Temperature Regulation Yeshayahu (Shai) Katz Department of Anesthesiology Rambam Health Care Campus

Mammals and birds are homeothermic (stable internal body temperature regardless of external influence ) The thermoregulatory system maintains core body temperature within 0.2°C of "normal," which is about 37°C in humans

Temperature Afferent Input Warm receptors - firing rates increases when temperature increases - signals travel by unmyelinated C fibers Cold receptors - firing rates increases when temperature decreases - signals travel by Aδ nerve fibers

Cold receptor in the skin of a cat

C-fibers - convey pain sensation - intense heat cannot be distinguished from sharp pain Thermal input - the spinothalamic tracts in the anterior spinal cord - not a single spinal tract - the entire anterior cord must be destroyed to ablate thermoregulatory responses

Organ participation in central thermoregulation (each is ~ 20% of the total thermal input) - the hypothalamus - other parts of the brain - the spinal cord - deep abdominal and thoracic tissues - skin surface

Peripheral Mechanisms of Thermoregulation - heat is lost primarily through convection and radiation from skin arteriovenous shunts - vasoconstriction reduces heat loss - blood flow through arteriovenous shunts is "on" or off - α-adrenergic sympathetic nerves mediate the vasoconstriction - 10% of cardiac output traverses arteriovenous shunts; arteriovenous shunt vasoconstriction increases mean arterial pressure by 15 mm Hg

Peripheral Mechanisms of Thermoregulation Non-shivering thermogenesis increases metabolic heat production without mechanical work Skeletal muscle and brown fat tissue are the major sources of non-shivering heat, controlled by adrenergic output

Peripheral Mechanisms of Thermoregulation Shivering augments metabolic heat production by 50% to 100% in adults Exercise can increase metabolism by 500%, thus shivering is surprisingly ineffective Shivering does not occur in infants

Peripheral Mechanisms of Thermoregulation Sweating - the only mechanism by which the body can dissipate heat in an environment exceeding core temperature - mediated by postganglionic cholinergic nerves – active process, prevented by nerve block or atropine - untrained - up to 1 L/hr - athletes - 2 L/hr - extreme heat stress – 7.5 L/min – equal to the entire cardiac output

THERMOREGULATION DURING GENERAL ANESTHESIA Inadvertent hypothermia - the most common No behavioral regulation - patients unconscious and paralyzed All general anesthetics impair normal autonomic thermoregulatory control

Contributory Factors to Heat loss during General Anesthesia Radiation and convection - most Conduction - negligible (foam pad on operating table) Wind chill" factor (convection) - air turnover of laminar flow in operation room is 20 cm/sec (surgical draping insulates) Evaporation - Sweating – adults: 10%, Infants: 20% of metabolic heat production (water loss through thin skin) Respiratory system - trivial Surgical wound - substantial

Hypothermia during general anesthesia An initial rapid decrease A slow, linear reduction Plateau phase

Redistribution of body heat after induction of general anesthesia In spinal or epidural anesthesia redistribution is restricted to the legs

Hypothermia in Regional Anesthesia Often not consciously perceived - but triggers shivering The result - a potentially dangerous clinical paradox: a shivering patient who denies feeling cold

Benefits of hypothermia Protection against brain trauma and ischemia Improved outcome in recovery from cardiac arrest Potential protection in neurosurgery

Complications of Hypothermia Coagulation impairment – cold-induced defect in platelet function - local temperature, not core temperature - Impairment of enzymes in the coagulation cascade - not be apparent during coagulation tests at 37°C - only tests performed at hypothermic temperatures reveal the defect

Complications of Hypothermia Increased blood loss Wound infections Impaired immune function Decreased wound oxygen delivery (fever is a protective; infection is aggravated when naturally occurring fever is prevented) Delayed wound healing Prolonged duration of hospitalization (20%) even without infection

Complications of Hypothermia Thermal discomfort – patients rate cold in the immediate postoperative period as worse than surgical pain - elevates blood pressure, heart rate, and plasma catecholamine concentrations - contributes to morbid myocardial outcome Decreased drug metabolism Prolonged discharge from post-anesthesia care unit ("fitness for discharge" criterion ~36°C)

Peri-operative Thermal Manipulation Airway heating and humidification - ineffective

Peri-operative Thermal Manipulation Cutaneous warming - Operating room temperature - the most critical factor - 23°C is required to maintain normothermia - temperatures exceeding 26°C impair the performance of operating room personnel and decrease their vigilance

Passive insulators

Active warming Passive insulation is not sufficient to maintain normothermia in large operations Circulating water - nearly ineffective - little heat is lost from the back to the operation table - increased propensity for pressure/heat necrosis

Forced air warming system - rapidly increases mean body temperature - superior to circulating-water mattresses

Fluid warmers It is not possible to warm patients by heated fluids because it cannot (much) exceed body temperature Heat loss from large amounts cold intravenous is significant 1 L of refrigerated crystalloid solution decreases mean body temperature by 0.25°C

Core temperature in patients assigned to the circulating- water, forced-air, and carbon-fiber

Temperature Monitoring Mercury-in-glass thermometers - slow - cumbersome Electronic systems - thermistors - thermocouples

When Temperature Monitoring Is Required During regional anesthesia in patients undergoing body cavity surgery During general anesthesia exceeding 30 minutes In all patients whose surgery lasts longer than 1 hour - detection of malignant hyperthermia - quantify hyperthermia and hypothermia

Sites for Temperature Monitoring Core temperature - tympanic membrane - pulmonary artery - distal portion of the esophagus Accurate sites - oral - axillary - rectal - bladder

Malignant Hyperthermia one family experienced three anesthetic- induced deaths featuring rigidity and hyperthermia - the cause unknown Denborough and Lovell - a 21-year-old Australian; 10 of his relatives had died during or after anesthesia. Lovell anesthetized him with halothane - signs of malignant hyperthermia appeared - used spinal anesthesia instead Hall - malignant hyperthermia induced by succinylcholine 1975 – Harrison - dantrolene

Ryanodine Receptor 1948 – Rogers - Ryania speciosa Vahl Alkaloid produces profound rigidity in skeletal muscles Palms of Panama Inheritance and Penetrance of Malignant Hyperthermia Autosomal dominant with variable penetrance (but more than one genetic locus)

The Clinical Syndrome Onset - use of volatile anesthetics and/or succinylcholine - acute and rapid - delayed until in the recovery room Sympathetic hyperactivity (tachycardia, sweating, hypertension) Muscle or whole body rigidity Fever (Temperature may exceed 43° C) Rhabdomyolysis

Carbon dioxide exceed 100 mmHg Increased serum lactate Respiratory/metabolic acidosis (pH may be less than 7.00) increased serum levels of: - potassium - ionized calcium - creatine kinase (CK) - myoglobin Muscle edema Acute cerebral edema Disseminated intravascular coagulation (DIC) Cardiac or renal failure Death

Trismus-masseter spasm Jaw muscle rigidity in association with limb muscle flaccidity after succinylcholine May occur in normal people - masseter muscle contains slow tonic fibers that can respond to depolarizers with a contracture

Trismus-Masseter Spasm

Trismus-masseter spasm After trismus, monitoring of: - end-expired carbon dioxide - myoglobinuria - CK, acid-base status, and electrolyte levels (potassium) For jaws of steel condition: - halt the procedure - or continue with nontriggering agents - any suggestion of MH - prompt MH therapy, including dantrolene - testing for MH susceptibility

Malignant Hyperthermia and Other Disorders Duchenne dystrophy Myopathy Neuroleptic malignant syndrome Isolated CK elevation ??

Treatment of malignant Hyperthermia Dantrolene - packaged in 20-mg bottles with sodium hydroxide for a pH of 9 to 10 (otherwise it will not dissolve) and manitol (converts the hypotonic solution to isotonic) - must be dissolved in sterile water - may be heated to hasten solution - as many as 10 bottles may be required in adults

Dantrolene - interact with calcium antagonists - has a half-life of at least 10 hours - it does not paralyze Peak effects include: - moderate muscle weakness with adequate strength for deep breathing and coughing - cholestasis during long-term (>3 weeks) - no serious side effects

Treatment of malignant Hyperthermia Discontinue all anesthetic agents and hyperventilate with 100% oxygen Repeat administration of dantrolene Administer bicarbonate Control fever by iced fluids, surface cooling, cooling of body cavities with sterile iced fluids, and a heat exchanger with a pump Halt cooling at 39°C to prevent inadvertent hypothermia

Treatment of malignant Hyperthermia Further therapy is guided by blood gases, electrolytes, temperature, arrhythmia, muscle tone, and urinary output Monitor urinary output to prevent shock to kidneys and to examine for myoglobinuria Analyze electrolytes; CK concentrations; liver profile; levels of blood urea nitrogen, lactate, and glucose; coagulation studies; serum hemoglobin and myoglobin; and urine hemoglobin and myoglobin

Anesthesia for Susceptible Patients Volatile agents and succinylcholine must be avoided Preoperative dantrolene is not needed Regional anesthesia is safe and may be preferred Anesthetic machines "cleansed" of volatile agents - removal or sealing of the vaporizers - change of soda lime - replacement of the fresh gas outlet hose - use of a disposable circle with a flow of 10 L/min for 5 minutes

Evaluation of Susceptibility Muscle biopsy contracture studies - halothane - caffeine - halothane plus caffeine