ARTERIAL BLOOD GASES WHEN, HOW AND WHAT DOES IT

MEAN?

Dr. N. S. Mani. Assistant Professor, Department of Paediatrics,

Governemnt Medical College, Mulamkunnathkavu, Valappaya PO
680596, Thrissur.

Blood gases are frequently requested for seriously ill surgical patients. Apart
from helping to establish a diagnosis, blood gases may also help to ascertain
the severity of a particular condition (e.g. metabolic acidosis in sepsis), the
direction that further interventions should take and the intensity of
monitoring required. It is therefore essential that the surgical trainee not only
appreciates the correct techniques involved in performing an arterial blood
gas (ABG) analysis, but also has an understanding of the changes in the
blood gas parameters in the commonly encountered clinical conditions. The
following is an attempt to explain the indications and technique of
performing an arterial blood gas sampling, the systematic analysis of a blood
gas report and an understanding of its implications. The theoretical basis of
respiratory pathophysiology and the biochemistry of acid base homoeostasis
have not been dealt with in this article. Also, certain concepts have been
explained in small print, only for the benefit of the curious reader.

Indications for an arterial blood gas analysis

Blood gas analyses are performed to evaluate the adequacy of ventilation,

oxygenation, oxygen-carrying capacity of the blood and acid-base levels.
ABGs are indicated in a number of clinical conditions to

1. Establish the diagnosis and severity of respiratory failure

2. Manage patients in intensive therapy units admitted for

· respiratory failure or dysfunction

· cardiac failure
· renal or hepatic failure
· poly trauma and multiorgan failure
· diabetic ketoacidosis
· sepsis and burns
· poisoning

3. Guide therapy in patients in the ITU, eg

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· oxygen administration
· mechanical ventilation
· alkali treatment

4. Monitor patients during

· cardiopulmonary surgery
· cardiopulmonary exercise testing
· sleep studies

5. Determine prognosis in critically ill patients

The aims of doing a blood gas analysis are to detect

1. the presence and severity of hypoxemia and hyper(hypo)capnia and the

amount of metabolic compensation.

2. changes in acid-base homeostasis, which might need further investigation

and intervention.

Arterial blood sampling

Blood can be drawn from an artery either via an indwelling arterial cannula
or by direct arterial puncture. The commonest artery used is the radial
followed by the dorsalis pedis; rarely the brachial and the femoral vessels (as
they are the principal sources of blood supply to the limbs). Time should
usually be allowed for the attainment of a steady state after alteration of
ventilatory parameters or the FiO2; at least 5 minutes for any patient without
obstructive lung disease and at least 30 minutes if he/she has obstructive
lung disease.

Direct arterial puncture is usually done with a 21G or smaller needle. If the
radial artery is to be used, the collaterality of blood flow to the hand must be
checked by the Allen's test. The wrist is kept immobilized and if necessary
extended with a support just below the dorsum of the wrist. Under aseptic
precautions and with (out) local anaesthesia, the heparinised syringe with
needle is introduced at an angle of 450 to the horizontal. The blood can then
be aspirated in two ways. One is to penetrate the needle till it hits the bone
and then withdrawing the needle while maintaining suction in the syringe till
one sees bright red blood coming freely into the syringe. The other way is to
penetrate the tissues while maintaining suction so that the artery is not
pierced through and through. After drawing a sample, firm pressure must be
applied at the site of arterial puncture for at least two minutes.

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Reading of the report

Normal values in an ABG report. (Table 1)

paO2 in
paCO2 in Sat
kPa HCO3
kPa pH BD/BE O2
(mm mmols/L
(mm Hg) (%)
Hg)
11-13
Arterial 4.7-5.9 7.36 -
(80- 21-28 +/-2 >95%
Blood (35-45) 7.44
100)
Venous 5 - 5.6 5.6-6.7 7.34 -
Blood (37-42) (42-50) 7.42

Table 2

Normal Range
Anion Gap 8-16 mmols/L
Osmolar Gap 10 mmols/L
PaO2 (mmHg)/FiO2
More than 3
(%)

Note: The arterial pO2 reduces with age. A rough guideline is that above the
age of 40 years, paO2 = 105-age in years/2.

The pH of the blood is maintained within a normal range by a number of

compensatory mechanisms, the most important being the body buffer
mechanisms and the renal and respiratory systems. The degree of
compensation varies between individuals and depends on the severity and
duration of the primary problem and associated medical comorbidities.
Respiratory compensation for metabolic problems is usually rapid and
almost complete. The lungs respond quickly by increasing ventilation to
blow off excessive carbon-dioxide (in metabolic acidosis) or decreasing
ventilation to retain carbon-dioxide (in metabolic alkalosis). The latter
compensation is less complete than the former for obvious reasons. The
renal compensation for respiratory imbalances is slow and incomplete. The
kidneys regulate extracellular fluid H+ ion concentration by secretion of H+
ions, reabsorption of filtered HCO3- ions, and the production of new HCO3-
ions. Excess HCO3- is filtered into the renal tubules and eliminated in the
urine. Depending on the need to excrete either an acid or a base load, the
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kidneys can excrete urine with a pH ranging from 4.5 to 8.0. A rough guide
to the degree of compensation to primary changes in CO2 and HCO3 as a
result of respiratory and metabolic imbalances respectively is shown in table
3.

Table 3. Respiratory and renal compensation in acid-base imbalance (5)

Acid-base Carbon-dioxide (mm Plasma bicarbonate

imbalance Hg) (mmol/L)
Compensates
Metabolic
(decreases) by 1.25 x Decreases by X
acidosis
X
Metabolic Compensates
Increases by X
alkalosis (increases) by 0.75 x X

Acute respiratory
Increases by X Compensates (increases)
acidosis
by 0.1 x X
Chronic
Compensates (increases)
respiratory Increases by X
by 0.4 x X
acidosis
Acute respiratory Compensates (decreases)
Decreases by X
alkalosis by 0.2 x X
Chronic
Compensates (decreases)
respiratory Decreases by X
by 0.4 x X
alkalosis

Algorithm for Blood Gas Analysis

Step 1 - Look at the PaO2 and PaCO2 levels

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Note : if patient is on oxygen supplementation use PaO2/PiO2 instead of
PaO2

Step II

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To diagnoses associated respiratory abnormalities (if any) check if the
PaCO2 values are similar to or grossly different from the expected values
due to compensation by the lungs (Table 3)

Note : if the primary abnormality is in the PaCO2 and not in the standard
bicarbonate values - go to Step 1

Abnormalities of gas exchange

Follow step I of the algorithm. A few concepts are explained further.

Hypoxia: The first step is to detect the presence of hypoxia (i.e., less than 60
mm Hg on room air). Patients with clinically evident respiratory problems
who have been given oxygen supplementation before blood gas analysis
must be assumed to be hypoxic at this stage. If a patient is being given
oxygen supplementation, then the ratio of the paO2 (in mm Hg) to FiO2 (in
%) is used to detect hypoxia. Usually, the oxygen saturation of the blood is
also noted which correlates with the paO2 of the arterial blood and helps in
establishing the diagnosis of hypoxia. The saturation as obtained by a blood
gas analysis is more accurate than that obtained by a pulse oximetry, as it is
not influenced by shock states and skin pigmentation.
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Hypercapnia: The paCO2 level must then be noted, which will help in
differentiating between type I and type II respiratory failure. In type I
respiratory failure, the paCO2 will be normal or low (</=45) and in type II
respiratory failure, the paCO2 will be high (>45).

Table 2. Causes of respiratory failure

Type I Type II
CNS depression (drugs,
Atelectasis
sleep, head injury)
Pulmonary edema (cardiogenic and sssHigh spinal cord
non cardiogenic) lesions
Pneumonia Phrenic nerve lesions
Pleural effusion Neuromuscular disorders
Haemo/pneumothorax Severe kyphoscoliosis
COPD
Type I causes in an
advanced state

Causes of type I respiratory failure include conditions with an impaired gas

exchange and causes of type II respiratory failure include the causes of type
I in an advanced state and conditions with impaired ventilation as shown in
table II. Differentiation between types I and II failure is essential to
determine the aetiology and institute further treatment. It may also rarely be
used to restrict O2 supplementation in patients with type II disease because
such patients are dependent on hypoxia for the respiratory drive and
abolishing hypoxia might further suppress the CNS stimulation for
respiration. Patients with persistent hypoxia, rising CO2 levels and
respiratory acidosis require mechanical ventilation and are usually seen by
the anaesthetist at this stage.
In patients on a ventilator, hypoxia might indicate one of several things,
including

• accidental disconnection of the breathing circuit ( which should be

evident by the alarms, fall in O2, fall in saturation on pulse oximetry,
clinical evidence of respiratory distress, etc.)
• development of pneumothorax which could be detected clinically and
might need confirmation by X-ray before intercostal tube drainage
• development or worsening of pre-existing chest problems
(bronchopneumonia, ARDS, pulmonary contusion) might require
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 changes in settings of the ventilator like increasing FiO2 levels,
ventilatory rate or tidal volume, adding or increasing PEEP, or
changing to other modes of ventilation.

A high CO2 level is always associated with hypoxia unless the patient is on
oxygen supplementation. However, hypercarbia associated with a normal
oxygen level should also be approached with the same urgency as the patient
might deteriorate rapidly. The possibility of a venous sample as a cause of
unexpected hypercarbia and hypoxia should be kept in mind. In patients on a
ventilator, moderate rise in CO2 levels are currently considered acceptable
and interventions to correct these might be associated with significant side
effects including barotraumas and hypotension (permissive hypercarbia).
Similarly, patients with COPD have adapted to higher levels of carbon-
dioxide and might not require correction to normal levels.
Acute changes in paCO2 result in predictable changes in pH. For every
increase in paCO2 of 20 mm Hg (2.6 kPa) above normal, the pH falls
approximately by 0.1. For every decrease of paCO2 of 10 mm Hg (1.3 kPa)
below normal, the pH rises by 0.1. Any change in pH outside these
parameters is therefore metabolic in origin (1). The kidneys take time to
compensate for the change in pH the amount of renal compensation indicates
the chronicity of the problem and the need for urgent correction. Correction
will usually involve a combination of treatment of the cause, initiation of
mechanical ventilation or modification of the settings and reduction of CO2
production.

Alveolar-arterial oxygen gradient (A-a)PO2: This is the difference in the

oxygen partial pressures between the alveolar and arterial sides. In patients
with type II respiratory failure, it may help to determine whether the patient
has associated lung disease or just reduced respiratory effort.

The A-a gradient increases a little with age, but should be less than 2.6kPa
(20mmHg). A normal gradient would imply conditions like CNS depression
and neuromuscular disorders as the cause and a high gradient would imply
some lung disease (1).

Abnormalities of acid base balance

Follow Step II of the algorithm. The concepts in the algorithm are explained
further.

PH of the blood: The pH is usually maintained within a narrow range by a

number of buffer systems in the body. A normal pH value may still be due to
a well-compensated imbalance or a mixed acid base disorder and an

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abnormal value is definitely due to a poorly compensated acid base problem
or due to both metabolic and respiratory derangements causing an imbalance
in the same direction. A rough guide to the amount of compensation that can
be expected for a given primary alteration in CO2 or HCO3 is given in table
3.
Serum bicarbonate: The actual bicarbonate is the value calculated from the
blood gas sample. The standard/corrected bicarbonate is the value obtained
after correction of CO2 levels to 40mm Hg and at room temperature. It gives
a better estimate of the metabolic problem causing acid base imbalance. The
base deficit/excess is the amount of deviation of the standard bicarbonate
from the normal. The metabolic problem could either be a low (base deficit
or metabolic acidosis) or high (base excess or metabolic alkalosis) standard
bicarbonate.

Compensation: As discussed earlier, a primary metabolic derangement will

be accompanied by some degree of respiratory compensation. The ability to
detect the primary abnormality and the amount of compensation is hindered
by other co-existing conditions causing respiratory acidosis and/or alkalosis.
Also, coexisting medical problems can cause both metabolic acidosis and
alkalosis. Step II of the algorithm gives a rough idea to determine the main
features of the acid base imbalance.

Metabolic acidosis
Metabolic acidosis can be due to a variety of conditions. Treatment of
metabolic acidosis is treatment of the cause. Direct administration of alkali
(sodium bicarbonate) is reserved for severe cases. A number of conditions
can result in metabolic acidosis, the most important among them being the
under perfusion of tissues resulting in accumulation of lactic acid.
Differentiation of the causes of metabolic acidosis requires the estimate of
an entity called the 'anion gap'.

Anion gap

Body fluids including blood may contain a variable number of ions, but the
total number of anions (negative ions) and cations (positive ions) are roughly
the same. The ions that are usually measured in blood are cations like
sodium and potassium and anions including chloride and bicarbonate. There
are unmeasured ions in both groups (cations and anions), which also
contribute to the ionic constitution of blood. The measured cations are
usually greater than the measured anions by about 8-16mmol/L. This is
because the unmeasured anions constitute a significant proportion of the

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total number of anions in blood. Proteins make this up predominantly, but
also included are sulphates, phosphates, lactate and ketones.

Causes of a decreased anion gap include hypoalbuminaemia and severe

haemodilution. Rarer causes include increase in minor cation concentrations
like calcium and magnesium. Causes of a raised anion gap include
dehydration and any cause of raised unmeasurable anions, like lactate,
ketones and renal acids, along with treatment with drugs given as organic
acids such as penicillin, salicylates and poisoning with methanol, ethanol
and paraldehyde. Rarely it may be due to decreased minor cation
concentrations such as calcium or magnesium.

Raised anion gap metabolic acidosis:

As documented above, accumulation of a number of acids can result in

raised anion gap metabolic acidosis. In such cases, the reduction in serum
HCO3- matches the anion gap. If not, a second acid base disorder should be
kept in mind. When metabolic acidosis and alkalosis coexist, as in vomiting
and ketoacidosis, the plasma HCO3- may be normal, and a raised anion gap
may be the initial evidence of an underlying acid-base disturbance (2).

To differentiate between the many causes of 'increased anion gap metabolic

acidosis', we measure the osmolar gap that is the difference between the
measured osmolarity and the calculated osmolarity.

Normal anion gap (hyperchloraemic) metabolic acidosis

This usually results from conditions wherein there is a loss of alkali

(i.e.HCO3-) or metabolic equivalent (eg, excretion of salts of organic anions
in proportionate excess of chloride) or an accumulation of HCl or metabolic
equivalent (eg, NH4Cl and chloride salts of amino acids) (2).
Loss of HCO3- can occur either due to GI causes or due to renal causes
(renal excretion or insufficient generation). In many surgical conditions, the
cause is usually obvious.

Examples of extrarenal causes are excessive diarrhoea or drainage of

gastrointestinal secretions, NH4Cl administration, parenteral nutrition, rapid
saline infusion and congestive cardiac failure. Generation of large amounts
of organic anions can sometimes produce this type of metabolic acidosis
(and not one with a raised anion gap), if the kidneys can prevent their
accumulation by rapid excretion.
Examples of renal causes include the various types of renal tubular acidosis

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(type I, type II and type IV).

Metabolic acidosis (M Ac.)

Examples of different types of renal tubular acidosis (RTA)

Type IV (def.
Type I (distal) Type II (proximal)
NH4+ production)
Urinary tract
Fanconi's syndrome Cortisol deficiency
obstruction
Interstitial Myeloma light Urinary tract
nephritis chain nephropathy obstruction
K+ sparing
Nephrotoxins
diuretics
Genetic diseases

Metabolic Alkalosis

Metabolic alkalosis can result from the loss of acid, addition of alkali or both
in the kidneys or elsewhere. Extrarenal sites include stomach (loss of acid),
redistribution of alkali from the intracellular stores to the ECF (as in
potassium or chloride depletion), oral administration (antacids, ion-exchange
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resins, milk alkali syndrome, oral HCO3-) and parenteral administration of
alkali (citrate in blood transfusions, bicarbonate in severe metabolic
acidosis). Renal causes of alkali excess include mineralocorticoid excess,
response to long-standing hypercapnia (persists even after correction of
respiratory acidosis), hypokalemia (promotes H+ secretion in the distal
nephron) and ECF volume depletion (impaired HCO3- excretion). Certain
conditions can cause metabolic alkalosis by a number of mechanisms (eg
diuretic use causes both ECF depletion and hypokalemia).
Respiratory Alkalosis
The principal cause of respiratory alkalosis (hypocapnia) is hypoxia and its
causes (type I respiratory failure), further treatment of which has been
detailed before. Other causes of acute respiratory alkalosis include anxiety,
fever, pain, sepsis, hepatic failure, CNS disorders (stroke, infections),
pulmonary disorders without hypoxia (infections and interstitial lung
disease), delirium tremens and drugs (salicylate intoxication). Chronic
causes include high altitude hypoxia, chronic hepatic failure, chronic
pulmonary disease, CNS trauma, anaemia, hyperthyroidism, beriberi and
pregnancy (2,4). Treatment should be directed towards the cause.

Problems with arterial blood gas analysis

ABG analysis is associated with a number of problems including 3

· Pain
· Preanalytical errors: air contamination, heparin dilution, storage, excessive
delay before analysis
· Analytical errors: accurate differences between models of blood gas
analysers
· Postanalytical errors: transcription errors, delays in reporting results
· Infection risk to patient (particularly with arterial catheter)
· Infection risk to clinician (particularly with arterial puncture)
· Thrombosis and distal embolization (particularly with arterial catheter) and
ischemia
· Blood loss (particularly with arterial catheter), arterial spasm, hematoma
· Intermittent information
· Spontaneous variability of blood gas levels without clinical change in the
patient
· Cost

Conclusion

Arterial blood gases can provide invaluable clinical information in critically

ill surgical patients. It must however be remembered that they are static
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measurements and do not necessarily reflect the changing physiologic status
of a sick patient. Therefore, any decision-making should be directed keeping
in mind the overall condition of the patient and not the blood gas report
alone. Picking up a major acid base disorder might not be as difficult as
identifying other coexisting acid base imbalances which might be masked by
the main disorder, but might also require active treatment.

Glossary

PaO2 Partial pressure of oxygen in arterial blood

Fraction of oxygen in inspired air (0.21 for
FiO2
atmospheric air)
Partial pressure of carbon dioxide in arterial
PaCO2
blood
Hydrogen ion concentration expressed in
H+
nmol/L
Negative logarithm of (H+) expressed in
pH
nmol/L
Percentage of haemoglobin which oxygenated
SaO2
(oxyhaemoglobin), i.e. oxygen saturation
HCO3 serum concentration of bicarbonate in mmol/L
Quantity of acid or base necessary to titrate 1
Base excess litre of blood to pH 7.4 at 370C with a PaCO2
of 5.3kPa
Base deficit Negative base excess
The state in which the pH of the blood is
Acid-base balance maintained at approximately between 7.35 and
7.45
Underlying acidosis/alkalosis, but the pH of the
Compensated
blood has been returned to normal by
acidosis/alkalosis
compensatory mechanisms.

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