Thermoregulation

Clinical approach: perioperative temperature management

• Define the problem early: core temperature, trend, and context (anaesthesia type, duration, exposure, fluids, ambient temperature, sepsis/thyroid disease)
  • Core sites: oesophageal (distal), nasopharyngeal, tympanic (true), bladder (if high urine flow), PA catheter (gold standard but rare)
  • Peripheral sites (less reliable): axillary, oral, temporal artery; skin temperature reflects vasomotor tone and environment
• Immediate actions for hypothermia (<36°C): active forced-air warming, warm IV fluids/blood, minimise exposure, increase ambient temperature, humidify/warm gases if prolonged case
  • Treat causes: haemorrhage/shock, sepsis, endocrine (hypothyroid/adrenal), drug effects, cold irrigation
• Immediate actions for hyperthermia: stop warming devices, check probe placement, assess for malignant hyperthermia, sepsis, thyroid storm, transfusion reaction, neuroleptic malignant syndrome
  • If MH suspected: call for help, stop triggers, 100% O2, dantrolene, active cooling, treat hyperkalaemia/acidosis, ICU
• Regional anaesthesia: anticipate impaired thermoregulation and redistribution hypothermia; monitor temperature for long blocks/sedation
  • Shivering may be absent below block; patient may feel warm despite falling core temperature
• Targets: maintain core ≥36°C; pre-warm high-risk patients and long cases
  • High-risk: elderly, neonates, trauma, burns, major abdominal/thoracic surgery, large exposure, cold theatre, large volume fluids/blood

Core concepts and definitions

• Thermoregulation maintains core temperature around 36.5–37.5°C via behavioural and autonomic responses
• Core vs shell: core (trunk/brain) relatively constant; shell (skin/limbs) varies with vasomotor tone and environment
• Heat balance: heat production (metabolism, shivering, non-shivering thermogenesis) vs heat loss (radiation, convection, conduction, evaporation)
• Thermal inputs: peripheral thermoreceptors (skin) and central receptors (hypothalamus, spinal cord, viscera)

Control system: hypothalamus and efferent responses

• Integrator: preoptic anterior hypothalamus compares afferent thermal signals to a set point and drives efferent responses
• Efferent responses (cold defence): cutaneous vasoconstriction → reduced heat loss; shivering → increased heat production; behavioural responses
  • Non-shivering thermogenesis: mainly brown adipose tissue (infants) via sympathetic stimulation (UCP1 uncoupling)
• Efferent responses (heat defence): vasodilation; sweating (sympathetic cholinergic); behavioural responses
  • Sweating effectiveness depends on evaporation; reduced by high humidity and occlusive drapes
• Thermoregulatory thresholds: temperatures at which vasoconstriction, shivering, vasodilation, sweating are triggered; normally tight interthreshold range (~0.2–0.4°C)

Mechanisms of heat loss and gain (exam numbers and key determinants)

• Radiation: infrared heat transfer to cooler objects; typically the largest component in theatre
  • Depends on temperature gradient and exposed surface area
• Convection: heat loss to moving air; increased by draughts, laminar flow, and large exposed areas
• Conduction: direct transfer to contacting surfaces; usually smaller contribution unless cold tables/fluids/irrigation
• Evaporation: latent heat loss from skin and respiratory tract; increased by surgical exposure, skin prep, open cavities, high minute ventilation with dry gases
• Heat gain: metabolism (basal metabolic rate), muscle activity, shivering; external warming devices; warmed fluids and gases

Perioperative hypothermia: patterns and mechanisms under anaesthesia

• Typical GA temperature pattern: (1) rapid initial fall (first 30–60 min) due to redistribution from core to peripheral compartments; (2) slower linear decline due to heat loss > production; (3) plateau when vasoconstriction threshold reached (if not profoundly impaired)
  • Redistribution is the dominant early mechanism; vasodilation from anaesthetics increases peripheral blood flow and heat transfer
• General anaesthesia: widens interthreshold range and lowers vasoconstriction and shivering thresholds (dose-dependent) → impaired cold defence
• Neuraxial anaesthesia: blocks sympathetic vasoconstriction and afferent thermal input from blocked segments; shivering threshold reduced; patient may not perceive hypothermia
  • Core temperature can fall despite patient feeling warm; vasodilation below block increases heat loss and redistribution
• Risk factors: cold ambient temperature, large exposure, long duration, major cavity surgery, large volumes of unwarmed fluids/blood, low BMI, extremes of age, high ASA, trauma, sepsis

Physiological effects of hypothermia (perioperative relevance)

• Cardiovascular: initial sympathetic activation (tachycardia, hypertension) then bradycardia, reduced CO; arrhythmias increase as temperature falls (AF/VT/VF at lower temps)
• Respiratory: left shift of oxyhaemoglobin dissociation curve; reduced CO2 production; impaired mucociliary function; increased pulmonary vascular resistance possible
• Coagulation: platelet dysfunction and impaired enzyme activity → increased bleeding; hypothermia contributes to trauma triad (hypothermia, acidosis, coagulopathy)
• Drug effects: reduced hepatic metabolism and renal clearance; increased potency/prolonged duration of many agents (notably neuromuscular blockers); MAC decreases with hypothermia
• Infection and wound healing: increased surgical site infection risk and impaired wound healing (vasoconstriction → reduced tissue oxygenation; immune dysfunction)
• Shivering: increases O2 consumption and CO2 production markedly; can worsen myocardial ischaemia and raise ICP

Hyperthermia and fever: mechanisms and perioperative causes

• Fever: raised hypothalamic set point (pyrogens → cytokines → PGE2) leading to vasoconstriction and shivering until new set point reached
• Hyperthermia: temperature rise without set-point change (heat production > loss or impaired loss); sweating and vasodilation may be present but overwhelmed
• Perioperative differentials: malignant hyperthermia, sepsis, thyroid storm, transfusion reaction, drug-induced (e.g. serotonin syndrome, NMS), overheating from warming devices, iatrogenic (warm irrigation/fluids)

Temperature monitoring: sites, accuracy, and pitfalls

• Core monitoring recommended for cases >30 min under GA or where significant temperature change is expected
• Oesophageal probe: good estimate of core if placed in distal third (behind heart); falsely low if too proximal (influenced by inspired gases)
• Nasopharyngeal: good if positioned correctly; can be affected by cold/warm gases and poor placement
• Tympanic: accurate only if measures tympanic membrane (infrared canal devices often unreliable)
• Bladder: reflects core when urine flow is high; lags during low flow or rapid temperature changes

Prevention and treatment strategies (practical physiology)

• Pre-warming (e.g. 20–30 min forced-air) reduces core-to-peripheral gradient → reduces redistribution hypothermia after induction
• Forced-air warming: effective for maintaining normothermia; ensure correct blanket type/placement; avoid underbody overheating/pressure risks
• Warmed IV fluids/blood: important when large volumes; fluid warmers reduce conductive heat loss; rapid infusers require warming
• Warmed/humidified gases: modest benefit in routine cases; more useful in prolonged ventilation, paediatrics, major burns
• Shivering management: treat hypothermia; consider meperidine (pethidine), clonidine, dexmedetomidine, magnesium, tramadol; ensure adequate analgesia
  • Exclude MH if hypercapnia, rigidity, rapid rise in temperature, acidosis, hyperkalaemia