Omdlenie
Patofizjologia i mechanizm

Omdlenie (syncope) to przejściowa utrata przytomności spowodowana nagłym, krótkotrwałym spadkiem przepływu krwi przez mózg, trwającym około 6-8 sekund, co prowadzi do hipoksji tkanki mózgowej i utraty napięcia posturalnego. Kluczowymi mechanizmami patofizjologicznymi są obniżenie rzutu serca, zmniejszenie oporu naczyniowego oraz spadek średniego ciśnienia tętniczego poniżej dolnej granicy autoregulacji (60 mmHg), co skutkuje niedostateczną perfuzją mózgową. Najczęstszą przyczyną jest omdlenie wazowagalne, wynikające z nadmiernej aktywacji nerwu błędnego i jednoczesnej wazodylatacji, prowadzącej do bradykardii i hipotensji. Inne typy to omdlenie ortostatyczne, kardiogenne (zaburzenia rytmu, dysfunkcje skurczowe, przeszkody odpływu), a także rzadkie formy związane z kaszlem, mikcją czy połykaniem. W patomechanizmie istotną rolę odgrywa dysfunkcja autonomicznego układu nerwowego, nieprawidłowa regulacja baroreceptorów oraz sygnalizacja purynergiczna z udziałem adenozyny i jej receptorów A1 i A2, wpływających na bradykardię i wazodylatację. Genetyczne predyspozycje, m.in. zmiany w receptorach adrenergicznych i transporterze norepinefryny, również modulują ryzyko omdleń.

Mechanizm omdlenia – podstawy patofizjologiczne

Omdlenie (syncope) to przejściowa utrata przytomności spowodowana chwilowym zmniejszeniem przepływu krwi przez mózg, której towarzyszy utrata napięcia posturalnego z następującym samoistnym powrotem do świadomości. Mechanizm omdlenia opiera się na niedostatecznej perfuzji mózgowej, która prowadzi do hipoksji tkanki mózgowej. Mózg wymaga stałego dopływu krwi dostarczającej tlen i glukozę, a nawet krótkotrwałe przerwanie tego dopływu (6-8 sekund) powoduje utratę przytomności.123

Utrzymanie prawidłowego przepływu mózgowego zależy od złożonego mechanizmu obejmującego:

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Defekt w jednym lub kilku z tych systemów może prowadzić do zmniejszenia przepływu krwi przez mózg. Krążenie mózgowe jest autoregulowane, co umożliwia utrzymanie stałego przepływu mózgowego przy zmianach średniego ciśnienia tętniczego w zakresie 60-160 mmHg lub ciśnienia perfuzji mózgowej w zakresie 50-150 mmHg. Kiedy ciśnienie spada poniżej dolnej granicy autoregulacji, dochodzi do omdlenia na skutek hipoksji mózgu.2

Hipoperfuzja mózgowa jako bezpośrednia przyczyna omdlenia

Nagłe przerwanie przepływu mózgowego na 6-8 sekund wystarczy, aby wywołać utratę przytomności. Omdlenie występuje, gdy przepływ mózgowy spada do około połowy wartości prawidłowej. Wiąże się to z niedostatecznym dostarczaniem tlenu i glukozy – podstawowych substratów energetycznych dla mózgu. Tkanka mózgowa, w przeciwieństwie do innych tkanek, nie posiada zdolności magazynowania energii w postaci wysokoenergetycznych fosforanów, co czyni ją szczególnie wrażliwą na niedokrwienie.132

Obniżenie rzutu serca może być spowodowane przeszkodą w odpływie krwi z serca, dysfunkcją skurczową lub rozkurczową, istotnym hemodynamicznie zaburzeniem rytmu serca lub defektem przewodnictwa. Zmniejszenie oporu naczyń obwodowych może wynikać z niestabilności naczynioruchowej, niewydolności autonomicznej lub reakcji wazodepresyjnej/wazowagalnej.3

Główne typy omdleń i ich mechanizmy patofizjologiczne

Omdlenie wazowagalne (wazowagarny mechanizm omdlenia)

Omdlenie wazowagalne (vasovagal syncope) jest najczęstszym typem omdlenia, odpowiedzialnym za ponad połowę wszystkich epizodów. Nazywane również neurokardiogennym lub odruchowym omdleniem, występuje, gdy organizm nieprawidłowo reaguje na określone bodźce. Mechanizm tego typu omdlenia obejmuje nadmierną aktywację nerwu błędnego, który spowalnia akcję serca, oraz jednoczesne rozszerzenie naczyń krwionośnych, co prowadzi do nagłego spadku ciśnienia tętniczego i zmniejszenia przepływu krwi do mózgu.123

W patomechanizmie omdlenia wazowagalnego kluczową rolę odgrywa interakcja pomiędzy autonomicznym układem nerwowym a układem krążenia. Bodźce wyzwalające (np. stres emocjonalny, widok krwi, intensywny ból, długotrwałe stanie) powodują aktywację jądra pasma samotnego w pniu mózgu, co prowadzi do:

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Te zmiany w autonomicznym układzie nerwowym prowadzą do dwóch podstawowych efektów hemodynamicznych:

  • Komponent kardiodepresyjny – spadek częstości akcji serca (efekt chronotropowy ujemny) oraz zmniejszenie kurczliwości mięśnia sercowego (efekt inotropowy ujemny), co skutkuje obniżeniem rzutu serca
  • Komponent wazodepresyjny – rozszerzenie naczyń krwionośnych (wazodylatacja) spowodowane głównie zmniejszeniem napięcia współczulnego oraz uwalnianiem tlenku azotu, prowadzące do spadku ciśnienia tętniczego

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Większość osób z omdleniem wazowagalnym wykazuje mieszaną odpowiedź, łączącą elementy kardiodepresyjne i wazodepresyjne. Charakterystyczną cechą jest początkowy wzrost aktywności współczulnej (tachykardia, poty, drżenie, zwężenie naczyń skórnych), po którym następuje nagłe przerwanie tej aktywności z towarzyszącym wzrostem aktywności przywspółczulnej, co prowadzi do bradykardii lub asystolii oraz znacznej hipotensji.23

Omdlenie ortostatyczne

Omdlenie ortostatyczne (określane również jako hipotensja ortostatyczna) występuje, gdy ciśnienie tętnicze gwałtownie spada w wyniku zmiany pozycji ciała, najczęściej przy wstawaniu z pozycji leżącej. W normalnych warunkach, gdy osoba wstaje, grawitacja powoduje przemieszczenie krwi do dolnych części ciała, poniżej przepony. Układ autonomiczny i serce reagują wtedy zwiększeniem częstości akcji serca oraz wazokonstrykcją, aby utrzymać stabilne ciśnienie tętnicze.23

W hipotensji ortostatycznej mechanizmy kompensacyjne zawodzą i nie są w stanie przeciwdziałać grawitacyjnemu przemieszczeniu krwi, co prowadzi do obniżenia powrotu żylnego, zmniejszenia rzutu serca i w konsekwencji spadku ciśnienia tętniczego poniżej poziomu niezbędnego do utrzymania prawidłowej perfuzji mózgowej. Hipotensja ortostatyczna może być spowodowana odwodnieniem, lekami rozszerzającymi naczynia, długotrwałym unieruchomieniem lub dysfunkcją autonomicznego układu nerwowego.23

Omdlenie kardiogenne

Omdlenie kardiogenne występuje, gdy serce nie jest w stanie zapewnić wystarczającego przepływu krwi do mózgu z powodu zaburzeń strukturalnych lub czynnościowych. Może być ono spowodowane:

  • Zaburzeniami rytmu serca – zbyt szybki rytm serca (tachyarytmie) uniemożliwia odpowiednie napełnianie komór, a zbyt wolny rytm (bradyarytmie) nie zapewnia wystarczającego rzutu serca
  • Przeszkodą w odpływie krwi z serca – jak w kardiomiopatii przerostowej czy stenozie aortalnej
  • Dysfunkcją skurczową mięśnia sercowego – niewydolność serca prowadząca do zmniejszenia rzutu serca
  • Dysfunkcją zastawek – upośledzając przepływ krwi przez serce

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W przypadku zaburzeń rytmu serca, omdlenie występuje, gdy częstość akcji serca jest zbyt szybka (powyżej 150-180 uderzeń/min), co nie pozwala na odpowiednie napełnianie komór, lub zbyt wolna (poniżej 30-35 uderzeń/min), co nie zapewnia odpowiedniego rzutu serca. Bloki przewodzenia w sercu mogą prowadzić do asystolii lub znacznej bradykardii, co również zmniejsza przepływ mózgowy.12

Czynniki wpływające na mechanizm omdlenia

Rola autonomicznego układu nerwowego

Autonomiczny układ nerwowy odgrywa kluczową rolę w regulacji funkcji sercowo-naczyniowych i utrzymaniu homeostazy wewnętrznej, w tym regulacji ciśnienia tętniczego, częstości akcji serca, równowagi płynów i elektrolitów oraz temperatury ciała. Zaburzenia w funkcjonowaniu tego układu mogą prowadzić do nieadekwatnych odpowiedzi na zmiany pozycji ciała czy inne bodźce.12

W kontekście omdlenia wazowagalnego, dysfunkcja odruchów z baroreceptorów jest często wymieniana jako potencjalny mechanizm. Baroreceptory kontrolują dwie zmienne determinujące ciśnienie tętnicze: rzut serca i całkowity opór obwodowy. W odpowiedzi na spadek ciśnienia tętniczego, zmniejszona aktywność baroreceptorów powinna skutkować pobudzeniem współczulnym serca, zahamowaniem przywspółczulnych włókien sercowych oraz wzrostem całkowitego oporu obwodowego, prowadząc do zwiększenia częstości akcji serca i rzutu serca.1

Jednak w przypadku omdlenia wazowagalnego obserwuje się paradoksalną regulację, w której początkowo występuje nadmierna aktywacja współczulna (tachykardia), po której następuje nagłe jej przerwanie i dominacja układu przywspółczulnego. To prowadzi do bradykardii i rozszerzenia naczyń krwionośnych, skutkując znacznym spadkiem ciśnienia tętniczego i zmniejszeniem przepływu mózgowego.12

Dokładny mechanizm tej nagłej zmiany z wazokonstrykcji i tachykardii na wazodylatację i bradykardię pozostaje nie w pełni wyjaśniony. Przez długi czas uważano, że jest to wynik nadmiernej stymulacji mechanoreceptorów wywołanej intensywnym skurczem niedostatecznie napełnionej lewej komory (odruch Bezoldt-Jarischa). Jednak najnowsze dowody wskazują na inne mechanizmy, takie jak nieprawidłowa regulacja autonomiczna, obecność endogennych substancji rozszerzających naczynia, funkcjonalne upośledzenie odruchów z baroreceptorów oraz paradoksalna regulacja w ośrodkowym układzie nerwowym.12

Czynniki predysponujące i wyzwalające omdlenie

Omdlenie może być wywołane przez różne czynniki wyzwalające, które wpływają na funkcjonowanie układu sercowo-naczyniowego i autonomicznego. Do najczęstszych należą:

  • Długotrwała pozycja stojąca – sprzyja zaleganiu krwi w dolnych częściach ciała, zmniejszając powrót żylny
  • Podwyższona temperatura otoczenia – prowadzi do rozszerzenia naczyń obwodowych
  • Odwodnienie – zmniejsza objętość krwi krążącej
  • Spożycie posiłku – powoduje przemieszczenie krwi do naczyń trzewnych (hipotensja poposiłkowa)
  • Silny stres emocjonalny – wpływa na regulację autonomiczną
  • Intensywny ból – może stymulować nerw błędny
  • Widok krwi, igły – silny bodziec dla omdlenia wazowagalnego
  • Kaszel, mikcja, defekacja – zwiększają ciśnienie wewnątrz klatki piersiowej (manewr Valsalvy)

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Osoby są bardziej podatne na omdlenie w pozycji stojącej, gdy pozostają nieruchomo, w cieple, po posiłkach, przy odwodnieniu lub w stanie stresu emocjonalnego. Czynniki te mogą być zaangażowane w niektóre omdlenia odruchowe, w tym omdlenia związane z mikcją i defekacją. Objętość osocza ma także znaczący wpływ, a jej zwiększenie poprzez interwencje takie jak zwiększenie podaży soli, trening fizyczny, a nawet spanie z uniesionym wezgłowiem łóżka może przynieść korzyści kliniczne.12

Szczególne mechanizmy niektórych typów omdleń

Pewne szczególne typy omdleń charakteryzują się unikalnymi mechanizmami patofizjologicznymi:

Omdlenie kaszlowe (tussive syncope) – występuje bezpośrednio po gwałtownym kaszlu lub przedłużonych napadach kaszlu. Mechanizm obejmuje:

  • Wzrost ciśnienia wewnątrz klatki piersiowej podczas kaszlu, co zmniejsza powrót żylny, napełnianie komór, rzut serca i ciśnienie tętnicze
  • Przeniesienie podwyższonego ciśnienia wewnątrz klatki piersiowej na płyn mózgowo-rdzeniowy, powodujące nagły wzrost ciśnienia wewnątrzczaszkowego i upośledzenie perfuzji mózgowej
  • Możliwe wywoływanie arytmii serca przez nerw błędny, w tym zatrzymanie zatokowe i blok przedsionkowo-komorowy

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Omdlenie związane z mikcją (micturition syncope) – występuje podczas lub bezpośrednio po oddaniu moczu, szczególnie w nocy po wstaniu z głębokiego snu:

  • Łączy spadek ciśnienia tętniczego związany z nagłym wstaniem z efektem opróżnienia pełnego pęcherza
  • Szybkie opróżnienie pęcherza może wywołać nagły spadek ciśnienia tętniczego
  • Często występuje u starszych mężczyzn

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Omdlenie po przełknięciu (swallow syncope) – rzadka forma omdlenia występująca po spożyciu pokarmu:

  • Odruchy inicjowane podczas połykania wyzwalają złożony mechanizm, w którym mózg wysyła sygnał do serca aby zwolniło (bradykardia) i do naczyń aby rozszerzyły się (wazodylatacja)
  • Prowadzi to do niskiego ciśnienia tętniczego i zmniejszonego przepływu krwi do mózgu
  • Dokładny mechanizm wciąż nie jest w pełni poznany

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Rola adenozyny w patogenezie omdlenia

W ostatnich latach zwrócono uwagę na rolę adenozyny (AD) i jej receptorów w patofizjologii omdlenia. Adenozyna jest neurotransmiterem, który wpływa na czynność serca i naczyń krwionośnych, a jej stężenie wzrasta w przypadkach zwiększonego zapotrzebowania metabolicznego w tkankach, szczególnie przy niskim przepływie krwi lub hipoksji.12

Dwa typy receptorów odgrywają kluczową rolę w mechanizmie omdlenia:

  • Receptory A1 – o wysokim powinowactwie, zlokalizowane głównie w węźle zatokowo-przedsionkowym i węźle przedsionkowo-komorowym, odpowiedzialne przede wszystkim za omdlenia związane z bradykardią
  • Receptory A2 – o niskim powinowactwie, w szczególności receptory A2A, występujące w dużym zagęszczeniu w naczyniach krwionośnych, odpowiedzialne za wazodylatację podczas omdlenia

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Interakcja między adenozyną lub ATP (adenozynotrifosforanem) a ich receptorami tworzy tzw. sygnalizację purynergiczną, która często występuje w patomechanizmie omdlenia. Poziomy ADP (adenozynodifosforanu) i ekspresja receptorów adenozynowych mogą wpływać na wynik testu pochyleniowego (HUTT) oraz testu adenozynowego (ADT), stosowanych w diagnostyce przyczyn omdleń.23

Badania wykazały, że test adenozynowy może rzucić światło na profil purynergiczny pacjentów z omdleniami, a wyniki mogą mieć implikacje terapeutyczne, choć jego wartość predykcyjna jest kwestionowana. Nadal nie jest jasne, czy pozytywny wynik testu adenozynowego wskazuje na klinicznie istotne omdlenie kardiodepresyjne, czy ujawnia głównie uśpioną chorobę układu przewodzącego, która może spontanicznie objawiać się napadami omdleń lub stanu przedomdleniowego.34

Genetyczne aspekty omdleń

Coraz więcej dowodów wskazuje na komponenty genetyczne w patofizjologii omdleń, szczególnie omdleń wazowagalnych. Obserwacje kliniczne wskazują, że pacjenci z omdleniami wazowagalnymi często mają krewnych pierwszego stopnia również dotkniętych tym problemem, co sugeruje dziedziczną predyspozycję.123

Jednym z głównych genetycznych komponentów omdleń wazowagalnych są receptory adrenergiczne. Badania molekularne wykazały różnice w ekspresji i funkcjonowaniu tych receptorów u osób z predyspozycją do omdleń. Dodatkowo, obserwuje się występowanie omdleń wazowagalnych u pacjentów z zespołem Ehlersa-Danlosa typu III z hipermobilnością stawów, co również sugeruje podłoże genetyczne.32

Innym aspektem genetycznym jest zmieniona aktywność transportera norepinefryny, który odpowiada za wychwyt zwrotny norepinefryny w szczelinie synaptycznej. Zwiększona aktywność tego transportera, szybciej usuwającego neurotransmiter, może ograniczać kompensacyjną wazokonstrykcję, predysponując do hipotonii posturalnej i omdleń.1

Najnowsze odkrycia w patofizjologii omdleń

Ostatnie badania na myszach zidentyfikowały specyficzną grupę neuronów czuciowych odpowiedzialnych za omdlenie. Komórki te, nazywane neuronami czuciowymi NPY2R nerwu błędnego, znajdują się w nerwie błędnym, który łączy mózg z sercem i innymi narządami. Aktywacja tych komórek u myszy swobodnie poruszających się powodowała omdlenie w ciągu kilku sekund. Obserwowano rozszerzenie źrenic, odruch oczny oraz spadek częstości akcji serca, ciśnienia tętniczego i częstości oddechów. Badacze odkryli również, że za powrót do przytomności po omdleniu odpowiada region podwzgórza.1

Tradycyjnie uważano, że omdlenie wazowagalne jest wywołane nadmierną stymulacją mechanoreceptorów mięśnia sercowego, co prowadzi do odruchu Bezold-Jarischa. Jednak najnowsze dowody wskazują na alternatywne mechanizmy, takie jak:

  • Nieprawidłowa regulacja autonomiczna
  • Obecność endogennych substancji rozszerzających naczynia
  • Funkcjonalne upośledzenie odruchów z baroreceptorów
  • Paradoksalna regulacja ośrodkowego układu nerwowego

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Nowsze badania wskazują również, że omdlenie wazowagalne może być powiązane z nieprawidłową odpowiedzią naczyń mózgowych na stres ortostatyczny. Podejrzewa się, że nieprawidłowości w ośrodkowym układzie nerwowym, zarówno funkcjonalne jak i strukturalne, mogą odgrywać kluczową rolę w patogenezie omdleń neurogennych.1

Pojawiła się również teoria poliwagaralna, sugerująca, że nerw błędny (część autonomicznego układu nerwowego) może stać się nadmiernie ochronny w pewnych sytuacjach, powodując utratę przytomności jako sposób ochrony przed postrzeganym zagrożeniem. Ta perspektywa ewolucyjna może wyjaśniać, dlaczego ludzie mdleją w obliczu stresu emocjonalnego lub na widok krwi.12

Nowa klasyfikacja fenotypowa omdleń

W ostatnich latach pojawiło się innowacyjne podejście do diagnostyki i leczenia omdleń, skoncentrowane na mechanizmie hemodynamicznym leżącym u podstaw omdlenia. Zaproponowano nową klasyfikację omdleń, która definiuje dwa główne fenotypy o różnych przeważających mechanizmach:

  • Fenotyp hipotensyjny – gdzie dominuje hipotensja lub wazodepresja
  • Fenotyp bradykardyczny – gdzie dominuje kardioinhibicja

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Identyfikacja fenotypu omdlenia (bradykardyczny lub hipotensyjny/wazodepresyjny) stanowi pierwszy krok w kierunku spersonalizowanego podejścia do zarządzania omdleniami, charakteryzującego się dostosowanymi interwencjami profilaktycznymi. To podejście opiera się na założeniu, że znajomość mechanizmu omdlenia jest warunkiem wstępnym skutecznej profilaktyki i leczenia.1

Implikacje kliniczne mechanizmów omdlenia

Zrozumienie mechanizmów patofizjologicznych omdleń ma istotne znaczenie dla ich diagnostyki i leczenia. Dobór leczenia w omdleniach zależy od zidentyfikowanej przyczyny i mechanizmu omdlenia. Leczenie zawsze koncentruje się na przyczynie podstawowej.12

W omdleniach wazowagalnych, które są najczęstszą przyczyną omdleń, kluczowe jest rozpoznanie czynników wyzwalających i ich unikanie. Pacjentom zaleca się utrzymanie odpowiedniego nawodnienia, unikanie długotrwałego stania oraz naukę technik mających na celu zapobieganie spadkowi ciśnienia tętniczego, takich jak manewry przeciwzaciśnieniowe (np. krzyżowanie nóg, zaciskanie pięści).12

Farmakoterapia w omdleniach wazowagalnych może obejmować:

  • Agonistów alfa-1-adrenergicznych – zwiększających ciśnienie tętnicze
  • Kortykosteroidy – pomagające podnieść poziom sodu i płynów
  • Selektywne inhibitory wychwytu zwrotnego serotoniny (SSRI) – pomagające regulować odpowiedź układu nerwowego
  • Midodryna
  • Fludrokortyzon

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W omdleniach kardiogennych leczenie skupia się na podstawowej chorobie serca:

  • W przypadku zaburzeń rytmu serca może być konieczne wszczepienie rozrusznika serca lub kardiowertera-defibrylatora
  • Ablacja cewnikowa może być stosowana w leczeniu tachyarytmii
  • W przypadku chorób strukturalnych serca może być wymagane leczenie interwencyjne, takie jak implantacja stentu lub wymiana zastawki

12

Beta-blokery były tradycyjnie stosowane w leczeniu omdleń wazowagalnych, choć ich skuteczność jest kwestionowana. Najnowsze badania sugerują, że mogą być one rozsądną opcją terapeutyczną dla pacjentów z omdleniami wazowagalnymi i współistniejącym nadciśnieniem tętniczym.12

Znaczącą rolę odgrywa również edukacja pacjenta dotycząca natury omdleń, rozpoznawania objawów prodromalnych oraz technik zapobiegających utracie przytomności. Dla pacjentów z nawracającymi omdleniami ważne jest unikanie urazów, które mogą powstać w wyniku upadku podczas omdlenia.12

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

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

Materiały źródłowe

  • #1 Syncope – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK442006/
    Syncope is caused by decreased cerebral blood flow leading to transient loss of consciousness and postural tone, associated with spontaneous recovery. […] The brain needs a constant supply of glucose (through adequate cerebral blood flow) to function and any interruption to this even for few seconds can lead to loss of consciousness or syncope. Cerebral blood flow is maintained by a complex mechanism involving cardiac output, systemic vascular resistance, mean arterial pressure, and intravascular volume. Any defect in one or more of these systems leads to decreased cerebral blood flow. […] Terms near syncope or presyncope are confusing in that they may convey a different meaning to different practitioners. However, when a practitioner defines near syncope as a feeling that you were going to pass out but did not then, near syncope and syncope are both thought to be related to cerebral hypoperfusion, and therefore, any disease process which decreases blood flow can cause syncope and near syncope.
  • #1 Pathophysiology of syncope – PubMed
    https://pubmed.ncbi.nlm.nih.gov/15480926/
    Syncope or near-syncope is a not uncommon effect of gravitational or other stresses and it occurs when cerebral blood flow falls to below about half the normal value. […] The ability to vasoconstrict powerfully is important in resisting syncope; heart rate responses are of much less physiological significance. […] The intriguing unanswered question is what suddenly changes vasoconstriction and tachycardia to vasodilatation and bradycardia. […] People are more likely to faint when upright, motionless, warm, following meals, dehydrated or emotionally stressed, and these factors may be involved in some reflex syncopes including micturition and defaecation syncopes. […] Plasma volume is of considerable importance and increasing this by interventions such as salt loading, exercise training, and even sleeping with the bed head raised can often be of clinical benefit.
  • #1 Vasovagal syncope – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/vasovagal-syncope/symptoms-causes/syc-20350527
    Vasovagal syncope occurs when you faint because your body overreacts to certain triggers. […] The vasovagal syncope trigger causes your heart rate and blood pressure to drop suddenly. That leads to reduced blood flow to your brain, causing you to briefly lose consciousness. […] Vasovagal syncope occurs when the part of your nervous system that regulates heart rate and blood pressure overreacts to a trigger. […] During a vasovagal syncope episode, your heart rate slows, and the blood vessels in your legs widen. This allows blood to pool in your legs, which lowers your blood pressure. The drop in blood pressure and slowed heart rate quickly reduce blood flow to your brain, and you faint.
  • #1 Reflex syncope – Wikipedia
    https://en.wikipedia.org/wiki/Reflex_syncope
    Reflex syncope is a brief loss of consciousness due to a neurologically induced drop in blood pressure and/or a decrease in heart rate. […] The underlying mechanism involves the nervous system slowing the heart rate and dilating blood vessels, resulting in low blood pressure and thus not enough blood flow to the brain. […] Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes. The nucleus tractus solitarii of the brainstem is activated directly or indirectly by the triggering stimulus, resulting in simultaneous enhancement of parasympathetic nervous system (vagal) tone and withdrawal of sympathetic nervous system tone. […] This results in a spectrum of hemodynamic responses: On one end of the spectrum is the cardioinhibitory response, characterized by a drop in heart rate (negative chronotropic effect) and in contractility (negative inotropic effect) leading to a decrease in cardiac output that is significant enough to result in a loss of consciousness. It is thought that this response results primarily from enhancement in parasympathetic tone.
  • #1 Syncope: Symptoms, Causes & Treatments
    https://my.clevelandclinic.org/health/diseases/17536-syncope
    Cardiac syncope can occur if you have a heart or blood vessel condition that affects blood flow to your brain. […] Neurologic syncope can happen when you have a neurological condition such as a seizure, stroke or transient ischemic attack (TIA). […] The cause of syncope is unknown in about 33% of people who have it. However, an increased risk of syncope is a side effect of some medications. […] Treatment options will depend on whats causing your syncope and the results of your evaluation and testing. The goal of treatment is to keep you from having episodes of syncope. […] Medicines for syncope include: Midodrine. Fludrocortisone (Astonin or Florinef). […] Although most episodes of syncope arent dangerous, they can be life-threatening if you have abnormal heart rhythms or a neurologic cause. People with a heart or neurologic issue need to follow up with a provider who can help.
  • #1 Patient education: Syncope (fainting) (Beyond the Basics) – UpToDate
    https://www.uptodate.com/contents/syncope-fainting-beyond-the-basics/print
    A number of disturbances in the rate and/or rhythm of the heart can cause syncope. These disturbances are called „arrhythmias.” […] Syncope can occur because of problems at several places in the heart’s electrical system. The problems may be due to primary heart rhythm problems, underlying heart disease, use of a medication, or a transient abnormal communication between the heart and the nervous system. […] Bradycardia means a slow heart rate. In sinus bradycardia, the heart rate is slower than normal. In most cases, sinus bradycardia (usually defined as a heart rate under 50 beats/min) is innocent and may be associated with excellent physical fitness. However, a dramatically slowed heart rate (usually less than 35 beats/min) can decrease the output of blood, thereby reducing the blood supply to the brain by reducing the amount of blood that the heart can pump per minute.
  • #1
    https://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/syncope/
    The pathophysiology of syncope involves the interaction between the circulatory system and the autonomic nervous system. The autonomic nervous system is vital for the maintenance of internal homeostasis including regulation of blood pressure, heart rate, fluid and electrolyte balance, and body temperature. If one considers orthostatic intolerance, postural hypotension, and syncope/presyncope as a continuum, it becomes possible to link them all to a disturbance of homeostasis. […] Syncope or presyncope occurs as a result of brain hypoxia, which is usually secondary to a reduction of cerebral perfusion pressure. However, not every reduction in blood pressure leads to brain hypoxia. This is because the cerebral circulation is autoregulated so that brain perfusion is maintained in the face of significant changes in mean blood pressure. This homeostatic mechanism allows regional cerebral blood flow to remain constant over a range of cerebral perfusion pressure (CPP) of 50 to 150 mm Hg or mean arterial pressure (MAP) of 60 to 160 mm Hg. So, as MAP or CPP increases, resistance in small cerebral arteries increases via vasoconstriction and vice versa. Blood pressure above the upper level of autoregulation can cause cerebral edema, like that seen in hypertensive encephalopathy and blood pressure below the lower level result in syncope secondary to brain hypoxia. […] The pathophysiology of syncope is summarized as a reduction in systemic blood pressure that causes a decrease in the global cerebral blood flow, which results in loss of consciousness. A sudden cessation of cerebral blood flow for 6 to 8 seconds has been shown to cause loss of consciousness.
  • #1 Pathophysiology of neurally-mediated syncope | Neurología (English Edition)
    https://www.elsevier.es/es-revista-neurologia-english-edition–495-articulo-pathophysiology-neurally-mediated-syncope-S2173580816301006
    The BR controls the 2 variables determining BP: cardiac output and total peripheral resistance. In response to a drop in BP, the decrease in baroreceptor activity results in cardiac sympathetic excitation, inhibition of the cardiac vagal efferent which causes an increase in total peripheral resistance, and tachycardia with increased cardiac output. […] The mechanism responsible for vasodilatation and bradycardia has long been assumed to be excessive stimulation of mechanoreceptors mediated by intense contraction of an insufficiently full left ventricle, which transmits paradoxical signals to the CNS (Bezoldt-Jarisch reflex). However, current evidence points to other mechanisms, such as aberrant autonomic regulation, presence of endogenous vasodilators, functional impairment of the BR, and paradoxical regulation of the CNS.
  • #1 Recurrent Cough Syncope Due to Pertussis in Adults: Report of Three Cases and Review of the Literature | Kogan | Journal of Medical Cases
    https://www.journalmc.org/index.php/JMC/article/view/2537/1888
    Cough syncope, also called tussive syncope, is a well-recognized syndrome for about 70 years, in which loss of consciousness usually occurs immediately after a violent cough or prolonged bouts of violent coughing, lasting for seconds with rapid restoration of full consciousness. Its precise pathophysiologic mechanism is not fully understood and remains a matter of debate. […] The precise pathophysiologic mechanism of cough syncope is not fully understood, and remains a matter of debate. Several mechanisms have been proposed in this regard. With continuous coughing, intra-thoracic pressure increases resulting in decrease in venous return, ventricular filling, cardiac output, and blood pressure. […] Other suggested mechanisms indicates that the increased intra-thoracic pressure during coughing is transmitted to the cerebrospinal fluid, causing an acute pressure increase in the skull, compromising cerebral perfusion and resulting in syncope. […] In our three patients, no significant decrease in blood pressure or heart rate was observed during their syncopal attacks, suggesting that decrease in cerebral perfusion due to increased intra-thoracic pressure seems the likely mechanism for their syncope.
  • #1 Fainting during urination (micturition syncope): What causes it?
    https://www.mayoclinic.org/diseases-conditions/vasovagal-syncope/expert-answers/micturition-syncope/faq-20058084
    Micturition syncope, also known as post-micturition syncope, is fainting while urinating or immediately after urinating. This is likely due to a sudden, severe drop in blood pressure. Micturition syncope is most common in older men. It happens most often when getting up at night from a deep sleep. […] The exact cause of micturition syncope isn’t fully understood. But it may be related to a fall in blood pressure when you get up suddenly and stand at the toilet. Or this may happen when a full bladder empties very quickly. This is thought to cause a sudden drop in blood pressure. […] Prevention of micturition syncope depends on recognizing the factors that contribute to micturition syncope and avoiding them.
  • #1 Fainting after eating – why does it happen? | Top Doctors UK
    https://www.topdoctors.co.uk/medical-articles/swallow-syncope-what-causes-fainting-after-swallowing
    Swallowing syncope is a rare form of syncope which takes place when a patient feels faint after eating. It occurs when the patient swallows food, which then causes them to faint, or pass out. […] The reflexes which are started or initiated at the point of swallowing are what causes syncope. Swallowing syncope is rare, and may not occur every single time a patient swallows. Certain specific situations, with all the triggers lining up as it were, are what cause swallow syncope to occur. This can trigger a complex reflex in which the brain then sends a signal to the heart to slow down (bradycardia) and to the vessels to pool blood (vasodilatation) which results in a low blood pressure, which causes patients to feel lightheaded, and if severe, to pass out completely. However, the mechanism behind swallow syncope is still not completely understood.
  • #1 Adenosine Test in Syncope of Unknown Origin | AER Journal
    https://www.aerjournal.com/articles/adenosine-test-obsolete-clinical-assessment-syncope-unknown-origin?language_content_entity=en
    Syncope is a common clinical condition affecting 50% of the general population; however, its exact pathophysiology and underlying mechanisms remain elusive. The adenosine test (ADT) has been proposed as a complementary diagnostic test in the work-up of syncope of unknown origin aiming to further elucidate the underlying pathogenetic mechanism of spontaneous syncope. […] The adenosine (AD) test (ADT) has been proposed as a useful tool in investigating the pathogenesis of SUO. By exhibiting different responses to ADT, distinct subgroups may show a differential involvement of AD and its receptors in the pathophysiology of syncope helping to decide group-targeted therapeutic strategies. […] AD seems to increase in cases of exaggerated metabolic demand in local tissue and, more specifically, in cases of low blood flow or hypoxia.
  • #1 Adenosine Test in Syncope of Unknown Origin | AER Journal
    https://www.aerjournal.com/articles/adenosine-test-obsolete-clinical-assessment-syncope-unknown-origin?language_content_entity=en
    This interaction between AD or ATP and their receptors, makes up the so-called purinergic signalling, usually found in the pathogenetic mechanism of syncope. […] Two types of receptors seem to play a crucial role in syncope, the high-affinity A1R and the low-affinity A2R. A1R are mostly located in the sinoatrial node and the AV node and are mainly responsible for bradycardia-induced syncope. A2R and more specifically A2AR are located in high densities in vessels and are responsible for vasodilation during syncope. […] Several studies have investigated the role of AD as a modulator of syncope via A1R and A2R and how ADP levels and adenosine receptors expression might affect the outcome of the head-up tilt table test (HUTT) and ADT. […] Such an adjustment seems to play a specific and critical role in the pathogenesis and manifestation of syncope and in the outcomes of ADT.
  • #1 Role of the sympathetic nervous system in vasovagal syncope and rationale for beta-blockers and norepinephrine transporter inhibitors – Medwave
    http://viejo.medwave.cl/link.cgi/English/Updates/Supplements/6842.act?ver=sindiseno
    In a review, Raj and Coffin propose that beta-blockers may be a reasonable therapeutic option for patients with vasovagal syncope and systemic arterial hypertension. […] As mentioned, the reuptake of norepinephrine in the synaptic cleft, made possible by the norepinephrine transporter, is the main mechanism of inactivation of norepinephrine. […] An increased activity of the norepinephrine transporter, clearing faster the neurotransmitter, would reduce the compensatory vasoconstriction predisposing to postural hypotension.
  • #1 Daily briefing: We finally know what causes fainting
    https://www.nature.com/articles/d41586-023-03466-9
    Experiments in mice have identified a specific group of sensory neurons that is responsible for syncope, the brief loss of consciousness during fainting. The cells called NPY2R vagal sensory neurons are found in the vagus nerve, which connects the brain to the heart and other organs. Scientists activated these cells in mice that were roaming about, which then fainted within a few seconds. Their pupils dilated, their eyes rolled back and their heart rate, blood pressure and breathing rate all dipped. The team also found that a region of the brains hypothalamus is responsible for recovery from fainting.
  • #1 Neurally Mediated Syncope | Vanderbilt Autonomic Dysfunction Center
    https://www.vumc.org/autonomic-dysfunction-center/neurally-mediated-syncope
    More than 35 years ago, some authors indicated that patients with NMS exhibit an abnormal cerebral vascular response to orthostatic stress. […] Results of some studies raise the possibility that abnormalities within the CNS, either functional or structural, play a pivotal role in the pathogenesis of NMS.
  • #1 Situational syncope: why we faint under stress | Top Doctors
    https://www.topdoctors.co.uk/medical-articles/situational-syncope-why-we-faint-under-stress
    Fainting is essentially caused by two things: low blood pressure and a low heart rate. This reduces the perfusion of blood and oxygen to the brain and leads to a transient loss of consciousness. […] The type of fainting we are referring to is known as situational syncope or vasovagal syncope and occurs because your body overreacts to a certain trigger; whether that be at the sight of blood or any kind of emotional distress. It causes your heart rate to drop and blood to rush to your legs which lowers your blood pressure. As a result, less blood flows to your brain and you experience a transient loss of consciousness. […] There is an evolutionary aspect to why humans faint. The polyvagal theory suggests that the vagus nerve (part of your nervous system) can become very protective in certain situations, causing you to lose consciousness as a way to protect you from an observed threat.
  • #1 Syncope: new solutions for an old problem | Rivasi | Polish Heart Journal (Kardiologia Polska)
    https://journals.viamedica.pl/polish_heart_journal/article/view/86433
    Syncope is a frequent event in the general population. […] In recent years, diagnosis and treatment have further evolved according to an innovative approach focused on the hemodynamic mechanism underlying syncope, based upon the assumption that knowledge of the syncope mechanism is a prerequisite for effective syncope prevention and treatment. […] Therefore, a new classification of syncope has been proposed, which defines two main syncope phenotypes with different predominant mechanisms: the hypotensive phenotype, where hypotension or vasodepression prevails, and the bradycardic phenotype, where cardioinhibition prevails. […] Identification of syncope phenotype bradycardic or hypotensive/vasodepressive represents the first step towards personalized management of syncope, characterized by customized interventions for prevention. […] The present review aims to illustrate these new developments in the diagnosis and therapy of non-cardiac syncope within a mechanism-based perspective. […] Diagnosis and therapy of bradycardic and hypotensive phenotypes are discussed, with a focus on recent evidence.
  • #1 Syncope – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK442006/
    A thorough history and physical examination alone may yield a diagnosis in up to 50% of patients presenting with syncope. […] Testing rarely leads to a diagnosis as the most common cause is vasovagal and benign. […] Treatment of underlying cause is the focus of treatment in syncope. […] The most common cause of syncope is vasovagal and is self-limiting. […] Mental illness and substance abuse should be considered in syncope patients where the etiology of syncope remains unclear.
  • #1 Vasovagal Syncope: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/23325-vasovagal-syncope
    If your blood pressure drops too much, this causes vasovagal syncope. You pass out because your brain isnt getting enough blood flow. […] A vasovagal syncopal episode can happen again, especially if you stand within 30 minutes of the first fainting episode. […] Most people who have vasovagal syncope will recover on their own. […] Knowing what causes vasovagal syncope can help you avoid that trigger or at least be ready for it. […] If you can recognize an episode before it happens, you may be able to stop it. Your healthcare provider can teach you techniques that keep your blood pressure high enough so that you dont pass out.
  • #1 Syncope (Fainting) – Heart Rhythm CentreHeart Rhythm Centre
    https://heartrhythm.com.au/symptom/syncope/
    Syncope occurs when the brain does not receive sufficient blood flow to maintain its normal function. […] Insufficient blood flow to the brain can occur either because the heart is beating too slowly or because the blood vessels dilate allowing the blood pressure to fall. […] Abnormal heart rhythms can cause syncope. When the heart beats too slowly, insufficient blood may be pumped to the brain. […] Syncope can occur when the heart cannot pump blood to the brain because of an obstruction. […] Postural hypotension occurs when the blood pressure is insufficient when standing. […] The most important aspect of treatment of vasovagal syncope is to avoid situations that trigger syncope. […] When syncope is caused by slow heart rhythms the usual treatment is a pacemaker. […] Many fast heart rhythms can be cured with the technique of catheter ablation. […] When syncope is due to ventricular tachycardia the treatment may be catheter ablation as described above or an implantable defibrillator.
  • #1 Role of the sympathetic nervous system in vasovagal syncope and rationale for beta-blockers and norepinephrine transporter inhibitors – Medwave
    http://viejo.medwave.cl/link.cgi/English/Updates/Supplements/6842.act?ver=sindiseno
    The semi-quantitative analysis of adrenergic innervations showed a significantly lower H/M (heart/mediastinum) ratio in the syncopal patients compared with the control group. […] It has been well demonstrated that patients with vasovagal syncope frequently have a first-degree relative who is also affected. […] Although genetic participation in the vasovagal syncope has been debated, some evidence suggests that there is one major genetic component: the adrenergic receptors. […] Based on the information previously presented, it is not a surprise that beta-blockers were employed in the treatment of vasovagal syncope from the very beginning. […] However, it should be noted that a fixed dose of metoprolol was used for all the patients, without individualizing the dosage, which probably justifies the absence of positive results.
  • #1 Vasovagal Syncope | Cedars-Sinai
    https://www.cedars-sinai.org/health-library/diseases-and-conditions/v/vasovagal-syncope.html
    Vasovagal syncope is a condition that leads to fainting in some people. It’s also called neurocardiogenic syncope or reflex syncope. It’s the most common cause of fainting. It’s usually not harmful and not a sign of a more serious problem. […] Many nerves connect with your heart and blood vessels. These nerves help control the speed and force of your heartbeat. They also regulate blood pressure by controlling whether your blood vessels widen or tighten. Usually, these nerves coordinate their actions so you always get enough blood to your brain. Under certain situations, these nerves might give an inappropriate signal. This might cause your blood vessels to open wide. At the same time, your heartbeat may slow down. Blood can pool in your legs which leads to a drop in blood pressure, and not enough of it may reach the brain. If that happens, you may briefly lose consciousness. When you lie or fall down, blood flow to the brain resumes. […] Vasovagal syncope is the most common cause of fainting. It happens when the blood vessels open too wide or the heartbeat slows, causing a temporary lack of blood flow to the brain.
  • #2
    https://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/syncope/
    The pathophysiology of syncope involves the interaction between the circulatory system and the autonomic nervous system. The autonomic nervous system is vital for the maintenance of internal homeostasis including regulation of blood pressure, heart rate, fluid and electrolyte balance, and body temperature. If one considers orthostatic intolerance, postural hypotension, and syncope/presyncope as a continuum, it becomes possible to link them all to a disturbance of homeostasis. […] Syncope or presyncope occurs as a result of brain hypoxia, which is usually secondary to a reduction of cerebral perfusion pressure. However, not every reduction in blood pressure leads to brain hypoxia. This is because the cerebral circulation is autoregulated so that brain perfusion is maintained in the face of significant changes in mean blood pressure. This homeostatic mechanism allows regional cerebral blood flow to remain constant over a range of cerebral perfusion pressure (CPP) of 50 to 150 mm Hg or mean arterial pressure (MAP) of 60 to 160 mm Hg. So, as MAP or CPP increases, resistance in small cerebral arteries increases via vasoconstriction and vice versa. Blood pressure above the upper level of autoregulation can cause cerebral edema, like that seen in hypertensive encephalopathy and blood pressure below the lower level result in syncope secondary to brain hypoxia. […] The pathophysiology of syncope is summarized as a reduction in systemic blood pressure that causes a decrease in the global cerebral blood flow, which results in loss of consciousness. A sudden cessation of cerebral blood flow for 6 to 8 seconds has been shown to cause loss of consciousness.
  • #2 Syncope: Symptoms, Causes & Treatments
    https://my.clevelandclinic.org/health/diseases/17536-syncope
    Vasovagal syncope happens when you have a sudden drop in blood pressure, which causes a drop in blood flow to your brain. It often occurs after standing for a while or under emotional distress. Normally, when you stand up, gravity makes blood settle in the lower part of your body, below your diaphragm. When that happens, your heart and autonomic nervous system work to keep your blood pressure stable. […] In vasovagal syncope, your heart rate and blood pressure inappropriately decrease severely. This causes decreased blood flow to your brain and leads to passing out. Typically, vasovagal syncope is benign. […] Postural syncope (also called postural hypotension or orthostatic hypotension) happens when your blood pressure drops suddenly due to a quick change in position, such as standing up after lying down. Certain medications and dehydration can lead to this condition.
  • #2 Pathophysiology of neurally-mediated syncope | Neurología (English Edition)
    https://www.elsevier.es/es-revista-neurologia-english-edition–495-articulo-pathophysiology-neurally-mediated-syncope-S2173580816301006
    Neurally mediated syncope is a frequent complication that can present at any age. It is both genetic and familial and has been observed in patients with EhlersDanlos syndrome type III with joint hypermotility. […] From a pathophysiological viewpoint, NMS is characterised by an initial state of sympathetic hyperactivity which translates clinically into tachycardia, sweating, tremor, and cutaneous vasoconstriction. At the time syncope occurs, sympathetic hyperactivity, both at the heart and resistance vessel levels, stops abruptly. There is an increase in cardiac vagal activity which can cause asystole or marked bradycardia; furthermore, deactivation of sympathetic activity to the blood vessels (vasoconstriction reflex) can elicit pronounced vasodilation with severe hypotension. […] The most plausible hypothesis hinges on the presence of an intermittent dysfunction of BR control over BP and HR, which can occur at the peripheral or the central level.
  • #2 Reflex syncope – Wikipedia
    https://en.wikipedia.org/wiki/Reflex_syncope
    On the other end of the spectrum is the vasodepressor response, caused by a drop in blood pressure (to as low as 80/20) without much change in heart rate. This phenomenon occurs due to dilation of the blood vessels, probably as a result of withdrawal of sympathetic nervous system tone. […] The majority of people with vasovagal syncope have a mixed response somewhere between these two ends of the spectrum.
  • #2 Patient education: Syncope (fainting) (Beyond the Basics) – UpToDate
    https://www.uptodate.com/contents/syncope-fainting-beyond-the-basics/print
    Sometimes, part of the conduction system between the sinus node and the rest of the heart becomes disrupted due to heart disease. Most often, this occurs in the middle of the heart where a special set of fibers conduct the electrical impulse to the pumping chambers (the ventricles), preventing the normal flow of electrical impulses. If the electrical signal from the sinus node fails to get through the entire conduction pathway, the heartbeat can be markedly slowed or totally interrupted. If the interruption is significant and the heart rate is too slow, it can impair blood flow to the brain. […] Any problem with the structure of the heart that interferes with the flow of blood can cause syncope. The two most common causes of outflow obstruction are hypertrophic cardiomyopathy and aortic stenosis.
  • #2 Syncope – Cardiovascular Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/cardiovascular-disorders/symptoms-of-cardiovascular-disorders/syncope
    Most syncope results from insufficient cerebral blood flow. […] Some cases involve adequate flow but with insufficient cerebral substrate (oxygen, glucose, or both). […] Most deficiencies in cerebral blood flow result from decreased cardiac output (CO). […] Decreased CO can be caused by cardiac disorders that obstruct outflow, cardiac disorders of systolic dysfunction, cardiac disorders of diastolic dysfunction, arrhythmias (too fast or too slow), and conditions that decrease venous return. […] Outflow obstruction can be exacerbated by exercise, vasodilation, and hypovolemia (particularly in aortic stenosis and hypertrophic cardiomyopathy), which may precipitate syncope. […] Arrhythmias cause syncope when the heart rate is too fast to allow adequate ventricular filling (eg 150 to 180 beats/minute) or too slow to provide adequate output (eg, 30 to 35 beats/minute).
  • #2 Vasovagal Syncope: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/23325-vasovagal-syncope
    Vasovagal syncope happens when your nervous system overreacts and your blood pressure and heart rate drop suddenly, causing you to faint or pass out. […] This is the most common type of reflex syncope, which happens automatically for reasons you cant control. People also sometimes call it neurocardiogenic syncope because factors involving your heart, brain or both cause it. […] Vasovagal syncope is a reflex reaction to something going on around you. But the reflex is either too strong or happens at the wrong time. This all starts in the part of your nervous system that works without you having to think about it your autonomic nervous system. […] One of the key nerves in this system is the vagus nerve, which controls your heart rate and blood pressure. If your vagus nerve becomes too active, it can cause your heart rate and blood pressure to drop too much or too quickly (or both).
  • #2 Pathophysiology of neurally-mediated syncope | Neurología (English Edition)
    https://www.elsevier.es/es-revista-neurologia-english-edition–495-articulo-pathophysiology-neurally-mediated-syncope-S2173580816301006
    The BR controls the 2 variables determining BP: cardiac output and total peripheral resistance. In response to a drop in BP, the decrease in baroreceptor activity results in cardiac sympathetic excitation, inhibition of the cardiac vagal efferent which causes an increase in total peripheral resistance, and tachycardia with increased cardiac output. […] The mechanism responsible for vasodilatation and bradycardia has long been assumed to be excessive stimulation of mechanoreceptors mediated by intense contraction of an insufficiently full left ventricle, which transmits paradoxical signals to the CNS (Bezoldt-Jarisch reflex). However, current evidence points to other mechanisms, such as aberrant autonomic regulation, presence of endogenous vasodilators, functional impairment of the BR, and paradoxical regulation of the CNS.
  • #2
  • #2
    https://link.springer.com/article/10.1007/s10286-004-1004-2
    Syncope or near-syncope is a not uncommon effect of gravitational or other stresses and it occurs when cerebral blood flow falls to below about half the normal value. […] The ability to vasoconstrict powerfully is important in resisting syncope; heart rate responses are of much less physiological significance. […] It is now known not to be due to stimulation of cardiac receptors and some cerebral signal is more probable. […] People are more likely to faint when upright, motionless, warm, following meals, dehydrated or emotionally stressed, and these factors may be involved in some reflex syncopes including micturition and defaecation syncopes. […] Plasma volume is of considerable importance and increasing this by interventions such as salt loading, exercise training, and even sleeping with the bed head raised can often be of clinical benefit.
  • #2 Cough syncope | MedLink Neurology
    https://www.medlink.com/articles/cough-syncope
    Several pathophysiologic processes may cause or contribute to cough-related syncope, including Valsalva-induced decreased cardiac output, increased intracranial pressure, cardiac arrhythmias, stimulation of a hypersensitive carotid sinus, cough-triggered neural reflex-mediated hypotension-bradycardia, laryngospasm, augmentation of left ventricular outflow obstruction, impaction of a brainstem herniation, decreased cerebral blood flow, internal jugular vein valve insufficiency, and rarely seizures. […] Cough is a defensive mechanism designed to remove mucous and foreign material from the airways. A cough begins with a spontaneous deep inspiration that increases lung volume and decreases intrathoracic pressure. Then the thoracic and abdominal wall muscles contract with the glottis closed (ie, Valsalva maneuver), greatly increasing intrathoracic pressure without changing lung volume. When the glottis opens, an explosive decrease in both intrathoracic pressure and lung volume occurs.
  • #2 Common causes of syncope (fainting) | GoHealth Urgent Care
    https://www.gohealthuc.com/library/common-causes-of-syncope-fainting
    Researchers think micturition syncope happens because the combination of standing up plus relaxing the bladder muscles leads to a sudden drop in blood pressure, resulting in loss of consciousness. […] Vasovagal syncope is the most common cause of syncope. It typically happens when the body overreacts to stress or fear, which causes a sudden drop in blood pressure. Common triggers of vasovagal syncope in the medical setting include the sight of blood or needles. […] Vasovagal syncope can often be prevented by adequate hydration, and by laying patients with a history of vasovagal syncope flat during procedures like blood draws or injections.
  • #2 Fainting after eating – why does it happen? | Top Doctors UK
    https://www.topdoctors.co.uk/medical-articles/swallow-syncope-what-causes-fainting-after-swallowing
    Treatment for swallow syncope focuses on the management of swallowing properly. This means taking small, bite-size pieces of food, chewing properly, and making sure to swallow at the right moment. […] Rarely, syncope occurs unpredictably with swallowing, and if this is a recurring problem, and interferes with quality of life, AND if the heart is shown to stop / slow during swallowing associated with reproduction of syncope symptoms, then a pacemaker may be beneficial.
  • #2 Adenosine Test in Syncope of Unknown Origin | AER Journal
    https://www.aerjournal.com/articles/adenosine-test-obsolete-clinical-assessment-syncope-unknown-origin?language_content_entity=en
    This interaction between AD or ATP and their receptors, makes up the so-called purinergic signalling, usually found in the pathogenetic mechanism of syncope. […] Two types of receptors seem to play a crucial role in syncope, the high-affinity A1R and the low-affinity A2R. A1R are mostly located in the sinoatrial node and the AV node and are mainly responsible for bradycardia-induced syncope. A2R and more specifically A2AR are located in high densities in vessels and are responsible for vasodilation during syncope. […] Several studies have investigated the role of AD as a modulator of syncope via A1R and A2R and how ADP levels and adenosine receptors expression might affect the outcome of the head-up tilt table test (HUTT) and ADT. […] Such an adjustment seems to play a specific and critical role in the pathogenesis and manifestation of syncope and in the outcomes of ADT.
  • #2 Situational syncope: why we faint under stress | Top Doctors
    https://www.topdoctors.co.uk/medical-articles/situational-syncope-why-we-faint-under-stress
    In humans, when we face similar threats, such as the sight of blood or extreme emotional distress, or in the cases of many medical students after seeing graphic sights in the operating theatre, our body can overreact and we behave similarly to the possum. […] Before fainting, you may experience presyncope. Usually, there is a strong adrenaline surge that brings about a hot flush, cramps, shortness of breath, palpitations, feeling weak at the knees, dizzy, etc. It happens when your brain isn’t getting enough oxygen due to the change in blood flow. […] Fainting can come on fairly abruptly for some, but for others, they may very well recognise that it is about to happen, so they can adopt strategies to abort the faint, for example, by sitting or laying down. […] If you are prone to fainting when having your blood taken or from prolonged standing and you can recognise the feeling, you should act accordingly; either by sitting or lying down to avoid it getting worse.
  • #2 Syncope: Symptoms, Causes & Treatments
    https://my.clevelandclinic.org/health/diseases/17536-syncope
    Cardiac syncope can occur if you have a heart or blood vessel condition that affects blood flow to your brain. […] Neurologic syncope can happen when you have a neurological condition such as a seizure, stroke or transient ischemic attack (TIA). […] The cause of syncope is unknown in about 33% of people who have it. However, an increased risk of syncope is a side effect of some medications. […] Treatment options will depend on whats causing your syncope and the results of your evaluation and testing. The goal of treatment is to keep you from having episodes of syncope. […] Medicines for syncope include: Midodrine. Fludrocortisone (Astonin or Florinef). […] Although most episodes of syncope arent dangerous, they can be life-threatening if you have abnormal heart rhythms or a neurologic cause. People with a heart or neurologic issue need to follow up with a provider who can help.
  • #2 Situational syncope: why we faint under stress | Top Doctors
    https://www.topdoctors.co.uk/medical-articles/situational-syncope-why-we-faint-under-stress
    Fainting can be dangerous, especially, if you are walking alone in the street or standing at the top of a flight of stairs. […] A very helpful exercise, and one that can work immediately, is called an isometric counterpressure manoeuvre. When you experience presyncope symptoms, you should hold your hands together and pull them slightly apart; clench your teeth; tense your buttocks, quadriceps and calves and cross your legs. It is an effective strategy in stabilising blood pressure by squeezing blood from your legs back to your heart. […] Many people underestimate how important it is to drink sufficient amounts of water throughout the day and how well it can help prevent episodes of syncope.
  • #2 Vasovagal Syncope: Causes, Symptoms, and Treatment
    https://www.healthline.com/health/vasovagal-syncope
    There is no standard treatment that can cure all causes and types of vasovagal syncope. Treatment is individualized based on the cause of your recurrent symptoms. […] Some of the medications used to treat vasovagal syncope include: alpha-1-adrenergic agonists, which raise blood pressure; corticosteroids, which help raise sodium and fluid levels; selective serotonin reuptake inhibitors (SSRIs), which help to regulate the nervous system response. […] Vasovagal syncope is the most common cause of fainting. Its typically not connected to a serious health problem, but its important to see a doctor who can rule out any underlying conditions that could be causing you to faint. […] This type of fainting episode is usually caused by certain triggers, like the sight of something that scares you, an intense emotion, getting overheated, or standing for too long.
  • #2 Syncope > Fact Sheets > Yale Medicine
    https://www.yalemedicine.org/conditions/syncope
    Cardiac syncope occurs when the heart is not pumping enough blood to the brain. This can occur because of an abnormal heart rhythm that is either too slow or too fast. This can also occur if there is a problem with heart structure or function that causes the pumping function to become ineffective. […] The treatment for syncope depends on what is found to be the underlying problem. If an abnormal heart rhythm is found, doctors determine which treatments to administer for each patient. If the problem is an underlying heart abnormality, such as a blocked artery or heart-valve problem, our cardiologists may recommend a stent or a valve-replacement procedure. […] For vasovagal syncope, the first step is understanding lifestyle factors that cause fainting, such as excess caffeine or alcohol. Physical maneuvers, like pressing the palms together at chest level, can sometimes be helpful. Occasionally, the patient will require medication.
  • #2 Role of the sympathetic nervous system in vasovagal syncope and rationale for beta-blockers and norepinephrine transporter inhibitors – Medwave
    http://viejo.medwave.cl/link.cgi/English/Updates/Supplements/6842.act?ver=sindiseno
    In a review, Raj and Coffin propose that beta-blockers may be a reasonable therapeutic option for patients with vasovagal syncope and systemic arterial hypertension. […] As mentioned, the reuptake of norepinephrine in the synaptic cleft, made possible by the norepinephrine transporter, is the main mechanism of inactivation of norepinephrine. […] An increased activity of the norepinephrine transporter, clearing faster the neurotransmitter, would reduce the compensatory vasoconstriction predisposing to postural hypotension.
  • #2 Fainting and Vaccines | Vaccine Safety | CDC
    https://www.cdc.gov/vaccine-safety/about/fainting.html
    Fainting, also called syncope, is a temporary loss of consciousness caused by a decreased blood flow to the brain. […] Fainting can happen after many types of vaccinations. […] Fainting after getting a vaccine is most commonly reported after three vaccines given to adolescents: HPV, MCV4, and Tdap. Because the ingredients of these three vaccines are different, yet fainting is seen with all of them, scientists think that fainting is due to the vaccination process and not to the vaccines themselves. […] Reports from VAERS shows that fainting after vaccinations is common in adolescents. […] Fainting itself is generally not serious, but harm from related falls or other accidents can cause injury. […] Although fainting itself might or might not be preventable, it is important to prevent injuries when people do faint.
  • #3 Syncope: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/811669-overview
    Syncope occurs as a consequence of global cerebral hypoperfusion. Brain parenchyma depends on adequate blood flow to provide a constant supply of glucose, the primary metabolic substrate. Brain tissue cannot store energy in the form of the high-energy phosphates found elsewhere in the body; consequently, a cessation of cerebral perfusion lasting only 3-5 seconds can result in syncope. […] Cerebral perfusion is maintained relatively constant by an intricate and complex feedback system involving cardiac output (CO), systemic vascular resistance (SVR), mean arterial pressure (MAP), intravascular volume status, cerebrovascular resistance with intrinsic autoregulation, and metabolic regulation. A clinically significant defect in any one of these systems or subclinical defects in several of them may cause syncope.
  • #3 Syncope: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/811669-overview
    CO can be diminished secondary to mechanical outflow obstruction, pump failure, hemodynamically significant arrhythmias, or conduction defects. SVR can drop secondary to vasomotor instability, autonomic failure, or vasodepressor/vasovagal response. MAP decreases with all causes of hypovolemia. Medications can affect CO, SVR, or MAP. […] Other conditions can mimic syncope. A central nervous system (CNS) event, such as a hemorrhage or an unwitnessed seizure, can present as syncope. Syncope can occur without reduction in cerebral blood flow in patients who have severe metabolic derangements (eg, hypoglycemia, hyponatremia, hypoxemia, hypercarbia).
  • #3 Vasovagal Syncope: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/23325-vasovagal-syncope
    Vasovagal syncope happens when your nervous system overreacts and your blood pressure and heart rate drop suddenly, causing you to faint or pass out. […] This is the most common type of reflex syncope, which happens automatically for reasons you cant control. People also sometimes call it neurocardiogenic syncope because factors involving your heart, brain or both cause it. […] Vasovagal syncope is a reflex reaction to something going on around you. But the reflex is either too strong or happens at the wrong time. This all starts in the part of your nervous system that works without you having to think about it your autonomic nervous system. […] One of the key nerves in this system is the vagus nerve, which controls your heart rate and blood pressure. If your vagus nerve becomes too active, it can cause your heart rate and blood pressure to drop too much or too quickly (or both).
  • #3 Reflex syncope (neurally-mediated syncope) | MedLink Neurology
    https://www.medlink.com/articles/reflex-syncope-neurally-mediated-syncope
    The vasodilation that contributes to the vasodepressor components of vasovagal syncope is caused largely by centrally initiated diminution of sympathetic vasoconstrictor tone (ie, passive vasodilation), but there can also be a sympathetically mediated vasodilatory component resulting from release of nitric oxide. […] Clustering of vasovagal syncope in some families suggests a genetic component.
  • #3 Pathophysiology of neurally-mediated syncope | Neurología (English Edition)
    https://www.elsevier.es/es-revista-neurologia-english-edition–495-articulo-pathophysiology-neurally-mediated-syncope-S2173580816301006
    Neurally mediated syncope is a frequent complication that can present at any age. It is both genetic and familial and has been observed in patients with EhlersDanlos syndrome type III with joint hypermotility. […] From a pathophysiological viewpoint, NMS is characterised by an initial state of sympathetic hyperactivity which translates clinically into tachycardia, sweating, tremor, and cutaneous vasoconstriction. At the time syncope occurs, sympathetic hyperactivity, both at the heart and resistance vessel levels, stops abruptly. There is an increase in cardiac vagal activity which can cause asystole or marked bradycardia; furthermore, deactivation of sympathetic activity to the blood vessels (vasoconstriction reflex) can elicit pronounced vasodilation with severe hypotension. […] The most plausible hypothesis hinges on the presence of an intermittent dysfunction of BR control over BP and HR, which can occur at the peripheral or the central level.
  • #3 Patient education: Syncope (fainting) (Beyond the Basics) – UpToDate
    https://www.uptodate.com/contents/syncope-fainting-beyond-the-basics/print
    Orthostatic hypotension refers to low blood pressure that occurs when a person stands or sits up or remains standing for a long time. In people who are susceptible, due to the effects of gravity, an excessive amount of blood is displaced from the upper part to the lower part of the body, causing an inadequate amount of blood flow to the brain, leading to syncope.
  • #3 Syncope – Cardiovascular Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/cardiovascular-disorders/symptoms-of-cardiovascular-disorders/syncope
    Venous return can be decreased by hemorrhage, increased intrathoracic pressure, increased vagal tone (which can also decrease heart rate), and loss of sympathetic tone (eg, from medications, carotid sinus pressure, autonomic dysfunction). […] Syncope involving these mechanisms (except for hemorrhage) is often termed vasovagal or neurocardiogenic and is common and benign. […] Orthostatic hypotension, a common benign cause of syncope, results from failure of normal mechanisms (eg, sinus tachycardia, vasoconstriction, or both) to compensate for the temporary decrease in venous return that occurs with standing. […] The central nervous system (CNS) requires oxygen and glucose to function. […] Even with normal cerebral blood flow, a significant deficit of either will cause loss of consciousness.
  • #3 Syncope – Cardiovascular Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/cardiovascular-disorders/symptoms-of-cardiovascular-disorders/syncope
    Most syncope results from insufficient cerebral blood flow. […] Some cases involve adequate flow but with insufficient cerebral substrate (oxygen, glucose, or both). […] Most deficiencies in cerebral blood flow result from decreased cardiac output (CO). […] Decreased CO can be caused by cardiac disorders that obstruct outflow, cardiac disorders of systolic dysfunction, cardiac disorders of diastolic dysfunction, arrhythmias (too fast or too slow), and conditions that decrease venous return. […] Outflow obstruction can be exacerbated by exercise, vasodilation, and hypovolemia (particularly in aortic stenosis and hypertrophic cardiomyopathy), which may precipitate syncope. […] Arrhythmias cause syncope when the heart rate is too fast to allow adequate ventricular filling (eg 150 to 180 beats/minute) or too slow to provide adequate output (eg, 30 to 35 beats/minute).
  • #3 Fainting: Causes, Types, and Prevention
    https://www.healthline.com/health/fainting
    Fainting, or the temporary loss of consciousness, can occur if your brain isnt getting enough oxygen. Fainting may be triggered by a number of factors, including dehydration, low blood sugar, standing up too quickly, or certain medications. […] Fainting happens when you lose consciousness for a short amount of time because your brain isnt getting enough oxygen. […] Fainting can be triggered by a number of factors, including: fear or other emotional trauma, severe pain, a sudden drop in blood pressure, low blood sugar due to diabetes, hyperventilation, dehydration, standing in one position for too long, standing up too quickly, physical exertion in hot temperatures, coughing too hard, straining during a bowel movement, consuming drugs or alcohol, seizures. […] Medications that can cause your blood pressure to drop also increase your chance of fainting.
  • #3 Cough syncope | MedLink Neurology
    https://www.medlink.com/articles/cough-syncope
    Several pathophysiologic processes may cause or contribute to cough-related syncope: Valsalva-induced decreased cardiac output. Cough acts like a strong Valsalva maneuver, increasing intrathoracic pressures by up to 300 mm Hg, which causes decreased venous return to the atria with resultant decreased stroke volume, decreased blood pressure, and decreased cerebral perfusion. Increased intracranial pressure. Cough-induced increased intrathoracic pressure is transmitted to the cerebrospinal fluid with resultant sudden increased intracranial pressure that may act like a cerebral concussion or may force blood out of the closed cranial vault and cause decreased cerebral blood flow or even transient cerebral circulatory arrest. Cardiac arrhythmias. Cough may produce vagally mediated cardiac arrhythmias, including sinus arrest and atrioventricular conduction block. Stimulation of hypersensitive carotid sinus. Cough may stimulate a hypersensitive carotid sinus and cause reflex hypotension or vagally mediated, high-grade, atrioventricular block and syncope. Cough-triggered neural reflex-mediated hypotension-bradycardia. Many patients with cough syncope exhibit prolonged hypotension in response to cough or Valsalva maneuver, and in at least some cases, this appears to be mediated via a neural reflex mechanism. Laryngospasm. Patients with severe gastroesophageal reflux disease can develop severe laryngospasm and syncope, particularly in association with a recent or concurrent respiratory infection that contributes to protracted cough and an increased amount of refluxate. Tracheal compression. A single case of cough syncope and tracheal compression due to a retrosternal goiter has been reported, but the case was confounded by a concomitant pulmonary embolus from a deep vein thrombosis. Augmentation of left ventricular outflow obstruction. Cough may dynamically augment left ventricular outflow obstruction in patients with idiopathic hypertrophic subaortic stenosis, partly due to reflex sympathetic stimulation. Impaired left ventricular diastolic filling. Cough may augment impaired diastolic filling and produce a marked decrease in cardiac output in patients with constrictive pericarditis. Impaction of a brainstem herniation. Cough or sneezing may cause impaction of a brainstem herniation in the foramen magnum in patients with a Chiari malformation with resulting compression of efferent sympathetic and parasympathetic cardiovascular pathways in the brainstem, dysfunction of the midbrain reticular activating system, craniospinal pressure dissociation, transient increased intracranial pressure, and vertebrobasilar compression with brainstem ischemia. Decreased cerebral blood flow. Cough may further impair cerebral circulation in patients with already compromised cerebral blood flow because of extracranial or intracranial arterial stenosis or occlusion. Internal jugular vein valve insufficiency. Cough syncope can result from transient increases in intracranial pressure and consequent reduction in cerebral blood flow due to abnormally high internal jugular vein pressures transmitted from the thoracic cavity because of incompetent internal jugular vein valves. Seizure. Rarely, cough and its associated changes in cerebral blood flow or other pathophysiologic processes may actually trigger a seizure with resultant loss of consciousness followed by a postictal state.
  • #3 Adenosine Test in Syncope of Unknown Origin | AER Journal
    https://www.aerjournal.com/articles/adenosine-test-obsolete-clinical-assessment-syncope-unknown-origin?language_content_entity=en
    ADT has never gained wide clinical acceptance because it has been challenged by studies that doubted the clinical significance of asystole or a high-degree AV block occurring during the test, as being the predominant mechanism responsible for spontaneous syncope. […] According to the above findings, it was concluded that ADT does not provide predictive value for patients with SUO or when selecting patients that would benefit from pacemaker implantation. […] ADT could have an additional role to HUTT in the diagnostic work-up of syncope. Although data from studies have failed to prove a consistent correlation between ADT and the rhythm disturbances occurring during spontaneous syncope, ADT can shed further light on the purinergic profile of syncopal patients and the results can have therapeutic implications.
  • #3 Role of the sympathetic nervous system in vasovagal syncope and rationale for beta-blockers and norepinephrine transporter inhibitors – Medwave
    http://viejo.medwave.cl/link.cgi/English/Updates/Supplements/6842.act?ver=sindiseno
    The semi-quantitative analysis of adrenergic innervations showed a significantly lower H/M (heart/mediastinum) ratio in the syncopal patients compared with the control group. […] It has been well demonstrated that patients with vasovagal syncope frequently have a first-degree relative who is also affected. […] Although genetic participation in the vasovagal syncope has been debated, some evidence suggests that there is one major genetic component: the adrenergic receptors. […] Based on the information previously presented, it is not a surprise that beta-blockers were employed in the treatment of vasovagal syncope from the very beginning. […] However, it should be noted that a fixed dose of metoprolol was used for all the patients, without individualizing the dosage, which probably justifies the absence of positive results.
  • #4 Patient education: Syncope (fainting) (Beyond the Basics) – UpToDate
    https://www.uptodate.com/contents/syncope-fainting-beyond-the-basics/print
    Syncope is caused by a short, temporary episode of low blood pressure. […] To remain conscious, a supply of oxygen-rich blood must be pumped to the brain without interruption. If the brain is deprived of this blood supply, even for a brief period, loss of consciousness (passing out) will occur. […] Vasovagal syncope is by far the most common type of a group of conditions called reflex syncope. A variety of conditions can trigger vasovagal syncope, including physical or psychological stress, dehydration, bleeding, or pain. The heart rate may slow dramatically at the time of the faint, and the blood vessels (mainly the veins) in the body expand, causing blood to pool in the lower extremities and the bowels, resulting in less blood return to the heart and a low blood pressure (hypotension). This causes a decrease in blood flow to the brain which causes near or complete loss of consciousness.
  • #4 Adenosine Test in Syncope of Unknown Origin | AER Journal
    https://www.aerjournal.com/articles/adenosine-test-obsolete-clinical-assessment-syncope-unknown-origin?language_content_entity=en
    A major challenge regarding the ADT is the interpretation of a positive test result. It remains unclear whether a positive ADT indicates an underlying clinically significant cardioinhibitory NMS or unveils a mostly dormant conduction system disease that may spontaneously present with syncopal or presyncopal attacks. […] ADT may possess a surrogate role in identifying this specific group of patients with asystolic syncope, especially when an ILR implantation is not feasible, and serve as a supplementary, easily performed and low-cost diagnostic test that can facilitate clinical decision-making. […] ADP and AD receptor levels have been used to identify patients with syncope without structural heart disease in two distinct subgroups.