Arterial Blood Gases Made Easy

lain A M Hennessey

MBCha (Ho,n)'" Senior House Officer, Ne()noll)na/ E.dih'"') Brili$h 1.......uyCatAl..S'''''1l. in ..... bllc"ho.. Oau Acnto'lngue r«ord fc.w tillS book is ....a,Loble from the

KTlt~<Jl

Libruy

l.ibrwy 01 Consn- e.taJosb's in f>ublicatiM D..... AQtalos n-o:ined If1 thos book. It is thr.o n:sp<JnlIibility of t1.. laallng prKti~ "'lyin,l; on indcpl~ldenl~''''Kl knowl~ge of U'" pat~t. to OtlaDWv-lhe mllreatrnrtamly agn..~ on the first pomt: ABC analysis now play:.

il/1

indispensablf' role in the assessment and manilKcmcnt of pahf'nh; wltll a huge range of acute moollal and surgu"al problems. AccuratE' ABG interpretation is undoubtedly a fundamental skill U1 modem clink'" medianl::. On the SI.'('ond pomt, we hope this book ran bto of a~sislance. Throughout. our aim~ have ~,\ to emphasirial blood. From these values we can ass....s ttwo state of tJdJ--buse bolanCt in blood and how well lungs are ~riorming their job of gll5 ,:xc}Ul11gt.

Already the~ afC questions: what is meant by 'acid-base status'? What is.:l 'partial pressure'? Why do they matter? It helps to break things cJown.

Part 1 of this book is designed to answer the:;e questions. We start with a few p:2 con be

meU-venhlat~ alveoli :md not all vt:ntilatcd alveoli ilrt' pt'rfused with blood - E"Speeially Ul tht> prest>ncp of lung disc~. This problem is known as ventilation I perfusion (V /Q) mi'lmatch. lmagme if alveoli in one area of lung are puorly venbJittPd (e.g. duc to collapse or consolidation). Blood pitssmg thot' alveoli n>tum.~ to the arterial circulation With Ie::;:; 0, and more ('01 than normal This is knuwn as shunting l Now, hy hyperventilnting. we can shift more air in and out of our remaining 'good alveoli'. nUs allows them to blow-uff eXlra C~ SO that the blood passing ttwm can offload more CU:!. 'The luwer Co, in non-shuntrtl blood compertSittH fOf" the higher COl in ..hunted blood, m;untaming tht! poleD,. The :,ame docs NOT apply to uxygt!J\i1lion. Blood passing 'good alveoli' is not able to carry more 0, Mause ils hM>moglobin i::. alrt>itdy maximally :xIturatcd \,nth for the low O:z levels in shuntt"d blood. and the p~ falle;.

Key point V/Q mismatch allows poorly ol()'genated blood tu re-cnter the arteriill circulation, thull low~ring Pao" and Sao2" Provid~ ov~rall

does not

I~ad

il)veolar ventilation is main~ed, V/Q mismatdt to an inC~ilse in PacOr

'Tl\(> tPTITI also applies to bluud lh"t bypasses alveoli altogelher (anatomICal ~'W1IUlg)

14

PULMONARY GAS EXCHANGE: THE BASIC",S,--_

.J=~=I ''''''''' O2

so, 11m

so,

",,.

..CO2

'"

'''"'

.....- -

--

so,

so,

....... CO2

15

PUlMONARY GAS ~CHANGE. ,~

mr BASICS

and oxygenation

The fraction of inspired oxygen (FiO:J refers to the percentage of 0: m the air we breathe In. The FiOz in room air IS 21 %, bul can increast"d wIth supplementaJ~.

"*

Aluw PacJ.z may result from t'ithcr VIQ mismatl..:h or inadequate vrnblabon and, in both ca~, increusi.njl, the F~ will improve the PaOz. 'l~ ~)(act r~ rcquirem..nt vane!:> depending nn how severely oxygenation is impalrM and will help to d ~ the chokP of deli...,cry device (figure 8). When thf' cause is inadequate ventilation it must be remE>mbered that incrc3Sing riO, wIll not rev~ the rise in P~. Supplemental ~ makes ABC analysis more complex as it can be difficult to Judgc whether the P/Kh is appropriately high for th~ F~ and, hE"llet", whl.>thcr oxygt"nabon lS impaired. A useful rule ot thumb is that thp diffeft'J)(.'C betwffn r~ and POOl (in kPa) should not normally be ~r~ater than 10. Howevpr there is often a d€'gree of uncertamty as to !he pl"€'Cise FiO,. and, if subtle impaU"lucol is suspected, thf' ABC should be ~..ated on room air.

OXYgMI et.livery

devic.,

Nasol fNO"gt. f~ < .. ~. ComfOl'tol:h ond comenient FiO, specific: depends on flaw rem t1-6 Vmin) and venhlabon

n0n-

Stondard fm;" mask: fiO, 30-50% at flow rotel6-10 Vmln bul ImpuKise Mot COllie CO:! relention ot flow, < 5 Vmin ('rebreolhing'). not 1IJefu1 Jar providing 10- ft0:2

100

~ rno~ F~

24--00%. Ddivers fUced, prediclabl. Fi0 2• Ideol for providing controlled, occurote O:z therapy allow CorN;ef\lfQl;QI1S fixH p«fOiilNilKe (high&wl

meuk wiIh re••nooi. ft0:2 6IJ...8O".li.. Con ochie¥e _ higher fiO:z with IighHifhng rnosJc Useful for ano.llefm UM in respiratory foe.

emergencIes fndotracheGl intubation: fi0 2 21-100%. Uled In soyerely un......11 potierlb with very high ~ requiremenls, especioMy wifh venhlolory !oillire. Patient is sedoltid ond InlInfusion.

11

rnsoRDERS OF GAS EXCHANGt:

5pee*-(e.g. "'JOC*cIIl ila.......,)

.,

.
olccompamed by a rise in bicarbonate (HCO~), which pr~rvcs aCidbase balancp. Howcwr, p"tiPTlts with chJ'()r'lic type 2 irnpaUID\.'n1 who expcrienn> a further sharp decline in ventilation will also holYC a rapid rise in PaC02 tacute Oil chronic), le~ding to aCid .I.ccum\llation .md low blood pH (Table 1.3.2). Supplemental ()2 improves hypoxaemiJ; bUI nol hypercapma, ~ trf'atment of type 2 ft>Spuulory impainncnl should also include measures to improw \'ffitilation (e_g. w.ersal of sedation, reJjpf of airway" ~Iruclion, a';si"tetJ ventilation). Thc OVPrzealous lldTlunistration of supplemental 0,. to som!' patients with chnmic ty'pf' 2 impainnent may furthcrdep~'iventilation by abolishing hypoxic drin> (p. 7). Pulse oximetry provides no mfurmation on PIICOz so is nut a suitahle sub:.tilutC' for ABC monitoring in tyJXl: 2 ~uatory impairment.

22

OIS, -

A 7.45), there is an alkalaemia. An acidosll'l .." any pnx:ess thallow~ blood pH whereas an alkalosIS

is any pt'ClCeS6 that

2'

r3lSeS

blood pH.

AClD-aASE BAlANCE: THE 8ASICS

What as pH? The pH (power 01 hydroget'l) Kale l~ a ~Implln.d 'W'a'f of expreuing large ~ in H' =ncerflluhoo, though if you'... not corne ouou jf before you

might think. II 'NO$ d.t.iglMd iuu to

confu~ you!

It i$ a MgUtive logarithmic KoIc fFigvfe 101. The 'negative' meon$!hut pH ~ get lower as !he H' concentration increoMli flO a pH 01 7 1 ;$ more

OCIdic thon 7.21. The 'Iogarilhmic.' meons thol a Mlift in pH by one numbel r.prelents a 10-f01d chonge in H' concenlfolron (so 7 Ii 10 times more ocidic than B)

Why i.

aci~s. bolance

important?

J;or cellular pI"0CCSS4.'S to occur effiCIently. Ihf. II' concentration lJ\USl be kcpl within tight limit!!. Failure to maintain pH baJarn.."C Ical.!s 10 lIlefficient cellular reactions and ultimately death (Figure lO).

pH

..

735 6.9

'16

7JJ

100

I.'

12

""

6J.l

7.3

1.45

I I

75

1.6

71

1~.6

25.1

20.0

7A

I

Sl

:5.8

"

35

I~

'5.8 Alu'csis

... , is

..... , . pHM """

27

ACID-BASE BAl.ANCe THE BASICS

MAINTAINING 4CID-8ASE BALANCE What generates H+ ions in our bodies?

n.e breakdown of fats and SUgMS for energy generates ~ which, when dis:dvro In blood, fOf"DlS carbonic acid (see Box on page 211). M~abolism

of pmtPin produces hydrochJonc, :lulphurit: and other so-called 'metabolic acids'

H· ions mu.st, therefore, be rcmovL'd. to maintain normal blood pi!. What removes H+ ion. from aur badies7

Respiratory mechanisms Our lungs are responsibl~ for removillK CO2_P'ICO:!, the parti..,1 pressure of carbon dioxidt> in our blood, is determinoo by alvL'Olar vCl1tllo:ation. If C~ production is altt"red, we adjust our breathing 10 exhale more or k'SS COg as IlI.'."CSSary. 10 maintain PlIC'O;z within oormallimifs. The bulk of the acid prodlK.L'd by our bOO.ies is in the form of COz, so it is our lungs that excrete the vast majority of the o:aud load.

Renal (mefobollc) mechanisms The kidneys art' r(>$poru;ible for eXcrelmg rnmbolic acids. TIleY ~'l,;rctc H' ions inio urint> and reabsorb HC0.'l from urine. HCo, io:t a base (and therduA:' taoolic rcspou!>eS tak(> days to develop.

Jwt one equation•••

~--This one eqoolion is c:rucial to understanding ocid-ba.se bolonc:.; ~o +

CO2 +-+ ""Cal .... H' + He0s

Firs/ly It show51hot C~, when dissolved In blood, becon'lfts on ls of lc.ctoncs in the unne, It would be obvious thai Ih... melabolic acid~ls was a primary pJ"O("~ (diabetic ketuadJosis).

It ;$ not ~ «)$Y kl ~ two pnmory oppoo$Ong p«X:flM$ from a «WTlperuoted d,w.bonce ;. more pr«:iMl

method Ihon !hot de~

obo.... involvM cakvlating Ihe ellpoc.oo compensatory response lor ony g,ven primary di1turbonce. Howevtlr the~ colculations are usually unneceuaryond ale not required for the case ~r~ in Pan 2.

ACID-BASE BALANCE: THE BASICS

-----,

""""'" """""

rtgUre 14 Fully compemoNJd meIOboIic ocidc)JIJ

33

ACID-BASE BALANCE: THE BASICS

MIXED ACID-SASt DISTUIlBANCt When d primary re.piratory disturbance and primary metabolic diduced. renal excretIOn) or through exct'SSi"'e loss of base (HC~). c.l1culaling the

anion gap (sec over) may help to ~tab~h the caU1Ie uf a metabolic acidosis. Metabolic aridOf;is is recognised on an AI}(; by low HCo, (and negative bas 70) may lead to arculal0'1' shod:, ~ dysfuncLion, and, uILimatcly death. Specific caU$CS or mdabolic aadlY.>1S are chscussed in greater detail ill the relevant Casel in Part 2.

36

DISORDERS OF ACID-BASE BALANCE

The anion gap In bkxxl, posilivefy charged ions (cations} musl be balanced by negotivefy chorged ions (onions} 10 maintoin flhtctron8lJlmlily_ Bul when lhe moin colions [Na' + K') are compared with the main onions (et" appears 10 be a shortoge 01 onions or an anion gop.

Anion gap

-+-

HCOJt there

=(NG + K) - (el + HC03) {Nonnal = 10 -

18 mnlOl/L]

The eop b mod.. up of unmeo""red onions wei, u, p1,u>pIKJ'" UIlJ >ulpIKJIt;

and negativefy cholged proteins (these are difficult to measure}.

A raIsed onion gap (> 18 mmol/L) therflfarfl indicates the presence 01 increased unmeasured anions, "9. !octole, solicylalc.

A note on .,. Iodic: ocido!5i!5 This cornman cause 01 melobolic <xidosis <Xcurs whCfl lissues roceive on inooequa", wpply 01 0 1 due 10 e!lh"," hypo.wemia or impaired perfusion. Norma! oelobic metabolIsm {which relies on 0 21 is then reploced by anaerobic metabolism (which generales lactic odd). lactic acidosis;s l!Ierelore 0 markIN 01 tiSSlIe hypoxia ond a useful indicator 01 ~firy in "voriety of conditiOM, ,,,dudir>g \oeVCfitct a mf'taboh ,11kalosis

RI:SPIRATORY ALKALOSIS A rl>SPllMl1ry ill!.;IlIMI::i III ii n

~~.

,n P

anJ

15 cau~' ('oliMeral circulation from ulnM arteryl (rigure 20).

• Position the p,ltknl's h 10 insprt the need Ie slowly to minimise the risk of arterial spasm.

• When the llt.wle is in the artery a flash of pulsatile blood will appear in the barrel of the needle. Most ABC syringes will th('tl fill under arterial pr"'SSllr(> (see info box over page). •

Obtain at least 3 UlL of blood before withdrawing.

'However, the value of routinely pedorming a modified Allen's test prior to arterial puncture has been questioned, in part due to its poor SP1lSitivity and specificity for identifying inade.l' ,atE' col1aleral cin:ulalion. (Slogoff S, Kc-"ts AS, Arlund C. On the s..... fcty of cadi"l artL'rY (;;lJUlul"tiOIl. An"esthesioloj;\Y 1983;59:42---47). 44

ABG SAMPLING TECHNIQUE

ngure 19 PO$jtioning 01 _i511ot A8G sompIing.

Arleriol sampling !porticvlor/y from the rodiol ortery) can be extremely pain/vI; dlscomforf can be reduced by inj.cring 1 ml 011 % lidocaine, at !he needle inMtrtion ~ite priOJ 10 wmpling

Venous _ &16.iaI lilac II?

Ooft. non.pul,otil. blood that requirti monuoI wction 10 os.pimle often inctocole$ a Y8OOt.I$ ~ ~ In _ e modVcOl'dioc orr.g). AnoIher dve " when ~ on A8G OldywS 's ''9n~1!y lower than 500: on pulse Wtirnelry.

.,

ABG SAMPliNG TfCHNIQUE

AFTER SAMPLING

•

Once duequatc blood has bft>n obtamed, remo,'c the needle and apply firm, d1rect pn.'S:iourc to the samplp ~lle for at least 5 minutes (and until bl~ing has cea:x'd).

•

lliposc of all sharps and contammated matcrials approprialply.

•

l'nsHrt> that no air bubbles are present in the samph~, as thcy may compromise results. Any sample with more than very fili~ bubbk--s should be discard:d.

• The sample Iohould be ;lnaly~ promptly: if the transit lime is likely 10 exl'ffd 10 minute'S, then the syringf' c;hould be blon.'\.! on crushed ice, •

..

If sampling IS WlSu«cssfuJ it is often advbablc 10 repeat lhe test on the OPPOSite wnst ib e\'Cfl sliW11 irritation of the artery on the first n'pntilahon. It also u.lltlllifics the pn>sencp of metabolic lkidosis and alkalosis.

2. TO ASSESS ILLNESS SEVERITY Thp four ABC valUel> l>hown in the t.1ble bl:>low, In aJditiun to owrall clinical QSHSSmm/, may help id\;~lIti{y critically \lnwpl1 patients rt:y,uiring Llq~ent inteTVf>ntion. Pao, < 8 kPa

"'0,

Bdow 8 fo{l~ in Pro, produce a marked redudion in Sox>, Ithe 'sleep' port of 1M 0, dl$KIClOlion curvel and hence 0, content 01 bbod Rising P0c0 2 Since .eool compem.ation occurs ewer dayJ 10 weeks,

ocu~

riS&s in PocO]

prodoce 0 cOf.espooding drop in pH. In respiratory distress, rising POCO] often signifies exhaustion and

,e:ve!$01 of !he

-

proefl~,

at: < -10/HC01

c

15

on omil'lOl./S s'gn. Polienls require Ulgen!

Ieoding to ven"lotory foilure or auisted venhlahon

15

This ....:rtu. is included in -..01 ~_...Iy 5COring syVelns arK!, when d""" kl Iodio: ocide»is, indicates 5e\Iere hypoluO of cenuktr IeYeI H+ > 55/pH


lcriorabun and jl1d~e the cffeness of therapeutic inlprventiol\:>, It i:o essential for tilrating 0, therapy in patients with chronic tyl't! 2 rt'Spiratory f.lilurc and for optimising \'enhlator YffinKS.

Box 1.7.1

Clinkal scenorios In which an ABO is us.ful

Establishing dtagnosb ond aSMsstng i1lneu MYel ilt 5u~ hypercoptiio

It PocoJ

Drowsiness, Roppmg Iremol', bounding pvI:IC~ Clinkol dete.iorotion in polient with chrOflic type 2 re$.pirOiOry impoirm.nl Of' prediipO$ing condItion le.g. chronic ob~ud1Ve pulmonory diseas.e\ Suspeded severe hypoxoemlO Very low Of unrecordable 0, saturaTion; CYOrlO$i~ Severe. prolonged or WOfSflning m,plrQlory distress Smok.e Inhalotion Ica.boxyhuemoglobln level) Hypervenlilonon (confirm I P~, check kw- UIldertying m.lOboIic ocidoslsl At,. detel'lOl'ohon III consciousne!oS Any leVu.ely unweH potient' Pulso oximetry unreliable 01 $U~piclouS re~ull As port of a 'A 45 = ocidoemio Concentration of free hydrogen ions: lhis is a measure of how addle or i1lkalinc a ~lution IS.

pH (7 35-7.45)


96% on room oir)

0 1 saturation of haemoglobin: the ~tage of o,.-binding site> on lib proteins occupied by ~ molecules. This is a measure of how much of lhc blood's ~-earrying capacity is being used. Sao-l refers ~ifical1y to the 0" saturation of rJrtmol blood.

,.

COMMON VALUES AND THEIR MEANINGS

HCOJocl (22-28 rnmol/ll Actual bicarbonate: the plasma bicarbon.:ttc concentratiun caiclilutcd from the actual pe02 allu pH JIlepiratory compensaoon takes minutes. Overcompensation does not occur. An apparent compensatory response could repl"e5ent an opposing primary process. •

Note that with a very mild acidaemia or alkalacmia both PaC0 2 and HCO) may be just within the "normal range" (considered to be a mIld mixed aad-base dISturbance).

-,-

PlCD,- 4, 7-U kPiI or

~5mm1-1g

BEj-llOo2j ~11 (22-28 ~

pH (7.35-7 45)

If' (35-45 Md4)

~ ~ . z

~ >

§ ~

MAKING A!G INTERPRETATION EASY

••

APPENDIX 1

The A-o erodi«llillhe difference Dtt.o.een !he ~ in oNeoIi IPAo"l ond the Po, in ortef"ioI biood lPa011. p~ is meowred Of! A6G bur PAc" hos to be calculated us.ng !be oIveoIor gc» equation 1- box beIowj. A-

G

flruclien' • f1'~ - ,..."

1111 noflnolly bs thon 2.6 i.:Po (20 mmHg). oIIhough it increo~ with oge

and F~, This meam Ihat: I. the l'lOl'moI range fOf Poo, IoUs wilh oge 2 me A-o grodient is most accurate when performed on room air

PAo, (kPo)

= (1;0, • 93.1) - (Poco, • 1.2) ~

Neo:2 ImmHg) = l'iD, • 713) -

5.

(I'ato, .. 1.2)

THE ABG IN PRACTICE CASE 1

History A 25-ye-ar-01d man, with no significant past medical ~toI)', presents to the emergency de-partment with a 2-day history of fever. productive rough and woT5elling breathlessness.

Examination He is hot and flushed with a temperature of39.3"C. He does not appear distressed but is using accessory muscles of respiration. There is diminished chest expansion on the left with dullness to percussion, bronchial breathing and coarse crackles in the left lower zone posteriorly.

""'"

lte:5pirotory role BIoodpn=~ ~ lroom airj

58

HM beats/min 28 breaths/min 118/70 mmHg

"""

Arleriol blood go~ 23/7/2006 Unit no,: 00654545

On room air

ID- John Simpson

No 98%) (0." - 1.51

13.5--51

QueSt101U

1. a) Describe her gas exchange.

b) Describe her actd-base status. 2. \\'hat is the likeliest diagnosis?

801

THE A8G IN PRACTICE

CASE 4

History A 78-year-old male on a surgical ward is found unresponsi\'e, having returned, a few hours previously, from a complicated open cholecysteclomv.

Re...iew of his charts J'e\'eals he has recetved three 10 mg injections morphine since returning to the ward, in addition to the morphine delivered by his patient-controUed analgesia device. Examination

The patient is unresponsive with ~llow respirations and bilateral pinpoint ptJpils. PlIlsll role Respirolorl' role

90 beob/min 5 breatlu/mirl

98/64 mmHg

8Iood preullle 500,

....

8M

5.6 mmol/l

u

..

i

THE ABG IN PRACTlCE

,Ivftwel blood gos 18/09/2006 l}r1it (lCl.: 6799986 [l Henry Spc~~

".

pH

"'"

""

Bicarb

"

,"'"

~No

a ;Co'

'*'

Glucose

On 28%0"

Normel 65.4 nmcl/l 7.18 B.2 ~Pe 62 mmHg 11.76 kJ'e 87 mmHg 22.4 mmoVL -1.5 mmol/l 99.8~

1

4.4 mmol/l 137 mmol/l 103 mmoI/L 1.16 mmeVl 11 g/dl 3.9 mmol/L

{35-45/

(7.35-7.45) (47...o.0J {35-451

I> 10 61 [> SOl

[22-28)

1-2-+21 (> 98'l.j 10..4-1 5) p.5-5J 1135-1451 (95-1051

11-1.251 !I3-181 (3.5-5.5)

Questions

1. a) De$(:ribe his gas exchange. b) Describe his acid-base status.

t What IS the m06t Wc:ely diagnosis? 1 What treatment does this patient require?

ThE ABG IN PRACTICE

CASE 5

History A 75-year-old man IS brought into the emergency department by his family. He is extremely short of breath and struggling to speak. Following a conversation wilh his family it emerges that he has a long history of chronic obstructi\'C pulmonary disease.

o.'Cf the lasl 3 day'S his breathing has worsened consideTably and he has expectorated increased \'oIumes of sputum.

Examination The patient is struggling for breath and appears extremely dis,lre". He exhibits signs of chest h)-pcrinflation and is breathing through pursed lips. Breath sounds are generally diminished but there are added sounds.

PulMi

120 beals/min

Re~rak:Hy JU'tI

26 bnlolls/min

8Iaod preuure

150/80 ll'ImHg

Temperature

36·C

Sa0 2%

'I"

..

THE A8G IN PRACTICE Arterial blood gas 10/07/2005 Unit no.: 77655349 ID: Joseph Spielmol1

H' pH Pto"

Po, Bicorb BE SPO, lactate K

No CI iCa'

Hb Glxose

39.5 tlmol/l 7.40 4.9 kPo 36 mrnHg 5.6 kPo 44 mmHg 23 mmol/l -1.2 mmol/l 80% 1.0 4.1 mmol!l 137 mmol/l 99 mmol/l 1.1 mmoljl 16.5g/dl 3.8 mmol/l

On oir

Norma! (35-45) [7.35-7.45) [4.7-6·01 (35-45) [;. 10.6J [> aOJ [22-2a} {-2-+21 I;. 98%) {O.4-1.5] (3.5--5)

(135--145J {95~105]

(1-1.25) (13-18) (J.N.51

Que5tions

1. a) Describe his gas exchange. b) Describe his acid-base status. 2. Should you provide him with oxygen?

.7

THE ABO IN PRJI.cllCE

CASt 6 History

The pabent from the pre"ious case is treated in the emergency department with nebuliscd bronchodibtors, oral prednisolone and antibiotics. He is then transfened to a respiratory ward where he it administered 28% oxygen by a fixed concentration mask. Despite this, his Sa0 2 (as measured by pulse oximetry) increases only marginally and there is no imprO\'ement in his symptoms. Examination

Examination findings in the chest are unchanged but he now appoool emausted and slightly confused.

--- - - ---

Re~loIory mle

120 beats/min 16 breath~/mln

8bxl pressure SoO,

120/80mmHg 83'X.1on 28% Q,]

Temp.... alure

Moe

Pulle

-

A repe.1t ABG is performed (6 hours after the first ABG).

THE ABO IN PRACTICE ,ArMori'" b£ood gas 11/07/2005 Unit no.: 77655349 10 joseph Spielman

On 28% OJ

N~ma1

rwnoI/l

W

51.4

oM

7.29 6.9 kPo

"'" II>,

-'" "

511>, lactate K No d

..."".

Gtuco~e

52 mmHg 6..4 kPo 48 IfImHg 24 mmot!1. -0.9 mnol/l

....

1.0 4.0 mmol/l 137 mmol/l. 99 mmai/l 1.1 mmol/L 16.5 g/dl 4.2 mmol/l

13>-- 10.61 (> 80) f22-281 1-2-+2} I> 98'%) (0.4-1.51 (3·5-51 (135-I45J (95-105) 11-1.25) 113-181

13.5-5.5}

Questions

l.a} Describe his gas exchange. b) Describe his acid--bi'lsc ~t"tus. 2. Should his oxygen now be stopped?

••

THE ABG IN PRAcnc:e

CASE 7

History A 77-year-old woman is admitted to the stroke ward with right-sid weakness, visual disturbance and slurred speech. She is commenced on nasogastric feeding due to swalJO\\ing problems but has a large vornlt 24 hours later. She initially appeal'S well but oyer the next few hours develops .....orsening breathing difficulties. Examination

She is agitated, distressed and pyrexial. A dull percussion note and coarse crackles are evident at both lung bases. Other than acute confusion, neuroIogkal findings are unchanged from admission. Pul$e Re$j>irolory ro)e

Blood preUl,,Ire SaO, '''''' 0,)

70

92 beob/mln 28 breotlu/min 112/65 mmHg

.,,,

THE ABG IN PRACTICE ·Merial blood go$

On 60"4 O 2

23/7/2006 Uril no.: 00654545

II). Mrory Woteo

No""" W

38.8 nlrlOllt

f.l5-45J

pi
sscd. Other than t1lchypnoea and a mild sinus tachycardia, cardiorespiratory examination is unremarkable. Electrocardiogram, chest X-ray and peak tlow measurements are all normal. Pulr.e Iod gas

Oneir

12/11/2006 l)roil no.: 12534943 !O Tril'lllY Forqhuof

... pH Ito,

29 nmolfL 7.53 3.1HPo

Ib,

24 mmHg 1".3 ~Po

Bicorb

108 mmHg 24 mmol/L -1.8 mmol/L

No<mal (35-45) {7.35-1.451 (.4 7-6.01 135-45) I> 10.61 I> BO) 122-2BI

BE 500,

99%

1-2-+21 (> 98%)

eoc-

1

10·4-1.51


2. What is the most likely cause of her breathlessness? 3. What would be the most effe...·th,e way of improving ~ delivery 10 her li.%u('S?

83

THE ABC IN PRACTICE

CASE 14 History A 78-year-old woman is admilled to the emergency department wit sudden-onset, g('fll."ralised, severe. abdominal pain. She describes the pain as being colicky with no particular f 10.6}

I> 801 (22-2.) {-2-+2) (> 98%1

3.2

10.4-1.5)

4.6 mmol/l 135 mmol/l 96 mmol/l. 1.16 mmol/l 12 g/dl 3.8 mmol/l

13.5-5) 1135-1451 [95-I05} {I-US] 113-181 (3.5-.5.51

Questions

1. a) Describe her gas exchange. b' Describe her acid-base status. 2. What is the most likely diagnosis?

IS

THE ABG IN PRACTICE

CASE lS History A 35-year-old woman with type 1 diabetes is brought to the emergency department by ambulance after being found in her hou severely unwell. Following a discussion with her parlner it emerg(>'S ~ has not been eating for the past fe-.\' days due to a vomiting illness and, as a precaution. has also been omitting her insulin.

Examination On examination, she appears drowsy and peripherally shut-down, with very dry mucous membranes. Her breath smells of acetone an her respirations are deep and sighing.

I M" Blood

preswf.

Resplfatory fOIe

! ~ (blood glLlOO5eI

130 beob/min 100/60 mmHg 26 breaths/min :>- 25 mmol/l

Ph}"Sical examination of her chest and ..bdomen is unremarkable.

••

THE ABG IN PRACTICE On 10 L ~ by mask

Arterial blood 9Q$

27/02/2005 Unit 1'10•. 7773S566 10: IlJa Tonner

Normal

H' pH

-.

Bicarb

BE SA>,

""K No C! jCo~

Hb Gi... :;o~

88.9 nmol/L 7.05 I 5 !.Po II ml'llHg 28.4 kYo 187 mmHg 6.0 mmoI/l -25.2 mmoI/l

99."" I 4.6 mmol/l 141 ",moI/l 96 mmol/l 1.25 mrno!/l 12 g/dl 35 mmoI/l

135-451 {7.35--7 ....S} (4.7-6·01

135-451 I> 10.6) I> aO) 12.4-30J 1-2_2} (> 98%1 (0.4-1.5)

IU-51 (135-14.51 (9S-105J

{I-1.25J 113-18)

(3.5-5.51

Questions 1. a) Describe her gas exchange. bl Describe her acid-b."\Se status.

2. Calculate the anion gap

3. What is the m05t likely diagnosis?

•

.7

THE ABG IN PRACTICE CASE 16

History A 37-year-old well-known local vagrant is brought into the department unconscious. He was fowld near a bottle of vodka and half-empt)' bottle of what appears to be methanol. It is unclear if he has drunk any of the contents. Exomination

The patient is unkempt with a significantly reduced conscious level (Glasgow coma scale score:= 9). There are no apparent focal neurological abnormalities.

II

THE ABG IN PRACTICE Arteriol blood gos

On air

10/07/2006 Unit rlO,: 35477899 ID: Gary Sooness Normol

W

63.3 rlmol/l

(35~451

pH

(7.35~7.45)

Bicorb

7,20 3.3 kPa 25 mmHg 12.8 U'a 96 mmHg 9.5 mmol/l

BE

-16,2 mmol/l

Sit>,

97.8% 1.3 4.5 mmotjL 136 mmol/l

Pco,

lactate

K No

(I

iCo' Hb Glocose

99 mmol/l \.1 mmol/L 13.5 g/dl

3.8 mmol/l

{4.7---6.0] (35--4':::')

(> 10.6) (> 80) (22-28) (-2...-+2) (> 98%) (0,4..-1.5) (3,5-51 (135-145) (95-1051 fl-L25] 113-18) P.5-5·51

Questions 1. a) Describe his gas exchange.

b) Describe his ilcid-base status.

2 What is the anion gap? 3. Is the acid-base status consistent with methanol ingestion?

.9

THE ABC IN PRACTlCE

CASE 17 History A 52-year-old man is being investigated on the urology ward fOT recurrent renal stones. He also complains of mild fatigue and lethargy. There is no history of gastrointestinal disturbance and he is not on any regular medi1:ations. Examination The patient is weU and clinical examination reveals no abnormalities

As part of the investigations an ABC is obtained.

90

THE ABG IN PRACTICE ArrcrioJ blood go~ 23/04/2006 U",JI no.: 27634943 10: Roger Porry

On air

Nonnol

H'

pH Ito,

""

S801 122-281 1-2-+21 I> 98%1

10..4-1.51 (3.5-51 [135-145) [95-105)

(1-1.251 1l1.5-15.5)

13.5-551

Questions

1. a) Descnbe his gas exchange. b) Describe his add--base status. 2. CakWate the anion gap_ 3. What is the likeliest diagnosis?

.,

THE ABG IN fl:ACTlCE

CASE 18 History An 18-year-old is admilled to the toxicology unit ha\ing taken a large overd06e of an unknown substarKe 5 hours earlier. She complains of nausea and a high-pitched noise in her ears.

Examination On examination, she is mildly confused. Her respirations are increased In both fale 10,6) (> 80l (22-281

160 nmol/l

6.' 4.8 kPa 36 mmHg 32 \;Pa 240 mmHg 3.8 mmol/l -20 mmol/l 100% 9 4.5 mmol/l 136 mmol/l 96 mmol/l 1.1 mmol/l 14.0g/dl 4 mmoJ/t

1-2-~2)

I> 98%1 {0.4-1.5) (3.5-5) 1135-1451 {95-1 051 11-1.25) 113.5-18.5) (3.5-55)

Questions

1. a) Describe his gas exchange. b) Describe his acid-base status.

2. 'vVha1 is his prognosis?

97

THE ABG IN PRACTICE CASE 21

History A 59-year-old male with a history' of alcohol excess presents to the emergeocy departmc:nt with a 3-day history of 5e\'e"re uppc:r abdominal pain. He now also reels \'ery' breathless. He ddmits to drinking up to 100 units of alcohol per week for the past few wee

Examination appears very unwell. He is tachycardic (120 beats/min) and hypotensive (75/60 mmHg). Th is marked epigastric tenderness.

Th{' p.."\tient is in f'vi(jpnt

(ji, Bicarb BE 51'>, lactate K

No

On air

Normal 135--451 17.35-7.45} 14.7--6.0)

135-451

I>

10.6)

I> BO)

122-281 l-2-+2} I> 98%1 10..4--1.5) p.5-5} 1135-1451 195-105) 11-1.25) 111.5-15.5) 13.5-5.5)

Questions 1. a) Describe her gas exchange.

b) Describe her acid-base status. 2. \Vhat electrolyte abnormalities are present?

3. \Vhat lreatment will correct the acid-base and projectile vomiting. The paIT'nts report that he had an uncomplicated delivery with no postpartum complications. He initially fed well, appeared to be thriving and gave no cause for concern but has deteriorated markedly over the past 2 weeks, vomiting all of his meals and now losing weight.

Examination The child is agitated, crying and is malnourished. His mucous membranes are dry and oncxamination of his abdomen a small m is found in the epigastrium.

102

THE ABG IN PRACTICE capillary blood g05 05/10/2005 U"iIIlO.: 28734943 ID: Richard Barter W pH

Pw,

BiUlrb

BE

"'"

laerate

K No (I iCo'

Hb

29 Ilmol/l 7.54 6.1 1&'0 .45.8 mmHg 11.2 ~Po 80 mmHg 37.5 mmo!/l +14 mmol/l

99% 1 2.5 mmol/l 135 mmol/l 86 mmo!/l 1 mmol/l 1B,O gJdl

On air

Normol {35-451 17.35-7..451 14.7-6.0} tJ5-451 (> 10.6) (> BOl (22-2BI (-2-+21. (> 98%1 (0.4-1.5)

13·5-51 (135-1451 (95-105) (1-1.251 (13.5-18.5)

Quesfions

1. a) Describe his gas exchange. b) Describe his acid-basc status. 2. Considering the pH and He03: is the PaC~ IUgher or lower than you would expect? 3. What is the underlying diagnosis?

'03

THE ABG IN PRACTICE

CASE 24

History A 36-year-old pregnant woman 011 the maternity ward complains feeling short of breath. She ha~ no other symptoms and no relevant past medical history.

Examination On examination, the patient is heavily pregnant but appears otherwise well. Examination of her chest re....eals no abnormalities.

Pube Respiratory role Blood prenure

110 beots/mirl 20 breaths/min 112/100 mmHg

Temperature

36.6"(:

0,%

99%

An AI3G is performed.

104

THE ABG IN

AfMriol b600d gas 18/08/2005 l,klill'lO.: 27634943 10 julie Dcnoldson H"

pH Ito, Po, Bicarb

"_Ie , SIb,

No

C; iCa' tf> GI. 98%l 10·4-1.51 13.5-5) (135-1451 (95-105J 1I-1.2S) (11.5-15.5j (3.5-5.5)

Questions 1. a) Describe her gas exchange. b) Describe her itdd-base status. 2......'hat is the mosllikely ell.ptanation lor the low

P~?

'0'

THE ABC IN PRACTICE

CASE 25

History A 55-year-old woman on till> orthopaedic ward complains of suddcn-onset breathlessness and pain on the left-hand. side of her chest. She underwent elccti\·e knee replacement surgery 4 days previously and has!x.'('3\ immobile in bed since the operation. She is otherwise well with no rele...· ant past medical history. Examination

The patient appears well but slightly short of breath. Other than mild tachycardia and tachypnoea, examination of the cardiovascul and respiratory systems yields no positi....e findings and there is no clinical evidence of deep-vein thrombosis. A chest X-ray reveals no abnormalities and an electrocardiogram shows only sinus tachycardia

""~ Re1piratofy rlJlelltal oxyg~ to COtTfft the hypoxaemia and appruprialP antibiotic; to ~at the infection. In a patient sIKh as tlus, with moderate hypoxaemia and no vt'fltilalory impairment, monitoring by pulse oximetry is more appropriolte than n>peated ABG sampling. lru.lications for further ABC analysis would include f'igns of exhaustion or hypen:apnia (p. 23) or a further :.igmficant ~ in ~

109

ANSWE~S

CASE 2 1. 2.

01

QfOflic I)'pe 2 respirolofy impoirmenl

b)

Compell$Oled

f~irolofy ocidosh

Chrooic type 2 respirorory irrpoirment due 10 morbid obesity

At first glance it may be difficult to determine whether this ABC rcp~ts respiratory acidosis with metabolic compensation or metabolic alkalosis with respiratory compensation, as both give a high HC03 and high PtiCOz. The best due is the pH (or H') which, ahhough just within the normal range, is on the brink of acidaemia. ThIS would represent overcompensation for an alkalosis and. therefore, sugg~ an acidosis as the primary abnormality (overcompensation does not occur). The mildJ}' impaired o)()'genation is consistent with the degn.-e of h}l>o'H,:ntilation. 1be likeliest caU5e of chronic type 2 respiratory impairment in this case is se\"ere obesity. Around 20% of individuals with a body mass index greater than 40 have chronic hypercapnia from restricted ventilation (pickwickian syndrome).

110

ANSWERS

CASE 3 1.

01

Mild Iype I fespirotory impairment (wirfl morhd hyperventilation)

hi 2

Uncompensated resplfclory olkalosis Putmonory embolism

This poltient is a young. fit. non-smoker with no history of lung problems but, despite hyperventilating (low PacOV. has a P~ below the normal range. indicating impaired oxygenn.tion. Given the recent long-haul flight and absence of clinical and X-ray abnormalities. the most likely cause of her breathlessness and impaired oxygenation is pulmonary embolism and she must be investigated accordingly. This is oneaf the clinical situations wheTe ukulation of the .\-a gradient can be helpful (more so when the P~ is just .....' ithin the normal range). As shown below, it is signiflcantly elevated, indicating the presence of VIQ mismatch.

I

A-<J grodient - PA~ - Po~ PAD2 _ (0.2/ l< 93.81- (3.9 l< 1.2) _19.7_4.7 _ 15/t;Po A-o grodienl_ 15 - 10 3

.4.7 ;aorm V with normaJ oxygenation (nannal pQO:z) and a normal A-a gradient. Note that the HC~ (and BEl is norma.l as there has been insufficient hme for metabolic compensation to OCXUf. Consequently the rt'duction in FiKOz has caused a marked alkalaemia. Anothet" point to noll' is that the concentJation of ionized calcium m the blood is afft>eled by the pH of the specimen. since H' ions compete with cakium for binding sites on albumin and other proteins. Therefore, as the number of H+ ions drops (alkalaemia), more caldum is bound to albumin, causing serum Ionized calcium levels to fall. This is the most likely cause of the numbness and tingling. Care must be taken in ruling out other cardiovascular and respiratory pathologies before ascribing s)mptoms of chest pain and shortness of breath to psychogenic hyperventilation.

119

ANSWERS

CASE 12 I.

0)

Normol- bul w.ere hypoxaelftio

bl

2.

J.

COlTIpeoSOled metobolic ocidosil COfbon monoxide poisoning Soc,

Carbon monoxide (CO) poisoning commonly presents with nausea, vomiting. headache and ronfU5ion. CO saturations correlate poorly with symptoms but levels above 5O'r~ may cause cardiac arrest and seiz.ures.

Why is the patient hypoxaemic? CO binds to hacmogJobin (Hb) with 200 timts the affinity of ~ so is carried on the Hb molecule (as carboxyhaemoglobin) in preference to ~. As a consequence. the perrentagc of Hb saturated with Oz - the ~ - is maTIcOOI~' redl.K."'ed in CO poisoning. f",'cn when the p~ is very high. Since the overall Oz content of blood is determined by the Sooz and Hb concentration, ~ dclivcry to tissues is inadequate (tissue hypoxia), le."lding to lactic acidOl'iis.

Why does .5cJo, appear to be normal? Most pulse oximeter.> are unable to distinguish carboxyhac:moglobin from oxyhaemoglobin, so fail to reflect the truc ~ in CO poisoning In ABC analysis. the ~ is not norrnaUy measured but simply COlIeu1atro from the measured PaOz. The Jailer parametcr is based only on free, unlxlUnd O 2 molccules SO is unaffected b}' the presence of CO.

120

ANSVVERS

CAS! 13 I.

01

HyperverJtilation _ 00 impairment of oxygenol;Of\ bul hypoxoemio

seolation is extremely unlikely.

128

ANSWEIlS

CASE 21

2.

Type I relpiratory impairmenl 1~V'8fel bl Severe fl'Ieklbolic acidosil with partial compen$Olion 0.6-0.8 f- p. 161

3

AcIOO par'lCfealllil

0)

The diagnosis of acute pancreatitis is based on the history. exam findings and increased serum amylase: the main use of the ABC is in :Jelping to assess illness severity. The severe lactic acidosis (high anion gap and incremled lactate) indicates m.uked tissue h)'J'Oxia. The main caUS(' is impaired blood supply to bssuesdue 10 circulatory collapse. This occurs as part of the systemic inflammatory response in pancreatitis and must be urgently corrected with aggressive fluid resuscitation:t. vasopressor agents. A POO:1 of 10.8 with an FiO:z of 0.6--0.8 implies severe respiratory imp.linnent, and together with chest X-ray appeara.nces, suggests the devclopment of acute respiratory distress syndrome (an Inflammatory lung condition). Although PaC>]. is currently adcquate, 1m:. p.ltient may require ventilatory support if he deteriorates further ('r tires from the increased work of breathing. Finally, the ABG also shows a high glucose and low calcium concentration - both of which are adverse prognostic fadors in acute pancreatitis. Th£ patient should be transferred immediately to a critical care ('TWlronment for intensive moniloring and supportive treatment.

129

ANSWERS

CAS022 I.

2.

3.

Mild type 2 re~1ofy impairment f
INDEX aspiration pneumoniil 70-1, 115 aspirin (Sil.I~btl.') poisorung J.l,

92-J,126 assessment of illness S('\tl'rity, ABC in 48 l'~amples 49 iBthm..ll,life.-threat~ng 76--7, WI atmosphenc pres.o;ure 5

base excess (51::) allSeiSment of illness se..'erity 48 commOil ,"alul"S 51 in metabolic acidom 36 bicaroonate (~) actu,d (plasma) (HCo,.act) 51 ~tandard (HCO)o'>t)51 bkarlxmiltc (HCO:J) balance In add-base balance 28, 29 tr'I chronic hypen:apnia 22 ind~is4B

in hypt'l"'Cl\lilatiofl24 in metabolic ilcidosis 36 In mebbohc .llkalosis 38 in respiIilIOry impairmt'Tlt 23, 25 blood samples handling 46 venous ll$ arterial blood 44, 101--5, J3l buffers 26

caldum concentration, plasmil IOf\ised (iCa) common values 51 low 78-9, 98-9,119, 129 carbon dw,xidc (CO~ effect of shunting 15 elimination 6 and alveolar ventilation 13 in pulmorulry gas ~ 4

"6

carbotl dio~de partial prt'Slrurt' (PCOz)5 in air 5 in arterial blood (POlWJ.l 5 common values 50 III diagnosis 48 IDCrcased 6 Ul metabohc alkalosis 38 in mixed acidoW 41 r'l'a'ptocs 6, 7 in respiratOf)' addosi~!

alkalosis 40 in re6piratory irnpairmcnl20. 22 and VIQ mismatch 14

common values 50 and H' ;on remo.:al2B in rt'5J>iraloX)' iJnpainnerlt 23, 25 carboft monoxide poisoning 80-1, 110 cardiac arrest %-7, 128 chloride (CI") ions in met.moltc alkalosis 38 pIa5ma Jeoveis. oommon values for: 31 chronic ob!;tructive pulmonary dISeaSe 66-9, 72-5, lJ3-14, rt6-17 CI ion~ sef' chloride iOllS compensation '19,32-3 full ~ partial 32, 33 In metabolic alkalosis 38

(en

predicting 34 respiratory tIS metabolic 54 COIltraindicat;om to ABC anal}"sis43

diabetes rnelhluis

type 1 86-7. 113 type 2 60-1, J 10 diabettc ketoacidosis 32. 86-7, J2J diagnosis. ABC in 46, 49 disordeP.l of l\Cid-base balance 36-t 1 disorders of g3S exchange 18--25 dJuretic drugs 38

INDl'X

hydrogen ions (H') e1ec:trol)'be rq>laCl'.ment therapy IJl) eodotracheal intubation 16, 17 exh.a~

gas

composition during respiration

cycle 13 effec:t of shunting 15

fan" masks, oxygen deli'.(>I')' 16, 1; FiO" s« o.w.ygen concentration in ,nspired air nuid replaC'm'Ol.'nt therapy 130

gas exchange disorders 18-25 sununary2S g.u exchangE', pulmonary

assessment 52-3 basics 4-17 defLnition 4 glUCO!lt', fa."iting. plasma ~e1s, (OlllU'lOn values for 51

H' ions s« hydrogen tons (W) hilemoglobin (Hb) plasma ronct'nlration 8

rommon values 51 haemoglobin oxygen saturation (SOJ8-11 in arterial bkx>d (~8, SO fal5ely high 81, 120 and V/Q mismatch 14

common values 50 lncrelO5e with tr.msfusion/lron supplements 82-3, 121 HeOl ba\:lnce U'l bicarl:>onate (HCO;J balance

rommon valUl"'li 50 generation 28 in pH ZJ ~~211

hypercapnia 6 aS5eSSment of 5Il?'-"erily 52

chronic t'S ocutt! 7 clinical signs 23 in obesity no in respiratory impilIrmcnt 22 hypen::hlQr.lcmic itd~s 90-1,125 hyperventilation 12, 14,24,25,58-9,

109 in adrenallnsuffidcncy 94-5,127 causes 24 in diabetic kdoacidOSlS 86--7, 123 diagnosis 48 in mesenteric ischaemia 84--5,122

and metabolic acidosis 36 in methanol poisoning 88--9, 124 p;ychogcnic:M, 78--9, 11.'J in renal tubular aodOl>is 90-1. l25 in ~\icylate poOwning 92-3, 126 hyponatf;W'mja~, 127 hypme.aemia 96-7, 118 1ll anaMtia 82-3 asst'$SIr\eJlt of $t'\"erily 52 definition 18 ~ 10 :maemia 127 ~ere80-l, 120

h:.poxia 18, 19 hypm.ic respiration 36

Nil.' ions Ii!« 5Qdium (Nj,°) >OOS nJ~1 prongs 16, 17

ladnte. C(IfJUnOfl values for 51 lactic lIC1dosis 37 III iIoCUle paf\C1'e'antis 98-9,11" In cardiac arrnt 96-7, 128

itl mescnlt>rlc ischaemia

8~';.

122

obtsity 60-1, 1]0 optold lonc:'ly 64-5. 112 olC)'g.:n 10::) Cllncefltrahoo in inspired air (FiOJ 16

mC"enlcric isoehaemia 84--5, III md:,lbolic acidosIS 30, 36--7 in aC\ll~ pilrlCrt"ltilis 98-9. 129

in adrmallll5utficioency 9+-5.717 anicon gap In 39 asst'SSID('flt of .wveritr 54 definition 36 in diabetic keloacidosis 86-7, 123 d,agnosili 4B hyperventilation in 24 in meseoto"!ric iso:) gen oxygen partial pre5SUIl:' (PO.z) 5 in air 5 In arterial blood (PdoJ 5 iilfId ah-ro1ar ventilation 12-161: common values SO in diagnosis 48 III lmxed aodOSIS 41 in oxyhllemoglobill dissociation 10-11

-'

in respiratn'y unpairmetlt20 common vllues 50 in oxyhaemoglobi.n dis'iOCiiltiOll 10--11 in respiratory impainnenl 25 o")'gemrion 8-11 and ah"eOl.1r vmtilatim> lJ impaired ~~ in..clequale 18

INDEX and oxygen coocentnltion 1f\ inspired air (FiOiI16 oxyhaemoglobin dis5ocialion curve 10-11 in respiratory impairment 20

PlfCO:! s« carbon dIoxide pam",1 pl1'S9ure, in arterial

blood pancreatitis, acute 98-9, J29 P.tOz Sn! oxygen. partial pressure, in artedal blood p.lrtW ~\tres5 sn /il$o carbon dioxide parti.1.1 pressun>; oxygen partial pnossure Pcoz ~ arbon dioxide partial ".,.,."~

pH

blood rommon values 50 in diagnosis 48 IlOrmal26 in respiratory impairment 2J dl!!inition ?J ~le27

_ al$() acid-baSt' balance pickwidian syndrome ItO pneum.orua, aspiration 70-1.115

pOz!# oxygen partial pressure potassium (K') ions in metabolic alkalosis 38 plasm", levels, common values fO!"

51 psychogenic hyperventiiatiOfl 24, 78-9,119 pu1mQnlIry ~lism 62-3, 106-7, 111,13J pulmonary gas exchange us smnent 52-3 bilSics 4--17 definition 4

pulge ox.imetry 8, 59, 109 pylork stCl'l(tiis 102-3, 131

radial artery sampling 44-5 local atllH':5l1wtic 43 wrist position 45 renal mechanisms in metabolic alkalosis 38 pH maintenaru:e 28, 29 renal tubular addaMs, type I 90-7, 125

respiratory acidosis 30, 40 in chronk obslmctive pulmona.f)' ~ 72-5, It4,1J617

chronic us acute 40

COOlpeOS3tedJ2,33 mixed with metabolic acic:b;is

"

in opkrid toxicity 64-5, 112 in I)"e' 2 diabetes 6O--J, no resp;ratory alkalosis 30, 40 in anaemia 82-3,121 in