IO0

POSTGRAD. MED. J., 1961, 37, 10

BLOOD GAS MEASUREMENTSIN CLINICAL PRACTICE

E. J. M. CAMPBELL, M.D., M.R.C.P.Assistant, The Professorial Medical Unit, The Middlesex Hospital, London, W.I

UNTIL recent years methods of blood gas measure-ment have been difficult and they were thereforenot widely available. Their possible value inroutine clinical practice was consequently largelyunknown and unexplored, and many clinicianshave forgotten their basic knowledge of oxygen andcarbon dioxide physiology.The sequence is now in reverse. There are easy

methods which could be widely available.Clinicians are learning their value in practice andin the process are relearning respiratory physiology.The aim of this article is to catalyse this chainreaction by indicating the most practicable methodsand by describing the use of the measurements inpractice.

There is now no need for physicians to relyentirely on clinical judgment in assessing, forexample, methods of treating respiratory de-pression in cases of poisoning. They would beunhappy without measurements of blood sugar indiabetic coma, urea in renal failure or sodium inadrenal failure. They are now entitled to requireknowledge of the Pco2 in respiratory failure.

Blood Collection for Gas AnalysisThis presents the first difficulty which has dis-

tinguished blood gas measurements from otherbiochemical investigations. The exchanges ofoxygen and carbon dioxide between blood andtissues prevent samples taken from the antecubitalveins in the usual manner from having much value.Venous blood can be used for the estimation ofcarbon dioxide content (see below) and even,with special precautions, for the estimation ofcarbon dioxide tension (Pco2) and pH (Brooksand Wynn, I959), but arterial blood is preferablefor these and, of course, essential for meaningfulestimates of oxygen. Arterial puncture continuesto be viewed askance partly because of allegeddifficulty and partly because of fear of damage.Like all clinical procedures, arterial puncture isbest learned by example and after half a dozensuccessful attempts one is almost as good as themost expert. A syringe lubricated by heparin(5,000 units/ml.) should be used with heparinfilling the deadspace of nozzle and needle. Mercuryis unnecessary. The blood should be allowed tofill the syringe under its own pressure; it should

not be drawn by suction because this is liable tointroduce bubbles of air. The period of samplingshould be between one and two minutes and thepatient should be relaxed and breathing naturallyto ensure that the sample reflects steady-state con-ditions as far as possible. Temporary fluctuationsin the breathing may otherwise cause the state ofthe arterial blood gases to be unrepresentative.After withdrawal, the site of puncture should becompressed sufficiently firmly to obliterate thedistal pulse for at least five minutes.

Discomfort or complications following com-petent arterial sampling are unrecorded. I havebeen told of damage to the median nerve in thecourse of a ' search' for the brachial artery by aninexperienced person, and I have known an alarm-ing haematoma to develop in a confused patientwho was allowed to flex the elbow repeatedly whilean indwelling arterial needle was in place. Therecan be few clinical procedures that are free fromsuch hazards. I have not heard or read of anyother serious complications following arterial punc-ture in the total experience of several workersamounting to over 25,000 punctures.Storage and Transport of Arterial BloodSamplesThe overriding consideration in the care of

blood samples is that they be kept out of contactwith the air. Measurements of Po2, Pco2 and pHmust usually be made within a few minutes ofcollection so the blood is most conveniently keptin the syringe. Neither cooling nor the additionof fluoride is satisfactory in preventing the meta-bolism of the cells. Early analysis of blood keptin the syringe is the best arrangement.These considerations do not apply to blood to be

analysed for carbon dioxide content which is notseriously affected by the metabolism of the cellsnor by minor degrees of contact with the air.Blood for carbon dioxide content can be trans-ferred to tubes (by 'filling from the bottom'),which should be completely filled and then stop-pered. Blood for oxygen content or saturationpresents an intermediate problem. Analysis can bedeferred up to an hour or so (depending on theaccuracy required) if the blood is cooled. Suchblood is preferably and conveniently kept in the

copyright. on M

arch 26, 2020 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.37.423.10 on 1 January 1961. D

ownloaded from

January 1961 CAMPBELL: Blood Gas Measurements in Clinical Practice II

syringe. If it is transferred to another containergreater care is required than for carbon dioxidecontent and the transfer should be anaerobic.

MethodsUnder this heading I propose to review the

practicability of the various available methodsbearing in mind cost, technical skill, time andreliability.Blood Oxygen

(i) Content and Saturation. For accuracy,reliability and cheapness the Van Slyke method(Van Slyke and Neill, I924) remains supreme.Unfortunately, it requires more skill and timethan most routine biochemical techniques, so othermethods should be considered if the number ofanalyses is large or the analyst's time is precious.For large numbers one of the many spectrophoto-metric or reflectrometric methods is probably bestand can be set up at reasonable cost (Refsum andHisdal, 1958; Verel, Saynor and Kesteven, 1960).

(2) Tension. Until recently the only practicablemethod for measuring blood oxygen tension wasthe microtonometric or ' bubble ' method of Riley(Riley, Campbell and Shepard, I957). Theapparatus is inexpensive, but each analysis re-quires about 40 minutes of skill and concentration.It should soon be replaced by the polarographicmethods (e.g. Severinghaus and Bradley, 1958;Bishop, I960), which promise to be sufficientlyinexpensive, reliable and rapid for routine use.

External OximetrySpectrophotometric techniques for the estima-

tion of the arterial oxygen saturation in vivo(Nilsson, 1960) are unfortunately not very accuratewith respect to absolute values, but can be usedto follow changes (see Campbell and Dickinson,1960, p. I20). The instruments are still moderatelyexpensive and temperamental.Carbon Dioxide

(I) Content. As in the case of oxygen, the VanSlyke method is the most accurate and thecheapest. The analysis for carbon dioxide contentis less laborious than that for oxygen, so thedemands on time and skill are not so great. Never-theless, automatic chemical analysers promise toreplace the Van Slyke method in busy laboratories.

(2) Tension. Until recently there have been onlytwo practicable methods for the measurement ofblood carbon dioxide tension. First, the ' direct'microtonometric bubble method of Riley, andsecondly, the 'indirect' method in which Pco2is calculated from the pH and carbon dioxidecontent. Both methods require time, skill andattention far above that generally available in

routine laboratories; although with improve-ments in pH meters this statement is becomingless true.With the development ofmore stable and reliable

pH meters two further methods of estimatingblood Pco2 have been introduced. First, theinterpolation method of Astrup (1956) and,secondly, the titration electrode method ofSeveringhaus and Bradley (1958). These havebrought Pco2 measurements within the reach ofroutine laboratories, although the skill required isstill above that demanded by most routine chemicalprocedures.

The Rebreathing Method for Estimating MixedVenous and Arterial Carbon Dioxide Tension.Collier's (1956) introduction of the rebreathingmethod for estimating blood carbon dioxide tensionis the greatest practical advance in clinical respira-tory physiology of the last 20 or 30 years. Thismethod abolishes all analytical problems of Pco2estimation. Using a rapid continuous carbondioxide gas analyser, the method is extremelysimple. Without this instrument it is still, givenslightly greater understanding, possible to applythe method using simple and cheap equiprient(Campbell and Howell, 1960). The whole pro-cedure, including preparation and analysis occupiesio minutes.

Practical ConclusionsAll general hospitals should today be able to

provide facilities for the following methods:(I) Arterial oxygen saturation by the Van Slyke

method.(2) Mixed venous carbon dioxide tension by the

rebreathing method.(3) Blood carbon dioxide content by the Van

Slyke method.With these and an understanding of the under-

lying physiology the clinician can evaluate anydisturbance of blood gas regulation. With par-ticular reference to respiratory disease, thepossession of a recording spirometer in additionto the above enables the vast majority of respira-tory problems to be adequately assessed.

Supplementation of these four essentials shouldbe governed by the particular interests to beserved.

Physiological Principles Underlying ClinicalInterpretation

Like most laboratory measurements, values forblood gas concentrations cannot be interpretedclinically without appreciation of the biologicalfactors affecting them. An adequate expositionof the physiology of the blood gases is far beyondthe scope of this article, but there are certain im-

copyright. on M

arch 26, 2020 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.37.423.10 on 1 January 1961. D

ownloaded from

12 POSTGRADUATE MEDICAL JOURNAL January 1961

u o50 /

030 '

a.20

I0

so

10

0 20 40 60 80 100 120 140OXYGEN PRESSURE mm.H9

FIG. i.-Oxygen dissociation curve of blood.

portant principles which deserve mention becauseof their practical significance.OxygenThe relationship between oxygen saturation and

tension is given by the dissociation curve (Fig. i).The normal arterial tension is about go mm. Hg,giving a saturation of about 97%. The shape of thedissociation curve is such that the saturation ofarterial blood does not fall below 90% until thetension falls below 60 mm. Hg, whereas furtherreduction in tension causes increasingly severedesaturation. The practical implications of thisrelationship are: firstly, that respiratory functionhas to be seriously disordered before measure-ments of saturation become unequivocally ab-normal; secondly, when the saturation falls below90% it becomes so sensitive to small changes intension that variations in breathing and bodilyactivity cause the saturation to vary considerably,making isolated measurements unreliable indica-tions of the average level. These facts partlyexplain the eagerness with which methods of con-tinuous or frequent oxygen tension determinationsare being developed.

Exercise increases oxygen consumption, in-creases the flow of blood through the lungs andcauses the blood entering the lungs to have alower saturation. These changes all tend to

increase the oxygen tension difference between thealveolar air and the pulmonary capillary blood andthus to reduce arterial oxygen tension. When thisfalls below 60 mm. Hg, the saturation falls rapidly.Hence, in a subject whose resting saturation isover go%, exercise can be used to stress respiratoryfunction and the amount of exercise (as judged bythe oxygen uptake) required to cause the arterialsaturation to fall below 85-90% provides a usefulmethod of detecting and assessing many types ofdisorder. In lung diseases it is an excellent sub-stitute for measurements of diffusing capacity towhich it is in some ways superior and which itcan be used to calculate (Shepard, 1958).Carbon Dioxide

Interpretation of changes in blood carbon di-oxide depends upon appreciation of two relation-ships:

(I) Arterial carbon dioxide tension is governedby the ratio of carbon dioxide production toeffective, i.e. alveolar, ventilation:

Arterial Pco, =CO2 productiona polr tion X barometric pressurealveolar ventilation

If alveolar ventilation is halved, arterial Pco2 isdoubled and vice versa.

(2) The proportion of carbon dioxide in the

copyright. on M

arch 26, 2020 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.37.423.10 on 1 January 1961. D

ownloaded from

January 1961 CAMPBELL: Blood Gras Measurements in Clinical Practice 13

... ?· ?,.-,· ...atl : ..... . .-.,,v...

0 3~~G0IZ 0 5

45 '-I...:',-;.' .'.':.~.· · ·'. ....,·

4mfiH.02

,.4 69 70.. 7. 7 7.3 7.4. :7.. 76 7..A779

.,.pH .UNIS

.!'.!" ,''.1.'' j. . . . .

'~l .. ".', ' ·.·-ru · .' " , '. .'

'Z,'.

·~~~~·' "i ,.:'. . · . ·· '"·

'/.':.

· ' .pHUNT' , .:".~'..~%il '.",

FIG. 2.-Bicarbonate/pH diagram. The numbers refer to the cases described in the text.

form of dissolved carbon dioxide, the proportionin the form of bicarbonate and the pH are inter-dependent. This interdependence is expressed inthe Henderson-Hasselbalch equation:

H =p l bicarbonate concentrationpH = pk' d- log. CO2 concentrationAs the concentration of dissolved carbon dioxide

is a constant function of the partial pressure ofcarbon dioxide, the equation can be written:p ' + l, bicarbonate concentrationpH =- pk' +- log.

0.03 x Pco2This equation enables the third variable to be

calculated from knowledge of the other two. Thisis valuable technically and also important clinicallybecause it shows that the full effects of a disturb-ance of any one of the three depends upon theother two. This is illustrated by Cases 3, 7, 8 andio described later.There are several ways of expressing the

Henderson-Hasselbalch relationship graphically,ofwhich one ofthe most popular is the bicarbonate:pH diagram (Fig. 2). Its use is indicated by thecase histories.

Clinical ValueSome overall judgments are required before

describing the illustrative cases if these are to beseen in true perspective.

Arterial Oxygen Measurements(None of the following remarks can necessarily be

applied to cases with intracardiac shunts whichpresent special problems.) It is still uncertain howvaluable arterial oxygen measurements are orwould be outside special cardiopulmonary units.They have been essential to the elucidation of thefunctional disturbance in many diseases, butevidence is still lacking about their value in themanagement of the individual patient. This viewcan be elaborated under three headings.

(I) Diagnosis. Cases in which a measurementof arterial oxygen saturation is essential to thediagnosis are very uncommon. The use of suchmanoeuvres as exercise and/or varying the oxygenconcentration of the inspired air to supplementclinical and radiological evidence will enable adiagnosis to be reached on nearly all occasions.Cases I and 2 described below may seem to beexceptions to this general rule, but, in fact, thediagnosis in both was strongly suspected andcould have been made by other methods. Thediagnosis in the patient with polycythaemia (Case5) depended on the estimation of Pco2 rather thanon the oxygen saturation.

(2) Prognosis. Evidence is still scanty thatmeasurements of arterial oxygenation add muchto the assessment of prognosis in either acute or

copyright. on M

arch 26, 2020 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.37.423.10 on 1 January 1961. D

ownloaded from

POSTGRADUATE MEDICAL JOURNAL

chronic respiratory disease (Cotes, I960). Suchevidence must await the introduction of adequatemethods for assessing the variability of arterialoxygenation.

(3) Treatment. If anoxic anoxia is suspectedduring an acute illness, the inspired air can andshould be enriched with oxygen. If anaemic orstagnant anoxia is suspected during an acute illnessthe inspired air should be Ioo% oxygen. Thesedecisions can be made clinically without recourseto measurements of blood oxygenation. Para-doxically, the oxygen concentration to give apatient is better judged from the arterial or mixedvenous Pco2 (see Case 4 below). In patientssuffering from chronic anoxia the value of oxygencan be adequately judged on clinical grounds,particularly by observing the effects on exercisetolerance.

Blood Carbon Dioxide MeasurementsMeasurements of blood carbon dioxide content

are, of course, essential to the assessment ofmetabolic (i.e. non-respiratory) disorders of acidbase metabolism (e.g. Cases 8, 0o and i ) and arerequired for the full assessment of respiratory dis-turbances (e.g. Cases 3 and 7).

Estimations of arterial or mixed venous Pco2are of great clinical value and provide informationwhich often cannot be obtained by other methods.The management of Cases 6, 9 and i was par-ticularly helped by having such facilities immedi-ately and continuously available.There is no substitute for measurements

of Pco2 when the adequacy of ventilation is indoubt. Anyone who attempts to forecast theadequacy of ventilation on the basis of clinicalevidence finds that he is very often wrong. Further-more, although there are other measurementswhich may help, none of them is as simple as therebreathing method for estimating Pco2.

In metabolic disturbances of hydrogen ion regu-lation the Pco2 is valuable in combination with theblood carbon dioxide content in providing anestimate of the pH. This topic is further discussedelsewhere in this issue (Ashby and Campbell,196I).Illustrative Cases

It has been easy to recollect patients in whommeasurements of Pco2 were of great value andradically affected the management. It has beendifficult to think of cases in which measurements ofarterial oxygen saturation were important, althoughmany could be found in which the measurementwas interesting and added to rather than changedthe picture.

CASE I.-Differentiation of Cardiac and RespiratoryCause of Breathlessness. A woman of 25 had had severekyphoscoliosis since childhood. In the preceding fewmonths she had become increasingly breathless andblue on exertion. The heart was enlarged and therewas a widely split second sound in the pulmonary area.The arterial saturation at rest breathing air was 72%,and while breathing 00o% oxygen it was 86%. ThePco, was normal.CommentThese figures illustrate the difficulty of inter-

pretation of changes in saturation in this range.The patient's colour changed unequivocally fromblue to -pink on receiving oxygen, an observationwhich had led to the belief that her anoxia waspulmonary in origin. In fact, she had a truevenous-arterial shunt and the findings are explic-able as follows: firstly, at a saturation of 72%cyanosis is easily seen, whereas at 86% it may beundetectable. Secondly, the data breathing airsuggested that there was a shunt equal to 50 to 70%of the cardiac output. This implies that 30 to 50%of the blood traversed the lungs, where, whilebreathing Ioo% oxygen, it could take up z ml./Ioo ml. extra oxygen in solution. This would besufficient to account for an increase in arterialsaturation of about Io%. The remaining 4%would readily be attributable to overcoming the'distribution' effect of her chest deformity,which, while breathing air, probably caused theblood flowing through parts of her lungs to beinadequately oxygenated.None of this difficulty would have arisen if 30%

oxygen had been used instead of Ioo% (see Case 2).Subsequently this patient was found to have an

atrial septal defect and progressive pulmonaryhypertension, causing a ' reversed ' shunt.

CASE 2.-Acute Cerebral Disease and a LocalizedPulmonary Lesion. A woman of 53 developed an acuteneurological illness with evidence of a focal cerebrallesion and meningeal irritation. The cerebro-spinalfluid contained many polymorphs but no organisms.The differential diagnosis included meningitis, brainabscess and cerebral tumour. X-ray of the chestshowed a lobulated shadow in the left lower lobe withprominent vascular connection. Arterial blood wassampled while the patient was breathing 30% oxygenand was found to have an oxygen saturation of 85%.Comment

Arterial unsaturation while breathing 30%oxygen can only be due to anatomical venous-arterial shunt. (Desaturation due to generalizedlung disease is corrected by 30% oxygen.) Thisfinding provided the lynch-pin of the diagnosis ofpulmonary arterio-venous fistula, a conditionknown to predispose to meningo-encephalitis. In-vestigation for cerebral tumour was therefore notpursued. The patient recovered.

CASE 3.-Combined Respiratory and Metabolic Dis-order in Emergency Surgery. A neurotic woman of 38

January I96I14copyright.

on March 26, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.37.423.10 on 1 January 1961. Dow

nloaded from

CAMPBELL: Blood Gas Measurements in Clinical Practice

was admitted with suspected peritonitis of four days'duration and physical signs of congestion or pneumoniaof the lower lobes. There was clinical evidence ofdehydration, sodium depletion, hyperventilation andarterial desaturation. The arterial blood (Fig. 2,point 31) Pco2 was 26 mm.Hg; plasma carbon dioxidecontent was I9.i mM./l.; pH 7.40; oxygen saturationwas 87%.

Exploratory laparotomy showed retroperitonealhaemorrhages and cedema but no ruptured viscus. Theoperation, which took one hour, had just finishedwhen the heart stopped. After cardiac massage througha thoracotomy, the heart started beating normally.

Arterial blood taken at this time had a pH of 7.00and a Pco2 of 90 mm.Hg (Fig. 2, point 32). Shortlyafterwards the heart stopped again and she died.Autopsy showed the intestine to contain large quan-tities of broken glass which she had apparentlyswallowed.CommentThe pre-operative findings for pH, Pco2 and

carbon dioxide content were similar to those in thepatient with salicylate poisoning (Case io) in thatthere was a combined metabolic acidosis andrespiratory alkalosis with a normal pH. Themetabolic acidosis was probably in part due to theelectrolyte disturbance caused by her abdominalcondition, but may have been partly due to therespiratory alkalosis. That the respiratory alkalosiswas not simply a consequence of the metabolicacidosis, but was probably due to the anoxia causedby the pneumonia, is indicated by the high normalpH.The combination of a low arterial Pco2 and a

low arterial oxygen saturation is the pattern ofblood gas changes seen in conditions causing mal-distribution of pulmonary blood flow. The dataindicate that over 40% of the blood flowing throughthis patient's lungs was ' shunted ', i.e. exchangedno oxygen or carbon dioxide. The consequentarterial hypoxia causes hyperventilation whichblows off carbon dioxide from the relatively nor-mal parts of the lungs, but cannot correct thehypoxia.The combination of a high alveolar ventilation

and maldistribution of pulmonary blood flowalmost certainly means that this patient required avery large total ventilation. This she obviouslydid not receive during the operation because anarterial Pco2 of 90 mm. Hg can only be reached byfairly prolonged underventilation. The effects ofsuch a respiratory acidosis on the pH was greatlyaggravated by the pre-existing metabolic acidosis(see Fig. 2).

It may be suggested that this patient presenteda hopeless case, but if such patients are to be savedgreater attention must be paid to respiratory func-tion and less absolute reliance placed on clinicaljudgment. The anaesthetist thought he had over-ventilated this patient. In fact, the cardiac arrest

may well have been attributable to under-ventilation.

CASE 4.-Management of Anoxia in RespiratoryFailure. A man of 55 with severe chronic obstructivelung disease was admitted with pneumonia. He wasslightly confused and there was central cyanosis. Thearterial Pco2 was 8I mm.Hg and the oxygen saturationwas 44%. He was given 34% oxygen to breathe whichincreased the saturation to 82.5% but caused him tobecome semi-comatose due to underventilation andaggravation of the respiratory acidosis-the Pco2 roseto 99 mm.Hg. Reduction of the inspired oxygen con-centration to 28% improved his mental state and thePco2 fell to 86.5 mm.Hg. with restoration of someanoxic drive to his ventilation as the saturation fellto 66%. The inspired oxygen concentration was sub-sequently gradually increased without ill effect.CommentThis case illustrates the paradox that knowledge

of the Pco2 is more helpful than knowledge of theoxygen saturation in managing the treatment ofanoxia in such a patient. He clearly had to receiveoxygen. The question was: how much? Theanswer is: as much as can be tolerated withoutallowing severe respiratory depression as indicatedby a serious increase in the Pco2.

CASE 5.-Polycythcemia. An obese man of 46 wasfound to have polycythaemia (Hb. i8 g./loo ml.). Hisdusky colour was attributed to a combination of thepolycythaemia and a colourful racial origin. After atime, however, the presence of undue cyanosis wasappreciated and the arterial oxygen saturation wasfound to be about 50%. A cardiac cause was excludedand he was referred for pulmonary function studies asa suspected case of chronic lung disease. His venti-latory capacity as judged by spirometry was found tobe normal but the arterial Pco2 was 85 mm.Hg.CommentThe combination of underventilation in the

presence of normal ventilatory capacity is diag-nostic of the syndrome of primary underventilation(Burwell, Robin, Whaley and Bickelman, 1956),which is usually accompanied by polycythamiaand obesity. (I am indebted to Dr. J. B. L. Howellfor the description of this case.)CASE 6.-Failure to Breathe Post-operatively. A

woman of 33 was operated on for a subphrenic abscess.The exposure was difficult and the anaesthetist main-tained controlled ventilation with the patient fullyparalysed by curare. After operation the patient wouldnot breathe. The possibility of carbon dioxide retentionwas considered and the artificial ventilation givenmore vigorously but the blood pressure fell. Themixed venous Pco2 was estimated by the rebreathingmethod and found to be about I50 mm.Hg. Over-ventilation was therefore given with greater confidenceand the Pco2 maintained at about 70 mm.Hg. Thepatient began to breathe and recovered completely.CommentThe patient's toxaemia and the various drugs

used in the course of anaesthesia had made any

January I96i I5copyright.

on March 26, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.37.423.10 on 1 January 1961. Dow

nloaded from

POSTGRADUATE MEDICAL JOURNAL

reliance on 'signs of carbon dioxide retention'unjustifiable. The anaesthetist did not knowwhether the patient was being over- or under-ventilated.Anybody who measures Pco2 in 'complicated'

cases who are ' not doing well' after operation canreport similar experiences (see also Cases 3 and 7).

CASE 7.-Distress After Thoracotomy, Cardiac By-pass and Aortic Surgery. A man of 21 had his aorticstenosis relieved with the aid of hypothermia andcardiac by-pass. In the immediate post-operativeperiod his condition was satisfactory, but after threehours it began to deteriorate. He was distressed andbreathless with rapid shallow breathing and had anincreasing tachycardia. The mixed venous Pco2 wasestimated by the rebreathing method and found to be68 mm.Hg, corresponding to an arterial Pco2 ofabout 62. Assisted ventilation was not tolerated sotracheostomy was performed. His condition imme-diately improved and his Pco2 fell to about 40.CommentAn arterial Pco2 of 62 mm. Hg is not dangerous,

but the plasma bicarbonate concentration was laterreported to have been 22 mEq/l. at the time of hisdeterioration. This is apparently a' normal' value,but when considered in conjunction with the Pco2(Fig. 2, point 7) it can be seen to represent asignificant metabolic acidosis, being well belowthe normal range of the bicarbonate buffer line.Thus the patient had both a respiratory and ametabolic acidosis giving a severe acidaemia (pH7. 9) and improvement in ventilation was thereforedoubly important.

CASE 8.-Resistant ' Heart Failure '. A woman of 60had gross cedema presumed to be due to ischaemicheart disease although the history and ECG wereequivocal. Initially she responded well to mercurialdiuretics, but oedema recurred and the plasma 'alkalireserve' was found to be 33 mEq./l. Although theplasma potassium concentration was normal she wasthought to be suffering from metabolic alkalosissecondary to potassium depletion caused by overuseof the mercurial diuretics. The arterial pH was foundto be 7.31, implying a Pco2 of about 65 mm.Hg (Fig. 2,point 8). A review of the case showed that she was,in fact, suffering from severe obstructive lung disease.Comment

Patients who develop 'cor pulmonale' almostalways have carbon dioxide retention. Thisempirical observation, whatever its explanation(Campbell and Short, I960), can provide a usefulaid to diagnosis in 'heart failure' of uncertaincause.

CASE 9.-Barbiturate Poisoning. An unconsciouswoman of 33 was admitted one Sunday evening. Shehad swallowed an apparently large amount of cyclo-barbitone early in the day. Her respiration rate was8/min. and she was considered by most observers to bevery blue. Preparations were made for the administra-tion of a stimulant drug and the arterial Pco2 was

measured so that the effects of this drug could bedocumented. The Pco2 was found to be 32 mm.Hg.No drug was given and the patient woke up eighthours later.CommentNow that easy methods of Pco2 estimation are

available, comparisons of methods of treatingrespiratory depression should become more con-vincing.

CASE io.-Salicylate Poisoning. A woman of 52swallowed 25 g. of aspirin and was admitted to hos-pital two days later with oliguria. There was obvioushyperventilation. The plasma bicarbonate concentra-tion was 13 mEq/l. and the arterial Pco2 17 mm.Hg,giving a calculated pH of 7.46. The blood urea was255 mg./Ioo ml. and the plasma salicylate concentrationwas 55 mg./xoo ml. A diuresis began shortly afteradmission. She was treated conservatively with waterand electrolyte replenishment governed by her urinarylosses and weight changes. Her blood urea, bicarbonate,Pco2 and pH were little changed two days later, butsubsequently she recovered rapidly.CommentAt the time of the measurements this patient

still had the respiratory alkalosis characteristic ofthe early stages of salicylate intoxication (Singer,I954). She also was in severe metabolic acidosis,which may have been due either to the salicylatepoisoning or the renal failure. The resultant was aslight alkalemia. Correction of the respiratoryalkalosis by the administration of carbon dioxideor by reducing ventilation would have caused afairly severe acidaemia; correction of the metabolicacidosis by the administration of alkali would havecaused a severe alkasemia. Either of these stepsmight have been unfortunate in such an ill patient.This case, therefore, illustrates the importance ofa full evaluation of acid-base disturbances. (Thiscase has been fully described elsewhere: Campbelland MacLaurin, I958.)CASE II.-Renal Asthma. This case, described else-

where (Ashby and Campbell, I96I) (p. 43), illustratesmany points, the most important lesson for routinepractice probably being the value of a simple methodof estimating Pco2 in supporting a clinical impressionwhich, by itself, carried little conviction. The diag-nosis of bronchial asthma had the blessing of sixdoctors who had seen the patient previously. Thepossibility that it was wrong and the patient was reallyoverbreathing was not taken sufficiently seriously tojustify spending time on arterial blood analyses in themiddle of a busy day. In fact, the first reading of avery low mixed venous Pco2 was disbelieved, but thesimplicity of the method allowed it to be checked inten minutes.

Summary(i) Practical problems and methods of blood gas

analysis are discussed.(2) Some physiological principles underlying

clinical interpretation are emphasized.

January I96I16copyright.

on March 26, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.37.423.10 on 1 January 1961. Dow

nloaded from

January 1961 CAMPBELL: Blood Gas Measurements in Clinical Practice

(3) Eleven illustrative cases are described.

AcknowledgmentsI am grateful to Professor A. Kekwick, Dr.

J. D. N. Nabarro, Mr. T. Holmes-Sellors andMr. L. P. Le Quesne for permission to describethese cases and to Mr. M. Hobsley, F.R.C.S., andDr. J. B. L. Howell for reading the manuscript.

REFERENCESASHBY, R. R., and CAMPBELL, E. J. M. (I96I): A Case of Renal Asthma, Postgrad. med. J., 37, 43.ASTRUP, P. (1956): A Simple Electrometric Technique for the Determination of Carbon Dioxide Tension in Blood

and Plasma, Total Content of Carbon Dioxide in Plasma, and Bicarbonate Content in ' Separated ' Plasma at aFixed Carbon Dioxide Tension (40 mm.Hg), Scand. . . din. Lab. Invest., 8, 33.

BISHOP, J. M. (1960):-Measurement of Blood Oxygen Tension, Proc. roy. Soc. Med., 53, 177.BROOKS, D., and WYNN, V. (1959): Use of Venous Blood for pH and Carbon Dioxide Studies, Lancet, i, 227.BURWELL, C. S., ROBIN, E. D., WHALEY, R. D., and BICKELMAN, A. G. (1956): Extreme Obesity Associated with

Alveolar Hypoventilation-a Pickwickian Syndrome, Amer. J. Med., 21, 8 1.CAMPBELL, E. J. M., and DICKINSON, C. J. (I960): Clinical Physiology, p. 120. Oxford: Blackwells.

, and HOWELL, J. B. L. (1960): Simple Rapid Methods of Estimating Arterial and Mixed Venous Pco2, Brit.med..., i, 458., and MACLAURIN, R. E. (1958): Acute Renal Failure in Salicylate Poisoning, Ibid., i, 503., and SHORT, D. S. (1960): The Cause of CEdema in ' Cor Pulmonale ', Lancet, i, 1I84.

COLLIER, C. R. (1956): Determination of Mixed Venous Carbon Dioxide Tensions by Rebreathing, Y. appl. Physiol.,9, 25.

COTES, J. E. (I960): Respiratory Function and Portable Oxygen Therapy in Chronic Non-specific Lung Disease inRelation to Prognosis, Thorax, 15, 244.

NILSSON, N. J. (1960): Oximetry, Physiol. Rev., 40, I.REFSUM, H. E., and HISDAL, B. (1958): Construction and Use of a Simple Reflectometer for Determination of Haemo-

globin Oxygen Saturation in Blood, Scand. . clin. Lab. Invest., 10, 439.RILEY, R. L., CAMPBELL, E. J. M., and SHEPARD, R. H. (1957): A Bubble Method for Estimation of Pco2 and Poein Whole Blood, J. appl. Physiol., II, 245.SEVERINGHAUS, J. W., and BRADLEY, A. F. (1958): Electrodes for Blood Po2 and Pco2 Determination, Ibid., 13, 515.SHEPARD, R. H. (1958): Effect of Pulmonary Diffusing Capacity on Exercise Tolerance, Ibid., 12, 487.SINGER, R. B. (1954): The Acid-base Disturbance in Salicylate Intoxication, Medicine (Baltimore), 33, I.VAN SLYKE, D. D., and NEILL, J. M. (1924): The Determination of Gases in Blood and other Solutions by VacuumExtraction and Manometric Measurement (I), J. biol. Chem., 6I, 523.VEREL, D., SAYNOR, R., and KESTEVEN, A. B. (1960): A Spectrophotometric Method of Estimating Blood OxygenUsing the Unicam SP 600, J. clin. Path., 13, 361.

EXTRA BIBLIOGRAPHYDAVENPORT, H. W. (1958): The ABC of Acid-base Chemistry, 4th ed. Chicago: University of Chicago Press.MOLLER, B. (I959): The Hydrogen Ion Concentration in Arterial Blood, Acta med. scand., 165, supp. 348.WOOLMER, R. F. (I959): pH and Blood Gas Measurement. A Ciba Foundation Symposium. London: J. & A.

Churchill.

copyright. on M

arch 26, 2020 by guest. Protected by

http://pmj.bm

j.com/

Postgrad M

ed J: first published as 10.1136/pgmj.37.423.10 on 1 January 1961. D

ownloaded from