BETA SAÚDE
Chills
Texto da Wikipédia (en), licença CC BY-SA. O BETARUBI mostra o verbete inteiro nesta página — a leitura não continua fora do site.
 | This article needs more reliable medical references for verification or relies too heavily on primary sources. (September 2019) |
| Chills | |
|---|---|
| Specialty | Infectious disease |
Chills is a feeling of coldness occurring usually during a high fever but sometimes alone in specific people. It occurs during fever as a result of the release of cytokines and prostaglandins as part of the inflammatory response, which increases the set point for body temperature in the hypothalamus. The increased set point causes the body temperature to rise (pyrexia), but also makes the patient feel chilled until the new set point is reached. The patient will also shiver because their body produces heat during muscle contraction in a physiological attempt to increase body temperature to the new set point.[1] Chills not accompanying a high fever are normally mild.
A scare, especially one of fear, may cause a chill of medium power and short duration; this is commonly interpreted as or confused with trembling.
Severe chills with violent shivering are called rigors.
Pathophysiology
Chills occur when the hypothalamic temperature set point is suddenly elevated[2] for one or more of several causes, including tissue destruction, pyrogenic substances, or dehydration.[2] Since the body temperature is below the new set point, body mechanisms of raising body temperature, including vasoconstriction, and shivering ensue.[2] The patient experiences cold, even extreme cold, although they may have a body temperature higher than normal.[2] As their temperature rises and reaches the new set point, chills stop and the patient feels neither hot nor cold.[2] If the factor elevating their temperature is then removed, their hypothalamic set point decreases, triggering body cooling mechanisms to reduce body temperature to the new set point and causing sweating, which may be severe, and hot skin due to vasodilation. This phase of the febrile state is known as the "crisis" or the "flush."[2]
In rats, prostaglandin E2 (PGE2), a pyrogenic mediator produced in the brain during infection, has been shown to induce warmth-seeking behavior by enhancing cold-sensory transmission to the central amygdaloid nucleus (CeA), an emotion center of the limbic system. This mechanism potentially generates the unpleasant cold sensation of chills. This effect of PGE2 is mediated by EP3 receptors expressed in CeA-projecting neurons in the lateral parabrachial nucleus.[3]
See also
References
- ↑ Huether, Sue E. (2014). Pathophysiology: The Biologic Basis for Disease in Adults and Children (7th ed.). Elsevier Health Sciences. p. 498. ISBN 978-0323293754.
- 1 2 3 4 5 6 Hall, John E.; Hall, Michael E.; Guyton, Arthur C. (2021). Guyton and Hall Textbook of Medical Physiology (14th ed.). Philadelphia, PA: Elsevier. p. 910. ISBN 978-0-323-59712-8.
- ↑ Yahiro, Takaki; Nakamura, Yoshiko; Nakamura, Kazuhiro (March 2026). "The pyrogenic mediator prostaglandin E2 elicits warmth seeking via EP3 receptor‐expressing parabrachial neurons: a potential mechanism of chills". The Journal of Physiology. 604 (5): 2110–2130. doi:10.1113/JP289466. ISSN 0022-3751. PMC 12953009. PMID 41664914.