Arterial blood gases made easy , SÁCH VỀ KHÍ MÁU ĐỘNG MẠCH DỄ HIỂU NHẤT

lain A M Hennessey

MBCha (Ho,n)'"
Senior House Officer, Ne()nolRoyol United HosPIIaI, Bath, UK

Alan G Ja pp

MIlCh. iHoNl SS< IHomI MlCP

Clinical Research Fellow in Cordiology
University 01 Edinburgh, UK

bLSEVlFR

IH='I M'eS


CHURCHILL
LNTNGSTONE
CLSEVlER

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Preface
If you've taken the time to open Arfnwl Blood Gases Mnd, l-:tJsy, you
must believe that artenal blood gases (AHtJi) are unportant. but not
Pntirely:,lraightforward.
We ft>rtamly 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 emphasi<:l' the key concept~,
fnrus on priKtical and useful aspects of ABG analysi!! and dvoid
extrant"Ous detal1. \Vc believe lThlny medical and nursing students,
JWlior doctors and specmhst nurses will benefit from a dear, roncise
guide to performing thl? te<:hnl4uc and interpN>tmg the results
lain A M HeJUlCSSCY
Alan Glapp

•

Contents
Prefcx:e

v

Acknowledgements

V"

1

Port 1 The ABG explained
1.1

3

Introduction

1.2 Pulmonary gas excnange: the basics
1.3

Disorders of gas exchange

1.4
1.5
16
1.7
1.8

19

Acid-bose balance: the basics
Disorders of ocid--bo$e balance

ABG $Ompliog technique

When and why IS
Common values

on

ABG required?

Making ABG inlefprctolion easy

Appendix
Pori 2 The ABG in practice

•

4
18
26
36
42
48
50
52
56

57

Answers

58
109

l<>de.

135

Cases 1-25



1. 1

..

INTRODUCTION
Arterial blOOl"l ~,\S (ABC) analysis ~fers 10 the mcasuremE'nt of pi I
and the partial pn:s~.m:s of oxygen (Oz) and carbon dioxide (Co,) in
artt>rial 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 pbase physIology: plel1St' do not skip them! If you understand these COT@
concepts, thf' rest wlll follow seamles.s1y. Part 1 abo t:xplainll how,
when and why 10 obtain an ABC sample, bcforeconduding with a
'iimple step by-step guide to intcrpretin~ABG data.
Part 2 tht-n allows you to put aU of this into practice with a senes
of case ~arios involving ABG analysis. You may already have a
method fOT interpreting ABGs but we lUge you to try our system (set
NIt in section 1.9) that offers a logical, rndhodical and consistent way
of approachmg ABGs.. By sceinM: how this system can idt'Jltify all of
~ majOr patterns of ABG abnonnalities. we hope you will gain the
necf"
3


PULMONARY GAS
EXCHANGE: THE BASICS
OUf ~lls use oxygpn (0,) to generate CJ\cq:;y and produce carbon
dioxide (COz) as waste. Blood <;upphes cdb with the O 2thfoy need
and dears the unwanted COt. This p~<; d~ds on the ability of
our lungs to f'nnch blood with O:z and rid it of Co,
Pulmonary Ras rxcllatlg' ",fel'S to the ttdusfer of O:z from the
atmosphe~ t~) the bloodstream (oxygenation) and CO 2 born thp
bloodstrp-am to the aunosphcl'c (C02 e-limination).

TIle cxchan~e lakl"S plal'"P between uny air sacs call1''d alvroll and
blood. \'t$scls called mpilfl1n~. Because ~y carll haxe exlTf'mely
thin walls and rome into very d06E' conmct (the al\'coIar-capillary

membrane), Co, and O:z arc able to move (diffu~) betw~ them
(Figure 1).

-'"
bI ollctliole

I

02 and co, lranSlBr
occurs at the aM!dar
A
F~ure 1 Ra.pimloty (Jnolomy.

•

B

capIafy l,lfl!OOrar,I


PULMONARY GAS EXCHANGE: THE BASICS

ABC.s help us to assess the ~ltectivencssof gas exchange by
providing measurernt"tlts of the partial pmiSurn of O 2 and COz in
arterial blood - thE" PflOz. and Pa~.
Partial pressure dcscribe5 thE" contribution of on~ individual gas
within a gas IJ\i.Jl.ture (such as air) to the total pre;sure. When a gas
dissol\l~ m liquid (e.g. blood), the amount dissolved depcnili; on the
partial pt'PllSUTe.

Nole
~.

partial pressure of 0 1
PalJl '" partial pre$5ure of O 2 in

D.rl~ri.l

blood

Gases move from areas of higher partial pressure to lowE"I' partial
pICSSW\!. At the alveolar-higher 1\7 and lower Pro, than capillary blood. Thus, Oz molecuJe:o;
moVE" from alveoli lu blood and CO:z molecules move from blood to
alveoli until the partial pressures arc equal.

A~on··· . . .

AI

:leO

P_uU""

1eYeI, otmospherk. pro!oSUfe (klkJl p"euure of gases

alrno$pn..1 - 10 1 lPo

Of

in

the

760 mmHg

o? oompriSC5 21 % of air, so the porliol pre$sure of ~ In oir
• 21% of otmospheric. pnmure

.21 kPoor l60mmHg
Co, mcJI,;~ up
in~,ed

aIr IS

fV1l a

til"/)'

frodioil 01 air, so the pamol pressure of C~ in

negligible

•


f'Ut.MONARY GAS eXCHANGE; THE 8ASICS

CARlON DIOXIDE WM''''ATION
Diffusion of co, from lhe bluodstrPam to alveoli is so dficient that

COl elimination is actually limited by how quickly we can "blowoff" the CO2 10 our alveoli. Thus, the PilC02 (which reflE'Cts the
overall amount of C~ in arterial blood) is dttermined by al'Ot.'Olar
Drnhlahon - the total volume of air transported bctwt.:cn alveoli and
the outside world every minute.
Vmtilation IA regulated by an area m the bralnstf>m called the
respiratory centre. 'This area containS specialised rca::ptun. that sense
the PtlCOz and cvnnect with the muscles involved in breathing. If
it is abnormal, the respiratory centre adju~ts the rate and depth of
breathing acrordingIy (Figure 2).

Normally, hmgs can maintAIn a normal P~ even in rondltioru;
where Co, production i!'l unusually high (e.~. sepsIS). Consequently
an increased PIKOz (hypercapnia) always lD1plies reduced alveolar
ventilation.

Key point

PaCo1 is controlled by vtnlil.llion ~nd the level of v..ntilation is
ildju5ted to m.aintilin PaCo1 within tight Iimils..

•

I
•


PUlMONARY GAS EXCHANGE: THE BASICS
~Paco2" +V&nlilatioo

t PaC02 " tVentla\loll

Figure 2 Control of ventilation.

~ note on ••• hypoxic

drive

In patients with chronicolfy high PoC02 levels (chronic hypercapnia), the
~iali-ed reo:;eptors thot deled CO 2 kmlls can become de$ensilbed. The
body then relies on receptors that detect the POiJ-l to gouge the adequocy of
ventilation and low POOJ becomes the principal Vflnlilotory stimulus. This is
referred to as hypoxic drive.
In patients who rely on h~ic drive, overzealous cOfrection of
hypoxoemio, with supplemental O:z, may depress ventilation, leading
to a colastrophlc riM in POCO:!. Patients with chronic hypercapnia
must therefore ~ given wpplementol O 2 in a controlled fashion with
careful ABG monitoring. The same does not oppfy to potienb with ocut.
hypercapnia.
7


PULMONARY GAS EXCHANGE: THE BASICS
HAEMOG~O.'N

OXYGEN SAtURATION (SO,)

Oxygenation is marc complicated than C~ t'liminabon. 1lte first
thing to realiSE' lS that the Po:!. does not actually teU llS how much
~ is in blood. It only fTlf'asures free, unbound ~ moIecules- a tiny
proportion of !he total

In fact, almost all 0,. molecules in blood are bound to a protem called
hamwgfobin Hb (Pigure 3). Becau~ of !.his, the amount of O 2 In blood
depends on two facton.:
1. Hb concentration: this determines how much O 2 blood. has the
capaCIty to carry.
2. Saturation of lib with 02 ($0,): this is the pcrccntaj.;c of
available bindin~ sites on lib that ront3m an 02 molecule - i.e.
how much of the carrying capacity is btrng used (Figure 4).

Note

Soz:: O 2 wtueation in (;my) blood
$Q:O:!. ""

O 2 "tueation in Q:rlmal blood

It. note on ... pulM ~i t

So::>:2 con be

me<»ured using

0

Pfobe

(pul!oe o..imelerl opplied /Q the

finger or earlobe. In most case$ it Pfovide$ odeqUQte informatioo
Q,ll,ygenarion,

but it

10 901.19-

iller.s occurate witn saturatlon1 below 75% and

00e$ not provide
infoflTlOlion on f'acQ) w ~hwklllQr be u~ 0$ 0 wbditute for A8G onolyJis

unre!iQble when plIfipherat perf",lion il poot. Oximetry

In

ventitololy impoir",..l.

Key point

.Po,. is not a m('uu~ of the unount of O 2 in bJuod - ultimately the
SaO:!;;md Hb concentration determine the D,. confent of arterial
blood.

•


PUlMONARY GAS EXCHANGE: THE BASICS

O:!tnnlklHb(M)

Ft,ure 3 Relative fXoporliom of Ire. 0, moIecot.s and O 2 moIecuUu

boHaemogIobil
1TlOIea.M

Fre9 QIl)9lll
rnoIecUe

Boln:I axygen
~

•

,

,

•

,!,

•

i

,!
,,

•

"

!

,

•
I,

•

I

•
•

I
,,

• •

11::'=1
Figu... 4 Haemoglobm

11~~=1

I
I

I~=I

OX)IQ~ sol!Jfation.

•


PUlMONARY GAS EXCHANGE: THE BASICS

OXYHAEMOGLOBIN DISSOCIATION CURVI
Vk now know that the amount of ~ in blood depenWi on the Hb
COTKt.>nlcation and the~. So what is the significance of the PQ:l?

Po;. can be thought of IlS the driving force for O! molC'Cull.'$ to bind
to Hb: as such it regulates the Soz. The oxyhapmoglobin dissociation
CUC'Ye (Figure 5) shows the So,. thai will result from any giV01 Po,..
In genern,

higher the Paz, the highel" the Sov but Iht CUrtlt is not
littttlr. Tfw. green line is known as the 'flat part of the cwve': changes
in ~ over this rangf' have relatively little effect on the 50:1. In
contrast, the red line is known as the 'steep part of thf' curve': even
small c.hanges in PO]. over this rangf" may have a major impact on~.
~

Note that, with a 'normal' PIlO:l of around 13 kPa (100 mmHg), Hb is,
more oc less, nUlximally stlhmdm (~> 95%). This means blOl.X1 has
uwd up its D,-t:acryinK capacity and any further rise in Pao, willlWt
significantly increase arterial D.z content

Key point

Po" is not the amount of O 2 in blood but is the driving force for
5.lItunting Hb with 02"

I.


PUlMONARY GAS EXCHANGE: THE BASICS
100

Cww shifts to IIfl wtleft:

!pH.IPro,
*lemperaIln,

80 RJDPG

Curve sIllfta k) righI wMri:

IpH.lPoCO"
i'twnper.lIllI'e,
12,3OPG

"
o+-,-~-=~_~_~--,_,~
o
5
10
15
20
80 ~~

,

o

37.5

7S

112.5

150

600 ~rrmtg

Figuro S ~Jobjn disso:iotioIl anotl. The CUfVe defines the
,J.m.,,,sJ.ip beMun Po, and the percfflJloGe so1uI"ation 01 haemoglobm
WIth 0")'9$l (~_ NoIe the sigmoId sho~: it is relolive/y Rot when P01 's >

80 mmHg flO 6lPa) but sleep whoM Po, foils below 60 mmHg fS lPo)

Key point

When Hb approaches maximal O 2 saturalion, furth~r increalles in
Paz uu not significantly increase blood O! cuntent.


PUlMONARY GAS EXCHANGE: THE BASICS

AlVEOUR Vllffll.ATlON AND ~

We hav*, now seen. how

P«>z re,;;uJa~ the ~. But what dcl'erlniJ'w>
P«>z'
There are three major factors that dictate the Pac,;:
1, Alveolar ventilation

2. Matching of ventilation with ~rfusion (VIQ)

3. ConCUltntion ot 0 1 in inspired air (FiOa)
Alveolar ••ntilation
O:z moves rapidly from alveoli to till: bloodstream - so lhe hIgher thr
uluwwr Po" Ihe hixhtr the PIlOz·

Unlikp air in the atmosphere, alveolar air rontain.'l significant
amounts of CO:z (Figure 6). More CO:! means a lower p~ (remember
the partial pressure of a ga" reflects Its share of the total \'olume).
An mcrease in alvoo1acventilation allows more CO:z to be 'blown oH',

resulting in a ~ alVl."'Olar ~. If, on the other hand, vcntilatiorl.
declines. L~ accumulate; at the cxpenw of O:z and alveolar ~
falls.
Whereas hyperventiation can mcrea!le alveolar pO:! only slightly
(bringing it closer to the Po:z of inspin>d air), there is no limit to how
tar alveolar f'oz (and hence P~ can fall with inadequate v.:ntilation.

12

PULMONARY GAS EXCHANGE: THE BASteS

""
75"

NftgIl.

"'-'

""""".......
.....

-

75"

.....

,tgur. 6 Composrlfon 01 inhaled ond ..."haled 905& at voriou$

~$

oJ

respiration.

K.y point
Both uxygen.ation .and COl elimination depend on alveol.u
ventil.ation: impail'e'd vcntiJiiltion cau5e5 PliO, to fall and Plica, tu

ri,..

13


PUlMONARY GAS EXCHANGE: THE BASK:S

Ventilation/perfusion mismott:h and .fhunring
Not all blood flowing thmugh the lung meets wt>U-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 <-1:1 (remember: flat part of curvt:,
page 11). Thf' non·shunt~ blood lhenofoN' carumt rompensah> 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 InlI<::hookolly ventiloted.

,.


PULMONAAY GAS EXCHANGE: THE BA5K.:S

Fbled pelb Ifs ... milt:

VaoobIc perforrnarx:e mask

Figun a Oxygen deJ,WKY clevius,

17

DISORDERS OF GAS
EXCHANGE
HYPOXIA, HYPOXAEMIA AND IMPAIRED
OXYGENATJON
The above lerms aN': often used interchangeably but mean different
thmgs.
Hypoxia refer.; tu any stld~;11 whIch tissUt'S M:'riot lI1I iruzdeqlUlk supply
of 0 1 to support nOrmQIlJt7'Obic mrl/lbolism l (Figwe 9). It may result

from either hypoxl!emia (!lee below) or impaired blood supply to
tis~ues (isl.:hacmia). It is ('Iften associated with lactic acidosis as cells
resort to anaerobic metabolism.

tmy slQf~ in wIridr 1M O 2rontent ofQrlmal blood
is reduced. II may remit hom impaired oxygenation (see below), low
haemoglobin (anaemia) Of reducw affutity of ha~mog1obin for Oz
(e_g. carbon monoxide).
Hypoxa~mla refers

to

Imp.tired oxygr:nation refers to hyporMmJII fC>.41tingJrom rtduaJ.
tnlmfer of D1from lungs to the bloodstrtflm. It is identified by a low P/Kl:!,
« 10.7 kPa; < 80 rnmHg).
It is important 10 note Ihc distinction betWt:'ell impaired oxygenation
(which results in hypoxaemia) and IrwdLqllllteoxygcnation (whkh
re;ults in hypoxia). Constder a palimt with a PlIU:!. of 85 kPa. He M..'l
impaIred oxygenation. suggesting the prcsmce of irnportanllung
diSE'OlSf'. NeveI"lhtllt.-ss, his Pao.z would usually result in an ~ > 90%
and, protlidt'd th£ haemoglobin and (llrdiac output are normQl, adequate

0:l: delivery to tiS$Uell.

lit" often m.lvisabl(' to u.'\t! the term 'm.."uc hypoxia' to avoid any l't>nfusion.

11


rnsoRDERS OF GAS EXCHANGt:

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

.,

.<

.,

iJ

t_I__~_ _-t
HoomogIobil

low /1QernagIObi'I

low ~

I.WlIlbIe 10 carry ~

(~)

(1IIp"oed
arygemIion)

(e.g. CO poisoIwlg)

figuN 9 Cau.seJ 01 hypo;ua

••


DI~DERS

OF GAS EXCHANGE

TYPE 1 RESPIRATORY IMPAIRMENT
Typt! 1 respiratory impairment' is defined as low P~ with norum!
or low P~. This implies defective oxygelation despite adequate
ventilation. V,Q mismatch is usually responsibl4" and may tc5ult
from ;1 numbt"r of causes (Box 1.3.1). The PIIJCO.z is often low due to
compt!J1satory hyperventilation.
If the ABG is drawn from a patient on supplM'lf>tltal Oz. the Pl7O-z may
not be below the normal rangt", but will be inappropnately low for
the FiO,.

The Sf>verity of type 1 respiratory impainnent i~ judgt..'l:1 according
to the scale of ~ resulting hypoxaemiol and, ultimately, the
presence of hypoxia (fable 13.1). Hpre it IS important to rernmilicr
the 0,. dissociation curve. Reductions in PtIOJ as far as 8 kJ'a have
a relatively minor effect on Sao:z and are well tolerat~. Beyond

this threshold, we reach th£' 'steep part' of lh£' curv£' and further
reductions in PtIOJ will lead 10 much greater falls in ~ significantly
lowt'ring the ~ content of arterial blood.
Initial treabm.. . .l l of type' 1 resplJatvry impairment is a~ at
achieVing an adequate Pac;. and Sat~ Witll supplemf'ntal O 2 while
atlcmpting to COIn:d Ute W\derlying cause. In many ca5f'1l pube
Olomt'try can be used as an alternativE' 10 repeated Aac; sarnplmg to
monItor progress.

'We USl' thf. lftm 'inlpairu-."ll' ralMr than 'fai.lure' hL-rc as t~ diaSJ'OSlS 01
re5pU"ilkw)' failUT# requires I Pao:z < 8 kPa « 60 rnmIiX).


DISORDERS Of GAS EXCHANGE

So;.:

1.3.1 Common CQU5e'5 of~ 1 respUoIwy lmpai.....ent· ~
Acula osllullo
Acvte re$piratory disben syndrome
Flbrosing ohieolitis
Chronic OO'l'U<:llve pulmonary diseose

Pneumonio
Pulmonary emboli$ll\

........ho<=
Pulmonory oedema

Table 1.3.1 Auesdng MYerity of type 1 respiratory

impai,""*"t

POOz {kPol

POO2lmmHgj
Sao, 1%1

Mild

~Clte

Sovwe

8-10.6
6f>-79

53-79
40-59
7>-89

<53

~94

at". _ken of .....e... intpo........t
•
•
•

<40

<75

.

H'9h f~ reqoJiremenl$ to maintain odeqvole Paa,
loctic: ocidl)$i$ lindicOling tissue hypolliol
Orgot'! dysfunction (drOWSlnen. confulion, reool fo,luf., hoemodynamlC
coIIopMl. como]

21