Temperature regulation and monitoring

Mammals and birds are homeothermic They require a nearly constant internal body temperature When internal temperature deviate significantly from normal : metabolic functions deteriorate death Thermoregulatory system maintains core body temperature within 0.2 C of normal (37) /.Anesthetic induced inhibition of thermoregulation /.cold operating room /.cold operating room /.unwarmed patiients /.unwarmed patiients Hypothermic Hypothermic

Mild hypothermia 1-2 C 1) Triples(3) morbid cardiac outcom 2) Triples(3) surgical wound infection 3) Prolonges recovery time -hospitalization 4) Increases surgical blood loss and the need for allogeneic transfusion by about 20%

Normal thermoregulation 1. Afferent thermal sensing(input) 2. Central regulation 3. Efferent response

Afferent input Cold-sensitive cells are anatomically and physiologically distinct from those that detect warmth Cold: A delta nerve fibers warm: unmyelinated C fibers (pain)

Most ascending thermal information traverses the spinothalamic tracts in the anterior spinal cord, but no single spinal tract is critical for conveying thermal information. Consequently, the entire anterior cord must be destroyed to ablate thermoregulatory responses.

1 /Hypothalamus 20% total thermal input 2 /Other parts of brain to the 3 /Spinal cord (ant) central regulatory system 4 /Deep abdominal and thoracic tissues 5 /Skin surface

Central control Temperature is regulated by central structures (primarily the hypothalamus) that compare integratd thermal inputs from the skin surface, neuraxis, and deep tissues with threshold temperatures for each thermoregulatory response. Most thermal information is "preprocessed" in the spinal cord and other parts of the central nervous system.

The slope of response intensity versus core temperature defines the gain of a thermoregulatory response. and time-dependent effects This system of thresholds and gains is a model for a thermoregulatory system that is further complicated by interactions between other regulatory responses (i.e., vascular volume control) and time-dependent effects.

How the body determines absolute threshold temperatures is unknown, but the mechanism appears to be mediated by norepinephrine, dopamine, S-hydroxytryptamine, acetylcholine, prostaglandin E" and neuropeptides.

Thresholds vary daily in both sexes (circadian rhythm) and monthly in women by approximately 0.5°C. Exercise, food intake, infection, hypothyroidism and hyperthyroidism, anesthetic and other drugs (including alcohol, sedatives, and nicotine), and cold and warm adaptation alter threshold temperatures.

Control of autonomic responses is approximately 80% determined by thermal input from core structures (Fig) In contrast, a large fraction of the input controlling behavioral responses is derived from the skin.

interthreshold range The interthreshold range (core temperatures not triggering autonomic thermoregulatory responses) is only 0.2°C. This range is bounded by the sweating threshold at its upper end and by vasoconstriction at the lower end.

Both sweating and vasoconstriction thresholds are 0.3°C to 0.5 C higher in women than men, even during the follicular phase of the monthly cycle (first 10 days). Differences are even greater during the luteal phase.

Central thermoregulatory control is apparently intact even in somewhat premature infants. In contrast, thermoregulatory control is sometimes impaired in the elderly."

Efferent responses The body responds to thermal perturbations (body temperatures differing from the appropriate threshold) by activating effector mechanisms that increase metabolic heat production or alter environmental heat loss.

Each thermoregulatory effector has its own threshold and gain, so there is an orderly progression of responses and response intensities in proportion to need.

In general, energy-efficient effectors such asvasoconstriction are maximized before metabolically costly responses such as shivering are initiated.

Effectors determine the ambient temperature range that the body will tolerate while maintaining a normal core temperature.

When specific effector mechanisms are inhibited (e.g., shivering prevented by the administration of muscle relaxants), the tolerable range is decreased. Still, temperature will remain normal unless other effectors can not compensate for the imposed stress.,behavioral regulation (e.g., dressing appropriately, modifying the environmental temperature, assuming positions that oppose skin surfaces and voluntary movement) is the most important effector mechanism.

Infants regulate their temperatures remarkably well. In contrast, advanced age, infirmity, or medications can diminish the efficacy of thermoregulatory responses & increase the risk of hypothermia. Mr: min tolarable ambient temperature (inhibit shivering) Anticholinergics: max tolarable teper… (inhibit sweating)

Cutaneous vasoconstriction is the most consistently used autonomic effector mechanism. Metabolic heat is lost primarily through convection and radiation from the skin surface, and vasoconstriction reduces this loss. Total digital skin blood flow is divided into nutritional (mostly capillary) and thermoregulatory (mostly arteriovenous shunt) components. The arteriovenous shunts are anatomically and functionally distinct from the capillaries supplying nutritional blood to the skin (thus vasoconstriction does not compromise the needs of peripheral tissues).

Control of blood flow through arteriovenous shunts tends to be "on" or "off.“ In other words, the gain of this response is high. Local alfa-adrenergic sympathetic nerves mediate constriction in the thermoregulatory arteriovenous shunts, and flow is minimally affected by circulating catecholamines. 10% of cardiac output traverses arteriovenous shunts; consequently, shunt vasoconstriction increases mean arterial pressure approximately 15 mm Hg.

Nonshivering thermogenesis increases metabolic heat production without producing mechanical work. It doubles heat production in infants but increases it only slightly in adults.

Skeletal muscle and brown fat tissue are the major sources of nonshivering heat in adults. 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 50% to 100% in adults. This increase is small in comparison to that produced by exercise (which can, at least briefly, increase metabolism 500%)and is thus surprisingly ineffective. Shivering does not occur in newborn infants and is probably not fully effective until children are several years old

Sweating is mediated by postganglionic cholinergic Nerves. It is thus an active process that is prevented by nerve block or atropine administration. Sweating is the only mechanism by which the body can dissipate heat in an environment exceeding core temperature. fortunately, the process is remarkably effective, with 0.58 kcal of heat dissipated per gram of evaporated sweat.

Active vasodilation is apparently mediated by nitric oxide.

Active vasodilation requires intact sweat gland function, so it is also largely inhibited by nerve blocks. The threshold for active vasodilation is usually similar to the sweating threshold, but the gain may be less. maximum cutaneous vasodilation is generally delayed until core temperature is well above that provoking the maximum sweating intensity.

THERMOREGULATION DURING GENERAL ANESTHESIA

Behavioral regulation is not relevant during general anesthesia because patients are unconscious and frequently paralyzed. All general anesthetics tested thus far markedly impair normal autonomic thermoregulatory control. Anesthetic-induced impairment has a specific form: warmresponse thresholds are elevated slightly whereas coldresponse thresholds are markedly reduced.

the interthreshold range is increased from its normal values near 0.3°C to approximately 2°C to 4°c. The gain and maximum intensity of some responses remain normal, whereas others are reduced by general anesthesia.

Response Thresholds Propofol, alfentanil, and dexmedetomidine all produce a slight linear increase in the sweating threshold a marked linear decrease in the vasoconstriction and shivering thresholds. Isoflurane and desflurane also slightly increase the sweating threshold; they decrease the cold-response thresholds nonlinearly.

the volatile anesthetics inhibit vasoconstriction and shivering (less than propofol does at low concentrations, but more than propofol does at typical anesthetic doses.) In all cases (except during meperidine and nefopam administration), vasoconstriction and shivering decrease synchronously and thus maintain their normal approximate 1°C difference. In all cases (except during meperidine and nefopam administration), vasoconstriction and shivering decrease synchronously and thus maintain their normal approximate 1°C difference..

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

Halothane, enflurane,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. However, the effect of these drugs on sweating or shivering remains unknown. Cl0nidine 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 do.

The only sedative or anesthetic drug tested that minimally influences thermoregulatory control is midazolam. Painful stimulation slightly increases vasoconstriction thresholds. thresholds will be somewhat lower when surgical pain is prevented by simultaneous local or regional anesthesia.

Responses in Infants and the Elderly Thermoregulatory vasoconstriction is comparably impaired in infants, children, and adults given isoflurane or halothane (Fig. 40_4). In contrast, the vasoconstriction threshold is about 1°C less in patients aged 60 to 80 years than in those between 30 and 50 years old (Fig. 40_5).

Thermoregulatory vasoconstriction is comparably impaired in infants, children, and adults given isoflurane or halothane.

the vasoconstriction threshold is about 1°C less in patients aged 60 to 80 years than in those between 30 and 50 years old

Nonshivering thermogenesis does not occur in anesthetized aduIts, which is unsurprising because this response is not particularly important in unanesthetized adults. In contrast to adult humans, nonshivering thermogenesis is an important thermoregulatory response in animals and human infants. However, nonshivering thermogenesis in animals is inhibited by volatile anesthetics and it fails to increase the metabolic rate in infants anesthetized with propofol.

Gain and Maximum Response Intensity Both the gain and maximum intensity of sweating remain normal during isoflurane and enflurane anesthesia. The gain of arteriovenous shunt vasoconstriction is reduced threefold during desflurane anesthesia,even though the maximum vasoconstriction intensity remains normal.

Shivering is rare during surgical doses of general anesthesia, its threshold being roughly 1°C less than the vasoconstriction threshold. (Vasoconstriction usually prevents additional hypothermia, so even unwarmed patients rarely become cold enough to shiver.) shivering can be induced by sufficient active cooling.

Gain and maximum shivering intensity remain normal during both meperidine and alfentanil administration Gain also remains nearly intact during nitrous oxide administration, although maximum intensity is reduced. Isoflurane changes the macroscopic pattern of shivering to such an extent that it is no longer possible to easily determine gain. The drug does, however, reduce maximum shivering intensity.

Sweating appears to be the thermoregulatory defense that is best preserved during anesthesia. Not only is the threshold only slightly increased, but the gain and maximum intensity are also well preserved. In contrast, the thresholds for vasoconstriction and shivering are markedly reduced, and furthermore, these responses are less effective than normal even after being activated.

DEVELOPMENT OF HYPOTHERMIA DURING GENERAL ANESTHESIA Inadvertent hypothermia during anesthesia is by far the most common perioperative thermal disturbance. Hypothermia results from a combination of anesthetic impaired thermoregulation and exposure to a cold operating room environment. Of these two causes, impaired thermoregulation is much more important. Of these two causes, impaired thermoregulation is much more important.

Heat Transfer Heat can be transferred from a patient to the environment in four ways: (1) radiation, (3) convection, (2) conduction (4) evaporation Among these mechanisms, radiation and convection contribute most to perioperative heat loss. All surfaces with a temperature above absolute zero radiate heat; similarly, all surfaces absorb radiant heat from surrounding surfaces. It is likely that radiation is the major type of heat loss in most surgical patients.

Conductive heat loss is proportional to the temperature difference between two adjacent surfaces.. In general, conductive losses are negligible during surgery because patients usually only directly contact the foam pad (an excellent thermal insulator) covering most operating room tables.

convective loss is usually the second most important mechanism by which heat is transferred from patients to the environment Sweating increases cutaneous evaporative loss enormously but is rare during anesthesia. In the absence of sweating, evaporative loss from the skin surface is limited to less than 10% of metabolic heat production in adults. In contrast, infants lose a higher fraction of their metabolic heat from transpiration of water through thin skin. The problem becomes especially acute in premature infants, who may lose one fifth of their metabolic heat production via transcutaneous evaporation. [.

only trivial amounts of heat are lost from the respiratory system. Evaporation inside surgical wounds may contribute substantially to total heat loss but has never been quantified in humans. Evaporation inside surgical wounds may contribute substantially to total heat loss but has never been quantified in humans.

Patterns of Intraoperative Hypothermia Hypothermia during general anesthesia develops with a characteristic pattern. 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.

Hypothermia during general anesthesia develops with a characteristic pattern. An initial rapid decrease in core temperature results from a core-to-peripheral redistribution of body heat. This is followed by a slow, linear reduction in core temperature that results simply from heat loss exceeding heat production. Finally, core temperature stabilizes and subsequently remains virtually unchanged. This plateau phase may be a passive thermal steady state or result when sufficient hypothermia triggers thermoregulatory vasoconstriction. Results are presented as means ± SD.

Thermoregulatory vasoconstriction during anesthesia significantly decreases cutaneous heat loss,but this decrease alone is usually insufficient to produce a thermal steady state. Furthermore, neither adults nor infants appear to be able to increase intraoperative heat production in response to hypothermia.

An additional mechanism must therefore contribute to the core temperature plateau. Evidence suggests that a primary factor is constraint of metabolic heat to the core thermal compartment. In this scenario, the distribution of metabolic heat (which is largely produced centrally) is restricted to the core compartment to maintain its temperature

Peripheral tissue temperature, in contrast, continues to decrease because it is no longer being supplied with sufficient heat from the core. core temperature plateau resulting from thermoregulatory vasoconstriction is thus not a thermal steady state, and body heat content continues to decrease even though core temperature remains nearly constant.

NEURAXIAL ANESTHESIA Autonomic thermoregulation is impaired during regional anesthesia, and the result is typically intraoperative core hypothermia. this hypothermia is often not perceived by patients, but it nonetheless triggers shivering. The result is frequently a potentially dangerous clinical paradox: a shivering patient who denies feeling cold.

Epidural anesthesia and spinal anesthesia each decrease the thresholds triggering vasoconstriction and shivering (above the level of the block) about 0.6°C. this decrease does not result from recirculation of neuraxially administered local anesthetic because: 1- the impairment is similar during epidural and spinal anesthesia.

2-lidocaine administered intravenously in doses producing plasma concentrations similar to those occurring during epidural anesthesia has no thermoregulatory effect 3- neuraxial administration of 2-chloroprocaine, a local anesthetic that has a plasma half-life near 20 seconds, also impairs thermoregulatory control.

The vasoconstriction and shivering thresholds are comparably 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

The key factor here is that tonic cold signals dominate thermal input at leg skin temperatures in typical operating room environments. Regional anesthesia blocks all thermal input from the blocked regions, which in the typical case is primarily cold information. Regional anesthesia blocks all thermal input from the blocked regions, which in the typical case is primarily cold information.

The brain may then interpret decreased cold information as relative leg warming. Because 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 same reduction in cold-response thresholds in an unanesthetized subject as produced by regional anesthesia. Moreover, the reduction in thresholds is proportional to the number of spinal segments blocked Moreover, the reduction in thresholds is proportional to the number of spinal segments blocked

Because neuraxial anesthesia prevents vasoconstriction and shivering in blocked regions, it is not surprising that epidural anesthesia decreases the maximum intensity of shivering. However, epidural anesthesia also reduces the gain of shivering, which suggests that the regulatory system is unable to compensate for lower body paralysis. Thermoregulatory defenses, once triggered, are thus less effective than usual during regional anesthesia.

Neuraxial anesthesia is frequently supplemented with sedative and analgesic medications that impair thermoregulatory control. Such inhibition may be severe when combined with the intrinsic impairment produced by regional anesthesia and other factors, including advanced age and preexisting illness.

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 rather than core temperature. During regional anesthesia, core hypothermia is accompanied by a real increase in skin temperature The reason is that thermal perception (behavioral regulation) is largely determined by skin rather than core temperature. During regional anesthesia, core hypothermia is accompanied by a real increase in skin temperature

The result is typically a perception of continued or increased warmth accompanied by activation of autonomic thermoregulatory responses including shivering neuraxial anesthesia inhibits numerous aspects of thermoregulatory control. neuraxial anesthesia inhibits numerous aspects of thermoregulatory control.

The vasoconstriction and shivering thresholds are reduced by regional anesthesia and further reduced by adjuvant drugs and advanced age. Even once triggered, the gain and maximum response intensity of shivering are about half-normal.

Finally 1) cold defenses are triggered at a lower temperature than normal during regional anesthesia, 1) cold defenses are triggered at a lower temperature than normal during regional anesthesia, 2) defenses are less effective once triggered, and 2) defenses are less effective once triggered, and 3) patients frequently do not recognize that they are hypothermic. 3) patients frequently do not recognize that they are hypothermic.

Because core temperature monitoring remains rare during regional anesthesia, substantial hypothermia often goes undetected in these patients. Because core temperature monitoring remains rare during regional anesthesia, substantial hypothermia often goes undetected in these patients.

Heat Balance

Hypothermia is common during regional anesthesia and may be nearly as severe as during general anesthesia. Core temperature typically decreases O.5 to 1.0°C shortly after induction of anesthesia. However, the vasodilation induced by regional anesthesia only slightly increases cutaneous heat loss. Furthermore, metabolic heat production remains constant or increases because of shivering thermogenesis. This rapid decrease in core temperature, similar to that noted after induction of general anesthesia also results from an internal core-to-peripheral redistribution of body heat.

As during general anesthesia, redistribution hypothermia during regional anesthesia can be minimized by cutaneous warming before induction.

Unlike patients given general anesthesia, however, core temperature does not necessarily plateau after several hours of surgery. Not only is the vasoconstriction threshold centrally impaired by regional anesthesia, but more importantly, vasoconstriction in the legs is also directly prevented by nerve block.

core temperature during combined regional/general anesthesia continues to decrease throughout surgery. core temperature monitoring and thermal management are particularly important in patients given simultaneous regional and general anesthesia.

Shivering Shivering-like tremor in volunteers given neuraxial anesthesia is always preceded by core hypothermia and vasoconstriction (above the level of the block). At least in nonpregnant individuals-that the temperature of injected local anesthetic does not influence the incidence of shivering during major conduction anesthesia.

Shivering during neuraxial anesthesia can sometimes be treated by warming sentient skin. Because the entire skin surface contributes 20% to thermoregulatory controls and the lower part of the body contributes about 1O%, sentient skin warming is likely to compensate for only small reductions in core temperature The same drugs that are effective for postanesthetic tremor are also useful for shivering during regional anesthesia; these drugs include meperidine ( 25 mg intravenously or epidurally ), clonidine ( 75 /lgIV ),ketanserin ( 10 mg IV ), and magnesiumsulfat. ( 30 mg/kg iv )

The risk of shivering during neuraxial anesthesia is markedly diminished by maintaining normothermia. there is a distinct incidence of low- intensity, shivering-like tremor that occurs in normothermic patients and is not thermoregulatory. The cause of this muscular activity remains unknown, but it is associated with pain and may thus result from activation of the sympathetic nervous system.

CONSEQUENCES OF MILD INTRAOPERATIVE HYPOTHERMIA Perianesthetic hypothermia produces potentially severe complications as well as distinct benefits. Thermal management thus deserves the same thoughtful analysis of potential risks and benefits as other therapeutic decisions do.

Benefits protection against cerebral ischemia and hypoxia Similar benefits have been demonstrated for acute myocardial infarction in human. Mild hypothermia reduces intracranial pressure but randomized studies have yet to demonstrate that therapeutic hypothermia improve outcomes in patients with brain trauma, stroke, or subarachnoid hemorrhage. Improve outcome is during recovery from cardiac arrest

Protection ? The approximately 8%/oC linear reduction in tissue metabolic rate. other factors (e.g., decreased release of excitatory amino acids) explain the protective action of hypothermia. there is no reason to expect protection to decrease linearly with temperature, and in animals it appears that much of the total benefit from moderate hypothermia occurs within the first couple of degrees.

complications Coagulation is impaired by mild hypothermia. 1) The most important factor appears to be a cold-induced defect in platelet function. the defect in platelet function is related to local temperature, not core temperatur, 2) Perhaps, hypothermia directly impairs enzymes of the coagulation cascade. Mild hypothermia significantly increases blood loss.

Hypothermia can contribute to wound infections both by directly impairing immune function and by triggering thermoregulatory vasoconstriction, which in turn decreases wound oxygen delivery. hypothermia delayed wound healing and prolonged the duration of hospitalization 20%, even in patients without infection. urinary nitrogen excretion remains elevated for several postoperative days in patients allowed to become hypothermic during surgery

Patients, asked years after surgery, often identify feeling cold in the immediate postoperative period as the worst part of their hospitalization-sometimes rating it worse than surgical pain. Drug metabolism is markedly decreased by peri operative hypothermia.

Postanesthetic Shivering 40% oxygen consumption increased increasing intraocular and intracranial pressure postoperative shivering probably aggravates wound pain by stretching incisions.

Over the years, postanesthetic tremor has been attributed to uninhibited spinal reflexes, pain, decreased sympathetic activity, pyrogen release, adrenal suppression, respiratory alkalosis, and most commonly, simple thermoregulatory shivering in response to intraoperative hypothermia. Unfortunately, the etiology of postanesthetic shivering-like tremor remains unclear.

at least two distinct tremor patterns : (1) a tonic pattern resembling normal shivering, typically with a 4- to 8-cycle/min waxing-and-waning component, (2) a phasic, 5- to 7-Hz bursting pattern resembling pathologic clonus.

The tonic pattern is apparently a simple thermoregulatory response to intraoperative hypothermia. In contrast, the clonic pattern is not a normal component of thermoregulatory shivering and appears to be specific to recovery from volatile anesthetics. Although the precise etiology of this tremor pattern remains unknown.

treatment Skin surface warming Drugs: clonidine (75 micg IV), ketanserin (10 mg IV), tramadol, physostigmine (0.04 mg/kg IV), and magnesium sulfate (30 mg/kg iV). the specific mechanisms by which ketanserin, tramadol, physostigmine, and magnesium sulfate stop shivering remain unknown. Similarly, how clonidine arrests shivering also remains unknown, but clonidine and dexmedetomidine comparably reduce the vasoconstriction and shivering thresholds (central > peripherally).

Alfentanil, a pure µ-receptor agonist, significantly impairs thermoregulatory control. Meperidine is reportedly considerably more effective in treating shivering than equianalgesic doses of other µ- agonists are. The action of this drug is mediated by non--µ-opioid receptors. Meperidine possesses considerable K activity and also has central anticholinergic activity. However, neither mechanism appears to mediate meperidine's special antishivering activity. Instead, it may result from agonist activity at central a-adrenoceptors. Whatever the mechanism, meperidine appears to be considerably more effective in the treatment of postoperative shivering than other opioids are.

PERIOPERATIVE THERMAL MANIPULATIONS Intraoperative thermoregulatory vasoconstriction, once triggered, is remarkably effective in preventing further core hypothermia. Nonetheless, most patients are poikilothermic during surgery because they do not become sufficiently hypothermic to trigger thermoregulatory responses. Therefore, intraoperative hypothermia can be minimized by any technique that limits cutaneous heat loss to the environment as a result of cold operating rooms, evaporation from surgical incisions,and conductive cooling produced by the administration of cold intravenous fluids

Effects of Vasomotor Tone on Heat Transfer Intraoperative vasoconstriction thus slightly impedes peripheral-to-core transfer of cutaneous heating and cooling. intraoperative thermoregulatory vasoconstriction is opposed by direct anesthetic-induced peripheral vasodilation.

During postanesthetic recovery, however, the situation differs markedly. Here, anesthetic-induced peripheral dilation dissipates, with thermoregulatory vasoconstriction left unopposed. As might be expected, this vasoconstriction then becomes an important factor and significantly impairs transfer of peripherally applied heat to the core thermal compartment. Patients with a residual spinal anesthetic block warm considerably faster than those recovering from general anesthesia alone (Fig).

postoperative thermoregulatory vasoconstriction decreases peripheral-to-core transfer of heat, applied warming is most effective during surgery when patients are vasodilated. this means that it is easier to maintain intraoperative normothermia (when most patients are vasodilated) than to rewarm them Postoperatively (when virtually all hypothermic patient are vasoconstricted). intraoperative warming is more appropriate than postoperative treatment of hypothermia because it prevents the complications resulting from hypothermia Patients unavoidably becoming hypothermic during surgery should nonetheless be actively heated postoperatively to increase thermal comfort, decrease shivering,and haste rewarming

Preventing Redistribution Hypothermia The initial o.5 C to l.5 C reduction in core temperature is difficult to prevent because it results from redistribution of heat from the central thermal compartment to cooler peripheral tissues. Consequently, surface warming usually fails to prevent hypothermia during the first hour of anesthesia. Lack of efficacy during this period results because the central-to-peripheral flow of heat is massive and because transfer of applied cutaneous heat to the core requires nearly an hour, even in vasodilated patients. Although redistribution can not be treated effectively,it can be prevented.

Intravenous fluids It is not possible to warm patients by administering heated fluids because the fluids cannot (much) exceed body temperature. On the other hand, heat loss from cold intravenous fluids becomes significant when large amounts of crystalloid solution or blood are administered. One unit of refrigerated blood or 1 L of crystalloid solution administered at room temperature decreases mean body temperature approximately 0.2S°C. Fluid warmers minimize these losses and should be used when large amounts of intravenous fluid or blood are administered.

Skin surface warming before induction of anesthesia (30 min ) does not significantly alter core temperature (which remains well regulated), but it does increase body heat content.

Simple thermodynamic calculations indicate that less than 10% of metabolic heat production is lost through the respiratory tract. The loss results from both heating and humidifying inspiratory gases, but humidification requires two thirds of the heat. Because little heat is lost through respiration, even active airway heating and humidification minimally influence core temperature. Airway Heating and Humidification

Airway heating and humidification are more effective in infants and children than adults, cutaneous warming is also more effective in these patients and transfers more than 10 times as much heat. Hygroscopic condenser humidifiers and heat- and moisture-exchanging filters ("artificial noses") retain substantial amounts of moisture and heat within the respiratory system. In terms of preventing heat loss, these passive devices are about half as good as active systems.

Intravenous Fluids It is not possible to warm patients by administering heated fluids because the fluids cannot (much) exceed body temperature. On the other hand, heat loss from cold intravenous fluids becomes significant when large amounts of crystalloid solution or blood are administered. One unit of refrigerated blood or 1 L of crystalloid solution administered at room temperature decreases mean body temperature approximately 0.25°C. Fluid warmers minimize these losses and should be used when large amounts of intravenous fluid or blood are administered.

1) Operating room temperature is the most critical factor influencing heat loss because it determines the rate at which metabolic heat is lost by radiation and convection from the skin and by evaporation from within surgical incision room temperatures exceeding 23°C are generally required to maintain normothermia in patients undergoing procedures; most operating room personnel find such temperatures uncomfortably warm. Infants may require ambient temperatures exceeding 26°C to maintain normothermia. Cutaneous Warming

2) 2) The easiest method of decreasing cutaneous heat loss is to apply passive insulation to the skin surface.: cotton blankets, surgical drapes, plastic sheeting, and reflective composites ("space blankets"). A single layer of each reduces heat loss approximately 30% the amount of skin covered is more important than which surfaces are insulated.

Passive insulation alone is rarely sufficient to maintain normothermia in patients undergoing large operations; 3) active warming will be required in these cases : A) circulating water more effective-and safer-when placed over patients rather than under them and, in that position, can almost completely eliminate metabolic heat loss. The most common perianesthetic warming system is B) forced air. The best forced-air systems transfer more than 30 W across the skin surface, which rapidly increases mean body temperature. Forced air usually maintains normothermia even during the largest operationsand is superior to circulating-water mattresses.

Induction of Mild Therapeutic Hypothermia ( ( 32°C or 33°C) Cold water – forced air cooling – endovascular cooling Cold water – forced air cooling – endovascular cooling Inducing therapeutic hypothermia during surgery is relatively easy because anesthetics profoundly impair thermoregulatory responses. In contrast, unanesthetized patients-even those who have suffered a stroke vigorously defend core temperature by vasoconstricting and shivering. It is thus necessary to pharmacologically induce tolerance to hypothermia. The best method thus far identified is the combination of buspirone and meperidine, drugs that synergistically reduce the shivering thresholdto approximately 34°C without provoking excessive sedation or respiratory toxicity. The combination of dexmedetomidine and meperidine may also be helpful,

DELIBERATE SEVERE INTRAOPERATIVE HYPOTHERMIA l0 to 15°C below normal. (i.e., 28°C) Organ function :.. Ischemia damages tissues. more toxic metabolic waste products (e.g., lactate and superoxide radicals).Hypothermia decreases the whole-body metabolic rate by approximately 8%/oC to approximately half the normal rate at 28°C..Cerebral blood flow also decreases in proportion to the metabolic rate during hypothermia because of an autoregulatory increase in cerebrovascular resistance..Cerebral function is well maintained until core temperatures reach around 33°C, but consciousness is lost at temperaturesbelow 28°C.,. Respiratory strength is diminished at core temperatures less than 33°C, but the ventilatory CO2 response is minimally affected... Nerve conduction decreases, but peripheral muscle tone increases, and rigidity and myoclonus ensue at temperatures near 26°C..acid-base changes.acid-base changesThe pH of neutral water (lOWI = [WI) increases U for each 1°C reduction in temperature; the pH of bloodin a closed system (e.g., test tube or artery) changes similarly.

Hypothermia is by far the most common perianesthetic thermal perturbation. However, hyperthermia is more dangerous than a comparable degree of hypothermia. 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. Hyperthermia can result from a variety of causes and usually indicates a problem of sufficient severity that physician intervention is required. Hyperthermia

Passive Hyperthermia and Malignant hyperthermia Passive intraoperative hyperthermia results from excessive patient heating and is most common in infants and children. It is especially frequent when effective active warming is used without adequate core temperature monitoring. it can easily be treated by discontinuing active warming and removing excessive insulation.

The increase in body temperature during malignant hyperthermia results from an enormous increase in metabolic heat produced by both internal organs and skeletal muscle. Central thermoregulation presumably remains intact during acute crises, but efferent heat loss mechanisms may be compromised by the intense peripheral vasoconstriction resulting from circulating catecholamine concentrations 20 times normal.

fever fever results when endogenous pyrogens increase the thermoregulatory target temperature ("set point"). Identified endogenous pyrogens include interleukin-l, tumor necrosis factor,interferon-a, and macrophage inflammatory protein-1. Although it was initially believed that these factors acted directly on hypothalamic thermoregulatory centers, there is increasing evidence for a more complicated system involving vagal afferents.

Fever is relatively rare during general anesthesia because volatile anesthetics per se inhibit the expression of fever as do opioids. fever may reflect preexisting infection or result, for example, from urologic manipulations. perioperative fever also occurs in response to mismatched blood transfusions, blood in the fourth cerebral ventricle, and allergic reactions. In addition, some degree of fever is typical after surgury.

In general, patients with fever and increasing core temperature will have constricted fingertips, whereas those with other types of hyperthermia will be vasodilated. Treatment: 1)cause 2)antipyreyic medications 3)active cooling

TEMPERATURE MONITORING Core temperature measurements (e.g., tympanic membrane,pulmonary artery, distal portion of the esophagus, and nasopharynx) are used to monitor intraoperative hypothermia, prevent overheating, and facilitate detection of malignant hyperthermia. Both core and skin surface temperature measurements are required to determine the thermoregulatoryeffects of different anesthetic drugs. Temperaturesare not uniform within the body; consequently, temperatures measured at each site have different physiologic and practical significance.

When Temperature Monitoring Is Required core temperature should be measured during regional anesthesia in patients likely to become hypothermic (e.g., those undergoing body cavity surgery). Core temperature monitoring is appropriate during the administration of most general anesthetics both to facilitate detection of malignant hyperthermia and to quantify hyperthermia and hypothermia.

More common than malignant hyperthermia is intraoperativ hyperthermia of other etiologies,including excessive warming, infectious fever,blood in the fourth cerebral ventricle, and mismatched blood transfusions. Core temperature perturbations during the first 30 minutes of anesthesia are thus difficult to interpret,and measurements are not usually required. Body temperature should, however, be monitored in patients undergoing general anesthesia exceeding 30 minutes in duration and in all patients whose surgery lasts longer than 1 hour.

Temperature-Monitoring and Thermal Management Guidelines