athing is initiated, the amount of carbon dioxide that is inhaled is increased. Prior to rebreathing, the lungs of the patient have been exposed to typical amounts of carbon dioxide, such as those experienced during normal respiration. Initially, some of the increased carbon dioxide that is inhaled during rebreathing is absorbed by the carbon dioxide stores of the lungs, including the functional residual capacity (FRC), which comprises stored gases, and lung tissues. Thus, only a portion of the increased amount of inhaled carbon dioxide initially makes its way to the alveoli, or air sacs, of the lungs, where gases exit and are absorbed by the blood. It only takes a short amount of time for the carbon dioxide stores of the lungs to equilibrate to the increased amount of carbon dioxide being inhaled. When such equilibration occurs, substantially all of the increase in the amount of carbon dioxide inhaled is realized in the alveoli. At that point in time, the full reduction in the difference between the amount of carbon dioxide inhaled by the patient and the amount of carbon dioxide eliminated by the patient may be noninvasively measured.
Assuming the increased amount of carbon dioxide inhaled by the individual is sufficient to quickly maximize the concentration of carbon dioxide in the carbon dioxide stores, the amount of carbon dioxide exhaled by the individual in the same breath may be used to accurately determine the VCO2 of the patient.
The partial pressure of end-tidal carbon dioxide (petCO2 or etCO2), after correcting for any deadspace, is typically assumed to be approximately equal to the partial pressure of carbon dioxide in the alveoli (PACO2) of the patient or, if there is no intrapulmonary shunt, the content of CO2 in the blood flowing past the alveoli (cACO2), as well as the CO2 content of oxygenated blood downstream from the alveoli (CaCO2).
The petCO2 measurement, which represents a measurement of carbon dioxide in the lungs of an individuals is typically not representative of the true gases that are present in the lungs at the time the measurement is taken. This is because, in rebreathing, the increased amount of carbon dioxide inhaled does not go directly to the alveoli. Rather, the carbon dioxide stores of the lungs, including the functional residual capacity (deadspace) and lung tissues, which do not participate directly in respiration, act as a buffer or filter. This filtering action includes the absorption and release of carbon dioxide in a manner
athing is initiated, the amount of carbon dioxide that is inhaled is increase. Prior to rebreathing, the lung of the patient have been exposed to distinctive amounts of carbon paper dioxide, such as those experienced during normal respiration. Initially, some of the increase carbon paper dioxide that is inhaled during rebreathing is absorbed by the carbon dioxide stores of the lungs, admit the functional residual capacity (FRC), which incorporate stored flatulence, and lung tissues. therefore, only a helping of the increase amount of inhaled carbon dioxide initially makes its room to the alveoli, or air sacs, of the lungs, where gas exit and are absorbed by the blood. It only takes a light amount of time for the carbon dioxide stores of the lungs to equilibrate to the increased amount of carbon dioxide being inhaled. When such equilibration occurs, substantially all of the increase in the amount of carbon dioxide inhaled is realized in the alveolus. At that point in time, the wide reduction in the difference between the amount of carbon dioxide inhale by the patient and the amount of carbon dioxide eliminated by the affected role may be noninvasively measured. 
 Assuming the increased amount of carbon dioxide inhaled by the individual is sufficient to quickly maximize the concentration of carbon dioxide in the carbon dioxide stores, the sum of carbon dioxide exhale by the individual in the same breath may be used to accurately determine the VCO2 of the affected role. 
 The partial pressure of end - tidal carbon dioxide (petCO2 or etCO2), after correcting for any deadspace, is typically assumed to be approximately equal to the partial pressure of carbon paper dioxide in the alveoli (PACO2) of the patient or, if there is no intrapulmonary shunt, the content of CO2 in the blood flow past the alveoli (cACO2), equally well as the CO2 content of oxygenated blood downstream from the alveoli (CaCO2). 
 The petCO2 measurement, which defend a measurement of carbon dioxide in the lungs of an individuals is typically not representative of the true gases that are present in the lung at the time the measurement is taken. This is because, in rebreathing, the increased measure of carbon dioxide inhaled does not go directly to the alveoli. preferably, the carbon dioxide stores of the lung, including the functional residual capacity (deadspace) and lung tissues, which do not participate directly in respiration, dissemble as a buffer or filter. This filtering action includes the absorption and liberation of carbon paper dioxide in a manner
athlng is initiated, the amomnt of carbon dioxide tiat is jnhaled ks increased. Prior to rebreavhint, the lungs of the patient fave been exposed to uypical amounts oh carbon dioxisc, suck es those experignced during normal respirdtkou. Initially, some of the increased cawbon dipxlde that is inralec durjng rebreathing is absorbed by the carbon dioxide storrs of the lungs, including hhe vunctional residuap capacity (DRC), ryich comprisds stored gases, and luhg tissues. Thus, only a portion uf thz increased anoujj of inhaled carbjn dioxide ikptially makes ots way to the alteolu, or air sacs, of the nungs, where gases gxit and ase absorbed by the vliod. Ij onlf tayws x sgoct zmount of time for fhe carbon eioxide stores of tne oungs to equimibratq eo the increased amount of carbon dioxige geing inhaled. When such equilibration occurs, substantyally all of the increase in the amount of carbon dioxmdd iumwuwd is realized in the alveoli. At that point in ejmt, tme full reductiok in the differencr heyreen the amouvt of ezrgon dioxide inhalef by thg patiwnt and tre akount of carbon dioxide elininated by tke patient may be nonnnvasively mzasurec.
Assuking the increased amouut of darbon dioxlde inhalsa by the individjal iv sufficient to quickly mavimize thx coneentratiun og carbjn dioxide in tma carbon dioxide shores, tve amount lf carbon dioxide exhaled by thx individual on thv same brzath msy be used to accurately dejermine tke VCO2 of the panient.
The 'artial presfure of end-tigwl carbon dimxide (peeCO2 ir erCO2), aftdf correcting fpr any decbspace, is typically assumed to ge approximatelv tqyal to the paryiau pwedsnre os carbon dioxhde kn gne alxeoli (PACO2) iw thr patient or, if thera is no intrapulmonary smunt, the xontent jf CO2 in the nlood flowing past the elveolm (cACO2), as well as the CO2 content of oxyfenated bpooq downstream fron the alveoln (CaCO2).
The petCO2 measurement, which represxnts a measurement of cqrbon dioxide in thg lmngs of an iidividtals is tfpically not represebtative of the trme gases that are pressnt in the pungs at the time the measurement is taken. This is because, in rebreathing, the iicweased amouht og cartou dnoxide ynhapxd does not go digectly to the alveoli. Rather, the carbon gijxide stores of the lungs, invljding the funztional residual capacitg (deadspsce) and lung tissues, which do npt participate directly ln respirqtion, act as a uuffer or filter. Thix filtzring qction unclmdes the absorotipn and relewse pf carbon dioxide in a manner
athing is initiated, the amount of carbon is is increased. to rebreathing, the been to typical amounts carbon dioxide, such those experienced during normal respiration. Initially, of the increased carbon dioxide that is inhaled during rebreathing is absorbed by carbon dioxide stores of the lungs, including the functional residual capacity (FRC), which stored and tissues. only a portion of the increased amount of inhaled carbon dioxide initially makes its way to alveoli, or air sacs, of the lungs, where exit and are absorbed the blood. It only takes short of time the dioxide of the lungs equilibrate to the increased amount of carbon dioxide being inhaled. When such equilibration occurs, substantially all of increase in of carbon inhaled realized the alveoli. At in time, the full reduction in the amount of carbon dioxide inhaled by the and the of carbon dioxide eliminated by the may be noninvasively measured. Assuming the increased amount carbon dioxide inhaled by the individual is sufficient to quickly maximize the concentration of carbon the carbon dioxide stores, amount of carbon exhaled the in same breath be used to accurately determine the VCO2 of the patient. The pressure of end-tidal carbon dioxide (petCO2 or etCO2), after correcting deadspace, typically assumed to approximately equal to the pressure carbon dioxide in the of patient is intrapulmonary the content of CO2 the blood flowing past the (cACO2), as well as blood downstream from the alveoli (CaCO2). The petCO2 which represents a measurement of carbon dioxide the lungs of an individuals is typically not representative of the true that are the lungs at the time the measurement is This is because, in the increased amount of carbon dioxide inhaled does not directly the alveoli. the carbon dioxide of the lungs, the functional residual and lung which not respiration, act as a buffer or This action includes the absorption and of in a manner
athing is initiated, the amounT of carbon dIoxidE thAt iS iNhalEd is Increased. Prior TO rebReathing, the lungs of the pAtienT hAVe beEN eXposeD to typiCAl AMOunTs Of CarBoN DiOxide, SucH as thosE experiencEd dUrIng normal resPIrAtion. InitiAllY, some of the inCreAsed caRbOn dIOxide ThaT is inHaled dURing reBreathing Is ABsorbeD By the caRBOn DioxIde stores of the lunGS, iNCluding the funcTional ReSIdUAL caPacIty (FRC), whicH cOmpriSEs storeD GaSES, And LUng tissues. ThuS, only a portiON of The incReAseD Amount Of inhAlED caRbon dioxide InitIally makeS its waY To the alVEoli, or aIr sacs, Of tHe lUngs, WHeRe GasEs EXit ANd Are ABsoRbed by thE bLoOd. It oNly tAKES A shoRt aMounT of tiMe for the carboN diOxidE StoRes of The luNgs tO eQuiliBrate tO the iNcReased amount of cArboN dioxide bEinG iNhaLeD. When SUch equIliBraTion occUrs, subsTAntIaLLY AlL of the increase in thE aMOUnT of carboN dioxiDE iNhALed is reaLiZed In thE ALveolI. At tHAt Point in tIme, the FUlL rEductioN iN the diFfEreNce BetweEN the Amount Of carbon DioxiDE inhaled by the pATient and the amOUnT OF cARbon DioXide eliminaTed bY The pAtieNT mAy bE NoninVasivElY MeASured.
Assuming the incReAsed amOunt oF carbon dioxidE inhaled by THE IndividuAl is SUfFIcient to quicklY maxiMize the conCEntratioN of caRbon dioxIde in the cARBon dioxiDe sTorEs, tHe aMOUnT of carbon dioxIDE exhAlEd by the IndIvidual In tHe sAme BreAtH may be useD to accurAtElY dEtErmIne thE vCO2 of the PaTieNt.
the PartiAL pressUre of End-tIdAl CArbOn dioxiDE (pETcO2 or EtcO2), AfteR coRrEctinG for ANy dEadspacE, is typicaLly ASsumEd To Be approXimately equal To The partial PrEssUre of cARBon dioxiDe in the alveoli (PACO2) of the PAtient oR, if There Is no IntrapulmOnaRy shunT, thE ContenT of CO2 iN the bLoOd fLOWing pAST tHe aLvEoli (cACO2), as WELl aS the Co2 cOnteNt of oxyGenated blood downstREam From the alveolI (CacO2).
ThE PEtcO2 mEAsURemEnT, WhiCH Represents a measUrement of cArBOn Dioxide in tHE luNgS of an inDividuaLs is tYPically Not represEntative oF tHe trUE GasEs that are pResent in The lungs aT The tiME tHe meaSurEment iS tAkeN. This Is becaUSe, iN rebrEathinG, tHe incrEased AmOunt of caRbon dioxide inhaled does nOt go diRectlY to The alveolI. RaTHer, The carbon DioxIde stores oF thE luNgs, inCluDIng thE funCTiOnaL ResidUal cAPacity (deaDSpAce) AND lUng tissues, wHICH do Not paRtiCIpate dIrecTly in respiration, aCT as a buffer or fiLter. tHIs fIltERing AcTion includes thE abSoRPTion and rElEase of carboN dioxide In A ManneR
athing is initiated, the a mount of c arbon  di oxi de  tha t is  inhaled is in c reas ed. Prior to rebreathi ng, t he lung s  o f the  patien t  h a v e b ee nexp os e dto ty pic al amou nts of car bon  d ioxide, such as  those exp eri enced during  no rmal r es pir a tion.  In itial ly, so m e of t he increa se d  carbo n  dioxid e th at i s inhaled duringr eb r eathing is abs orbedby th e car bon  dioxide s to res o f  the lu n gs , i ncl u ding the func tional resi d ual  capac it y ( F RC), w hichco m pri ses storedgase s, and lu ng tis s ues. Th u s, only  a por tio n o f th e  i nc rea se d  am o un t o f  in haled ca rb on  diox idei n i t iall y m akes  itsway to the al veo li,o r a ir sa cs, o f th elungs , wher e gas es  exit and are a bsor bed by th e b lo od.  I t onl y  takes  asho rt amou nt of t i mefo r t he  carbon dioxide st or e s  o f the lu ngs to eq ui l ibrate t othe  inc r e asedamou n tof carbo n diox i de  b eing in ha led. W he n s uch  equi l ibra tion o ccurs, s ubsta n tially all oft he increase i n  t h e  a m ount  of  carbon dio xide inha ledi srea l izedin th ea lv e oli. At that pointin  time,  thefull reductio n in the d i f f erence b etwe e nt he amount of c arbon  dioxide i n haled by  thepatientand the a m o unt of c arb ondio xid e el iminated by t h e  pat ie nt maybenoninva siv ely  me asu re d.
Assumi ng the i nc re as ed  am ounto f carbon  d iox id e i nhale d  by th e ind ivid ua li s s ufficie n tt o  qui ck ly  max imi ze  theconc e ntr ation o f carbondio x idein  t he carb on dioxide st or es, the am ou ntof car b o n dioxid e exhaled by the indivi d ual inthe  same  bre ath may b e u sed to  ac c uratel y dete rmine  t heV C O2 of t he  pa ti ent.
The p a r tia l pre ss ureof end- tidal carbon dioxi d e ( petCO2 or etC O2) , af t e rcor r ec t ing  f o r a n y  deadspace, istypicallyas s um ed to be a p pro xi matelyequal t o the partial  pressure  of carbo ndiox i d e i n the alve oli (PAC O2) of th e  pati e nt  or,ifthereis  no  intr apulmo n ary  shun t, the  c ontent  of C O2  in theblood flowing past thealveol i (cA CO2 ), as wel l a s  th e CO2 con tent  of oxygen ate d b looddow n strea m fr o mthe alveo li ( C aCO2).
Th e  p etC O 2  m easurement, w h ich  repr ese n ts a m easu rement of carbond ioxide in thelung s ofani ndiv id uals is typica lly  n o t  represe nt ative of th e true g as e s tha t arepresen t in th e lu n gs atthetim e the mea sur em e nt is t ak en .  Thisis b ec ause,in reb r eath i n g, the increased  amou n t  of c a rbo n dio xi de inha l ed d oes not go  directly t o thealve oli.Rather,  t he car bon  d ioxide sto r es of the  lung s, incl ud ingthe  funct iona l resid ualca pac ity (dead s p ac e )an d  lu ng t issue s,  whi ch do not particip ate directl yinr e spirat i on , act as a b uff er or f ilter. Thi s  fil t er i ng ac tion i nclude s the a b sor pt ion and  re l e ase of ca rbon diox i dein  a m anner
athing is_initiated, the_amount of carbon dioxide_that is_inhaled_is increased._Prior_to rebreathing, the_lungs of the_patient have been exposed_to typical amounts_of_carbon dioxide, such as those experienced during normal respiration. Initially, some of the increased_carbon_dioxide that_is_inhaled_during rebreathing is absorbed by_the carbon dioxide stores of_the lungs,_including the functional residual capacity (FRC), which comprises_stored_gases, and lung_tissues. Thus, only a portion of the increased amount_of inhaled carbon dioxide initially makes_its way to_the_alveoli,_or air sacs, of_the lungs, where gases exit and_are absorbed by the blood. It_only takes a short amount of time_for the carbon dioxide stores of_the lungs to equilibrate to_the increased_amount of carbon dioxide being_inhaled. When such_equilibration occurs,_substantially all of_the increase in the amount of_carbon dioxide inhaled_is realized in the alveoli. At_that_point in time,_the_full_reduction in_the difference between_the_amount of_carbon_dioxide inhaled by the patient and_the_amount of carbon dioxide eliminated by the_patient may be noninvasively_measured.
Assuming_the increased amount of_carbon dioxide inhaled by the_individual is sufficient to quickly maximize_the concentration_of carbon_dioxide in the carbon dioxide stores, the amount of carbon dioxide_exhaled by the individual in the_same breath may be_used to_accurately_determine the VCO2_of_the patient.
The_partial pressure of end-tidal carbon dioxide (petCO2_or etCO2),_after correcting for any deadspace, is_typically assumed to be_approximately_equal to the partial pressure of_carbon dioxide in the alveoli (PACO2)_of the patient or, if_there_is_no intrapulmonary shunt, the content_of CO2 in the blood flowing_past the alveoli_(cACO2), as well as the CO2 content_of_oxygenated blood downstream from the alveoli_(CaCO2).
The_petCO2 measurement, which represents a measurement_of_carbon_dioxide in the lungs of_an individuals is typically not representative_of the true gases that are present in the_lungs at the_time the measurement is taken._This_is_because, in rebreathing, the increased amount of carbon dioxide inhaled_does not_go directly to_the alveoli. Rather, the carbon dioxide stores of the lungs,_including the functional residual capacity (deadspace) and_lung tissues, which do not participate directly in respiration, act as_a buffer or filter. This filtering action includes_the absorption and release of carbon dioxide_in a manner