Thermoregulation-physiology, anaesthetic effects, hypothermia,hyperthermia and fever, malignant hyperthermia,temperature monitoring,guidelines

1. THERMOREGULATION
PRESENTOR:- DR. KANIKA CHAUDHARY
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2. 2
OVERVIEW
• INTRODUCTION
• CORE TEMPERATURE AND SKIN TEMPERATURE
• HEAT PRODUCTION AND HEAT LOSS
• NORMAL THERMOREGULATION
• CHANGES IN GENERAL ANESTHESIA
• CHANGES IN REGIONAL ANESTHESIA
• EFFECTS OF HYPOTHERMIA
• CONSEQUENCES OF MILD INTRAOP HYPOTHERMIA
• INDUCTION OF MILD HYPOTHERMIA
• DELIBERATE SEVERE HYPOTHERMIA
• MAINTAINING INTRAOP HYPOTHERMIA
• HYPERTHERMIA & FEVER
• MALIGNANT HYPERTHERMIA
• TEMPERATURE MONITORING
• GUIDELINES

3. INTRODUCTION
• Humans are homeothermic and require a nearly constant internal body
temperature for maintaining normal physiological functions.
• The homeostatic mechanisms for regulating body temperature represents the
thermoregulatory system. Body temperature is controlled by balancing heat
production against heat loss.
• The thermoregulatory system usually maintains core body temperature with
in 0. 2° C of normal, which is about 37° C in humans .
3

4. CORE TEMPERATURE AND SKIN TEMPERATURE
• The temperature of the deep tissues of the body— the “core” of the body—remains very
constant, within ± 0.6°C
• No single core temperature can be considered normal. Range:- 36.5–37.5°C . Core
temperature gradually decreases with age
• Core temperature measurements (e.g. tympanic membrane, pulmonary artery, distal
esophagus, and nasopharynx) are used to monitor intraoperative hypothermia,prevent
overheating, and facilitate detection of malignant hyperthermia
• The core thermal component is composed of highly perfused tissues whose temperature is
uniform and high compared with the rest of the body
4

5. • The skin temperature, in contrast to the core temperature, rises and falls with the
temperature of the surroundings.
• Body temperature shows circadian rhythm, highest in the afternoon or in the evening and
least at 5:00 A.M in the morning and vary by 0.5 to 1°C.
• Rectal temperature is 0.5°C more than core temperature.
• In children, body temperature is 0.5°C higher.
• Non-pregnant women in their reproductive phase of life show 0.5°C higher body
temperature in the luteal phase of menstrual cycle.
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How body temperature is controlled?
• When the rate of heat production in the body is
greater than the rate at which heat is being lost, heat
builds up in the body and the body temperature rises.
Conversely, when heat loss is greater, both body heat
and body temperature decrease .
• Body temperature is controlled by balancing heat
production against heat loss.

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HEAT PRODUCTION
(1) Basal rate of metabolism of all the cells of the body
(2) extra rate of metabolism caused by muscle activity, including muscle contractions caused
by shivering
(3) extra metabolism caused by the effect of thyroxine (and, to a less extent, other hormones,
such as growth hormone and testosterone) on the cells
(4) extra metabolism caused by the effect of epinephrine, norepinephrine, and sympathetic
stimulation on the cells
(5) extra metabolism caused by increased chemical activity in the cells themselves,
especially when the cell temperature increases
(6) extra metabolism needed for digestion, absorption, and storage of food

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HEAT LOSS
• Most of the heat produced in the body is generated in the deep organs,
especially in the liver, brain, and heart, and in the skeletal muscles during
exercise. Then this heat is transferred from the deeper organs and tissues to
the skin, where it is lost to the air and other surroundings.
• The rate at which heat is lost is determined by two factors:
(1)how rapidly heat can be conducted from where it is produced in the
body core to the skin
(2) how rapidly heat can then be transferred from the skin to the
surroundings

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How heat is lost from the skin surface?
1. RADIATION
• At normal room temperature, about 60 percent of total
heat loss is by radiation
• Loss of heat by radiation means loss in the form of
infrared heat rays, a type of electromagnetic wave
• The human body radiates heat rays in all directions.
Heat rays are also being radiated from the walls of
rooms and other objects toward the body.

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2. CONDUCTION
• About 3 percent, are normally lost from the body by direct conduction from the surface of
the body to solid objects, such as a chair or a bed
• Loss of heat by conduction to air is 15 percent

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3. CONVECTION
• The removal of heat from the body by convection
air currents is commonly called heat loss by
convection. Actually, the heat must first be
conducted to the air and then carried away by the
convection air currents
• About 15 percent of total heat loss occurs by
conduction to the air and then by air convection
away from the body

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4. EVAPORATION
When water evaporates from the body surface, 0.58
Calorie of heat is lost for each gram of water that
evaporates. Even when a person is not sweating, water
still evaporates insensibly from the skin and lungs at a
rate of about 600 to 700 ml/day. This causes continual
heat loss at a rate of 16 to 19 Calories per hour

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NORMAL THERMOREGULATION
• Thermoregulation is similar to other physiologic control systems in that the
brain uses negative and positive feedback to minimize perturbations from
preset, “normal” values
• The processing of thermoregulatory information occurs in three phases:-
i. Afferent thermal sensing
ii. Central regulation
iii. Efferent responses

15. AFFERENT SENSING
15
Cold receptors
Aδ fibres
Warm receptors
C fibres
Anterior spinothalamic tract
Hypothalamus

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CENTRAL REGULATION
•Temperature is regulated by central structures (primarily the hypothalamus) that
compare integrated thermal inputs from the skin surface, and deep tissues with threshold
temperatures for each thermoregulatory response. Although integrated by hypothalamus,
most thermal information is “preprocessed” in the spinal cord and other parts of the CNS
•The preoptic nuclei in the hypothalamus contains temperature sensitive neurons(cold and
heat sensitive neurons). Preoptic nucleus of anterior hypothalamus integrates input from
peripheral and central thermoreceptors.
•Approximately 80% of this thermal input is derived from core body temperature. There
is evidence however that some thermoregulatory functions occur at the level of the
spinal cord not involving the hypothalamus.
•The interthreshold range (core temperatures not triggering autonomic thermoregulatory
responses) is 0.2 degree centigrade. This range is bounded by the sweating threshold at
its upper end and by vasoconstriction at the lower end.

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18. 18

19. EFFECTOR RESPONSE
Autonomic response
• Determined by the core temperature
Behavioural alteration
• Determined by the peripheral
temperature
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TEMPERATURE DECREASING MECHANISM:- When body is too HOT

22. nerves
Less heat generated
More water covers the
skin.
More evaporation
and hence heat loss
Skin arteries dilate
More blood to the
skin.
Heat loss by More
radiation &
conduction
Muscles of
skin arteriole
walls relax
Sweat
glands
increase
secretionMuscles
reduce
activity
Core body
temperature
>37°C
Hypothalamus
Thermoreceptors
22

23. RESPONSE TO HEAT
1. Hypothalamic mechanism: there is vasodilatation and sweating
starts when temperature exceeds 37.1˚C.
2. Behavioural adjustment:
•Bathing in cold shower.
•Circulation of air by fan
•Voluntary muscular activities diminish and muscle tone is reduced.
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24. RESPONSE TO HEAT
SWEATING:
• Is mediated by post-ganglionic cholinergic fibres which is an active
process where body can dissipate heat in an environment, exceeding
core temperature.
• 0.58 kcal dissipated per gram of evaporated sweat
•Threshold for sweating is temperature>37˚C
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25. RESPONSE TO HEAT
VASODILATION
• Caused by inhibition of sympathetic centers in the posterior
hypothalamus that causes vasoconstriction
•Is an active process mediated by Nitric oxide.
•Has a similar threshold but lower gain when compared to sweating.
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TEMPERATURE INCREASING MECHANISM:- When body is too COLD

27. More heat
generated
Less water covers
the skin.
Less evaporation
Skin arteries
constrict
Less blood to the
skin.
Less radiation &
conduction of heat
Muscles of
skin arteriole
walls
constrict
Sweat
glands
decrease
secretion
Muscles
shivering
Core body
temperature
<37°C
Thermoreceptors
Hypothalamus
27

28. RESPONSE TO COLD
1. Cutaneous vasoconstriction:
•Most consistently used autonomic effector response.
•Threshold for vasoconstriction is 36.5˚C
• Caused by stimulation of posterior hypothalmic sympathetic centers
•First response to a decrease in core temperature below the normal
range(36.5-37.0˚C)
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29. RESPONSE TO COLD
2.Shivering:
•it is involuntary oscillatory, unsynchronised muscular contractions.
•Threshold for shivering is 36 to 36.2˚C
• When the environmental temperature is 23˚C (critical temperature), shivering
begins and increases heat production by 50 to 100%.
•Shivering does not occur in infants and not fully effective in children until they
are seven years old.
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30. RESPONSE TO COLD
3.Piloerection: this leads to standing up of the body hair due
to posterior hypothalamus stimulation. In between the erect
hair, considerable amount of air is trapped and helps to
preserve body temperature.
4.Adipose tissue lipolysis: cause heat generation.
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Non shivering thermogenesis
• Nonshivering thermogenesis, produce heat in response to cold stress. This type of
thermogenesis is stimulated by sympathetic nervous system activation, which releases
norepinephrine and epinephrine, which in turn increase metabolic activity and heat
generation.
• Brown fat, sympathetic nervous stimulation causes liberation of large amounts of heat. This
type of fat contains large numbers of mitochondria and many small globules of fat instead
of one large fat globule. In these cells, the process of oxidative phosphorylation in the
mitochondria is mainly "uncoupled."
• When the cells are stimulated by the sympathetic nerves, the mitochondria produce a large
amount of heat but almost no ATP, so almost all the released oxidative energy immediately
becomes heat.
.

33. THERMOREGULATION IN PAEDIATRICS
Loss of heat in neonates is much greater due to following reasons
i. large surface area to body mass ratio (term neonate 1 and adult 0.4)
ii. Greater thermal conductance (less subcutaneous fat)
iii. Greater evaporative heat loss (less keratin content)

34. THERMOREGULATION IN PAEDIATRICS
• Infants are especially vulnerable to hypothermia because of the large
ratio of body surface area to weight, the thinness of the skin, and a
limited ability to cope with cold stress.
• Cold stress causes increased oxygen consumption and a metabolic
acidosis, particularly in preterm infants because of even thinner skin
and limited fat stores
• The head comprises of 20% surface area and shows highest regional
heat flux. hence covering of head is very important

35. Prevention:
•Heat loss by radiation is decreased by use of double shelled isolates
during transport.
•Heat loss by conduction is reduced by placing baby on a warming
mattress and warming the OT room.
•Heat loss through convection is minimized by keeping the infant in
an incubator, covered by blankets and by covering head.
•Heat lost through evaporation is lessened by humidification of
inspired gases, use of plastic wrap to decrease water loss through
skin.

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THERMOREGULATION DURING GENERALANESTHESIA
• Anesthetic- induced normal autonomic thermoregulatory impairment has a specific form:
 warm-response thresholds are elevated slightly
 cold-response thresholds are markedly reduced
 The inter- threshold range is increased from its normal values near 0.2° C to
approximately 2° C to 4° C

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Interthreshold range is distance between first
cold response(vasoconstriction) and the first
warm response(sweating); temperature with
in this range will not elicit autonomic
thermoregulatory compensation
During GA, the thresholds for
vasoconstriction and non-shivering
thermogenesis are shifted down to
34.5°C and thresholds for vasodilation
and sweating increased to 1°C .
Interthreshold range thus increases
from 0.2°C to 4°C

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RESPONSE THRESHOLD
• Propofol, alfentanil, and dexmedetomidine all produce a slight, linear increase in the
sweating threshold combined with a marked and linear decrease in the vasoconstriction and
shivering thresholds.
• Isoflurane and desflurane also slightly increase the sweating threshold; however, they
decrease the cold-response thresholds non- linearly.
• The volatile anesthetics inhibit vasoconstriction and shivering less than propofol at low
concentrations, but more than propofol at typical anesthetic doses. In all cases (except after
meperidine and nefopam administration), vasoconstriction and shivering decrease
synchronously and maintain their normal approximate 1° C difference.

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The combination of increased
sweating thresholds and
reduced vasoconstriction
thresholds increases the inter
threshold range approximately
20-fold, from its normal value
near 0.2° C to approximately
2° C to 4° C. Temperatures
within this range do not trigger
thermoregulatory defenses; by
definition, patients are
poikilothermic within this
temperature range

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• Isoflurane, desflurane, enflurane, halothane, and the combination of nitrous oxide and
fentanyl decrease the vasoconstriction threshold 2° C to 4° C from its normal value near
approximately 37° C. The dose dependence is nonlinear (i.e., greater concentrations
produce disproportionate threshold reductions). The shivering thresholds decrease
synchronously. In contrast, these drugs increase the sweating threshold only slightly
• Clonidine synchronously decreases cold-response thresholds, while slightly increasing the
sweating threshold. Nitrous oxide decreases the vasoconstriction and shivering thresholds
less than equipotent concentrations of volatile anesthetics. In contrast, midazolam only
slightly impairs thermoregulatory control
• The vasoconstriction threshold is approximately 1° C less in patients 60 to 80 years old
than in those between 30 and 50 years old

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INADVERTANT HYPOTHERMIA DURING GENERAL
ANESTHESIA
• Hypothermia= core body temperature<36 ˚C
1. Mild:- 35˚C -32.2 ˚C
2. Moderate:- 32.2˚C - 28˚C
3. Severe:- <28˚C
• Inadvertent hypothermia during anesthesia is the most common perioperative thermal
disturbance. Hypothermia results from a combination of anesthetic-impaired thermoregulation
and exposure to a cold operating room environment.
• Common in patients at extremes of age, and in those undergoing abdominal surgeries or
procedures of long duration

42. CAUSES OF INTRA-OP HYPOTHERMIA
• OT temperature of <21˚C
• Administration of cold blood or IV fluids
• Prolonged surgery.
• Intraabdominal surgery or intrathoracic surgery due to exposure to large viscera,
body cavities.
• Use of repeated large volumes of irrigating fluids.
• Direct effect of anaesthetic drugs

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Patterns of intraoperative hypothermia

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• General anaesthesia typically results in mild core hypothermia (1–3°C).
• Phase 1 is a rapid reduction in core temperature of 1.0–1.5°C within the first 30–45
min. This is attributable to vasodilatation and other effects of general anaesthesia.
Vasodilatation inhibits normal tonic vasoconstriction resulting in a core-to-peripheral
temperature gradient and redistribution of body heat from core to peripheral tissues.
• Phase 2 is a more gradual, linear reduction in core temperature of a further 1°C over the
next 2–3 h of anaesthesia. This is due to heat loss by radiation, convection and
evaporation exceeding heat gain which is determined by the metabolic rate.
• Phase 3 is a ‘plateau’ phase where heat loss is matched by metabolic heat production.
This occurs when anaesthetised patients become sufficiently hypothermic to reach the
altered threshold for vasoconstriction which restricts the core-to- peripheral heat
gradient.

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HYPOTHERMIA DURING REGIONALANESTHESIA
• Epidural and spinal anesthesia each decrease the thresholds triggering vasoconstriction and shivering
(above the level of the block) approximately 0.6° C
• The vasoconstriction and shivering thresholds are decreased during regional anesthesia, suggesting an
alteration in central, rather than peripheral control. The mechanism by which peripheral administration of
local anesthesia impairs centrally mediated thermoregulation may involve alteration of afferent thermal
input from the legs
• Regional anesthesia blocks all thermal input from blocked regions, which in the typical case is primarily
cold information. The brain may then interpret decreased cold information as relative leg warming. This
appears to be an unconscious process because perceived temperature does not increase. Leg warming
proportionately reduces the vasoconstriction and shivering thresholds. Consistent with this theory, a leg
skin temperature near 38° C is required to produce the reduction in cold-response thresholds in an
unanesthetized subject that is produced by regional anesthesia. Furthermore, reduction in the thresholds is
proportional to the number of spinal segments blocked

46. 46
• Core hypothermia during regional anesthesia may not trigger a perception of cold. The
reason is that thermal perception (behavioral regulation) is largely determined by skin
temperature, rather than core temperature.
• Because redistribution during spinal or epidural anaesthesia is usually confined to the
lower half of the body, the initial core hypothermia is not as pronounced as in general
anaesthesia (approximately 0.5°C).
• Subsequent hypothermia results simply from heat loss exceeding metabolic heat
production. Unlike patients given general anesthesia, however, core temperature does not
necessarily plateau after several hours of surgery. Because the legs constitute the bulk of
the peripheral thermal compartment, an effective plateau cannot develop without
vasoconstriction in the legs and the resulting decrease in cutaneous heat loss and
constraint of metabolic heat to the core

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49. 49
CONSEQUENCES OF MILD INTRAOP HYPOTHERMIA
BENEFITS:-
• Substantial protection against cerebral ischemia and hypoxia is provided by just 1° C to
3° C of hypothermia. Protection initially was thought to result from the approximate
8%/°C linear reduction in tissue metabolic rate. Other actions (e.g., decreased release of
excitatory amino acids) also explain the protective action of hypothermia.
• Rapid induction of hypothermia is thus becoming routine for patients after recovery from
cardiac arrest. The other situation in which therapeutic hypothermia appears beneficial is
in asphyxiated neonates
• The potential protection afforded by mild hypothermia is so great that reduced core
temperature (i.e., ≈34° C) is sometimes used during neurosurgery and other procedures in
which tissue ischemia can be anticipated

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• Hypothermic protection against ischemia may extend to other organs. For example, mild
hypothermia markedly reduced infarct size in experimental studies.
• Acute malignant hyperthermia is more difficult to trigger in mildly hypothermic than in
those kept normothermic. Furthermore, once triggered, the syndrome is less severe. Various
data suggest that active warming should be avoided in patients known to be susceptible to
malignant hyperthermia; instead, these patients should be allowed to become slightly
hypothermic during surgery

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ADVERSE EFFECTS OF HYPOTHERMIA:-
1.Wound infection:-the most common serious complication, due to
• Impaired immune function
• decreased cutaneous blood flow
• decreases wound oxygen delivery
• decreased synthesis of collagen
2.REVERSIBLE COAGULOPATHY
• Hypothermia reduces platelet function and decreases the activation of the coagulation
cascade
• Hypothermia directly impairs enzymes of the coagulation cascade. This is not apparent
during routine coagulation screening because the tests are performed at 37° C
• Increases blood loss and the need for allogenic transfusion during elective primary hip
arthroplasty

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3.PROLONGED RECOVERY
•Mild hypothermia decreases the metabolism of most drugs
•Propofol ---during constant infusion, plasma conc. is 30% greater than normal with a 3 ℃
fall in temperature
•Atracurium---a 3 ℃ reduction in core temp. increase the duration of muscle relaxation by
60 percent
4.DRUG METABOLISM
•Prolongation of NDMR : – vecuronium > atracurium
•Reduction in MAC for volatile anaesthetics
•Hypothermia increases the solubility of volatile anaesthetics

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5.SHIVERING
• The best thermoregulatory response to counteract a decrease in body temperature is through
shivering.
•A 2 fold increase in metabolic heat production can be sustained over increased durations.
•Uncomfortable, psychologically distressing
•May exacerbate wound pain, increase intracranial and intraocular pressure
6.OTHERS
•Altered mental status.
•DIC
•Hypoglycemia
•Decrease renal perfusion.
•Respiratory depression
•Increased pulmonary vascular resistance

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Postanesthetic shivering
• The incidence of postoperative shivering-like tremor reportedly is approximately 40%, but it
now appears to be less as more patients are kept normothermic and opioids are administered
more frequently and in larger doses than in the past
• Shivering is an involuntary, oscillatory muscular activity that augments metabolic heat
production upto 600% above basal level.
• Shivering occurs in approximately 40% of unwarmed patients who are recovering from
general anaesthesia and in about 50% of patients with a core temperature of 35.5 degree
centigrade and in 90% of patients with a core temperature of 34.5 degree centigrade
• The tonic pattern consistently demonstrated the waxing-and-waning pattern of four to eight
cycles/ minute that characterizes normal shivering and apparently it is a simple
thermoregulatory response to intra- operative hypothermia

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• Although the precise etiology of shivering remains unknown, the cause may be
anesthetic-induced disinhibition of normal descending control over spinal reflexes
• Consequences of postanesthetic shivering:-
 Increased oxygen consumption and carbon dioxide production.
 Catecholamine release and Sympathetic stimulation.
 Increased CO and HR and BP
 Increased intraocular pressure, increased intracranial pressure.
 Patient discomfort.

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Prevention:
• Intra-operative use of forced air warming device
• Heating and humidifying inspired gases
• Warmed I.V. fluids
• Covering the skin with surgical drape
• OT room temperature increased to 25˚C

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Treatment:
• Pethidine more effective in the treatment of postoperative shivering than other opioids
• Tramadol 50mg IV
• Clonidine 75 μg IV
• Ketanserine 10mg IV
• Physostigmine 0.04mg/kg IV
• Magnesium sulphate 30mg/kg IV

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INDUCTION OF MILD HYPOTHERMIA
• Hypothermia is occasionally used during neurosurgery or acute myocardial infarction.
Target core temperatures are 32° C to 34° C, and it is thought to be important to reach the
target temperature quickly
• Administration of refrigerated intravenous fluids also is effective and reduces mean body
temperature 0.5° C/L
• Forced-air cooling is easy to implement, but it is relatively slow, taking approximately 2.5
hours to cool neurosurgical patients to 33° C
• Newer circulating-water systems include garment-like covers or “energy exchange pads”
that cover far more skin surface and transfer large amounts of heat and are fairly effective

59. 59
• The best way to induce therapeutic hypothermia rapidly is probably endovascular cooling.
These systems consist of a heat-exchanging catheter, usually inserted into the inferior vena
cava via the femoral artery, and a servo- controller. They can decrease core temperatures at
rates approaching 4° C/hour
• Pharmacologically, the best method so far identified is the combination of buspirone and
meperidine, drugs that synergistically reduce the shivering threshold to approximately 34°
C without provoking excessive sedation or respiratory toxicity.

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DELIBERATE SEVERE INTRAOP HYPOTHERMIA
• Severe hypothermia may be induced deliberately to confer protection against tissue
ischemia, specifically during cardiac surgery and, occasionally, neurosurgery.
• Drugs such as barbiturates and volatile anesthetics provide considerably less protection
than even mild hypothermia
• Cardiac surgery is increasingly performed at either “tepid” temperatures (i.e., 33° C) or
normothermia.
• Outcomes of bypass surgery, whether on or off pump, are improved by maintaining
normothermia or near normothermia. Deep hypothermia (i.e., 18° C) remains routine for
cases of intentional circulatory arrest.

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ORGAN FUNCTION
• Hypothermia decreases whole-body metabolic rate by approximately 8%/°C, to
approximately half the normal rate at 28° C. Whole-body oxygen demand diminishes, and
oxygen consumption in tissues that have higher than normal metabolic rates, such as the
brain, is especially reduced.
• Low metabolic rates allow aerobic metabolism to continue during periods of compromised
oxygen supply; toxic waste production declines in proportion to the metabolic rate. This
decreased metabolic rate certainly contributes to the observed protection against tissue
ischemia, other effects of hypothermia, including “membrane stabilization” and decreased
release of toxic metabolites and excitatory amino acids, appear to be most important.
• Cerebral blood flow also decreases in proportion to metabolic rate during hypothermia
because of an autoregulatory increase in cerebrovascular resistance.

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• Cerebral function is well maintained until core temperatures reach approximately 33° C,
but consciousness is lost at temperatures lower than 28° C
• Primitive reflexes such as gag, pupillary constriction, and monosynaptic spinal reflexes
remain intact until approximately 25° C
• Hypothermic effects on the heart include a decrease in heart rate, increased contractility,
and well-maintained stroke volume. Cardiac output and blood pressure both decrease.
• At temperatures lower than 28° C, sinoatrial pacing becomes erratic, and ventricular
irritability increases. Fibrillation usually occurs between 25° C and 30° C, and electrical
defibrillation is usually ineffective at these temperatures. Because coronary artery blood
flow decreases in proportion to cardiac work, hypothermia per se does not cause
myocardial ischemia.

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• Hypothermia decreases blood flow to the kidneys by increasing renovascular resistance.
• Respiratory strength is diminished at core temperatures less than 33° C, but the
ventilatory CO2 response is minimally affected.
• Hepatic blood flow and function also decrease, thus significantly inhibiting metabolism
of some drugs

64. MAINTAINING INTRA-OP HYPOTHERMIA
Prevention and treatment of mild peri-operative hypothermia
•There are 3 basic strategies
1. Minimizing redistribution of heat
2. Cutaneous warming during anaesthesia
3. Internal warming
64

65. 65
Minimizing redistribution of heat
• The initial 0.5° C to 1.5° C reduction in core temperature is diffcult to prevent
because it results from redistribution of heat from the central thermal
compartment to cooler peripheral tissues .Although redistribution is diffcult to
treat,but it can be prevented
• This may be achieved by:
1. pre-operative warming of peripheral tissue
2. pre-operative pharmacological vasodilatation

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1.Pre-operative warming of peripheral tissue
This reduces the normal core-to-peripheral temperature gradient so that induction of anaesthesia
does not result in the sudden core hypothermia seen in Phase 1. However, to be effective, this
would require subjecting patients to over 1 h of exposure to a source of radiated heat pre-
operatively
2. Pre-operative pharmacological vasodilatation
This facilitates core-to-peripheral redistribution of heat before anaesthesia; it does not
compromise core temperature because patients are not anaesthetised and their thermoregulatory
responses are intact.
Oral nifedipine, taken pre-operatively, has been shown to reduce effectively the extent of the
initial redistribution hypothermia by 50%.

67. 67
Cutaneous warming during anaesthesia
1.Passive insulation
A single layer of any insulator (e.g. space blanket) reduces cutaneous heat loss by
approximately 30% because it traps a layer of still air between it and the skin. Adding
further layers of passive insulation does little or nothing to preserve core temperature.
2.Active warming
Active warming systems maintain normothermia much more effectively than passive
insulation.
-electrically powered air heater fan
- circulating water mattress
- active warming by resistive heating blankets

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1.Fluid warming
Fluids should be warmed to body temperature prior to infusion. The administration of one
litre of fluid at room temperature decreases core temperature by 0.25°C. Warm fluids
should be used when large amounts of fluid or blood replacement are anticipated.
2.Airway humidification
• Airway heating and humidification are more effective in infants and children than in
adults.
• Hygroscopic condenser humidifiers and heat-and-moisture exchanging filters
(“artificial noses”) retain substantial amounts of moisture and heat within the
respiratory system
INTERNAL WARMING

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3.Invasive internal warming techniques
Cardiopulmonary bypass transfers heat at a rate and magnitude not seen in any other situation.
Peritoneal dialysis is also very effective but neither technique is relevant to mild peri-
operative hypothermia.
4.Amino acid infusion
Amino acid infusion during anaesthesia increases metabolic rate and patients are less
hypothermic compared with those given the same volume of crystalloid. This technique has
not gained wide-spread acceptance because of doubts about the effect on cardiac outcome of
increased metabolic rate during anaesthesia.

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HYPERTHERMIAAND FEVER
• Hyperthermia is a generic term simply indicating a core body temperature exceeding
normal values.
• Hyperthermia:- hypothalamic set point is normal but peripheral mechanisms are unable
to maintain body temperature that matches the set point
• Fever occurs when the hypothalamic set point is increased by the action of circulating
pyrogenic cytokines, causing intact peripheral mechanism to conserve and generate heat
until the body temperature increases to elevated set point
• In general, patients with fever and increasing core temperature have constricted
fingertips whereas those with other types of hyperthermia are vasodilated.

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• Causes of perioperative hyperthermia:- dehydration, fever, premedication with
anticholinergic drugs, excessive surgical draping, malignant hyperthermia, thyroid storm,
neuroleptic syndrome, septicaemia, excessive heat delivery from the radiant warmers
• Treatment of hyperthermia depends on the etiology, with the critical distinction being
between fever and the other causes of hyperthermia.
• Treatment of hyperthermia should be directed at prompting heat dissipation and
terminating excessive heat production (e.g dantrolene for malignant hyperthermia)
• Treatment of fever should be directed at identification and eradication of pyrogens and
lowering the thermoregulatory set point with antipyretic drugs such as aspirin,
acetaminophen and cyclooxygenase inhibitors
•

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MALIGNANT HYPERTHERMIA
• Malignant hyperthermia(MH) is a pharmacogenetic clinical syndrome that, in its classic
form, occurs during anesthesia with a volatile halogenated alkane such as halothane and/or
the administration of the depolarizing muscle relaxant succinylcholine.
• MH, first described by Denborough and Lovell in 1960, is an inherited clinical syndrome
characterized by elevated core temperature, tachycardia, tachypnea, hypercarbia, muscle
rigidity and rhabdomyolysis, acidosis and hyperkalemia
• The incidence of fulminant MH was reported to be 1 case per 62,000 anesthetics adminis-
tered when triggering agents were not used, but the number of suspected cases was 1 case
per 4500 anesthetics administered when triggering agents were administered

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Excitation-contraction coupling

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Pathophysiology of malignant hyperthermia
• The most common genetic defect is a defective calcium channel “RYR1” located in the
membrane of the sarcoplasmic reticulum of skeletal muscle.
• More than 70% of MH cases are linked to the RYR1 located on chromosome 19. Less than
2% are related to mutations in the gene coding for dihydropyridine receptor(DHPR) known
as CACNA1s
• The MH syndrome results from an abnormal and uncontrolled elevation of intracellular
calcium levels in skeletal muscle.
• During an MH episode, the mutated RYR1 calcium channel is remained in an open position
, leading to an uncontrolled release of calcium with elevation of intracytoplasmic calcium
levels and continous muscle activation as well as ATP breakdown. ATP breakdown during
this process aggravates heat production further.

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Acute management for MH is as follows:-
1.Discontinue all anesthetic agents and hyperventilate with 100% O2 with a fresh flow to at
least 10 L/min. With increased aerobic metabolism, normal ventilation must increase.
However, CO2 production is also increased because of neutralization of fixed acid by
bicarbonate; hyperventilation removes this additional CO2.
2.Reconstitute dantrolene in sterile water (not saline), and administer rapidly (2.5 mg/kg
intravenously [IV] to a total dose of 10 mg/kg IV) every 5 to 10 minutes until the initial
symptoms subside.
3.Administer bicarbonate (1 to 4 mEq/kg IV) to correct the metabolic acidosis with frequent
monitoring of blood gases and pH.

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4.Control fever by administering iced fluids, cooling the body surface, cooling body
cavities with sterile iced fluids, and, if necessary, using a heat exchanger with a pump
oxygenator. Cooling should be halted when the temperature approaches 38° C to prevent
inadvertent hypothermia.
5.Monitor urinary output, and establish diuresis if urine output is inadequate. Administer
bicarbonate to alkalinize urine to protect the kidney from myoglobinuria- induced renal
failure.
6.Blood gases, electrolytes, CK, temperature, arrhythmia, muscle tone, and urinary output
guide further therapy. Hyperkalemia should be treated with bicarbonate, glucose, and
insulin. Effective doses of dantrolene to reverse MH are the most effective way to lower
serum potassium levels. In severe cases, calcium chloride or calcium gluconate may be
used.
7.Analyze coagulation studies (e.g., international normalized ratio [INR], platelet count,
prothrombin time, fibrinogen, fibrin split degradation products).

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• The clinical course will determine further therapy , dantrolene should probably be
repeated at least every 10 to 15 hours, since its half-life is at least 10 hours .The total dose
of dantrolene that can be used is up to 30 mg/kg .
• Follow the initial dosing regimen with a dose of 1 mg/kg IV or 2 mg/kg orally four times
daily for 3 days. Treatment is extended to 3 days to prevent recurrences.
• The most common side effect of dantrolene is muscle weakness, particularly grip
strength, which usually resolves in 2–4 days after the drug is discontinued

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• Dantrolene is packaged in 20-mg in 70ml vial with sodium hydroxide for a pH of 9.5
(otherwise, it will not dissolve) and 3 g of mannitol, which converts the hypotonic
solution to isotonic.. Dantrolene must be reconstituted in sterile water rather than salt
solutions or it will precipitate. Warming the sterile water to 40°C immediately prior to
mixing can speed up the process and also help drawing the drug in a syringe because the
solution is fairly viscous.
• In 2009, a newer, rapid soluble dantrolene(Ryanodex) is a nanocrystalline dantrone
sodium suspension(DSS) that allow for a much larger dose of 250mg to be dispensed in
a vial that requires only 5ml of sterile water to dissolve it in solution. It reconstitutes in
approximately 20 seconds, which is significantly faster than the older version

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TEMPERATURE MONITORING
INDICATIONS FOR TEMPERATURE MONITORING :-
• The monitoring guidelines of the American Society of Anesthesiologists state that “Every
patient receiving anesthesia shall have temperature monitored when clinically significant
changes in body temperature are intended, anticipated or suspected.”
• Temperature monitoring should be performed whenever large volumes of cold blood
and/or intravenous fluids are administered, when the patient is deliberately cooled and/or
warmed, for pediatric surgery of substantial duration, and in hypothermic or pyrexial
patients or those with a suspected or known temperature regulatory problem such as
malignant hyperthermia.
• Major surgical procedures, especially those involving body cavities, should be
considered a strong indication for temperature monitoring.

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MEASURING DEVICES:-
A.Thermistor:-
A thermistor is composed of a metal (i.e., manganese, nickel, cobalt, iron, or zinc) oxide
sintered into a wire or fused into a rod or bead
• Measure temperature change by changing electrical resistance.
• Resistance of the metal oxide increases as the temperature decreases and vice versa so the
resistance can be converted to a temperature
• Advantages of thermistors include small size, rapid response time, continuous readings,
and sensitivity to small changes in temperature. They are inexpensive. Probes can be
interchangeable and disposable.

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B.Thermocouple :-
A thermocouple consists of an electrical circuit that has two dissimilar metals welded together
at their ends . One of the two metal junctions remains at a constant temperature. The other is
exposed to the area being measured, producing a voltage difference that is measured and
converted to a temperature reading.
Advantages of thermocouples include accuracy, small size, rapid response time, continuous
readings, stability, and probe interchangeability. The materials are inexpensive, so the probes
can be made disposable.

86. C.Liquid crystal probes:-
• They change colour as a function of temperature, used for measuring skin temperature. use
the thermal optic transmission qualities of crystals.
•Advantages:
Commercial kits are available.
Ease of application
Continuous information output
Simplicity in screening for MH
•Disadvantages: need for subjective observer interpretation and the inability to interface with a
recording system. They are less accurate than other devices. Extreme ambient temperature,
humidity, and air movement can cause inaccuracy.

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88. D.Infrared sensors:-
• Detect electromagnetic heat radiation from the body. Used to measure tympanic membrane
temperature.
•Advantage:
Response time is <5 seconds
Very good index of core temperature
Disposable thin plastic film cover reduces risk of infection
• Disadvantage:
Probe must be accurately placed aimed at the tympanic membrane.
Only intermittent spot checks can be made
Bleeding can occur from around tympanic membrane
Trauma to the tympanic membrane

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90. SITES FOR MONITORING
CENTRAL/ CORE
•Oesophageal
•Pulmonary artery
•Tympanic membrane
•Nasopharynx

91. SITES FOR MONITORING
PERIPHERAL:
•Oral
•Axilla
•Skin
OTHERS:
•Rectum
•Bladder

92. CORE TEMPERATURE MONITORING
•Oesophageal: probe is placed 20cm below from pharyngo-
esophageal junction, which shows accurate core-temperature because
of closer proximity with heart and descending aorta.
•Pulmonary artery: temperature probes can be incorporated into the
pulmonary artery (Swan-Ganz) catheters. Electrical safety standards
have to be met with respect to leakage currents.

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94. CORE TEMPERATURE MONITORING
•Tympanic Membrane: it approximates brain temperature better than
any other tissue. The blood supply to tympanic membrane is by
internal carotid artery which also supplies hypothalamus.
•Nasopharynx: The temperature is in close approximation with brain
temperature. the danger of causing epistaxis is a consideration
especially in patients who are on anticoagulants.

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96. CORE TEMPERATURE MONITORING
•Jugular Bulb: done by inserting 5 French Swan-Ganz catheter into
jugular bulb. Gold standard in cardiac bypass surgery.
•Spinal subarachnoid space: in neurosurgical and cardiovascular
procedures. Intrathecal temperature with a thermocouple incorporated
catheter in subarachnoid space.

97. PERIPHERAL MONITORING
•Oral: The location of temperature probe is sublingual on either side
of frenulum, affected by cold and hot food, mouth breathing, crying.
•Axilla: 1˚C lower than core temperature.
•Skin: it is not a reliable index of core temperature because the degree
of vasoconstriction or vasodilatation can significantly affect the
measurements obtained.

98. •Bladder: It is reliable index of core temperature, during steady state. But
drawback is that it is dependant on the urine output.
•Rectum: It is an adequate indicator of core temperature, during steady state. But
drawback is that it seldom reflects the actual core temperature in anaesthetised
patient when temperature changes are relatively rapid.

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GUIDELINES
Thermal management guidelines as proposed by “Outcome Research Consortium”
1) Core body temperature should be measured or reliably estimated in most patients given
general anesthesia for more than 30 minutes.
2) Temperature should also be measured or reliably estimated during regional anesthesia when
changes in body temperature are intended, anticipated, or suspected.
3) Unless hypothermia is specifically indicated (e.g., for protection against ischemia), efforts
should be made to maintain intra-operative core temperature >36°C.

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• According to ASA Standards, “every patient receiving anesthesia shall have
temperature monitored when clinically significant changes in body
temperature are intended, anticipated or suspected”.
• For office-based sedation, regional anesthesia, or general anesthesia, the
ASA also requires that "the body temperature of pediatric patient shall be
measured continuously.

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•Temperature monitoring should always be directed toward the core temperature. —
Preventive measures should be instituted against inadvertent hypothermia.
•In adult patients who are at risk for malignant hyperthermia or who are under general
anesthesia for a period exceeding 30 minutes, temperature should be monitored.
•Ambient temperature should be kept between 21 degrees C and 24 degrees C for adults; and
between 21 degrees C and 26 degrees C for children, with a relative humidity level of 40-60
percent.
•Warming of infusion fluids to 38 degrees C is always recommended in children. In adults, the
use of this preventive measure should be assessed on a case-by-case basis.
Italian society of Anesthesiologists recommends:-

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•Active external warming systems are always recommended. — The forced-air
warming system is always recommended for use in children by reason of its
proven effectiveness, even under conditions of reduced usable surface.
•In adults, the use of a forced-air warming system should be considered when
the intervention will last longer than 30 minutes or when the core body
temperature falls below 36 degrees C.
•The patient should never be discharged from the recovery room until
normothermia is restored, or if signs of hypothermia are present.

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In 2007, American college of cardiology and American heart
association published a guidelines for care of patients undergoing
non-cardiac surgery. They recommended that “Maintenance of body
temperature in a normothermic range is recommended for most
procedures other than during periods in which mild hypothermia is
intended to provide organ protection (e.g, during high aortic cross-
clamping)”

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SUMMARY
• General anesthetics decrease the thresholds (triggering core temperatures) for vasoconstriction and shivering by 2° C to 3° C.
• Anesthetic-induced impairment of thermoregulatory control, combined with a cool operating room environment, makes most
patients hypothermic.
• The major initial cause of hypothermia in most patients is core-to-peripheral redistribution of body heat.
• Neuraxial anesthesia impairs both central and peripheral thermoregulatory control and is associated with substantial
hypothermia.
• Body temperature should be monitored in patients having surgery lasting more than 30 minutes, and core temperature should
be maintained at 36° C or higher whenever possible. Forced-air warming currently offers the best combination of high efficacy,
low cost and remarkable safety
• Malignant hyperthermia (MH) is an anesthetic-related disorder of increased skeletal muscle metabolism. It is an inherited
condition in an autosomal dominant pattern.
• Dantrolene significantly attenuates myoplasmic calcium (Ca2+) concentrations and thereby allows restoration of normal
metabolism, with a reversal of the signs of metabolic stimulation

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REFERENCES:-
1. Miller’s Anesthesia 8th edition & 6th edition
2. Guyton and Hall textbook of Medical Physiology 12th edition
3. Wylie and Churchill-Davidson's A Practice of Anesthesia 7th edition
4. Yao & Artusio’s Anesthesiology, 8th edition
5. Morgan and Mikhail's Clinical Anesthesiology, 5th edition
6. Stoelting pharmacology and physiology, south asia edition, 5th edition
7. Understanding Anesthesia Equipment(Dorsch and Dorsch), 5th edition
8. Harrison’s principle of internal medicine, 19th edition
9. David A Kirkbride, Donal J Buggy; Thermoregulation and mild peri‐operative hypothermia, BJA CEPD
Reviews, Volume 3, Issue 1, 1 February 2003, Pages 24–28
10. Luthra A, Dube SK, Kumar S, Goyal K. Intraoperative hyperthermia: Can surgery itself be a cause?.
Indian J Anaesth 2016;60:515-7
11. Bhattacharya PK, Bhattacharya L, Jain RK, Agrarwal RC. Post anaesthesia shivering (PAS): A
review. Indian J Anaesth. 2003;47(2):88–93
12. http://www.or.org/temp_monitoring.htm
13. ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery:
a report of the American College of Cardiology/American Heart Association Task Force on Practice
Guidelines

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THANK YOU