iindaba

Unyango lweoksijini yenye yeendlela ezisetyenziswa ngokuqhelekileyo kumayeza anamhlanje, kodwa kusekho ukungaqondi kakuhle malunga nezalathiso zonyango lweoksijini, kwaye ukusetyenziswa ngokungafanelekanga kweoksijini kunokubangela ukusabela okunetyhefu enkulu.

Uvavanyo lweklinikhi ye-tissue hypoxia

Iimpawu zeklinikhi ze-tissue hypoxia ziyahlukahluka kwaye azichanekanga, kunye neempawu ezibalaseleyo ezibandakanya i-dyspnea, ukuphefumula okufutshane, i-tachycardia, uxinzelelo lokuphefumula, utshintsho olukhawulezayo kwimeko yengqondo, kunye ne-arrhythmia. Ukumisela ubukho be-tissue (visceral) hypoxia, i-serum lactate (ephakanyisiweyo ngexesha le-ischemia kunye nokunciphisa i-cardiac output) kunye ne-SvO2 (iyancipha ngexesha lokunciphisa i-cardiac output, i-anemia, i-arterial hypoxemia, kunye nesantya esiphezulu se-metabolic) luncedo kuvavanyo lweklinikhi. Nangona kunjalo, i-lactate inokunyuswa kwiimeko ezingekho phantsi kwe-hypoxic, ngoko ukuxilongwa akunakwenziwa kuphela ngokusekelwe ekuphakameni kwe-lactate, njengoko i-lactate inokunyuswa kwiimeko zokunyuka kwe-glycolysis, ezifana nokukhula ngokukhawuleza kwamathumba anobungozi, i-sepsis yokuqala, ukuphazamiseka kwe-metabolic, kunye nokulawulwa kwee-catecholamines. Amanye amaxabiso aselabhoratri abonisa ukungasebenzi kakuhle kwelungu elithile nawo abalulekile, njenge-creatinine ephakamileyo, i-troponin, okanye i-enzymes yesibindi.

Uvavanyo lweklinikhi ye-arterial oxygenation status

I-Cyanosis. I-Cyanosis idla ngokuba luphawu oluthi lwenzeka ekupheleni kwe-hypoxia, kwaye luhlala lungathembeki ekuxilongeni i-hypoxemia kunye ne-hypoxia kuba ayinakwenzeka kwi-anemia kunye ne-perfusion ephantsi kwegazi, kwaye kunzima kubantu abanolusu olumnyama ukuba baqaphele i-cyanosis.

Ukujongwa kwe-Pulse oximetry. I-non invasive pulse oximetry monitoring isetyenziswe ngokubanzi ukujonga zonke izifo, kwaye i-SaO2 yayo eqikelelwayo ibizwa ngokuba yi-SpO2. Umgaqo wokujongwa kwe-pulse oximetry ngumthetho weBill, othi ukuxinwa kwezinto ezingaziwayo kwisisombululo kunokumiselwa ngokufunxa ukukhanya. Xa ukukhanya kudlula kuzo naziphi na izicwili, uninzi lwayo lufunxwa zizinto zezicubu kunye negazi. Nangona kunjalo, nge-heartbeat nganye, igazi le-arterial lihamba nge-pulsatile flow, livumela ukuba i-pulse oximetry monitor ibone utshintsho ekufakweni kokukhanya kwi-wavelengths ezimbini: i-660 nanometers (obomvu) kunye ne-940 nanometers (infrared). Amazinga okufunxa kwehemoglobin encitshisiweyo kunye nehemoglobin eneoksijini ahlukile kula maza mabini. Emva kokuthabatha ukufunxwa kwezicwili ezingatsaliyo, ukuxinana kwehemoglobin eneoksijini xa kuthelekiswa nehemoglobin iyonke ingabalwa.

Kukho imida ethile ekubekeni iliso kwi-pulse oximetry. Nayiphi na into esegazini efunxa la maza obude inokuphazamisana nokuchaneka komlinganiselo, kuqukwa ne-hemoglobinopathies efunyenweyo - i-carboxyhemoglobin kunye ne-methemoglobinemia, i-methylene blue, kunye nokwahluka kwe-genetic hemoglobin. Ukufunxwa kwe-carboxyhemoglobin kumgama ongama-660 nanometers kuyafana naleyo yehemoglobin eneoksijini; Ukufunxa okuncinci kakhulu kumgama wamaza angama-940 nanometers. Ngoko ke, kungakhathaliseki ukuba i-carbon monoxide i-saturated hemoglobin kunye ne-oksijini egcwele i-hemoglobin, i-SpO2 iya kuhlala ihleli (90% ~ 95%). Kwi-methemoglobinemia, xa i-iron ye-heme ifakwe kwi-oxidized kwi-ferrous state, i-methemoglobin ilingana ne-coefficients yokufunxa yobude obubini bobude. Oku kubangela ukuba i-SpO2 yohluke kuphela phakathi koluhlu lwama-83% ukuya kuma-87% phakathi koluhlu olubanzi loxinaniso lwe-methemoglobin. Kule meko, amaza amaza okukhanya amane ayafuneka kumlinganiselo we-oksijini yegazi le-arterial ukwahlula phakathi kweendlela ezine ze-hemoglobin.

Ukujongwa kwe-pulse oximetry kuxhomekeke ekuhambeni kwegazi okwaneleyo kwe-pulsatile; Ke ngoko, ukujongwa kwe-pulse oximetry akunakusetyenziswa kwi-hypoperfusion yothuso okanye xa kusetyenziswa izixhobo zokuncedisa i-ventricular non-pulsatile (apho i-cardiac output ibala kuphela inxalenye encinci ye-cardiac output). Kwi-tricuspid regurgitation eqatha, ukuxinana kwe-deoxyhemoglobin kwigazi le-venous kuphezulu, kwaye ukutyhalwa kwegazi le-venous kunokukhokelela kufundo olusezantsi lwe-oksijini yegazi. Kwi-hypoxemia enzima ye-arterial (SaO2 <75%), ukuchaneka kunokunciphisa kwakhona njengoko obu buchule bungakaze buqinisekiswe ngaphakathi kolu luhlu. Okokugqibela, baya besanda abantu abaqaphela ukuba ukujongwa kwe-pulse oximetry kunokuthi kugqithise ukugcwala kwe-arterial hemoglobin saturation ukuya kuthi ga kwi-5-10 yeepesenti yeepesenti, kuxhomekeke kwisixhobo esithile esisetyenziswa ngabantu abantsundu.

PaO2/FIO2. Umlinganiselo we-PaO2 / FIO2 (ngokuqhelekileyo ubizwa ngokuba ngumlinganiselo we-P / F, ukusuka kwi-400 ukuya kwi-500 mm Hg) ibonisa iqondo lokutshintshiselana kwe-oksijini engaqhelekanga kwimiphunga, kwaye iluncedo kakhulu kulo mongo njengoko umoya we-mechanical unokusetha ngokuchanekileyo i-FIO2. Umlinganiselo we-AP/F ongaphantsi kwe-300 mm Hg ubonisa ukungaqhelekanga kokutshintshiselana kwegesi okubalulekileyo ngokweklinikhi, ngelixa umlinganiselo we-P/F ongaphantsi kwe-200 mm Hg ubonisa i-hypoxemia enzima. Izinto ezichaphazela umlinganiselo we-P / F zibandakanya izicwangciso zokungenisa umoya, uxinzelelo olulungileyo lokuphelelwa umoya, kunye ne-FIO2. Impembelelo yeenguqu kwi-FIO2 kumlinganiselo we-P / F iyahluka ngokuxhomekeka kwimeko yokulimala kwemiphunga, i-shunt fraction, kunye noluhlu lweenguqu zeFIO2. Ukungabikho kwe-PaO2, i-SpO2/FIO2 inokusebenza njengesalathisi esifanelekileyo.

Uxinzelelo lwe-alveolar arterial oksijini inxenye (Aa PO2) umahluko. Umlinganiselo we-Aa PO2 ngumahluko phakathi kwe-alveolar oksijini yoxinzelelo oluyinxenye ye-alveolar kunye nomlinganiselo we-arterial oksijini yoxinzelelo oluyinxenye, esetyenziselwa ukulinganisa ukusebenza kakuhle kotshintshiselwano lwegesi.

Umahluko "oqhelekileyo" we-Aa PO2 wokuphefumla umoya ojikeleze elwandle uyahluka ngokweminyaka, ukusuka kwi-10 ukuya kwi-25 mm Hg (2.5 + 0.21 x ubudala [iminyaka]). Into yesibini enempembelelo yiFIO2 okanye i-PAO2. Ukuba enye yezi zinto zimbini zinyuka, umahluko kwi-Aa PO2 uya kwanda. Oku kungenxa yokuba utshintshiselwano lwegesi kwii-alveolar capillaries lwenzeka kwindawo ethe tyaba (slope) ye-hemoglobin oxygen dissociation curve. Ngaphantsi kweqondo elifanayo lokuxutywa kwe-venous, umahluko kwi-PO2 phakathi kwegazi elixubekileyo le-venous kunye negazi le-arterial liya kwanda. Ngokuchasene noko, ukuba i-PO2 ye-alveolar iphantsi ngenxa yokungonelanga komoya okanye ukuphakama okuphezulu, ukuhlukana kwe-Aa kuya kuba ngaphantsi kunesiqhelo, oku kunokukhokelela ekunciphiseni okanye ukuxilongwa ngokuchanekileyo kwe-pulmonary dysfunction.

Isalathisi se-Oxygenation. Isalathiso se-Oxygenation index (OI) singasetyenziselwa izigulane ezinomshini wokuvavanya umoya ofunekayo wokuxhasa umoya wokugcina i-oxygenation. Ibandakanya uxinzelelo lwe-airway (MAP, kwi-cm H2O), i-FIO2, kunye ne-PaO2 (kwi-mm Hg) okanye i-SpO2, kwaye ukuba idlula i-40, ingasetyenziselwa njengomgangatho we-extracorporeal membrane oxygenation therapy. Ixabiso eliqhelekileyo elingaphantsi kwe-4 cm H2O / mm Hg; Ngenxa yexabiso elifanayo le-cm H2O / mm Hg (1.36), iiyunithi zihlala zingabandakanyi xa zibika lo mlinganiselo.

Iimpawu zonyango lwe-oxygen ebukhali
Xa izigulane zifumana ubunzima bokuphefumla, ukuxhaswa kwe-oksijini ngokuqhelekileyo kuyadingeka ngaphambi kokuxilongwa kwe-hypoxemia. Xa uxinzelelo lwe-arterial lwe-oksijeni (i-PaO2) lungaphantsi kwe-60 mm Hg, esona sibonakaliso sicacileyo sokufumana i-oksijini yi-hypoxemia ye-arterial, ehambelana ngokuqhelekileyo ne-arterial oxygen saturation (SaO2) okanye i-peripheral oxygen saturation (SpO2) ye-89% ukuya kwi-90%. Xa i-PaO2 yehla ngaphantsi kwe-60 mm Hg, ukugcwala kwe-oksijini yegazi kunokuncipha ngokukhawuleza, okukhokelela ekunciphiseni okukhulu kwe-oksijeni ye-arterial kwaye kunokubangela i-tissue hypoxia.

Ukongeza kwi-arterial hypoxemia, ukuxhaswa kwe-oksijini kunokufuneka kwiimeko ezinqabileyo. I-anemia enkulu, umonzakalo, kunye nezigulana ezibalulekileyo zotyando zinokunciphisa i-tissue hypoxia ngokunyusa amanqanaba omoya we-arterial. Kwizigulane ezine-carbon monoxide (CO) enetyhefu, ukongeza i-oksijini kunokunyusa umxholo we-oksijini echithiweyo egazini, indawo ye-CO ebophelelwe kwi-hemoglobin, kwaye yandise umlinganiselo we-hemoglobin ene-oxygen. Emva kokuphefumla ioksijini ecocekileyo, isiqingatha sobomi be-carboxyhemoglobin yimizuzu engama-70-80, ngelixa isiqingatha sobomi xa ukuphefumla umoya ojikeleze yimizuzu engama-320. Ngaphantsi kweemeko ze-oxygen ye-hyperbaric, i-half-life ye-carboxyhemoglobin iyancipha ibe ngaphantsi kwemizuzu ye-10 emva kokuphefumla i-oksijini ecocekileyo. I-oksijini ye-Hyperbaric isetyenziswa ngokuqhelekileyo kwiimeko ezinamazinga aphezulu e-carboxyhemoglobin (> 25%), i-ischemia ye-cardiac, okanye i-sensory abnormalities.

Nangona ukungabikho kwedatha exhasayo okanye idatha engachanekanga, ezinye izifo zinokuthi zizuze ngokuncedisa i-oksijeni. Unyango lweoksijini luqhele ukusetyenziselwa intloko ebuhlungu yeqela, ingxaki yeentlungu ze-sickle cell, ukukhululeka koxinzelelo lokuphefumla ngaphandle kwe-hypoxemia, i-pneumothorax, kunye ne-mediastinal emphysema (ukukhuthaza ukufunxa komoya wesifuba). Kukho ubungqina obubonisa ukuba i-oxygen ephezulu ye-intraoperative inokunciphisa iziganeko zosulelo lwendawo yotyando. Nangona kunjalo, ukongeza i-oksijini akubonakali kunciphisa ngokufanelekileyo isicaphucaphu / ukuhlanza emva kokusebenza.

Ngokuphuculwa kwamandla okubonelela nge-oxygen ngaphandle, ukusetyenziswa kwexesha elide lonyango lwe-oxygen (LTOT) nalo luyanda. Imigangatho yokuphumeza unyango lwe-oksijini yexesha elide sele icacile. Unyango lwexesha elide lweoksijini luqhele ukusetyenziswa kwizifo ezingapheliyo zemiphunga (COPD).
Izifundo ezimbini kwizigulane ezine-COPD ye-hypoxemic zibonelela ngedatha yenkxaso ye-LTOT. Uphononongo lokuqala lwaluyi-Nocturnal Oxygen Therapy Trial (NOTT) eyenziwa kwi-1980, apho izigulane zabelwa ngokungenamkhethe nokuba ubusuku (ubuncinci iiyure ze-12) okanye unyango oluqhubekayo lwe-oxygen. Kwiinyanga ze-12 kunye ne-24, izigulane ezifumana kuphela unyango lwe-oxygen ebusuku zinezinga eliphezulu lokufa. Uvavanyo lwesibini lwaluyi-Medical Research Council yeFamily Trial eyenziwa kwi-1981, apho izigulane zahlulwa ngokungenamkhethe zibe ngamaqela amabini: abo bangazange bafumane i-oksijini okanye abo bafumana i-oksijini ubuncinane iiyure ze-15 ngosuku. Ngokufanayo novavanyo lwe-NOTT, izinga lokufa kwiqela le-anaerobic laliphezulu kakhulu. Izifundo zezilingo zombini zizigulane ezingabhemiyo ezifumene unyango oluphezulu kwaye zineemeko ezizinzileyo, kunye ne-PaO2 ngaphantsi kwe-55 mm Hg, okanye izigulane ezine-polycythemia okanye isifo senhliziyo se-pulmonary nge-PaO2 ngaphantsi kwe-60 mm Hg.

Ezi zilingo zimbini zibonisa ukuba ukongeza i-oksijini ngaphezu kweeyure ze-15 ngosuku kungcono kunokuba ungayifumani ngokupheleleyo i-oksijini, kwaye unyango oluqhubekayo lwe-oksijini lungcono kunokunyanga kuphela ebusuku. Iikhrayitheriya zokubandakanywa kwezi zilingo zisisiseko kwiinkampani ze-inshurensi yezonyango zangoku kunye ne-ATS ukuphuhlisa izikhokelo ze-LTOT. Kunengqiqo ukucacisa ukuba i-LTOT yamkelwe nakwezinye izifo ze-hypoxic ze-cardiovascular, kodwa okwangoku kukho ukungabikho kobungqina obufanelekileyo bokulinga. Ulingo lwamva nje lwe-multicenter alufumananga mahluko kwimpembelelo yonyango lwe-oksijini ekufeni okanye umgangatho wobomi kwizigulane zeCOPD ezine-hypoxemia ezingazange zihlangabezane neendlela zokuphumla okanye zibangelwa kuphela ngumsebenzi.

Ngamanye amaxesha oogqirha banikezela nge-oksijini yokuncedisa ebusuku kwizigulana eziye zehla kakhulu kwi-oksijini yegazi ngexesha lokulala. Okwangoku akukho bungqina obucacileyo bokuxhasa ukusetyenziswa kwale ndlela kwizigulane ezine-apnea ephazamisayo yokulala. Kwizigulana ezine-obstructive sleep apnea okanye ukutyeba kwe-hyopnea syndrome ekhokelela ekuphefumleni kakubi ebusuku, ukuphefumla umoya ongonwabiyo ongowonayo endaweni yokongezwa kweoksijini yeyona ndlela yonyango.

Omnye umba omele uqwalaselwe kukuba ingaba i-oxygen supplementation iyafuneka ngexesha lokuhamba emoyeni. Uninzi lweenqwelomoya zentengiso ziye zonyusa uxinzelelo lwekhabhin ukuya kumphakamo olingana neemitha ezingama-8000, kunye noxinzelelo lweoksijini ephefumleyo malunga ne-108 mm Hg. Kwizigulane ezinezifo zemiphunga, ukuncipha kwe-oxygen tension (PiO2) e-inhaled (PiO2) kunokubangela i-hypoxemia. Ngaphambi kokuhamba, izigulane kufuneka zenze uvavanyo olubanzi lwezonyango, kubandakanywa novavanyo lwegesi yegazi. Ukuba i-PaO2 yesigulane emhlabeni i-≥ 70 mm Hg (SpO2> 95%), ngoko i-PaO2 yabo ngexesha lokuhamba inokuthi idlule i-50 mm Hg, ngokuqhelekileyo ibonwa ngokwaneleyo ukujamelana nomsebenzi omncinci womzimba. Kwizigulane ezine-SpO2 ephantsi okanye i-PaO2, uvavanyo lokuhamba ngomzuzu we-6 okanye uvavanyo lwe-hypoxia simulation lungaqwalaselwa, ngokuqhelekileyo ukuphefumula i-15% ye-oxygen. Ukuba i-hypoxemia yenzeka ngexesha lokuhamba emoyeni, i-oksijini inokulawulwa nge-cannula yeempumlo ukwandisa ukungena kwe-oxygen.

Isiseko sebhayoloji yetyhefu yeoksijini

Ubuthi beoksijini bubangelwa kukuveliswa kweentlobo ze-oxygen esebenzayo (ROS). I-ROS i-oksijini ephuma kwi-radical yamahhala kunye ne-electron engabonakaliyo ye-orbital enokuthi iphendule ngeeprotheni, i-lipids, kunye ne-nucleic acids, iguqule isakhiwo sayo kwaye ibangele umonakalo weselula. Ngexesha le-metabolism ye-mitochondrial eqhelekileyo, inani elincinci le-ROS liveliswa njenge-molecule yokubonisa. Iiseli zamajoni omzimba zikwasebenzisa iROS ukubulala iintsholongwane. I-ROS ibandakanya i-superoxide, i-hydrogen peroxide (H2O2), kunye ne-hydroxyl radicals. I-ROS egqithisileyo iya kudlula ngokungaguquguqukiyo imisebenzi yokukhusela iselula, ekhokelela ekufeni okanye ekubangeleni umonakalo weseli.

Ukunciphisa umonakalo owenziwe sisizukulwana se-ROS, indlela yokukhusela i-antioxidant yeeseli inokunciphisa i-radicals yamahhala. I-Superoxide dismutase iguqula i-superoxide ibe yi-H2O2, ethi ke iguqulwe ibe yi-H2O kunye ne-O2 nge-catalase kunye ne-glutathione peroxidase. I-Glutathione yi-molecule ebalulekileyo ethintela umonakalo we-ROS. Ezinye i-antioxidant molecules ziquka i-alpha tocopherol (i-vitamin E), i-ascorbic acid (i-vitamin C), i-phospholipids, kunye ne-cysteine. Izicubu zemiphunga yomntu ziqulethe ukugxila okuphezulu kwe-antioxidant ye-extracellular kunye ne-superoxide dismutase isoenzymes, iyenza ingabinatyhefu xa ibonakaliswe kwindawo ephezulu yeoksijini xa kuthelekiswa nezinye izicubu.

I-Hyperoxia eyenziwa yi-ROS yokulimala kwe-lung mediated inokwahlulwa ibe ngamanqanaba amabini. Okokuqala, kukho isigaba se-exudative, esibonakaliswa ngokufa kwe-alveolar yohlobo lwe-1 yeeseli ze-epithelial kunye neeseli ze-endothelial, i-edema ye-interstitial, kunye nokuzaliswa kwe-neutrophils exudative kwi-alveoli. Emva koko, kukho isigaba sokwandisa, ngexesha apho iiseli ze-endothelial kunye nohlobo lweeseli ze-epithelial ze-2 zanda kwaye zigquma i-membrane engaphantsi evezwe ngaphambili. Iimpawu zexesha lokubuyisela ukulimala kwe-oksijeni kukunyuka kwe-fibroblast kunye ne-interstitial fibrosis, kodwa i-capillary endothelium kunye ne-alveolar epithelium isagcina ukubonakala okuqhelekileyo.
Ukubonakaliswa kweklinikhi ye-pulmonary oxygen toxicity

Inqanaba lokuvezwa apho ubuthi lwenzeka khona alikacaci. Xa i-FIO2 ingaphantsi kwe-0.5, ubuthi beklinikhi ngokuqhelekileyo abukho. Izifundo zabantu zakwangoko ziye zafumanisa ukuba ukuvezwa kwi-oksijini ephantse ibe yi-100% kunokubangela ukungahambi kakuhle kweemvakalelo, isicaphucaphu, kunye ne-bronchitis, kunye nokunciphisa umthamo wemiphunga, amandla okusasazwa kwemiphunga, ukuthotyelwa kwemiphunga, i-PaO2, kunye ne-pH. Eminye imiba enxulumene netyhefu ye-oksijini ibandakanya i-atelectasis yokufunxa, i-hypercapnia eyenziwe nge-oksijini, i-acute breathing distress syndrome (ARDS), kunye ne-neonatal bronchopulmonary dysplasia (BPD).
I-atelectasis engapheliyo. I-nitrojeni yigesi engasebenziyo esasazeka ngokucothayo kwigazi xa kuthelekiswa neoksijini, ngaloo ndlela idlala indima ekugcineni ukwandiswa kwe-alveolar. Xa usebenzisa i-oxygen eyi-100%, ngenxa yezinga lokufunxa i-oksijini elidlula izinga lokuhanjiswa kwegesi entsha, ukusilela kwe-nitrogen kunokukhokelela ekuweni kwe-alveolar kwiindawo ezinomlinganiselo ophantsi we-alveolar ventilation perfusion ratio (V / Q). Ngokukodwa ngexesha lotyando, i-anesthesia kunye nokukhubazeka kunokukhokelela ekunciphiseni komsebenzi wemiphunga eseleyo, ukukhuthaza ukuwa kweendlela ezincinci zomoya kunye ne-alveoli, okubangelwa ukuqala ngokukhawuleza kwe-atelectasis.

I-hypercapnia ebangelwa yioksijini. Izigulana ezimandundu zeCOPD zithambekele ekubeni ne-hypercapnia enzima xa bevezwe kwindawo ephezulu yeoksijini ngexesha lokuwohloka kwemeko yabo. Inkqubo yale hypercapnia kukuba ukukwazi kwe-hypoxemia ukuqhuba ukuphefumla kuvinjelwe. Nangona kunjalo, kuso nasiphi na isigulana, kukho ezinye iindlela ezimbini ezidlalayo ukuya kumanqanaba ahlukeneyo.
I-hypoxemia kwizigulane ze-COPD yisiphumo soxinzelelo oluncinci lwe-alveolar ye-oxygen (PAO2) kwindawo ephantsi ye-V / Q. Ukuze kuncitshiswe impembelelo yale mimandla ye-V / Q ephantsi kwi-hypoxemia, iimpendulo ezimbini ze-pulmonary circulation - i-hypoxic pulmonary vasoconstriction (HPV) kunye ne-hypercapnic pulmonary vasoconstriction - iya kudlulisela ukuhamba kwegazi kwiindawo ezinomoya. Xa ukuxhaswa kwe-oksijini kwandisa i-PAO2, i-HPV iyancipha kakhulu, inyusa i-perfusion kule mimandla, okubangelwa kwiindawo ezine-V / Q ratios ephantsi. Ezi zicubu zemiphunga ngoku zizityebi kwioksijini kodwa zinamandla abuthathaka okuphelisa i-CO2. Ukunyuka kwe-perfusion kwezi zicubu zemiphunga kuza kwiindleko zokubingelela iindawo ezinomoya ongcono, ezingenako ukukhulula izixa ezikhulu ze-CO2 njengangaphambili, ezikhokelela kwi-hypercapnia.

Esinye isizathu sisiphumo esibuthathaka se-Haldane, oku kuthetha ukuba xa kuthelekiswa negazi le-oksijini, igazi le-deoxygenated lingathwala i-CO2 eninzi. Xa i-hemoglobin i-deoxygenated, idibanisa iiprotons ezininzi (H +) kunye ne-CO2 ngendlela yee-amino esters. Njengoko ingxinano ye-deoxyhemoglobin iyancipha ngexesha lonyango lwe-oksijini, umthamo we-buffering we-CO2 kunye ne-H + nawo uyancipha, ngaloo ndlela unciphisa amandla egazi le-venous ukuthutha i-CO2 kunye nokukhokelela ekwandeni kwe-PaCO2.

Xa unikezela i-oksijini kwizigulane ezinokugcinwa kwe-CO2 ezingapheliyo okanye izigulane ezinobungozi obuphezulu, ngokukodwa kwimeko ye-hypoxemia enzima kakhulu, kubaluleke kakhulu ukulungelelanisa i-FIO2 kakuhle ukugcina i-SpO2 kwi-88% ~ 90%. Iingxelo ezininzi zeemeko zibonisa ukuba ukungaphumeleli ukulawula i-O2 kunokukhokelela kwimiphumo emibi; Uphononongo olungacwangciswanga olwenziwa kwizigulane eziye zaqatsela kakhulu i-CODP endleleni eya esibhedlele ibonakalise ngokungathandabuzekiyo oku. Xa kuthelekiswa nezigulane ezingenamthintelo we-oksijeni, izigulane ezabelwe ngokungenamkhethe ukuba zongeze i-oksijini ukugcina i-SpO2 ngaphakathi kwinqanaba le-88% ukuya kwi-92% yayinezinga lokufa eliphantsi kakhulu (7% vs. 2%).

I-ARDS kunye ne-BPD. Abantu kudala befumanisa ukuba ubutyhefu beoksijini bunxulunyaniswa ne-pathophysiology ye-ARDS. Kwizilwanyana ezincancisayo ezingezizo ezomntu, ukuvezwa kwe-oksijini eyi-100% kunokukhokelela kumonakalo we-alveolar kunye nokufa. Nangona kunjalo, ubungqina obuchanekileyo bobutyhefu be-oxygen kwizigulane ezinezifo ezinzima zemiphunga kunzima ukwahlula kumonakalo obangelwa zizifo eziphantsi. Ukongeza, izifo ezininzi ezivuthayo zinokubangela ukulawulwa komsebenzi wokukhusela i-antioxidant. Ke ngoko, uninzi lwezifundo ziye zasilela ukubonisa unxibelelwano phakathi kokuvezwa kweoksijini egqithisileyo kunye nokulimala okukhulu kwemiphunga okanye i-ARDS.

Isifo se-pulmonary hyaline membrane sisifo esibangelwa ukungabikho kwezinto ezisebenzayo zomhlaba, ezibonakaliswe ngokuwa kwe-alveolar kunye nokuvuvukala. Abantwana abasandul’ ukuzalwa ngaphambi kwexesha abanesifo se-hyaline membrane badla ngokufuna ukuphefumlelwa ioksijini ephezulu. Ubuthi beoksijini buthathwa njengeyona nto iphambili kwi-pathogenesis ye-BPD, nokuba kwenzeka kwiintsana ezisanda kuzalwa ezingadingi kungena komoya ngoomatshini. Iintsana ezisanda kuzalwa zichaphazeleka ngakumbi kumonakalo omkhulu weoksijini ngenxa yokuba imisebenzi yazo yokukhusela i-antioxidant yeselula ayikakhuli ngokupheleleyo kwaye ikhule; I-retinopathy ye-prematurity sisifo esihambelana nokuphindaphindiweyo kwe-hypoxia / hyperoxia yoxinzelelo, kwaye esi siphumo siqinisekisiwe kwi-retinopathy ye-prematurity.
Impembelelo ye-synergistic ye-pulmonary oxygen toxicity

Kukho amachiza amaninzi anokonyusa ubutyhefu beoksijini. I-oksijeni yonyusa i-ROS eveliswa yi-bleomycin kwaye ingasebenzi i-bleomycin hydrolase. Kwii-hamsters, uxinzelelo oluphezulu lwe-oksijini oluphezulu lunokwandisa i-bleomycin eyenza ukulimala kwemiphunga, kunye neengxelo zecala ziye zachaza i-ARDS kwizigulane ezifumene unyango lwe-bleomycin kwaye zavezwa kwi-FIO2 ephezulu ngexesha le-perioperative. Nangona kunjalo, ulingo olulindelekileyo lwasilela ukubonisa unxibelelwano phakathi kokuvezwa kweoksijini ephezulu, ukuvezwa kwangaphambili kwi-bleomycin, kunye nokungasebenzi kakuhle kwemiphunga emva kokuhlinzwa. IParaquat sisitshabalalisi sorhwebo esesinye isixhasi setyhefu yeoksijini. Ngoko ke, xa ujongene nezigulane ezinetyhefu yeparaquat kunye nokuvezwa kwe-bleomycin, i-FIO2 kufuneka incitshiswe kangangoko kunokwenzeka. Ezinye iziyobisi ezinokwandisa ubutyhefu beoksijini ziquka i-disulfiram kunye ne-nitrofurantoin. Ukunqongophala kweeprotheyini kunye nezondlo kunokukhokelela kumonakalo ophezulu we-oksijini, onokuthi ngenxa yokunqongophala kwe-thiol equkethe i-amino acids ebalulekileyo kwi-glutathione synthesis, kunye nokungabikho kwe-antioxidant vitamin A kunye ne-E.
Ubuthi beoksijini kwezinye iinkqubo zamalungu

I-Hyperoxia inokubangela ukusabela okunetyhefu kwizitho ezingaphandle kwemiphunga. Uphononongo olukhulu lwe-multicenter retrospective cohort lubonise unxulumano phakathi kokunyuka kokufa kunye namanqanaba aphezulu e-oksijini emva kokuphumelela kwe-cardiopulmonary resuscitation (CPR). Uphononongo lufumene ukuba izigulane ezine-PaO2 ezinkulu kune-300 mm Hg emva kwe-CPR zine-in-hospital risk risk ratio ye-1.8 (95% CI, 1.8-2.2) xa kuthelekiswa nezigulane ezinegazi eliqhelekileyo le-oksijeni okanye i-hypoxemia. Isizathu sokunyuka kwezinga lokufa kukuwohloka kwenkqubo ye-nervous system emva kokubanjwa kwentliziyo okubangelwa yi-ROS edibanisa ukulimala okuphezulu kwe-oxygen. Uphononongo olutshanje luphinde luchaze izinga lokufa kwabantu abanyukayo kwizigulane ezine-hypoxemia emva kwe-intubation kwisebe elingxamisekileyo, elihambelana ngokusondeleyo kwinqanaba le-PaO2 ephakamileyo.

Kwizigulane ezinokulimala kwengqondo kunye ne-stroke, ukubonelela ngeoksijini kwabo bangenayo i-hypoxemia kubonakala kungenanzuzo. Uphononongo olwenziwa liziko le-trauma lifumene ukuba xa kuthelekiswa nezigulane ezinezinga eliqhelekileyo le-oksijeni yegazi, izigulane ezinokulimala kwengqondo ebuhlungu ezifumene i-oksijeni ephezulu (i-PaO2> i-200 mm Hg) yonyango inezinga eliphezulu lokufa kunye ne-Glasgow Coma Score ephantsi ekuphumeni. Olunye uphononongo kwizigulane ezifumana unyango lwe-hyperbaric oksijini lubonise ukungahambi kakuhle kwe-neurological prognosis. Kwilingo elikhulu le-multicenter, ukongeza i-oksijini kwizigulane ze-stroke ezibukhali ngaphandle kwe-hypoxemia (i-saturation enkulu kune-96%) yayingenayo inzuzo ekufeni okanye kwi-prognosis yokusebenza.

Kwi-acute myocardial infarction (AMI), ukuxhaswa kwe-oksijini yonyango olusetyenziswa ngokuqhelekileyo, kodwa ixabiso lonyango lwe-oxygen kwizigulane ezinjalo lisaphikisana. Ioksijini iyimfuneko kunyango lwezigulane ze-acute myocardial infarction ezine-concomitant hypoxemia, njengoko inokusindisa ubomi. Nangona kunjalo, izibonelelo zokuncedisa i-oksijini yendabuko ngokungabikho kwe-hypoxemia ayikacaci. Ngasekupheleni kweminyaka yee-1970, uvavanyo oluyimfama oluphindwe kabini lwabhalisa izigulane ze-157 ezine-infarction ye-myocardial enzima kwaye zithelekisa unyango lwe-oxygen (6 L / min) ngaphandle konyango lwe-oxygen. Kwafunyaniswa ukuba izigulane ezifumana unyango lwe-oksijeni zineziganeko eziphezulu ze-sinus tachycardia kunye nokunyuka okukhulu kwi-enzymes ye-myocardial, kodwa kwakungekho mmahluko kwizinga lokufa.

Kwi-ST segment elevation acute myocardial infarction izigulane ezingenayo i-hypoxemia, unyango lwe-nasal cannula oksijini kwi-8 L/min alunanzuzo xa kuthelekiswa nokuphefumla umoya okhoyo. Kwesinye isifundo kwi-oxygen inhalation kwi-6 L / min kunye ne-inhalation yomoya we-ambient, akukho mahluko kwi-1-year-death kunye namazinga okufunda phakathi kwezigulane ezine-acute myocardial infarction. Ukulawula i-oxygen saturation phakathi kwe-98% ukuya kwi-100% kunye ne-90% ukuya kwi-94% ayinayo inzuzo kwizigulane ezinokubanjwa kwentliziyo ngaphandle kwesibhedlele. Iimpembelelo ezinobungozi ezinokuthi zibe ne-oksijini ephezulu kwi-acute myocardial infarction ibandakanya ukunyanzeliswa kwe-coronary artery, ukuphazamiseka kokuhamba kwegazi kwe-microcirculation, ukunyuka kwe-oxygen shunt esebenzayo, ukunciphisa ukusetyenziswa kwe-oksijeni, kunye nokwanda komonakalo we-ROS kwindawo yokubuyisela ngempumelelo.

Ekugqibeleni, izilingo zeklinikhi kunye nohlalutyo lwe-meta luphande amaxabiso ekujoliswe kuwo afanelekileyo e-SpO2 kwizigulana ezigula kakhulu esibhedlele. Iziko elilodwa, iileyibhile ezivulekileyo zolingo ngokuthelekisa unyango lwe-oxygen olulondolozayo (i-SpO2 ekujoliswe kuyo 94% ~ 98%) kunye nonyango lwendabuko (ixabiso le-SpO2 97% ~ 100%) lenziwe kwizigulane ze-434 kwiyunithi yokunyamekela kakhulu. Izinga lokufa kwiyunithi yokhathalelo olunzulu lwezigulane ezinikezelwe ngokungenamkhethe ukufumana unyango lwe-oksijini olulondolozayo luye lwaphuculwa, kunye namazinga aphantsi othusayo, ukusilela kwesibindi, kunye ne-bacteremia. Uhlalutyo lwe-meta olwalandelayo lubandakanya izilingo zeklinikhi ze-25 eziye zafumana izigulane ezingaphezu kwe-16000 esibhedlele ezinokuxilongwa okuhlukeneyo, kubandakanywa ukubetha, ukwenzakala, i-sepsis, i-myocardial infarction, kunye noqhaqho olungxamisekileyo. Iziphumo zolu hlalutyo lweemeta zibonise ukuba izigulane ezifumana izicwangciso zonyango lwe-oxygen zinomlinganiselo wokufa kwabantu esibhedlele (umngcipheko ohlobene, 1.21; 95% CI, 1.03-1.43).

Nangona kunjalo, izilingo ezimbini ezalandelayo aziphumelelanga ukubonisa nayiphi na impembelelo yeendlela zonyango lwe-oksijini olugcinayo ngenani leentsuku ngaphandle kwee-ventilators kwizigulana ezinesifo semiphunga okanye izinga lokusinda kweentsuku ezingama-28 kwizigulana ze-ARDS. Kutshanje, uphononongo lwezigulane ezingama-2541 ezifumana umoya wokuphefumla ngoomatshini zifumene ukuba ukuxhaswa kwe-oksijini ekujoliswe kuyo phakathi kweendlela ezintathu ezahlukeneyo ze-SpO2 (88% ~ 92%, 92% ~ 96%, 96% ~ 100%) azizange zichaphazele iziphumo ezinjengeentsuku zokuphila, ukufa, ukubanjwa kwentliziyo, i-arrhythmia, i-myocardial infarction, i-myocardial infarction Iintsuku ezingama-28. Ngokusekelwe kule datha, izikhokelo ze-British Thoracic Society zincoma uluhlu olujoliswe kuyo lwe-SpO2 lwe-94% ukuya kwi-98% kwizigulane ezininzi zabantu abadala. Oku kunengqiqo kuba i-SpO2 ngaphakathi kolu luhlu (ukuqwalasela i-± 2% ~ 3% yephutha le-pulse oximeters) ihambelana noluhlu lwe-PaO2 lwe-65-100 mm Hg, olukhuselekileyo kwaye lwanele amanqanaba e-oxygen yegazi. Kwizigulane ezisengozini yokungaphumeleli kokuphefumula kwe-hypercapnic, i-88% ukuya kwi-92% yinjongo ekhuselekileyo yokuphepha i-hypercapnia ebangelwa yi-O2.