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 The thermoregulatory system maintains core body temperature
which is approximately 37° C.
 mild hypothermia under anaesthesia
(1) triples the incidence of morbid cardiac outcomes,
(2) triples the incidence of surgical wound infections,
(3) increases surgical blood loss and the need for
allogeneic transfusions by approximately 20%, and
(4) prolongs postanesthesia recovery and the duration of
hospitalization.
 Thermoregulation is based on multiple,
redundant signals from nearly every type of
tissue.
 The processing of thermoregulatory
information occurs in three phases:
1. afferent thermal sensing,
2. central regulation
3. efferent responses
 Each thermoregulatory effector has its own
threshold and gain, so an orderly progression of
responses and response intensities occurs in
proportion to need.
 Effectors determine the ambient temperature
range that the body will tolerate while maintaining
normal core temperature.
 When specific effector mechanisms are inhibited
(e.g., when shivering is prevented by
administration of muscle relaxants), the tolerable
range is decreased.
 Quantitatively, behavioral regulation is the most
important effector mechanism.
 Behavioral compensations include
› dressing appropriately
› modifying environmental temperature
› assuming positions that appose skin surfaces
› moving voluntarily
 Infants regulate their temperatures remarkably
well.
 In contrast, advanced age, infirmity, or
medications can diminish the efficacy of
thermoregulatory responses and increase the risk
of hypothermia.
 Cutaneous vasoconstriction is the most
consistently used autonomic effector mechanism.
 Total digital skin blood flow devided into
› Nutritional- mostly capillaries (10µ)
› Thermoregulatory- A-V shunts(100µ)
 The A-V shunts do not have nutritional role and
are regulated by local alpha adrenergic system
 Shunts receive 10% of cardiac output and
increase mean BP by 15 mmHg on constriction
 Control of blood flow through the arteriovenous
shunts tends to be “on” or “off.”
 Nonshivering thermogenesis increases metabolic
heat production without producing mechanical work.
 It doubles heat production in infants, but increases it
only slightly in adults.
 The intensity of nonshivering thermogenesis
increases in linear proportion to the difference
between mean body temperature and its threshold.
 Sources
› Skeletal muscle
› brown fat tissue
 The metabolic rate in both tissues is controlled
primarily by norepinephrine release from adrenergic
nerve terminals and is further mediated locally by an
uncoupling protein.
 Sustained shivering augments metabolic heat
production by 50% to 100% in adults. This
increase is small compared with that produced by
exercise (500%) and is thus surprisingly
ineffective.
 Shivering does not occur in newborn infants & not
fully effective in children.
 The rapid tremor (≤250 Hz) and unsynchronized
muscular activity of thermogenic shivering suggest
no central oscillator.
 However, superimposed on the fast activity is
usually a slow (four to eight cycles/ minute),
synchronous “waxing-and-waning” pattern that
presumably is centrally mediated.
 Sweating is mediated by postganglionic,
cholinergic nerves. It is an active process that is
prevented by nerve block or atropine
administration.
 Even untrained individuals can sweat up to 1
L/hour, and athletes can sweat at twice that rate.
 Sweating is the only mechanism by which the
body can dissipate heat(0.58 kcal/gm of
evapourated sweat) in an environment
exceeding core temperature.
 Active vasodilation is apparently mediated by nitric
oxide. Because active vasodilation requires intact
sweat gland function, it also is largely inhibited by
nerve block.
 The threshold for active vasodilation usually is
similar to the sweating threshold, but the gain may
be less.
 During extreme heat stress, blood flow through
the top millimeter of skin can reach 7.5 L/minute—
equaling the entire resting cardiac output.
 Consequently, maximum cutaneous vasodilation
usually is delayed until core temperature is clearly
higher than that provoking maximum sweating
intensity
 The thresholds vary daily in both sexes
(circadian rhythm) and monthly in women by
approximately 0.5° C.
 Both sweating and vasoconstriction thresholds are
0.3° C to 0.5° C higher in women than in men,
even during the follicular phase of the monthly
cycle (first 10 days).
 Differences are even greater during the luteal
phase.
 Exercise, food intake, infection, hypo and
hyperthyroidism, anesthetic and other drugs
(alcohol, sedatives, and nicotine), and cold and
warm adaptation alter threshold temperature
 Control of autonomic responses is 80%
determined by thermal input from core structures
,but input controlling behavioral responses is
derived from the skin surface.
 The interthreshold range (core temperatures not
triggering ANS responses) is a few tenths of a
degree centigrade (0.2˚C).This range is
bounded by the sweating threshold at its
upper end and by vasoconstriction at the
lower end.
 The slope of response intensity versus core
temperature defines the gain of a
thermoregulatory response.
 Response intensity no longer increasing with
further deviation in core temperature identifies the
maximum intensity.
 The mechanism of threshold fixation is unknown
but appears to be mediated by
› norepinephrine,
› dopamine,
› 5-hydroxytryptamine,
› acetylcholine,
› prostaglandin E1,
› and neuropeptides.
Core temperature (Tc) is maintained within the range of temperatures bound by the core
threshold temperatures for shivering and sweating, defined as the interthreshold zone, or
thermoeffector threshold zone.
Igor B. Mekjavic, and Ola Eiken J Appl Physiol
2006;100:2065-2072
DECREASED
MUSCLE MASS
NEUROMUSCULAR
DISEASE
MUSCLE
RELAXANTS
INHIBIT
SHIEVERING
INCREASE
MINIMUM
TOLERABLE
AMBIENT
TEMPERATU
RE
ANTICHOLINERGIC
DRUGS
INHIBIT SWEATING
DECREASE
MAXIMUM
TOLERABLE
TEMPERATURE
 Behavioral regulation is not relevant during general
anesthesia because patients are unconscious and
frequently paralyzed.
 All general anesthetics markedly impair normal autonomic
thermoregulatory control.
 Anesthetic induced impairment has a specific form: warm-
response thresholds are elevated slightly, whereas cold-
response thresholds are markedly reduced.
 Consequently, the interthreshold range is increased from
its normal values near 0.2° C to approximately 2° C to 4°
C.
 The gain and maximum intensity of some responses
remain normal, whereas other responses are reduced by
general anesthesia
Anaesthetic drugs Threshold of
sweating
Threshold of
vasoconsrtiction/
shievering
Propofol
Alfentanil
Dexmedetomidine
Slight increase marked decrease
(linear )
Isoflurane
Desflurane
Enflurane
Halothane
N2O+fentanyl
Slight increase Decrease
(non-linear)
N2O only - Slight decrease
Clonidine slight increase Decrease
Painfiul stimuli - Slight increase
In all cases (except after meperidine and Nefopam administration), vasoconstriction and
shivering decrease synchronously and maintain their normal approximate 1° C
difference.
 Thermoregulatory vasoconstriction is
comparably impaired in infants, children, and
adults when isoflurane or halothane is given
 In contrast, the vasoconstriction threshold is
approximately 1° C less in patients 60 to 80
years old than in those between 30 and 50
years old
 Non shivering thermogenesis fails to increase
the metabolic rate in infants anesthetized with
propofol .
Drugs Gain Max. shievering intensity
Meperidine
Alfentanil
Normal Normal
N2O Normal Decreased
Isoflurane Not easily determined Decreased
Shivering is rare during surgical doses of general
anesthesia. This finding is consistent with the shivering
threshold being roughly 1° C less than the
vasoconstriction threshold.
 Sweating is the best preserved major
thermoregulatory defense during anesthesia. Not only
is the threshold only slightly increased, but the gain
and maximum intensity remain normal.
 In contrast, the thresholds for vasoconstriction and
shivering are markedly reduced, and furthermore, the
efficacy of these responses is diminished even after
being activated.
Anaesthetic agents Gain Max intensity of
sweating
Isoflurane
Enflurane
Normal Normal
Desflurane Decreased Normal
 Inadvertent hypothermia is by far the most
common perioperative thermal disturbance during
anesthesia.
Hypothermia
anesthetic-impaired
thermoregulation
cold operating room
environment.
HEAT TRANSFER
 Heat can be transferred from a patient to the
environment four ways:
(1) Radiation- major type of heat loss
mechanism
(2) Convection : second most important mechanism
(3) Conduction:
(4) evaporation:
Heat loss (radiation) (T1- T2)
Heat loss (Convection) √ air speed
Conductive loss (T1-T2)
 An initial rapid decrease in core temperature is
followed by a slow, linear reduction in core
temperature. Finally, core temperature stabilizes and
subsequently remains virtually unchanged
 Anesthetic induced vasodilation increases cutaneous
heat loss only slightly.
 Anesthetics reduce the metabolic rate 20% to 30%.
 However, even the combination of increased heat
loss and reduced heat production is insufficient to
explain the 0.5° C to 1.5° C decrease in core
temperature usually observed during the first hour of
anesthesia
 The first hour decrease is
explained by core-
peripheral temperature
gradient.
 Core temperature
represents only
approximately half
the body mass (mostly
the trunk and head);
the remaining mass is
typically 2° C to 4° C
cooler than the core.
 This core-to-peripheral tissue temperature
gradient is normally maintained by tonic
thermoregulatory vasoconstriction.
 Anesthetic-induced vasodilation allows core heat
to flow peripherally. This flow warms the arms and
legs, but it does so at the expense of the core .
 This redistribution reduces core temperature
depends on the core-to-peripheral tissue
temperature gradient at the time of induction.
 Temperature usually decreases in a slow, linear
fashion for 2 to 4 hours. This reduction results
simply from heat loss exceeding metabolic heat
production.
 After 3 to 4 hours of anesthesia, core
temperature usually reaches a plateau.The core
temperature plateau may simply represent a
thermal steady state (heat production equaling
heat loss).
 Distribution of metabolic heat (which largely is
produced centrally) is restricted to the core
compartment, thus maintaining its temperature.
Peripheral tissue temperature continues to
decrease because it is no longer being supplied
with sufficient heat from the core.
 Autonomic thermoregulation is impaired during
regional anesthesia resulting in intraoperative core
hypothermia.
 The vasoconstriction and shivering thresholds are
reduced by regional anesthesia and they are
further reduced by adjuvant drugs and advanced
age.
 Even once triggered, the gain and maximum
response intensity of shivering are approximately
half normal.
 Finally, behavioral thermoregulation is impaired.
 The result is that cold defenses are triggered at a
lower temperature than normal during regional
anesthesia, defenses are less effective once
triggered, and patients frequently do not recognize
that they are hypothermic.
 Epidural and spinaL anesthesia each decrease the
thresholds triggering vasoconstriction and shivering
(above the level of the block) approximately 0.6° C.
 This decrease is due to central effect than due to
recirculation of neuraxially administered local
anesthetic because impairment is similar during
epidural and spinal anesthesia.
 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.
 Given that skin temperature is an important input to
the thermoregulatory control system, 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 in an unanesthetized subject that is
produced by regional anesthesia.
 Reduction in the thresholds is proportional to
number of spinal segments blocked.
 Neuraxial anesthesia prevents vasoconstriction
and shivering in blocked regions.
 epidural anesthesia decreases the maximum
intensity of shivering & the gain of shivering,
 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.
 vasoconstriction, once triggered, produces a
core temperature plateau during general
anesthesia.
 In regional anesthesia,the vasoconstriction
threshold is centrally impaired but
vasoconstriction in the legs is directly
prevented by nerve block.
 Because the legs constitute the bulk of the
peripheral thermal compartment, an effective
plateau cannot develop without
vasoconstriction in the legs.
SHIVERING
 Shivering-like tremor,typical in neuraxial
anesthesia, is preceded by core hypothermia and
vasoconstriction (above the level of the block).
 Electromyographic analysis indicates that the
tremor has the waxing-and waning pattern of 4
to 8 cycles/minute that characterizes normal
shivering.
 The temperature of injected local anesthetic does
not influence the incidence of shivering during
major conduction anesthesia.
 The risk of shivering during neuraxial anesthesia
is markedly diminished by maintaining strict
normothermia
 Perianesthetic hypothermia produces potentially severe
complications, as well as distinct benefits.
BENEFITS
 Protection was thought to result from the approximate
8%/°C linear reduction in tissue metabolic rate.
 Rapid induction of hypothermia is now becoming routine
for patients after recovery from cardiac arrest.
 therapeutic hypothermia appears beneficial is in
asphyxiated neonates.
 The reduced core temperature (i.e 34°C) is sometimes
used during neurosurgery and other procedure in which
tissue ischemia can be anticipated.
 Transfusion requirement and blood loss are
significantly increased.
 Hospitalization prolonged &wound healing
delayed
 Enzymes of the coagulation cascade & platelet
function are impaired.:- defective coagulation
 Reversal from anaesthesia prolonged
 Metabolism of drugs:- markedly decreased
› Vecuronium -action is prolonged(doubled),
› propofol - plasma concentration is increased by 30%,
› volatile anaesthetics:- MAC is reduced by 5%/°c
› Atracurium :- not much affected
› neostigmine:- onset is delayed
 Infection of wound:- due to
› directly impairing immune function
› by triggering thermoregulatory vasoconstriction that, in
turn, decreases wound oxygen delivery.
 Abnormal haemodynamics :- elevating blood
pressure, heart rate, and plasma catecholamine
concentrations due to thermal discomfort.
 INCIDENCE – 40%
 Now decreased due to usage of opiods and
normothermic measures
 It increases intraocular,intracranial pressures and
also aggravates wound pain
 Determinants of shivering risk
› young age
› core temperature.
Much postoperative tremor is simply normal shivering
 Postanesthetic tremor causes
› uninhibited spinal reflexes,
› pain,
› decreased sympathetic activity,
› pyrogen release,
› adrenal suppression,
› respiratory alkalosis,
› intraoperative hypothermia.
Although the precise etiology is unknown, the cause may
be anesthetic-induced disinhibition of normal
descending control over spinal reflexes.
 Postoperative tremor has the following patterns:
(1) a tonic pattern resembling normal shivering,
typically having a waxing and- waning component of
4 to 8 cycles/minute;
(2) a phasic, 5- to 7-Hz bursting pattern resembling
pathologic clonus.
 The tonic pattern is simple thermoregulatory
response to intraoperative hypothermia.
 In contrast, the clonic pattern is not a normal
component of thermoregulatory shivering and
appears specific to recovery from volatile
anesthetics.
 Postanesthetic shivering treatment
› skin surface warming :- It contributes only 20% to
control of shivering and available skin surface warmers
increase mean skin temperature only a few degrees
centigrade.
› Drugs
1. clonidine (75 μg IV),
2. ketanserin(10mg IV),
3. tramadol,physostigmine (0.04 mg/kg IV),
4. nefopam (0.15 mg/kg),
5. Dexmedetomidine,
6. magnesium sulfate (30 mg/kg IV).
7. Meperidine
 Heat production during anesthesia is approximately
0.8 kcal/kg/hour. Because the specific heat of the
human body is approximately 0.83 kcal/kg
 body temperature decreases approximately
1°C/hour when heat lost to the environment is twice
metabolic production.
 Normally, approximately 90% of metabolic heat is lost
through the skin surface.
 During anesthesia, additional heat is also lost directly
from surgical incisions and by administration of cold
intravenous fluids.
 Although redistribution is difficult to treat , it can be
prevented.
 Skin surface warming before induction of
anesthesia does not much increase core
temperature but it does increase body heat
content.
 Most of the increase is in the legs, the most
important component of the peripheral thermal
compartment.
 Active pre-warming for 30 minutes likely
prevents considerable redistribution.
 Less than 10% of metabolic heat production is lost
via the respiratory tract due to heating and
humidifying inspiratory gases.
 Airway heating and humidification
-minimally influence core temperature.
-more effective in infants and children than in
adults.
 Hygroscopic condenser humidifiers and heat-
and-moisture exchanging (HME) filters (“artificial
noses”) retain substantial amounts of moisture
and heat within the respiratory system.
 One unit of refrigerated blood or 1 L of crystalloid
solution administered at room temperature each
decreases mean body temperature approximately
0.25° C.
 Fluid warmers minimize these losses.
 Most warmers allow fluid to cool in the tubing
between the heater and the patient, this cooling is
of little consequence in adults.
 Special high-volume systems with powerful
heaters and little resistance to flow are available
when large amounts of fluid must be administered
quickly
 Operating room temperature determines the rate
at which metabolic heat is lost by radiation and
convection from the skin and by evaporation from
within surgical incisions.
 Room temperatures exceeding 23° C are
generally required to maintain normothermia
 Infants may require ambient temperatures
exceeding 26° C to maintain normothermia.
Passive warming Active warming
•easiest & commomnly used
method
•Insulator readily available in
most operating rooms include
•cotton blankets,
•surgical drapes,
•plastic sheeting,
•reflective composites
(“space blankets”).
•A single layer of each reduces
heat loss approximately 30%,
•For patients undergoing large
operations
•Warming methods
•1. Circulating watersystem:
more effective—and safer—
when it is placed over patients,
it can almost completely
eliminate metabolic heat loss
•2. forced-air systems: it
completely eliminate heat loss
from the skin surface
Cutaneous warming
 Hypothermia is occasionally used during neurosurgery or
acute myocardial infarction. Typically, target core
temperatures are 32° C to 34° C.
 Methods
1. Forced Air cooling: easy to implement . Takes approx 2.5
hrs to cool neurosurgical patients to 33°C.
2. Passive Body cooling :Immersion in cold water is the
quickest noninvasive method of actively cooling patients.
3. Circulating-water systems: It includes garment-like
covers or “energy exchange pads” that cover far more
skin surface and transfer large amounts of heat and are
effective.
4. Pharmacological/ Drugs :
combination of buspirone and meperidine
combination of dexmedetomidine and meperidine
5. Endovascular cooling:
› The best way to induce hypothermia
› These systems consist of a heat-exchanging
catheter, usually inserted into the inferior vena cava
via the femoral vein, and a servo controller.
6.Cold IV Fluids: Administration of refrigerated
intravenous fluids also is effective and reduces
mean body temperature 0.5° C/L.
 Hypothermia decreases whole-body metabolic rate by
approximately 8%/°C,to approximately half the normal
rate at 28° C.
 Whole-body oxygen demand diminishes.
 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.
 CNS changes
 Cerebral function is well maintained until core
temperatures reach approximately 33° C
 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.
 Nerve conduction decreases, but peripheral
muscle tone increases, resulting in rigidity and
myoclonus at temperatures near 26° C.
 Somatosensory- and auditory-evoked potentials
are temperature dependent, but they are not
significantly modified at core temperatures of 33°
C or higher.
 CVS changes
 decrease in heart rate,
 increased contractility,
 Cardiac output and blood pressure both
decrease. But stroke volume is well-maintained.
 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.
 Renal changes
 renal blood flow decreases by increasing
renovascular resistance.
 Inhibition of tubular absorption maintains normal
urinary volume.
 As temperature decreases, reabsorption of
sodium and potassium is progressively inhibited,
causing antidiuretic hormone–mediated “cold
diuresis.”
 Despite increased excretion of these ions, plasma
electrolyte concentrations usually remain normal.
 Kidney functions return to normal when patients
are rewarmed.
 Hyperthermia is a generic term simply indicating
a core body temperature exceeding normal
values.
 In contrast, fever is a regulated increase in the
core temperature targeted by the
thermoregulatory system.
 In general, patients with fever and increasing core
temperature have constricted fingertips whereas
those with other types of hyperthermia are
vasodilated.
 Treatment of hyperthermia
 The first- and second-line treatments are
1. amelioration of the underlying cause
2. administration of antipyretic medications.
 The second strategy often fails or is only partially
effective, perhaps because some fever is
mediated by mechanisms that bypass
conventional antipyretics.
 In these patients, third-line treatment is most likely
to be implemented: active cooling. Active cooling
of febrile patients should thus be instituted with
considerable care, to be sure that the benefits
outweigh the stress induced by activation of
thermoregulatory defenses.
HYPERTHERMIA DURING EPIDURAL
ANALGESIA
 Hyperthermia frequently complicates epidural
analgesia for labor and delivery,as well as in
nonpregnant postoperative patients.
 This is especially the case when labor is long,
more than 8 hours
 A clinical consequence of this hyperthermia is that
women given epidural analgesia are more often
given antibiotics than are women treated
conventionally, and their infants are more
commonly treated for sepsis.
 Core temperature measurements are used to monitor
› intraoperative hypothermia,
› prevent overheating
› facilitate detection of malignant hyperthermia.
 Muscle or skin surface temperatures may be used
› to evaluate vasomotion,
› to ensure the validity of peripheral neuromuscular monitoring.
 Both core and skin surface temperature measurements
are required
› to determine the thermoregulatory effects of different anesthetic
drugs.
› to estimate mean body temperature& body heat content.
THERMOMETERS
 Mercury-in-glass thermometers are slow and
cumbersome and thus have universally been
replaced with electronic systems.
 The most common electronic thermometers are
thermistors and thermocouples.
 Deep tissue thermometers are based on actively
reducing cutaneous heat flux to zero.
 Infrared monitors that extrapolate tympanic
membrane temperature from outer ear
temperature are unreliable, as are infrared
systems that scan forehead Skin.
 Normal range
 Oral temp- 35.6˚C -37.8˚ C
 Core temp- 0.5˚ C higher than oral
temperature
 Scrotal temp- 32 ˚C
 Circadian fluctuation – 0.5 -0.7 ˚C
 Menstual variation – 0.5 ˚C
 Rectal temperature is considered an
“intermediate” temperature in deliberately cooled
patients.
 During cardiac surgery, bladder temperature is
equal to rectal temperature (and therefore
intermediate) when urine flow is low, but it is equal
to pulmonary artery temperature (and thus core)
when flow is high.
 The adequacy of rewarming is best evaluated by
considering both “core” and “intermediate”
temperature
1. to facilitate detection of malignant hyperthermia.
2. to quantify hyperthermia and hypothermia.
 The most common perioperative thermal disturbance
is inadvertent hypothermia.
 Conditions
› general anesthesia exceeding 30 minutes in duration
› surgery lasting longer than 1 hour
› during regional anesthesia in which patients likely to
become hypothermic ,example body cavity surgery.
 The objectives of temperature monitoring and perioperative
thermal management are to detect thermal disturbances and to
maintain appropriate body temperature during anesthesia.
 Available data suggest the following guidelines:
1. Core body temperature should be measured in most patients
given general anesthesia for longer than 30 minutes.
2. Temperature should also be measured 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
intraoperative core temperature higher than 36° C.
 AHA & American College of Cardiology
recommend 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).”
 Based on evidence of hypothermia induced
complications,maintaining perioperative
normothermia became one of the first
anesthetic “pay-for-performance”measures.
THANK YOU
 Guyton & Hall medical physiology,13th
edition,Chapter 74,p911-922
 Miller Anaesthesia 8th edition p1335, p1622-
1644
 http://www.ncbi.nlm.nih.gov/pubmed/204214
77
 Internet sources

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Physiology of thermoregulation & monitering of temperature

  • 1.
  • 2.  The thermoregulatory system maintains core body temperature which is approximately 37° C.  mild hypothermia under anaesthesia (1) triples the incidence of morbid cardiac outcomes, (2) triples the incidence of surgical wound infections, (3) increases surgical blood loss and the need for allogeneic transfusions by approximately 20%, and (4) prolongs postanesthesia recovery and the duration of hospitalization.
  • 3.  Thermoregulation is based on multiple, redundant signals from nearly every type of tissue.  The processing of thermoregulatory information occurs in three phases: 1. afferent thermal sensing, 2. central regulation 3. efferent responses
  • 4.
  • 5.
  • 6.
  • 7.
  • 8.
  • 9.  Each thermoregulatory effector has its own threshold and gain, so an orderly progression of responses and response intensities occurs in proportion to need.  Effectors determine the ambient temperature range that the body will tolerate while maintaining normal core temperature.  When specific effector mechanisms are inhibited (e.g., when shivering is prevented by administration of muscle relaxants), the tolerable range is decreased.
  • 10.  Quantitatively, behavioral regulation is the most important effector mechanism.  Behavioral compensations include › dressing appropriately › modifying environmental temperature › assuming positions that appose skin surfaces › moving voluntarily  Infants regulate their temperatures remarkably well.  In contrast, advanced age, infirmity, or medications can diminish the efficacy of thermoregulatory responses and increase the risk of hypothermia.
  • 11.  Cutaneous vasoconstriction is the most consistently used autonomic effector mechanism.  Total digital skin blood flow devided into › Nutritional- mostly capillaries (10µ) › Thermoregulatory- A-V shunts(100µ)  The A-V shunts do not have nutritional role and are regulated by local alpha adrenergic system  Shunts receive 10% of cardiac output and increase mean BP by 15 mmHg on constriction  Control of blood flow through the arteriovenous shunts tends to be “on” or “off.”
  • 12.  Nonshivering thermogenesis increases metabolic heat production without producing mechanical work.  It doubles heat production in infants, but increases it only slightly in adults.  The intensity of nonshivering thermogenesis increases in linear proportion to the difference between mean body temperature and its threshold.  Sources › Skeletal muscle › brown fat tissue  The metabolic rate in both tissues is controlled primarily by norepinephrine release from adrenergic nerve terminals and is further mediated locally by an uncoupling protein.
  • 13.  Sustained shivering augments metabolic heat production by 50% to 100% in adults. This increase is small compared with that produced by exercise (500%) and is thus surprisingly ineffective.  Shivering does not occur in newborn infants & not fully effective in children.  The rapid tremor (≤250 Hz) and unsynchronized muscular activity of thermogenic shivering suggest no central oscillator.  However, superimposed on the fast activity is usually a slow (four to eight cycles/ minute), synchronous “waxing-and-waning” pattern that presumably is centrally mediated.
  • 14.  Sweating is mediated by postganglionic, cholinergic nerves. It is an active process that is prevented by nerve block or atropine administration.  Even untrained individuals can sweat up to 1 L/hour, and athletes can sweat at twice that rate.  Sweating is the only mechanism by which the body can dissipate heat(0.58 kcal/gm of evapourated sweat) in an environment exceeding core temperature.  Active vasodilation is apparently mediated by nitric oxide. Because active vasodilation requires intact sweat gland function, it also is largely inhibited by nerve block.
  • 15.  The threshold for active vasodilation usually is similar to the sweating threshold, but the gain may be less.  During extreme heat stress, blood flow through the top millimeter of skin can reach 7.5 L/minute— equaling the entire resting cardiac output.  Consequently, maximum cutaneous vasodilation usually is delayed until core temperature is clearly higher than that provoking maximum sweating intensity
  • 16.  The thresholds vary daily in both sexes (circadian rhythm) and monthly in women by approximately 0.5° C.
  • 17.  Both sweating and vasoconstriction thresholds are 0.3° C to 0.5° C higher in women than in men, even during the follicular phase of the monthly cycle (first 10 days).  Differences are even greater during the luteal phase.  Exercise, food intake, infection, hypo and hyperthyroidism, anesthetic and other drugs (alcohol, sedatives, and nicotine), and cold and warm adaptation alter threshold temperature  Control of autonomic responses is 80% determined by thermal input from core structures ,but input controlling behavioral responses is derived from the skin surface.
  • 18.  The interthreshold range (core temperatures not triggering ANS responses) is a few tenths of a degree centigrade (0.2˚C).This range is bounded by the sweating threshold at its upper end and by vasoconstriction at the lower end.
  • 19.
  • 20.  The slope of response intensity versus core temperature defines the gain of a thermoregulatory response.  Response intensity no longer increasing with further deviation in core temperature identifies the maximum intensity.  The mechanism of threshold fixation is unknown but appears to be mediated by › norepinephrine, › dopamine, › 5-hydroxytryptamine, › acetylcholine, › prostaglandin E1, › and neuropeptides.
  • 21. Core temperature (Tc) is maintained within the range of temperatures bound by the core threshold temperatures for shivering and sweating, defined as the interthreshold zone, or thermoeffector threshold zone. Igor B. Mekjavic, and Ola Eiken J Appl Physiol 2006;100:2065-2072
  • 23.  Behavioral regulation is not relevant during general anesthesia because patients are unconscious and frequently paralyzed.  All general anesthetics markedly impair normal autonomic thermoregulatory control.  Anesthetic induced impairment has a specific form: warm- response thresholds are elevated slightly, whereas cold- response thresholds are markedly reduced.  Consequently, the interthreshold range is increased from its normal values near 0.2° C to approximately 2° C to 4° C.  The gain and maximum intensity of some responses remain normal, whereas other responses are reduced by general anesthesia
  • 24. Anaesthetic drugs Threshold of sweating Threshold of vasoconsrtiction/ shievering Propofol Alfentanil Dexmedetomidine Slight increase marked decrease (linear ) Isoflurane Desflurane Enflurane Halothane N2O+fentanyl Slight increase Decrease (non-linear) N2O only - Slight decrease Clonidine slight increase Decrease Painfiul stimuli - Slight increase
  • 25. In all cases (except after meperidine and Nefopam administration), vasoconstriction and shivering decrease synchronously and maintain their normal approximate 1° C difference.
  • 26.  Thermoregulatory vasoconstriction is comparably impaired in infants, children, and adults when isoflurane or halothane is given  In contrast, the vasoconstriction threshold is approximately 1° C less in patients 60 to 80 years old than in those between 30 and 50 years old  Non shivering thermogenesis fails to increase the metabolic rate in infants anesthetized with propofol .
  • 27. Drugs Gain Max. shievering intensity Meperidine Alfentanil Normal Normal N2O Normal Decreased Isoflurane Not easily determined Decreased Shivering is rare during surgical doses of general anesthesia. This finding is consistent with the shivering threshold being roughly 1° C less than the vasoconstriction threshold.
  • 28.  Sweating is the best preserved major thermoregulatory defense during anesthesia. Not only is the threshold only slightly increased, but the gain and maximum intensity remain normal.  In contrast, the thresholds for vasoconstriction and shivering are markedly reduced, and furthermore, the efficacy of these responses is diminished even after being activated. Anaesthetic agents Gain Max intensity of sweating Isoflurane Enflurane Normal Normal Desflurane Decreased Normal
  • 29.  Inadvertent hypothermia is by far the most common perioperative thermal disturbance during anesthesia. Hypothermia anesthetic-impaired thermoregulation cold operating room environment.
  • 30. HEAT TRANSFER  Heat can be transferred from a patient to the environment four ways: (1) Radiation- major type of heat loss mechanism (2) Convection : second most important mechanism (3) Conduction: (4) evaporation: Heat loss (radiation) (T1- T2) Heat loss (Convection) √ air speed Conductive loss (T1-T2)
  • 31.  An initial rapid decrease in core temperature is followed by a slow, linear reduction in core temperature. Finally, core temperature stabilizes and subsequently remains virtually unchanged  Anesthetic induced vasodilation increases cutaneous heat loss only slightly.  Anesthetics reduce the metabolic rate 20% to 30%.  However, even the combination of increased heat loss and reduced heat production is insufficient to explain the 0.5° C to 1.5° C decrease in core temperature usually observed during the first hour of anesthesia
  • 32.  The first hour decrease is explained by core- peripheral temperature gradient.  Core temperature represents only approximately half the body mass (mostly the trunk and head); the remaining mass is typically 2° C to 4° C cooler than the core.
  • 33.  This core-to-peripheral tissue temperature gradient is normally maintained by tonic thermoregulatory vasoconstriction.  Anesthetic-induced vasodilation allows core heat to flow peripherally. This flow warms the arms and legs, but it does so at the expense of the core .  This redistribution reduces core temperature depends on the core-to-peripheral tissue temperature gradient at the time of induction.  Temperature usually decreases in a slow, linear fashion for 2 to 4 hours. This reduction results simply from heat loss exceeding metabolic heat production.
  • 34.  After 3 to 4 hours of anesthesia, core temperature usually reaches a plateau.The core temperature plateau may simply represent a thermal steady state (heat production equaling heat loss).  Distribution of metabolic heat (which largely is produced centrally) is restricted to the core compartment, thus maintaining its temperature. Peripheral tissue temperature continues to decrease because it is no longer being supplied with sufficient heat from the core.
  • 35.  Autonomic thermoregulation is impaired during regional anesthesia resulting in intraoperative core hypothermia.  The vasoconstriction and shivering thresholds are reduced by regional anesthesia and they are further reduced by adjuvant drugs and advanced age.  Even once triggered, the gain and maximum response intensity of shivering are approximately half normal.
  • 36.
  • 37.  Finally, behavioral thermoregulation is impaired.  The result is that cold defenses are triggered at a lower temperature than normal during regional anesthesia, defenses are less effective once triggered, and patients frequently do not recognize that they are hypothermic.  Epidural and spinaL anesthesia each decrease the thresholds triggering vasoconstriction and shivering (above the level of the block) approximately 0.6° C.  This decrease is due to central effect than due to recirculation of neuraxially administered local anesthetic because impairment is similar during epidural and spinal anesthesia.
  • 38.  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.  Given that skin temperature is an important input to the thermoregulatory control system, 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 in an unanesthetized subject that is produced by regional anesthesia.
  • 39.  Reduction in the thresholds is proportional to number of spinal segments blocked.  Neuraxial anesthesia prevents vasoconstriction and shivering in blocked regions.  epidural anesthesia decreases the maximum intensity of shivering & the gain of shivering,  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.
  • 40.
  • 41.  vasoconstriction, once triggered, produces a core temperature plateau during general anesthesia.  In regional anesthesia,the vasoconstriction threshold is centrally impaired but vasoconstriction in the legs is directly prevented by nerve block.  Because the legs constitute the bulk of the peripheral thermal compartment, an effective plateau cannot develop without vasoconstriction in the legs.
  • 42. SHIVERING  Shivering-like tremor,typical in neuraxial anesthesia, is preceded by core hypothermia and vasoconstriction (above the level of the block).  Electromyographic analysis indicates that the tremor has the waxing-and waning pattern of 4 to 8 cycles/minute that characterizes normal shivering.  The temperature of injected local anesthetic does not influence the incidence of shivering during major conduction anesthesia.  The risk of shivering during neuraxial anesthesia is markedly diminished by maintaining strict normothermia
  • 43.  Perianesthetic hypothermia produces potentially severe complications, as well as distinct benefits. BENEFITS  Protection was thought to result from the approximate 8%/°C linear reduction in tissue metabolic rate.  Rapid induction of hypothermia is now becoming routine for patients after recovery from cardiac arrest.  therapeutic hypothermia appears beneficial is in asphyxiated neonates.  The reduced core temperature (i.e 34°C) is sometimes used during neurosurgery and other procedure in which tissue ischemia can be anticipated.
  • 44.  Transfusion requirement and blood loss are significantly increased.  Hospitalization prolonged &wound healing delayed  Enzymes of the coagulation cascade & platelet function are impaired.:- defective coagulation  Reversal from anaesthesia prolonged
  • 45.  Metabolism of drugs:- markedly decreased › Vecuronium -action is prolonged(doubled), › propofol - plasma concentration is increased by 30%, › volatile anaesthetics:- MAC is reduced by 5%/°c › Atracurium :- not much affected › neostigmine:- onset is delayed  Infection of wound:- due to › directly impairing immune function › by triggering thermoregulatory vasoconstriction that, in turn, decreases wound oxygen delivery.  Abnormal haemodynamics :- elevating blood pressure, heart rate, and plasma catecholamine concentrations due to thermal discomfort.
  • 46.  INCIDENCE – 40%  Now decreased due to usage of opiods and normothermic measures  It increases intraocular,intracranial pressures and also aggravates wound pain  Determinants of shivering risk › young age › core temperature. Much postoperative tremor is simply normal shivering
  • 47.  Postanesthetic tremor causes › uninhibited spinal reflexes, › pain, › decreased sympathetic activity, › pyrogen release, › adrenal suppression, › respiratory alkalosis, › intraoperative hypothermia. Although the precise etiology is unknown, the cause may be anesthetic-induced disinhibition of normal descending control over spinal reflexes.
  • 48.  Postoperative tremor has the following patterns: (1) a tonic pattern resembling normal shivering, typically having a waxing and- waning component of 4 to 8 cycles/minute; (2) a phasic, 5- to 7-Hz bursting pattern resembling pathologic clonus.  The tonic pattern is simple thermoregulatory response to intraoperative hypothermia.  In contrast, the clonic pattern is not a normal component of thermoregulatory shivering and appears specific to recovery from volatile anesthetics.
  • 49.  Postanesthetic shivering treatment › skin surface warming :- It contributes only 20% to control of shivering and available skin surface warmers increase mean skin temperature only a few degrees centigrade. › Drugs 1. clonidine (75 μg IV), 2. ketanserin(10mg IV), 3. tramadol,physostigmine (0.04 mg/kg IV), 4. nefopam (0.15 mg/kg), 5. Dexmedetomidine, 6. magnesium sulfate (30 mg/kg IV). 7. Meperidine
  • 50.  Heat production during anesthesia is approximately 0.8 kcal/kg/hour. Because the specific heat of the human body is approximately 0.83 kcal/kg  body temperature decreases approximately 1°C/hour when heat lost to the environment is twice metabolic production.  Normally, approximately 90% of metabolic heat is lost through the skin surface.  During anesthesia, additional heat is also lost directly from surgical incisions and by administration of cold intravenous fluids.
  • 51.  Although redistribution is difficult to treat , it can be prevented.  Skin surface warming before induction of anesthesia does not much increase core temperature but it does increase body heat content.  Most of the increase is in the legs, the most important component of the peripheral thermal compartment.  Active pre-warming for 30 minutes likely prevents considerable redistribution.
  • 52.  Less than 10% of metabolic heat production is lost via the respiratory tract due to heating and humidifying inspiratory gases.  Airway heating and humidification -minimally influence core temperature. -more effective in infants and children than in adults.  Hygroscopic condenser humidifiers and heat- and-moisture exchanging (HME) filters (“artificial noses”) retain substantial amounts of moisture and heat within the respiratory system.
  • 53.  One unit of refrigerated blood or 1 L of crystalloid solution administered at room temperature each decreases mean body temperature approximately 0.25° C.  Fluid warmers minimize these losses.  Most warmers allow fluid to cool in the tubing between the heater and the patient, this cooling is of little consequence in adults.  Special high-volume systems with powerful heaters and little resistance to flow are available when large amounts of fluid must be administered quickly
  • 54.  Operating room temperature determines the rate at which metabolic heat is lost by radiation and convection from the skin and by evaporation from within surgical incisions.  Room temperatures exceeding 23° C are generally required to maintain normothermia  Infants may require ambient temperatures exceeding 26° C to maintain normothermia.
  • 55. Passive warming Active warming •easiest & commomnly used method •Insulator readily available in most operating rooms include •cotton blankets, •surgical drapes, •plastic sheeting, •reflective composites (“space blankets”). •A single layer of each reduces heat loss approximately 30%, •For patients undergoing large operations •Warming methods •1. Circulating watersystem: more effective—and safer— when it is placed over patients, it can almost completely eliminate metabolic heat loss •2. forced-air systems: it completely eliminate heat loss from the skin surface Cutaneous warming
  • 56.
  • 57.  Hypothermia is occasionally used during neurosurgery or acute myocardial infarction. Typically, target core temperatures are 32° C to 34° C.  Methods 1. Forced Air cooling: easy to implement . Takes approx 2.5 hrs to cool neurosurgical patients to 33°C. 2. Passive Body cooling :Immersion in cold water is the quickest noninvasive method of actively cooling patients. 3. Circulating-water systems: It includes garment-like covers or “energy exchange pads” that cover far more skin surface and transfer large amounts of heat and are effective.
  • 58. 4. Pharmacological/ Drugs : combination of buspirone and meperidine combination of dexmedetomidine and meperidine 5. Endovascular cooling: › The best way to induce hypothermia › These systems consist of a heat-exchanging catheter, usually inserted into the inferior vena cava via the femoral vein, and a servo controller. 6.Cold IV Fluids: Administration of refrigerated intravenous fluids also is effective and reduces mean body temperature 0.5° C/L.
  • 59.  Hypothermia decreases whole-body metabolic rate by approximately 8%/°C,to approximately half the normal rate at 28° C.  Whole-body oxygen demand diminishes.  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.
  • 60.  CNS changes  Cerebral function is well maintained until core temperatures reach approximately 33° C  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.  Nerve conduction decreases, but peripheral muscle tone increases, resulting in rigidity and myoclonus at temperatures near 26° C.  Somatosensory- and auditory-evoked potentials are temperature dependent, but they are not significantly modified at core temperatures of 33° C or higher.
  • 61.  CVS changes  decrease in heart rate,  increased contractility,  Cardiac output and blood pressure both decrease. But stroke volume is well-maintained.  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.
  • 62.  Renal changes  renal blood flow decreases by increasing renovascular resistance.  Inhibition of tubular absorption maintains normal urinary volume.  As temperature decreases, reabsorption of sodium and potassium is progressively inhibited, causing antidiuretic hormone–mediated “cold diuresis.”  Despite increased excretion of these ions, plasma electrolyte concentrations usually remain normal.  Kidney functions return to normal when patients are rewarmed.
  • 63.  Hyperthermia is a generic term simply indicating a core body temperature exceeding normal values.  In contrast, fever is a regulated increase in the core temperature targeted by the thermoregulatory system.  In general, patients with fever and increasing core temperature have constricted fingertips whereas those with other types of hyperthermia are vasodilated.
  • 64.  Treatment of hyperthermia  The first- and second-line treatments are 1. amelioration of the underlying cause 2. administration of antipyretic medications.  The second strategy often fails or is only partially effective, perhaps because some fever is mediated by mechanisms that bypass conventional antipyretics.  In these patients, third-line treatment is most likely to be implemented: active cooling. Active cooling of febrile patients should thus be instituted with considerable care, to be sure that the benefits outweigh the stress induced by activation of thermoregulatory defenses.
  • 65. HYPERTHERMIA DURING EPIDURAL ANALGESIA  Hyperthermia frequently complicates epidural analgesia for labor and delivery,as well as in nonpregnant postoperative patients.  This is especially the case when labor is long, more than 8 hours  A clinical consequence of this hyperthermia is that women given epidural analgesia are more often given antibiotics than are women treated conventionally, and their infants are more commonly treated for sepsis.
  • 66.  Core temperature measurements are used to monitor › intraoperative hypothermia, › prevent overheating › facilitate detection of malignant hyperthermia.  Muscle or skin surface temperatures may be used › to evaluate vasomotion, › to ensure the validity of peripheral neuromuscular monitoring.  Both core and skin surface temperature measurements are required › to determine the thermoregulatory effects of different anesthetic drugs. › to estimate mean body temperature& body heat content.
  • 67. THERMOMETERS  Mercury-in-glass thermometers are slow and cumbersome and thus have universally been replaced with electronic systems.  The most common electronic thermometers are thermistors and thermocouples.  Deep tissue thermometers are based on actively reducing cutaneous heat flux to zero.  Infrared monitors that extrapolate tympanic membrane temperature from outer ear temperature are unreliable, as are infrared systems that scan forehead Skin.
  • 68.  Normal range  Oral temp- 35.6˚C -37.8˚ C  Core temp- 0.5˚ C higher than oral temperature  Scrotal temp- 32 ˚C  Circadian fluctuation – 0.5 -0.7 ˚C  Menstual variation – 0.5 ˚C
  • 69.
  • 70.  Rectal temperature is considered an “intermediate” temperature in deliberately cooled patients.  During cardiac surgery, bladder temperature is equal to rectal temperature (and therefore intermediate) when urine flow is low, but it is equal to pulmonary artery temperature (and thus core) when flow is high.  The adequacy of rewarming is best evaluated by considering both “core” and “intermediate” temperature
  • 71. 1. to facilitate detection of malignant hyperthermia. 2. to quantify hyperthermia and hypothermia.  The most common perioperative thermal disturbance is inadvertent hypothermia.  Conditions › general anesthesia exceeding 30 minutes in duration › surgery lasting longer than 1 hour › during regional anesthesia in which patients likely to become hypothermic ,example body cavity surgery.
  • 72.  The objectives of temperature monitoring and perioperative thermal management are to detect thermal disturbances and to maintain appropriate body temperature during anesthesia.  Available data suggest the following guidelines: 1. Core body temperature should be measured in most patients given general anesthesia for longer than 30 minutes. 2. Temperature should also be measured 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 intraoperative core temperature higher than 36° C.
  • 73.  AHA & American College of Cardiology recommend 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).”  Based on evidence of hypothermia induced complications,maintaining perioperative normothermia became one of the first anesthetic “pay-for-performance”measures.
  • 75.  Guyton & Hall medical physiology,13th edition,Chapter 74,p911-922  Miller Anaesthesia 8th edition p1335, p1622- 1644  http://www.ncbi.nlm.nih.gov/pubmed/204214 77  Internet sources

Notas do Editor

  1. Core temperature (Tc) is maintained within the range of temperatures bound by the core threshold temperatures for shivering and sweating, defined as the interthreshold zone, or thermoeffector threshold zone. The responses of sweating and shivering are characterized by the Tc values at which they are activated and the gain of the response. Nonthermal factors may influence both of these characteristics, namely the threshold and gain. Changes in the former would alter the magnitude of the interthreshold zone, whereas changes in the gain would alter the intensity of the response.