ICU · first-part-physiology

Thermoregulation — Comprehensive

Also known as Thermoregulation · Body temperature regulation · Hypothalamic set point · Preoptic anterior hypothalamus · Heat production · Heat loss · Shivering thermogenesis · Non-shivering thermogenesis · Brown adipose tissue · Targeted temperature management · Therapeutic hypothermia · Fever · Hyperthermia · Heat stroke · Poikilothermia

Thermoregulation — the integrated hypothalamic control of body temperature by balancing heat production against heat loss. HEAT PRODUCTION: basal metabolic rate (70-80% of resting heat), shivering thermogenesis (skeletal muscle — up to 5x BMR increase), non-shivering thermogenesis (brown adipose tissue / uncoupling protein 1 — dominant in neonates, reactivated in adult humans), voluntary exercise, and hormonal calorigenesis (thyroid hormone T3/T4 — slow genomic up-regulation of Na+/K+ ATPase; catecholamines — rapid beta-adrenergic stimulation of metabolism). HEAT LOSS: radiation 60% (infrared transfer to cooler surroundings — dominant at rest in a temperate room), convection 12% (air currents carry heat away — basis of forced-air cooling and wind chill), conduction 3% (direct contact — basis of cooling blankets and ice/water immersion), evaporation 25% (sweat 0.58 kcal/g water vaporised + respiratory water loss), and respiration (latent heat of vaporisation + warming of inspired gas). HYPOTHALAMIC CONTROL: the preoptic area of the anterior hypothalamus (PO/AH) houses the central thermoregulatory integrator — it is itself warm-sensitive, contains the defended set point (~37 degrees C core), and integrates central (blood) temperature with peripheral (skin/cold) afferent input to generate autonomic outputs (sweating, shivering, cutaneous vasodilation/vasoconstriction) and behavioural outputs (clothing, seeking shade/shelter). NORMAL RANGE: 36-37.5 degrees C core. RESPONSE TO COLD: peripheral vasoconstriction (sympathetic — reduces shell conductance) → shivering (skeletal muscle) → non-shivering thermogenesis (brown fat) → piloerection (trapped air layer) → TSH/catecholamine release (raise metabolic rate). RESPONSE TO HEAT: cutaneous vasodilation (active vasodilation via cholinergic/nitric oxide — opens arteriovenous anastomoses) → sweating (eccrine glands, sympathetic cholinergic) → behavioural cooling. TARGETED TEMPERATURE MANAGEMENT (TTM): controlled hypothermia 32-36 degrees C after cardiac arrest — reduces cerebral metabolic rate by 6-7% per degree C fall → reduces cerebral O2 demand, attenuates excitotoxicity, reperfusion injury, seizure activity and free-radical generation → neuroprotection. FEVER: prostaglandin E2 (PGE2) synthesised in the PO/AH (via COX-induced conversion of arachidonic acid, driven by endogenous pyrogens IL-1, IL-6, TNF-alpha acting on the organum vasculosum of the lamina terminalis) RAISES the hypothalamic set point → the patient feels cold → shivering + vasoconstriction raise core temperature to the new set point. Antipyretics (paracetamol, NSAIDs) work by BLOCKING PGE2 synthesis (COX inhibition). HYPERTHERMIA: the set point is NORMAL — body temperature exceeds the set point due to excessive external heat, exercise, or uncontrolled heat production (malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome, heat stroke) — antipyretics are INEFFECTIVE because the set point is not elevated; treatment is active cooling. POIKILOTHERMIA: loss of hypothalamic thermoregulation — high spinal cord injury (loss of sympathetic outflow below the lesion), brain death — body temperature drifts passively towards ambient temperature.