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Patofiziologija ružičastog pjenastog sputuma kod plućnog edema

Patofiziologija ružičastog pjenastog sputuma kod plućnog edema



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Plućni edem je stanje u kojem je tekućina curenja u alveolarne prostore. To može biti posljedica hemodinamskih uzroka kao što su zatajenje lijevog srca i opstrukcija plućnih vena ili mikrovaskularna ozljeda ili povećana propusnost kapilara.

Klinički smo naučeni razlikovati različite vrste sputuma. Sputum kod plućnog edema je karakteristično ružičast i pjenast.

Ovdje je važno napomenuti da je tekućina koja curi u alveolarne prostore transudat, a ne krv. Stoga nipošto nije da je ružičasta posljedica krvi. Inače bi se zvalo hemoptiza.

Moje pitanje je zašto je ispljuvak ružičast ako krv nema nikakvu ulogu?


Iako je tekućina u plućnom edemu transudat, u njoj ima krvi. To je potkrijepljeno činjenicom da postoje mikrohemoragije u akutnoj plućnoj kongestiji i makrofagi opterećeni hemosiderinom ili 'stanice zatajenja srca' u dugotrajnoj plućnoj kongestiji na histologiji. To znači da su eritrociti pobjegli iz vaskulature kako bi ušli u tkivo (i nisu se uspjeli vratiti u krv), dok su ih makrofagi kasnije potrošili.

Budući da gubitak krvi nije jako velik, boja je ružičasta, a ne crvena kao što se vidi kod hemoptize.

Razlog za to vjerojatno je u značajnim razlikama u hidrostatskim i onkotskim tlakovima u usporedbi s ostatkom tijela. U plućima, jedan rub kapilare je nasuprot jedne, iznimno tanke alveolarne stanice koja pruža vrlo mali pritisak kako bi uravnotežila povećane sile prisutne u plućnom edemu. Bez ovog unutarnjeg pritiska za stabilizaciju stijenke kapilare, dolazite do situacije u kojoj se male rupture javljaju na slabim točkama AC membrane, za razliku od drugdje u tijelu gdje su pritisci izjednačeniji i promjena je osmotski proces, a ne stanični poremećaj.

Iako makrofagi napunjeni hemosiderinom mogu biti dokaz da eritrociti napuštaju krvožilni sustav, važno je napomenuti da se mogu naći i u drugim organima. Jedan primjer je kronična venska kongestija jetre, gdje hipoksija (zbog kongestije) može dovesti do oštećenja endotela koji ispušta eritrocite, koje kasnije progutaju makrofagi.


Patofiziologija ružičastog pjenastog sputuma kod plućnog edema - Biologija

Plućni edem definira se kao abnormalno nakupljanje ekstravaskularne tekućine u plućnom parenhima. Dvije glavne vrste su kardiogeni i nekardiogeni plućni edem. Ova aktivnost naglašava ulogu interprofesionalnog tima u dijagnostici i liječenju ovog stanja.

  • Navedite znakove i simptome različitih vrsta plućnog edema.
  • Pregledati patofiziologiju različitih vrsta plućnog edema.
  • Opišite liječenje različitih tipova plućnog edema.
  • Sažmite važnost interprofesionalnog pristupa za učinkovito liječenje bolesnika s plućnim edemom.

Uvod

Plućni edem se može definirati kao abnormalno nakupljanje ekstravaskularne tekućine u plućnom parenhimu. Ovaj proces dovodi do smanjene izmjene plinova na alveolarnoj razini, napredujući do potencijalnog zatajenja disanja. Njegova etiologija je ili posljedica kardiogenog procesa s nemogućnošću uklanjanja dovoljne količine krvi iz plućne cirkulacije ili nekardiogene precipitirane ozljedom plućnog parenhima. To je važno patološko obilježje u mnogim procesima bolesti, pa je stoga učenje temeljnog procesa bolesti ključno za upravljanje njegovim liječenjem. Kliničke značajke uključuju progresivno pogoršanje dispneje, hropove pri auskultaciji pluća i pogoršanje hipoksije.[1]

Etiologija

Plućni edem se općenito može podijeliti na kardiogeni i nekardiogeni plućni edem.

Kardiogeni ili volumno preopterećeni plućni edem nastaje zbog brzog porasta hidrostatskog tlaka plućnih kapilara. To se obično vidi kod poremećaja koji uključuju sistoličku i dijastoličku funkciju lijeve klijetke (akutni miokarditis uključujući druge etiologije neishemične kardiomiopatije, akutni infarkt miokarda), funkciju zalistaka (aortna/mitralna regurgitacija i stenoza u umjerenom do teškom rasponu), fibrilacija atrija s brzim ventrikularnim odgovorom, ventrikularna tahikardija, visoki stupanj i srčani blok trećeg stupnja).[2]

Nekardiogeni plućni edem uzrokovan je ozljedom pluća s posljedičnim povećanjem plućne vaskularne permeabilnosti što dovodi do kretanja tekućine bogate proteinima u alveolarne i intersticijske odjeljke. Akutna ozljeda pluća s teškom hipoksemijom naziva se sindrom akutnog respiratornog distresa (ARDS) i viđa se u različitim stanjima koja izravno zahvaćaju pluća, kao što su upala pluća, inhalacijske ozljede ili neizravno, kao što su sepsa, akutni pankreatitis, teška trauma s šokom, višestruke transfuzije krvi.[3]

Epidemiologija

Svake se godine primi više od milijun pacijenata s dijagnozom plućnog edema uzrokovanog srčanim uzrocima (zatajenje srca).[4] Procjenjuje se da se kod 190 000 pacijenata svake godine dijagnosticira akutna ozljeda pluća.[5] Oko 1,5 do 160 do 160. 3,5 slučajeva/100 000 stanovnika ima dijagnozu ARDS-a.

Patofiziologija

Posljedična patologija povećanog sadržaja ekstravaskularne tekućine u plućima ostaje uobičajena za sve oblike plućnog edema. Međutim, temeljni mehanizam koji dovodi do edema proizlazi iz poremećaja različitih složenih fizioloških procesa, održavajući osjetljivu ravnotežu filtracije tekućine i otopljene tvari kroz plućnu kapilarnu membranu. Ova neravnoteža može biti uzrokovana jednim ili više sljedećih čimbenika:

  • Porast intravaskularnog hidrostatskog tlaka koji se retrogradno prenosi na plućnu mikrovaskulaturu
  • Povećanje intersticijskog hidrostatskog tlaka
  • Ozljeda endotela i poremećaj epitelnih barijera
  • Smanjenje onkotskog tlaka zbog osnovnih stanja jetre, bubrega, pothranjenosti i drugih stanja s gubitkom proteina. 
  • Limfna insuficijencija
  • Povećan negativni intersticijski tlak 

Odnos između hidrostatskih i onkotskih sila u odnosu na neto filtraciju tekućine najbolje se objašnjava jednadžbom Ernesta Starlinga&rsquosa. Brzina filtracije tekućine određena je razlikama u hidrostatskom i onkotskom tlaku između plućnih kapilara i intersticijalnog prostora.[1][3][6]

Povijest i fizička

Progresivno pogoršavanje dispneje, tahipneje i hripanja (ili pucketanja) na pregledu s povezanom hipoksijom kliničke su značajke zajedničke i kardiogenom i nekardiogenom plućnom edemu.

Kašalj s ružičastim pjenastim ispljuvakom koji je zabilježen zbog hipoksemije zbog poplave alveola i auskultacije S3 galopa može ukazivati ​​na kardiogeni edem. Slično, prisutnost šumova, povišenog jugularnog venskog tlaka, perifernog edema može ukazivati ​​na srčanu etiologiju.

U bolesnika s nekardiogenim plućnim edemom treba pažljivo procijeniti simptome infekcija kao što su vrućica, kašalj s iskašljavanjem, dispneja koja ukazuje na vjerojatnu upalu pluća, nedavne traume, transfuzije krvi jer ti bolesnici mogu napredovati u sindrom akutnog respiratornog distresa. & #160

Auskultacija ostaje temelj za procjenu uz krevet u svih bolesnika s respiratornim simptomima. Točnije, čuje se fino ili grubo pucketanje ključno je za određivanje sljedećih koraka u upravljanju. Kod kardiogenog plućnog edema čuje se fino pucketanje. Čuju se isključivo u fazi udisaja kada se mali dišni putovi, koji su bili zatvoreni tijekom izdisaja, naglo otvaraju.[7]

Evaluacija

Uz temeljitu anamnezu i fizikalni pregled, elektrokardiogram pomaže u dijagnosticiranju srčane ishemije ili infarkta miokarda. To je brz, jeftin i relativno manje specijaliziran test koji se može napraviti uz krevet.

Slijede različiti dijagnostički alati koji se koriste za dijagnosticiranje plućnog edema i, što je još važnije, za razlikovanje njegovih različitih tipova. 

Laboratorijsko ispitivanje

Natriuretski peptid moždanog tipa (BNP) luče srčani miociti lijeve klijetke kao odgovor na istezanje uzrokovano povećanim volumenom ventrikularne krvi ili povećanim intrakardijalnim tlakom. Povišene razine BNP koreliraju s krajnjim dijastoličkim tlakom lijeve klijetke, kao i tlakom plućne okluzije i mogu se vidjeti u bolesnika s kongestivnim zatajenjem srca.[3] BNP razine manje od 100 pg/ml sugeriraju da je zatajenje srca manje vjerojatno, a razine su manje vjerojatno da je zatajenje srca manje od 160. veći od 500 pg/ml ukazuju na veliku vjerojatnost zatajenja srca. Razine između 100 i 500 pg/ml ne pomažu u dijagnozi zatajenja srca i često se viđaju u kritično bolesnih pacijenata.[3] 

Povišenje troponina obično se bilježi u bolesnika s oštećenjem miocita, kao što je akutni koronarni sindrom. Međutim, također je zabilježeno da su oni povišeni u bolesnika s teškom sepsom.[3]

Hipoalbuminemija (&le3,4 g/dL) je neovisni pokazatelj povećane bolničke smrtnosti i smrtnosti nakon otpusta za pacijente s akutnim dekompenziranim zatajenjem srca.[8]  Nizak albumin u izolaciji ne dovodi do edema pluća jer postoji. istovremeni pad razine plućnog intersticija i albumina u plazmi sprječavajući stvaranje transpulmonalnog gradijenta onkotskog tlaka.[9] 

Dobivanje razine elektrolita u serumu, uključujući bubrežnu funkciju, osmolarnost seruma, toksikološki probir, pomaže u bolesnika s plućnim edemom zbog toksičnog gutanja. Dobivanje razine lipaze i amilaze pomaže u dijagnosticiranju akutnog pankreatitisa.  

Radiografsko ispitivanje

Koriste se i posteroanteriorni i lateralni pogledi u standardnim slikama ili anteroposteriorni pogledi u prijenosnim slikama. Kardiogeni plućni edem karakterizira prisutnost središnjeg edema, pleuralnih izljeva, Kerley B septalnih linija, peribronhijalne manžete i povećane veličine srca. Kod nekardiogene etiologije, uzorak edema je tipično pjegav i periferan što može pokazati prisutnost zamućenja brušenog stakla i konsolidacije na zračnim bronhogramima.[10] Pleuralni izljevi češće se vide kod kardiogenog tipa.[1]

Ehokardiografija 

Pomaže u dijagnostici sistoličke disfunkcije lijeve klijetke i valvularne disfunkcije. Modalitetima, uključujući tkivnu doplersku sliku mitralnog anulusa, može se procijeniti prisutnost i stupanj dijastoličke disfunkcije.[3]

Ultrazvuk pluća

Novija tehnika koja je neinvazivna i ne uključuje izlaganje zračenju. Najčešće se koristi u jedinicama intenzivne njege, hitnoj pomoći i operacijskim sobama. Pomaže u otkrivanju nakupljanja ekstravaskularne plućne vode (EVLW) prije kliničkih manifestacija.[10]

Kateterizacija plućne arterije

Često se smatra zlatnim standardom u određivanju etiologije plućnog edema, to je invazivni test koji pomaže u praćenju sistemskog vaskularnog otpora, minutnog volumena srca i tlaka punjenja. Povišeni tlak okluzije plućne arterije preko 18 mm Hg pomaže u određivanju kardiogenog plućnog edema.[3]

Transpulmonalna termodilucija

To je invazivni modalitet testiranja koji se provodi u pacijenata koji su obično podvrgnuti velikim srčanim, vaskularnim ili torakalnim operacijama. Također se koriste u septičkom šoku i prate nekoliko hemodinamskih indeksa kao što su srčani indeks, miješana venska zasićenost kisikom, indeks udarnog volumena i EVLW.[10]

Liječenje / upravljanje

Terapijski ciljevi u bolesnika s plućnim edemom uključuju ublažavanje simptoma i liječenje osnovnog patološkog stanja.

Diuretici ostaju glavni oslonac liječenja, a furosemid je najčešće korišteni lijek. Više doze su povezane s većim poboljšanjem dispneje, međutim, također povezane s prolaznim pogoršanjem bubrežne funkcije.[11]

Vazodilatatori se mogu dodati kao pomoćna terapija diureticima u liječenju plućnog edema.[12] IV nitroglicerin (NTG) je lijek izbora, a smanjuje predopterećenje i plućnu kongestiju. NTG se smije koristiti samo kada je sistolički krvni tlak (SBP) > 110 mm Hg. Nesiritid je rekombinantni moždani natriuretski peptid koji ima vazodilatatorna svojstva. Pokazalo se da značajno smanjuje pritisak plućne kapilare (PCWP) i tlak punjenja, ali nije zabilježeno naknadno poboljšanje dispneje.[13] Noviji lijekovi kao što je serelaksin, rekombinantni ljudski oblik relaksina, inducirana aktivacija dušikovog oksida, što uzrokuje vazodilataciju. Klevidipin je blokator kalcijevih kanala ultra kratkog djelovanja, koji je započeo vrlo rano u prezentaciji, povezan je sa smanjenom duljinom boravka, poboljšanom dispnejom i rjeđim prijemom u intenzivnu terapiju.[14] 

Nifedipin se koristi u profilaksi i liječenju plućnog edema velikih visina (HAPE). Ovaj blokator kalcijevih kanala djeluje protiv vazokonstrikcije plućne vaskulature uzrokovane hipoksijom. To dovodi do sniženja plućnog arterijskog tlaka s naknadnim poboljšanjima u razmjeni plinova, sposobnosti vježbanja i radiografiji prsnog koša.[15] Nifedipin se koristi samo kao profilaktička strategija kada se visinska aklimatizacija ne može postići u visokorizičnim osobama i situacijama. , uključujući brzu stopu uspona, ekstremne fizičke napore, nedavnu infekciju dišnog trakta i nisku nadmorsku visinu domaćeg mjesta stanovanja.[16]

Inotropi, kao što su dobutamin i dopamin, koriste se u liječenju plućne kongestije kada su povezani s niskim SBP i znakovima hipoperfuzije tkiva. Značajne nuspojave uključuju tahiaritmije, ishemiju i hipotenziju. Milrinon je IV inotrop s vazodilatacijskim svojstvima, ali je povezan s povećanjem smrtnosti nakon otpuštanja.[17]

Morfin smanjuje sistemski vaskularni otpor i djeluje kao analgetik i anksiolitik. Koristi se u liječenju plućnog edema koji je posljedica akutnog koronarnog sindroma. Međutim, može uzrokovati respiratornu depresiju za koju je potrebna intubacija i općenito se ne preporučuje.[11]

Ventilacijska potpora, kako neinvazivna tako i invazivna, koristi se za poboljšanje oksigenacije, usmjeravanje alveolarnih i intersticijskih tekućina natrag u kapilare, poboljšanje hiperkarbije, a time i preokretanje respiratorne acidoze, i konačno, oksigenaciju tkiva. Također ima za cilj smanjenje rada disanja. Odluka o pružanju respiratorne potpore temelji se na kliničkom poboljšanju uz ispitivanje gore navedenih lijekova, psihičkom statusu pacijenta, ukupnoj energiji ili nedostatku istih. U bolesnika na invazivnoj mehaničkoj ventilaciji neophodno je kontinuirano praćenje hemodinamike jer smanjenje predopterećenja može dovesti do smanjenog minutnog volumena srca, a time i pada SBP-a. Neinvazivna mehanička ventilacija, kada se započne rano u liječenju plućnog edema, povezana je s manjom pojavom umora respiratornih mišića i, prema tome, smanjenjem invazivne ventilacije.[11]

Diferencijalna dijagnoza

Imerzioni plućni edem od utapanja, neurogeni plućni edem od moždanog udara, traume glave, preosjetljivosti na lijekove ili uzimanja toksičnih tvari, transfuzije krvi koje dovode do akutne ozljede pluća povezane s transfuzijom (TRALI), bolesti jetre, plućne embolije ili infarkta i uremije.[18]

Prognoza

Plućni edem je akutno dekompenzirano stanje zbog srčane ili nesrčane etiologije. Privremene mjere kao što su dodatna oksigenacija, diuretici, nitrati i morfin pomažu u upravljanju dispnejom, hipoksemijom. Međutim, potrebno je definitivno liječenje temeljnih uzroka kako bi se spriječilo njegovo ponavljanje. Prognostička predviđanja teško je kvantificirati, s obzirom na veliki broj kardiogenih i nekardiogenih etiologija plućnog edema i podataka o njihovoj individualnoj smrtnosti. Uznapredovalo stanje plućnog edema u ARDS-u imalo je progresivno poboljšane ishode. Bolnička smrtnost se smanjila sa 60% od 1967. do 1981. na raspon od 30% do 40% u 1990-ima.[19]  Nadalje, analiza studija smrtnosti od ARDS-a pokazala je pad ukupne smrtnosti od oko 1,1% godišnje od 1994. godine. do 2006. Prognoza koja koristi podatke o smrtnosti uvelike je varijabilna i ovisi o precipitirajućem procesu ARDS-a.[20] 

Komplikacije

Budući da je plućni edem posljedica složenih fizioloških poremećaja, bilo da se radi o zahvaćenosti srca, jetre, višeorganskih sustava, toksičnim podražajima, komplikacije koje proizlaze iz njega su uglavnom sekundarne u odnosu na prethodno navedene patofiziološke procese. Kardiogeni plućni edem može napredovati do respiratornog zatajenja što zahtijeva korištenje mehaničkog ventilatora. ARDS je komplikacija akutne ozljede pluća s progresivnom hipoksemijom, koja također zahtijeva intubaciju i mehaničku ventilaciju.

Odvraćanje i edukacija pacijenata

Bolesnike s ishemijskom ili valvularnom srčanom bolešću u anamnezi potrebno je educirati o simptomima plućnog edema prilikom svakog posjeta klinici kod svojih liječnika. Mora se naglasiti savjetovanje o prehrani s malo soli, redovitoj tjelovježbi i pridržavanju lijekova.

Poboljšanje rezultata tima za zdravstvo

Plućni edem može biti posljedica zahvaćenosti više organa, pa se stoga preporuča uključivanje interprofesionalnog tima kao što su internisti, kardiologi, pulmologi u ranoj fazi tečaja za pravodobno započinjanje ciljane terapije radi poboljšanja ishoda bolesnika. Medicinske sestre, studente medicine, studente medicinskih sestara moraju redovito informirati o znakovima respiratornog zatajenja radi ranijeg prepoznavanja bolesnika s prijetećom respiratornom dekompenzacijom. Moraju se prakticirati dobre vještine uzimanja povijesti kako bi se identificirali čimbenici kao što su nepridržavanje lijekova, loša socioekonomska situacija, korištenje nedopuštenih droga kako bi se izbjegle recidivi ili ponovni prijem. [Razina 5]


Neurogeni plućni edem

Prasanna Udupi Bidkar, Hemanshu Prabhakar, u Komplikacije u neuroanesteziji, 2016.

Uvod

Plućni edem karakterizira nakupljanje tekućine u zračnim prostorima i intersticiju pluća. Može biti posljedica intrinzične patologije pluća ili sustavnih čimbenika. Stoga se plućni edem tradicionalno dijeli na kardiogene i nekardiogene uzroke. Kardiogeni plućni edem nastaje zbog akutnog zatajenja lijeve klijetke, nakon raznih inzulta poput infarkta miokarda. Nekardiogeni plućni edem može biti uzrokovan akutnom ozljedom pluća ili sindromom respiratornog distresa odraslih (ARDS). Kardiogeni plućni edem uzrokovan je povišenim plućnim hidrostatskim tlakom, sekundarnim uz povišeni plućni venski tlak.


Što uzrokuje ružičasti pjenasti sputum kod zatajenja srca?

Znakovi i simptomi Najčešći simptom od plućni edem je teškoće u disanju, ali može uključivati ​​i druge simptome kao što su iskašljavanje krvi (klasično se vidi kao ružičasti, pjenasti ispljuvak), prekomjerno znojenje, tjeskoba i blijeda koža.

Osim navedenog, koji je najčešći uzrok plućnog edema? The najčešći uzrok plućnog edema je kongestivno zatajenje srca (CHF). Zatajenje srca se događa kada srce više ne može pravilno pumpati krv po cijelom tijelu. Time se stvara rezervni pritisak u malim krvnim žilama pluća, koji uzroci žile da propuštaju tekućinu.

S obzirom na to, zašto imam pjenasti sputum?

Pjenasti sputum ponekad može biti znak: kronične opstruktivne plućne bolesti (KOPB) gastroezofagealne refluksne bolesti (GERB) upale pluća.

Što uzrokuje krvavi ispljuvak kod plućnog edema?

Ozbiljnije uzroci od krv-obojeni sputum može uključivati: plućne embolija, ili a krv ugrušak u plućima. plućni edemili imate tekućinu u plućima. plućne aspiracija ili udisanje stranog materijala u pluća.


Možda će vam se također svidjeti

@anon 6: Gusta, bijela, pjenasta sluz može biti znak plućnog edema. Plućni edem može se pojaviti kao posljedica preeklampsije u trudnoći, kao i glavobolje, smetnje vida, bol na mjestu jetre i oteklina. Preeklampsija se može javiti i postnatalno, ali je dijelom uzrokovana posteljicom. Malo je vjerojatno nakon 72 sata nakon porođaja i vrlo je malo vjerojatno da se radi o preeklampsiji osam tjedana nakon rođenja. Potencijalno, zato su liječnici napravili krvnu pretragu, potvrdili da nije preeklampsija i poslali vas na put. Međutim, ovo je nagađanje i vaši simptomi nisu ohrabrujući, a mogu biti znak nečeg drugog, stoga nastavite tražiti liječničku pomoć dok vas netko ne sasluša. anon990072 4. travnja 2015

Idem na šesti tjedan ovoga i dišem sve teže i teže, ali liječnici samo pošalju RT i onda mi prepišu još jednu dozu albuterola i inhalator. Jedini test koji su napravili je rendgen. Bojim se da jednog dana uskoro neću moći doći do daha. Što trebam učiniti da dobijem pomoć koja mi je potrebna? anon334843 16. svibnja 2013

Iskašljao sam gustu bijelu pjenušavu sluz s mrljama krvi i imam vruću i hladnu zimicu i groznicu. Moji mišići kao da su u plamenu. Također imam jaku glavobolju i oticanje ruku, stopala i lica. Moje tijelo kao da se gasi.

Bio sam u bolnici šest puta, i svaki put su mi rekli da imam samo postporođajnu depresiju ili migrenu, jer liječnici rade samo jednostavnu analizu krvi i onda mi kažu da nije u redu. Zahtijevao sam da se napravi test sluzi, ali su me brzo poslali. Bolestan sam već osam tjedana. Zdravstveni sustav me iznevjerava. Postoji li netko tko me može uputiti u pravom smjeru da dobijem pomoć koja mi je potrebna? anon332154 27. travnja 2013

Različite vrste tuberkuloze su zarazne, dok druge nisu. Živim s atipičnom tuberkulozom koja, na moju sreću, nije zarazna, iako me iz dana u dan jako tuguje. orangey03 31. siječnja 2013

Moj tata je imao pjenasti ispljuvak i tekućinu u plućima kada je imao upalu pluća. Morao je biti hospitaliziran jer mu je bilo jako teško disati.

Imao je stalni kašalj koji mu jednostavno nije dopuštao da dobro udahne. Mogao je umrijeti bez pomoći liječnika. kylee07drg 30. siječnja 2013

Jedan od simptoma KOPB-a mog djeda bio je iskašljavanje bijelog pjenastog sputuma. Pušio je dugi niz godina, ali se istinski razbolio tek u svojoj osamdesetoj.

Počelo je sporo, samo s upornim kašljem i blagim nedostatkom daha kada bi bio aktivan. U samo nekoliko godina to je napredovalo do točke u kojoj je često iskašljavao ispljuvak i nije mogao ni otići u kupaonicu, a da ne završi bez daha.

Napokon je morao biti premješten u starački dom. Kad je stigao tamo, uopće nije dugo poživio. Trebao mu je samo stalni nadzor i pomoć tijekom posljednjih dana. Perdido 29. siječnja 2013

@Kristee – Tuberkuloza je zarazna, ali ako se netko već liječio od nje, nije vjerojatno da će je širiti. Većina ljudi koji ga imaju traže liječenje, jer im to daje temperaturu i jak kašalj, a to su dvije stvari s kojima se teško dugo nositi.

Svaki put kad sam imao ispljuvak iz pluća ili bronhija, bio sam više nego spreman otići liječniku. Ako je infekcija bakterijska, uvijek mogu dobiti antibiotike i odmah mi može biti bolje. Kristee 29. siječnja 2013

Čuo sam da tuberkuloza može izazvati ružičasti pjenasti ispljuvak. Prestrašio bih se kad bih iskašljao nešto što je izgledalo kao da ima krvi.

Zna li netko je li tuberkuloza zarazna? To nije nešto s čime sam se ikada susreo, pa se pitam može li se uopće širiti s osobe na osobu.


Liječenje plućnog edema

  1. Terapija kisikom: Prioritet je dati kisik kako bi se poništila hipoksija ili uskraćivanje opskrbe kisikom u tijelu. Teška hipoksija može zahtijevati korištenje mehaničke ventilacije kako bi se osigurao pozitivan tlak u dišnim putovima. : Kako bi se smanjila tekućina koja se nakupila u srcu i plućima, obično se daju diuretici poput furosemida (Lasix).
  2. Antihipertenzivi: Hipertenzija može na kraju dovesti do plućnog edema. Lijekovi za snižavanje krvnog tlaka uključuju beta blokatore (npr. bisoprolol) i ACE inhibitore (npr. ramipril).
  3. Reduktori predopterećenja i reduktori naknadnog opterećenja: lijekovi kao što je nitroglicerin mogu se koristiti za smanjenje tlaka koji ide u srce.
  4. Lijekovi protiv kolesterola: Za kardiogeni plućni edem mogu se propisati lijekovi protiv kolesterola kako bi se smanjio LDL ili loš kolesterol koji začepljuje srčane arterije.
  5. Antivirusni ili antibiotici: Bakterije i virusi su česti temeljni uzroci nekardiogenog plućnog edema.

Testovi za procjenu sputuma

Sputum se može analizirati u laboratoriju kako bi se odredio njegov sadržaj kako bi se procijenile infekcije ili tražio rak. Testovi mogu uključivati:

  • Kultura sputuma: Kultura sputuma se radi stavljanjem uzorka sputuma u medij za uzgoj (posuda s agarom) i traženje prisutnosti rasta. To se može učiniti kako bi se odredila određena vrsta bakterije koja uzrokuje upalu pluća. Nakon što se utvrdi bakterijski soj, laboratorij može napraviti daljnja ispitivanja kako bi utvrdio koji je antibiotik najučinkovitiji protiv te bakterije (testiranje osjetljivosti).
  • Sputum za tuberkulozu: može se uzeti uzorak sputuma za traženje tuberkuloze, iako je često potrebno nekoliko uzoraka kako bi se pronašao onaj koji je dijagnostički.
  • Citologija sputuma: U citologiji sputuma uzorak sputuma se procjenjuje pod mikroskopom. To se može učiniti za traženje znakova tuberkuloze ili znakova stanica raka. Nekada se smatralo da citologija sputuma može otkriti rak pluća, ali nije učinkovit alat za probir. Međutim, ako se pronađu stanice raka, to može biti dijagnoza raka pluća. Zatim će se morati učiniti daljnji testovi kako bi se otkrilo mjesto raka.

Dobivanje uzorka sputuma (umjesto sluzi) može biti donekle izazovno, jer zahtijeva da osoba iskašljava ispljuvak iz dubine pluća.


Patofiziologija ružičastog pjenastog sputuma kod plućnog edema - Biologija

Kongestivno zatajenje srca

Diferencijalna dijagnoza

Kongestivno zatajenje srca

Ukupna specifičnost sistematski pregled je 90% s osjetljivošću od 10-30%

Laboratorijski podaci u smislu dijagnoze.

Dodatne istrage

EKG: Nema specifičnog za CHF. Korisno za dijagnosticiranje ishemije srca, IM, aritmija, ventrikularne hipertrofije, abnormalnosti elektrolita, toksičnosti Dig itd.

ehokardiografija: Pomaže u identifikaciji regionalnih abnormalnosti gibanja stijenke, funkcije lijeve klijetke, tamponade srca, bolesti zalistaka srca.

Radionuklidna ventrikulografija: Izbačajna frakcija, veličina komore i abnormalnosti regionalnog gibanja stijenke.

Swna-Ganz kateter: Tlak punjenja LV, minutni volumen U teško bolesnog bolesnika s plućnim edemom.

Kompenzacijski pokušaji

Povećan učinak simpatičkog živčanog sustava:

Pomaci Starlingove krivulje: Srce pokušava kompenzirati nizak minutni volumen ili dilatacijom (za povećanje krajnjeg dijastoličkog tlaka) ili hipertrofijom (povećanom potražnjom za kisikom). Starlingova krivulja je pomaknuta prema dolje udesno i ima spljoštenu konturu u bolesnika sa smanjenom kontraktilnošću srca. Usklađenost se odnosi na tlak potreban za punjenje ventrikula do određenog volumena. Kod CHF ventrikule postaju krute (nesukladne) što zahtijeva viši LVEDP da bi se postiglo dijastoličko punjenje koje je dovoljno za održavanje minutnog volumena srca.

Renin angiotenzinski sustav: Smanjena bubrežna perfuzija dovodi do zadržavanja soli i vode. Elevacija LVEDP.

Inoptropno djelovanje koje rezultira povećanim minutnim volumenom srca

Zatajenje srca također bi se pogoršalo verapmilom i esmololom.

Budući da bi ton vagusa bio nizak, atropin bi imao mali učinak.

Mjera za smanjenje nakon opterećenja

Nitroprusid je dilatator arteriola kao i venodilatator. Ovaj lijek bi trebao poboljšati minutni volumen srca (smanjen nakon opterećenja), kao i smanjiti venski tlak i kapilarni hidrostatski tlak.

Etiologija kongestivnog zatajenja srca

Terapijske strategije za liječenje bolesnika s kongestivnim zatajenjem srca

Smanjite metaboličke potrebe. Omjer ponude kisika: Mirovanje u krevetu, kisik, smanjenje aktivnosti kateholamina (beta-blokatori)

Za smanjenje venskog povratka (prethodno opterećenje): Podignite glavu kreveta, nitrati, diuretici (furosemid) (stari trikovi: naizmjenični podvez, flebotomija)

Povećajte minutni volumen srca: inotropni agensi: dopamin, dobutamin, amrinon, milrinon, digoksin (kronični chf) nitropress,

Smanjite radno opterećenje: Smanjite naknadno opterećenje: , Periferni vaskularni otpor. Dilatacija arterija (nitrati, nitropres) IABP

Osnovni uzrok: Dijastolička disfunkcija (smanjenje krvnog tlaka) Zamjena stenotičnog ventila.

Uklonite čimbenike koji doprinose: Anemija

Suprotstavljanje štetnim kompenzacijskim naporima: Renin agiotenzinski sustav. Ograničenje soli i vode, ACE inhibitori (Captopril, Enalpril)

Analgetici i anksiolitici: morfij (plućni edem)

Transplantacija srca: Posljednje sredstvo za potpuno propalo Srce otporno na terapiju.

Mehanička ventilacija: U teškim slučajevima plućnog edema. Za podršku ventilaciji. Omogućite odmor miokardu. Za kontrolu plućnog edema.


P&A: Etiologije akutnog plućnog edema

P: Kada je prikladno kodirati i flash ili akutni plućni edem i akutni kronični zatajenje srca (dijastoličko, sistoličko ili drugo)? Koje druge etiologije dovode do bljeskavog plućnog edema i kako mogu znati kada se treba raspitati?

O: Počnimo s razgovorom o kongestivan zatajenje srca (CHF) s plućnim edemom u odnosu na akutni plućni edem iz drugih uzroka. Etiologije plućnog edema podijeljene su u dvije kategorije: kardiogeni i nekardiogeni.

Kad god pacijent ima akutnu epizodu CHF, smatra se da je akutni plućni edem inherentan pogoršanju CHF. Stoga se akutni plućni edem koji ima kardiogenu etiologiju ne šifrira zasebno.

Međutim, kada dokumentacija podržava akutni plućni edem nekardiogenog porijekla, može se šifrirati zasebno.

Pregled/patofiziologija

Mehanizmi za nekardiogeni plućni edem uključuju povećanu propusnost kapilara i promjene u gradijentu tlaka unutar plućne vaskulature koje uzrokuju upalu.

Kako bi se razlikovao nekardiogeni plućni edem od kardiogenih uzroka, postoji nekoliko područja koja stručnjak za CDI može potražiti u dokumentaciji. Najvažnije, rendgenske snimke prsnog koša mogu otkriti bilateralne infiltrate s odsutnošću vaskularne kongestije, odsutnošću jugularne venske distenzije (JVD) kao i odsutnošću perifernog edema. Ako se dokumentira plućni kapilarni pritisak, očekivalo bi se da je manji od 18 mmHg.

Kada postaviti upit

"Blic" plućni edem opisuje akutni iznenadni početak, ali nažalost, trenutno ne postoji ICD-10 kod za pojam "bljesak" i bilo bi potrebno pojašnjenje za oštrinu ako postoji dokumentiran nekardiogeni uzrok. Međutim, imajte na umu da se ova terminologija obično povezuje s kardiogenim uzrocima.

Važno je da nekardiogena etiologija bude jasno dokumentirana. Ako je dokumentacija nejasna, potrebno je pojašnjenje.

Iako jezik povezivanja nije potreban, najbolja je praksa povezati etiologiju s akutnim plućnim edemom, ne ostavljajući pitanja o njegovom temeljnom uzroku, a pružatelje treba educirati kao takve.

Primjeri nekardiogene etiologije

Primjeri nekardiogene etiologije uključuju (ali nisu ograničeni na):

  • Sindrom akutnog respiratornog distresa (ARDS)
  • Plućna embolija
  • Sepsa
  • Pankreatitis
  • Udisanje toksina
  • Predoziranja (osobito opijati)
  • Trauma
  • Akutne ozljede pluća povezane s transfuzijom
  • Teške infekcije, posebno gram-negativne upale pluća
  • Promjene nadmorske visine i tlaka (poznate kao plućni edem velike nadmorske visine ili HAPE)
  • Neurogeni plućni edem
  • Radiation pneumonitis

Patient presentation

The onset of acute pulmonary edema often has a sudden onset, but it can be gradual as well. A patient with acute pulmonary edema typically demonstrates a variety of symptoms such as shortness of breath, especially while lying flat or with activity, wheezing, bilateral infiltrates on chest x-ray (ARDS), a feeling of drowning, tachypnea, tachycardia, dizziness, restlessness, anxiety/agitation, frothy and/or pink tinged sputum, cyanosis and a variety of additional symptoms based on the underlying etiology.

Treatment will be based on the underlying etiology in addition to oxygen supplementation that can include non-invasive or mechanical ventilation depending on the severity and the underlying cause. Prompt identification of the underlying etiology is necessary due to the rapid progression that can occur without treatment.


Sažetak

Background—

Swimming-induced pulmonary edema (SIPE) occurs during swimming or scuba diving, often in young individuals with no predisposing conditions, and its pathophysiology is poorly understood. This study tested the hypothesis that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise than in the general population and are reduced by sildenafil.

Methods and Results—

Ten study subjects with a history of SIPE (mean age, 41.6 years) and 20 control subjects (mean age, 36.2 years) were instrumented with radial artery and pulmonary artery catheters and performed moderate cycle ergometer exercise for 6 to 7 minutes while submersed in 20°C water. SIPE-susceptible subjects repeated the exercise 150 minutes after oral administration of 50 mg sildenafil. Work rate and mean arterial pressure during exercise were similar in controls and SIPE-susceptible subjects. Prosječno o 2 and cardiac output in controls and SIPE-susceptible subjects were: o 2 2.42 L·min –1 versus 1.95 L·min –1 , P=0.2 and cardiac output 17.9 L·min –1 versus 13.8 L·min –1 , P=0.01. Accounting for differences in cardiac output between groups, mean pulmonary artery pressure at cardiac output=13.8 L·min –1 was 22.5 mm Hg in controls versus 34.0 mm Hg in SIPE-susceptible subjects (P=0.004), and the corresponding pulmonary artery wedge pressure was 11.0 mm Hg versus 18.8 mm Hg (P=0.028). After sildenafil, there were no statistically significant differences in mean pulmonary artery pressure or pulmonary artery wedge pressure between SIPE-susceptible subjects and controls.

Zaključci—

These observations confirm that SIPE is a form of hemodynamic pulmonary edema. The reduction in pulmonary vascular pressures after sildenafil with no adverse effect on exercise hemodynamics suggests that it may be useful in SIPE prevention.

Clinical Trial Registration—

Uvod

Immersion pulmonary edema, also known as swimming-induced pulmonary edema (SIPE), is a condition in which cough, dyspnea, hemoptysis, and hypoxemia develop after surface swimming or diving, often in young, healthy individuals. Wilmshurst et al 1 first described SIPE in 11 healthy recreational divers. Although first believed to be extremely rare, nearly 300 cases have since been published, including several that describe the syndrome in healthy military recruits during strenuous swimming. 2–7 Among military recruits, its prevalence in 2.4- to 3.6-km open sea swimming trials has been reported as between 1.8% and 60%, depending on severity. 2,6 In triathletes, 1.4% have reported symptoms consistent with SIPE. 8

Editorial, see p 951

Clinical Perspective on p 996

SIPE usually resolves spontaneously within 24 hours, or with β2-adrenergic agonist or diuretic therapy, but it can be fatal. 9,10 Individuals who develop SIPE often have recurrences under the same conditions. 1,2,6,11,12 Proposed risk factors for SIPE include cold water, 1,11,12 negative static lung load, 5,13 exertion, 4,6,7,11,12 fluid loading, 7 and low vital capacity. 6 Many who experience SIPE have chronic hypertension or develop it later, 1,8,14–16 but many cases occur among individuals without hypertension, especially young military recruits, who undergo careful medical screening. 2–7

The pathophysiology of SIPE is not fully understood. In 1 study, an analysis of specimens obtained via bronchoalveolar lavage ruled out an inflammatory process. 17 Some instances of SIPE appear to have been precipitated by ventricular dysfunction, 5,9 and, indeed, transient cardiac abnormalities have been described immediately after an event. 16 However, in most cases, cardiac function during recovery is normal. 5,10–12,14,16–18 A hemodynamic cause cannot be reasonably excluded on the basis of post hoc resting measurements on dry land, particularly in view of both plausible rationale and physiological and observational evidence. During immersion in water, central redistribution of blood from the extremities occurs 19 and is augmented when the water is cold. 20 The resulting engorgement of the central veins, heart, and pulmonary vessels causes increased right-sided intravascular pressures. 21 Wilmshurst and colleagues 1 demonstrated that a greater increase in forearm vascular resistance in response to exposure of the head and neck to ice-cold water is greater in SIPE-susceptible individuals than in control subjects. They proposed that hydrostatic pulmonary edema occurs in susceptible individuals because of a combination of immersion-induced central redistribution of blood and idiosyncratic increase in afterload response attributable to cold. When swimming in the lateral decubitus position, predominantly unilateral edema occurs in the dependent lung, suggesting a hemodynamic mechanism. 3,4

This study was performed to advance the understanding of SIPE pathogenesis by testing the hypothesis that SIPE-susceptible individuals have higher mean pulmonary artery pressure (MPAP) and pulmonary artery wedge pressure (PAWP) during exercise in cold water in comparison with the general population. We also tested whether prophylactic sildenafil can attenuate the increase, with the aim of reducing the risk of SIPE.

Metode

Predmeti

After institutional approval and informed consent, 10 healthy individuals 18 to 55 years old, with a history of ≥1 episodes of SIPE, were recruited from a group of 71 who were screened for the study (ClinicalTrials.gov NCT00815646). Findings were compared with 20 controls who had no history of SIPE and who had participated in other institutional review board–approved studies, which, in part, have been previously reported. 21,22 All subjects had a normal physical examination, chest radiograph, spirometry (forced vital capacity forced expiratory volume in the first second of expiration and forced expiratory flow, midexpiratory phase), and 12-lead ECG. Before recruitment, 9 SIPE subjects had been evaluated for coronary artery disease by the use of exercise stress echocardiogram, nuclear imaging, or coronary angiography. For the control subjects, exclusion criteria were cardiovascular disease, abnormal spirometry (forced vital capacity forced expiratory volume in the first second of expiration and forced expiratory flow, midexpiratory phase), maximum oxygen consumption (V o 2max) <30 mL·kg –1 ·min –1 , estimated body fat >3% higher than age- and sex-based upper limits, abnormal ECG, age >55 years, or pregnancy. The same exclusions, with the exception of the body fat criterion, applied to the SIPE subjects. SIPE subjects with a history of mild hypertension were admitted to the study if blood pressure was normal while taking medication.

Instrumentacija

Methods have been previously described. 21,22 In brief, on the morning of the study, each subject was instrumented with radial artery and pulmonary artery catheters placed via an antecubital or arm vein. Placement of the catheter tip in the pulmonary artery was confirmed radiographically. Pressure transducers (Hospira, Lake Forest, IL) were calibrated immediately before each run, with the use of an aneroid gauge that had been precalibrated against a mercury manometer. All signals were digitized with a data acquisition board (PCI 6014, National Instruments, Austin, TX) and recorded on a personal computer using Labview (version 6.1, National Instruments, Austin, TX).

Protokol

On the day before the study, the capacity of each subject to perform dry exercise was tested on a cycle ergometer for 12 minutes to a maximum of 150 W. Subjects were then familiarized with the immersed environment by exercising for 9 to 12 minutes in the water to a maximum of 125 W external power.

On the day of the study, SIPE subjects were first evaluated during supine dry rest. Dry resting measurements in control subjects were conducted in the upright position (sitting on an exercise bike) with the transducers situated 5 cm inferior to the sternal angle. To measure the hemodynamic effect of rapid submersion, 10 of the control subjects and all of the SIPE subjects were placed in the prone position on a rescue litter breathing via a scuba regulator and immersed as quickly as possible in cold water for 2 to 3 minutes (dunk see Figure 1 in Wester et al 21 ). Heart rate, mean arterial pressure, MPAP, and PAWP were measured immediately before submersion and at 1 minute afterward. During this preexercise maneuver, pressure transducers were positioned at the level of the subject’s midthorax until the subject hit the water, at which point the transducer position was maintained at the water surface level. During underwater exercise, the transducer level was positioned at the level of the water surface. Pressures were averaged over several respiratory cycles. Effective arterial elastance was calculated as (2 × Psys+Pdia)/(3 × stroke volume), 23 where Psys i Pdia represent systolic and diastolic arterial pressures. Pulmonary artery compliance was calculated as stroke volume/pulmonary artery pulse pressure. 24

Exercise on an electronically braked cycle ergometer was then performed for 6 minutes at 60 rpm while prone and fully submersed to a depth of ≈50 cm in a pool (volume, 4.42 m 3 ) filled with water at 18°C to 20°C, as previously described. 21 The external work rate was set according to the estimated exercise capacity of each subject, which was typically 100 to 125 W (150–175 W total work rate including the work of moving the legs through the water, previously estimated at 50 W). Heart rate, mean arterial pressure, MPAP, and PAWP were measured immediately before the sixth minute of exercise. In control subjects, resting measurements were also taken, several minutes after the dunk. Resting measurements were not obtained in SIPE subjects to minimize the time of exposure to cold water and the risk of SIPE.

Expired gas volume was collected in Douglas bags over 1 minute during the fifth and sixth minutes of exercise, and the volume of each was measured using a calibrated gasometer (model DTM 325-4, American Meter, Nebraska City, NE). Samples of mixed O2 i CO2 expired gas were collected from each bag and measured using mass spectrometry (model 1100 medical gas analyzer, Perkin-Elmer, Pomona, CA), confirmed with gas chromatography (model 3800, Varian, Palo Alto, CA). Arterial and mixed venous blood samples were collected anaerobically in heparinized glass syringes over a 15- to 20-second period during the sixth minute and chilled on ice. Within 15 minutes, the blood samples were analyzed by using a blood gas analyzer (Synthesis 15, Instrumentation Laboratory, Lexington, MA) and CO-oximeter (model 682, Instrumentation Laboratory). Concentrations of expired O2 i CO2 were measured by using mass spectrometry (model 1100 medical gas analyzer, Perkin-Elmer, Pomona, CA) and confirmed with gas chromatography (model 3800, Varian, Palo Alto, CA). Standard equations were used to calculate oxygen consumption, which was then used to calculate cardiac output in the Fick equation.

Following the first exercise, the SIPE subjects were given 50 mg sildenafil orally (Pfizer, New York, NY). Approximately 150 minutes after sildenafil administration, the protocol was repeated. After each exercise, SIPE subjects were examined for clinical evidence of SIPE and performed spirometry.

Statističke metode

Neupareno t tests were used to compare continuous variables between groups obtained under identical circumstances, with correction for multiple comparisons (Tukey-Kramer) paired t tests were used for comparisons within each group. Categorical variables were compared by using the Fisher exact test. Hemodynamic responses that depended on cardiac output (CO), ie, systemic and pulmonary vascular pressures and vascular resistances, were compared among the 3 conditions (controls, SIPE-susceptible before and after sildenafil) by using a repeated-measures analysis of covariance, where the covariable was CO (PROC MIXED, SAS 9.3, SAS Institute, Cary, NC). This model allowed pairwise comparisons among the 3 conditions, adjusted for post hoc multiple comparisons (Tukey-Kramer), while accounting for the repeated measures within subjects and adjusting for the variable levels of exercise (CO). Given the linear relationship between MPAP and PAWP versus CO within the range of COs in this study, 25 model estimates between SIPE-susceptible and control subjects were made at the CO of the SIPE-susceptible subjects (13.8 L·min –1 ). P<0,05 smatra se statistički značajnim.

Role of the Funding Sources

The funding agencies for this study funded the development of the experimental system and the costs of each study. The funding agencies played no role in study design, data acquisition, or analysis. The investigators and all authors had sole discretion in the data analysis and interpretation, writing of the manuscript, and the decision to submit for publication.

Rezultati

Subject Characteristics

A summary of subject recruitment and baseline characteristics is shown in Tables 1 and 2. Table 3 provides details on each SIPE-susceptible subject. The SIPE-susceptible group had a greater proportion of females than the control group, but otherwise, there were no statistically significant demographic differences between the 2 groups. o 2max of the control group was 44.8±8.2 mL·kg –1 ·min –1 . Two subjects had experienced SIPE while diving, 5 during a triathlon or in training for a triathlon and 2 during both. Another subject experienced SIPE when she fell off her windsurfer into a cold river. Echocardiography showed mild left ventricular hypertrophy in subjects 1 and 5. Both ran regularly one was a triathlete and marathon runner. The echo findings were consistent with athlete’s heart. All other subjects had normal echocardiography. Coronary artery disease had previously been excluded by exercise stress echocardiography in 6 subjects, nuclear stress testing in 2 subjects, and coronary angiography in 1 subject. Stress testing was not performed in 1 subject because of her young age (31 years) and regular high-level exercise. One subject was taking candesartan for hypertension. Blood pressure was normal in all subjects during the screening assessment and before the study.

Stol 1. SIPE-Susceptible Subject Recruitment

SIPE indicates swimming-induced pulmonary edema.

* Pulmonary hypertension (2), sleep apnea and obesity (1).

Tablica 2. Subject Characteristics

Results shown as mean±SD. BMI indicates body mass index SD, standard deviation and SIPE, swimming-induced pulmonary edema.

Tablica 3. Subjects with Previous SIPE

BP indicates blood pressure BMI, body mass index BNP, brain natriuretic peptide CT, computed tomography echo, echocardiography EF, ejection fraction HR, heart rate LV, left ventricle LVEF, LV ejection fraction LVH, left ventricular hypertrophy MET, metabolic equivalent MR, mitral regurgitation PDA, patent ductus arteriosus PR, pulmonary regurgitation ProBNP, probrain natriuretic peptide RA, room air RBBB, right bundle-branch block RV, right ventricle SIPE, swimming-induced pulmonary edema and TR, tricuspid regurgitation.

All subjects completed the study with no adverse effects and with no symptoms, abnormal breath sounds, or changes in spirometry to suggest pulmonary edema.

Supine, Dry Measurements in SIPE-Susceptible Group and Cold-Water Dunk

Hemodynamic variables of the SIPE-susceptible volunteers in the dry, supine position were normal (Table 4). We have previously observed that sitting at rest on an exercise bicycle, where there is little peripheral muscle tone, often induces low right-sided pressures. Thus, dry measurements in the control subjects are not directly comparable with the supine measurements in the SIPE-susceptible group, although they were within normal limits (see Wester et al 21 for 10 of these control measurements). Following sildenafil administration, heart rate and CO were higher (P=0.0141 and 0.0053) systemic vascular resistance (SVR) and pulmonary vascular resistance were lower (P=0.0007 and 0.017 Table 4). During the preexercise dunk, pulmonary artery pressure was greater in the SIPE-susceptible group (P=0.0032, Table 5). Sildenafil significantly attenuated the systemic and pulmonary hypertensive responses to rapid immersion in cold water.

Tablica 4. Resting, Supine Characteristics of SIPE Subjects in Dry Conditions

Results shown as mean±SD. CO indicates cardiac output CGODIŠNJE, pulmonary artery compliance (see Methods) CVP, central venous pressure Ea, effective arterial elastance MAP, mean arterial pressure MPAP, mean pulmonary artery pressure PAWP, pulmonary artery wedge pressure PVR, pulmonary vascular resistance SD, standard deviation SIPE, swimming-induced pulmonary edema and SVR, systemic vascular resistance.

* Statistically significant in comparison with presildenafil.

Tablica 5. Hemodynamic Effects of Rapid Submersion in 20°C Water (Dunk) in All Subjects

Results are shown as mean±SD. C indicates control CVP, central venous pressure DBP, diastolic blood pressure HR, heart rate MAP, mean arterial pressure MPAP, mean pulmonary artery pressure PAWP, pulmonary artery wedge pressure S, Sildenafil, SD, standard deviation SBP, systolic blood pressure and SIPE, swimming-induced pulmonary edema.

Exercise Measurements

Hemodynamic and ventilatory parameters during exercise are listed in Table 6. Mean external work rate for the control subjects was 107.8 W (range, 50–170 W) and 112.5 W (range, 75–200 W) for the SIPE-susceptible subjects. o 2 during exercise was lower in the SIPE-susceptible group, but the difference was not statistically significant. Tidal volume during exercise was lower in the SIPE-susceptible group (P=0.0036) with no significant difference in respiratory minute volume. Ventilatory frequency was not different between the 2 groups. CO was lower in the SIPE group (P=0.01). SVR was higher in the SIPE-susceptible group (P=0.0106). Blood gases were not significantly different between groups except after sildenafil, when pH was slightly higher in comparison with both control (P=0.0087) and presildenafil (P=0.02), and Pa o 2 was higher in the SIPE-susceptible group in comparison with presildenafil (P=0.0337).

Table 6. Hemodynamics and Gas Exchange Measurements in Controls and SIPE Subjects During Exercise, Unadjusted for Cardiac Output

Results shown as mean±SD. BTPS indicates body temperature and pressure C, control CO, cardiac output CVP, central venous pressure HR, heart rate MAP, mean arterial pressure MPAP, mean pulmonary artery pressure Pa o 2, Pa co 2, arterial P o 2 and P co 2, respectively (see Methods) PAWP, pulmonary artery wedge pressure PVR, pulmonary vascular resistance S, Sildenafil SD, standard deviation SIPE, swimming-induced pulmonary edema STPD, standard temperature and pressure, dry SVR, systemic vascular resistance o 2, oxygen consumption E, respiratory minute volume Vf, ventilatory frequency and Vt, tidal volume.

* Not including resistive work because of the motion of legs through the water, which adds ≈50 W.

After accounting for differences in CO, both MPAP and PAWP were higher in the SIPE group than in controls during exercise (P=0.004 and P=0.028, respectively), as shown in Figure. After sildenafil, there was a significant decrease in PAP, and neither MPAP nor PAWP in the SIPE group were significantly different from controls. Differences in mean arterial pressure or central venous pressure among groups were not statistically significant. Similarly, when SVR and pulmonary vascular resistance in the control group were model estimated at the CO of the SIPE-susceptible group, there were no differences between SIPE-susceptible individuals and controls, and no effect of sildenafil. During immersed exercise there was no difference between controls and SIPE-susceptible subjects in pulmonary artery compliance, either before or after sildenafil.

Lik. Mean PAP and PAWP vs cardiac output. Control subjects were studied at rest and during exercise, whereas SIPE-susceptible subjects were studied only during exercise. Accounting for differences in cardiac output, mean PAP and PAWP were significantly higher in the SIPE-susceptible group than in controls (P=0.004 and P=0.028, respectively). After sildenafil, mean PAP was significantly reduced (P=0.025). During the postsildenafil exercise, neither mean PAP nor PAWP was significantly different from controls. PAP indicates pulmonary artery pressure PAWP, pulmonary artery wedge pressure and SIPE, swimming-induced pulmonary edema.

Rasprava

Our findings indicated an exaggerated increase in MPAP and PAWP during exercise in individuals who have experienced SIPE, supporting the Wilmshurst findings. 1 Despite similar external work rates, o 2, VE, heart rate, CO, and arterial pH measures indicated that SIPE-susceptible subjects were not working as hard as the control subjects even though their MPAP and PAWP values were higher. The greater MPAP and PAWP during exercise provide a hemodynamic explanation for SIPE susceptibility. Possible explanations for the lower metabolic rate in the SIPE-susceptible subjects despite similar external work rates include lower baseline oxygen consumption and differences in the rate of pedaling or in leg diameter, either of which would affect the work necessary to move the legs through the water.

The elevation in pulmonary vascular pressures during submersion is primarily attributable to central redistribution of blood from the extremities, 19,26 which engorges the central veins, heart, and pulmonary vessels, causing higher intracardiac and intravascular pressures, 21,26–28 This increase is augmented in cold water. 20,21 In a normal lung, PAWP that acutely exceeds a critical value of 18 to 25 mm Hg can cause hydrostatic alveolar edema. 29–31 Pulmonary capillary pressure has a value between MPAP and PAWP 32 thus, acute elevation in either parameter could cause a critical pressure at the alveolar interface because of immersion-related blood redistribution.

Several possible explanations could account for an exaggerated increase in pulmonary vascular pressures in SIPE-susceptible individuals.

Higher blood volume. Increased blood volume and the accompanying increase in cardiac filling pressures are induced by immersion and could be augmented by previous fluid loading, which, importantly, is sometimes encouraged before exercise, particularly in naval recruits before swim training. 7 However, SIPE has been reported without fluid loading. 6 Moreover, subjects in this experiment did not specifically consume excess fluid before the study.

Higher venous tone. This determines the degree to which capacitance vessels in the arms and splanchnic bed can accommodate blood displaced from the legs. Low venous tone (high venous capacitance) would allow more blood to be accommodated in these veins and thus attenuate immersion-related increases in MPAP and PAWP. 28 Conversely, high venous tone, attributable to increased activity of the sympathetic nervous system 33,34 or mild hypertension, 35 would result in higher blood volume in the heart and intrathoracic vessels because of peripheral to central redistribution. Indeed, previous studies in our laboratory have demonstrated that pulmonary artery and pulmonary artery wedge pressures are higher in thermoneutral water in comparison with the dry exercise and even higher in cold water. 21 Among experimental subjects we observed high variability in this response (nearly 2-fold), consistent with a variable degree of venous tone. It is plausible that those with a greater increase in pulmonary vascular pressures may represent the subpopulation at greatest risk for SIPE. 36 The reduction in MPAP after sildenafil suggests that there may have been active vasoconstriction, perhaps because of excessive sympathetic tone, possibly cold-related. Pulmonary artery compliance was similar between controls and SIPE-susceptible subjects, and was not affected by sildenafil, thus does not appear to play a role in SIPE susceptibility.

Impaired left ventricular (LV) systolic function. Transient global myocardial dysfunction with normal coronary arteries has been reported in cases of SIPE. 5,9,37 However, in most cases of SIPE, resting echocardiography after the event is normal 16–18 and indeed, all SIPE-susceptible subjects in the present study had normal echocardiography, including LV systolic function.

Low diastolic LV compliance. Although there was no diastolic dysfunction in their dry echocardiographic studies, central blood redistribution in the face of a stiffer LV would lead to a higher LV end-diastolic pressure, PAWP, and pulmonary artery pressure. In healthy individuals, exercising on dry land, end-diastolic volume increases without a change in end-diastolic pressure. 38 However, in individuals who have heart failure with preserved ejection fraction, the greater LV chamber stiffness causes LV end-diastolic pressure during exercise to increase. 39 Although none of our volunteers had clinical heart failure, the analogy is that, with augmented preload attributable to immersion in cold water, a slightly greater LV wall stiffness in SIPE-susceptible individuals could be the cause of higher LV filling pressure during exercise in cold water. Small increases in E/A and E/e′ ratios in extremely fit athletes have been attributed to LV remodeling attributable to prolonged exercise 40 and, indeed, 7 of the 10 SIPE-susceptible subjects in this study were extremely physically fit. It has been proposed that increased arterial stiffness may predispose to diastolic dysfunction, especially among women. 41–43 We did not observe a difference in arterial elastance between SIPE-susceptible and control populations during exercise, although sildenafil did induce a statistically significant reduction in arterial elastance in the SIPE-susceptible group during rest.

In comparison with controls, the SIPE-susceptible group had a higher SVR during exercise and a greater increase in systolic blood pressure during the cold-water dunk, which is consistent with an exaggerated peripheral vasoconstrictive response to cold. 1 However, because CO during exercise was lower in the SIPE-susceptible subjects, the calculated SVR values in the 2 groups are not directly comparable. When SVR in the control group was model estimated at the CO of the SIPE-susceptible group, there was no difference in SVR. Therefore, although cold exposure augmented afterload effects (blood pressure) to a greater degree in SIPE-susceptible subjects during the dunk at rest, during exercise the increased MPAP and PAWP in SIPE-susceptible subjects could not be attributed to high afterload. It is more likely that the higher MPAP and PAWP in the SIPE-susceptible group during exercise are attributable to enhanced venoconstriction, which elicits increased preload, or lower LV diastolic compliance. These effects, singly or in combination, would cause greater LV filling pressure and, hence, higher MPAP and PAWP.

Sildenafil has pharmacological effects that probably account for the reduction in MPAP and PAWP in SIPE-susceptible individuals during exercise in cold water. A selective inhibitor of phosphodiesterase-5, sildenafil leads to an increase in intracellular cyclic GMP and relaxation of vascular smooth muscle, and has a small and transient effect on blood pressure and systemic vascular resistance. 44 In our subjects, sildenafil administration was associated with a decrease in resting mean arterial pressure and SVR and an increase in CO. During exercise, sildenafil reduced pulmonary vascular pressures and pulmonary vascular resistance but had no effect on other hemodynamic variables. Although we did not assess it in this study, others have demonstrated that sildenafil induces an increase in venous compliance. 44 Thus, the sildenafil-induced reduction in pulmonary vascular pressures observed in this study during submersed exercise is likely attributable to vasodilatation of both pulmonary vessels and peripheral veins. This study demonstrated a hemodynamic effect of sildenafil that may plausibly reduce the likelihood of pulmonary edema in SIPE-susceptible swimmers.

A multicenter randomized trial in patients with a history of heart failure with preserved ejection fraction failed to observe an increase in exercise capacity (peak oxygen uptake during an incremental test) in response to sildenafil treatment. 45 However, hemodynamic studies in this population have demonstrated reduced pulmonary artery pressure, PAWP, increased cardiac index, isovolumic relaxation time, and increased CO and endothelial function. 46–48 Whereas in this study we are focusing on factors that may promote pulmonary edema, there are probably other factors limiting peak oxygen consumption in chronic heart failure, such as deconditioning, on which sildenafil is unlikely to have an effect. Although we cannot conclude from this study that sildenafil provides prophylaxis against SIPE, one of our study subjects (subject 3) who had experienced several episodes of SIPE during triathlons, has had no further episodes since using prerace sildenafil.

There are several shortcomings of our study. Although our subjects were not randomly selected from the SIPE-susceptible or general population, we believe that the 2 groups are similar. In particular, potential subjects with comorbidities associated with SIPE were excluded. Further, the hypertensive pulmonary vascular response to exercise in cold water that was observed in our subjects may likely be even more exaggerated in the general SIPE-susceptible population, which includes many individuals with hypertension. 5 The control group was 90% male, in comparison with 40% male in the SIPE-susceptible group, raising the possibility that the differences may be caused by a fundamental sex-related phenomenon that is not connected with SIPE susceptibility. We believe this is unlikely, because a previous study showed no sex-related effect on MPAP during rest or exercise in a previous study on 255 males and 101 females. 49 The SIPE-susceptible group may also have been fitter than the controls. Although none of the controls had experienced SIPE while swimming or diving, the possibility that some of them by chance may have been SIPE susceptible cannot be excluded. However, this is unlikely because, in a fit civilian population (triathletes), only 1% to 2% report SIPE symptoms. 8 Although the immersed exercise protocol was identical for both groups, preexercise measurements were obtained under different conditions (supine versus sitting). Thus, the congruence of the groups at baseline cannot be established with absolute certainty. Because it was not possible to randomize the order of the sildenafil administration we cannot exclude acute adaptation to the cold as the mechanism for postsildenafil attenuation of the hemodynamic responses to the dunk and submersed exercise. We believe this is unlikely because the reduction in intravascular pressures during exercise after sildenafil was confined to MPAP and PAWP and others have reported constant norepinephrine response to cold-water (20°C) exposure during repetitive immersions during the same day. 50 Furthermore, in our study the change in intravascular pressures during exercise in the second cold-water exposure was confined to MPAP and PAWP, with no effect on systemic blood pressure. It could be argued that differences in exercise ventilation might have affected PAP and PAWP, but both PAP and pulmonary vascular resistance were lower in the control group despite lower pH, which would be expected to increase both parameters. Although the observed change in PAWP after sildenafil was not statistically significant, because of the small sample size, the possibility that sildenafil can reduce PAWP in this setting cannot be excluded.

In summary, we have observed that during submerged exercise in cold water, individuals with a history of swimming-induced pulmonary edema have higher MPAP and PAWP than those with no such history. We further demonstrated that these pressures can be reduced with a single 50-mg oral dose of sildenafil.

Acknowledgments

We are grateful to the following experts for their technical assistance: Albert Boso, Barry Castle, Owen Doar, Tommy Edwards, Eric Schinazi, and Aaron Walker and to the volunteers who were willing to donate their time to participate in the study. We appreciate Kathy Gage’s constructive suggestions on the manuscript. Contributors: Dr Moon, S.D. Martina, and Drs Peacher, Potter, Wester, Cherry, and Freiberger contributed to the study concept, design, and conduct, analysis of data and writing of the manuscript. Drs Otteni and Kernagis and M. J. Natoli participated in the study conduct and data acquisition. W. D. White performed the statistical analysis.

Izvori financiranja

This study was funded by the Divers Alert Network and US Naval Sea Systems Command Contracts N61331-03-C-0015 and N0463A-07-C-0002 .