ARTERIAL BLOOD GAS MONITORING

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  • 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 bodys 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.L1).

    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 termmetabolic acids includes all of the bodys 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 L1 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 mEqL1. 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.L1. An increase in

    1. Professor & Head.2. Associate Professor

    Dept. of Anaesthesiology &Intensive Care, NIMS, HyderabadCorrespond to :Prof. S. Manimala RaoNizams 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 = 10pH

    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 mmolL1). 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 HCO3and 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 HCO3from 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 H2CO3 H + + HCO3(1.2mmol.l1) (mol.l1) (40mmol.l1) (24mmol.l1)

    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)

  • INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2002292

    presence of H+ reduces haemoglobins 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.gl.

    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.dl1, 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 concentrationremains 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 patients 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.5With 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 nmolL1, pH less than 7.36

    Acidosis A process that would cause acidemia, if notcompensated

    Alkalemia A H+ below the range of 36-44 nmolL1, pHgreater than 7.44

    Alkalosis A process that w...

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