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C O N T I N U I N G P R O F E S S I O N A L D E V E LO P M E N T

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Arterial blood gas analysis

NS227 Woodrow P (2004) Arterial blood gas analysis. Nursing Standard. 18, 21, 45-52.
Date of acceptance: December 1 2003.

Aim and intended learning outcomes
This article aims to give nurses an understanding
of the main gas and acid-base measurements derived
from an arterial sample, so that they can interpret
results of samples from patients in their care. After
reading this article you should be able to:
■ Describe what acid-base balance is, and its sig-
nificance for homeostasis of the blood.
■ Discuss with junior colleagues the significance
of carbon dioxide measurement.
■ Explain to a junior colleague how compensation
occurs, and how it can be identified from blood
gas samples.
Introduction
With increasing numbers of acutely ill patients in
most wards, nurses often see arterial blood gases
(ABGs) being taken by medical colleagues and, in
some areas, by other nurses. ABGs can aid medical
diagnosis, but nurses may be the first clinical staff
to receive the results. Understanding the signifi-
cance of these results, and knowing when medical
help needs to be summoned urgently, can improve
patient care. Nurses taking samples need to be able
to interpret results. Understanding diagnostic results
can make nursing care more holistic for the patient
and rewarding for nurses. This article describes how
nurses can analyse ABG samples.
Blood gases may be analysed from capillary sam-
ples. Differences between arterial and capillary results
are so slight that for practical purposes they can be
considered identical. Information in this article there-
fore also applies to analysing capillary samples.
Although commonly referred to as ‘blood gases’
or ‘ABGs’, most machines supply other results, such
as electrolytes and metabolites, that are useful for
patient care, but which are not gases or necessarily
related to respiratory function. This article describes
how to interpret the main ABG results. It does not In brief
discuss how to take samples, errors that can occur
when taking samples, or care of arterial lines. Author
Philip Woodrow MA, RGN,
DipN, Grad Cert Ed, is Practice
The sample Development Nurse, Critical
Care, East Kent Hospitals NHS
In a few specialist areas, such as intensive care units, Trust, Canterbury, Kent.
patients may have an arterial line inserted, which Email: philip.woodrow@
enables samples to be obtained easily and painlessly. ekht.nhs.uk
However, arterial lines are dangerous and should
not be used where the patient is not monitored and Summary
observed continuously by staff familiar with the With increasing use of arterial
potential dangers. In most wards and departments, blood gas analysis in various
obtaining an ABG sample necessitates an ‘arterial ward and other hospital
stab’ – taking blood with a syringe and needle from settings to aid medical
diagnosis and management,
an artery (usually the radial artery) in a similar way
nurses who can interpret
to taking blood from a vein. As arteries are deeper
results are often able to
than veins, arterial stabs are painful. Local anaes- initiate earlier interventions
thetics should be used (Hope et al 1998), but in the and understand the reasons
author’s experience rarely are. Arterial bleeds take for medical interventions. This
longer to stop than venous ones. Sheehy and Lombardi article enables nurses to
(1995) recommend pressing on arterial sites for five interpret such results.
minutes, although if patients have prolonged clot-
ting or bleeding disorders, pressure may be needed Key words
for longer. Removing pressure too soon may cause ■ Oxygen therapy
haematoma or bruising. ■ Respiratory disorders
Once the sample has been obtained, nurses may
These key words are based
be asked to transport, or arrange transport for, the
on subject headings from the
sample. Because cells in blood are living, gas exchange British Nursing Index. This
and metabolism continue, so delays in analysing article has been subject to
samples cause increasingly inaccurate results. double-blind review.
Beaumont (1997) recommends analysing samples
kept at room temperature within 15 minutes. Unless
blood gas analysers are available in or very near Online archive
the ward, samples should therefore be cooled to
reduce metabolism, so prolonging the time avail- For related articles visit our
able for reliable analysis. Common practice has online archive at:
been to insert the syringe into some ice. Clutton- www.nursing-standard.co.uk
Brock (1997) suggests that this prolongs the reli- and search using the key
words above.
able sampling time to 60 minutes. However, some

february 4/vol18/no21/2004 nursing standard 45

p45-52w21 1/27/04 5:50 PM Page 46
monitoring patients
Box 1. pH (overall acid-base balance)
normal 7.35-7.45
■ <7.35 = acidosis
■ >7.45 = alkalosis
anecdotal claims have been made that ice imme-
diately against the syringe wall causes haemolysis
(breakdown of erythrocytes), causing inaccurate
results: lower pH and oxygen (PaO2), higher car-
bon dioxide (PaCO2) and potassium (K+) (Gosling
1995). So anecdotal recommendations are to place
the syringe in iced water. However, if transporting
a container of iced water causes a further delay, it
is debatable whether this method achieves any
greater accuracy.
Delay before measurement may also cause inac-
curacies from separation of blood cells and plasma.
Which way measurements are affected depends on
whether mainly plasma or mainly cells are inserted
into the machine. Samples should therefore be mixed
well during transportation, by rolling the syringe (like
a cement mixer). Vigorous shaking should be avoided,
as this may cause haemolysis.
TIME OUT 1
Re-read the above paragraph; identify
what you would need to safely transport
a sample to the nearest usable blood gas
analyser. If you identify any items that are
not available in your clinical area, inform
your ward manager.
Analysis
Measured results, suggested ‘normal’ values and
the sequence of printing results vary between
machines, largely depending on how they have
been programmed locally. This article identifies the
most important results for most adult patients, but
if additional measurements are used in your place
of work, you should find out the normal range and
what abnormalities may suggest about patients’
conditions. There are four main groups of results
that will be analysed on most samples:
■ pH.
■ Respiratory function (oxygen, carbon dioxide,
saturation).
■ Metabolic measures (bicarbonate, base excess).
■ Electrolytes and metabolites.
This article focuses on the first three aspects.
Electrolyte and metabolite measurements are use-
ful but are additional to, rather than part of, gas
analysis, so are not discussed here. When results
are analysed, information about the patient, such
as his or her identification number and body tem-
perature, may be fed into the machine. Depending
on how the machine is programmed, some infor-
46 nursing standard february 4/vol18/no21/2004
mation may be optional, but will be printed above
the analysed results. As with any machine, there
can be slight differences between different meas-
urements (‘drift’), so changes of less than 10 per
cent are generally not considered significant.
Temperature Machines provide the option to meas-
ure results at the patient’s own temperature or at
a default temperature of 37°C. Dissociation of
gases, and therefore all results derived from gases,
are affected by temperature. This can be illustrated
by re-analysing samples at different temperatures.
Therefore, some people consider that gases should
be measured at the patient’s temperature. However,
body temperature varies between different sites,
and if the recorded temperature changes because
a different site is used, for example, axilla is replaced
by tympanic measurement, or if recording of tem-
perature was inaccurate then results may differ
without any change in the patient. Thus, it is gen-
erally considered safer to measure all samples at
the default temperature of 37°C, where any trends
will be from a consistent baseline. The author’s own
preference is to sample all results at 37°C; how-
ever, to avoid variation in readings between dif-
ferent practitioners, it is important that all people
measuring ABGs in a clinical area follow the same
practice. Wards and units should therefore make
team decisions about whether or not to enter
patients’ temperatures.
TIME OUT 2
Obtain a printout, or copy down results,
from an ABG analysis (if none is available
in the notes of any patients on your
ward, specialised areas such as critical
care may be able to provide you with a
copy). Note down why the patient was
admitted, any other relevant history and
treatment, and why the gas sample was
taken. If you obtain more than one
printout, select one to use while reading
this article. Was the sample analysed at
37°C or at the patient’s temperature? If
you have the opportunity, ask why.
pH
The normal range is 7.35-7.45 (Box 1). Potential
hydrogen (pH) concentration of ions measures acid-
ity or alkalinity. Acids are chemicals that can release
(donate) hydrogen ions (H+), while alkalis are chem-
icals that can absorb (receive) hydrogen ions. The
pH scale measures moles per litre, and ranges
between 1 (absolute acid) and 14 (absolute alkali):
car batteries contain strong acids, with a pH of
about 2.0; resting gastric pH is less than 3; many
citrus fruits have a pH of 4; sodium hydroxide, a
strong alkali, has a pH of 13. Such extremes of acid-
ity or alkalinity in blood would be fatal. The main
acid in blood, carbonic acid, is fortunately weak.
Chemically, neutral pH is 7.0. But human blood
p45-52w21 1/27/04 5:50 PM Page 47
is slightly alkaline, normally ranging between 7.35
and 7.45. Therefore, blood pH below 7.35 is termed
acidotic and that above pH 7.45 is alkalotic.
The pH scale is a negative logarithm. A logarithm
presents large numbers in a few, more easily
managed, figures. A negative logarithm similarly
represents small numbers, with many decimal points,
in a more manageable and safer form. There are
only 0.000004millimole (40 nanamoles, nmol) of
hydrogen ions in each litre of blood. However, slight
changes in concentration can be life-threatening
– doubling or halving acid concentration alters pH
by 0.3 (Box 2), while moving one whole figure on
the pH scale causes a tenfold change in hydrogen
ion concentration (Fletcher and Dhrampal 2003).
The normal blood pH of 7.35-7.45 means that the
hydrogen ion concentration is normally 3.5 x 10-8
to 4.5 x 10-8 per litre of blood.
Slight changes in pH affect enzyme activity (Hornbein
1994), while acidity increases oxygen dissociation
from haemoglobin (the Bohr effect) and impairs
cardiac contraction (= negative inotrope). Blood
pH below 7.0 or above 8.0 makes survival very
unlikely. Acidosis occurs more often than alkalosis,
but both are life-threatening. Complications are
cumulative as blood pH moves progressively fur-
ther from the normal range.
pH measures the overall acid-base balance of the
blood sample. Acid-base balance is affected by
both respiratory and metabolic function. An abnor-
mal pH does not identify whether problems are
respiratory or metabolic (or both) in origin. In health,
the body attempts to maintain homeostasis. As
homeostasis of blood pH is to maintain 7.35-7.45,
an abnormality of one component (for example,
metabolic acidosis) may stimulate an opposing
abnormality of the other component (for example,
respiratory alkalosis) to maintain a normal pH. This
is called compensation, and it can only be identified
by looking at pH together with both respiratory
and metabolic results.
Anaerobic metabolism from poor perfusion, such
as during shock, produces lactic acid (Babb and
Farmery 2003). Although this is a weak acid, increased
levels can cause life-threatening metabolic acidosis.
Lactate is a metabolite measured by some analysers.
Normal blood lactate level is 1mmol/l or less.
TIME OUT 3
Look at the sample results you have
selected. Is the acid-base balance
normal? If not, is it acidic or alkalotic?
Respiratory function
Blood gas analysis measures
■ PaCO2 (partial pressure of arterial carbon diox-
ide).
■ PaO2 (partial pressure of arterial oxygen).
■ SaO2 (saturation of haemoglobin by oxygen).
monitoring patients
Box 2. Hydrogen ion concentration
■ pH 7.7 = 20nmol/l H+
■ pH 7.4 = 40nmol/l H+
■ pH 7.1 = 80nmol/l H+
■ pH 6.8 =160nmol/l H+
(= 0.000016mmol/l)
Box 3. PaCO2
■ Normal: 4.5-6.0kPa
■ <4.5 = hypocapnia, respiratory alkalosis
■ >6.0 = hypercapnia, respiratory acidosis
(Cornock 1996)
Some printers omit the lower case ‘a’. With capil-
lary or venous samples, if the machine is informed
of the source of the sample, a small ‘c’ or’v’ may
be printed. Venous samples are very rarely taken,
but might be used to measure electrolytes and
metabolites.
In the UK, gases are almost always measured in
kilopascals (kPa), however, some countries, includ-
ing the United States, use millimetres of mercury
(mmHg). As US texts, and old texts from the UK,
give gases in mmHg, you may need to be able to
convert these figures. One millimetre of mercury
(1mmHg) equals 0.133kPa, so dividing mmHg by
7.5 approximates to kPa.
Carbon dioxide (PaCO2) The normal range is 4.5-
6.0kPa (Box 3). The amount of carbon dioxide in
the atmosphere is normally insignificant (about
0.04%). Carbon dioxide is produced by body cells
as a waste product of metabolism. The respiratory
centres in the brainstem respond primarily to the
level of arterial carbon dioxide. So, with healthy
respiratory centres and lung function, hypercapnia
(>6.0kPa) stimulates respiratory centres to increase
the rate and depth of breathing, which removes
more carbon dioxide. Similarly, hypocapnia (<4.5kPa)
reduces the stimulus to breathe, so decreasing the
respiratory rate and depth. Arterial carbon dioxide
levels therefore indicate ventilation, the amount of
air moving in and out of the alveoli. In health, res-
piratory responses can restore a life-threatening pH
of 7.0 to 7.2/7.3 in three to 12 minutes (Guyton
and Hall 2000).
Hypoventilation, which may occur in conjunction
with respiratory failure, may lead to hypercapnia
and hypoxia, because of the inability to remove suf-
ficient carbon dioxide to maintain normal levels.
Inadequate ventilation may necessitate ventilatory
support, such as non-invasive ventilation (BTS 2002)
or the respiratory stimulant doxapram (BTS 1997).
Hypocapnia occurs with hyperventilation. This is
only likely to be seen with:
february 4/vol18/no21/2004 nursing standard 47
p45-52w21 1/27/04 5:50 PM Page 48
monitoring patients
■ Panic attacks.
■ Artificial (over-)ventilation.
■ Compensation for metabolic acidosis.
With panic attacks, causes should be identified and
if possible resolved, and the patient reassured. If
hypocapnia causes problems, it can be reversed by
the patient rebreathing his or her own carbon
dioxide (using a paper bag), but this is usually only
necessary in first-aid situations. Artificial over-
ventilation can be adjusted by reducing ventilator
settings (rate and/or volume). Compensatory meta-
bolic acidosis should usually not be treated, as the
compensation maintains haemostasis; however,
the cause of acidosis often requires treatment.
Carbon dioxide is often referred to as a ‘potential
acid’. Chemically, an acid has to contain hydrogen
ions, which carbon dioxide does not. However,
when carbon dioxide produced by cells diffuses
into capillary blood it mixes with water (the main
component of blood) to form carbonic acid:
CO2 + H2O ↔ H2CO3.
Arterial carbon dioxide therefore indicates the
amount of carbonic acid, so hypercapnia creates a
respiratory acidosis, while hypocapnia creates a res-
piratory alkalosis.
Carbonic acid has two useful properties for human
blood physiology: it is weak and unstable. Being a
weak acid, large amounts of carbonic acid would be
needed to create a life-threatening acidosis, so res-
piratory acidosis occurs only if excessive amounts of
carbon dioxide are retained. Its instability means that
it dissociates (breaks down) easily, which is why the
arrow in the above formula points both ways. Carbonic
acid usually dissociates back into water and carbon
dioxide, carbon dioxide being removed through the
lungs and excess water being removed in urine.
Oxygen (PaO2) The normal range is 11.5-13.5kPa
(Cornock 1996). Oxygen is literally vital for cells,
and so for organs and the body, to survive. However,
prolonged use of high concentrations can cause
toxic damage. Precise levels for oxygen toxicity are
debated but are often considered to be >60%
oxygen for >24 hours (Hinds and Watson 1996).
So if a patient is hyperoxic (PaO2 >13.5kPa), sup-
plementary oxygen for prolonged use should be
reduced. Significant hyperoxia almost never occurs
unless patients are given high concentration sup-
plementary oxygen. More often, patients have
hypoxia (PaO2 <11.5kPa), as a result of respiratory
Box 4. Respiratory failure
Type 1
■ PaO2 <8kPa
■ PaCO2 <6kPa
Type 2
■ PaO2 <8kPa
■ PaCO2 >6kPa
(BTS 2002)
48 nursing standard february 4/vol18/no21/2004
failure, and need supplementary oxygen to main-
tain adequate tissue oxygenation. For short-term
use during acute crises, such as during or immedi-
ately after cardiac arrest, oxygen toxicity is not an
issue, so maximal (100%) oxygen should be given.
Hypoxia may be caused by hypoventilation, in
which case carbon dioxide will be raised. But
oxygen is far less soluble than carbon dioxide, so
any disease increasing the fluid barrier between
alveolar air and pulmonary blood (for example, pul-
monary oedema, chest infection) may cause hypoxia
while carbon dioxide remains normal (normocapnia).
Hypoxic patients need oxygen; without oxygen,
tissue cells die. Contrary to widespread belief, only
10-15 per cent of patients with COPD may become
apnoeic if given more than 28% oxygen (Bateman
and Leach 1998). However, medical gases are drugs,
which legally require a prescription. Nurse-initiated
oxygen therapy may be covered in some areas by
patient group directions, but in other areas nurses
initiating oxygen should remember their individual
accountability (NMC 2002). Where urgent treat-
ment is necessary to preserve life, there is a legal
(Dimond 2002) and professional (NMC 2002) expec-
tation that nurses will act in patients’ best interests.
Saturation (SaO2) The normal level is about 97%.
Most readers will be familiar with oxygen saturation
from pulse oximetry. Pulse oximeter probes meas-
ure saturation of haemoglobin in peripheral (capil-
lary) blood (SpO2). The saturation measured in an
ABG sample is the SaO2. However, differences between
SpO2 and SaO2 are in practice negligible, both often
being referred to as SO2. Oximetry readings may be
falsely high as a result of:
■ Carbon monoxide (for example, from smoking
a cigarette) (Dobson 1993).
■ Bright light, especially fluorescent light and heat
lamps (Fox 2002, Ralston et al 1991).
Whereas most oximeter finger probes have effec-
tive light shields, ear probes do not, and finger
probes are contoured for a finger, not the ear.
Shading probes with the hand may result in a more
accurate, lower, reading.
Falsely low oximetry readings may be caused by:
■ Poor perfusion (Jensen et al 1998), such as from
vascular disease, vasoconstriction (Keenan 1995),
severe shock (Keenan 1995) or very irregular
heart rhythms.
■ Shivering (Stoneham et al 1994).
■ High blood bilirubin levels (bilirubinaemia) (Dobson
1993).
■ Dark nail varnish, especially blue or black (Wahr
and Tremper 1996).
■ Intravenous dyes, such as methylene blue (Fox
2002).
The relationship between partial pressure of oxy-
gen in arterial blood (PaO2) and saturation of haemo-
globin in arterial blood by oxygen (SaO2) is complex,
shown graphically by the oxygen saturation curve
(Figure 1). This S-shaped curve represents signifi-
cant changes in PaO2 with minimal changes in SaO2
p45-52w21 1/27/04 5:50 PM Page 49
at higher levels (the ‘plateau’ of the curve); changes
in SaO2 accelerate while changes in PaO2 reduce
at lower levels (the ‘steep’ part of the curve).
Saturation measures the percentage of haemo-
globin (Hb) that is saturated by oxygen. It does not
measure Hb. So, if two patients both have oxygen
saturations of 97%, but one has an Hb of 14g/dl and
the other has an Hb of 7g/dl, the first has 97% of
14g/dl saturation and the second has 97% of 7g/dl,
giving the first patient nearly twice the amount of
oxygen in the arterial blood. Blood gas samples usu-
ally measure Hb, so the Hb should be checked when
considering the significance of oxygen saturation.
Respiratory failure
Respiratory failure results in inadequate oxygen in
the blood. The British Thoracic Society (2002) defines
respiratory failure as an arterial oxygen level below
8kPa (Box 4).
With respiratory failure, arterial carbon dioxide
levels may be low, normal or high. Carbon dioxide
is 20 times more soluble than oxygen (Waterhouse
and Campbell 2002), so diseases that increase the
fluid barrier between alveolar air and pulmonary
blood, such as pulmonary oedema, may cause
hypoxia while carbon dioxide levels remain normal
(normocapnia). This is called type 1 respiratory fail-
ure, and is defined as PaO2 below 8kPa and PaCO2
below 6kPa (BTS 2002).
When breathing is shallow (for example, in COPD)
or slow, insufficient carbon dioxide will be removed
from the blood, causing high blood carbon dioxide
(hypercapnia) in addition to hypoxia. This is called
type 2 respiratory failure, and is defined as PaO2
below 8kPa and PaCO2 above 6kPa (BTS 2002).
TIME OUT 4
Review the respiratory function of the
patient whose results you are analysing.
Is the respiratory acid-base balance
normal? If not, does the patient have a
respiratory acidosis or alkalosis? What
does this imply about his or her
respiratory function? Identify whether you
consider the oxygen status to be
satisfactory. Does the patient have
respiratory failure? If so, is it type 1 or type
2? Remember to check the Hb. Do you
think there should be any change in the
patient’s oxygen therapy? If so, describe
what you recommend. How do these
findings compare with what you know of
the patient’s respiratory function?
Metabolic measures
Bicarbonate (HCO3-) The normal range is 24-
27mmol/l (Coombs 2001). Bicarbonate is the main,
although not the only, chemical buffer in plasma,
so levels indicate metabolic acid-base status.
monitoring patients
Bicarbonate is produced in various parts of the
body, including the liver and kidneys. Low levels of
bicarbonate are caused either by extensive buffer-
ing or by impaired/delayed response to produce
sufficient buffer, such as with liver failure.
Carbonic acid, the main acid in blood, can dis-
sociate into bicarbonate and a free hydrogen
radical, resulting in production of bicarbonate from
respiratory acidosis. Conversely, bicarbonate and a
hydrogen radical (a single H+ atom) can form car-
bonic acid:
CO + H O ↔ H CO ↔ HCO - + H+
2 2 2 3 3
So bicarbonate, used to measure metabolic acid-
base balance, can be increased as a result of hyper-
capnia. Therefore, from the measured bicarbonate
and carbon dioxide, analysers calculate how much
bicarbonate results from respiratory dysfunction and
subtract this from the actual bicarbonate, to provide
a computer estimation. This is the standardised bicar-
bonate (SBC; standardised figures are sometimes
identified by ‘std’) and represents a more accurate
estimation of metabolic function. When gases are
relatively normal, actual and SBC are similar or iden-
tical, but abnormal carbon dioxide levels can cause
significant differences. Using standardised rather
than actual levels is therefore logical; however, all
staff should use the same measurement, as alter-
nating between standardised and actual levels could
result in patients being treated for differences in
interpretation rather than for any physiological change.
Base excess (BE) The normal level is ±2 (Cornock
1996). Metabolic acid-base balance is also repre-
sented by base excess. BE measures the number of
Figure 1. Oxygen dissociation curve
100
97
Arterial
Shift to the right, eg from
pyrexia or acidosis, which
decreases the affinity of
haemoglobin for oxygen
Normal oxygen
dissociation curve
SaO2 %
70
Venous
5.3 13.3
PO2(kPa)
february 4/vol18/no21/2004 nursing standard 49
p45-52w21 1/27/04 5:50 PM Page 50
monitoring patients
Box 5. Metabolic acid-base balance
Metabolic acidosis
■ ↓ HCO3-/SBC
■ ↓ BE/SBE
Metabolic alkalosis
■ ↑ HCO3-/SBC
■ ↑ BE/SBE
Box 6. Compensation (pH in normal range)
■ Respiratory acidosis
(PaCO2 >6kPa)
■ Metabolic alkalosis
(SBC >28, SBE >+2)
■ Respiratory alkalosis
(PaCO2 <4.5kPa)
■ Metabolic acidosis
(SBC <22, SBE <-2)
moles of acid or base needed to return 1 litre blood
to pH 7.4 (assuming PaCO2 remains constant at
5.3kPa). It is derived from measured bicarbonate.
However, like bicarbonate, it can be affected by res-
piratory function, so standardised base excess (SBE)
is calculated, removing the respiratory element to
provide a purely metabolic estimation.
BE means an excess of base (alkali). With meta-
bolic alkalosis, there is an excess of base. But with
metabolic acidosis, there is a negative BE (Box 5).
Sometimes printouts fail to clearly show a minus
sign, but if bicarbonate is low, BE will be negative.
Compared with the pH scale, BE measurement is
simple. Its neutral is zero. Unlike the negative loga-
rithmic pH scale, the BE scale is linear. The normal
range is usually given as +2 to -2.
TIME OUT 5
Review the metabolic results from the
patient whose results you are analysing.
Is the metabolic acid-base balance
normal? If not, does the patient have a
metabolic acidosis or alkalosis? What
does this imply about his or her
metabolic function? How do these
findings compare with what you know
of the patient’s renal and other metabolic
functions? Are there significant
differences between actual and
standardised measurements? If so, note
how abnormal carbon dioxide is.
Compensation
In health, the body maintains homeostasis. Homeostasis
of blood pH is 7.35-7.45. Therefore, provided the
50 nursing standard february 4/vol18/no21/2004
body remains healthy enough to respond, imbal-
ance of either respiratory or metabolic function will
be compensated for by an opposite imbalance of
the other (Box 6). However, while altering respira-
tory rate and depth can (with a healthy respiratory
system) normalise blood pH in a few minutes, meta-
bolic responses take considerably longer (hours or,
sometimes, days). A patient’s history often indi-
cates which way, if any, compensation is occurring
(Table 1). For example, people with COPD, and
therefore hypercapnia with a chronic respiratory
acidosis, often develop compensatory chronic meta-
bolic alkalosis. Reducing respiratory acidosis (for
example, using non-invasive ventilation) in these
patients may result in continuing metabolic (over-)
compensation, causing overall alkalosis that per-
sists for some days. Attempts to compensate may
also be incomplete, failing to normalise pH.
Respiratory effects on acid-base balance, through
removal of carbon dioxide, is at least as powerful
as all chemical buffers combined, and may be twice
as powerful (Marieb 2004). Doubling or halving
the amount of air reaching the alveoli (ventilation)
can alter pH by 0.2 (Marieb 2004), enough to return
a severe acidosis of 7.2 to normal in three to 12
minutes (Guyton and Hall 2000). With healthy
lungs, ventilation can increase 15-fold (Marieb
2004), as experienced by some athletes during vig-
orous exercise.
Metabolic control is more complex, relying on:
■ Hydrogen loss in urine.
■ Production and re-absorption of chemical buffers
(bicarbonate, phosphate, proteins), mainly by
the liver, kidneys and gut.
■ Production of metabolic acids from cells and in
the stomach.
■ Absorption of acids and alkalis from the diet (and
other routes, such as intravenous infusions).
Most intravenous infusions are acidic; for example,
in the author’s workplace the pH of normal saline
(0.9%) is 5.0, while the pH of 5% glucose is 4.15.
TIME OUT 6
Is compensation occurring in the result
you have analysed? If so, from the
patient’s history, identify whether
respiratory function is compensating for
a metabolic problem or vice versa. Is
compensation achieving normal pH?
TIME OUT 7
Having completed your analysis of the
results, discuss your findings and ideas
with a colleague who is used to
interpreting ABGs. If nursing and medical
colleagues in your area are not used to
interpreting ABG results, ask the critical
care outreach team. You may like to use
the case study in box 7 as an example.
p45-52w21 1/27/04 5:50 PM Page 51

monitoring patients

Table 1. Three examples of successful and unsuccessful compensation

Metabolic acidosis (compensated) Respiratory acidosis with (excessive) Uncompensated metabolic acidosis
metabolic compensation

Temperature 36.1 (Not temperature corrected) ■ pH 7.296

■ pH 7.361 ■ pH 7.584 ■ PaCO2 5.10kPa
■ PaCO2 3.15kPa ■ PaCO2 4.86kPa ■ PaO2 12.55kPa
■ PaO2 30.9kPa ■ PaO2 9.24kPa ■ HCO3– act 18.2mmol/l
■ HCO3– act 33.3mmol/l ■ BE -8.3mmol/l
Temperature corrected: ■ BE 11.6mmol/l ■ K+ 7.07mmol/l
■ pH 7.351 ■ Hb 10.9g/dl ■ Lactate 3.65mmol/l
■ PaCO2 3.14kPa ■ SaO2 97.9%
■ PaO2 30.4kPa
■ HCO3–act 21.6mmol/l This patient has an alkalosis. Ventilation This patient has a severe acidosis. Gases
■ HCO3–std 21.7mmol/l (PaCO2) is adequate, as the patient is are normal, so the patient is ventilating
■ BE – act -3.5mmol/l receiving non-invasive ventilation for adequately. There is a severe metabolic
■ BE – std -3.4mmol/l respiratory failure caused by pneumonia. acidosis, and lactate is high. Potassium is
■ Hb 13.5g/dl Oxygen is poor. The ventilator is currently also life-threateningly high.
■ SaO2 100.6% delivering only air, so supplementary
■ K+ 4.1mmol/l oxygen needs to be added. The patient had had a cardiac arrest, and
■ Na+ 139mmol/l at the time this gas was taken was being
■ Ca2+ (calcium) 1.15mmol/l He or she has a metabolic alkalosis. hand-ventilated following successful
■ Cl- (chloride) 108mmol/l Before admission, the pneumonia had resuscitation.
■ Glu (glucose) 5.1mmol/l presumably caused increasing respiratory
■ Lac (lactate) 0.5mmol/l acidosis, initiating metabolic
compensation to maintain normal pH.
This patient has a normal pH, but is Now that ventilation has removed the
hyperventilating (PaCO2). Oxygenation respiratory acidosis, metabolic alkalosis
(PaO2, SaO2) is excessive, partly from remains, causing an overall alkalosis.
hyperventilation, and partly from the
three litres of nasal oxygen the patient
was receiving. Oxygen can be
discontinued, and monitored using pulse
oximetry.
The 100.6% saturation is machine error.
Changes in gas measurements from
temperature correction and in metabolic
measurements from standardisation are
small and insignificant.

The patient has a slight metabolic

acidosis. This would be the underlying
problem, for which respiratory
compensation is occurring.
This patient had type 1 diabetes and was
recovering from diabetic ketoacidosis.
While blood glucose level is now normal,
metabolic acidosis is reducing but persists.
Lactate is normal.

Conclusion Like any other investigation, blood gas analysis

ABG analysis provides useful monitoring, especially
for carbon dioxide. In most wards, taking arterial
samples has traditionally been a medical role, but
some specialist nurses are now taking samples and
so need to be able to interpret measurements.
Nurses who are not taking samples may be able
to initiate earlier intervention if they are able to
interpret results. Understanding results can help
nurses to understand treatments and interventions,
so making nursing more interesting.
may provide information that can be useful for
treating patients.
This article has described how to interpret the
most important results. It has not covered every
possible measurement machines may make (which
vary according to programming). As you develop
your skills further, you may benefit from finding
out the significance, or otherwise, of other meas-
urements.
Interpreting ABG samples is a skill which, like
any other, improves with practice. Unfortunately,

february 4/vol18/no21/2004 nursing standard 51

p45-52w21 1/27/04 5:50 PM Page 52

monitoring patients

Box 7. Case study

Mr Watts is admitted with bronchopneumonia. He has no history of chronic respiratory disease. He

has a non-productive cough. His oxygen saturation is below 86% and he is very dyspnoeic. On
100% oxygen, his blood gases are:
■ pH 7.32
■ pCO2 7.44kPa
■ pO2 6.78kPa
■ SBC 26.0mmol/l
■ SBE 2.4mmol/l
■ SO2 89%

This result shows an overall acidosis, with respiratory acidosis but no metabolic compensation. This
indicates a new respiratory problem. Raised carbon dioxide indicates poor ventilation, which also
contributes to severe hypoxia. The sample confirms that the pulse oximetry measurement was
accurate, and he is started on bilevel non-invasive ventilation.

Following prn (pro re nata, or when required) salbutamol and ipratropium nebulisers, his cough
becomes productive. A physiotherapist is called, achieving effective sputum clearance. One hour
after physiotherapy, with bilevel non-invasive ventilation delivering 60% oxygen, his gases are:
■ pH 7.425
■ pCO2 5.47kPa
■ pO2 15.54kPa
■ SBC 26.0mmol/l
■ SBE 2.0mmol/l
■ SO2 99%

Mr Watts’ metabolic status remains unchanged, as would be expected. His carbon dioxide (and
acid-base balance) levels have been restored to normal, so it is decided to discontinue bilevel non-
invasive ventilation. His oxygenation is greatly improved, but it is decided to maintain 60% oxygen
as non-invasive ventilation is being discontinued. Further changes can be guided by pulse oximetry.
These ABGs have enabled prompt (and probably earlier than might otherwise have occurred)
interventions and, following the second gas, early discontinuation of non-invasive ventilation.

Mr Watts will need active treatment for his bronchopneumonia, including antibiotics, regular
physiotherapy, and probably other medications and investigations. Nursing care should include
frequent (at least four-hourly) respiratory observations, including rate and depth of breathing and
oxygen saturation.

samples are often taken when patients’ conditions TIME OUT 8

are too poor to spend time practising interpreta- Now that you have completed the
tion. Making a second copy of the printout from article you might like to write a
the machine, or copying results on to notepaper, practice profile. Guidelines to help you
enables nurses to practise interpretation at a more are on page 55.
convenient time

REFERENCES
Babb M, Farmery A (2003) Haemorrhagic
shock. Surgery. 21, 8, 208a-208e.
Bateman N, Leach R (1998) Acute oxygen
therapy. British Medical Journal. 317,
7161, 798-801.
Beaumont T (1997) How to guides:
arterial blood gas sampling. Care of
the Critically Ill. 13, 1, centre insert.
British Thoracic Society (2002) Non
invasive ventilation in acute respiratory
failure. Thorax. 57, 3, 192-211.
British Thoracic Society (1997) Guidelines
for the management of chronic
obstructive pulmonary disease. Thorax.
52, Supplement 5.
Clutton-Brock T (1997) The assessment
and monitoring of respiratory function.
In Goldhill D, Withington P (Eds)
Textbook of Intensive Care. London,
Chapman & Hall.
Coombs M (2001) Making sense of
arterial blood gases. Nursing Times.
97, 27, 36-38.
Cornock M (1996) Making sense of
arterial blood gases and their
interpretation. Nursing Times. 92, 6,
30-31.
Dimond B (2002) Legal Aspects of
Nursing. Third edition. Harlow,
Longman/Pearson Education.
Dobson F (1993) Shedding light on pulse
oximetry. Nursing Standard.
7, 46, 4-11.
Fletcher S, Dhrampal A (2003) Acid-base
balance and arterial blood gas analysis.
Surgery. 21, 3, 61-65.
Fox N (2002) Pulse oximetry. Nursing
Times. 98, 40, 65.
Gosling P (1995) How to guides: blood
gas analysis. Care of the Critically Ill.
11, 1, centre insert.
Guyton A, Hall J (2000) Textbook of
Medical Physiology. Tenth edition.
Philadelphia PA, WB Saunders.
Hinds C, Watson D (1996) Intensive Care.
Second edition. London, WB Saunders.
Hope R et al (1998) Oxford Handbook of
Clinical Medicine. Fourth edition.
Oxford, Oxford University Press.
Hornbein T (1994) Acid-base balance. In
Miller R (Ed) Anesthesia. Fourth
edition. New York NY, Churchill
Livingstone.
Jensen L et al (1998) Meta-analysis of
arterial oxygen saturation monitoring
by pulse oximetry in adults. Heart and
Lung. 27, 6, 387-408.
Keenan J (1995) Pulse oximetry. Nursing
Standard. 9, 35, 55.
Marieb E (2004) Human Anatomy and
Physiology. San Francisco CA,
Benjamin/Cummings.
Nursing and Midwifery Council (2002) Code
of Professional Conduct. London, NMC.
Ralston A et al (1991) Potential errors in
pulse oximetry. Anaesthesia. 46, 4,
291-295.
Sheehy S, Lombardi J (1995) Emergency
Care. Fourth edition. St Louis MO,
Mosby.
Stoneham M et al (1994) Knowledge
about pulse oximetry among medical
and nursing staff. Lancet. 344, 8933,
1339-1342.
Wahr J, Tremper K (1996) Oxygen
measurement and monitoring
techniques. In Prys-Roberts C, Brown B
Jr (Eds) International Practice of
Anaesthesia. Oxford, Butterworth
Heinemann.
Waterhouse J, Campbell I (2002)
Respiration: gas transfer. Anaesthesia
and Critical Care. 3, 9, 340-343.

52 nursing standard february 4/vol18/no21/2004