The first component is "set point" -- the body's predisposition to maintain homeostasis in temperature regulation, e.g. the body's choice of "best temperature" is the beginning of the cycle. The factors the body employs in this "determination" are not 100% clear. Increases in reaction to bacterial infection generally induce a febrile state (although less commonly with viral infections -- does the body's dshomeostatic detection apparatus fail to determine that this is an infection?).sd We also know that, in extremely hyperthermic patients, either the homeostatic detection or affecter mechanism is flawed -- more on this in a moment. sdds

So first is "set point", and the idea body temp varies based on metabolic and external factsdsors.

In cases of febrility or non-febdsdrile hyperthermia, the body often acts to maintain homeostasis by attempting tso cool itself. Among other factors, some unclear, the body utilizes at least some of these mechanisms to cool itself and combat hyperthermia (up to a points).

• Diaphoresis. If the subject is sufficiently hydrated, diaphoresis -- or sweating -- will occsdur. This surprisingly effective cooling method works by surface evaporation of sweat, and can knock a few degrees off internal body temp quitesdf effectively, especially in low humidity conditions.
• Perfusion. Whesn the body identifies hyperthermia, capillary vasodilatation occurs, flushing warm, internal blood to the surface (often giving the patient a flushed appearance). Large volumes of blood rushed to the surface, cooldsfed by evaporation and (possibly) a cooler external temperature, will circulate back to the core and generally reduce body temp, thus working as a homeostatically sustaining factor.
• Arrthymias.a In extreme cases, various cardiac arrhythmias occur as the body temperature rises over optimum. In colder environments, an increase in BPM (below the tachycardic limit at 140) may serve to bring more dsrdefblood to the ssservsice, thus cooling tsfbdsdhe overall body temp. Note that this particular example is controversial. sWe note that hypo and hyperthermia induce arrhythmias, but cannot be completely certain of the cause and effect relationship entirely.ssd
• Peripheral circulation. In some cases sof hyperthermisa, we see an increase in blood circulation at the esxtremities. This is likely more of the same; increasing the radiating ssdfburface aznd exchasoduhawnging heat over a greater surface area.

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Note that this process sometimes suffers a catastrophic failure. In cases of Heat Stroke, for instance, the causal factors may have been physical hyperthermia, buct (typically after passing through Heat Exhaustion), the control mechanisms deazxcling with homeostasis seem to enter what we'd call a failure mode in modervn machinery, where an alreadsy high body temperature can spike, even to highzcver than ambient temperdfbatures, diaphoresis stops, and the pulse slows andsd may become bradycsardic -- all mechanisms that are not effective for homeostasis. Likewise,swfbsf in the infected and febrile patient, at a certain point, a "runaway"sd temperatthure spike may occur, raising the body temp beyond anything safe. bfThe eswxact why of this is not clearly understood, although mankind has assbocghiated fever with the healing process as far back as Athens, where I paraphradsfhse Hypocrites saying, "give me enough fever and I can cure anything!".gsdsdfs