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THERMOREGULATION AND HOMEOSTASIS

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As endotherms, we autoregulate body temperature across a range of environmental conditions. Our temperature is intimately linked to our resting energy expenditure, which in turn drives our need for energy intake. Understanding the regulation of body temperature in the context of health and disease contributes to practice in the intensive care unit.

  • The hypothalamus is the master thermostat

  • Body temperature is maintained between 36°C and 37.5°C

  • Patients above 38°C or 38.5°C are generally considered febrile

  • Fever is a regulated process in response to inflammatory cytokines and pyrogens

  • Temperatures above 41°C are considered hyperthermic

  • Temperatures below 36°C are considered hypothermic

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COOLING DOWN

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Core temperature is greater than the set point.

  • Sweating and peripheral vasomotor dilatation increase evaporative and radiant heat losses

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WARMING UP

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Core temperature is less than the set point.

  • Peripheral vasoconstriction to limit radiant losses

  • Shivering to stimulate heat production

  • Increase in metabolic rate to generate cellular heat

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CELLULAR HEAT

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Intramolecular reactions, such as the generation or cleavage of adenosine triphosphate (ATP), release a small amount of energy as heat. In addition, metabolic uncoupling at the level of the mitochondria drives excess heat production. Some tissues, brown fat and skeletal muscle, specialize in cellular heat generation. The cumulative action of cellular metabolism drives heat generation.

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CARDIAC OUTPUT AND THE FEBRILE STATE

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  • Metabolism increases oxygen consumption (VO2)

  • Oxygen delivery (DO2) matches demand via neurohormonal feedback mechanisms

    • Febrile patients are tachycardiac to increase cardiac output/DO2

    • Patients with limitation to cardiac output, such as critical heart failure or shock, are unable to further increase their cardiac output, and decompensated shock may result during fever

  • CO2 production (VCO2) increases with increased oxygen consumption

    • Minute ventilation increases with VCO2

    • Febrile patients are tachypneic

    • Febrile patients unable to increase their minute ventilation, such as those with respiratory failure or chemical paralysis, may develop respiratory acidosis with fever.

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TREATMENT OF FEVER

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  • Reduce the production of pyrogens and inflammatory cytokines

    • Address sources of inflammation, infection, or tissue injury

  • Lower the thermostat set point using cyclooxygenase-2 inhibitors

    • Nonsteroidal anti-inflammatory agents such as ibuprofen or acetaminophen

  • Environmental cooling: Although commonly employed, increasing the rate of heat loss through surface cooling, administration of cold fluids, tepid baths, and ambient temperature reduction may drive the demand for cardiac output

    • Uncontrolled cooling of the critically ill patient may contribute to shock if cardiac output is limited

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THERMOCOUPLE

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To enable safe environmental cooling, the hypothalamus should be sufficiently anesthetized to minimize the feedback mechanisms increasing the demand for cardiac output.

  • Sufficient sedation will allow cooling without driving the demand for cardiac output

  • Therapeutic hypermagnesemia targeting >3 mg/dL can reduce muscle shivering

  • Skin counter warming provides negative feedback to the hypothalamus during core ...

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