Wyczerpanie cieplne
Patofizjologia i mechanizm

Wyczerpanie cieplne jest umiarkowaną formą choroby związanej z przegrzaniem organizmu, charakteryzującą się temperaturą ciała w zakresie 37-40°C, co odróżnia je od udaru cieplnego (>41°C). Patofizjologia obejmuje zaburzenie równowagi między produkcją a rozpraszaniem ciepła, głównie przez nadmierne pocenie i rozszerzenie naczyń skórnych, co prowadzi do odwodnienia (utrata do 2 litrów płynów na godzinę) i zaburzeń elektrolitowych. Wyczerpanie cieplne wiąże się z redystrybucją krwi do skóry, hipowolemią, hipotonią, tachykardią oraz łagodnymi objawami neurologicznymi (ból głowy, zawroty, drażliwość). Na poziomie molekularnym aktywowane są białka szoku cieplnego (HSP), które chronią komórki przed uszkodzeniem, jednak przy długotrwałym stresie cieplnym dochodzi do aktywacji kaskady zapalnej, stresu oksydacyjnego i zaburzeń bariery jelitowej, co może predysponować do progresji do udaru cieplnego i niewydolności wielonarządowej.

Patogeneza wyczerpania cieplnego

Wyczerpanie cieplne (ang. Heat exhaustion) jest umiarkowaną formą choroby związanej z wysoką temperaturą, występującą w sytuacji, gdy organizm nie jest w stanie skutecznie się ochłodzić. Stanowi ono część kontinuum chorób związanych z ciepłem, które w przypadku braku odpowiedniego leczenia może prowadzić do udaru cieplnego – stanu zagrażającego życiu.12 Temperatura ciała w przypadku wyczerpania cieplnego zazwyczaj mieści się w zakresie od 37°C do 40°C, co odróżnia je od udaru cieplnego, gdzie temperatura przekracza 41°C.34

Mechanizmy termoregulacji i ich zaburzenia

Kluczowym elementem patofizjologii wyczerpania cieplnego jest zaburzenie równowagi między wytwarzaniem a rozpraszaniem ciepła przez organizm. W warunkach normalnych, temperatura ciała jest utrzymywana w wąskim zakresie dzięki zrównoważeniu obciążenia cieplnego z rozpraszaniem ciepła.56 Gdy temperatura rdzenia ciała wzrasta, jądro przedwzrokowe przedniego podwzgórza stymuluje włókna eferentne autonomicznego układu nerwowego do produkcji potu i rozszerzenia naczyń skórnych – głównych mechanizmów ochładzania organizmu.78

Mechanizm chłodzenia ciała ludzkiego opiera się głównie na poceniu się. Parowanie potu reguluje temperaturę ciała, ale gdy wykonywane są intensywne ćwiczenia lub dochodzi do nadmiernego wysiłku w gorącej, wilgotnej pogodzie, zdolność organizmu do skutecznego chłodzenia się ulega pogorszeniu.9 W upalne dni organizm zwiększa przepływ krwi do skóry nawet do 8 litrów na minutę, co stanowi znaczną część objętości wyrzutowej serca, aby rozpraszać ciepło.10

Wyczerpanie cieplne pojawia się, gdy organizm nie jest w stanie skutecznie rozpraszać nadmiaru ciepła, co może wynikać z czynników zewnętrznych utrudniających rozpraszanie ciepła (np. ekstremalne temperatury, wysiłek fizyczny, warunki środowiskowe o wysokiej wilgotności) lub ograniczeń fizjologicznych organizmu.1112

Rola odwodnienia i zaburzenia elektrolitowe

Jednym z kluczowych mechanizmów patogenetycznych wyczerpania cieplnego jest utrata płynów i elektrolitów, głównie przez nadmierne pocenie się. Wyczerpanie cieplne występuje, gdy płyny utracone przez pocenie nie są odpowiednio uzupełniane.13 Przy intensywnym poceniu organizm może tracić do 2 litrów płynów na godzinę, co prowadzi do odwodnienia.14 Jeśli osoba nie przyjmuje wystarczającej ilości płynów, organizm nie ma potrzebnych zasobów do produkcji odpowiedniej ilości potu, co osłabia zdolność termoregulacji.15

Umiarkowane lub ciężkie odwodnienie może prowadzić do niedoboru zarówno wody, jak i soli, które są niezbędnymi składnikami potu. W przypadku wyczerpania cieplnego z dominującym niedoborem wody, głównymi objawami są pragnienie, postępująca hipowolemia, hiperosmolarność i hipertermia. Natomiast gdy dominuje niedobór soli (np. gdy utrata wody przez pocenie jest uzupełniana, ale utracone sole nie są), prowadzi to do hipoosmolarności i jej konsekwencji, takich jak obrzęk komórek.16

Kaskada zapalna i efekty komórkowe

Najnowsze badania zidentyfikowały kaskadę zapalnych zdarzeń patologicznych, która rozpoczyna się od łagodnego wyczerpania cieplnego i, jeśli nie zostanie przerwana, może ostatecznie prowadzić do niewydolności wielonarządowej i śmierci.17 Przy długotrwałym narażeniu na wysoką temperaturę dochodzi do aktywacji odpowiedzi ostrej fazy, która moderuje odpowiedź zapalną poprzez stymulację produkcji białek zmniejszających produkcję wolnych rodników i hamujących uwalnianie enzymów proteolitycznych.18

Podwyższona temperatura rdzenia ciała wywołuje również ekspresję białek szoku cieplnego (HSP). Białka te przejściowo zwiększają tolerancję na ciepło poprzez słabo poznane mechanizmy (np. poprzez zapobieganie denaturacji białek) oraz poprzez regulację odpowiedzi sercowo-naczyniowej.1920 Przy przedłużającym się lub ekstremalnym podwyższeniu temperatury, mechanizmy kompensacyjne zostają przytłoczone, co umożliwia wystąpienie stanu zapalnego i zespołu dysfunkcji wielonarządowej.21

W przypadku ciężkiego wyczerpania cieplnego, które może prowadzić do udaru cieplnego, obserwuje się podobieństwa do patofizjologii sepsy. Dochodzi do uszkodzenia bariery jelitowej, zwiększenia jej przepuszczalności i uwolnienia lipopolisacharydów (LPS) z jelita do krwiobiegu, co może wyzwolić ogólnoustrojową odpowiedź zapalną.2223

Model dwuścieżkowy wyczerpania cieplnego i udaru

W kontekście zrozumienia patogenezy wyczerpania cieplnego i jego progresji do udaru cieplnego, istotny jest tzw. model dwuścieżkowy (Dual Pathway Model, DPM). Model ten sugeruje, że udar cieplny jest wyzwalany przez dwie niezależne ścieżki, które są aktywowane sekwencyjnie wraz ze wzrostem temperatury rdzenia ciała powyżej 40°C.24

  1. Ścieżka „sepsy cieplnej” – związana z endotoksemią, ogólnoustrojowym zapaleniem i odpowiedzią podobną do sepsy, dominująca przy temperaturze rdzenia ciała poniżej 42°C.25
  2. Ścieżka „toksyczności cieplnej” – związana z bezpośrednim, termolitycznym działaniem wysokiej temperatury, która samodzielnie może powodować uszkodzenie i dezintegrację struktur komórkowych i narządów w organizmie, dominująca przy temperaturze rdzenia ciała powyżej 42°C.26

W przypadku wyczerpania cieplnego, pierwsza ścieżka jest zwykle aktywowana, ale nie w stopniu prowadzącym do pełnoobjawowego udaru cieplnego, chociaż niektóre mechanizmy zapalne mogą już być obecne.27

Wpływ na układ krążenia i narządy wewnętrzne

Podczas wyczerpania cieplnego dochodzi do rozszerzenia naczyń obwodowych, co skutkuje zmniejszeniem powrotu żylnego i spadkiem ciśnienia tętniczego. Krew jest przekierowywana z krążenia trzewnego do skóry i mięśni, co prowadzi do niedokrwienia przewodu pokarmowego i zwiększonej przepuszczalności błony śluzowej jelit.28

Wzrost temperatury ciała wiąże się ze zwiększonym zużyciem tlenu i podwyższonym metabolizmem, co prowadzi do hiperwentylacji i tachykardii. Układ sercowo-naczyniowy musi pracować wydajniej, pompując więcej krwi do skóry, aby umożliwić rozpraszanie ciepła. U pacjentów z wyczerpaniem cieplnym obserwuje się przyspieszony, słaby puls oraz szybki, płytki oddech.29

Jeśli wyczerpanie cieplne nie jest leczone, może dojść do uszkodzenia narządów wewnętrznych. Hepatocyty, śródbłonek naczyniowy i tkanka nerwowa są najbardziej wrażliwe na podwyższone temperatury rdzenia ciała, ale wszystkie narządy mogą ostatecznie zostać dotknięte.30 Dodatkowe obciążenie układu sercowo-naczyniowego może prowadzić do zaostrzenia chorób przewlekłych, w tym chorób układu krążenia, oddechowego i cukrzycy.31

Czynniki ryzyka i podatność

Wyczerpanie cieplne, jako stan pośredni między przegrzaniem a udarem cieplnym, może wystąpić u każdej osoby, jednak pewne grupy są szczególnie narażone na jego rozwój ze względu na specyficzne czynniki ryzyka.32

Czynniki osobnicze

Szczególnie podatne na wyczerpanie cieplne są:3334

  • Osoby starsze – z powodu zmniejszonej zdolności do aklimatyzacji, osłabionej odpowiedzi białek szoku cieplnego związanej ze starzeniem się oraz często występujących chorób współistniejących
  • Dzieci – ze względu na niższą zdolność termoregulacji i większy stosunek powierzchni ciała do masy ciała
  • Osoby z nadciśnieniem tętniczym – bardziej narażone na zaburzenia krążenia przy podwyższonej temperaturze
  • Osoby z przewlekłymi chorobami – zwłaszcza chorobami sercowo-naczyniowymi, neurodegeneracyjnymi i metabolicznymi
  • Osoby pracujące lub ćwiczące w gorącym środowisku – zwiększone wytwarzanie ciepła wewnętrznego podczas wysiłku fizycznego
  • Osoby przyjmujące niektóre leki – szczególnie diuretyki, które mogą zwiększać ryzyko odwodnienia

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Czynniki środowiskowe

Warunki środowiskowe znacząco wpływają na rozwój wyczerpania cieplnego:37

  • Wysoka temperatura otoczenia – zwłaszcza powyżej 38°C
  • Wysoka wilgotność powietrza – utrudniająca parowanie potu i efektywne ochładzanie ciała
  • Słaba cyrkulacja powietrza – ograniczająca konwekcyjne odprowadzanie ciepła
  • Długotrwała ekspozycja na wysoką temperaturę – szczególnie bez dostępu do klimatyzowanych pomieszczeń
  • Intensywny wysiłek fizyczny w wysokiej temperaturze – zwiększający wewnętrzne wytwarzanie ciepła

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Rola aklimatyzacji

Aklimatyzacja, czyli proces adaptacji organizmu do wysokich temperatur, odgrywa kluczową rolę w zapobieganiu wyczerpaniu cieplnemu. Proces ten obejmuje:40

  • Poprawę wydolności układu sercowo-naczyniowego
  • Aktywację osi renina-angiotensyna-aldosteron
  • Oszczędzanie soli przez gruczoły potowe i nerki
  • Zwiększenie zdolności do wydzielania potu
  • Rozszerzenie objętości osocza
  • Zwiększenie wskaźnika filtracji kłębuszkowej
  • Zwiększenie odporności na rabdomiolizę wysiłkową

41

Osoby nieaklimatyzowane lub dopiero co przybywające do gorącego klimatu są bardziej narażone na wyczerpanie cieplne, gdyż ich organizm nie zdążył jeszcze dostosować mechanizmów termoregulacyjnych do nowych warunków.42

Progresja do udaru cieplnego

Wyczerpanie cieplne, jeśli nie jest odpowiednio leczone, może szybko rozwinąć się w udar cieplny – stan zagrażający życiu, charakteryzujący się temperaturą rdzenia ciała przekraczającą 41°C oraz dysfunkcją ośrodkowego układu nerwowego.4344

Mechanizm przejścia od wyczerpania do udaru

Przejście od wyczerpania cieplnego do udaru cieplnego wiąże się z kilkoma kluczowymi procesami patofizjologicznymi:4546

  1. Niewydolność termoregulacji – gdy mechanizmy chłodzenia organizmu całkowicie zawodzą, temperatura ciała gwałtownie wzrasta
  2. Uszkodzenie komórkowe przez ciepło – nadmierne ciepło denaturuje białka, destabilizuje fosfolipidy i lipoproteiny oraz upłynnia lipidy błonowe
  3. Zespół ogólnoustrojowej reakcji zapalnej (SIRS) – podobnie jak w sepsie, dochodzi do kaskady zapalnej z uwalnianiem cytokin prozapalnych
  4. Koagulopatia – zaburzenia krzepnięcia mogą prowadzić do rozsianego wykrzepiania wewnątrznaczyniowego (DIC)
  5. Uszkodzenie śródbłonka naczyniowego – prowadzące do zaburzeń mikrokrążenia

Podczas udaru cieplnego dochodzi do całkowitego załamania się mechanizmu pocenia, co eliminuje główny sposób rozpraszania ciepła przez organizm. Temperatura ciała może wzrosnąć do 41°C lub wyżej w ciągu 10-15 minut.47

Różnice między wyczerpaniem cieplnym a udarem cieplnym

Kluczowe różnice między wyczerpaniem cieplnym a udarem cieplnym obejmują:4849

Parametr Wyczerpanie cieplne Udar cieplny
Temperatura ciała 37-40°C >41°C (często >42°C)
Stan świadomości Prawidłowy lub lekko zmieniony Wyraźne zaburzenia (splątanie, majaczenie, śpiączka)
Funkcja OUN Zachowana Zaburzona
Pocenie Obfite Często zahamowane (anhydroza)
Skóra Chłodna, wilgotna, blada Gorąca, sucha, zaczerwieniona
Funkcja narządów Zwykle zachowana Niewydolność wielonarządowa
Rokowanie Dobre przy odpowiednim leczeniu Poważne, wysokie ryzyko zgonu

Pacjenci z wyczerpaniem cieplnym zachowują zdolność do rozpraszania ciepła i mają prawidłową funkcję ośrodkowego układu nerwowego, podczas gdy w udarze cieplnym obserwuje się wyraźne zaburzenia neurologiczne i często zahamowanie pocenia.5051

Maksymalne obciążenie termiczne

Pojęcie „maksimum termicznego” (thermal maximum) zostało wprowadzone do określenia wielkości i czasu trwania obciążenia cieplnego, które komórki mogą wytrzymać, zanim ulegną uszkodzeniu. Ludzkie maksimum termiczne zostało ustalone jako temperatura rdzenia ciała około 42°C (107,6°F) utrzymywana przez okres od 45 minut do ośmiu godzin.52

Przy wyższych temperaturach, zniszczenie komórek następuje szybciej i bardziej kompleksowo. Uwalniane są czynniki zapalne, a przepuszczalność przewodu pokarmowego zwiększa się, co może pozwolić endotoksynom na przedostanie się do krwiobiegu. Dochodzi również do zmian hematologicznych i śródbłonkowych przypominających rozsiane wykrzepianie wewnątrznaczyniowe.53

W przypadku wyczerpania cieplnego, temperatura rdzenia ciała zazwyczaj pozostaje poniżej tego krytycznego progu, ale jeśli schładzanie organizmu nie zostanie podjęte, możliwe jest przekroczenie wartości maksimum termicznego i rozwój udaru cieplnego.54

Uszkodzenia narządowe przy wyczerpaniu cieplnym

Chociaż wyczerpanie cieplne jest zwykle stanem odwracalnym, długotrwała ekspozycja na wysoką temperaturę lub progresja do cięższych form choroby związanej z ciepłem może prowadzić do uszkodzeń różnych układów i narządów.55

Wpływ na ośrodkowy układ nerwowy

Podwzgórze, a szczególnie jądro przedwzrokowe przedniego podwzgórza, pełni kluczową rolę w regulacji temperatury ciała. Ostatnie badania wskazują, że w przypadku progresji do udaru cieplnego, podwzgórze może doznawać mikrouszkodzeń naczyniowych i ostrych zmian nekrotycznych, co zaburza centralną regulację temperatury.56

Objawy ze strony OUN przy wyczerpaniu cieplnym są zwykle łagodne i obejmują:57

  • Ból głowy
  • Zawroty głowy
  • Drażliwość
  • Osłabienie
  • Zaburzenia koncentracji

58

W przeciwieństwie do udaru cieplnego, przy wyczerpaniu cieplnym nie występują poważne zaburzenia świadomości ani dysfunkcja OUN, chociaż niektórzy pacjenci mogą wykazywać łagodne zaburzenia poznawcze.59

Układ sercowo-naczyniowy

Przy wyczerpaniu cieplnym układ sercowo-naczyniowy jest poddawany znacznemu obciążeniu z powodu konieczności zwiększenia przepływu krwi do skóry przy jednoczesnym utrzymaniu odpowiedniego przepływu przez narządy trzewne. Objawia się to:60

  • Tachykardią – jako odpowiedź na zwiększone zapotrzebowanie na przepływ krwi
  • Hipotonią – z powodu rozszerzenia naczyń obwodowych i zmniejszonego powrotu żylnego
  • Słabym napięciem tętniczym – z powodu względnej hipowolemi

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U osób z istniejącymi wcześniej chorobami serca, wyczerpanie cieplne może zwiększać ryzyko incydentów sercowo-naczyniowych. Wzrost częstości akcji serca i zwiększone obciążenie mogą być czynnikami wyzwalającymi zawał serca, szczególnie u osób starszych i osób z chorobami serca.62

Nerki i rola rabdomiolizy

Nerki są szczególnie narażone na uszkodzenie w czasie wyczerpania cieplnego z kilku powodów:63

  • Zmniejszony przepływ krwi przez nerki z powodu redystrybucji krwi do skóry
  • Odwodnienie prowadzące do zmniejszonej filtracji kłębuszkowej
  • Zwiększone stężenie produktów przemiany materii wymagających eliminacji

W ciężkich przypadkach wyczerpania cieplnego może dojść do rabdomiolizy – rozpadu tkanki mięśniowej z uwolnieniem mioglobiny do krwiobiegu. Mioglobina może zatkać kanaliki nerkowe, prowadząc do ostrego uszkodzenia nerek.64 Powtarzające się epizody wyczerpania cieplnego mogą również zwiększać ryzyko przewlekłej choroby nerek, szczególnie u osób pracujących regularnie w wysokich temperaturach bez odpowiedniego nawodnienia.65

Układ pokarmowy i wątroba

Podczas wyczerpania cieplnego krew jest przekierowywana z krążenia trzewnego do skóry, co może prowadzić do niedokrwienia narządów jamy brzusznej. Skutki tego obejmują:66

  • Nudności i wymioty – typowe objawy wyczerpania cieplnego
  • Ból brzucha – związany z niedokrwieniem jelit
  • Zwiększoną przepuszczalność bariery jelitowej – potencjalnie prowadzącą do endotoksemii

67

Wątroba, jako główny organ metaboliczny, jest również narażona na uszkodzenie w wyniku hipertermii. Hepatocyty są szczególnie wrażliwe na podwyższone temperatury rdzenia ciała.68 Chociaż poważne uszkodzenie wątroby jest rzadkie przy typowym wyczerpaniu cieplnym, może ono wystąpić przy progresji do udaru cieplnego, gdzie wątroba odgrywa kluczową rolę w eliminacji endotoksyn.69

Biochemiczne mechanizmy wyczerpania cieplnego

Na poziomie komórkowym i molekularnym, wyczerpanie cieplne wywołuje szereg procesów biochemicznych, które mogą prowadzić do zaburzeń homeostazy i potencjalnie do uszkodzenia komórek.70

Rola białek szoku cieplnego

Białka szoku cieplnego (HSP) są grupą białek opiekuńczych, których ekspresja jest indukowana przez stres termiczny. Pełnią one kluczową rolę w ochronie komórek przed uszkodzeniami wywołanymi przez ciepło:71

  • HSP70 – jedno z najważniejszych białek szoku cieplnego, pozwala komórce znosić stres środowiskowy
  • HSP działają jako „opiekunowie” białek, zapobiegając ich denaturacji
  • Hamują szlaki zapalne, w tym szlak NF-κB
  • Regulują odpowiedź sercowo-naczyniową

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W przypadku wyczerpania cieplnego, aktywowana jest odpowiedź białek szoku cieplnego, choć może być ona niewystarczająca do całkowitego zapobieżenia uszkodzeniom. Przy przedłużonym stresie cieplnym lub progresji do udaru cieplnego, ekspresja HSP może być zaburzona, co prowadzi do zmniejszonej ochrony komórek.74

Stres oksydacyjny i mitochondria

Ekspozycja na wysoką temperaturę zwiększa metabolizm komórkowy, co prowadzi do zwiększonej produkcji reaktywnych form tlenu (ROS). Nadmiar ROS może prowadzić do:75

  • Uszkodzenia DNA, białek i lipidów komórkowych
  • Aktywacji inflammasomu NLRP3 – kluczowego kompleksu białkowego w procesach zapalnych
  • Zaburzenia funkcji mitochondriów – głównych producentów energii w komórce
  • Inicjacji programowanej śmierci komórki, w tym apoptozy i piropozy

76

Mitochondria są szczególnie wrażliwe na stres cieplny. W warunkach hipertermii może dojść do kurczenia się mitochondriów, zwiększenia gęstości ich błon i zaburzenia fosforylacji oksydacyjnej, co ogranicza produkcję ATP i prowadzi do deficytu energetycznego w komórce.77

Mechanizmy śmierci komórek

Przy wyczerpaniu cieplnym, a szczególnie przy progresji do udaru cieplnego, aktywowane są różne szlaki śmierci komórkowej:78

  • Apoptoza – programowana śmierć komórki aktywowana przez stres cieplny, mediowana przez białka rodziny Bcl-2 i kaspazy
  • Piroptoza – zapalna forma śmierci komórki, zależna od aktywacji kaspazy-1 i inflammasomu
  • Ferroptoza – forma śmierci komórki zależna od żelaza i peroksydacji lipidów, nasilana przez stres oksydacyjny
  • Nekroptoza – programowana nekroza, zależna od receptorów TNF i TLR

79

W przypadku wyczerpania cieplnego, śmierć komórek jest zazwyczaj ograniczona, ale przy progresji do udaru cieplnego może dojść do masowej aktywacji szlaków śmierci komórkowej, co przyczynia się do niewydolności wielonarządowej.80

Zaburzenia bariery jelitowej i endotoksemia

Hipoteza „przeciekającego jelita” jest istotnym elementem patofizjologii chorób związanych z ciepłem. Stres cieplny powoduje:81

  • Nadmierne otwarcie połączeń ścisłych (tight junctions) w nabłonku jelitowym
  • Zniszczenie struktury i funkcji komórek jelitowych
  • Zwiększenie przepuszczalności błony śluzowej jelita
  • Przedostawanie się endotoksyn (LPS) do krwiobiegu

82

Bariera fizyczna tworzona przez połączenia ścisłe jest kluczowa dla zdrowia jelit i składa się z klaudyn, oklaudyn i wewnątrzkomórkowych białek płytki zonula occludens (ZO-1, ZO-2 i ZO-3). Przy stresie cieplnym, liczne kinazy i fosfatazy fosforylują białka połączeń ścisłych, co prowadzi do zmniejszonej interakcji oklaudyn i klaudyn z zonula-occludens, wpływając na przepuszczalność jelit.83

Endotoksyny uwolnione do krwiobiegu mogą aktywować białe krwinki, które atakują „skażenie” we krwi, tworząc skrzepy. Te skrzepy mogą prowadzić do niewydolności wielonarządowej.84

Choć najbardziej nasilone zaburzenia bariery jelitowej obserwuje się w udarze cieplnym, już na etapie wyczerpania cieplnego mogą występować początkowe zaburzenia integralności nabłonka jelitowego, stanowiące potencjalny czynnik ryzyka progresji do cięższych stanów.85

Podsumowanie patogenezy wyczerpania cieplnego

Wyczerpanie cieplne jest złożonym stanem patofizjologicznym, który rozwija się gdy obciążenie cieplne przekracza zdolność organizmu do rozpraszania ciepła, ale nie osiąga jeszcze poziomu powodującego całkowitą niewydolność termoregulacji i poważne uszkodzenia wielonarządowe, jak w udarze cieplnym.86

Główne mechanizmy patogenetyczne wyczerpania cieplnego obejmują:87

  • Zaburzenie równowagi między wytwarzaniem a rozpraszaniem ciepła
  • Utratę płynów i elektrolitów poprzez nadmierne pocenie się
  • Redystrybucję krwi do skóry kosztem narządów wewnętrznych
  • Względną hipowolemia i hipotonię
  • Aktywację odpowiedzi zapalnej i stresu oksydacyjnego
  • Indukcję białek szoku cieplnego jako mechanizmu ochronnego
  • Wczesne zaburzenia bariery jelitowej

88

Skuteczne rozpoznanie i leczenie wyczerpania cieplnego jest kluczowe, aby zapobiec jego progresji do udaru cieplnego, który stanowi zagrożenie dla życia. Przy odpowiednim leczeniu, większość pacjentów z wyczerpaniem cieplnym powraca do zdrowia w ciągu 24-48 godzin bez długotrwałych następstw.8990

Zrozumienie złożonych mechanizmów patogenetycznych wyczerpania cieplnego jest niezbędne dla opracowania skutecznych strategii profilaktycznych i terapeutycznych, zwłaszcza w kontekście globalnego ocieplenia i zwiększającego się ryzyka ekspozycji na wysokie temperatury.91

Kolejne rozdziały

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  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 The pathophysiology of heat exposure
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4843928/
    Heat exposure of the body can result in different physiological/pathological outcomes. Behavioral (e.g., cold seeking) and autonomic (e.g., skin vasodilation, sweating) warmth-defense effectors are recruited to maintain normal body temperature. Physiologically, successful activation of the effectors results in warmth tolerance. In case of repeated, chronic heat exposure the tolerance intensifies leading to heat acclimation. […] Heat-related illnesses develop when the pathological effects of heat load are not prevented. Syndromes vary from less severe, such as heat syncope to severe forms as lethal heat stroke. […] In severe hypovolemia, heat exhaustion develops with domination of water- or salt-depletion. The former is mainly due to insufficient fluid replacement and consists of thirst, progressive hypovolemia, hyperosmolarity and hyperthermia. Salt-depletion dominates when sweating-induced water loss is replaced, but salt is not (e.g., by soft drinks), leading to hypoosmolarity and its consequences (e.g., cell swelling).
  • #2 Heat exhaustion – PubMed
    https://pubmed.ncbi.nlm.nih.gov/30459023/
    Heat exhaustion is part of a spectrum of heat-related illnesses that can affect all individuals, although children, older adults, and those with chronic disease are particularly vulnerable due to their impaired ability to dissipate heat. […] If left uninterrupted, there can be progression of symptoms to heatstroke, a life-threatening emergency. Signs and symptoms of heat exhaustion may develop suddenly or over time. Exposure to a hot environment for a prolonged period and performing exercise or work in the heat can overwhelm the body’s ability to cool itself, causing heat exhaustion. Heat exhaustion can be worsened by dehydration due to inadequate access to water or insufficient fluid replacement. Heat exhaustion can be managed by the immediate reduction of heat gain by discontinuing exercise and reducing radiative heat source exposure. The individual should be encouraged to drink cool fluids and remove or loosen clothing to facilitate heat loss. In more extreme situations, more aggressive cooling strategies (e.g., cold shower, application of wet towels) to lower core temperature should be employed. Heat-related illnesses such as heat exhaustion can be prevented by increasing public awareness of the risks associated with exposure to high temperatures and prolonged exercise.
  • #3 Heat exhaustion – Wikipedia
    https://en.wikipedia.org/wiki/Heat_exhaustion
    Heat exhaustion is a heat-related illness characterized by the body’s inability to effectively cool itself, typically occurring in high ambient temperatures or during intense physical exertion. […] In heat exhaustion, core body temperature ranges from 37 C to 40 C (98.6 F to 104 F). Symptoms include profuse sweating, weakness, dizziness, headache, nausea, and lowered blood pressure, resulting from dehydration and serum electrolyte depletion. […] Heat exhaustion is a moderate form of heat-related illness characterized by increasingly overwhelmed thermoregulatory mechanisms. In heat exhaustion, the core body temperature rises to between 37 C and 40 C (98.6 F and 104 F). To dissipate heat, blood flow to the skin can increase up to 8 liters per minute, accounting for a significant proportion of the cardiac output.
  • #4 Heat exhaustion – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/heat-exhaustion/symptoms-causes/syc-20373250
    Heat exhaustion is a condition that happens when your body overheats. […] Without prompt treatment, heat exhaustion can lead to heatstroke, a life-threatening condition. […] In hot weather, your body cools itself mainly by sweating. The evaporation of your sweat regulates your body temperature. But when you exercise strenuously or otherwise overexert in hot, humid weather, your body is less able to cool itself efficiently. […] If heat exhaustion isn’t treated, it can lead to heatstroke. Heatstroke is a life-threatening condition. It happens when your core body temperature reaches 104 F (40 C) or higher. Heatstroke needs immediate medical attention to prevent permanent damage to your brain and other vital organs that can result in death.
  • #5 Heat Stroke: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/166320-overview
    Despite wide variations in ambient temperatures, humans and other mammals can maintain a constant body temperature by balancing heat gain with heat loss. When heat gain overwhelms the body’s mechanisms of heat loss, the body temperature rises, potentially leading to heat stroke. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death. […] The exact temperature at which cardiovascular collapse occurs varies among individuals because coexisting disease, drugs, and other factors may contribute to or delay organ dysfunction. Full recovery has been observed in patients with temperatures as high as 46C, and death has occurred in patients with much lower temperatures. Temperatures exceeding 106F or 41.1C generally are catastrophic and require immediate aggressive therapy.
  • #6 Nonexertional (classic) heat stroke in adults – UpToDate
    https://www.uptodate.com/contents/nonexertional-classic-heat-stroke-in-adults
    Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.
  • #7 Heat stress: what is it and how is it measured? | Copernicus
    https://climate.copernicus.eu/heat-stress-what-it-and-how-it-measured
    Heat stress refers to the build-up of body heat generated either internally by muscle use or externally by the environment. It occurs when the heat a body absorbs from the environment exceeds the body’s ability to dissipate it. […] Heat stress generally results from a combination of factors, such as high ambient temperatures, humidity, physical activity, and inadequate fluid intake. Various factors influence the human body’s ability to keep its core temperature within certain boundaries. The human heat budget results from the balance between the heat produced by the human body and the heat exchanged with the surrounding environment. This balance is controlled by the body’s thermoregulatory system (the hypothalamus, sweat glands, circulatory system, and skin), physiology (the way the body functions) and behaviour, which covers things like eating and drinking, activity and resting, clothing, and so on.
  • #8 Nonexertional (classic) heat stroke in adults – UpToDate
    https://www.uptodate.com/contents/nonexertional-classic-heat-stroke-in-adults
    Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.
  • #9 Heat exhaustion – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/heat-exhaustion/symptoms-causes/syc-20373250
    Heat exhaustion is a condition that happens when your body overheats. […] Without prompt treatment, heat exhaustion can lead to heatstroke, a life-threatening condition. […] In hot weather, your body cools itself mainly by sweating. The evaporation of your sweat regulates your body temperature. But when you exercise strenuously or otherwise overexert in hot, humid weather, your body is less able to cool itself efficiently. […] If heat exhaustion isn’t treated, it can lead to heatstroke. Heatstroke is a life-threatening condition. It happens when your core body temperature reaches 104 F (40 C) or higher. Heatstroke needs immediate medical attention to prevent permanent damage to your brain and other vital organs that can result in death.
  • #10 Heat exhaustion – Wikipedia
    https://en.wikipedia.org/wiki/Heat_exhaustion
    Heat exhaustion is a heat-related illness characterized by the body’s inability to effectively cool itself, typically occurring in high ambient temperatures or during intense physical exertion. […] In heat exhaustion, core body temperature ranges from 37 C to 40 C (98.6 F to 104 F). Symptoms include profuse sweating, weakness, dizziness, headache, nausea, and lowered blood pressure, resulting from dehydration and serum electrolyte depletion. […] Heat exhaustion is a moderate form of heat-related illness characterized by increasingly overwhelmed thermoregulatory mechanisms. In heat exhaustion, the core body temperature rises to between 37 C and 40 C (98.6 F and 104 F). To dissipate heat, blood flow to the skin can increase up to 8 liters per minute, accounting for a significant proportion of the cardiac output.
  • #11 Management of Heatstroke and Heat Exhaustion | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0601/p2133.html/1000
    Heat exhaustion and heatstroke are part of a continuum of heat-related illness. Both are common and preventable conditions affecting diverse patients. Recent research has identified a cascade of inflammatory pathologic events that begins with mild heat exhaustion and, if uninterrupted, can lead eventually to multiorgan failure and death. […] Heatstroke and heat exhaustion occur when the bodys thermoregulatory responses are inadequate to preserve homeostasis. This can result from extrinsic factors that make heat dissipation less efficient, such as extremes of temperature, physical effort, and environmental conditions. It also can result from physiologic limitations, putting children, elderly persons, and those who are chronically ill at increased risk. Chronic volume depletion, medication use, inability to increase cardiovascular output, normal deficiencies in heat shock protein responses associated with aging, and lack of acclimatization all can inhibit the bodys ability to respond to heat challenges.
  • #12 Heat Exhaustion: Symptoms, Causes, and Treatment | Red Cross
    https://www.redcross.org/take-a-class/resources/learn-first-aid/heat-exhaustion?srsltid=AfmBOooFCf5ajp5OYpJxuJ-ulN2_uhCZE3JD_3vdDjnMJHvtoa7TDop3
    Heat exhaustion occurs when fluids lost through sweating are not replaced. […] The body’s primary mechanism of cooling itself is through sweating. […] If a person does not take in enough fluids, the body does not have what it needs to make adequate amounts of sweat. […] Heat exhaustion is often accompanied by dehydration, as the body’s excessive production of sweat in an attempt to cool itself depletes fluid levels in the body. […] Also, humid environments and environments without good air circulation can make it difficult for the sweat to evaporate. Under these conditions, a person may develop heat exhaustion. […] The first is not getting enough fluids. Heat exhaustion occurs when fluids lost through sweating are not replaced. […] If a person does not take in enough fluids, the body does not have what it needs to make adequate amounts of sweat. Heat exhaustion is often accompanied by dehydration. […] Environmental temperatures that are greater than 100 F (38 C) increase risk. However, if someone is unaccustomed to labor or exercise in the heat, they can develop a heat-related illness at lower environmental temperatures.
  • #13 Heat Exhaustion: Symptoms, Causes, and Treatment | Red Cross
    https://www.redcross.org/take-a-class/resources/learn-first-aid/heat-exhaustion?srsltid=AfmBOooFCf5ajp5OYpJxuJ-ulN2_uhCZE3JD_3vdDjnMJHvtoa7TDop3
    Heat exhaustion occurs when fluids lost through sweating are not replaced. […] The body’s primary mechanism of cooling itself is through sweating. […] If a person does not take in enough fluids, the body does not have what it needs to make adequate amounts of sweat. […] Heat exhaustion is often accompanied by dehydration, as the body’s excessive production of sweat in an attempt to cool itself depletes fluid levels in the body. […] Also, humid environments and environments without good air circulation can make it difficult for the sweat to evaporate. Under these conditions, a person may develop heat exhaustion. […] The first is not getting enough fluids. Heat exhaustion occurs when fluids lost through sweating are not replaced. […] If a person does not take in enough fluids, the body does not have what it needs to make adequate amounts of sweat. Heat exhaustion is often accompanied by dehydration. […] Environmental temperatures that are greater than 100 F (38 C) increase risk. However, if someone is unaccustomed to labor or exercise in the heat, they can develop a heat-related illness at lower environmental temperatures.
  • #14 Heat stroke pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Heat_stroke_pathophysiology
    Heat stress means perceived discomfort and physiologic strains during heat exposure. A series of physiologic events occur to adapt heat. These events include thermoregulation (with acclimatization), an acute-phase response, and production of heat shock proteins. If these sequence of actions fails to prevents body from high temperature, heat stress progresses to heat stroke. […] The core body temperature is set to 37 C. Thermoregulatory center is located in hypothalamus, every 1 C in body temperature activates the peripheral and central receptors to maintain core body temperature at 37 C. […] Increased sweating will cause loss of salt and water up to 2 liters per hour. Therefore, dehydration may worsen thermoregulation. […] Acclimatization, involves enhancement of cardiovascular performance, activation of the reninangiotensinaldosterone axis, salt conservation by the sweat glands and kidneys, an increase in the capacity to secrete sweat, expansion of plasma volume, an increase in the glomerular filtration rate, and an increase in the ability to resist exertional rhabdomyolysis.
  • #15 Heat Exhaustion: Symptoms, Causes, and Treatment | Red Cross
    https://www.redcross.org/take-a-class/resources/learn-first-aid/heat-exhaustion?srsltid=AfmBOooFCf5ajp5OYpJxuJ-ulN2_uhCZE3JD_3vdDjnMJHvtoa7TDop3
    Heat exhaustion occurs when fluids lost through sweating are not replaced. […] The body’s primary mechanism of cooling itself is through sweating. […] If a person does not take in enough fluids, the body does not have what it needs to make adequate amounts of sweat. […] Heat exhaustion is often accompanied by dehydration, as the body’s excessive production of sweat in an attempt to cool itself depletes fluid levels in the body. […] Also, humid environments and environments without good air circulation can make it difficult for the sweat to evaporate. Under these conditions, a person may develop heat exhaustion. […] The first is not getting enough fluids. Heat exhaustion occurs when fluids lost through sweating are not replaced. […] If a person does not take in enough fluids, the body does not have what it needs to make adequate amounts of sweat. Heat exhaustion is often accompanied by dehydration. […] Environmental temperatures that are greater than 100 F (38 C) increase risk. However, if someone is unaccustomed to labor or exercise in the heat, they can develop a heat-related illness at lower environmental temperatures.
  • #16 The pathophysiology of heat exposure
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4843928/
    Heat exposure of the body can result in different physiological/pathological outcomes. Behavioral (e.g., cold seeking) and autonomic (e.g., skin vasodilation, sweating) warmth-defense effectors are recruited to maintain normal body temperature. Physiologically, successful activation of the effectors results in warmth tolerance. In case of repeated, chronic heat exposure the tolerance intensifies leading to heat acclimation. […] Heat-related illnesses develop when the pathological effects of heat load are not prevented. Syndromes vary from less severe, such as heat syncope to severe forms as lethal heat stroke. […] In severe hypovolemia, heat exhaustion develops with domination of water- or salt-depletion. The former is mainly due to insufficient fluid replacement and consists of thirst, progressive hypovolemia, hyperosmolarity and hyperthermia. Salt-depletion dominates when sweating-induced water loss is replaced, but salt is not (e.g., by soft drinks), leading to hypoosmolarity and its consequences (e.g., cell swelling).
  • #17 Management of Heatstroke and Heat Exhaustion | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0601/p2133.html
    Heat exhaustion and heatstroke are part of a continuum of heat-related illness. Both are common and preventable conditions affecting diverse patients. Recent research has identified a cascade of inflammatory pathologic events that begins with mild heat exhaustion and, if uninterrupted, can lead eventually to multiorgan failure and death. […] Heat exhaustion is characterized by nonspecific symptoms such as malaise, headache, and nausea. […] Untreated heat exhaustion can progress to heatstroke, a much more serious illness involving central nervous system dysfunction such as delirium and coma. […] Heatstroke and heat exhaustion occur when the bodys thermoregulatory responses are inadequate to preserve homeostasis. This can result from extrinsic factors that make heat dissipation less efficient, such as extremes of temperature, physical effort, and environmental conditions. It also can result from physiologic limitations, putting children, elderly persons, and those who are chronically ill at increased risk. Chronic volume depletion, medication use, inability to increase cardiovascular output, normal deficiencies in heat shock protein responses associated with aging, and lack of acclimatization all can inhibit the bodys ability to respond to heat challenges.
  • #18 Overview of Heat Illness – Injuries; Poisoning – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/injuries-poisoning/heat-illness/overview-of-heat-illness
    Patients with heat exhaustion maintain the ability to dissipate heat and have normal central nervous system (CNS) function. […] The body can compensate for large variations in heat load, but prolonged or excessive exposure to heat that exceeds capacity for heat dissipation increases core temperature. Modest, transient core temperature elevations are tolerable, but severe elevations (typically 41 C) can lead to protein denaturation and the release of inflammatory cytokines. As a result, cellular dysfunction may occur and an inflammatory cascade may be activated, leading to multiorgan dysfunction similar to that which follows prolonged shock. […] Compensatory mechanisms include an acute-phase response that moderates the inflammatory response (eg, by stimulating production of proteins that decrease production of free radicals and inhibit release of proteolytic enzymes). Also, increased core temperature triggers expression of heat-shock proteins. These proteins transiently enhance heat tolerance by poorly understood mechanisms (eg, possibly by preventing protein denaturation) and by regulation of cardiovascular responses. With prolonged or extreme temperature elevation, compensatory mechanisms are overwhelmed, allowing inflammation and multiple organ dysfunction syndrome to occur.
  • #19 Overview of Heat Illness – Injuries; Poisoning – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/injuries-poisoning/heat-illness/overview-of-heat-illness
    Patients with heat exhaustion maintain the ability to dissipate heat and have normal central nervous system (CNS) function. […] The body can compensate for large variations in heat load, but prolonged or excessive exposure to heat that exceeds capacity for heat dissipation increases core temperature. Modest, transient core temperature elevations are tolerable, but severe elevations (typically 41 C) can lead to protein denaturation and the release of inflammatory cytokines. As a result, cellular dysfunction may occur and an inflammatory cascade may be activated, leading to multiorgan dysfunction similar to that which follows prolonged shock. […] Compensatory mechanisms include an acute-phase response that moderates the inflammatory response (eg, by stimulating production of proteins that decrease production of free radicals and inhibit release of proteolytic enzymes). Also, increased core temperature triggers expression of heat-shock proteins. These proteins transiently enhance heat tolerance by poorly understood mechanisms (eg, possibly by preventing protein denaturation) and by regulation of cardiovascular responses. With prolonged or extreme temperature elevation, compensatory mechanisms are overwhelmed, allowing inflammation and multiple organ dysfunction syndrome to occur.
  • #20 Heat stroke pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Heat_stroke_pathophysiology
    Endothelial cells, leukocytes, and epithelial cells incorporate a variety of cytokines (mainly interleukin-1 and interleukin-6) to protect against tissue injury and promote repair. […] Heat-shock proteins are secreted in response to heat to protect cells from injury. Heat-shock proteins bind to proteins and act as chaperons to prevent them from denaturation. […] Severe heat stroke causes vascular congestion and/or hemorrhage, thrombi, increased inflammatory cells, and disruption of architecture in many internal organs including: liver, jejunum, spleen, lungs, and kidneys.
  • #21 Overview of Heat Illness – Injuries; Poisoning – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/injuries-poisoning/heat-illness/overview-of-heat-illness
    Patients with heat exhaustion maintain the ability to dissipate heat and have normal central nervous system (CNS) function. […] The body can compensate for large variations in heat load, but prolonged or excessive exposure to heat that exceeds capacity for heat dissipation increases core temperature. Modest, transient core temperature elevations are tolerable, but severe elevations (typically 41 C) can lead to protein denaturation and the release of inflammatory cytokines. As a result, cellular dysfunction may occur and an inflammatory cascade may be activated, leading to multiorgan dysfunction similar to that which follows prolonged shock. […] Compensatory mechanisms include an acute-phase response that moderates the inflammatory response (eg, by stimulating production of proteins that decrease production of free radicals and inhibit release of proteolytic enzymes). Also, increased core temperature triggers expression of heat-shock proteins. These proteins transiently enhance heat tolerance by poorly understood mechanisms (eg, possibly by preventing protein denaturation) and by regulation of cardiovascular responses. With prolonged or extreme temperature elevation, compensatory mechanisms are overwhelmed, allowing inflammation and multiple organ dysfunction syndrome to occur.
  • #22 Heat stroke – Wikipedia
    https://en.wikipedia.org/wiki/Heat_stroke
    The pathophysiology of heat stroke involves an intense heat overload followed by a failure of the body’s thermoregulatory mechanisms. More specifically, heat stroke leads to inflammatory and coagulation responses that can damage the vascular endothelium and result in numerous platelet complications, including decreased platelet counts, platelet clumping, and suppressed platelet release from bone marrow. […] Growing evidence also suggests the existence of a second pathway underlying heat stroke that involves heat and exercise-driven endotoxemia. Although its exact mechanism is not yet fully understood, this model theorizes that extreme exercise and heat disrupt the intestinal barrier by making it more permeable and allowing lipopolysaccharides (LPS) from gram-negative bacteria within the gut to move into the circulatory system. High blood LPS levels can then trigger a systemic inflammatory response and eventually lead to sepsis and related consequences like blood coagulation, multi-organ failure, necrosis, and central nervous system dysfunction.
  • #23 Heat Sepsis Precedes Heat Toxicity in the Pathophysiology of Heat Stroke—A New Paradigm on an Ancient Disease
    https://www.mdpi.com/2076-3921/7/11/149
    Heat stroke (HS) is an ancient illness dating back more than 2000 years and continues to be a health threat and to cause fatality during physical exertion, especially in military personnel, fire-fighters, athletes, and outdoor laborers. […] However, pathological and clinical reports from HS victims and research evidence from animal and human studies support the notion that heat alone does not fully explain the pathophysiology of HS and that HS may also be triggered and driven by heat- and exercise-induced endotoxemia. […] The dual pathway model (DPM) of HS proposed that HS is triggered by two independent pathways sequentially along the core temperature continuum of >40 °C. HS is triggered by heat sepsis at Tc < 42 °C and by the heat toxicity at Tc > 42 °C, where the direct effects of heat alone can cause cellular and organ damage. Therefore, heat sepsis precedes heat toxicity in the pathophysiology of HS.
  • #24 Heat Sepsis Precedes Heat Toxicity in the Pathophysiology of Heat Stroke—A New Paradigm on an Ancient Disease
    https://www.mdpi.com/2076-3921/7/11/149
    Heat stroke (HS) is an ancient illness dating back more than 2000 years and continues to be a health threat and to cause fatality during physical exertion, especially in military personnel, fire-fighters, athletes, and outdoor laborers. […] However, pathological and clinical reports from HS victims and research evidence from animal and human studies support the notion that heat alone does not fully explain the pathophysiology of HS and that HS may also be triggered and driven by heat- and exercise-induced endotoxemia. […] The dual pathway model (DPM) of HS proposed that HS is triggered by two independent pathways sequentially along the core temperature continuum of >40 °C. HS is triggered by heat sepsis at Tc < 42 °C and by the heat toxicity at Tc > 42 °C, where the direct effects of heat alone can cause cellular and organ damage. Therefore, heat sepsis precedes heat toxicity in the pathophysiology of HS.
  • #25 Heat Sepsis Precedes Heat Toxicity in the Pathophysiology of Heat Stroke—A New Paradigm on an Ancient Disease
    https://www.mdpi.com/2076-3921/7/11/149
    There is a growing body of evidence in the last three decades that supports the notion that heat- and exercise-induced endotoxemia may play important roles in the pathophysiology of HS independently from the effects of heat stress. […] The evidence presented suggests that endotoxemia may play important roles that are independent from heat in the pathophysiology of HS. […] The DPM suggests that HS is triggered by two independent pathways that are activated sequentially. The first pathway is due to endotoxemia, systemic inflammation and the sepsis response, and is labelled as the “heat sepsis” pathway. […] The second pathway in the DPM is due to the thermolytic effects of heat, which is also known as the heat toxicity pathway, where high temperature alone can cause disintegration and damage to cellular structures and organs in the body.
  • #26 Heat Sepsis Precedes Heat Toxicity in the Pathophysiology of Heat Stroke—A New Paradigm on an Ancient Disease
    https://www.mdpi.com/2076-3921/7/11/149
    There is a growing body of evidence in the last three decades that supports the notion that heat- and exercise-induced endotoxemia may play important roles in the pathophysiology of HS independently from the effects of heat stress. […] The evidence presented suggests that endotoxemia may play important roles that are independent from heat in the pathophysiology of HS. […] The DPM suggests that HS is triggered by two independent pathways that are activated sequentially. The first pathway is due to endotoxemia, systemic inflammation and the sepsis response, and is labelled as the “heat sepsis” pathway. […] The second pathway in the DPM is due to the thermolytic effects of heat, which is also known as the heat toxicity pathway, where high temperature alone can cause disintegration and damage to cellular structures and organs in the body.
  • #27 Heat Sepsis Precedes Heat Toxicity in the Pathophysiology of Heat Stroke—A New Paradigm on an Ancient Disease
    https://www.mdpi.com/2076-3921/7/11/149
    The suggestion of 42 °C as the Tc cross-over point between the two DPM pathways should be taken conceptually and not as an absolute and fixed cross-over point in the DPM. […] The DPM promotes giving equal emphasis to the level of heat stress and to protecting against the development of endotoxemia in the prevention of HS.
  • #28 Nonexertional (classic) heat stroke in adults – UpToDate
    https://www.uptodate.com/contents/nonexertional-classic-heat-stroke-in-adults
    Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.
  • #29 Heat Exhaustion and Heat Stroke – Mississippi State Department of Health
    https://msdh.ms.gov/page/43,3942,98,261.html
    Heat exhaustion is a milder form of heat-related illness that can develop after long exposure to high temperatures and inadequate water. […] Those most prone to heat exhaustion are elderly people, people with high blood pressure, and people working or exercising in a hot environment. […] The skin may be cool and moist. The victim’s pulse rate will be fast and weak, and breathing will be fast and shallow. If heat exhaustion is untreated, it may progress to heat stroke. […] Heat stroke occurs when the body’s temperature rises rapidly, the sweating mechanism fails, and the body is unable to cool down. Body temperature may rise to 106 degrees or higher within 10 to 15 minutes. Heat stroke can cause death or permanent disability if emergency treatment is not provided.
  • #30 Nonexertional (classic) heat stroke in adults – UpToDate
    https://www.uptodate.com/contents/nonexertional-classic-heat-stroke-in-adults
    Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.
  • #31
    https://www.who.int/news-room/fact-sheets/detail/climate-change-heat-and-health
    The bodys inability to regulate internal temperature and eliminate heat gain in such conditions increases the risk of heat exhaustion and heatstroke. […] The strain put on the body as it tries to cool itself also stresses the heart and kidneys. As a result, heat extremes can worsen health risks from chronic conditions (cardiovascular, mental, respiratory and diabetes related conditions) and cause acute kidney injury.
  • #32 Heat exhaustion – PubMed
    https://pubmed.ncbi.nlm.nih.gov/30459023/
    Heat exhaustion is part of a spectrum of heat-related illnesses that can affect all individuals, although children, older adults, and those with chronic disease are particularly vulnerable due to their impaired ability to dissipate heat. […] If left uninterrupted, there can be progression of symptoms to heatstroke, a life-threatening emergency. Signs and symptoms of heat exhaustion may develop suddenly or over time. Exposure to a hot environment for a prolonged period and performing exercise or work in the heat can overwhelm the body’s ability to cool itself, causing heat exhaustion. Heat exhaustion can be worsened by dehydration due to inadequate access to water or insufficient fluid replacement. Heat exhaustion can be managed by the immediate reduction of heat gain by discontinuing exercise and reducing radiative heat source exposure. The individual should be encouraged to drink cool fluids and remove or loosen clothing to facilitate heat loss. In more extreme situations, more aggressive cooling strategies (e.g., cold shower, application of wet towels) to lower core temperature should be employed. Heat-related illnesses such as heat exhaustion can be prevented by increasing public awareness of the risks associated with exposure to high temperatures and prolonged exercise.
  • #33 Heat Exhaustion and Heat Stroke – Mississippi State Department of Health
    https://msdh.ms.gov/page/43,3942,98,261.html
    Heat exhaustion is a milder form of heat-related illness that can develop after long exposure to high temperatures and inadequate water. […] Those most prone to heat exhaustion are elderly people, people with high blood pressure, and people working or exercising in a hot environment. […] The skin may be cool and moist. The victim’s pulse rate will be fast and weak, and breathing will be fast and shallow. If heat exhaustion is untreated, it may progress to heat stroke. […] Heat stroke occurs when the body’s temperature rises rapidly, the sweating mechanism fails, and the body is unable to cool down. Body temperature may rise to 106 degrees or higher within 10 to 15 minutes. Heat stroke can cause death or permanent disability if emergency treatment is not provided.
  • #34 Nonexertional (classic) heat stroke in adults – UpToDate
    https://www.uptodate.com/contents/nonexertional-classic-heat-stroke-in-adults
    Heat stroke is defined as an elevated core body temperature, usually in excess of 40.5°C (105°F), with associated central nervous system (CNS) dysfunction in the setting of a large environmental heat load that cannot be dissipated. It is a potentially fatal condition that requires rapid identification and treatment. […] Important risk factors for the development of nonexertional (classic) heat stroke include extremes of age, pregnancy, obesity, poor physical condition, lack of acclimatization, lack of air conditioning, and social isolation. Dehydration resulting from inadequate water intake to replace fluids lost by sweating is an important factor. […] The diagnosis of nonexertional (classic) heat stroke is made clinically based upon an elevated core body temperature (generally >40.5°C [105°F]), central nervous system (CNS) dysfunction (eg, altered mental status), and exposure to severe environmental heat.
  • #35 Nonexertional (classic) heat stroke in adults – UpToDate
    https://www.uptodate.com/contents/nonexertional-classic-heat-stroke-in-adults
    Heat stroke is defined as an elevated core body temperature, usually in excess of 40.5°C (105°F), with associated central nervous system (CNS) dysfunction in the setting of a large environmental heat load that cannot be dissipated. It is a potentially fatal condition that requires rapid identification and treatment. […] Important risk factors for the development of nonexertional (classic) heat stroke include extremes of age, pregnancy, obesity, poor physical condition, lack of acclimatization, lack of air conditioning, and social isolation. Dehydration resulting from inadequate water intake to replace fluids lost by sweating is an important factor. […] The diagnosis of nonexertional (classic) heat stroke is made clinically based upon an elevated core body temperature (generally >40.5°C [105°F]), central nervous system (CNS) dysfunction (eg, altered mental status), and exposure to severe environmental heat.
  • #36 Heat Exhaustion Symptoms & First Aid | St John Ambulance
    https://www.sja.org.uk/get-advice/first-aid-advice/effects-of-heat-and-cold/heat-exhaustion/
    Heat exhaustion is caused by a loss of salt and water from the body, usually through excessive sweating. […] Heat exhaustion isn’t always caused by weather and can be a consequence of the body producing more heat than it can lose during vigorous and/or endurance exercise. […] Some prescribed medication can make people more susceptible to heat illness (for example, Selective Serotonin Reuptake Inhibitors like Sertraline and Tricyclic Antidepressants like Amitryptaline).
  • #37 Heat Exhaustion: Symptoms, Causes, and Treatment | Red Cross
    https://www.redcross.org/take-a-class/resources/learn-first-aid/heat-exhaustion?srsltid=AfmBOooFCf5ajp5OYpJxuJ-ulN2_uhCZE3JD_3vdDjnMJHvtoa7TDop3
    Heat exhaustion occurs when fluids lost through sweating are not replaced. […] The body’s primary mechanism of cooling itself is through sweating. […] If a person does not take in enough fluids, the body does not have what it needs to make adequate amounts of sweat. […] Heat exhaustion is often accompanied by dehydration, as the body’s excessive production of sweat in an attempt to cool itself depletes fluid levels in the body. […] Also, humid environments and environments without good air circulation can make it difficult for the sweat to evaporate. Under these conditions, a person may develop heat exhaustion. […] The first is not getting enough fluids. Heat exhaustion occurs when fluids lost through sweating are not replaced. […] If a person does not take in enough fluids, the body does not have what it needs to make adequate amounts of sweat. Heat exhaustion is often accompanied by dehydration. […] Environmental temperatures that are greater than 100 F (38 C) increase risk. However, if someone is unaccustomed to labor or exercise in the heat, they can develop a heat-related illness at lower environmental temperatures.
  • #38 Heat stress: what is it and how is it measured? | Copernicus
    https://climate.copernicus.eu/heat-stress-what-it-and-how-it-measured
    Symptoms of heat stress include elevated core body temperature, increased heart rate, rapid breathing, excessive sweating, nausea, dizziness, and in severe cases, heat-related illnesses like heat exhaustion or heat stroke – a potentially life-threatening medical emergency. […] Heat strain refers to the physiological and psychological responses of the body to heat stress. It encompasses the measurable changes in the body’s functions and performance due to exposure to heat. Physiological responses like changes in heart rate, core body temperature, skin temperature and sweating rate are considered indicators of heat strain. […] Several key risk factors contribute to the susceptibility of individuals to heat stress. Environmental conditions, such as high temperatures and humidity levels, play a pivotal role in elevating the risk by decreasing sweat evaporation, which is the human body’s main cooling mechanism.
  • #39 Heat Illness Prevention | What Causes Heat Illness?
    https://www.dir.ca.gov/dosh/etools/08-006/whatcauses.htm
    Heat illness results when the body is out of heat balance. Heat balance means that the heat the body produces equals the heat it looses. When the body is out of Heat balance it produces and retains more heat than it looses causing heat illness. […] Heat building-up inside the body from moving muscles during physical work activities is the major source of heat build-up in the body. About 75% of the stored energy the body uses to do physical work is converted into heat. Only about 25% of the energy is converted into the movements required to perform work. The more strenuous the physical activity, the more internal heat the body produces. Performing physical work activities when risk factors for heat illness are present increases the internal heat the body produces. […] Heat build-up inside the body from physical work activities is the major source of heat load. In combination with this, working where the environmental and personal risk factors listed above are present, creates an even greater possibility that heat illness could occur.
  • #40 Heat stroke pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Heat_stroke_pathophysiology
    Heat stress means perceived discomfort and physiologic strains during heat exposure. A series of physiologic events occur to adapt heat. These events include thermoregulation (with acclimatization), an acute-phase response, and production of heat shock proteins. If these sequence of actions fails to prevents body from high temperature, heat stress progresses to heat stroke. […] The core body temperature is set to 37 C. Thermoregulatory center is located in hypothalamus, every 1 C in body temperature activates the peripheral and central receptors to maintain core body temperature at 37 C. […] Increased sweating will cause loss of salt and water up to 2 liters per hour. Therefore, dehydration may worsen thermoregulation. […] Acclimatization, involves enhancement of cardiovascular performance, activation of the reninangiotensinaldosterone axis, salt conservation by the sweat glands and kidneys, an increase in the capacity to secrete sweat, expansion of plasma volume, an increase in the glomerular filtration rate, and an increase in the ability to resist exertional rhabdomyolysis.
  • #41 Heat Stress | Mine Safety and Health Administration (MSHA)
    http://www.msha.gov/safety-and-health/safety-and-health-materials/heat-stress
    The objective of controls in a hot work site is to keep workers body core temperature from rising above 100F (38C). Excessive heat gained by the human body must be offset by adequate periods of heat loss. […] A combination of engineering controls and proper work practices is possibly the best solution. […] Acclimatization is a long-term adjustment of an individual to a stress. Repeated exposure to heat stress can increase many workers tolerance to heat.
  • #42 Heat Illness Prevention | What Causes Heat Illness?
    https://www.dir.ca.gov/dosh/etools/08-006/whatcauses.htm
    Being thirsty is not a good signal of the bodys need for water. By the time a person is thirsty they may have already lost too much water and their work performance has already declined. […] Alcohol increases dehydration and the bodys requirements for water. Sweating can cause the body to loose large amount of water. As the body becomes dehydrated more water is required to replace bodily fluids. Dehydration increases a persons susceptibility to heat illness and deteriorates their work performance. Therefore, it is important for employees working in warm or hot environments to drink sufficient amounts of water and avoid drinking any alcohol beverages. […] Acclimatization is important for all employees working in warm or hot temperatures or where other risk factors for heat illness are present. However, in any large group of workers, remember that there are wide differences in the ability of individuals to adapt to the heat. These differences in individuals can not be accurately predicted prior to exposure to warm or hot conditions. For these reasons even some acclimatized individuals may still develop heat illness given the temperatures and other risk factors present at a particular worksite at a given time.
  • #43 Heat exhaustion – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/heat-exhaustion/symptoms-causes/syc-20373250
    Heat exhaustion is a condition that happens when your body overheats. […] Without prompt treatment, heat exhaustion can lead to heatstroke, a life-threatening condition. […] In hot weather, your body cools itself mainly by sweating. The evaporation of your sweat regulates your body temperature. But when you exercise strenuously or otherwise overexert in hot, humid weather, your body is less able to cool itself efficiently. […] If heat exhaustion isn’t treated, it can lead to heatstroke. Heatstroke is a life-threatening condition. It happens when your core body temperature reaches 104 F (40 C) or higher. Heatstroke needs immediate medical attention to prevent permanent damage to your brain and other vital organs that can result in death.
  • #44 Hyperthermia (Heat-Related Illnesses) Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/22111-hyperthermia
    Heat exhaustion is a moderate form of heat illness that can quickly turn into heat stroke without treatment. It happens when you lose too much water and/or salt, typically when exerting yourself in the heat. Your internal body temperature is elevated but below 104 degrees F (40 degrees C). Symptoms include dizziness, nausea, vomiting and headache. […] Heat-related illnesses happen when your body’s usual mechanisms for managing heat get overwhelmed. This can occur due to hot and humid weather, metabolic heat (heat your body makes) or both. As a result, your body can’t get rid of heat efficiently enough to keep your temperature at a normal level. […] Treatment depends on the type of heat-related illness. You can usually manage heat rash and heat cramps on your own. You should seek medical attention for heat exhaustion and heat stroke while taking measures to cool your body. […] Your outlook depends on many factors, including the type of heat-related illness you have and its severity.
  • #45 Heat Stroke: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/166320-overview
    Despite wide variations in ambient temperatures, humans and other mammals can maintain a constant body temperature by balancing heat gain with heat loss. When heat gain overwhelms the body’s mechanisms of heat loss, the body temperature rises, potentially leading to heat stroke. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death. […] The exact temperature at which cardiovascular collapse occurs varies among individuals because coexisting disease, drugs, and other factors may contribute to or delay organ dysfunction. Full recovery has been observed in patients with temperatures as high as 46C, and death has occurred in patients with much lower temperatures. Temperatures exceeding 106F or 41.1C generally are catastrophic and require immediate aggressive therapy.
  • #46 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine
    https://bmjmedicine.bmj.com/content/1/1/e000239
    EHS pathophysiology is complex and involves an interaction of thermoregulatory and cardiovascular factors that lead to systemic inflammatory response syndrome. In catastrophic EHS events, systemic inflammatory response syndrome is likely initiated by endotoxaemia when the hepatic system fails to clear bacteria effectively. Coagulopathy is also present in the pathophysiology and manifests through disseminated intravascular coagulation, resulting in thrombosis or bleeding (or both).
  • #47 Heat Exhaustion and Heat Stroke – Mississippi State Department of Health
    https://msdh.ms.gov/page/43,3942,98,261.html
    Heat exhaustion is a milder form of heat-related illness that can develop after long exposure to high temperatures and inadequate water. […] Those most prone to heat exhaustion are elderly people, people with high blood pressure, and people working or exercising in a hot environment. […] The skin may be cool and moist. The victim’s pulse rate will be fast and weak, and breathing will be fast and shallow. If heat exhaustion is untreated, it may progress to heat stroke. […] Heat stroke occurs when the body’s temperature rises rapidly, the sweating mechanism fails, and the body is unable to cool down. Body temperature may rise to 106 degrees or higher within 10 to 15 minutes. Heat stroke can cause death or permanent disability if emergency treatment is not provided.
  • #48 Ask the Doc: Heat Stroke vs. Heat Exhaustion — What’s the Difference? | Health.mil
    https://www.health.mil/News/Articles/2022/06/27/Ask-the-Doc-Heat-Stroke-vs-Heat-Exhaustion
    Heat-related illnesses refer to a spectrum of conditions that worsen as the body loses its ability to compensate for the increased core temperature due to environmental heat or metabolic heat. […] Heat exhaustion occurs earlier in the spectrum of heat-related illnesses. If left unaddressed, heat exhaustion can rapidly progress to the medical emergency we call heat stroke. It can be difficult to differentiate the two without accurate diagnostic measurements. […] The primary difference between heat exhaustion and heat stroke has to do with core body temperature and persistent, severe neurologic manifestations. Heat stroke involves a core temperature above 104 F (40 C), and persistent neurologic dysfunction to include coma, seizure, and altered level of consciousness, confusion, or headache. If heat stroke has set in and there is a delay in cooling, this condition can be fatal.
  • #49 Heat Exhaustion/ Heat Stroke
    https://www.uspharmacist.com/article/heat-exhaustion-heat-stroke
    Heat exhaustion and heat stroke are two conditions that can result from exposure to high environmental temperatures for brief or extended periods of time. […] In these conditions, the body cannot compensate for the excess heat and cannot effectively cool itself through sweating. […] A person may develop heat exhaustion after several days of hot weather or high air temperatures and not drinking enough fluids, which leads to water and/or salt depletion and dehydration. Symptoms of heat exhaustion are pale, sweaty skin, muscle cramps, weakness, fainting, dizziness, headache, nausea, and vomiting. […] Heat stroke is potentially deadly, resulting from a rapid rise in body temperature and a failure of the body to sweat and cool itself. […] This condition can develop from heat exhaustion that is not treated.
  • #50 Overview of Heat Illness – Injuries; Poisoning – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/injuries-poisoning/heat-illness/overview-of-heat-illness
    Patients with heat exhaustion maintain the ability to dissipate heat and have normal central nervous system (CNS) function. […] The body can compensate for large variations in heat load, but prolonged or excessive exposure to heat that exceeds capacity for heat dissipation increases core temperature. Modest, transient core temperature elevations are tolerable, but severe elevations (typically 41 C) can lead to protein denaturation and the release of inflammatory cytokines. As a result, cellular dysfunction may occur and an inflammatory cascade may be activated, leading to multiorgan dysfunction similar to that which follows prolonged shock. […] Compensatory mechanisms include an acute-phase response that moderates the inflammatory response (eg, by stimulating production of proteins that decrease production of free radicals and inhibit release of proteolytic enzymes). Also, increased core temperature triggers expression of heat-shock proteins. These proteins transiently enhance heat tolerance by poorly understood mechanisms (eg, possibly by preventing protein denaturation) and by regulation of cardiovascular responses. With prolonged or extreme temperature elevation, compensatory mechanisms are overwhelmed, allowing inflammation and multiple organ dysfunction syndrome to occur.
  • #51 Heat-related illnesses – Knowledge @ AMBOSS
    https://www.amboss.com/us/knowledge/heat-related-illnesses/
    Heat exhaustion is a moderate heat-related illness characterized by dehydration, normal or slightly elevated body temperature (typically 40C), and normal mental status. […] Heat exhaustion is typically treated with rehydration, passive cooling, and, if needed, evaporative and convective cooling (e.g., mist and fan). […] Heat exhaustion is a heat-related illness characterized by all of the following: a decrease in blood volume and/or total body water caused by heat stress, normal or slightly elevated core body temperature (typically defined as 40C), and normal mental status. […] In contrast with heatstroke, the homeostatic thermoregulatory system retains partial function, and heat continues to actively dissipate. […] If heatstroke cannot be excluded clinically, begin intensive active cooling without delay.
  • #52 Management of Heatstroke and Heat Exhaustion | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0601/p2133.html/1000
    The term thermal maximum was developed to measure the magnitude and duration of heat that cells can encounter before becoming damaged. Human thermal maximum has been established as a core body temperature of approximately 42C (107.6F) for between 45 minutes and eight hours. Cellular destruction occurs more quickly and completely at higher temperatures. Inflammatory factors are released and gastrointestinal permeability increases, which may allow endotoxins into the circulation. Hematologic and endothelial changes resembling disseminated intervascular coagulation also occur.
  • #53 Management of Heatstroke and Heat Exhaustion | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0601/p2133.html/1000
    The term thermal maximum was developed to measure the magnitude and duration of heat that cells can encounter before becoming damaged. Human thermal maximum has been established as a core body temperature of approximately 42C (107.6F) for between 45 minutes and eight hours. Cellular destruction occurs more quickly and completely at higher temperatures. Inflammatory factors are released and gastrointestinal permeability increases, which may allow endotoxins into the circulation. Hematologic and endothelial changes resembling disseminated intervascular coagulation also occur.
  • #54 pathophysiology of heat-related illness and death :: www.forensicmed.co.uk
    https://www.forensicmed.co.uk/pathology/pathophysiology-of-heat-related-illness-and-death/
    The development of heatstroke and progression to multi-organ dysfunction is a complex interplay of several factors: acute physiological alterations associated with hyperthermia e.g. circulatory failure, hypoxia, increased cellular metabolic demands; direct cellular damage due to heat; the systemic inflammatory response; and failure of the coagulation system (Epstein and Roberts 2011, and Yan et al 2006). […] Multi-organ failure is the ultimate mode of death, and heat-related mortality is high ranging between 33 and 80%.
  • #55 Heat Exhaustion Symptoms, Signs, Treatment, Definition
    https://www.emedicinehealth.com/heat_exhaustion/article_em.htm
    Heat exhaustion is a condition that occurs when the body overheats. […] Heat exhaustion is caused by the failure of the body’s cooling mechanism to maintain a normal core temperature. […] The main cause of heat exhaustion is the failure of the body’s cooling mechanism (mainly evaporative sweating) to maintain a normal core body temperature, resulting in the body overheating. […] Complications of heat exhaustion include progression to heat stroke, a medical emergency that can lead to permanent organ damage and death. […] The diagnosis of heat exhaustion is generally made after obtaining the patient’s history and performing a physical exam. […] Treatment for heat exhaustion should begin immediately when a person is suspected of having heat exhaustion, and the primary treatment is evaporative cooling and removing the person from the hot environment. […] If heat exhaustion is not detected and treated, then heat stroke may develop resulting in possible organ damage, seizures, coma, and even death.
  • #56 A Hypothalamus centered Pathogenesis of Heat Stroke Deaths- A Postmortem-Based Human Study | medRxiv
    https://www.medrxiv.org/content/10.1101/2025.03.10.25323319v2.full
    Heat stroke deaths are increasing during the summer in tropical countries with hot climates. The pathogenesis mechanisms leading to death in heat stroke are not well established. […] Our observations indicate that the anterior hypothalamus may have a commanding role in the pathogenesis of heat stroke. Acute hemorrhage in the preoptic area of the anterior hypothalamus associated with microvascular injury and acute necrotic lesions of key organs involved in the hemodynamic circulation and temperature control, primarily the heart, lung, kidney, and liver should be considered in the forensic determination of the cause of death in such cases. […] The robust evidence of microvascular injuries and acute necrotic lesions localized to the heat-controlling region of the hypothalamus, accompanied by similar injuries in the internal organs, primarily in the heart, lung, kidney, and liver, is unraveled in our study. Our observations establish a unique tissue injury pattern in heat stroke deaths, which can be used as a signature for the forensic determination of the cause of death in autopsied cases. It also affirms a hypothalamus-mediated vascular overdrive of the organs involved in hemodynamic and temperature control as the key pathogenic mechanism leading to death in heat stroke cases.
  • #57 Heat-related Illnesses | Heat | CDC
    https://www.cdc.gov/niosh/heat-stress/about/illnesses.html
    Heat exhaustion is the body’s response to an excessive loss of water and salt, usually through excessive sweating. […] Symptoms of heat exhaustion include: Headache, Nausea, Dizziness, Weakness, Irritability, Thirst, Heavy sweating, Elevated body temperature, Decreased urine
  • #58 Heat-related illnesses: physiology, symptoms and management – The Pharmaceutical Journal
    https://pharmaceutical-journal.com/article/ld/heat-related-illnesses-physiology-symptoms-and-management
    Heat exhaustion is the result, typified by excessive sweating and rapid fluid and electrolyte loss. […] Thermoregulatory dysfunction, hypovolaemia and hypotension increase the risk of dehydration, particularly in individuals with comorbidities or pre-existing risk factors. […] Heat exhaustion is characterised by pale, moist skin and a fever (body temperature of more than 38°C). […] Gastrointestinal upset can also occur, which, coupled with fluid loss through sweat, increases the risk of dehydration. […] Headache and generalised fatigue are classic symptoms of heat exhaustion, as well as being early signs of dehydration. […] Management of heat exhaustion is the same as for heat cramps. […] If appropriately managed, symptoms of mild heat exhaustion should generally resolve within two to three hours.
  • #59 Heat-related illnesses – Knowledge @ AMBOSS
    https://www.amboss.com/us/knowledge/heat-related-illnesses/
    Heat exhaustion is a moderate heat-related illness characterized by dehydration, normal or slightly elevated body temperature (typically 40C), and normal mental status. […] Heat exhaustion is typically treated with rehydration, passive cooling, and, if needed, evaporative and convective cooling (e.g., mist and fan). […] Heat exhaustion is a heat-related illness characterized by all of the following: a decrease in blood volume and/or total body water caused by heat stress, normal or slightly elevated core body temperature (typically defined as 40C), and normal mental status. […] In contrast with heatstroke, the homeostatic thermoregulatory system retains partial function, and heat continues to actively dissipate. […] If heatstroke cannot be excluded clinically, begin intensive active cooling without delay.
  • #60 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine
    https://bmjmedicine.bmj.com/content/1/1/e000239
    A person’s ability to thermoregulate is closely linked to the ability of the cardiovascular system to cope with central and peripheral blood flow demands to support metabolic and thermoregulatory requirements. […] Effective thermoregulatory pathways must be active to provide means for heat loss to prevent EHS during severe or prolonged physical activity. […] A thermoregulatory failure underlying EHS would signify a suppressed ability to dissipate heat coupled with high rates of heat storage, which would result in a marked elevation in core temperature. […] The leaky gut hypothesis has been linked to EHS pathophysiology because of observations that in patients with extreme EHS, high levels of lipopolysaccharide (a cell wall component of Gram negative bacteria) are observed. […] Systemic inflammatory response syndrome is a dysregulated defence response of the body to a noxious stressor to localise and eliminate the source of the insult.
  • #61 Heat Exhaustion and Heat Stroke – Mississippi State Department of Health
    https://msdh.ms.gov/page/43,3942,98,261.html
    Heat exhaustion is a milder form of heat-related illness that can develop after long exposure to high temperatures and inadequate water. […] Those most prone to heat exhaustion are elderly people, people with high blood pressure, and people working or exercising in a hot environment. […] The skin may be cool and moist. The victim’s pulse rate will be fast and weak, and breathing will be fast and shallow. If heat exhaustion is untreated, it may progress to heat stroke. […] Heat stroke occurs when the body’s temperature rises rapidly, the sweating mechanism fails, and the body is unable to cool down. Body temperature may rise to 106 degrees or higher within 10 to 15 minutes. Heat stroke can cause death or permanent disability if emergency treatment is not provided.
  • #62 Heat kills in 3 main ways. Know the signs to protect yourself : Shots – Health News : NPR
    https://www.npr.org/sections/health-shots/2023/07/23/1189506023/heres-what-happens-to-the-body-in-extreme-temperatures-and-how-heat-becomes-dead
    Those toxins can activate white blood cells, says Camilo Mora, a climate scientist and professor at the University of Hawaii at Manoa who has researched how heat can turn fatal. „They say, Oh my God, we’re getting attacked right now. And the white blood cells are going to attack this contamination in the blood, creating coagulation” or blood clots, Mora says. Those clots can lead to multiple organ failure. […] The second way people die in high heat also has to do with your body pumping more blood to the skin. Your heart has to pump faster which can make you feel lightheaded to keep your blood pressure up. […] Those spikes in the heart rate can be triggers for a heart attack, he says, especially for the elderly and those with underlying heart conditions. […] The third deadly danger has to do with the fluids your body is losing in extreme heat. People can sweat as much as a liter and half per hour, Jay says. And if you don’t replenish those fluids, you get dehydrated and your blood volume shrinks, which makes it harder to maintain blood pressure. That can strain your heart and your kidneys.
  • #63
    https://www.who.int/news-room/fact-sheets/detail/climate-change-heat-and-health
    The bodys inability to regulate internal temperature and eliminate heat gain in such conditions increases the risk of heat exhaustion and heatstroke. […] The strain put on the body as it tries to cool itself also stresses the heart and kidneys. As a result, heat extremes can worsen health risks from chronic conditions (cardiovascular, mental, respiratory and diabetes related conditions) and cause acute kidney injury.
  • #64 Heat kills in 3 main ways. Know the signs to protect yourself : Shots – Health News : NPR
    https://www.npr.org/sections/health-shots/2023/07/23/1189506023/heres-what-happens-to-the-body-in-extreme-temperatures-and-how-heat-becomes-dead
    Rhabdomyolysis causes muscle tissue to break down, releasing proteins into the blood that can clog kidneys. This usually occurs in the acute phase of heatstroke. Jay says there’s also some evidence that habitually working outdoors in high heat without proper hydration can increase the risk of chronic kidney disease.
  • #65 The Difference Between Heat Exhaustion, Stroke | TIME
    https://time.com/6295531/heat-stroke-exhaustion-stress-differences/
    When the body has lost too much water and electrolytes due to excessive sweating, heat exhaustion can set in. Symptoms can include nausea, vomiting, fainting, slurred speech, physical weakness, a bad headache, irritability, clammy skin, and an elevated body temperature. Repeated incidents of heat exhaustion can also lead to organ damage, particularly for the kidneys. Severe heat exhaustion can bring on rhabdomyolysis, a breakdown of muscle tissues that can cause irregular heart rhythms, seizures, and acute kidney damage. […] Victims of apparent heat exhaustion should be immediately moved to a cool air conditioned if possible area, and encouraged to take small, frequent sips of cool liquids. Call 911 if the person cannot be taken to a medical clinic or emergency room. Remove shoes, socks, and any restrictive or heavy clothing, and bathe the head, face, neck, and wrists with water or cold compresses.
  • #66 Nonexertional (classic) heat stroke in adults – UpToDate
    https://www.uptodate.com/contents/nonexertional-classic-heat-stroke-in-adults
    Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.
  • #67 The mechanisms behind heatstroke-induced intestinal damage | Cell Death Discovery
    https://www.nature.com/articles/s41420-024-02210-0
    With the frequent occurrence of heatwaves, heatstroke (HS) is expected to become one of the main causes of global death. […] Intestinal damage plays an initiating and promoting role in HS. […] A large number of studies have shown that intestinal damage after HS involves the body’s stress response, disruption of oxidative balance, disorder of tight junction proteins, massive cell death, and microbial imbalance. […] The current view is that the mechanism of heat injury is due to direct damage from heat and systemic inflammatory response syndrome (SIRS) caused by heat stress and endotoxin leakage. […] It is believed that the disruption of the intestinal barrier contributes to and initiates HS. […] Therefore, the gastrointestinal tract has long been considered the motor of multiple organ failure and a key factor in various critical illnesses.
  • #68 Nonexertional (classic) heat stroke in adults – UpToDate
    https://www.uptodate.com/contents/nonexertional-classic-heat-stroke-in-adults
    Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.
  • #69 The pathogenesis and therapeutic strategies of heat stroke-induced liver injury | Critical Care | Full Text
    https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04273-w
    The liver, as the key line of defense for the collective elimination of endotoxin, may obtain surprises with specific treatment for HS-induced ALI. […] In brief, the mechanism of HS-induced liver injury is not only related to systemic factors such as systemic inflammatory reaction and coagulation dysfunction but also closely related to pathological mechanisms such as abnormal death of liver cells and abnormal function of KCs.
  • #70 Heat Stroke: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/166320-overview
    On a cellular level, heat directly influences the body by interfering with cellular processes along with denaturing proteins and cellular membranes. In turn, an array of inflammatory cytokines, interleukins and heat shock proteins (HSPs) are produced. In particular, HSP-70 allows the cell to endure the stress of its environment. Intense heat stress that is uncompensated leads to apoptosis and cell death. […] On a microvascular level, heat stroke resembles sepsis and involves inflammation, translocation of lipopolysaccharides from the gut, and activates the coagulation cascade. Certain preexisting factors, such as age, genetic makeup, and the nonacclimatized individual, may allow progression from heat stress to heat stroke, systemic inflammatory response syndrome (SIRS), multiorgan dysfunction syndrome (MODS), and ultimately death. Progression to heat stroke may occur through thermoregulatory failure, an amplified acute-phase response, and alterations in the expression of HSPs.
  • #71 Heat stroke pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Heat_stroke_pathophysiology
    Endothelial cells, leukocytes, and epithelial cells incorporate a variety of cytokines (mainly interleukin-1 and interleukin-6) to protect against tissue injury and promote repair. […] Heat-shock proteins are secreted in response to heat to protect cells from injury. Heat-shock proteins bind to proteins and act as chaperons to prevent them from denaturation. […] Severe heat stroke causes vascular congestion and/or hemorrhage, thrombi, increased inflammatory cells, and disruption of architecture in many internal organs including: liver, jejunum, spleen, lungs, and kidneys.
  • #72 Heat Stroke: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/166320-overview
    On a cellular level, heat directly influences the body by interfering with cellular processes along with denaturing proteins and cellular membranes. In turn, an array of inflammatory cytokines, interleukins and heat shock proteins (HSPs) are produced. In particular, HSP-70 allows the cell to endure the stress of its environment. Intense heat stress that is uncompensated leads to apoptosis and cell death. […] On a microvascular level, heat stroke resembles sepsis and involves inflammation, translocation of lipopolysaccharides from the gut, and activates the coagulation cascade. Certain preexisting factors, such as age, genetic makeup, and the nonacclimatized individual, may allow progression from heat stress to heat stroke, systemic inflammatory response syndrome (SIRS), multiorgan dysfunction syndrome (MODS), and ultimately death. Progression to heat stroke may occur through thermoregulatory failure, an amplified acute-phase response, and alterations in the expression of HSPs.
  • #73 The mechanisms behind heatstroke-induced intestinal damage | Cell Death Discovery
    https://www.nature.com/articles/s41420-024-02210-0
    Severe intestinal epithelial damage is also considered to be the main cause of death from HS. […] The body’s stress response, oxidative damage, destruction of intestinal tight junction (TJ) proteins, excessive cell death, and imbalance of intestinal flora are all challenges faced by the intestine under HS. […] The mechanism of intestinal damage is complex and interrelated. […] In HS, inflammation and cell death caused by heat stress can activate the coagulation cascade through the extrinsic and intrinsic pathways, ultimately leading to the formation of an inflammatory thrombus. […] The activated UPR can limit protein synthesis and increase HSP70, which inhibits the NF-B pathway and reduces inflammation. […] Excess ROS can impair intestinal barrier function by reducing epithelial cell viability and damaging intestinal TJs.
  • #74 The pathogenesis and therapeutic strategies of heat stroke-induced liver injury | Critical Care | Full Text
    https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04273-w
    Excessive ROS will be produced during heat stress, which has been proven to be a key stimulator of NLRP3 inflammasome and a potential target for negative regulation of cell pyroptosis. […] The previous studies have suggested that mitophagy is closely related to the occurrence and development of various liver diseases, including viral hepatitis, liver ischemia/reperfusion (I/R) injury, and drug-induced liver injury. […] In HS-induced liver injury, the important role of mitophagy has also been confirmed. […] The increased expression of HSP level is related to the better prognosis of HS patients. […] In HS-induced liver injury, PARP blockage has also emerged as a promising treatment. […] The pathophysiological mechanism of HS is similar to sepsis, and systemic inflammatory reaction is important pathogenesis.
  • #75 The pathogenesis and therapeutic strategies of heat stroke-induced liver injury | Critical Care | Full Text
    https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04273-w
    Excessive ROS will be produced during heat stress, which has been proven to be a key stimulator of NLRP3 inflammasome and a potential target for negative regulation of cell pyroptosis. […] The previous studies have suggested that mitophagy is closely related to the occurrence and development of various liver diseases, including viral hepatitis, liver ischemia/reperfusion (I/R) injury, and drug-induced liver injury. […] In HS-induced liver injury, the important role of mitophagy has also been confirmed. […] The increased expression of HSP level is related to the better prognosis of HS patients. […] In HS-induced liver injury, PARP blockage has also emerged as a promising treatment. […] The pathophysiological mechanism of HS is similar to sepsis, and systemic inflammatory reaction is important pathogenesis.
  • #76
    https://link.springer.com/article/10.1007/s10495-024-01979-w
    Severe heat stress is characterized by cell death of direct heat damage, excessive inflammatory responses, and coagulation disorders that can lead to multiple organ dysfunction (MODS) and even death. […] Various modes of cell death, including apoptosis, pyroptosis, ferroptosis, necroptosis and PANoptosis are involved in MODS induced by heatstroke. […] Understanding the mechanism of cell death provides new targets to protect multi-organ function in HS.
  • #77 The mechanisms behind heatstroke-induced intestinal damage | Cell Death Discovery
    https://www.nature.com/articles/s41420-024-02210-0
    Excessive activation of programmed cell death (PCD) is a significant reason for intestinal epithelium damage in HS-related intestinal damage, in addition to direct thermal stimulation-induced cell damage. […] Necroptosis, as a newly discovered form of PCD, exhibits unique morphological characteristics that are different from apoptosis or necrosis. […] The activation of necroptosis relies on a variety of receptors, such as TNF and TLR. […] In a high-heat environment, disruption of antioxidant balance, accumulation of ROS, shrinkage of mitochondria, and an increase in membrane density are all key features of cell ferroptosis. […] The occurrence of ferroptosis involves the transition metal iron, ROS, and PUFA-PLs. […] The massive production of ROS can facilitate p53’s phosphorylation at Ser46 and its entry into mitochondria via Pin1, which in turn encourages Bax to undergo a conformational shift and enter the mitochondria.
  • #78
    https://link.springer.com/article/10.1007/s10495-024-01979-w
    Severe heat stress is characterized by cell death of direct heat damage, excessive inflammatory responses, and coagulation disorders that can lead to multiple organ dysfunction (MODS) and even death. […] Various modes of cell death, including apoptosis, pyroptosis, ferroptosis, necroptosis and PANoptosis are involved in MODS induced by heatstroke. […] Understanding the mechanism of cell death provides new targets to protect multi-organ function in HS.
  • #79 The mechanisms behind heatstroke-induced intestinal damage | Cell Death Discovery
    https://www.nature.com/articles/s41420-024-02210-0
    Excessive activation of programmed cell death (PCD) is a significant reason for intestinal epithelium damage in HS-related intestinal damage, in addition to direct thermal stimulation-induced cell damage. […] Necroptosis, as a newly discovered form of PCD, exhibits unique morphological characteristics that are different from apoptosis or necrosis. […] The activation of necroptosis relies on a variety of receptors, such as TNF and TLR. […] In a high-heat environment, disruption of antioxidant balance, accumulation of ROS, shrinkage of mitochondria, and an increase in membrane density are all key features of cell ferroptosis. […] The occurrence of ferroptosis involves the transition metal iron, ROS, and PUFA-PLs. […] The massive production of ROS can facilitate p53’s phosphorylation at Ser46 and its entry into mitochondria via Pin1, which in turn encourages Bax to undergo a conformational shift and enter the mitochondria.
  • #80
  • #81 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine
    https://bmjmedicine.bmj.com/content/1/1/e000239
    A person’s ability to thermoregulate is closely linked to the ability of the cardiovascular system to cope with central and peripheral blood flow demands to support metabolic and thermoregulatory requirements. […] Effective thermoregulatory pathways must be active to provide means for heat loss to prevent EHS during severe or prolonged physical activity. […] A thermoregulatory failure underlying EHS would signify a suppressed ability to dissipate heat coupled with high rates of heat storage, which would result in a marked elevation in core temperature. […] The leaky gut hypothesis has been linked to EHS pathophysiology because of observations that in patients with extreme EHS, high levels of lipopolysaccharide (a cell wall component of Gram negative bacteria) are observed. […] Systemic inflammatory response syndrome is a dysregulated defence response of the body to a noxious stressor to localise and eliminate the source of the insult.
  • #82 The pathogenesis and therapeutic strategies of heat stroke-induced liver injury | Critical Care | Full Text
    https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04273-w
    The studies have shown that one of the important mechanisms of HS is the excessive opening of intestinal tight junctions, the destruction of intestinal cell structure and function, the increase in intestinal mucosal permeability, and the introduction of endotoxin into the blood. […] Cytokines are considered to be key mediators of SIRS in HS-induced systemic MODS and are closely related to the severity and outcome of HS. […] As one of the most ubiquitous, abundant, and evolutionarily conserved transcription and growth factors in eukaryotes, high mobility group box 1 (HMGB1) occupies an important position in the diagnosis and treatment of HS. […] The mechanism of HMGB1 in the HS liver injury model was further explored by Yan Geng et al. […] The most common pathological change of HS-induced liver injury is the massive degeneration of hepatocytes including abnormal cell death, while pyroptosis exerts an important role in abnormal cell death in HS-induced liver injury.
  • #83 The mechanisms behind heatstroke-induced intestinal damage | Cell Death Discovery
    https://www.nature.com/articles/s41420-024-02210-0
    The physical barrier formed by TJ is crucial to intestinal health, which is composed of claudins, occludins, and the intracellular plaque proteins zonula occludens (ZO-1, ZO-2, and ZO-3). […] Studies have shown that upon heat stress, multiple kinases and phosphatases will phosphorylate the TJ proteins, resulting in reduced interaction of occludins and claudins with zona-occludins, thereby affecting intestinal permeability. […] The activation of MLCK is related to various factors, for example, inflammatory pathways. […] After HS, the HSR takes effect, resulting in increased expression of HSP. […] In summary, a growing body of evidence demonstrates that the signaling pathways and regulatory processes involved in TJ protein expression are extremely complex, but it remains unclear whether HS directly or indirectly causes TJ dysfunction.
  • #84 Heat kills in 3 main ways. Know the signs to protect yourself : Shots – Health News : NPR
    https://www.npr.org/sections/health-shots/2023/07/23/1189506023/heres-what-happens-to-the-body-in-extreme-temperatures-and-how-heat-becomes-dead
    Those toxins can activate white blood cells, says Camilo Mora, a climate scientist and professor at the University of Hawaii at Manoa who has researched how heat can turn fatal. „They say, Oh my God, we’re getting attacked right now. And the white blood cells are going to attack this contamination in the blood, creating coagulation” or blood clots, Mora says. Those clots can lead to multiple organ failure. […] The second way people die in high heat also has to do with your body pumping more blood to the skin. Your heart has to pump faster which can make you feel lightheaded to keep your blood pressure up. […] Those spikes in the heart rate can be triggers for a heart attack, he says, especially for the elderly and those with underlying heart conditions. […] The third deadly danger has to do with the fluids your body is losing in extreme heat. People can sweat as much as a liter and half per hour, Jay says. And if you don’t replenish those fluids, you get dehydrated and your blood volume shrinks, which makes it harder to maintain blood pressure. That can strain your heart and your kidneys.
  • #85 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine
    https://bmjmedicine.bmj.com/content/1/1/e000239
    A person’s ability to thermoregulate is closely linked to the ability of the cardiovascular system to cope with central and peripheral blood flow demands to support metabolic and thermoregulatory requirements. […] Effective thermoregulatory pathways must be active to provide means for heat loss to prevent EHS during severe or prolonged physical activity. […] A thermoregulatory failure underlying EHS would signify a suppressed ability to dissipate heat coupled with high rates of heat storage, which would result in a marked elevation in core temperature. […] The leaky gut hypothesis has been linked to EHS pathophysiology because of observations that in patients with extreme EHS, high levels of lipopolysaccharide (a cell wall component of Gram negative bacteria) are observed. […] Systemic inflammatory response syndrome is a dysregulated defence response of the body to a noxious stressor to localise and eliminate the source of the insult.
  • #86 Heat Stress, Heat Stroke & Hypothermia | Emergency Management & Business Continuity | Western Washington University
    https://embc.wwu.edu/heat-stress-heat-stroke-hypothermia
    Heat stress is the bodys response to an excessive loss of the water and salt contained in sweat. If heat stress is untreated, it may progress to heat stroke. […] Heat stroke occurs when the body is unable to regulate its temperature. During heat stroke, the bodys temperature rises, the sweating mechanism fails, and the body is unable to cool down.
  • #87 Heat-related Illness Deep Dive — USF Emergency Medicine
    https://www.tampaemergencymedicine.org/blog/heat-related-illness-deep-dive
    The inability of the body to compensate for increases in heat storage is the source of heat-related illness. […] Uncompensated temperature rise leads to many deleterious consequences described in the various stages and forms of heat illness. […] If heat exhaustion continues without cooling, it can lead to a heat injury. […] Heatstroke, like heat injury, requires organ dysfunction but specifically needs to present with CNS involvement and a core temperature over 104F. […] The pathology of EHS is secondary to overexertion beyond the body’s ability to compensate in its ability to cool. […] The physiologic mechanism of heatstroke is very closely linked to that of SIRS in sepsis. […] This breakdown of the mucosa allows the permeation of endotoxins and bacterial lipopolysaccharides into the bloodstream.
  • #88 Heat Illness: Heat Exhaustion and Heat Stroke | 5-Minute Clinical Consult
    https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688398/all/Heat_Illness:_Heat_Exhaustion_and_Heat_Stroke?q=Obesity
    Heat exhaustion is a mild to moderate form of heat illness displaying dehydration-type symptoms with a normal to elevated temperature (1). […] Excess heat has direct cellular toxicity. Excess heat also leads to an imbalance between inflammatory and anti-inflammatory cytokines, vascular endothelial damage, and end-organ dysfunction. […] Interplay between failure of heat-dissipating mechanisms, an overwhelming heat stress, and an exaggerated acute-phase inflammatory response.
  • #89 Heat exhaustion Information | Mount Sinai – New York
    https://www.mountsinai.org/health-library/condition/heat-exhaustion
    Heat exhaustion occurs most often when you are exposed to high temperatures and become dehydrated, usually from not drinking enough fluids. It can also happen when you replace large volumes of sweat with fluids that do not contain enough salt. […] Heat stroke is classified as: […] Exertional heat stroke occurs despite normal functioning of the body’s heat regulation mechanisms. For example, exertional heat stroke may be experienced by young healthy people after strenuous physical work in warm and humid conditions. […] Non-exertional heat stroke occurs due to a failure of the body’s temperature regulation system. Non-exertional heat stroke is more likely to occur in older individuals who may have chronic health conditions. […] If you avoid heat stroke, recovering from heat exhaustion usually takes 24 to 48 hours. Depending on the severity of heat exhaustion, you may be hospitalized so doctors can monitor your fluid and electrolyte levels to avoid complications. Delayed access to cooling is the leading cause of complications among people with heat stroke. Heat exhaustion can exacerbate a wide range of medical conditions.
  • #90 Heat Exhaustion Symptoms, Treatment, Recovery
    https://www.medicinenet.com/heat_exhaustion/article.htm
    Heat exhaustion is one part of the spectrum of heat-related illness, and symptoms should be reversible with treatment. However, some affected individuals do not recognize their symptoms and if they are not removed from the hot environment, cooled, and rehydrated, the heat-related illness can progress to heat stroke, a life-threatening condition. […] Most individuals recover well from heat exhaustion. The key to recovery is recognizing symptoms before they progress to heat stroke. The earlier the activity is stopped, the individual is cooled and hydration begins, the greater the likelihood that complications will not occur.
  • #91 Heat stress: what is it and how is it measured? | Copernicus
    https://climate.copernicus.eu/heat-stress-what-it-and-how-it-measured
    The UTCI categorises thermal stress into different levels based on the feels-like temperature and corresponding physiological responses. This categorisation helps individuals, professionals, and policymakers better understand and manage the potential health impacts associated with various thermal stress levels. […] Severe strain on the body’s thermoregulation. This category is associated with an increased risk of heat-related health issues, and precautions are necessary to avoid heat-related illnesses.