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Boards: Monitoring > Thermoregulation > Flashcards

Thermoregulation Flashcards

1
Q

First Law of Thermodynamics

A

Energy can’t be created nor destroyed - can only change form

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2
Q

Second Law of Thermodynamics

A

Total entropy never decreases over time in an isolated system

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3
Q

Third Law of Thermodynamics

A

Absolute zero (T = 0 kelvin), zero entropy = unattainable

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4
Q

Physiology of Thermoregulation

A
  • Organism’s heat energy measured as body temp
    o Total amt of heat energy = function of temperature, patient mass
    o Most mammals: temperature relatively constant (homeothermic) despite continual metabolic heat production, environmental heat gain/loss
    o Temperature fluctuates with time of day, time of year (hibernating animals) hormonal influences, activity levels
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5
Q

Homeothermic

A

Maintain relatively constant temperature despite changes

Most mammals

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6
Q

Only non homeothermic/poikilothermic mammal?

A

Adult naked mole rat

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7
Q

Poikilothermic

A

species normally subject to significant environmental temperature influences

amphibians, reptiles, some fish

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8
Q

Normal Temperature Regulation

A

o Sensed by temperature-responsive cells t/o body
o thermal receptors in skin discharge when threshold reached
Most utilize cation channels: transient receptor potential (TRP) family
o Visceral receptors: brain (anterior hypothalamus, preoptic area), SC, abdomen (GIT, bladder)
o Afferent input to CNS via different nerve fiber types (A-delta, C) depending on whether signal hot, cold, noxious
 Signals –> ascending tracts of SC –> hypothalamus –> integrated, responses issued

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9
Q

Summary of Thermal Input to CNS

A

Averaging of temp allows for narrow thermal set point assoc with interthreshold range of +/- 0.2*C (temp variation when no compensatory mechanisms occur)

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10
Q

Role of Anesthetic Drugs and Altered Thermoregulation

A

Ax drugs alter thermoregulatory thresholds for compensatory responses
 Why perioperative patients fail to shiver even though mildly hypothermic
Increase in threshold range (approx. 3.5*C) caused by anesthetic agents (volatile agents, opioids, sedatives) somewhat drug, dose-dependent
 Key: ax reduces p’s ability to tightly regulate core body temp

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11
Q

Normal Core to Periphery Gradient

A

2-4*C

Significant longitudinal variation in limbs: greater away from trunk, greater difference

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12
Q

Mechanism of Maintenance of Core to Periphery Gradient

A

Heat transfer btw core, periphery = blood-borne convection, some tissue-to-tissue conduction

Factors that influence distribution of blood:
* Arteriovenous anastomoses
* Cutaneous VC/VD
* Countercurrent vascular heat exchange
* Sweating *in p’s that can do so
* Environmental temperature

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13
Q

Panting, Shivering

A

modify heat loss/gain (core temp > skin-to-core temp gradient)

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14
Q

How anesthetic drugs change body temperature

A

why p undergo rapid decrease in body temp following admin of ax drugs esp those that cause profound peripheral VD ie ACP, inhalants
* Drugs which cause less peripheral VD: less rapid decrease in temp
* Also important: body size/surface area-to-mass ratio can greatly influence change in core body temp
o Cats, small dogs: faster changes than larger patients (horses)

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15
Q

Hypothermia

A

Heat loss in excess of metabolic production or decreased thermoregulatory set-point, which delays shivering/other compensatory mechanisms

Heat loss/gain usually greatest in areas with large blood flow, low mass (limbs)

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16
Q

Three Phases of Heat Loss during Anesthesia

A
  1. Initial rapid hypothermic phase (0-2hr)
  2. Linear phase (2-4hrs)
  3. Plateau phase (>4hrs)
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17
Q

Initial rapid hypothermic phase

A
  • Rapid decline during first hr of GA DT redistribution of warm blood from lost through skin by radiation, convection
  • Transfer of core heat to periphery DT VD
  • Phase nearly impossible to prevent by application of external heat source following induction

Temp change: 0.5-1.5*C

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18
Q

Most effective way to mitigate initial rapid hypothermic phase?

A

prewarm patient skin, peripheral tissues
o Warm, ambient environment —> minimizes thermal gradient btw skin and core so once blood flow increases to periphery, heat energy required to re-establish equilibrium minimal
o Limitations: patient compliance, patient compensatory mechanisms

Temp change: 0.5-1.5*C

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19
Q

Linear Phase

A

Slower linear decline, ~2hr bc heat loss exceeding metabolic production

Rate of heat fall depends on difference btw heat lost, produced and size of patient

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20
Q

Plateau Phase

A

Pseudoequilibrium with environment, body temp stabilizes over 3-4hrs

Peripheral VC causes restriction of metabolic heat to the core

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21
Q

Four mechanisms of heat transfer?

A
  1. Radiation
  2. Convection
  3. Conduction
  4. Evaporation
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22
Q

Radiation

A

electromagnetic (photon) transfer of energy btw surfaces
—Does not depend on air around patient
—DOES depend on emissivity of involved surfaces, their temperature difference (in K) raised to 4th power

MAIN LOSS OF HEAT LOSS DURING SX

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23
Q

Emissivity

A

object’s capacity to exchange heat
* 1.0=perfect absorber of heat, 0=perfect reflector of heat, human skin=0.95

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24
Q

Conduction

A

direct heat transfer btw two adjacent surfaces, heat flow proportional to temperature difference btw two bodies/surfaces
 Examples of colder objects: OR tables, linens, surgical instruments, skin prep, irrigation, IVF
 Thermal insulation: reduce heat transfer
 Wetness: increases conductive heat loss

Think why have to use pot holder with warm pot handle

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25
Q

Convection

A

transfer of heat via intermediary, ie moving air or flowing liquid
—Eg heat lost when body surfaces exposed
—Movement of air (‘wind chill’) increases heat loss proportional to square root of air velocity
* Examples: clipping, initial prep, sterile prep in OR

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26
Q

Convection and Heat Loss During Sx

A

 Normally second most common cause of heat loss behind radiation (30%)
Most important cause of heat loss in environments with high air flow
 Use of air-trapping sheet, blanket around patient will limit air flow –> reduce effects of convection by around 30%
 Additional layers do little to decrease heat loss from convection: importance of decreasing air flow vs insulating capacity of cover

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27
Q

Evaporation

A

liquids from skin or body cavity surface results in patient heat loss DT ’donation’ of heat energy required to vaporize liquid

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28
Q

Evaporation - MOA

A

Heat loss greater with surgeries requiring large incisions with exposure of internal surfaces than with small incisions or non-invasive procedures
* Evap heat losses can reach 50% total heat loss for smaller animal patients (rabbits) with lrg surgical fields, less relative to skin loss with larger animals
 Also includes use of water or alcohol-based solutions to prep sx site
* Heat loss suggested to be less with water than alcohol

29
Q

Isaza et al VAA 2021: heat loss and prep solutions

A
  • Heat loss suggested to be less with water than alcohol
  • Isaza et al 2021 VAA: 48 intact female MBD puppies, 43 intact female kittens prepared for sx using 1.6% chlorhex then water or alcohol
    o No significant mean RT difference btw groups
    o Use of water, alcohol = same degree of temperature change
30
Q

Warmed IVF

A

When fluids introduced at less than blood temperature, heat energy transferred to solution to increase temp until reaches equilibrium with patient blood
* Avoid overheating: blood protein, enzyme damage
* Minor source of heat loss

31
Q

Limitations of Warmed IVF

A

Limitations: rate of fluid flow, distance positioned from patient

Specified range of fluid flow rates where fluid output at/near indicated temperature
* If rate too high: inadequate time to absorb heat, reach equilibrium with warmer surface = cooler than indicated fluid
* If rates too low: fluid loses significant heat to room air en route to patient

32
Q

In Line Warmer Examples

A

dry heat, microwave, water immersion, countercurrent heat exchangers, line inside convective warming device

33
Q

Preuse warmers

A

incubator, microwave, water bath – convenient, inexpensive
* Rapidly cools, do not use with dextrose containing solutions

34
Q

Forced Air Units

A

Heat out of unit = function of air temp, air flow volume at hose end
* Efficacy of system to warm patient mainly function of blanket design

‘Hosing’ patients (aiming blanket-end of hose toward p) inefficient, may result in overheating of objects in contact w/ p skin
 Most effective method – do not use a hair dryer

MOA of heating: CONVECTION

35
Q

Important Considerations with FAUs

A
  • Blanket: minimal temperature differences btw patient, blanket
  • Effectiveness = fxn of temp difference btw patient, blanket
  • Patient coverage by blanket
  • Use of blanket = important for distribution of heat
36
Q

Circulating Warm Water Blankets

A

 Water reservoir/heater/pump + replaceable blanket/pad
 Reduce risk of thermal injury by limiting water temperature, distributing water flow to areas of pad not under significant pressure

Conductive heat delivery device

37
Q

MOA Circulating Warm Water Blankets

A

MOA: water circulates through blanket in channels formed btw plastic layers
* Occlusion of some of channels by patient pressure: shunting of flow around area, reducing risk of heat accumulation at pressure points

38
Q

Advantages of Circulating Warm Water Blankets

A
  • Electrical safety features DT proximity of water, electricity
  • Limit water temp: ~140F/40C
  • Versatile: attached to several sizes, shapes of blankets
  • Generally less expensive
  • Reduced risk of burns at pressure points
39
Q

Disadvantages of Warm Water Blanket

A
  • Usually blanket placed btw patient, table; if more coverage desired, additional blankets, units needed
  • Failure/leakage of blanket = drenching of patient, significant evaporative heat loss during transport, recovery
  • Less effective vs forced air
40
Q

Resistive Polymer Electric Heating (eg HotDog)

A

Conductive heat delivery device

  • Several layers: polymer, padding, waterproofing, protective layer
    o Moisture can alter function, burn injury

Under ideal conditions, similarly effective or more effective than forced air

41
Q

Resistive Polymer Electric Heating - MOA

A

Polymer heating heats evenly, hot spots limited
o Resistance to electrical flow (which related to production of heat) monitored by controller, regulates heat delivery
o Temperature sensors in pad independently monitor temperature
o Must be in contact with patient skin for accurate measurement

42
Q

Advantages of Resistance Polymer Electric Heating

A
  • Less concern for sx site contamination vs forced air systems – no air flow
  • Lower disposable costs
  • Quiet
  • Simple to use
43
Q

Disadvantages of Resistance Polymer Electric Heating

A
  • Large initial purchase price
  • THERMAL INJURY - pad damage without obvious external signs
  • Over patient to limit more pressure points?
  • Limited by amt of body surface that can contact pad
44
Q

Passive Coverings

A

 Ex: thermal drapes, space blankets, reflective blankets, metallized plastic sheets, sheets, head coverings, blankets, socks
 Don’t prevent shivering, reduce cutaneous loss, will not maintain normothermia
 Inhibit access to patient
 Combustible

45
Q

Bad Management Strategies for Perioperative Heat Loss

A

 Do not distribute heat away from areas of pressure, hypoperfusion
 Resistive foam heating discs OK – reduce heat delivery when pad resistance increased
o Containers filled with warm H2O ie gloves, bottles, etc
o Microwaveable bags with cereal grains
o Conscious p able to sense impending thermal injury, move away from source, alter body position to limit exposure of pressure/heat –> mechanisms abolished by GA

46
Q

How Anesthesia Increases Risk of Thermal Injury

A

peripheral blood flow to skin decreases –> lower blood flow allows accumulation of heat energy at skin surface, increased risk of thermal injury

Cannot get away from source bc anesthetized

47
Q

Common Complications Assoc with Hypothermia

A
  1. Impaired hepatic metabolism of drugs
  2. Worsened VQ mismatch/hypoxemia
  3. MAC overdose
  4. Prolonged Recovery
  5. Post wound infections
  6. Impaired coagulation
  7. Increased blood viscosity
  8. Hypovolemia
  9. Cardiac complications: arrhythmias, arrest
  10. Increased shivering/discomfort during recovery
48
Q

Mild Hypothermia

A

p’s normal temp to 96.8*F, temp below which risk of complications thought to increase in most species
 Depends on patient’s entire status/overall clinical picture

49
Q

Worsening VQ Mismatch, hypoxemia

A
  • Shifting of oxygen dissociation curve to left

Decreased oxygen delivery to tissues - increased affinity of oxygen for hgb

50
Q

Risk of Ax Overdose

A

5-15% decrease in MAC with every 1C/1.8F decrease in body temp **

51
Q

Prolonged Recovery

A
  • Altered drug distribution
  • Decreased drug metabolism
  • Altered behavior of anesthetic drugs
  • Higher blood concentrations
  • Prolonged duration of action
  • Prolonged time to stand in horses
52
Q

Postop Wound Infection

A

Decreased peripheral tissue blood flow during recovery, decreased function of T cells, neutrophils

Other factors contribute: surgery time, surgery location, underlying health of p, ax-assoc hypoxemia (horses)

53
Q

Hypovolemia

A
  • For every degree (*C) of hypothermia, 2.5% IV volume may be lost
  • Cold-induced diuresis
  • When patient rewarms, VD  need more fluids to accommodate loss
  • Hypothermic patients: significantly greater fluid, transfusion requirements
  • More difficult peripheral catheter placement
54
Q

At what point do you have cardiac arrest from hypothermia?

A

core temp <70F/20-23C

55
Q

Cardiac Complications from Hypothermia

A
  • Hypotension, myocardial ischemia, arrhythmias DT increased MvO2 from shivering happen at MUCH higher temperatures
  • May increase catecholamine concentrations
  • Peripheral VC  body’s attempt to conserve heat = increased BP, cardiac workload, ECG changes
  • Cardiac dysrhythmias
  • Decreased contractility
  • Myocardial ischemia
  • Infarction
  • Increased requirements for vasoactive drugs
56
Q

Consequences of Rapid Rewarming of Patient

A

shock DT distribution of blood to periphery as tissues vasodilate

57
Q

Core Temps >96*F

A

 Often not associated with detrimental effects
 +/- immune system impairment –> increased risk of infection
 +/- altered coagulation/hemostatic abnormalities
 Possible shivering during recovery
 Increased non-shivering thermogenesis
 Should not prolong recovery?

58
Q

Core Temps 90-94

A

 Reduced anesthetic requirements
 Prolonged recovery
 Most animals will shiver
 Require artificial warming

59
Q

Core Temps 82-86

A

 Marked CNS depression
 Little if any anesthetic agent required
 Artificial rewarming
 +/- Atrial arrhythmias
 O2 consumption 50% normal
 HR, CO 35-40% normal
 Arterial BP 60% normal
 Cerebral metabolism 25% normal

60
Q

Core Temps 77-80

A

 Prolonged PR interval
 Widened QRS complexes
 ↑ myocardial automaticity
 ↓ tissue O2 delivery compared to consumption
 ↑ Blood viscosity (200%)

61
Q

Core Temp 72-74*F

A

Vfib, death

62
Q

Hyperthermia

A

Increase in temp, usually only IRT increased environmental temperature

Hyperthermia without a reset thermostat = pathologic
 Overzealous use of supplemental heat, large dogs cocooned on OR table, light levels of anesthesia, some drugs, large/heavily coated dogs in MRI

63
Q

Fever/Pyrexia

A

reset thermostat caused by release of endogenous pyrogens (IL-1) from monocytes IRT Infections, tissue damage, antibody-antigen reactions

64
Q

Malignant Hyperthermia

A

pigs, dogs, humans, horses

Rapidly, relentlessly progressive increase in body temperature: metabolic heat production associated with disturbed intracellular Ca cycling via RYR1

If hyperthermia associated with other signs of hypermetabolism, suspect MH or some variant of hypermetabolic disease
* Increased ETCO2
* Metabolic acidosis
* Hypoxia

65
Q

Mild Hyperthermia

A

<40C, <104F: Does not normally require treatment

66
Q

Severe Hyperthermia

A

o Cell death >42C, >108F - Oxygen delivery can no longer keep pace with increased metabolism, increased oxygen consumption

For every 1*C increase, 13% increase in metabolic rate

o Severe hyperthermia causes multiple organ dysfunction and failure: renal, hepatic, GI, myocardial, skeletal, cerebral edema, DIC, hypoxemia, metabolic acidosis, hyperkalemia

67
Q

Rectal Thermometer

A

o Pros: cheap, technically easy to use, access anus when oral cavity in sx field
o Cons: not core temperature, technically easy to use

68
Q

Esophageal Thermometer

A

o MOA: thermistor advanced to level of 5th rib (caudal axilla) near aorta, measurement of core temperature
o Pros: technically easy to use, measurement of core temp
o Cons: Interferences with procedures that include PO cavity, monitor with thermistor port, potential for esophageal damage if preexisting pathology (ME)

69
Q

Tympanic Thermometer

A

measure IR waveforms from tympanic membrane

Boards: Monitoring (19 decks)

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