arterial blood gas monitoring

RAO, NAGENDRANATH : ARTERIAL BLOOD GAS MONITORING 289Indian J. Anaesth. 2002; 46 (4) : 289-297

ARTERIAL BLOOD GAS MONITORINGProf. S. Manimala Rao1 Dr. V. Nagendranath2

IntroductionIn order to understand and interpret ABGs one has

to have a clear knowledge regarding the nomenclature,physiology and types of acid base disorders. These arefirst discussed, followed by the section “Rapidinterpretation of arterial blood gases”. Disorders of acidbase balance can complicate many disease states andoccasionally the abnormality may be so severe as to belife threatening. Monitoring of ABGs is an essential partin the anaesthetic management of the high-risk patients aswell as in the care of critically ill patients in the ICU.Since both areas manifest sudden and life threateningchanges in all systems concerned, a thorough understandingof acid base balance is mandatory for any physician, andthe anaesthesiologist is no exception.

Common terms and definitionspH : It is the negative logarithm of the hydrogen

ion concentration. A complete definition requires that thelogarithm is defined as being to the base ten and theconcentration measured as activity in moles per liter. Alinear change in logarithmic scale does not indicate alinear change in the variable. It indicates a proportionatechange.

Neutral pH : It is the pH at which there are equalnumbers of H+ ions and OH– ions. Water is more ionizedat body temperature than at room temperature; neutralpH is 6.8 rather than 7.0. This is also the average pHinside the cell. The body preserves neutrality (pH 6.8)inside our cells, where most of the body’s chemistryoccurs, and maintains the blood at pH 7.4, which is 0.6pH units on the alkaline side of neutral.

Logarithm : It is helpful to think of “power”.Thus 103 = 1000 and log (1000) = 3. When the pHchanges by 0.3 units, e.g., from 7.4 to 7.1 the hydrogenion concentration doubles (from 40 - 80 nmol.L–1).

Respiratory acid and respiratory acidosis : Carbondioxide is the respiratory acid – it is the only acid, whichcan be exhaled. Strictly speaking carbon dioxide is a gas,not an acid. Carbonic acid is only formed when combinedwith water. Nevertheless, clinicians customarily regardcarbon dioxide and respiratory acid as synonymous.Respiratory acidosis is a high PCO2 with a low pH.

Metabolic acids and metabolic acidosis : The term“metabolic acids” includes all of the body’s acids exceptcarbon dioxide. Metabolic acids are not respirable; theyhave to be neutralized, metabolized, or excreted via thekidney. Metabolic acidosis is a pH, which is more acidthan appropriate for the PCO2. This definition emphasizesthe importance of the respiratory component to the overallpH. The pH is always a product of the two components,respiratory and metabolic, and the metabolic componentis judged, calculated, or computed by allowing for theeffect of the PCO2, i.e., any change in the pH unexplainedby the PCO2 indicates a metabolic abnormality.

Acidosis and alkalosis : Acidosis is an abnormality,which tends to produce an acidic pH unless there is adominating, opposing alkalosis. Alkalosis is the oppositeand tends to produce an alkaline pH unless there is adominating, opposing acidosis.

Bicarbonate : In acid-base determinations, theconcentration (in millequivalents per liter) of thebicarbonate ion (HCO3

–) is calculated from the PCO2 andpH. Because it is also altered by both the respiratory andthe metabolic components (see below under physiology),it cannot be an ideal measure of either.

Base excess (BE) : It is a measure of metabolicacid level, and is normally zero. The blood base (totalbase) is about 48 mmol L–1 depending on the haemoglobinconcentration. Changes are termed excess or deficit. It ishelpful to remember that the phrase “this patient has abase excess of minus ten” means, “this patient has ametabolic acid excess (acidosis) of 10 mEqL–1”. The baseexcess may be used to estimate the amount of treatment(neutralization) required to overcome the metabolic acidosis(or alkalosis).

H+ ion and pHpH is the negative logarithm to the base 10 of the

hydrogen ion concentration in nmol.L–1. An increase in

1. Professor & Head.2. Associate Professor

Dept. of Anaesthesiology &Intensive Care, NIMS, HyderabadCorrespond to :Prof. S. Manimala RaoNizam’s Institute of Medical SciencesPanjagutta, Hyderabad – 500 082. (A.P.)

INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2002290

the pH indicates a proportionate decrease in the [H+] anda decrease in the pH indicates a proportionate increase inthe [H+].

pH = - log10[H+] H = 10–pH

Various rules of thumb have been proposed forinterconversion. Taking into account ease of calculationand range of clinical accuracy the best is the one proposedby Burden et al.1 The useful conversion range is pH 7.10to 7.60 (H+ concentration 79-25 mmolL–1). The methodworks by treating the two decimal digits of pH in thisrange as if they were a whole number between 10 and60. If this number is subtracted from 83, the result isvery close to H+ concentration. In reverse, subtractingH+ concentration from 83 yields two decimal digits ofthe corresponding pH, e.g. if H = 71; 83 - 71=12,therefore the pH = 7.12 (actual value is 7.15). If pH is7.50; 83-50=33, therefore [H+] = 33, pH 7.33 and theactual value is 7.32.

Table I - Represents the pH values and correspondingH ion concentrations

pH [H+] nmol/L pH [H+] nmol/L

6.70 200 7.40 40

6.75 178 7.45 35

6.80 158 7.50 32

6.85 141 7.55 28

6.90 126 7.60 25

6.95 112 7.65 22

7.00 100 7.70 20

7.05 89 7.75 18

7.10 79 7.80 16

7.15 71 7.85 14

7.20 63 7.90 13

7.25 56 7.95 11

7.30 50 8.00 10

7.35 45

The new generation of blood gas machines willreport the H+ as well as the pH. Acid is an H+ donor andbase is H+ acceptor. The intra and extracellular buffersystems minimize the changes in H+ that occur as a resultof addition of an acid or alkali load to the extracellularfluid (ECF), 60% of the acid load is buffered in the intracellular fluid (ICF). The most important buffer is the

imidazole ring of the histidine in the haemoglobinmolecule. The bicarbonate/carbonic acid is a weak buffer.However the presence of carbonic anhydrase, the highsolubility of CO2 and the ability of kidney to synthesizenew bicarbonate and above all the efficient removal ofCO2 by lungs make it a powerful buffer. All buffers ina common solution are in equilibrium with the sameH+ ion concentration. Therefore, whenever there is achange in the H+ ion concentration in the CSF, thebalance of all the buffer system changes at the sametime – the isohydric principle.2 It is therefore enough tostudy one buffer system in order to evaluate the acidbase status of ECF.

The Henderson-Hasselbalch equation, with itsreliance on logarithms and antilogarithms is long andcumbersome and when attempting to deal with clinicalsituations, this equation has been found wanting.Kassirer and Bliech have rearranged the Hendersonequation that relates H+ (instead of pH) to PCO2 andHCO3

– and have derived an expression, which has greatclinical utility.3

H+ = 24 x PCO2/HCO3–

It is important to emphasize that H+ ionconcentration is defined by the ratio of PCO2 to HCO3

–

and not by absolute value of either one alone.

ACID-BASENormal metabolism of proteins and nucleotides

generates about 100 mmol H+ per day in the form ofsulphuric and phosphoric acids. By comparison, hydrationof CO2 to form H2CO3 generates 12,500 mmol H+ perday.

Carbon dioxide transport1) In Dissolved form : Carbon dioxide is twenty times

more soluble in water than oxygen. One millilitreof plasma will dissolve 0.0006 ml of carbon dioxideper mmHg partial pressure. 100 ml of plasma witha PCO2 of 40 mmHg therefore carries about 2.4 mlCO2 in solution. This is about 5% of total CO2carriage.

2) As carbamino compounds : Carbon dioxide combinesdirectly with terminal amine groups in blood proteinsand haemoglobin. 5 -10% of CO2 carriage occurs inthis way. The exact figure depends on thehaemoglobin concentration.

3) As bicarbonate: The remaining 85 -90% of carbondioxide is carried by blood in the form ofbicarbonate ions. Carbonic anhydrase in red cellsaccelerates the formation of H2CO3 from dissolved

RAO, NAGENDRANATH : ARTERIAL BLOOD GAS MONITORING 291

carbon dioxide. The H2CO3 then dissociates intoH+ and bicarbonate ion. Histidine buffers in thehaemoglobin molecule accept the H+, andbicarbonate ions diffuse out of the red cell (aninward chloride shift occurs to maintainelectroneutrality). This removal of H+ and HCO3

–

from the red cell cytoplasm promotes further H2CO3formation and dissociation.

Control of hydrogen ion concentrationThe hydrogen ion environment is tightly controlled

over a variety of time periods:

1) Seconds: buffer systems

2) Minutes: CO2 excretion by the lungs

3) Hours to days: renal excretion of H+, reabsorptionof HCO3

Buffer systems consist of equilibrium mixtures ofweak acids and their salts, they provide a sink for H+ orOH- ions, minimizing the pH change in response to acid/alkali loads. Buffers are most effective when bothcomponents are present in equal concentration. This occurswhen the pH is equal to the negative logarithm of theequilibrium constant (PKa) for the reaction concerned.Useful buffering occurs over a range of one pH uniteither side of the optimum pH. The primary buffers inextracellular fluid are (in order of importance):

1) Carbonic acid/bicarbonate:H2CO3/HCO3 (pKa = 6.1)

2) Haemoglobin/histidine residues(38 per molecule): HHb/Hb (pKa = 6.8)

3) Plasma protein/histidine residues:HPr/Pr (pKa = 6.8)

4) Phosphate: H2PO4/HPO4 (pKa = 6.8)

Despite having a pKa distant from normal plasmapH, the carbonic acid/bicarbonate system has a very highbuffering capacity, since large quantities of carbonic acidcan be accumulated or disposed of by modification ofbreathing. At pH 7.4, histidine is the only amino acidresidue that readily accepts a hydrogen ion. The largenumbers of histidine in haemoglobin make it a veryeffective buffer. Plasma proteins contain fewer histidinesand are therefore less active as buffers. Phosphate ispresent in low concentrations in extracellular fluid, and istherefore of minimal importance. It is a primaryintracellular buffer however, and has an importantbuffering function in urine, facilitating H+ excretion.

The main buffer system, which is also the oneexamined by blood gas analysis, is the carbonic acid/bicarbonate buffer, with normal values shown here:

CO2+H2O Ö H2CO3 Ö H + + HCO3–

(1.2mmol.l–1) (�mol.l–1) (40mmol.l–1) (24mmol.l–1)

Carbonic acid itself quickly dissociates either intohydrogen ion and bicarbonate or carbon dioxide and water.It represents a transitional state and is present in onlymicromolar quantities.

OxygenationInterpretation of PO2 requires knowledge of the

sigmoid oxyhaemoglobin dissociation curve. The sigmoidshape derives from the fact that haemoglobin consists offour subunits, and binding of oxygen to one subunitfacilitates the binding of oxygen to the other units. Thecharacteristic points on the curve are:

1) The arterial point PO2=100mmHg(13.3kPa) SO2=97.5%

2) The mixed PO2=40mmHgvenous point (5.3kPa) SO2=75%

3) The P50 PO2=27mmHg(3.6kPa) SO2=50%

Binding of oxygen to haemoglobin results inconformational changes to the molecular subunits, makingthe histidine residues less ready to accept H+. Sodeoxyhaemoglobin is a better H+ acceptor than isoxyhaemoglobin, allowing deoxygenated blood totransport more CO2 (in the form of H+ + HCO3

–), fora given PCO2, than oxygenated blood does — this iscalled the Haldane effect. Deoxygenated haemoglobin isalso more ready to bind CO2 in the form of carbaminocompounds at terminal amine groups. Conversely, the

Oxygen Dissociation Curve

Hb

satu

ratio

n

PO2 (kPa)


presence of H+ reduces haemoglobin’s affinity foroxygen, so a low pH shifts the dissociation curve to theright, making haemoglobin more ready to give up O2 ata given PO2 — the Bohr effect.

The Bohr and Haldane effects make usefulphysiological sense - the high O2 environment of thelungs oxygenates haemoglobin and so causes H+ releaseand reformation of CO2 to be expired, while the highCO2 environment of the tissues acidifies red cells and sofacilitates oxygen release.

A summary of factors affecting the oxyhaemoglobindissociation curve is as follows:

Left shift Right shift(increase O2 affinity) (decreased O2 affinity)

Alkalosis AcidosisHypocarbia � Hypercarbia -Temperature � Temperature - 2,3 DPG � 2,3 DPG -

Acidosis, hypercarbia and increased temperatureare all features of the local circulation in metabolicallyactive tissues, and they all increase oxygen unloadingfrom haemoglobin. 2,3 DPG levels are low in storedblood, making it relatively ineffective at unloading oxygenin the tissues. The high affinity of HbF for oxygen is dueto its relative insensitivity to 2,3 DPG. Oxygen contentof blood depends on both haemoglobin saturation andhaemoglobin concentration, with an additional largelytrivial contribution from dissolved O2. Each gram ofhaemoglobin can combine, under ideal conditions, with1.39 ml of oxygen. But carboxyhaemoglobin andmethaemoglobin are both present in normal blood, so theconventional figure for oxygen carrying capacity ofhaemoglobin is 1.34 ml.g–l.

Oxygen dissolves in plasma to the extent of only0.00003 ml.l-1.mmHg-1, so that 100 ml of blood at normalarterial PO2 transports only 0.3 ml O2. In contrast, if thehaemoglobin concentration is 15 g.dl–1, the same 100 mlof arterial blood will carry 15 x 1.34x97.5%=19.6 ml ofoxygen associated with haemoglobin.

Effect of temperatureWhen blood is cooled, CO2 becomes more soluble

reducing its PCO2 by about 4.5% per oC fall intemperature and the pH rises by about 0.015 per oC fallin temperature. Available evidence suggests thathomeostatic mechanisms center around protein buffersand enzymes, specifically the alpha imidazole group onhistidine residues, the so called alpha stat regulation.This mechanism requires that, with hypothermia the pH

rises and PCO2 falls, whereas the HCO3– concentration

remains unchanged. The alpha stat concept refers to theuse of 37oC temperature-uncorrected pH and PCO2values, whereas the pH stat concept refers to the use ofpH and PCO2 values corrected to the patient’s coretemperature.4

Hiramatsu et al have used the pH stat strategy inDeep Hypothermic Circulatory Arrest (DHCA) and foundthat Cerebral Blood Flow (CBF) was greater during coolingwith a better preservation of cytochrome aa3 values.5

With few exceptions, the appropriate clinical interpretationof blood gas values is better accomplished using the alphastat strategy and this is an universal practice. Combinationof pH stat and alpha stat is adopted in complex congenitalcardiac lesions along with DHCA.

Acid base disordersSeveral definitions that are used to describe

disturbances in acid base status are useful in understandingacid base disorders

Acidemia – A H+ ion above the normal range of36-44 nmolL–1, pH less than 7.36

Acidosis – A process that would cause acidemia, if notcompensated

Alkalemia– A H+ below the range of 36-44 nmolL–1, pHgreater than 7.44

Alkalosis – A process that would cause alkalemia if notcompensated

There are mainly two types of disorders,respiratory and metabolic. They may be compensatoryor non compensatory. Changes in pH that are primarilya result of changes in PCO2 are termed respiratorydisorders. On the other hand changes in pH broughtabout by changes in bicarbonate and other buffer basesare termed primary metabolic disorders. Basically thereare four primary acid-base disorders viz. respiratoryacidosis, metabolic acidosis, respiratory alkalosis andmetabolic alkalosis. Compensation usually occurs in aprimary acid base disturbance with an appropriate changein other components, e.g. a primary metabolic acidosisis compensated for by secondary respiratory alkalosis(by hyperventilation). On the other hand primaryrespiratory acidosis as it occurs in chronic obstructiveairway disease (COPD) is secondarily compensated forby metabolic alkalosis brought about by H+ secretionand HCO3

– absorption by the kidneys. While the formertakes a few minutes to achieve the result, the latter maytake days to weeks to be fully established.


The changes in PCO2, pH and HCO3– depending

upon the type of disorder are given in table 2.

Table 2: Primary and expected compensatory changes inacid base disorders.

Primary disorder Characteristic Expected (“normal”)primary changes in vivo response

Metabolic acidosis [H+] - [HCO3–] � For each mmolL–1 fall in

[HCO3–], PaCO2

falls by 1 mmHg

Metabolic alkalosis [H+] � [HCO3–] - For each mmolL–1 rise in

[HCO3–], PaCO2 rises by

0.75 mmHg; however,PaCO2 does not exceed

55mmHg

Acute respiratory [H+] - PaCO2 - For each mmHg rise inacidosis PaCO2, plasma [H+]

rises by 0.75 nmolL–1

Chronic respiratory [H+] - PaCO2 - For each mmHg fall in acidosis PaCO2, plasma [H+]

falls by 0.30 nmolL-1

Acute respiratory [H+] � PaCO2 � For each mmHg fall inalkalosis PaCO2, plasma [H+]

falls by 0.75 nmolL–1

Chronic respiratory [H+] � PaCO2 � For each mmHg fall inalkalosis PaCO2, plasma [H+]

falls by 0.15 nmolL–1

Respiratory acidosisMain causes: sedation, coma, neuromuscular

disorders, severe kyphoscoliosis or obesity, pulmonaryfibrosis, sarcoidosis, pneumothorax or effusion, chronicobstructive airway disease, airway obstruction, severepulmonary parenchymal disease.

Retention of CO2 drives the bicarbonate bufferequilibrium towards production of H+ and HCO3

–. H+

is buffered by protein and haemoglobin, limiting the fallin pH.

Bicarbonate levels rise by about 1 mmol.l–1 forevery 10mmHg (1.3 kPa) rise in PCO2. Thereforeeven quite extreme hypercarbia will not push bicar-bonate over 32 mmol.l-1 acutely. After 6-12 hours,however, renal H+ excretion increases causing thegeneration and reabsorption of bicarbonate. Bicarbonatelevels then rise further, while pH returns towardsnormal. Chronic respiratory acidosis with metaboliccompensation will therefore raise bicarbonate by as muchas 4 mmol.l-1 for each 10 mmHg rise in CO2, but thiscompensation will take one or two days to becomecomplete.

Respiratory alkalosisMain causes: anxiety, encephalitis/meningitis,

salicylates, acute asthma, pulmonary embolus, hypoxia ataltitude.

Reduction in CO2 drives the bicarb bufferequilibrium towards the production of carbonic acid.Protein and haemoglobin buffers release H+, limiting therise in pH. Bicarbonate levels fall by about 2 mmol.l-1 forevery 10 mmHg fall in PCO2. After 6-12 hours, renal H+

excretion and bicarbonate reabsorption are reduced, pHfalls towards normal, and bicarbonate is further reduced.Chronic respiratory alkalosis with renal compensation istherefore associated with a bicarbonate fall of up to 5mmol.l-1 for each 10 mmHg fall in PCO2, but thiscompensation will take one or two days to becomecomplete.

Metabolic acidosisMain causes: hypovolaemia, cardiogenic or septic

shock, severe hypoxia, diabetic ketoacidosis, renal failure,diarrhoea, pancreatic fistula.

The presence of excess H+ is compensated tosome extent by protein and haemoglobin buffers.The bicarb buffer equilibrium is driven towardsCO2 production, which drives an initial increase inbreathing to maintain normal carbonic acid levels.Bicarbonate is consumed, and therefore falls. Over thenext 12-24 hours H+ diffuses into the brain, anddrives a further increase in ventilation, which lowerscarbonic acid levels and induces a compensatoryrespiratory alkalosis. (Lactic acid is produced by allcells, including brain cells, and therefore produces afaster respiratory response than do ketoacids, which areproduced by the liver and must diffuse into the brainacross the blood-brain barrier.) Once compensation isestablished, PCO2 is reduced by 1-1.3 mmHg (0.13-0.17 kPa) for each mmol.l–l fall in bicarbonate. Becauseof the slow equilibration of CSF H+ with blood pH,hyperventilation may persist for 12-24 hours after bloodpH returns to normal.

Metabolic alkalosisMain causes: vomiting, nasogastric suction,

gastric fistula, steroids, diuretic therapy, inappropriatesodium bicarbonate administration, massive bloodtransfusion (citrate metabolised to bicarbonate).

Reduction in H+ is compensated to some extentby release of hydrogen ions from protein andhaemoglobin buffers. The bicarb buffer equilibrium ispushed towards increasing bicarbonate levels anddecreasing carbonic acid. Ventilation falls immediately


to maintain normal carbonic acid levels. After 12-24hours, rising CSF pH may induce a further fall inventilation to produce a compensatory respiratoryacidosis - this rarely involves a rise in PCO2 to morethen 55 mmHg (7.3kPa), since oxygenation must bemaintained. Metabolically alkalotic patients may besufficiently sick from their underlying disease so thatthe respiratory compensation is absent andhyperventilation may occur instead.

Base excessFrom the above it is clear that CO2 and bicarbonate

levels are inextricably linked, and interpretation of mixedrespiratory/metabolic disorders is very complicated if onlypH, PCO2 and bicarbonate levels are available. What isrequired is a measure of metabolic acid/base status whichis separated from the effects of CO2. Several parametershave been used in the past, including standard bicarbonateand buffer base, but the most frequently used today isbase excess. Base excess is defined as the amount offully-ionised acid which would be required to return thepatient’s blood to pH 7.4 when the CO2 has been adjustedto 40 mmHg (5.3 kPa). It is derived from nomograms orcalculations, based on experimental results produced bySiggaard-Andersen. Units are mmol.l-l. Positive valuesindicate metabolic alkalosis, negative values metabolicacidosis.

To correct a metabolic acidosis, the followingquantity of sodium bicarbonate is suggested in theAdvanced Life Support manual:

NaHCO3 dose (mmol) = base excess (mmol.l–l) xbody weight (kg)/3

(8.4% sodium bicarbonate solution contains 1 mmolNaHCO3 per ml).

Body weight divided by three is a rather generousestimate of extra-cellular fluid volume, so this equation isestimating the bicarbonate dose to fully correct ECFacidosis. Bear in mind, however, that most of the ECFlacks the protein and haemoglobin buffers present in blood,and much of it equilibrates only slowly with blood.Therefore small doses of bicarbonate (50-100 ml) shouldbe titrated against repeated estimates of pH and base excess.

Anion gapThis is a useful concept in the assessment of the

cause of metabolic acidosis, though an understanding ofthe concept is probably of more use than the parameteritself.

Electrical neutrality in body fluids is attained bythe following balance:

Cations [+] mmol.l-1 Anions [-] mmol.l-1

Na+ 140 Cl- 104

K + 4.5 HCO3- 24

C a + + 5 Protein- 15

M g + + 1.5 Phosphate- 2

Sulphate- 1 Org. acid 5

Total 151 Total 151

Anion gap is calculated as [Na+]-([Cl–]+[HCO3–])

and is usually 12 mmol.l-l. It is increased if K+, Ca++

or Mg++ concentrations fall or if protein levels rise; itfalls if potassium, calcium or magnesium levels rise orplasma proteins decrease. But if these values are normal,the anion gap is due to the presence of metabolic acids.If there is a rise in metabolic acids, bicarbonate will beconsumed by association with H+ and there will thereforebe a shift in the anionic distribution from bicarbonate tometabolic acids, and the anion gap will increase. Thisoccurs classically in lactic acidosis, ketoacidosis andmost kinds of renal failure. However, if chloride risessimultaneously with the bicarbonate fall, the two effectsoffset each other, and no change in anion gap is seen.This is hyperchloraemic acidosis, which occurs in renaltubular acidosis, early renal failure, diarrhoea, uretericdiversions and carbonic anhydrase-inhibitor treatment.

Mixed acid base disordersSuppose a patient has low pH and is therefore

acidemic. In this setting, a low plasma HCO3– concentration

indicates metabolic acidosis and a high PCO2 indicatesrespiratory acidosis. Similar reasoning can lead to thediagnosis of a combined metabolic and respiratory alkalosisin a patient with an elevated pH, a high plasma HCO3

–

and a low PCO2.

A knowledge of the extent of renal and respiratorycompensations allows mixed disorders to be diagnosed,e.g. a patient with a salicylate overdose is found to havethe following result:

pH 7.45, PCO2 20, HCO3– 13

The slightly high pH indicated that the patient isalkalemic. This can be due to a high HCO3

– concentrationor a low PCO2. Since only the latter is present the primarydiagnosis is respiratory alkalosis, most likely acute, giventhe history. In this disorder, the body buffers will reduce


the plasma HCO3 concentration by 2 mEqL–1 for every 24to 20 mEqL–1 as the PCO2 drops acutely from 40 to 20Torr. The actual HCO3 of 13 mEqL–1 is lower thanexpected, suggesting that the patient has a combined,respiratory alkalosis and metabolic acidosis. Also, renaland respiratory compensations return the pH toward butrarely to normal. Thus, a normal pH in the presence ofchanges in the PCO2 and HCO3

– concentrationsimmediately suggests a mixed disorder.6

Blood gas monitorsThe pH, PCO2 and PO2 measurements are normally

accomplished by blood gas analysers using an arterialblood sample fed into the analyser as and when the acidbase status is required. Improvements in technology havepaved the way for blood gas monitors which display thesame results online.

A blood gas monitor is a patient dedicated devicethat measures arterial pH, PCO2 and PO2 withoutpermanently removing blood. A sensor that operates viaoptical detection of altered light is an optode. Eithertransmission based or fluorescence based chemistries canbe used as indicators for optode microsensing.

They are operable with a 20G arterial catheter anddo not negatively affect continuous pressure measurement,obtaining of blood samples or routine function of thearterial catheter system. They are stable and consistentfor at least 72 hours.

To avoid patient interface problems with intra-arterial devices, an extra-arterial fluorescent optode systemhas been developed. This device locates the pH, PCO2and PO2 fluorescent optodes within a sensor cassette thatis inserted in series with the arterial catheter tubing systemnear the patient’s wrist. To measure pH, PCO2 and PO2,a stopcock closes the system to the IV fluid source, whichthen allows arterial blood to flow into the sensor cassettewhen a sub-atmospheric pressure is created in an“upstream” reservoir. The placement of the reservoir issuch that only IV fluid enters the reservoir. The stopcockis then returned to its original position so that the reservoiris isolated and fluid flow from the pressurized bag isrestored, by allowing BP monitoring to continue. Theminimal blood flow occurring in the sensor cassette doesnot interfere with optode function. Results are displayedwithin 90 seconds.

Advantages1. They furnish immediate and continuing blood gas

trends.

2. They reduce blood loss incident to obtaining data.

3. They reduce the risks of nosocomial infection.

4, They reduce the exposure of personnel to patient’sblood.

Rapid interpretation of ABGThe fundamental for any interpretation is to

recognize the cause of the problem, which once evaluatedcan lead to a systematic management.

In approaching the evaluation of blood gas andacid-base disturbances in the body the following schemeis suggested:

1) The patient’s history and clinical condition shouldbe carefully reviewed. 2) The adequacy of alveolarventilation should be assessed. 3) The alveolar-to-arterialoxygen tension gradient should be calculated. 4) Plasmaelectrolytes should be measured and the anion gapcalculated. 5) The acid-base status of the body should bedetermined.

What are the components of an ABG report?

1) Patient data – I.P. No., sex, age. 2) Clinicalstatus – FiO2, R.R. or ventilatory settings. 3) Arterial O2tension (PaO2). 4) Arterial CO2 tension (PaCO2). 5) pH6) Bicarbonate in mEqL–1 7) Base excess 8) Haemoglobin9) O2 content 10) O2 saturation 11) Temperature12) Serum K+ values

The usual questions one asks after the availabilityof data for evaluation of acid-base status are:

1) Is there an acid-base disorder? 2) If so, is itprimary or compensatory? 3) Whether it is simple ormixed 4) And finally what is the aetiology?

A thorough history and careful evaluation of thepatient at the bedside yields clues to the understanding ofthe disorder. An acute disorder is not compensated andit may clearly be evident from the history. The evaluatingperson must thoroughly understand that compensation onlyattempts to restore the abnormal state to near normal butnever to a total correction. The respiratory compensationfor primary metabolic process and the renal compensationfor chronic respiratory acidosis are very effective whereasthe respiratory compensation for metabolic alkalosis hasa ceiling at a PaCO2 of 55mmHg.

Before understanding to interpret the arterial bloodgases one should be fairly thorough with the normal values,which are given in the following table.


S.No. Value Arterial blood Mixed venous

1. pH 7.40 (7.35 – 7.45) 7.36 (7.31 – 7.41)

2. PaO2 80-100 mmHg 35-40 mmHg

3. O2 saturation 95% - 70-75%

4. PaCO2 35-45 mmHg 41-51 mmHg

5. HCO3– 22-26 mEqL–1 22-26 mEqL–1

6. BE -2 to +2 -2 to +2

Arterial or venous blood sampleIt is traditional to draw arterial blood for PaO2,

PaCO2 and pH measurements. It is the best indicator ofhow well the lungs are oxygenating. However in thehaemodynamically unstable patient, mixed venous bloodis a close approximation of acid-base status of the times.It has been recommended that central venous blood canbe analysed in such situations.In analyzing the data follow a sequence of order1. Check pH. It indicates acidemia or alkalemia

pH <7.35 acidemia – the process causingacademia is acidosispH >7.45 alkalemia – the process causingalkalemia is alkalosisBoth processes may be occurring simultaneously,the pH indicates the stronger one

2. Check PO2, which indicates oxygenation.

3. Check PCO2, which indicates ventilation.Hypoventilation leads to more dissolved CO2 in bloodleading to higher PaCO2. Conversely hyperventilationis a state caused whenever there is not enoughdissolved CO2 in blood i.e. the lungs are excretingfar more CO2 by excessive ventilation. CO2 is alwaysconsidered an acid as it combines with H2O to formweak acid viz. H2CO3, which in turn breaks downto H+ and bicarbonate HCO3

–. H+ is buffered byplasma proteins, whereas CO2 is eliminated by thekidney as acid in urine and by lungs as CO2 gas.

4. Respiratory abnormalities - PCO2 – respiratory acidosis - � ventilation �PCO2 – respiratory alkalosis - - ventilation

5. Check bicarbonate and BE. These two indicatewhether the primary disorder is metabolic orrespiratory. These two are influenced only bymetabolic processes other than respiratorydisturbances that affect a patient’s pH. If metabolicprocess causes accumulation of acid or loss ofbicarbonate, the HCO3

- values drop below normal

and BE will become negative. On the other handloss of acid by vomiting or ingestion or accumulationof HCO3

- will lead to an increase in bicarbonate andBE values. BE values refer not only to bicarbonate,but also to proteins and haemoglobin which are theother buffer bases.

6. Metabolic abnormalities-HCO3

–or BE–metabolic alkalosis–acid�or HCO3- -

�HCO3–or BE–metabolic acidosis – acid-or HCO3�

pH is maintained for, by two major mechanisms.One is compensation i.e. it alters the component notprimarily responsible for the abnormality.

Secondly by correction, pH is normalized by alteringthe component that is primarily responsible for theabnormality. The body always strives to maintain abalance between HCO3 and PaCO2 of 20:1. At thisratio the pH is normal. For every 10 mmHg rise orfall in PaCO2 from 40 mmHg, there is an increaseor decrease in pH by 0.08 units.

For e.g. PCO2 - 20 (40 + 20 = 60 mmHg)pH � 0.08 x 2 = 0.16pH = 7.4 – 0.16 = 7.24

For studying states of academia or alkalemia onerequires all the measurements viz. pH, PaCO2 andbicarbonate.

Examples :1. pH 7.45, PCO2 26 and HCO3

– 19Here the pH is alkalotic, PCO2 indicates respiratoryalkalosis and bicarbonate is low. Acute CO2 excretion(acute respiratory alkalosis) drives the hydrationreaction more the left than normal, and HCO3

–

decreases slightly. Final interpretation is partiallycompensated respiratory alkalosis.

2. pH 7.48, PaCO2 55 and HCO3 38pH is alkalotic, PCO2 indicates respiratory acidosisand bicarbonate is high. Metabolic alkalosis ispartially compensated with PCO2 ceiling of 55mmHg.

3. pH 7.13, PCO2 82 and HCO3 24pH is acidotic, PCO2 indicates respiratory acidosisand a normal bicarbonate. This picture showsuncompensated respiratory acidosis.

4. pH 7.29, PCO2 25, HCO3 12Here the pH is low indicating academia and thebicarbonate is low indicating a metabolic origin.Final interpretation is metabolic acidosis partially


compensated by a fall in PCO2 in an attempt tobring the pH towards normal.

5. pH 7.45, PCO2 20, HCO3 13Here the pH suggests alkalemia. PCO2 is lowsuggesting a respiratory alkalosis. The actualbicarbonate is lower than expected suggesting acombined metabolic acidosis and respiratory alkalosis.

FiO2 is the fractional inspired oxygen concentration.PaO2 is always related to FiO2. Blood gas analysis withoutFiO2 marking, does not really make any sense. Ratio ofPaO2/FiO2 permits evaluating patients receiving variousamounts of oxygen. It gives an indirect method ofestimation of venous admixture. Increasing A-a gradientssignify deterioration in lung function.

A-aO2 gradient = 140 – (PO2 torr)5% should be substracted which is a normal

physiological shunt. An A-a ratio of 0.75 is normal,0.40-0.75 is acceptable, 0.20-0.39 is poor and less than0.20 is very poor. PaO2 denotes the O2 tension, whichdoes not directly relate to ventilation. But there is areciprocal relationship between PaCO2 and PaO2. Thenormal PaO2 varies with age and high altitudes.

Oxygen saturation (SaO2) can be calculated fromthe formula

O2 sat% = contentcapacity

e.g. In interpretation the saturation is very usefuland should give a clue to defective or abnormalhaemoglobins, when PaO2 and Hb% are within normallimits but O2 saturation and content are low.

Oxygen content is necessary when evaluating theadequacy of O2 delivery to tissues. To increase CaO2 onehas to improve the patient’s haemoglobin.

Table III illustrates a schematic representation forinterpretation of acid-base balance

Rapid interpretation of arterial blood gases maynot be a cakewalk. But with some basic understandingand perseverance, the student will be able to do itaccurately in many situations. Mixed acid-base disordersand complex conditions may pose a problem but righthistory and clinical evaluation may pave the way for easyinterpretation.

References1. Burden and McQuillan. BJA 1997; 78:479.2. Guyton AC, Hall JE. Textbook of Medical Physiology 9th ed.

1996: 390.3. Kassirer JP, Bleich HL. Rapid estimation of plasma CO2 from

pH and total CO2 content. N Engl J Med 1965; 272:1067.4. Shapiro BA, Peruzzi WT, Templin RK. Clinical application of

blood gases. 5th ed. 1994:230-31.5. Hiramatsu T et al. pH strategies and cerebral energetics before

and after circulatory arrest. J Thorac Cardiovasc Surg 1995;109: 948.

6. Burton David Rose. Clinical physiology of acid-base andelectrolyte disorders. 4th ed. 1994:508.

Dr. Sawant passed M.B.B.S. and D.A. from S.S.G. Hospital and MedicalCollege, Baroda in 1955 and 1957 respectively. He joined Tata Memorial Hospital,Mumbai in May 1959 and worked as Head of the Dept. from 1966 to 1990. Underhis dynamic leadership the dept. rose to international heights.

He was very popular amongst the residents, his colleagues and all other staffmembers of the hospital, for his ever helpful and co-operative nature.

His sudden and untimely demise on 8th April 2001, shocked not only TMH butthe whole of ISA, Mumbai branch.

May Almighty God give peace to the departed soul!

OBITUARY

Dr. Narayana S. Sawant(18-11-1928 to 08-04-2001)

arterial blood gas monitoring

Documents