Air movement increases heat loss via convection

Therefore - risk of hypothermia and cold injury increases with wind speed

When -29 degrees, with a wind chill it can be as cold as -44 degrees in which skin will freeze within 1-2 minutes

33-35 degrees

Thermoregulatory responses are normal:

1. Intense cold sensation

2. Peripheral vasoconstriction

3. Violent shivering

Shivering - changing tensions in the muscle of antagonistic pairs in attempt to generate heat, that when they go out of sync produce ocillations

30-33 degrees

Thermoregulatory responses begin to fail and spontaneous recovery becomes unlikely

1. Shivering gradually decreases

2. Joints become stiff, muscles rigid

3. Progressive reduction in metabolism and VO2

4. CNS cooling leads to dulling, irrational behaviour and eventually unconciousness

5. Cardiac cooling leads to decreasing heart rate and declining cardiac output

Ezymes arent working as well within the tissues so processes are slow

Semi-conciousness occurs

Below 30 degrees

The effects of moderate hypothermia become intensified:

1. Heart rate continues to decline as core temperature falls

2. Heart becomes prone to arrythmias

3. Cooling and dehydration increases blood viscocity

4. Respiration becomes slow and shallow

5. Ventricular fibrillation is the most common cause of death (about 27 degrees)

Active (above 34 degrees)

For fully conscious victims

Hot bath

Hot showers

Passive rewarming (below 34 degrees)

For unconcious victims

Sleeping bag and wrapping in blankets

Slow rate of rewarming to reduce risk of collapse

Extraneous heating may be necessary 

Hot water bottle/electric blanket

If temperature of exposed peripheral tissues falls below -0.55 degrees, tissue fluid may freeze

Mild - only skin freezes

Severe - deeper tissues freeze

Damage to affected cells results from mechanical action of ice crystals and from cell dehydration

Permeability of small blood vessels is increased by freezing - on thawing there is a loss of fluid from the circulation into the ISF

This may lead to sludging of RBC in the mitochondrion, which reduces or stops local blood flow, leading to gangrene and possible loss of fingers, toes etc

Tissue temperatures between 17 and -0.55 degrees lasting for a protracting period can result in NFCI

Feet are most commonly affected

Cold, wet feet lose heat rapidly which induces intense vasoconstriction

Local hypoxia and accumulation of toxic metabolites results in tissue death, with deeper tissues often affected

Blisters, ulcers and gangrene may develop and amputation of toes or even the foot may be necessary

Thermal conductivity of water is 27x greater than air

Rate of heat loss from resting subject in water is 2-5 x greater than in air

Although risk of hypothermia following accidental immersion in cold water is high, the victim must first survive the initial shock response and avoid drowning in first 30 mins

CSR lasts for about 1 minute after sudden immersion into cold water

First response to rapid skin cooling is involuntary gasp

Followed by hyperventilation which may lead to loss of consciousness

Peripheral vasoconstriction leads to increases afterload on heart

Main causes of death during this phase are drowning, cardiac arrest and cardiac arrythmias

Cold water incapacitation occurs within 5-15 minutes in cold water

Vasoconstriction decreases blood flow to the extremities allowing the periphery to cool rapidly

Muscle and nerve fibres lose function when cold

Within critical time frame you will lose meaningful movement in hand and feet and then arms and legs for floatation

Other importanr life-saving/survival activites become difficult and then impossible

It takes at least 30 mins for an adult to become even midly hypothermic following cold water immersion

Survival times are influenced by many factors:

1. Subcutaneous fat levels

2. SA:V ratio

3. Magnitude of shivering response

4. Activity levels and posture

5. Clothing (amount and type)

Collapse can happen just before, during or after rescue

The symptoms can range anywhere from fainting to death

Several factors involved:

Imminent rescue results in a mental relaxation, so levels of stress hormones decrease

Blood pressure can fall and muscular relaxation occurs

This can cause collapse, and in extreme cases, death as a result of cardiac arrest

Cardiac function is significantly affected by the way the victim is handled and removed from water

Transport casualty horizontally/slightly head down

Acute cold

Localised cold has direct effects on smooth muscle:

Cells disturb mitochondrial function and increase release of free radicals

This activates Rho kinase - a signalling molecule that can promote adrenergic receptors

Can also inhibit myosin light chain phospotase (MLCP) - which deactivates myosin light chain

This in conjunction with the adrenergic receptors causes vasoconstriction

Relaxation is switched off so contraction occurs

Recognised by trip receptors which signals back to dorsal root and trigeminal ganglion sensory neurons

This enhances metabolic heat production and vasoconstriction

Vasoconstriction is mediated by noradrenaline release (60-70%) and neuropeptide Y (20-30%) 

1. Reflex vasoconstriction

2. Local cooling

3. Response to core temperature reduction

Cold induced vasodilation - CIVD

Periodic fluctations in vasoconstriction/dilation to keep tissue alive

Centrally mediated and suppressed when core temperature falls

Enhances with exercise training

Metabolic enhancement:

Increased muscle tone

Recruitment of brown adipose tissue

Involuntary rhythmic contractions initiated by skin temperature fall then enhanced by core fall

Maximal at core temp of about 35 degrees but ceases at about 31 degrees

1. Decreased metabolic response to cold (shivering)

2. Increased thermal comfort

3. Faster fall in deep body temperature

Most evident at rest in the cold