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ABC of oxygenAssessing and interpreting arterial blood gases and acid-base balance

Adrian J Williams

One of the main factors determining oxygen delivery to cells isthe oxygen content of the blood. Blood gas tensions are

measured by direct blood sampling or transcutaneous diffusionand oxygen saturation of haemoglobin from pulse oximetry.Arterial blood gas analysis is widely available in hospitals and thedirect measurements (pH, Pao2, Paco2) are among the mostprecise in medicine. The value of such measurements, however,depends on the ability of doctors to interpret the results properly.

Arterial punctureArterial puncture may result in spasm, intraluminal clotting, orbleeding and haematoma formation, as well as a transientobstruction of blood flow. These factors may decrease thearterial flow in distal tissues unless adequate collateral arterialvessels are available. The brachial and femoral arteries do nothave adequate collateral supplies. The radial artery at the wristis the best site for obtaining an arterial sample because it is nearthe surface, relatively easy to palpate and stabilise, and usuallyhas good collateral supply from the ulnar arteries. This can beconfirmed by a modified Allens test.

It is kinder to patients to use local anaesthesia over theradial artery before puncture. Analgesic patches can be used forchildren. Use a 20 or 21 gauge needle with a preheparinisedsyringe. Express the heparin from the syringe before taking thesample; adequate heparin will remain in the 0.2 ml dead spaceof the barrel and needle. At least 3 ml of blood is required toavoid a dilution effect from the heparin.

Any sample with more than fine air bubbles should bediscarded. Air bubbles result in gas equilibration between the airand the arterial blood, lowering the arterial carbon dioxide

pressure (Paco

2) and increasing the arterial oxygen pressure(Pao2). The cellular constituents of blood remain metabolicallyactive so arterial gas tensions in the sample will change overtime. If the sample cannot be analysed quickly it should becooled to 5C immediately. The sample can then be stored forup to one hour with little clinically significant effect on the result.

Arterialised ear lobe samples provide an alternative toarterial puncture for occasional samples. A capillary tube isused to sample blood from a warmed, vasodilated earlobe. ThePaco2values agree well with those obtained from arterialsamples, but accuracy of the Pao2depends on good techniquein arterialisation of the ear lobe.

Analysers

Modern blood gas analysers are automated self diagnosticinstruments requiring minimal maintenance. The pH electrodemeasures the potential difference between a known solutionwithin the measuring electrode and the unknown (sample)solution at 37C.

The Paco2electrode measures carbon dioxide tensions byallowing carbon dioxide to undergo a chemical reactionproducing hydrogen ions. The hydrogen ion production causesa difference in potential that is measured by half cells similar tothose of the pH electrode. The Pao2electrode is apolarographic device that measures oxygen tensions byoxidation-reduction reactions, a chemical process that generatesmeasurable electric currents.

Problems of taking arterial blood samples

x Bleedingx Vessel obstructionx Infection

Normal values of arterial pH and Paco2

Mean 1 SD 2 SD Acceptable

pH 7.4 7.38-7.42 7.35-7.45 7.3-7.5

Paco2(kPa) 5.3 5.0-5.6 4.7-6.0 4-6.7

Taking arteria l blood sample

Allens test. The radial and ulnararteries are occluded by firmpressure while the fist is clenched.The hand is opened and the arteriesreleased one at a time to check theirability to return blood flow to thehand

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Calibration is important since the electrodes drift over time;a 1 point calibration adjustment to a single standard is madebefore each analysis or every 30 minutes. A 2 point calibrationusing two standards should be done every 2-8 hours.

Pulse oximetryThe development of simpler oximeters to measure oxygensaturation has been important in improving monitoring of

oxygen therapy. The sigmoid saturation curve for haemoglobindefines the relation between saturation and Pao2. Oximeterswork on the principle that desaturated haemoglobin andoxygenated haemoglobin absorb light of different wavelengths.The current devices use two wavelengths and measure theabsorption in the pulsatile element of the blood flow, thusproducing a measure of the oxygen saturation of arterial bloodseparate from the non-pulsatile venous blood.

The probe is applied to the finger or earlobe. The delay inregistration of central changes in saturation depends on thecirculation time from the lungs to the monitoring site. It isslightly greater for the finger (about 30 seconds). Oximeters tendto be less accurate with saturations below 75%, but for mostclinical situations changes above this range are more important.Some clinical situations can affect the accuracy of measurement.

Transcutaneous measurementsTranscutaneous electrodes with combined sensors can be usedto measure both oxygen and carbon dioxide pressures. Theseelectrodes rely on diffusion from vasodilated vessels in heatedskin. In neonates with thin, well vascularised skin the method isreliable, but it is less useful in adults. The transcutaneous carbondioxide pressure is slightly higher than the Paco2while thetranscutaneous oxygen pressure is often around 80% of thePao2. The results are easier to interpret if initial pressures arecompared with arterial gas pressures. A delay of around 5minutes in the signal is related to diffusion across the skinbarrier. This makes the method suitable for monitoring stable

measurements or slow trends rather than instantaneouschanges. The electrode needs to be moved every 4-8 hoursbecause heating of the skin may cause local burns.

Relation between pH and Paco2Acute changes in Paco2result in predictable changes in pH (thenegative log of hydrogen ion concentration) and plasmacarbonic acid. This represents the respiratory acid-base change.Although the relation is not completely linear, within clinicallyrelevant ranges it is sufficiently linear to allow the followingguideline to estimate the degrees of abnormality resulting fromacute changes in Paco2:x For every increase in Paco2of 20 mm Hg (2.6 kPa) above nor-mal the pH falls by 0.1

x For every decrease of Paco2 of 10 mm Hg (1.3 kPa) belownormal the pH rises by 0.1.

Any change in pH outside these parameters is thereforemetabolic in origin.

Anion gap conceptOrganisms exist in a state of electroneutrality with major andminor cations balanced by similar anions. The anion gap is anartificial disparity between the concentrations of the majorplasma cations and anions routinely measurednormallysodium, chloride, and bicarbonate. The anion gap is calculatedas Na+ (Cl+HCO3

).

Adult values for Pao2and oxygen saturation

Pao2(kPa) Sa o2(%)

Normal (range) 13 (>10.7) 97 (95-100)

Hypoxaemia < 10.7 < 95

Mild hypoxaemia 8-10.5 90-94

Moderate hypoxaemia 5.3-7.9 75-89

Severe hypoxaemia < 5.3 < 75

Problems with readings of pulse oximeters

Clinical situation Result

Carboxyhaemoglobin Falsely high saturation

Bilirubin Falsely low saturation

Melanotic skin Variable, reduced signal

Poor peripheral perfusion Low signal, unreliable results

Approximate relation between Paco2and pH

Paco2(mmHg kPa) pH Plasma bicarbonate (mmol/l)

80 10.6 7.2 28

60 8 7.3 26

40 5.3 7.4 24 (normal value)

30 4 7.5 22

20 2.7 7.6 20

Disturbances in acid-base balancex Respiratory acidosis(that is, ventilatory failure)the drop in pH is

explained by the change in Paco2x Respiratory alkalosis(that is, alveolar hyperventilation)the

decreased Paco2explains the increased pHx Metabolic acidosisreduced pH not explained by increased Paco2. It

is usually associated with an increased anion gap due to theaccumulation of renal acids, lactic acids, and ketoacids (fromdiabetes or starvation)

x Metabolic alkalosisraised pH out of proportion to changes inPaco2. It is associated with hypokalaemia, volume contraction, orexogenous alkali administration

Transcutaneous oxygen and carbon dioxide monitor

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The anion gap is normally 8-16 mmol/l, of which11 mmol/l is typically due to albumin. A decreased anion gap isusually caused by hypoalbuminaemia or severe haemodilution.Less commonly, it occurs as a result of an increase in minorcation concentrations such as in hypercalcaemia orhypermagnesaemia. Increased anion gap acidosis is caused bydehydration and by any process that increases theconcentrations of the minor anions, lactate, ketones, and renalacids, along with treatment with drugs given as organic salts

such as penicillin, salicylates, and with methanol and ethyleneglycol. Rarely an increased anion gap may result fromdecreased minor cation concentrations such as calcium andmagnesium.

Metabolic acidosis without an increased anion gap istypically associated with an increase in plasma chlorideconcentrations; chloride ions replace plasma bicarbonate.Hyperchloraemic acidosis is usually caused by gastrointestinalloss or renal wasting of bicarbonate.

Pathophysiology of acute respiratoryfailure

Alveolar ventilation and carbon dioxideVentilation can be defined in terms of movement of a volume ofair in to and out of the lungs, removing carbon dioxide fromthe blood and providing oxygen. Tidal volume (Vt) is the sumof alveolar volume (Va) and dead space volume (Vd). Thesedivisions are also appropriate to tidal ventilation, which includesthe component that takes part in gas exchange (alveolarventilation) and dead space ventilation.

Alveolar ventilation is best defined in terms of ventilation ofcarbon dioxide. Diffusion of carbon dioxide across thealveolocapillary membrane is more rapid than diffusion ofoxygen, and the carbon dioxide dissociation curve of blood islinear over a wide range of alveolar ventilation.

Changes in alveolar ventilation (Va) are accompanied bycorresponding linear changes in alveolar and thus arterial

carbon dioxide pressure. Since alveolar ventilation is theimportant variable, measurement of tidal ventilation andrespiratory rate can be misleading. A patient with hypercapniamay actually have a high tidal ventilation. For example, ifVt= 0.5 l/breath; Vd=0.2 l, and respiratory rate = 16breaths/min the minute ventilation is 8 l/min (16 0.5) butalveolar ventilation is 4.8 l/min (16 (0.5 0.2)). Assuming atypical Vco2of 0.2 l/in):

Paco2 = 0.2 863 = 36 mm Hg= 4.8 kPa4.8

If Vt = 0.3 l/breath, Vd= 0.2 l, and respiratory rate = 28breaths/min the minute ventilation is 8.4 l/min (28 0.3) butalveolar ventilation is 2.8 l/min (28 (0.3 0.2))

Paco2 = 0.2 863 = 62 mm Hg= 8.2 kPa.2.8

Thus, for a similar minute ventilation the patient is workingless efficiently and the Paco2is raised.

OxygenationOxygenation is the transfer of adequate oxygen from the

alveoli to the blood, where it exists mainly in the form ofoxyhaemoglobin. I will consider only respiratory causes ofinadequate oxygenation. However, haemoglobin may bedesaturated by other causesfor example, carbon monoxidepoisoning. An oxygen pressure above 8 kPa will be associatedwith saturation over 90% and adequate oxygen carryingcapacity if the packed cell volume is normal.

Minor anions and cations

Cations Anions

Potassium Phosphates

Calcium Sulphates

Magnesium Organic anions such as proteins

Assessment of alveolar ventilation is thekey to determining whether a patient isgetting enough oxygen

Calculation of alveolar ventilation

In a steady state:

Va=Vco2 863 or by transposition: Paco2 =Vco2 863

Paco2 VaWhereVco2 = carbon dioxide production by the body (l/min) corrected to

standard temperature and pressure dryVa= alveolar volume per unit of time corrected to body temperatureand pressure, saturated with water (BTPS)863 = conversion factor to express Vain l/min BTPSPaco2 = partial pressure of alveolar carbon dioxide (mm Hg, BTPS)

which is essentially equal to arterial carbon dioxide pressure (Paco2)

12

Partial pressure of oxygen (kPa)

%s

aturationofhaemoglobinwithoxygen

10864200

20

40

60

80

100

Oxygen saturation curve

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Alveolar-arterial oxygen gradientRespiratory failure is defined as type I when there ishypoxaemia without carbon dioxide retention and type II whenthere is hypercapnia. Calculation of the gradient between thealveolar and arterial oxygen tensions (the A-a gradient) in typeII respiratory failure will help to determine whether thepatient has associated lung disease or just reduced respiratoryeffort.

A raised Paco2reflects reduced alveolar ventilation. Broadly

speaking, this may be produced by reduction in minuteventilation (central or pump failure), obstruction of airflow, or amismatch with perfusion giving a relative increase in dead spaceventilation and reduction in alveolar ventilation. Disorders ofthe lung structure reduce the efficiency of oxygen transfer andwiden the A-a gradient.

The A-a gradient increases a little with age but should beless than 2.6 kPa so central respiratory depression should give aPao2over 7.3 kPa in this situation. A Pao2below this signifiesassociated lung disease. Prolonged respiratory depression maylead to collapse of some areas of lung and an increase in theA-a gradient.

Clinical approach to blood gasinterpretation

A structured approach to the interpretation of arterial bloodgases helps ensure that nothing is missed. Two basic stepsshould be followed. Firstly, Paco2and pH should be assessed. Inessence this is the ventilatory state (respiratory acid-basebalance) and will automatically lead to an assessment of themetabolic acid-base balance. Secondly, arterial oxygenationshould be assessed. This includes evaluation of hypoxaemia aswell as the arterial oxyhaemoglobin saturation along with theA-a gradient.

Alveolar hypoventilation (raised Paco2) with a normal pHprobably represents a primary ventilatory change present long

enough for renal mechanisms to compensate

as in chronicventilatory failure. A similar picture can result from carbondioxide retention from reduced ventilation compensatingfor a metabolic alkalosis, although such compensation isusually only partial. In acute respiratory failure the change inpH will be accounted for by the high carbon dioxideconcentration.

Alternatively if the pH is appropriately raised for thereduction in Paco2then acute alveolar hyperventilation ispresent. The renal system seldom compensates completely foran alkalosis, the pH is between 7.46 and 7.50 in chronic alveolarhyperventilation.

Alveolar hyperventilation (low Paco2) with a pH of 7.35 to7.40 indicates a primary metabolic acidosis in which therespiratory system has normalised the pH. Although not

impossible, it is very unusual for either the renal or therespiratory system to overcompensate. Alveolarhyperventilation in the presence of an arterial pH < 7.35suggests a severe metabolic acidosis or some limitation on theability of the respiratory system to compensate.

A normal Paco2accompanied by an arterial pH > 7.45represents a primary metabolic alkalosis to which theventilatory system has not responded. In the presence ofhypoxaemia, however, this might occur when patients withchronic carbon dioxide retention increase their usual level ofventilation. This may be seen when pulmonary emboli occur inchronic lung disease such as chronic obstructive pulmonarydisease.

Calculation of the alveolar-arterial difference for oxygen

(A-a)Po2 = Pao2 Pao2Pao2 = Pio2 Paco2/R

Where R = respiratory quotient = volume of CO2produced/ volumeof O2consumedR = 0.8 for a normal diet and approaches 1.0 as proportion ofcarbohydrates consumed increasesPio2 = (Pb Ph2o) Fio2Pio2 = partial pressure of inspired oxygen

Ph2o= water pressurePb=barometric pressureFio2 = fractional concentration of oxygen in inspired gas = 0.21

breathing airAssuming Pb = 101 kPa at sea levelPh

2o= 6.2 kPa as inspired air is fully saturated by the time it reaches

the carinaAssume Paco2 = Paco2because of the ease of exchange of carbondioxide

Therefore:Pao2 = (Pb Ph2o) Fio2 Paco2/R

= (1016.2) Fio2 Paco2/0.8 (at sea level)= 94.8 Fio2 1.25 Paco2

Breathing air with a Paco2of 8 kPaPao2 = 94.8 0.21 (1.25 8) = 10 kPa

Systematic assessment of arterial blood gas measurements

Step 1aDetermine whether the Paco2is low ( < 4.7 kPa) indicating alveolarhyperventilation, normal (4.7-6 kPa), or high ( > 6 kPa) as in

ventilatory failure. Calculate the respiratory pH to determine if thereis any metabolic compensation or additional disorder

Step 1bIn the presence of a metabolic acidosis, calculate the anion gap todetermine whether it has increased. No increase occurs withdiarrhoea or urinary loss of bicarbonate

Step 2aAssess arterial oxygenation. Arterial hypoxaemia in adults is definedas Pao2