izindaba

Ukwelashwa komoyampilo kungenye yezindlela ezisetshenziswa kakhulu kwezokwelapha zesimanje, kodwa kusenemibono eyiphutha mayelana nezinkomba zokwelashwa komoya-mpilo, futhi ukusetshenziswa okungafanele komoya-mpilo kungabangela ukusabela okunobuthi obukhulu.

Ukuhlolwa komtholampilo kwe-tissue hypoxia

Izimpawu zomtholampilo ze-tissue hypoxia ziyahlukahluka futhi aziqondile, ezinezimpawu ezigqame kakhulu ezihlanganisa i-dyspnea, ukuphelelwa umoya, i-tachycardia, ukucindezeleka kokuphefumula, izinguquko ezisheshayo esimweni sengqondo, kanye ne-arrhythmia. Ukunquma ukuba khona kwe-tissue (visceral) hypoxia, i-serum lactate (ekhuphuke ngesikhathi se-ischemia nokuncipha kokuphuma kwenhliziyo) kanye ne-SvO2 (eyehle ngesikhathi sokuncipha kokuphuma kwenhliziyo, i-anemia, i-arterial hypoxemia, kanye nezinga eliphezulu le-metabolic) ziwusizo ekuhlolweni komtholampilo. Kodwa-ke, i-lactate ingakhushulwa ezimweni ezingezona ze-hypoxic, ngakho-ke ukuxilongwa akunakutholakala kuphela ngokusekelwe ekuphakameni kwe-lactate, njengoba i-lactate ingase ikhuphuke ngaphansi kwezimo zokwanda kwe-glycolysis, njengokukhula okusheshayo kwezimila eziyingozi, i-sepsis yokuqala, ukuphazamiseka kwe-metabolic, nokuphathwa kwama-catecholamines. Amanye amanani aselabhorethri abonisa ukungasebenzi kahle kwezitho ezithile nawo abalulekile, njenge-creatinine ephakeme, i-troponin, noma ama-enzyme esibindi.

Ukuhlolwa komtholampilo kwesimo se-arterial oxygenation

I-Cyanosis. I-Cyanosis ivamise ukuba wuphawu olwenzeka ekupheleni kwesigaba se-hypoxia, futhi ngokuvamile ayithembeki ekuxilongeni i-hypoxemia ne-hypoxia ngoba ingase ingenzeki ku-anemia nokugeleza kwegazi okungekuhle, futhi kunzima kubantu abanesikhumba esimnyama ukuthola i-cyanosis.

Ukuqapha i-Pulse oximetry. I-non invasive pulse oximetry monitoring isetshenziswe kabanzi ukuqapha zonke izifo, futhi i-SaO2 yayo elinganiselwe ibizwa nge-SpO2. Umgomo wokuqapha i-pulse oximetry umthetho kaBill, othi ukuhlangana kwento engaziwa esixazululweni kunganqunywa ngokumunca kwayo ukukhanya. Lapho ukukhanya kudlula kunoma iyiphi izicubu, iningi lakho limuncwa izakhi zezicubu negazi. Kodwa-ke, ngokushaya kwenhliziyo ngakunye, igazi le-arterial lidlula ukugeleza kwe-pulsatile, okuvumela i-pulse oximetry monitor ukuthi ibone izinguquko ekungeneni kokukhanya kuma-wavelengths amabili: ama-nanometer angu-660 (obomvu) nama-nanometers angu-940 (infrared). Amazinga okumuncwa kwe-hemoglobin encishisiwe ne-hemoglobin ene-oksijini ahlukile kulawa maza wamaza amabili. Ngemva kokukhipha ukumuncwa kwezicubu ezingezona ipulsatile, ukugcwala kwe-hemoglobin ene-oxygen ehlobene nengqikithi ye-hemoglobin ingabalwa.

Kunemikhawulo ethile yokuqapha i-pulse oximetry. Noma iyiphi into esegazini emunca lawa maza obude ingaphazamisa ukunemba kokulinganisa, okuhlanganisa i-hemoglobinopathies etholiwe - i-carboxyhemoglobin ne-methemoglobinemia, i-methylene eluhlaza okwesibhakabhaka, nokunye okuhlukile kofuzo lwe-hemoglobin. Ukumuncwa kwe-carboxyhemoglobin ebangeni lamaza ama-nanometer angu-660 kufana ne-hemoglobin ene-oxygen; Ukumuncwa okuncane kakhulu kubude begagasi obungu-940 nanometers. Ngakho-ke, kungakhathaliseki ukuthi ingakanani i-carbon monoxide saturated hemoglobin kanye ne-oksijini egcwele i-hemoglobin, i-SpO2 izohlala injalo (90%~95%). Ku-methemoglobinemia, lapho i-heme iron yenziwe i-oxidized ibe yi-ferrous state, i-methemoglobin ilinganisa ama-coefficients okumuncwa ama-wavelengths amabili. Lokhu kubangela ukuthi i-SpO2 ihluke kuphela phakathi kwebanga lama-83% kuya ku-87% phakathi kwebanga elibanzi lokuhlushwa le-methemoglobin. Kulokhu, amaza amane okukhanya ayadingeka ukuze kulinganiswe umoya-mpilo we-arterial ukuze kuhlukanise phakathi kwezinhlobo ezine ze-hemoglobin.

Ukuqapha kwe-Pulse oximetry kuncike ekugelezeni kwegazi okwanele kwe-pulsatile; Ngakho-ke, ukuqapha kwe-pulse oximetry akukwazi ukusetshenziswa ku-hypoperfusion yokushaqeka noma lapho kusetshenziswa amadivaysi okusiza angewona ama-pulsatile ventricular (lapho ukuphuma kwenhliziyo kubala kuphela ingxenye encane yokuphuma kwenhliziyo). Ekubuyiseleni kabusha okunamandla kwe-tricuspid, ukugcwala kwe-deoxyhemoglobin egazini le-venous kuphezulu, futhi ukushaya kwe-venous kungaholela ekufundweni kokugcwala kokugcwala komoya-mpilo egazini okuphansi. Ku-arterial hypoxemia enzima (SaO2<75%), ukunemba kungase kuphinde kwehle njengoba le nqubo ingakaze iqinisekiswe ngaphakathi kwalolu banga. Okokugcina, abantu abaningi ngokwengeziwe bayaqaphela ukuthi ukuqapha i-pulse oximetry kungase kulinganisele ngokweqile ukugcwala kwe-arterial hemoglobin ngamaphuzu afika kumaphesenti angu-5-10, kuye ngokuthi idivayisi ethile esetshenziswa abantu abanesikhumba esimnyama.

I-PaO2/FIO2. Isilinganiso se-PaO2/FIO2 (esivame ukubizwa ngokuthi isilinganiso se-P/F, esisuka ku-400 siye ku-500 mm Hg) sibonisa izinga lokushintshaniswa komoyampilo okungavamile emaphashini, futhi siwusizo kakhulu kulo mongo njengoba umoya wokungena ngomshini ungasetha ngokunembile i-FIO2. Isilinganiso se-AP/F esingaphansi kuka-300 mm Hg sibonisa ukungahambi kahle kokushintshisana kwegesi okuphawulekayo, kuyilapho isilinganiso se-P/F esingaphansi kuka-200 mm Hg sibonisa i-hypoxemia enzima. Izinto ezithinta isilinganiso se-P/F zifaka izilungiselelo zokungenisa umoya, ukucindezela kokuphelelwa umoya kokuphela, kanye ne-FIO2. Umthelela wezinguquko ku-FIO2 kusilinganiso se-P/F uyahlukahluka kuye ngohlobo lokulimala kwamaphaphu, ingxenyenamba ye-shunt, kanye nobubanzi bezinguquko ze-FIO2. Uma ingekho i-PaO2, i-SpO2/FIO2 ingasebenza njengenye inkomba enengqondo.

Umehluko we-Alveolar arterial oxygen partial pressure (Aa PO2). Ukulinganisa okuhlukile kwe-Aa PO2 umehluko phakathi kwengcindezi eyingxenye ye-alveolar oxygen elinganisiwe kanye nokucindezela kwengxenye ye-arterial oxygen, okusetshenziselwa ukukala ukusebenza kahle kokushintshisana kwegesi.

Umehluko “ovamile” we-Aa PO2 wokuphefumula umoya osendaweni ezingeni lolwandle uyahlukahluka ngokuya ngeminyaka, kusukela ku-10 kuye ku-25 mm Hg (2.5+0.21 x ubudala [iminyaka]). Isici sesibili esinomthelela yi-FIO2 noma i-PAO2. Uma enye yalezi zici ezimbili inyuka, umehluko ku-Aa PO2 uzokwanda. Lokhu kungenxa yokuthi ukushintshana kwegesi kuma-alveolar capillaries kwenzeka engxenyeni eyisicaba (emithambekeni) yejiko lokuhlukanisa i-hemoglobin oxygen dissociation. Ngaphansi kwezinga elifanayo lokuxutshwa kwe-venous, umehluko ku-PO2 phakathi kwegazi le-venous elixubile negazi le-arterial uzokwanda. Ngokuphambene nalokho, uma i-alveolar PO2 iphansi ngenxa yokungeneli komoya okwanele noma ukuphakama okuphezulu, umehluko we-Aa uzoba ngaphansi kunokujwayelekile, okungase kuholele ekubukeni phansi noma ekuxilongeni okungalungile kokungasebenzi kahle kwamaphaphu.

Inkomba ye-oxygenation. Inkomba ye-oxygenation (OI) ingasetshenziswa ezigulini ezinomshini wokuphefumula ukuze kuhlolwe amandla okusekela umoya odingekayo ukuze kugcinwe umoya-mpilo. Ihlanganisa umfutho womoya omaphakathi (MAP, ku-cm H2O), i-FIO2, ne-PaO2 (ku-mm Hg) noma i-SpO2, futhi uma ingaphezu kuka-40, ingasetshenziswa njengendlela evamile yokwelapha i-extracorporeal membrane oxygenation. Inani elivamile elingaphansi kuka-4 cm H2O/mm Hg; Ngenxa yenani elifanayo lika-cm H2O/mm Hg (1.36), amayunithi ngokuvamile awafakwa lapho kubikwa lesi silinganiso.

Izinkomba zokwelashwa kwe-oxygen acute
Lapho iziguli zithola ubunzima bokuphefumula, ukufakwa kwe-oxygen ngokuvamile kuyadingeka ngaphambi kokuxilongwa kwe-hypoxemia. Uma ukucindezela kwengxenye ye-arterial ye-oxygen (PaO2) ingaphansi kuka-60 mm Hg, inkomba ecacile kakhulu yokuthatha umoya-mpilo i-arterial hypoxemia, ngokuvamile ehambisana nokugcwala kwe-arterial oxygen saturation (SaO2) noma i-peripheral oxygen saturation (SpO2) yama-89% kuya ku-90%. Lapho i-PaO2 yehla ngaphansi kuka-60 mm Hg, ukugcwala komoyampilo egazini kungase kwehle kakhulu, okuholela ekwehleni okukhulu kokuqukethwe komoyampilo we-arterial futhi okungase kubangele i-tissue hypoxia.

Ngaphezu kwe-arterial hypoxemia, ukwengezwa komoya-mpilo kungase kudingeke ezimweni ezingavamile. I-anemia enzima, ukuhlukumezeka, kanye neziguli ezibucayi ezihlinzayo zinganciphisa i-tissue hypoxia ngokwandisa amazinga e-arterial oxygen. Ezigulini ezinoshevu we-carbon monoxide (CO), ukugcwalisa umoya-mpilo kungakhuphula izinga lomoya-mpilo oncibilikisiwe egazini, kuthathe indawo ye-CO eboshwe ku-hemoglobin, futhi kwandise ingxenye ye-hemoglobin ene-oksijini. Ngemuva kokuhogela umoya-mpilo ohlanzekile, uhhafu wempilo ye-carboxyhemoglobin imizuzu engama-70-80, kanti uhhafu wempilo lapho uphefumula umoya osendaweni imizuzu engama-320. Ngaphansi kwezimo zomoya-mpilo we-hyperbaric, uhhafu wempilo ye-carboxyhemoglobin ufinyezwa ube ngaphansi kwemizuzu eyi-10 ngemuva kokuhogela umoya-mpilo omsulwa. I-hyperbaric oxygen ngokuvamile isetshenziswa ezimeni ezinamazinga aphezulu e-carboxyhemoglobin (>25%), ischemia yenhliziyo, noma ukungezwani kwezinzwa.

Naphezu kokuntuleka kwedatha esekelayo noma idatha engalungile, ezinye izifo zingase futhi zizuze ngokufaka umoya-mpilo. Ukwelashwa komoyampilo kuvame ukusetshenziselwa ubuhlungu bekhanda leqembu, inkinga yobuhlungu be-sickle cell, ukukhululeka kokucindezeleka kokuphefumula ngaphandle kwe-hypoxemia, i-pneumothorax, ne-mediastinal emphysema (ekhuthaza ukumuncwa komoya wesifuba). Kunobufakazi bokuthi i-oxygen ephezulu ye-intraoperative inganciphisa izehlakalo zokutheleleka kwezindawo zokuhlinza. Kodwa-ke, ukufaka umoya-mpilo akubonakali kunciphisa ngempumelelo isicanucanu/ukuhlanza ngemuva kokuhlinzwa.

Ngokuthuthukiswa komthamo wokunikezwa komoyampilo weziguli ezingaphandle, ukusetshenziswa kwe-oxygen therapy yesikhathi eside (LTOT) nakho kuyakhula. Izindinganiso zokuqalisa ukwelashwa komoya-mpilo isikhathi eside sezivele zicace kakhulu. Ukwelashwa kwe-oksijeni yesikhathi eside kuvame ukusetshenziselwa isifo esingamahlalakhona sokuvimbela amaphaphu (COPD).
Izifundo ezimbili ngeziguli ezine-hypoxemic COPD zinikeza idatha esekelayo ye-LTOT. Ucwaningo lokuqala lwaluyi-Nocturnal Oxygen Therapy Trial (NOTT) eyenziwa ku-1980, lapho iziguli zazinikezwa ngezikhathi zasebusuku (okungenani amahora angu-12) noma ukwelashwa kwe-oxygen okuqhubekayo. Ezinyangeni eziyi-12 nezingama-24, iziguli ezithola kuphela ukwelashwa komoyampilo ebusuku zinezinga eliphezulu lokufa. Ukuhlolwa kwesibili kwakuyi-Medical Research Council Family Trial eyenziwa ngo-1981, lapho iziguli zazihlukaniswa ngokungahleliwe zaba amaqembu amabili: lezo ezingazange ziwuthole umoya-mpilo noma lezo ezathola umoya-mpilo okungenani amahora angu-15 ngosuku. Ngokufanayo nokuhlolwa kwe-NOTT, izinga lokufa eqenjini le-anaerobic laliphezulu kakhulu. Izihloko zazo zombili izilingo kwakuyiziguli ezingabhemi ezithole ukwelashwa okuphezulu futhi zinezimo ezinzile, ezine-PaO2 ngaphansi kwe-55 mm Hg, noma iziguli ezine-polycythemia noma isifo senhliziyo se-pulmonary nge-PaO2 ngaphansi kwe-60 mm Hg.

Lezi zivivinyo ezimbili zibonisa ukuthi ukugcwalisa umoya-mpilo amahora angaphezu kwe-15 ngosuku kungcono kunokungawutholi ngokuphelele umoya-mpilo, futhi ukwelapha komoyampilo okuqhubekayo kungcono kunokwelapha ebusuku kuphela. Imibandela yokufakwa yalezi zivivinyo iyisisekelo sezinkampani zamanje zomshwalense wezokwelapha kanye ne-ATS ukuthuthukisa imihlahlandlela ye-LTOT. Kunengqondo ukuphetha ngokuthi i-LTOT iyamukelwa futhi kwezinye izifo ze-hypoxic zenhliziyo, kodwa okwamanje kukhona ukuntuleka kobufakazi obufanele bokuhlola. Uhlolo lwakamuva lwe-multicenter alutholanga mehluko kumthelela wokwelashwa komoya-mpilo ekufeni noma ikhwalithi yokuphila kweziguli ze-COPD ezine-hypoxemia engazange ihlangabezane nemibandela yokuphumula noma eyabangelwa ukuzivocavoca kuphela.

Ngezinye izikhathi odokotela banikeza iziguli ezithola ukwehla okukhulu kokugcwala komoyampilo ebusuku ngesikhathi sokulala. Okwamanje abukho ubufakazi obucacile bokusekela ukusetshenziswa kwale ndlela ezigulini ezine-obstructive sleep apnea. Ezigulini ezine-obstructive sleep apnea noma ukukhuluphala ngokweqile kwe-hyopnea syndrome okuholela ekuphefumuleni okubi ebusuku, ukungenisa komoya okungewona okuhlaselayo kunokwengezwa komoyampilo kuyindlela yokwelapha eyinhloko.

Olunye udaba okufanele lucatshangelwe ukuthi ingabe i-oxygen supplementation iyadingeka yini phakathi nokuhamba emoyeni. Izindiza eziningi zezentengiselwano ngokuvamile zikhuphula umfutho wekhabhini ukuya endaweni ephakeme elingana namafidi angu-8000, ngokudonsa komoyampilo okuhogeliwe okucishe kube ngu-108 mm Hg. Ezigulini ezinezifo zamaphaphu, ukwehla kwe-oxygen tension (PiO2) kungabangela i-hypoxemia. Ngaphambi kohambo, iziguli kufanele zihlole ukuhlolwa kwezokwelapha okuphelele, okuhlanganisa nokuhlolwa kwegesi legazi. Uma i-PaO2 yesiguli ephansi ingu-≥ 70 mm Hg (SpO2>95%), khona-ke i-PaO2 yabo ngesikhathi sendiza ingase yeqe ku-50 mm Hg, ngokuvamile okubhekwa njengokwanele ukubhekana nomsebenzi omncane womzimba. Ezigulini ezine-SpO2 ephansi noma i-PaO2, ukuhlolwa kokuhamba kwemizuzu engu-6 noma ukuhlolwa kwe-hypoxia simulation kungacatshangelwa, ngokuvamile ukuphefumula umoya-mpilo ongu-15%. Uma i-hypoxemia yenzeka phakathi nokuhamba emoyeni, umoya-mpilo ungalawulwa nge-cannula yamakhala ukuze kwandiswe ukungena komoyampilo.

Isisekelo se-biochemical of oxygen poisoning

Ubuthi be-oksijeni bubangelwa ukukhiqizwa kwezinhlobo ze-oxygen esebenzayo (ROS). I-ROS iyi-radical yamahhala etholakala komoya-mpilo ene-electron engahlanganisiwe ye-orbital engasabela ngamaprotheni, ama-lipids, nama-nucleic acid, aguqule isakhiwo sawo futhi abangele ukulimala kwamaselula. Ngesikhathi se-metabolism evamile ye-mitochondrial, inani elincane le-ROS likhiqizwa njenge-molecule yokubonisa. Amaseli omzimba aphinde asebenzise i-ROS ukuze abulale amagciwane. I-ROS ihlanganisa i-superoxide, i-hydrogen peroxide (H2O2), nama-hydroxyl radicals. I-ROS eyeqile izodlula njalo imisebenzi yokuvikela amaselula, okuholela ekufeni noma ekudaleni ukulimala kwamaseli.

Ukunciphisa umonakalo ophakathi kwesizukulwane se-ROS, indlela yokuvikela i-antioxidant yamaseli inganciphisa ama-radicals mahhala. I-Superoxide dismutase iguqula i-superoxide ibe yi-H2O2, bese iguqulwa ibe i-H2O ne-O2 nge-catalase ne-glutathione peroxidase. I-Glutathione iyi-molecule ebalulekile ekhawulela umonakalo we-ROS. Amanye ama-molecule e-antioxidant ahlanganisa i-alpha tocopherol (i-vitamin E), i-ascorbic acid (i-vitamin C), i-phospholipids, ne-cysteine. Izicubu zamaphaphu omuntu ziqukethe ukugxila okuphezulu kwama-antioxidant e-extracellular kanye ne-superoxide dismutase isoenzymes, okuwenza angabi nobuthi obuncane lapho evezwe ekugxilweni okuphezulu komoyampilo uma kuqhathaniswa nezinye izicubu.

I-Hyperroxia eyenzelwe ukulimala kwe-ROS okuphakathi kwamaphaphu kungahlukaniswa izigaba ezimbili. Okokuqala, kunesigaba se-exudative, esibonakala ngokufa kwamaseli e-alveolar ohlobo 1 namaseli e-endothelial, i-interstitial edema, kanye nokugcwaliswa kwama-neutrophils exudative ku-alveoli. Ngokulandelayo, kunesigaba sokwanda, lapho amaseli e-endothelial kanye nohlobo 2 lwamaseli e-epithelial anda futhi amboze ulwelwesi lwangaphansi oluvezwe ngaphambilini. Izici zenkathi yokululama yokulimala komoya-mpilo ziwukwanda kwe-fibroblast kanye ne-interstitial fibrosis, kodwa i-capillary endothelium ne-alveolar epithelium isalokhu ibukeka ngendlela evamile.
Ukubonakaliswa komtholampilo kobuthi be-oksijeni yamaphaphu

Izinga lokuchayeka okwenzeka kulo ubuthi alikacaci. Uma i-FIO2 ingaphansi kuka-0.5, ubuthi bomtholampilo ngokuvamile abukho. Ucwaningo lwabantu lwakuqala luthole ukuthi ukuchayeka cishe ku-100% komoyampilo kungabangela ukungezwani kwezinzwa, isicanucanu, kanye ne-bronchitis, kanye nokunciphisa umthamo wamaphaphu, amandla okusabalalisa amaphaphu, ukuthobela amaphaphu, i-PaO2, ne-pH. Ezinye izindaba ezihlobene nobuthi komoyampilo zifaka i-atelectasis yokumunca, i-hypercapnia eyenziwe komoya-mpilo, i-acute Respiratory Distress Syndrome (ARDS), kanye ne-neonatal bronchopulmonary dysplasia (BPD).
I-atelectasis ye-Absorbent. I-nitrogen iyigesi engasebenzi esakazeka kancane kancane egazini uma iqhathaniswa nomoya-mpilo, ngaleyo ndlela idlala indima ekugcineni ukunwetshwa kwe-alveolar. Uma usebenzisa i-oxygen engu-100%, ngenxa yezinga lokumuncwa komoyampilo elidlula izinga lokulethwa kwegesi entsha, ukushoda kwe-nitrogen kungaholela ekugoqekeni kwe-alveolar ezindaweni ezinezinga eliphansi le-alveolar ventilation perfusion ratio (V/Q). Ikakhulukazi ngesikhathi sokuhlinzwa, i-anesthesia kanye nokukhubazeka kungaholela ekwehleni komsebenzi wamaphaphu asele, okukhuthaza ukuwa kwemigudu yomoya encane kanye ne-alveoli, okuholela ekuqaliseni ngokushesha kwe-atelectasis.

I-hypercapnia ebangelwa umoya-mpilo. Iziguli ezinzima ze-COPD zithambekele ekubeni ne-hypercapnia enzima lapho zichayeka ekugxilweni okuphezulu komoyampilo ngesikhathi isimo sabo siba sibi kakhulu. Indlela yale hypercapnia iwukuthi ikhono le-hypoxemia lokushayela ukuphefumula liyavinjelwa. Kodwa-ke, kunoma yisiphi isiguli, kunezinye izindlela ezimbili ezidlalwa ngamazinga ahlukahlukene.
I-hypoxemia ezigulini ze-COPD ingumphumela wokucindezela okuncane kwe-alveolar ye-oxygen (PAO2) endaweni ephansi ye-V / Q. Ukuze kuncishiswe umthelela walezi zifunda eziphansi ze-V/Q ku-hypoxemia, ukusabela okubili kokujikeleza kwamaphaphu - i-hypoxic pulmonary vasoconstriction (HPV) kanye ne-hypercapnic pulmonary vasoconstriction - kuzodlulisela ukugeleza kwegazi ezindaweni ezinomoya omuhle. Lapho ukufakwa kwe-oxygen kwandisa i-PAO2, i-HPV iyancipha kakhulu, ikhulisa ukugcwala kulezi zindawo, okuholela ezindaweni ezinezilinganiso eziphansi ze-V/Q. Lezi zicubu zamaphaphu manje sezicebile nge-oxygen kodwa zinamandla abuthakathaka okuqeda i-CO2. Ukwanda kwe-perfusion yalezi zicubu zamaphaphu kuza ngezindleko zokudela izindawo ezinomoya ongcono, ongakwazi ukukhulula inani elikhulu le-CO2 njengangaphambili, okuholela ku-hypercapnia.

Esinye isizathu umphumela we-Haldane obuthakathaka, okusho ukuthi uma kuqhathaniswa negazi elifakwe umoya-mpilo, igazi elingenayo umoya-mpilo lingathwala i-CO2 eyengeziwe. Lapho i-hemoglobin ikhishwa umoya-mpilo, ibopha ama-proton amaningi (H+) kanye ne-CO2 ngendlela yama-amino esters. Njengoba ukugcwala kwe-deoxyhemoglobin kuncipha ngesikhathi sokwelashwa komoyampilo, amandla okubhafa we-CO2 ne-H + nawo ayancipha, ngaleyo ndlela enze buthaka amandla egazi le-venous ukuthutha i-CO2 futhi kuholele ekwandeni kwe-PaCO2.

Lapho kunikezwa umoya-mpilo ezigulini ezinokugcinwa kwe-CO2 okungapheli noma iziguli ezisengozini enkulu, ikakhulukazi esimweni se-hypoxemia eyedlulele, kubaluleke kakhulu ukulungisa kahle i-FIO2 ukuze kugcinwe i-SpO2 ebangeni lama-88%~90%. Imibiko yamacala amaningi ibonisa ukuthi ukwehluleka ukulawula i-O2 kungaholela emiphumeleni emibi; Ucwaningo olungahleliwe olwenziwa ezigulini ezinokwenyuka okukhulu kwe-CODP endleleni eya esibhedlela likuqinisekisile ngokungangabazeki lokhu. Uma kuqhathaniswa neziguli ezingenayo imingcele ye-oxygen, iziguli ezabelwa ngokungahleliwe ukuthi zengeze umoya-mpilo ukuze zigcine i-SpO2 phakathi kwe-88% kuya ku-92% yayinezinga lokufa eliphansi kakhulu (7% vs. 2%).

I-ARDS kanye ne-BPD. Sekuyisikhathi eside abantu bethola ukuthi ubuthi be-oxygen buhlotshaniswa ne-pathophysiology ye-ARDS. Ezilwaneni ezincelisayo okungezona abantu, ukuchayeka ku-100% komoyampilo kungaholela ekulimaleni kwe-alveolar futhi ekugcineni nokufa. Kodwa-ke, ubufakazi obuqondile bobuthi be-oxygen ezigulini ezinezifo ezinzima zamaphaphu kunzima ukuhlukanisa nomonakalo obangelwa izifo eziyisisekelo. Ngaphezu kwalokho, izifo eziningi ezivuthayo zingabangela ukulawulwa komsebenzi wokuzivikela we-antioxidant. Ngakho-ke, izifundo eziningi zehlulekile ukukhombisa ukuhlobana phakathi kokuchayeka komoyampilo okweqile kanye nokulimala okukhulu kwamaphaphu noma i-ARDS.

Isifo se-pulmonary hyaline membrane yisifo esibangelwa ukuntuleka kwezinto ezisebenzayo ezingaphezulu, ezibonakala ngokuwa kwe-alveolar nokuvuvukala. Izingane ezisanda kuzalwa ngaphambi kwesikhathi ezinesifo se-hyaline membrane ngokuvamile zidinga ukuhogela okugxilile komoyampilo. Ubuthi be-oksijeni bubhekwa njengesici esiyinhloko ku-pathogenesis ye-BPD, ngisho nasezinganeni ezisanda kuzalwa ezingadingi ukushaywa umoya ngemishini. Izingane ezisanda kuzalwa zisengozini enkulu yokulimala komoya-mpilo ngenxa yokuthi imisebenzi yazo yokuvikela i-antioxidant yamangqamuzana ayikakhuli ngokugcwele futhi ayikavuthwa ngokugcwele; I-retinopathy ye-prematurity yisifo esihambisana nokuphindaphinda kwe-hypoxia/hyperoxia, futhi lo mphumela uqinisekisiwe ku-retinopathy ye-prematurity.
Umphumela we-synergistic we-pulmonary oxygen toxicity

Kunezidakamizwa ezimbalwa ezingathuthukisa ubuthi be-oxygen. I-oksijeni inyusa i-ROS ekhiqizwa i-bleomycin futhi yenza i-bleomycin hydrolase isebenze. Kuma-hamster, ukucindezela kwengxenye ye-oksijini ephezulu kungabhebhethekisa ukulimala kwamaphaphu okubangelwa i-bleomycin, futhi imibiko yamacala iphinde yachaza i-ARDS ezigulini ezithole ukwelashwa kwe-bleomycin futhi zachayeka ku-FIO2 ephezulu ngesikhathi sokusebenza. Kodwa-ke, uhlolo olwaluzoba khona lwehlulekile ukukhombisa ukuhlobana phakathi kokuchayeka komoyampilo okugxilile, ukuchayeka ngaphambilini ku-bleomycin, kanye nokungasebenzi kahle kwamaphaphu kwangemva kokuhlinzwa. I-Paraquat isibulala-zinambuzane esithengiswayo esingesinye isithuthukisi sobuthi be-oxygen. Ngakho-ke, lapho usebenza neziguli ezinobuthi be-paraquat kanye nokuchayeka ku-bleomycin, i-FIO2 kufanele incishiswe ngangokunokwenzeka. Ezinye izidakamizwa ezingase zikhulise ubuthi be-oksijini zihlanganisa i-disulfiram ne-nitrofurantoin. Ukushoda kwamaprotheni nezakhi zomzimba kungaholela ekulimaleni okuphezulu komoyampilo, okungenzeka kube ngenxa yokuntuleka kwe-thiol equkethe ama-amino acid abalulekile ekuhlanganiseni kwe-glutathione, kanye nokuntuleka kwamavithamini A no-E ane-antioxidant.
Ubuthi be-oksijeni kwezinye izinhlelo zezitho

I-Hyperoxia ingabangela ukusabela okunobuthi ezithweni ezingaphandle kwamaphaphu. Ucwaningo olukhulu lwe-multicenter retrospective cohort lubonise ukuhlobana phakathi kokunyuka kokufa kanye namazinga aphezulu e-oxygen ngemva kokuvuselelwa kwe-cardiopulmonary (CPR) okuphumelelayo. Ucwaningo lwathola ukuthi iziguli ezine-PaO2 ezinkulu kune-300 mm Hg ngemuva kwe-CPR zinezinga lokufa kwesibhedlela se-1.8 (95% CI, 1.8-2.2) uma kuqhathaniswa neziguli ezine-oxygen evamile yegazi noma i-hypoxemia. Isizathu sokunyuka kwezinga lokufa ukuwohloka kokusebenza kwesistimu yezinzwa emaphakathi ngemva kokuboshwa kwenhliziyo okubangelwa ukulimala kwe-ROS okuxhumanise ne-high oxygen reperfusion. Ucwaningo lwakamuva luphinde lwachaza izinga lokufa elikhulayo ezigulini ezine-hypoxemia ngemva kokungena emnyangweni wezimo eziphuthumayo, okuhlobene eduze nezinga le-PaO2 ephakeme.

Ezigulini ezinokulimala kobuchopho kanye ne-stroke, ukunikeza umoya-mpilo kulabo abangenawo i-hypoxemia kubonakala kungenanzuzo. Ucwaningo olwenziwa isikhungo sokuhlukumezeka sathola ukuthi uma kuqhathaniswa neziguli ezinamazinga ajwayelekile e-oksijini yegazi, iziguli ezinokulimala kwengqondo okubuhlungu ezithole ukwelashwa kwe-oksijeni ephezulu (PaO2> 200 mm Hg) zinezinga eliphezulu lokufa kanye ne-Glasgow Coma Score ephansi lapho zikhishwa. Olunye ucwaningo ezigulini ezithola i-hyperbaric oxygen therapy lubonise ukubikezelwa okungalungile kwemizwa. Esivivinyweni esikhulu se-multicenter, ukugcwalisa i-oksijini ezigulini ze-stroke ezinzima ngaphandle kwe-hypoxemia (i-saturation enkulu kune-96%) yayingenayo inzuzo ekufeni noma ekubikezelweni okusebenzayo.

Ku-acute myocardial infarction (AMI), ukwengezwa komoya-mpilo kuwukwelapha okuvame ukusetshenziswa, kodwa ukubaluleka kokwelashwa komoya-mpilo ezigulini ezinjalo kuseyimpikiswano. Umoya-mpilo uyadingeka ekwelapheni iziguli ze-acute myocardial infarction ezine-hypoxemia ehambisanayo, njengoba ingasindisa izimpilo. Kodwa-ke, izinzuzo zokwengezwa kwe-oksijeni yendabuko lapho kungekho hypoxemia azikacaci. Ngasekupheleni kweminyaka yawo-1970, ukuhlolwa okungahleliwe okuphindwe kabili okuyizimpumputhe kwabhalisa iziguli ze-157 ezine-acute myocardial infarction enzima futhi kwaqhathanisa ukwelashwa komoya-mpilo (6 L/min) ngaphandle kokwelashwa komoyampilo. Kutholakale ukuthi iziguli ezithola ukwelashwa kwe-oksijini zinezinga eliphezulu le-sinus tachycardia kanye nokwanda okukhulu kwama-enzyme e-myocardial, kodwa kwakungekho umehluko ezingeni lokufa.

Esigabeni se-ST sokuphakama kwe-acute myocardial infarction iziguli ezingenayo i-hypoxemia, ukwelashwa kwe-nasal cannula oxygen ku-8 L/min akuzuzisi uma kuqhathaniswa nokuhogela umoya ozungezile. Kolunye ucwaningo mayelana nokuhogela komoyampilo ku-6 L/min kanye nokuhogela umoya osendaweni, kwakungekho mehluko ekufeni konyaka ongu-1 kanye namazinga okufunda phakathi kweziguli ezine-acute myocardial infarction. Ukulawula ukugcwala kwe-oxygen egazini phakathi kuka-98% kuya ku-100% no-90% kuya ku-94% akunayo inzuzo ezigulini ezinokuboshwa kwenhliziyo ngaphandle kwesibhedlela. Imiphumela engaba khona eyingozi yomoya-mpilo ophezulu ku-acute myocardial infarction ihlanganisa ukuvinjelwa komthambo we-coronary, ukuphazamisa ukugeleza kwegazi kwe-microcirculation, ukukhuphuka kokusebenza komoya-mpilo, ukwehla kokusetshenziswa komoyampilo, kanye nokwanda komonakalo we-ROS endaweni yokubuyisela kabusha ngempumelelo.

Ekugcineni, izivivinyo zemitholampilo kanye nokuhlaziywa kwemeta kuphenye amanani afanelekile e-SpO2 eziguli ezigula kakhulu esibhedlela. Isikhungo esisodwa, ilebula evulekile yokuhlola okungahleliwe okuqhathaniswa nokwelashwa komoya-mpilo okulondolozayo (i-SpO2 target 94%~98%) nokwelashwa kwendabuko (inani le-SpO2 elingu-97% ~ 100%) lwenziwa ezigulini ezingama-434 egunjini labagula kakhulu. Izinga lokufa egunjini labagula kakhulu leziguli ezabelwa ngokungahleliwe ukuthola ukwelashwa komoyampilo okonakele liye lathuthuka, ngezinga eliphansi lokushaqeka, ukwehluleka kwesibindi, kanye ne-bacterium. Ukuhlaziywa kwemeta okwalandela kwakuhlanganisa izivivinyo zemitholampilo ezingama-25 ezaqasha iziguli ezingaphezu kuka-16000 ezibhedlela ezinokuxilongwa okuhlukahlukene, okuhlanganisa ukushaywa unhlangothi, ukuhlukumezeka, i-sepsis, i-myocardial infarction, nokuhlinzwa okuphuthumayo. Imiphumela yalokhu kuhlaziywa kwe-meta ibonise ukuthi iziguli ezithola amasu okwelapha oksijini okulondolozayo zinezinga lokufa kwabantu esibhedlela (ingozi ehlobene, i-1.21; 95% CI, 1.03-1.43).

Kodwa-ke, izivivinyo ezinkulu ezimbili ezalandela zehlulekile ukukhombisa noma yimuphi umthelela wamasu okwelashwa komoyampilo okulondolozayo ngenani lezinsuku ezingenawo ama-ventilators ezigulini ezinesifo samaphaphu noma izinga lokusinda kwezinsuku ezingama-28 ezigulini ze-ARDS. Muva nje, ucwaningo lweziguli ezingama-2541 ezithola umoya wokungena ngomshini luthole ukuthi ukwengezwa komoyampilo okuhlosiwe phakathi kwezigaba ezintathu ezihlukene ze-SpO2 (88%~92%, 92%~96%, 96%~100%) akuzange kube nomthelela emiphumeleni efana nezinsuku zokusinda, ukufa, ukuboshwa kwenhliziyo, i-arrhythmia, i-myocardial infarction, i-myocardial infarction izinsuku ezingu-28. Ngokusekelwe kule datha, imihlahlandlela ye-British Thoracic Society incoma ububanzi obuqondiwe be-SpO2 obungu-94% ukuya ku-98% ezigulini eziningi zabantu abadala ezilaliswe esibhedlela. Lokhu kunengqondo ngoba i-SpO2 ngaphakathi kwalolu hlu (kucatshangelwa iphutha le-± 2%~3% lama-pulse oximeters) ihambisana nebanga le-PaO2 lika-65-100 mm Hg, eliphephile futhi elanele amazinga komoyampilo wegazi. Ezigulini ezisengozini yokwehluleka ukuphefumula kwe-hypercapnic, i-88% kuya ku-92% iyinhloso ephephile yokugwema i-hypercapnia ebangelwa i-O2.