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Misc - temp/procedures > Temperature and its measurement > Flashcards

Temperature and its measurement Flashcards

1
Q

What is thermoneutral zone

A

thermoneutral zone is the range of ambient temperature in which an person can maintain body temperature without increasing body heat production (metabolic rate) above resting level or at minmum oxygen consumption - at thermal equilibrium with environment

Minimum heat production is equal to minimum oxygen consumption as metabolism is primarily aerobic

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2
Q

WHat is is the thermoneutral zone for neonates

A

32-34 degrees

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3
Q

Thermoneutral zone for adults

A

25-30 degrees

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4
Q

Preterm babies have higher or lower thermoneutral zones and why?

A

Higher
Increased evaborative heat losses

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5
Q

Why are neonates particularly prone to heat stress (4) I.e why can’t they regulate when hot or cold

A

prone to getting too chold or too hot because of
- Large surface area to volume ratio
- thin subcutaneous tissue
- limited sweating capacity
- Limited ability to exert direct control on personal environment

This leads to higher proportionate evaporation from skin
Addit reealtive hgiher basal metabolic rate and therefore more heat to lose to maintain thermal equilibrium

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6
Q

Why is the thermoneutral zone less than body temperature

A

The body has a basal metabolic rate therefore producing more heat than its environment and requires a gradient to lose it too maintain equilibrium

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7
Q

What mechanisms arte used by a neonate to control its body temperature - in response to cold

A

Position and skin blood flow when within thermoneutral zone

In response to cold
- Behavioural - crying
- Skin vasoconstriction
- Non shivering thermogenesis (brown fat)
- Increased muscular acitivty and shivering - may also lead to removal of insulating materials
(shivering not well developed)

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8
Q

What is brown fat - how is it different to regular fat, where is it

A

Metabolically active fat tissue important for heat production in babies - increased metabolic activity producing heat (a type of non shivering thermogenesis)

Cytoplasm of ordinary fat cells have large fat globules and minimal mitochondria as they mainly store energy; however in brown fat many fat globules may be present but also large mitochondria

Some uncoupling of oxidative phosphorylation so more heat for a given amount of metabolism, and glycogen is contained which provides glucose

It is located in abdominal locations (perinephric), around large BV, interscapular, base of neck

2-6% of body weight

Total body heat production can be doubled by increased brown fat activity

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9
Q

What mechanisms arte used by a neonate to control its body temperature - in response to heat

A

Response to warmth
- Behaviorual - crying
- SKin vasodilation
- Sweating (limited compared to adults) but stil can double evaporative heat losses

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10
Q

How much brown fat does a neonate have as a proportion of weight?

How much metabolic acitivty can it account for

A

2-6% of body weight

Total body heat production can be doubled by increased brown fat activity

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11
Q

Why does brown fat produce so much heat

A

Some uncoupling of oxidative phosphorylation so more heat for a given amount of metabolism, and glycogen is contained which provides glucose

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12
Q

What key factors in brown fat being used for heat need to be kept in mind for neonates

A

Oxygen required for heat production - therefore if cold and hypoxic will struggle

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13
Q

What triggers brown fat metabolism?

A

RIch sympathetic innervation which acts via beta recepotrs to cause increased lipolysis and fatty acid oxidation

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14
Q

Define heat and give its SI units

A

Heat - a measure of the average kinetic energy of a substance per degree of freedom of its constituent molecules
* Quantity of thermal energy contained in a substance
* Specific heat of water 4.2 kJ/kg/degree
* The body is about 85% of th that at 3.6kJ/kg/degree Celsius
* SI unit for energy si the Joule

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15
Q

What is specific heat capacity?

A

Specific heat capacity - the heat required to raise unit mass of the substance by 1 degree of temperature

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16
Q

Define temperature

A

Temperature -physical state of a substance which determines whether or not the substance is in thermal equilibrium with its surroundings - heat energy is transfered from areas of high temperature of lower temperature
* Temperature is a mean energy fo the molecules
* SI unit is kelvin

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17
Q

Define core body temperature

A

Core temperature - deep body temperature o internal organs measured as the rectal temperature which is 0.5 degrees higher than axillary temperature

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18
Q

Optimal function of enzymes is between what degrees

A

35-41
Above 45 degrees denature

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19
Q

What does Q10 refer to

A

The rate of reaction is related to temperature
Ratio of velocity of reaction when temperature increased by 10 degrees
Enzyme reactionstend to increase 2.5x for each 10 degree rise

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20
Q

Draw a diagram representing magnitude of compensatory response against temperature

A
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21
Q

What are the basic physics principles by which heat transfers

A

Basic mechanisms of heat transference
* Conduction - flow of heat energy via direct collisions between atoms and molecules of warmer and cooler regions and the resultant transfer of kinetic energy
◦ the better a conductor of heat the faster the rate of transfer e.g. metal feels cold because heat is transferred quickly into it
* Convection the transfer of heat from a body by the liquid or gas which surrounds it
◦ Passive - hot object cooling in still air
◦ Active - blowing air
* Radiation
◦ Hot bodies emit thermal energy in the form of electromagnetic radiation
◦ A black body is a body that absorbs all radiation that falls upon it - the best absorber. They are also the best emitters, the amount of radiation depends on the termperatre (stefan Boltzmann law) the radiation energy per unit of time from a black body is proportional to the 4th power of the temperature

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22
Q

Define conduction

A

flow of heat energy via direct collisions between atoms and molecules of warmer and cooler regions and the resultant transfer of kinetic energy

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23
Q

Define convection

A
  • Convection the transfer of heat from a body by the liquid or gas which surrounds it
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24
Q

Define radiation

A

◦ Hot bodies emit thermal energy in the form of electromagnetic radiation

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25
Q

What are the mechanisms by which heat is lost form the body and what relative importance does each have

A

Radiation - 40-50% heat loss - emitting electromagnetic energy
◦ Higher rate of heat loss in neonates due to higher relative surface area
◦ Increased loss when peripheral circulation dilated

Convection and conduction
◦ 15% loss

Evaporation - 30% heat loss
◦ Skin ~20% - sweat as heat is required to turn water to vapour so thermal energy is removed
◦ Respiratory tract - 5% - 25% of which is through warming of the air, 75% by humidifying it
◦ Urination
◦ Defection

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26
Q

What proportion of total body heat loss does radiation contribute

A

40-50%

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27
Q

What proportion of body heat loss does evaporation contribute - wher eis most of this from

A

30%
Skin 20%
Respiratory tract 5%

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28
Q

How does the respiratory tract lose heat

A

25% from warming air
75% from humidifying it

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29
Q

What is the regulatory set point for temperature and its range

A

37 +/- 0.4

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30
Q

Where is the central regulator for temperature

A

hypothalamus

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31
Q

Interthreshold range define

A

the range of core temperature over which no autonomic thermoregulation responses occur

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32
Q

What factors cause variation in temperature normally

A

Circadian rhythm
Food
Thyroid
Drugs

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33
Q

Are temperature set points the same for mena dn women

A

no
Women 0.3 - 0.5 higher

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34
Q

How does the thyroid influence heat set points

A
  • Thyroid hormone act on mitochondrial and nuclear receptors regulating membrane bound Na/K ATPase balancing heat production with heat loss
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35
Q

During the day when is your temperature hgihest and lowest

A

temperature lowest in early hours of morning, highest in evening

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36
Q

When does the body have a reduced sensitivty to changes in temperature

A

Anaesthetised
Old
Unwell

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37
Q

First response to hot

A

sweat

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38
Q

First response to cold

A

Vasoconstriction

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39
Q

What temperature is the skin usually kept at

A

29-33 degrees

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40
Q

Anterior hypothalamus which region is involved in temperature regulation

A

pre optic

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41
Q

Anterior hypothalamus programs responses to hot or cold

A

hot - senstivie to local warming
Increases firing rate producing sweating and vasodialtion
Regulates heat loss!!

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42
Q

Posterior hypothalamus responds to hot or cold more

A

cold
Regulates heat retention and creation

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43
Q

Which area of the hypothalamus is more important for set point and control

A

Posterior

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44
Q

How is the posterior hypothalamic set point cellularly modified

Neurotransmitters involved

A

‣ Determined by ratio of sodium and calcium ions in the posterior hypothalamus with input from acetylcholine
‣ Neurotransmittters involved (anterior hypothalamus)
* Noradrenaline
* Seratonin
* Dopamine
* PG

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45
Q

Where is heat information afferent transmitted through the spinal cord

A

lateral spinothalamic tract in anterior spinal cord - synaoses with reticular system in medullar and reaches posterolateral and ventrolateral medullary nuclei

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46
Q

How does the skin sense heat - what kind of receptors

A

Temperature mediated ion channels

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47
Q

Name of cold receptors, what layer of the skin

A

bulbs of krause in the dermis/deep to the epidermis

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48
Q

Bulbs of Krausse mediate what sensation? What size fibres? What threshold

A

Cold
A delta
Increased discharge below 25 degrees - maximum discharge; active from 10-40 degrees

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49
Q

Bulb of kraus especially located where

A

face

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50
Q

Do cold receptors constantly fire or periodically, to what stimulus?

A

Static (regular, periodic) discharges at constant temperatures

at 25 degrees increased discharge occurs; active over the ranges 10-40 degrees

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51
Q

Warm receptors referred to as?

A

Bulbs of ruffini

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52
Q

Describe the structural appearance of a bulb of ruffini?

A

Elliptical

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53
Q

Where do you find bulbs of ruffini

A

SC and intestines, all membranes
Deep to the dermis

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54
Q

Bulbs of ruffini afferent receptors are what type of fibre?

A

Unmyelinated C fibres

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55
Q

Describe the physiology of bulbs of ruffini firing?

A
  • Static discharges between 30-40 degrees and maximal discharge at 44 degrees before ceasing at 46 degrees
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56
Q

Draw a diagram representing the relationship between thermoneutral zone and metabolic rate?

A
57
Q

What is a critical temperature

A

The lower end of the thermoneutral zone where metabolic rate must increase to maintain temperature

58
Q

Draw how evaporative heat loss, radiation, conduction and convection interplay over temperatures below, within and above the thermoneutral zone

A
59
Q

What are the effector systems for temperature control

A
  • Sympthatic system
    ◦ Cutaneous vasoconstriction and vasodilation
    ◦ SKin heat loss by sweating - sympathetic cholinergic
    ◦ Heat production by effects on metabolic rate - non shivering thermogenesis
  • Behavioural response - activity, posture, amount of clothing
  • Thyroid hormone secretion
  • Shivering
  • Piloerection
60
Q

How does the sympathetic system act in temperature control

A
  • Sympthatic system
    ◦ Cutaneous vasoconstriction and vasodilation
    ◦ SKin heat loss by sweating - sympathetic cholinergic
    ◦ Heat production by effects on metabolic rate - non shivering thermogenesis
61
Q

When is temperature highest physiologically?

A

Evening 37.3

62
Q

Which gender has a higher baseline core temperature

A

women - latter half of menstrual cycle 0.5 degrees higher

63
Q

What relationship does metabolic rate have to temperature when below the critical temperature?

A

Linear increase with temperature drop

64
Q

What is the thermoneutral zone

A

◦ This range at which metabolic rate and oxygen consumption is stable (minimal) is the THERMONEUTRAL ZONE

65
Q

What range does the thermoneutral zone have

A

22-28 degrees adult clothed
27-31 unchlothed 70kg adult male

66
Q

What is the critical temperature

A

the bottom end of the thermoneutral zone below which the metbaolic rate will begin increasing

67
Q

Neonatal critical temperature?

A

32-34 degrees

68
Q

What are the mechnaisms by which core temperature can be modulated?

A

◦ metabolic heat production
‣ Shivering and non shivering thermogenesis
* Shivering increases metabolic rate by 4x
◦ Active vasoconstriction - reduced heat production
◦ Behavioural change leading to reduced heat production
‣ Wearing clothing - reduces radiation and convection
◦ Increased heat loss
‣ Active vasodilation
‣ Sweating
‣ Behavioural change

69
Q

How mechanisms account for heat lost from the skin?

A

Convection
radiation
conduction

70
Q

How much cardiac output does the skin get

A

8%

71
Q

How much can blood flow vary per 100g of tissue for skin?

A

1-150mL/min

72
Q

What is the stucture of skin blood flow

A

◦ Superficial cutaneous arterioles, capillaries and venules and deep venous plexus (capacitance system holding up to 1.5L)

73
Q

What mechanism accounts for skin modulation of blood flow

A

alpha adrenergic sympathetic fibres - causing peripehral construction reducing skin blood flow from warm deep areas to superfiical, reducing heat loss to the environemnt

74
Q

What is a shunt vessel and how is it involved in heat regulation?

A

mainly in hands, feet, ears,nose, lips
‣ 50-100 micrometers diametre
‣ Smooth vascular muscle innervated by alpha adrenergic receptors regulated by SNS
‣ When body temp 30degrees or greater sympathetic activity decreases (anterior hypothalamus) causing vasodilation, enhanced by bradykinin from sweat glands (activated by cholinergic SNS), fall in total vascular resistance leads to increased cardiac output, massive increase in skin blood flow accommodated by AV shunts and deep venous plexus
‣ Increased area for heat transfer
‣ Cutaneous blood flow increasing 30 fold in heat stress, decreases 10 fold in cold stres - at maximum up to 60% of cardiac output

75
Q

How is heat conserved in cutaneous veins

A

counter current system
Calibre under control by noradrenaline
in cold conditions the blood returning from deep veins aquire heat from arteries reducing body heat loss

76
Q

What is shivering?
How increased does the metabolic rate become?

A
  • Shivering thermogenesis is involuntary contraction of muscles increasing the metabolic rate by up to 100% in adults
  • Rapid tremors up to a frequency 250Hz unsynchronised
  • Slow 4-8 cycles/min synchronous waves wax and wane are superimposed on tremors suggesting central control
  • Cyclical muscle rigours 10-20Hz appear as shivering becomes more intense
77
Q

What is non shivering thermogenesis? What mediates its action? What tissues does it occur in?

A
  • Increases metabolic heat production without mechanical work
  • Activated by Beta 3 sympathetic activity - uncouples oxidative phosphorylation in brown fat and skeletal muscle
  • Lipolysis o adipose tissue releases glycerol and free fatty acids —> energy source for skeletal muscle and myocardium
  • Newborn brown fat in interscapular areas, perinephric, and surrounding intrabaomdinal vessels
  • Brown fat is highly vascular, abundant mitochrondria and richly innervated by adrenergic fibres
  • Neonate brown fat metabolism can increase metabolic rate 2x normal - and in this situation TG are hydrolysed to glycerol and FFA —> FFA then resesterified to fatty acid acyl COA
    ◦ Acyl CoA broken down liberating heat
    ◦ Meanwhile fatty acid recycled by COA replaced with glycerol reforming TG
    ◦ As each molecule of fatty acid recycles one molecule of ATP is converted to heat
    ◦ Thus a small fraction of fatty acid is oxidised rather than re-esterified and this is reflected by raised O2 consumption
78
Q

Explain the chemical/metabolic components to non shivering thermogenesis

A

TG are hydrolysed to glycerol and FFA —> FFA then resesterified to fatty acid acyl COA
◦ Acyl CoA broken down liberating heat
◦ Meanwhile fatty acid recycled by COA replaced with glycerol reforming TG
◦ As each molecule of fatty acid recycles one molecule of ATP is converted to heat
◦ Thus a small fraction of fatty acid is oxidised rather than re-esterified and this is reflected by raised O2 consumption

79
Q

What occurs to the thermoregulatory set point in response to GA? What effector systems are still able to perform heat conservation?

A
  • Under GA interthreshold range widened to 4 degrees (from 0.4) and behavioural responses abolished - therefore thresholds for hypothalamic response lowered by 2-3 degrees
    ◦ Within this range the patient is poikilothermic as active thermoregulatory responses are absent so passive changes in proportion to metabolic heat production and heat loss
    ◦ The only responses available vasoconstriction and non shivering thermogenesis - and vasoconstriction is counteracted by many of the GA drugs used
80
Q

Explain the phases of intraoperative hypothermia

A
  • Intraoperative hypothermia under GA follows a triphasic pattern
    ◦ Phase 1 - redistribution
    ‣ Decrease in core temp 1.5-2 degrees over 30-45 minutes due to vasodilation (GA drugs vasodilating, indirect lowered vasoconstriction threshold in the hypothalamus)
    ‣ Cool blood from peripheries enters core circulation, warm blood redistributes towards peripheres
    ◦ Phase 2 - linear
    ‣ More gradual fall in core temperature 1 degree over 2-3 hours occurs when heat loss by
    * Radiation 40%
    * Convection 30%
    * Evaporation 25% (varies with surgery - highest in abdominal)
    * Conduction
    ‣ Metabolic rate reduced 15-40% under GA
    ‣ Ends because of maximal vasoconstriction so ongoing heat loss is balanced by metabolic heat production
    ◦ Phase 3 - plateau
    ‣ Core temperature reaches plateau because rate of loss is matched by production - however temp falls in core because maximal peripheral vasoconstriction ineffective
    ‣ Regional anaesthesia diminishes vasoconstriction and shivering below the level of the block - decreasing Afferent input, and initial redistribution of cool blood occurs because of vasodilation induced by regional anaesthesia
    * Vasoconstriction above the level of the block can compensate partially for a fall in temperature
81
Q

Phase 1 of intraoperative hypothermia

A

◦ Phase 1 - redistribution
‣ Decrease in core temp 1.5-2 degrees over 30-45 minutes due to vasodilation (GA drugs vasodilating, indirect lowered vasoconstriction threshold in the hypothalamus)
‣ Cool blood from peripheries enters core circulation, warm blood redistributes towards peripheres

82
Q

Phase 2 of intraoperative hypothermia explain

A

Linear
‣ More gradual fall in core temperature 1 degree over 2-3 hours occurs when heat loss by
* Radiation 40%
* Convection 30%
* Evaporation 25% (varies with surgery - highest in abdominal)
* Conduction
‣ Metabolic rate reduced 15-40% under GA
‣ Ends because of maximal vasoconstriction so ongoing heat loss is balanced by metabolic heat production

83
Q

Phase 3 of intraoperative hypothermia

A

◦ Phase 3 - plateau
‣ Core temperature reaches plateau because rate of loss is matched by production - however temp falls in core because maximal peripheral vasoconstriction ineffective
‣ Regional anaesthesia diminishes vasoconstriction and shivering below the level of the block - decreasing Afferent input, and initial redistribution of cool blood occurs because of vasodilation induced by regional anaesthesia
* Vasoconstriction above the level of the block can compensate partially for a fall in temperature

84
Q

What is hypothermia by definition

A

core temperature <35

85
Q

What are the responses to hypothermia

A
  1. Shivering thermogenesis
  2. Non shivering thermogenesis
  3. Behaviroual changes - insulation, curling up, goose pimples
  4. Cutaneous vasoconstriction
86
Q

Shivering thermogenesis produces heat how?

A
  • Shivering thermogenesis
    ◦ Involuntary muscle activity enahnces heat production by ATP hydrolysis associated with muscle fibre contraction (out of phase with one another)
    ‣ More pronounced in extensor and proximal muscles of upper limb, trunk and jaw in severe cases
    ‣ Increases heat production 5 fold - cannot be sustained due to energy reserves
    ‣ SKin receptors are the main stimulus, it does not occur readily with moderate fall in core temperature
    ‣ Poorly developed in neonates
87
Q

Non shivering thermogenesis generates heat how?

A

◦ BMR increases 2-3 fold
◦ Neonates occurs in brown fat - thermogenic capacity 150x muscle however muscle or skin 40% of total body mass
◦ Theories
‣ Large amounts of non esterified fatty acids uncouples mitochondrial phosphorylation from respiration and energy is lost as heat
‣ Reeling of TG and fatty acids leads to increased ATP turnover
◦ Stimulated by catecholamines , thyroid hormones have a permissive effect as they increase the catecholamine response
◦ Cold acclimitasion appears to occur with increased BMR despite brown fat mass remaining the same

88
Q

Cutaneous vasoconstriciton in response to cold preseves heat how? Mechanism?

A

SNS mediated
Reduced heat loss via conduction, convection and evaporation

89
Q

To prolonged severe cooling what paradoxical reaction can occur

A

◦ Prolonged cooling paradoxical vasodilation by direct cold induced paralysis of vessels becoming unresponsive to SNS thereafter vasoconstriction alternates with vasodilation serving to preventing tissue damage

90
Q

Frostbite mechanism

A

◦ Cell dehydration
◦ Mechanical damage from ice crystals
◦ Increased blood permeability
◦ MIld forms - skin freezes; moderate to severe muscle and tendons freeze ; prolonged cooling can cause neuromuscular damage

91
Q

Higher temperature > thermoneutral zone induce what response

A
  1. Behaviuoural - reduced acitvity, reduced feeding, reduced clothing
  2. Sweating
  3. Cutaneous vasodilation
92
Q

Sweat
- How many sweat glands, where are they, what is their maximum output by hour and day

A

‣ 2 million sweat glands
‣ 50% on chest and back
‣ Maximal rate 3L/hr this cannot be sustained - 12L per day max

93
Q

How is sweat made

A

‣ Proximal region of sweat gland produces hypotonic solution
‣ Solute reabsorption as the fluid moves along the duct towards the skin surface
‣ Low rates of secretion - Na content 5mmol/L
‣ High secretions can be 10x that value - less time for reabsorption
◦ Evaporation 2.4kJ/m energy loss at 37 degrees

94
Q

What effect does rising core temperature have on caridac output and BP

A
  • Rising core temperatures increased vasodilation and cardiac output with stable BP
95
Q

What is heat stroke

A
  • Loss of energy, irritability —> neurological disturbance.
    ◦ Cessation of sweating primary cause of loss o thermoregulation.
  • Unconscious once temp >42 with cellular damage and coagulation of proteins
96
Q

What is heat exhaustion

A

excessive water or salt loss; 10% dehydration mental deterioration. Cramps in legs, arms, back with salt losses

97
Q

Consequences of hypothermia

A

Compensatory
- Peripheral vasoconstriction
- Shivering - at 36 degrees
- Non shivering thermogeneiss
Cardiovascular
- J waves/osbourne waves, QT prolongation
- HR and BP decrease; cardiac output decreases
- Severe bradycardia below 28 degrees
- Increased arryhtmias below 28 degrees
- Oxyhaemoglobin curve shifted left reducing tissue oxyegn delivery
- Increased viscotiy inceasing LV work
- Coronary vasoconstriction
Respiraotry
- CO2 increasingly soluble so PaCO2 lower
- Decreased RR
CNS
- Confusion, irritability <34 degrees, LOC 32 degrees
- <20 degrees EEG appears as brain death
- Shivering - lost <27 degrees
- Cerebral metabolism aerobic at low temperatures so O2 delivery still important
- Increased seizure threshold
Metabolism
- BMR increases 6% fr every 1 degre
- Hyperglycaemia - reduced carbohydrate metabolism
- Enzyme reactinos slower including drug metabolism
Muscle weakness
Renal - cold diuresis due to suppression of ADH
Haematological
- Platalet and clotting dysfunction
- Decreased granulocyte and monocyte function
- neutroenia and thrombocytopenia
Acid base
- Alkalosis and hypocapnoea
Pharmacology
- Delayed absorption
- Decreased metabolism

98
Q

Cardiovascular effects of hypothermia

A
  • Cardiovascular
    ◦ J waves on ECG/Osbourne waves between QRS and T, phase 1 repolarisation + QT prolongation
    ◦ HR and BP decrease with decreasing temperature; severe bradycardia common below 28 degrees; decreased cardiac output (vasoconstriction + reduced HR)
    ‣ HR decreasing due to reduced conductance through cold conducting system
    ◦ Increased arrhythmias below 28 degrees - VF common; AF common
    ‣ Additionally resistance to defibrillation
    ◦ Oxyhaemoglobin dissociation curve shifted left increasing oxygen affinity and reducing tissue delivery
    ◦ Blood viscosity increases increased LV work but also with coronary vasoconstriction induced by cold can provoke massive coronar arterial events
    ◦ MI precipitated by above
99
Q

Respiratory effects of hypothermia

A
  • Respiratory - decreased RR and medullary sensitivty to CO2
    ◦ Addutionally solubuility of CO2 increased so PCO2 at actual body temperature appears even lower even accounting for reduced metabolic activity
100
Q

CNS effects of hypothermia

A

◦ Confusion, irritability at mild hypothermia 34 degrees
‣ LOC below 32 degrees
◦ Core temp 20 degrees EEG consistent with brain death
◦ Shivering - the ability to do so is lost once core temperature is <27. Initially begins as whole body metabolic rate and oxygen consumption increase which is counterporductive
◦ Increased seizure threshold - also likely protecting the brain from excitotoxic damage
◦ Cerebral metabolism is aerobic even at low temperatures - so ongoing oxygen supply is very important. The brain otherwise copes quite well with hypothermia

101
Q

Metabolic effects of hypothermia

A

◦ BMR reduces 6% for every 1 degree drop in core temperature –> decreased O2 consumption
‣ Decreased at 28 degrees to 50% of normal; suggesting at 32-33 degrees metabolism is 60-70% of noraml
‣ Note as much as the BMR % calculation is oft quoted it is proibably inaccurate as the graph is curved
◦ Hyperglycaemia due to reduced cellular uptakeof glucose and reduced carbohydrate metabolism
◦ Enzymatic reactions slowed including of drug metabolism; prolonged duration of muscle relaxant
◦ Gut motility is suppressed - thus feeds are often halted until rewarming occurs

102
Q

Renal effects of hypothermi

A

Suppression fo ADH so cold diuresis
Electrolytes unchanged

103
Q

Haematological effects of hypothermia

A

◦ Platelet and clotting dysfunction —>increased blood loss and transfusion requirement
‣ Major contributing feature to coagulopathy is fibrinogen synthesis failure as it is halved at 32 degrees and fibrinolysis is not affected so when the clot is formed it should not be any more prone to falling apart than usual
‣ In profound hypothermia however the most important factory incoagulopathy is acidosis
◦ Decreased granulocyte and monocyte acitvity as difficulty migrating into tissues –> Increased incidence of post operative wound infection
◦ Increased haemocrit and blood viscocity - reduced plasma volume, and reduced exchange between compartments
◦ Neutropenia and thrombocytopenia - sequestraton in low flow capillary beds of liver and spleen

104
Q

Acid base changes in hypothermia

A

◦ Alkalosis and hypocapnoea
‣ Interpret the pH, CO2 and PaO2 at 37 degrees without correction
‣ pH changes with temperature linearly - as dissociation is an endothermic reaction therefore more acid gets stuck as HA instead of dissociating to hydrogen ions but we have no reference ranges for normal values (PCO2)at other temperatures so correcting is full of problems. But at all temperatures the intracellular pH remains at levels of celclular function due to protein buffering intracellularly
‣ Rise of pH with falling temperature
‣ Fall of PCO2 with falling body temperature
◦ Increased oxygen solubility and O2 haemoglobin affinity
‣ So the lower the corrected PaO2 however oxygen content stable or increased both due to solubility and haemoglobin affinity rising (Hb affinity increases 22 fold as temperature drops from 37 to 0) BUT the oxygen carrying capacity still doesnt change at 1.37ml per 1g of Hb
‣ PaO2 however does not need to be corrected

105
Q

Pharmacology specifics in hypothermia

A

◦ Delayed absorption
◦ Decreased metabolism (esp hepatic)
‣ CYP450 enzymes slow down
‣ Hepatic blood flow also decreased affecting rapidly cleared drugs the most
‣ e.g. propoofol circulating levels increase by 30% for every 3 degrees below normal and 15% for fentanyl
‣ Key examples at 32 degrees
* Propofol reduced by 50% clearance, reduced intercompartmental clearance trapping it in brain tissue
* Fentanyl reduced to 75%
* Midazolam reduces to 1% of normal, effects marked after 35 degrees where metabolism is 1% or less
* Remifentanyl - reduced to 70%
* Rocuronium - reduced to 50%, duration of effect increased by 5 minutes for every 1 degree below 37 degrees.
* Gentamicin reduced clearance by 75-80% (due to GFR reductions)
* Antiarrhtyhmic drugs
◦ Delayed heaptic and renal clearance
◦ Poorer affinity of receptors (catecholamines)

106
Q

Specific drug changes at 32 degrees
- Propofol
- Fentanyl
- Midazolam
- Rocuronium
- gentamicin

A

‣ Key examples at 32 degrees
* Propofol reduced by 50% clearance, reduced intercompartmental clearance trapping it in brain tissue
* Fentanyl reduced to 75%
* Midazolam reduces to 1% of normal, effects marked after 35 degrees where metabolism is 1% or less
* Remifentanyl - reduced to 70%
* Rocuronium - reduced to 50%, duration of effect increased by 5 minutes for every 1 degree below 37 degrees.
* Gentamicin reduced clearance by 75-80% (due to GFR reductions)
* Antiarrhtyhmic drugs

107
Q

Antiarrhtyhmics and hypothermia

A

Certainly, studies on the early antiarrhythmic pharmacopoeia had confirmed that Class I agents (specifically, quinidine) were the most effective, whereas other agents were either useless or actually pro-arrhythmic. The pro-arrhythmic effect was found to be related to the QT prolongation effect of some antiarrhythmic agents, which is enhanced by the cold; particularly sotalol was found to be strongly pro-arrhythmic in hypothermia, and should not be used. Even good old amiodarone- the workhorse of the ICU- can prolong QTc by 100msec or so, and the Irish have recommended that you watch those patients carefully.

So which anti-arrhythmics are safe? Presently, there is no agreement. Lignocaine does not prolong the QT interval, and may be one of the answers, but its use in hypothermic patients is not well researched.

108
Q

ADrenaline use in hypothermic arrest

A

every 4th cycle due to reduced cleearance

109
Q

What basic mechanisms are there to measure temperature

A

Basic principle is measure a physical proprty that is consistent in its temperature dependence (thermometric property) - the devices are called thermometers
* Volume expansion
◦ Mercury in glass thermometers - expansion of liquid
◦ Bimetallic strip - expansion of solid
◦ Bourdon - pressure change of gas
* Chemical thermometer
◦ Liquid crystal
* Electrical
◦ Platinum wire - resistance change
◦ Thermister - resistance change
◦ Thermocouple - Seebeck effect

110
Q

Explain how a liquid in glass thermometer works

A
  • Uniform evacuated glass capillary tube connected to mercury resevoir - heating the reservoir causes expansion of the mercury (actually only 11-2% of the total volume) and the top of the colum will rest at a position unique to the particular temperature allowing interpretation via scale
    ◦ Constrictoin at bottom of tube just above the resevoir to maintain position of mercury column for a short period of time after movement
    ◦ Capillary tube small, uniform and evacuated - to allow for sensitvity and linear scaling
    ◦ Thermometer is shaped so the tube is the focal point of a parabolic mirror on the back of the thermometer greatly facilitating visualisation fo the small capillary tube and minimises error
    ◦ Size of mercury reservoir a compromise between sensitivity and thermal inertia so response is rapid to changes
    ◦ Now the resevoir used is a alcohol based liquid
111
Q

Advantages of a liquid in glass thermometer and disadvantages

A
  • Advantages
    ◦ Readily available
    ◦ Inexpensive
    ◦ easy to use
    ◦ Accurate
    ◦ Chemically sterilised
    ◦ Response time slow but suitable for most applications if steady temperature
  • Disadvantages
    ◦ Not suitable for remote recording or insertion into body caviities
    ◦ Cannot be made small
    ◦ No continuous reading
    ◦ Reading cannot be processed or connected to a recorder
    ◦ Slow response
    ◦ Risk fo cross infection
    ◦ Contains potentialy toxic sbstance
    ◦ Fragile
  • Number on the side represents time constant so the response time can be gauged
112
Q

What is a bourdon thermometer?
What law is it based on?

A
  • Measures high temperatures accurately
  • Based on Charle’s law - as the temperature of a gas increases the pressure proportionately changes with it
  • The gas is held in a resevoir or bulb, linked to a capillary tube to a hollow bourdon tube. As the temperature increases the pressure increases and the Bourdon tube uncoils which is linked to a pointer behind which is a temperature on a calibrated dial
113
Q

What is a thermister

A

temperature sensitive resistor whose resistance changes with temperature

114
Q

Draw a diagram to explain thermisters

A
115
Q

Explain how a thermister is constructed and used

A
  • Defined - temperature sensitive resistor whose resistance changes with temperature
  • Solid state thermometer composed of fused oxides of certain heavy metals e.g. cobalt
  • resistance changes with temperature - non linear but not difficult to design for this
  • Most thermisters in clinical use have a negative temperature coefficient i.e. resistance reduces with increased temperature (NEGATIVE thermal conductivity)
    ◦ Although platinum wires have positive coefficient - platinum resistance is linear however, but not as sensitive as other thermisters
  • Wheatstone bridge circuit used to measure resistanc accurately
116
Q

Advantages of a thermister thermometer - give examples

A
  • Advantages
    ◦ Very small
    ◦ Continuous
    ◦ Electronic processing easy
    ◦ Suitable for insertion .e.g oesophageal probes
    ◦ Robust and simple
  • e.g. urinary catheter, nasopharyngeal and oesophageal probes
117
Q

Thermocouple
Based on what effect
What metals are used
Advantages

A
  • Electrical thermometer based on Seebeck effect
    ◦ Small electrical potential develops at any junction between two dissimilar metals and the size of this is temperature dependent
  • In a thermocouple two metal wires typically copper and constantan, are joined at both ends
    ◦ The temperature of one junction is kept at constant reference and the other is used to measure, the potential difference therefore is measurement dependent
  • Can be made very small, very accurate, respond quickly
118
Q

How does a tympanic thermometer work?

A

Infrared manometer measuring infrared radiation

119
Q

What is the principle underlying tympanic thermometers? Flaws

A
  • Measures the temperature in the middle ear by detecting radiation from eardrum
    ◦ Thermopile - an electornic device which converts thermal energy to electrical energy
  • Tympanic membrane is used because blood supply is similar in temperature and location to the hypothalamus
  • However depending on the anatomy of the ear
    ◦ If the ear canal is the site that is recorded inaccurate - so ear canal needs to be patent and non tortuous
    ◦ Lifting the ear upwards helps

Poor correlation with other methods
Ear pathology distorts measurement

120
Q

What is the gold standard thermometer

A

PAC - intercardiac blood

121
Q

Where is the ideal place to measure temperature

A

Intracardiac or hypothalamic blood

122
Q

COmpare baldder, rectal and oesophageal thermoemters

A
  • Bladder
    ◦ Continuous measurement
    ◦ Minimally invasive
    ◦ Stable measurement regardless of urine flow rate
    ◦ Not as accurate as PAC but better than rectal and surface methods
    ◦ However - costly, needs monitor for display, source of infection
  • Rectal probe
    ◦ Intemrittent or continuous measurement
    ◦ Bacterial metabolism renders rectum slightly hotter than core temperature
    ◦ Invasive
    ◦ Risk fo traumatic insertion
    ◦ Potential source of bacteraemia
  • Oeosphageal
    ◦ Continuous
    ◦ Not as acurate as PAC but better than rectal or surface methods
    ◦ Issues
    ‣ Position depedent
    ‣ Risk of oesophageal trauma
    ‣ Uncomfortable
123
Q

Characteristics, advantage and disadvantages of PAC as a method of temperature measurement

A

Accurate
continuous measurement

Invasive

124
Q

Characteristics, advantage and disadvantages of Bladder temperature measurement

A

◦ Continuous measurement
◦ Minimally invasive
◦ Stable measurement regardless of urine flow rate
◦ Not as accurate as PAC but better than rectal and surface methods
◦ However - costly, needs monitor for display, source of infection

125
Q

Characteristics, advantage and disadvantages of rectal temperature measurement

A

◦ Intemrittent or continuous measurement
◦ Bacterial metabolism renders rectum slightly hotter than core temperature
◦ Invasive
◦ Risk fo traumatic insertion
◦ Potential source of bacteraemia

126
Q

Characteristics, advantage and disadvantages of oesophageal temperature measurement

A

◦ Continuous
◦ Not as acurate as PAC but better than rectal or surface methods
◦ Issues
‣ Position depedent
‣ Risk of oesophageal trauma
‣ Uncomfortable

127
Q

Characteristics, advantage and disadvantages of tympanic and nasopharyngeal temperature measurement

A
  • Tympanic
    ◦ Aims to reflect hypothalamic and core temperature
    ◦ However poor correlation with other methods
    ◦ Ear pathology distorts
  • Nasopharyngeal
    ◦ Similar to oesophageal in its advantages
    ◦ However risk of sinusitis, not able to use in base of skull, opsition dependent and may erroneously measure humidified gas temp from ETT
128
Q

Describe oral temperature measurement, its advantages and disavantages

A
  • Oral
    ◦ Safe, convenient, familiar
    ◦ Next best to PA catheter
    ◦ Needs cooperation
    ◦ Presence of ETT and orogastrics may limit in ICU
    ◦ Mouth breathing, drinking hot or cold fluids may distort
129
Q

Axillary temperature measurement vs PAC

A

Non invasive
Axillary temperature is lower than core body temperature

130
Q

Hyperthermia define

A

Hyperthermia is when core temperature exceeds that normally maintained by homeostatic mechanisms

131
Q

Fever vs hyperthermia

A

Fever or pyrexia is an elevation of body temperature above the normal range of 36.5–37.5 °C (97.7–99.5 °F) due to an increase in the temperature regulatory set point

Uncontrolled hyperthermia differs from fever in that the body temperature is elevated above the thermoregulatory set point due to excessive heat production and/or insufficient heat dissipation

132
Q

Physiological effects of hyperthermia

A

The threshold for cellular damage seems to be 41.6-42°C for 8 hours

Cardiac
- Increased cardiac output and HR
- Vasodiltion and SIRS response - cytokine release due to heeat stress, bacterial translocation and endotoxaemiaa, endothialial cell injury
- Tachyarrhthmias
- Hypotension
- QT prolongtion and ST segmental changes
- MI
Respirtory
- ARDS due to SIRS
- Respiratory alkalosis
Metabolic
- Increased O2 consumption and CO2 production
- Lactic acidosis
- Uncoupling of oxidative phosphorylation with failing enzyme system
- Hyperglycaemia
- Low phosphate
- High CK
Renal
- Rhabodmyolysis
- Renal failure - ATN and rhabdomyolysis cuasing myoglobin induced ATN
haematological
- DIC due to endothelial cell injury
Liver failure - direct tissue injury and splanchnic blood flow diversion
CNS
- Altered mental state
- Seizures
- Coma
Skin
- May no longer sweat
- May be hot or cool dependent of shocked - vasodilatory shock decompensates as ongoing dehydration occurs

133
Q

Heat stroke define

A

Heat stroke is hyperthermia with neurological dysfunction due to the failing thermoregulatory system
rectal temperature exceeds 40.6°C (definition varies between authors — in practice, don’t be too strict especially if prehospital cooling performed)

134
Q

Radiation heat loss principles

A

Radiative heat exchange:

Describes the loss of heat through EMR by all objects above 0°K
Radiative heat loss is proportional to temperature
Radiative heat loss does not require a transfer medium

135
Q

Principle sof conduction heat loss
- Define
- Requires what conditions to occur
- At baseline how much heat loss occurs via this mechanism
- How does the body use this principle to hold onto heat
- Who has a barrier to heat loss

A

Conduction is the transfer of heat (as kinetic energy) by direct contact from a higher temperature object to the lower temperature one. Conduction:

Requires physical contact between bodies to conduct heat
Solids conduct heat better than gases
There is no conduction in a vacuum
Heat loss via conduction is minimal in air but is a major cause of heat loss in immersion
As arteries and veins typically run next to each other, arterial heat tends to be transferred to the (cooler) veins, limiting further heat loss
This is similar to counter-current exchange in the kidney.
As fat is a poorer conductor of heat than muscle, increased body fat will slow heat loss by conduction

136
Q

Central temperatur esensors are located where

A

Abdominal visdcera
Spinal cord
Hypothalamus anterior
Brainstem

137
Q

SI unit for heat

A

heat is a form of energy
SI unit therefore is Joule

138
Q

SI unit of temperature

A

Kelvin

139
Q

Thermometers utilise what surrogate properties to measure temperature

A

They measure a temperature dependent property e.g.
Volume expansion
- Liquid in glass thermometer
- Bimetallic strip
Chemical thermoemeter
- Liquid crystal thermometer
Electric thermometers
- Platinum wire
- Thermister
- Thermocouple

Misc - temp/procedures (7 decks)

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