the trust in pulse oximeters

2
1130 7. Lanzavecctioa A, Roosnek E, Gregory T, et al. T cells can present antigens such as HIV gp120 targeted to their own surface molecules. Nature 1988; 334: 530-32. 8. Smith DH, Byrn RA, Marsters SA, et al. Blocking of HIV-1 infectivity by a soluble, secreted form of the CD4 antigen. Science 1987; 228: 1704-07. 9. Fisher RA, Bertonis JM, Meier W, et al. HIV infection is blocked in vitro by recombinant soluble CD4. Nature 1988; 331: 76-78. 10. Hussey RE, Richardson NE, Kowalski M, et al. A soluble CD4 selectively inhibits HIV replication and syncytium formation. Nature 1988; 331: 78-81 11. Deen KC, McDougal JS, Macker R, et al. A soluble form of CD4 (T4) protein inhibits AIDS virus infection. Nature 1988; 331: 82-84. 12. Trannecker A, Luke W, Karjalian K. Soluble CD4 molecules neutralise human immunodeficiency virus type 1. Nature 1988; 331: 76-78. 13. Manca F, Habeshaw JA, Dalgleish AG. HIV envelope glycoprotein, antigen-specific T-cell responses, and soluble CD4. Lancet 1990; 335: 811-15. 14. Watanabe M, Reimann KA, De Long PA, et al. Effects of recombinant CD4 in rhesus monkeys infected with simian immunodeficiency virus of macaques. Nature 1989; 237: 267-70. 15. Schosley RT, Merigan TC, Gant P, et al. Recombinant soluble CD4 therapy in patients with the acquired immunodeficiency syndrome (AIDS) and AIDS-related complex. A phase I-II escalating dosage trial. Ann Intern Med 1990; 112: 247-53. 16. Kalm JO, Allan JD, Hodges TL, et al. The safety and pharmacokinetics of recombinant soluble CD4 (rCD4) in subjects with the acquired immunodeficiency syndrome (AIDS) and AIDS-related complex. A phase 1 study. Ann Intern Med 1990; 112: 254-61. 17. Lamarre D, Capon DJ, Karp DR, et at. Class II MHC molecules and the HIV gp120 envelope protein interact with functionally distinct regions of the CD4 molecule. EMBO J 1989; 8: 3271-77. 18. Bym RA, Mordenti J, Lucas C, et al. Biological properties of a CD4 immunoadhesin. Nature 1990; 344: 667-70. 19. Dalgleish AG, Thomson BJ, Chanh TC, Malkovsky M, Kennedy RC. Neutralisation of HIV isolates by anti-idiotypic antibodies which mimic the T4 (CD4) epitope: a potential AID S vaccine. Lancet 1987; ii: 1047-50. 20. Johnson VA, Barlow MA, Chanh TC, et al. Synergistic inhibition of human immunodeficiency virus type 1 (HIV-1) replication in vitro by recombinant soluble CD4 and 3’ azido-3’ deoxythymidine. J Infect Dis 1989; 159: 837-44. THE TRUST IN PULSE OXIMETERS Pulse oximeters give a non-invasive continuous readout of the oxygen saturation of haemoglobin in arterial blood. They are widely accepted as sensitive and accurate instruments that produce clinically useful data and are used extensively in anaesthetic practice. Are we becoming too complacent about the accuracy of such monitors? These instruments rely on spectrophotometric analysis of light transmitted through tissues to measure haemoglobin oxygen saturations. A microprocessor is used to isolate the pulsatile component of the light signal, which is assumed to be solely of arterial origin. Two specific wavelengths of light suited to the detection of haemoglobin and oxyhaemoglobin are used to generate the sensor output. Haemoglobin saturation values are calculated by use of an inbuilt algorithm derived from human experimental data. Current models are unable to distinguish between chromophores other than haemoglobin and oxyhaemoglobin, so in practice all pulsatile signals are attributed to these two compounds. Since the introduction of pulse oximetry there have been several clinical reports of erroneous data generation. Oximeters process complex data from highly amplified signals and are therefore subject to interference from the hostile electromagnetic environment in which they are used. Sensor movement,l infrared2 and theatre lighting,3 and surgical diathermy may produce such interference, which is usually transient. However, a permanent instrument readout error following diathermy was lately reported 4 The assumptions that underlie the calculation of saturation may give rise to difficulties. Thus it is assumed that the pulsatile component of the sensor output indicates only events in the arterial circulation, yet venous pulsationl or anything that causes slight rhythmical changes in optical conduction can give spurious readings. Use of oximeters with a waveform display may allow the operator to reject artifactual readings obtained from non-arterial sources. The assumption that all absorption signals at the two wavelengths used by the instrument arise from haemoglobin or oxyhaemoglobin is potentially a more serious source of error since any other substance in the arterial blood that absorbs light at the detection wavelengths will be reported as being one of these two compounds. Substances of this type include carboxyhaemoglobin,s 5 methaemoglobin,6 and certain dyes such as methylene blue.7 Exclusive reliance on pulse oximeter readings in patients with raised blood concentrations of these interfering chromophores may be dangerous and therefore confirmatory investigations such as co-oximetry should be used if there is uncertainty. Skin dyes,8 dried blood,9 and nail polishlO have also affected the accuracy of readings, despite the fact that the absorbance they produce would be expected to be non-pulsatile. Pulse oximeters are widely thought to provide a measurement of oxygen saturation throughout the body. This generalisation may be true in the steady state, but under dynamic conditions oximetry gives an accurate assessment of arterial oxygen saturation only at the point of measurement-ie, simultaneous pulse oximeter readings taken from tissues with different perfusion rates show different saturation values after induced changes in arterial oxygen tension. Thus Severinghaus" induced decreases in arterial oxygen tension in normal subjects and found response lags of 50 s and 10 s for saturation readings obtained from pulse oximeter sensors placed on the finger and earlobe, respectively. Any factors that impair blood flow to the tissues onto which the sensor is placed may increase this response lag and further delay detection of arterial hypoxaemia. These effects will be greater in instruments with long averaging times. A computer model of the cardiorespiratory system has been used to assess the importance of time delays on the detection of hypoxic events. 12 Various causes of oxygen supply failure were examined and in most cases pulse oximetry, even with a 60 s delay, gave adequate warning of a fall in brain oxygen tension. However, when arterial oxygen saturation fell most rapidly-ie, during ventilation with a gas mixture containing no oxygen-severe brain hypoxia could occur before a pulse oximeter with finger sensor would alarm. If this computer simulation accurately represents human pathophysiology, over-reliance on finger pulse oximetry may, in this circumstance, result in an unacceptable risk of hypoxic damage. Pulse oximetry undoubtedly represents an important advance in patient monitoring technology and its use is strongly recommended by the Association of Anaesthetists.13 A survey of insurance claims resulting from over a thousand anaesthetic mishaps concluded that its addition to a monitoring system could have prevented over a third of avoidable incidents.14 Nevertheless, the limitations of the technique suggest that unqualified reliance on the values produced might sometimes be dangerously misleading. Technological advances may overcome some of these limitations; meanwhile, the effect of different sensor

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Page 1: THE TRUST IN PULSE OXIMETERS

1130

7. Lanzavecctioa A, Roosnek E, Gregory T, et al. T cells can presentantigens such as HIV gp120 targeted to their own surface molecules.Nature 1988; 334: 530-32.

8. Smith DH, Byrn RA, Marsters SA, et al. Blocking of HIV-1 infectivityby a soluble, secreted form of the CD4 antigen. Science 1987; 228:1704-07.

9. Fisher RA, Bertonis JM, Meier W, et al. HIV infection is blocked in vitroby recombinant soluble CD4. Nature 1988; 331: 76-78.

10. Hussey RE, Richardson NE, Kowalski M, et al. A soluble CD4

selectively inhibits HIV replication and syncytium formation. Nature1988; 331: 78-81

11. Deen KC, McDougal JS, Macker R, et al. A soluble form of CD4 (T4)protein inhibits AIDS virus infection. Nature 1988; 331: 82-84.

12. Trannecker A, Luke W, Karjalian K. Soluble CD4 molecules neutralisehuman immunodeficiency virus type 1. Nature 1988; 331: 76-78.

13. Manca F, Habeshaw JA, Dalgleish AG. HIV envelope glycoprotein,antigen-specific T-cell responses, and soluble CD4. Lancet 1990; 335:811-15.

14. Watanabe M, Reimann KA, De Long PA, et al. Effects of recombinantCD4 in rhesus monkeys infected with simian immunodeficiency virusof macaques. Nature 1989; 237: 267-70.

15. Schosley RT, Merigan TC, Gant P, et al. Recombinant soluble CD4therapy in patients with the acquired immunodeficiency syndrome(AIDS) and AIDS-related complex. A phase I-II escalating dosagetrial. Ann Intern Med 1990; 112: 247-53.

16. Kalm JO, Allan JD, Hodges TL, et al. The safety and pharmacokineticsof recombinant soluble CD4 (rCD4) in subjects with the acquiredimmunodeficiency syndrome (AIDS) and AIDS-related complex. Aphase 1 study. Ann Intern Med 1990; 112: 254-61.

17. Lamarre D, Capon DJ, Karp DR, et at. Class II MHC molecules and theHIV gp120 envelope protein interact with functionally distinct regionsof the CD4 molecule. EMBO J 1989; 8: 3271-77.

18. Bym RA, Mordenti J, Lucas C, et al. Biological properties of a CD4immunoadhesin. Nature 1990; 344: 667-70.

19. Dalgleish AG, Thomson BJ, Chanh TC, Malkovsky M, Kennedy RC.Neutralisation of HIV isolates by anti-idiotypic antibodies whichmimic the T4 (CD4) epitope: a potential AID S vaccine. Lancet 1987; ii:1047-50.

20. Johnson VA, Barlow MA, Chanh TC, et al. Synergistic inhibition ofhuman immunodeficiency virus type 1 (HIV-1) replication in vitro byrecombinant soluble CD4 and 3’ azido-3’ deoxythymidine. J Infect Dis1989; 159: 837-44.

THE TRUST IN PULSE OXIMETERS

Pulse oximeters give a non-invasive continuous readout ofthe oxygen saturation of haemoglobin in arterial blood.They are widely accepted as sensitive and accurate

instruments that produce clinically useful data and are usedextensively in anaesthetic practice. Are we becoming toocomplacent about the accuracy of such monitors?These instruments rely on spectrophotometric analysis of

light transmitted through tissues to measure haemoglobinoxygen saturations. A microprocessor is used to isolate thepulsatile component of the light signal, which is assumed tobe solely of arterial origin. Two specific wavelengths of lightsuited to the detection of haemoglobin and oxyhaemoglobinare used to generate the sensor output. Haemoglobinsaturation values are calculated by use of an inbuilt

algorithm derived from human experimental data. Currentmodels are unable to distinguish between chromophoresother than haemoglobin and oxyhaemoglobin, so in practiceall pulsatile signals are attributed to these two

compounds.Since the introduction of pulse oximetry there have been

several clinical reports of erroneous data generation.Oximeters process complex data from highly amplifiedsignals and are therefore subject to interference from thehostile electromagnetic environment in which they are used.Sensor movement,l infrared2 and theatre lighting,3 andsurgical diathermy may produce such interference, which isusually transient. However, a permanent instrument

readout error following diathermy was lately reported 4The assumptions that underlie the calculation of

saturation may give rise to difficulties. Thus it is assumedthat the pulsatile component of the sensor output indicatesonly events in the arterial circulation, yet venous pulsationlor anything that causes slight rhythmical changes in opticalconduction can give spurious readings. Use of oximeterswith a waveform display may allow the operator to rejectartifactual readings obtained from non-arterial sources. Theassumption that all absorption signals at the two

wavelengths used by the instrument arise from haemoglobinor oxyhaemoglobin is potentially a more serious source oferror since any other substance in the arterial blood thatabsorbs light at the detection wavelengths will be reported asbeing one of these two compounds. Substances of this typeinclude carboxyhaemoglobin,s 5 methaemoglobin,6 andcertain dyes such as methylene blue.7 Exclusive reliance onpulse oximeter readings in patients with raised bloodconcentrations of these interfering chromophores may bedangerous and therefore confirmatory investigations such asco-oximetry should be used if there is uncertainty. Skindyes,8 dried blood,9 and nail polishlO have also affected theaccuracy of readings, despite the fact that the absorbancethey produce would be expected to be non-pulsatile.

Pulse oximeters are widely thought to provide a

measurement of oxygen saturation throughout the body.This generalisation may be true in the steady state, butunder dynamic conditions oximetry gives an accurate

assessment of arterial oxygen saturation only at the point ofmeasurement-ie, simultaneous pulse oximeter readingstaken from tissues with different perfusion rates showdifferent saturation values after induced changes in arterialoxygen tension. Thus Severinghaus" induced decreases inarterial oxygen tension in normal subjects and foundresponse lags of 50 s and 10 s for saturation readingsobtained from pulse oximeter sensors placed on the fingerand earlobe, respectively. Any factors that impair blood flowto the tissues onto which the sensor is placed may increasethis response lag and further delay detection of arterialhypoxaemia. These effects will be greater in instrumentswith long averaging times. A computer model of thecardiorespiratory system has been used to assess the

importance of time delays on the detection of hypoxicevents. 12 Various causes of oxygen supply failure wereexamined and in most cases pulse oximetry, even with a 60 sdelay, gave adequate warning of a fall in brain oxygentension. However, when arterial oxygen saturation fell mostrapidly-ie, during ventilation with a gas mixture

containing no oxygen-severe brain hypoxia could occurbefore a pulse oximeter with finger sensor would alarm. Ifthis computer simulation accurately represents human

pathophysiology, over-reliance on finger pulse oximetrymay, in this circumstance, result in an unacceptable risk ofhypoxic damage.Pulse oximetry undoubtedly represents an important

advance in patient monitoring technology and its use is

strongly recommended by the Association ofAnaesthetists.13 A survey of insurance claims resulting fromover a thousand anaesthetic mishaps concluded that itsaddition to a monitoring system could have prevented over athird of avoidable incidents.14 Nevertheless, the limitationsof the technique suggest that unqualified reliance on thevalues produced might sometimes be dangerouslymisleading. Technological advances may overcome some ofthese limitations; meanwhile, the effect of different sensor

Page 2: THE TRUST IN PULSE OXIMETERS

1131

application sites on reducing the time to detection ofdesaturation warrants further study.

1. Taylor MB. Erroneous actuation of the pulse oximeter. Anaesthesia 1987;42: 1116.

2. Brooks TD, Paulus DA, Winkle WE. Infrarad heat lamps interfere withpulse oximeters. Anesthesiology 1984; 61: 630.

3. Costarino AT, Davies DA, Keon TP. Falsely normal saturation readingwith the pulse oximeter. Anesthesiology 1987; 67: 830-31.

4. Broome IJ. A dangerous failure of a pulse oximeter. Anaesthesia 1990; 45:166.

5. Hodges MR, Preece LP, Downs JB. Clinical experience with pulseoximetry in the presence of elevated carboxyhemoglobin.Anesthesiology 1989; 71: A369.

6. Rieder HU, Frei FJ, Zbinden AM, Thomson DA. Pulse oximetry inmethaemoglobinaemia. Anaesthesia 1989; 44: 326-27.

7. Gorman ES, Shnider MR. Effect of methylene blue on the absorbance ofsolutions of haemoglobin. Br J Anaesth 1988; 60: 439-44.

8. Goucke R. Hazards of henna. Anesth Analg 1989; 69: 416-17.9. Hopkins PM. An erroneous pulse oximeter reading. Anaesthesia 1989; 44:

868.

10. Cote CJ, Goldstein EA, Fuchsman WH, Hoaglin DC. The effect of nailpolish on pulse oximetry. Anesth Analg 1988; 67: 683-86.

11. Severinghaus JW, Naifeh KH. The accuracy of six pulse oximeters toprofound hypoxia. Anesthesiology 1987; 67: 551-58.

12. Verhoeff F, Sykes MK. Delayed detection of hypoxic events by pulseoximeters: computer simulations. Anaesthesia 1990; 45: 103-09.

13. Recommendations for standards of monitoring during anaesthesia andrecovery. London: Association of Anaesthetists of Great Britain andIreland, 1988.

14. Dull DL, Tinker JH, Caplan RA, Ward RJ, Cheney FW. ASA closedclaims study: can pulse oximetry and capnometry prevent anestheticmishaps? Anesth Analg 1989; 68: S74.

RADIAL KERATOTOMY

Patients with myopic (shortsighted) eyes can achieve cleardistance vision reliably and safely with spectacles or contactlenses. Over the past decade radial keratotomy (the mostwidespread form of refractive surgery) has emerged asanother way of correcting low to moderate myopia; the aimof the operation is to provide good unaided distance acuity.The sight-threatening consequences of myopia (risk ofretinal detachment and macular degeneration), which aremore common in moderate to high myopia, are not affectedby refractive surgery.

Radial keratotomy was developedl in the USSR and isbecoming established in the USA but it is not widelyavailable in the UK. The value of this technique is defined,as with any surgical procedure, by the balance betweenpotential benefits and risks compared with the consequencesof conservative treatment. Specifically, its results need to beassessed in relation to the accuracy, predictability, andstability of refractive correction; the proportion of patientswho can subsequently do without spectacles; and thefrequency and severity of postoperative complications.Deep radial cuts are made into the cornea (sparing an opticalclear zone of 3-4 mm), which reduce the steepness of thecorneal curvature and therefore the eye’s refractive power.The structure of the (healthy) cornea is irreversibly altered,so the operation cannot be undone if the patient finishes upworse off, and inevitably there are risks of infection andperforation.The relation between refractive error and visual acuity

alters after radial keratotomy, and both components mustbe assessed to measure success adequately. Four-yearresults from the PERK study3 show that although themyopic error is reduced in most patients and uncorrectedvisual acuity generally improves considerably, the

outcome tends to be unpredictable. Uncorrected acuitybetter than 6/60 was found in 31% of eyes preoperativelyand in 98% at 4 years. The percentage of eyes withuncorrected acuity of 6/12 or better (approximately the legaldriving standard) increased from 0-25% to 76% at 4 yearspostoperatively, but 19% of eyes lost at least one line ofbest-corrected acuity. Between 16% and 40% of all eyesbecame hypermetropic by more than 05 D, indicating thatimproved distance acuity required accommodative effort insome cases; these patients will become presbyopic early andtherefore require glasses once again, this time for reading,which they might have avoided without surgery.Astigmatism increased (36%) more often than it decreased(16%), and 36% of patients still wear a spectacle or contactlens before one or both eyes. "Starburst" glare (mosttroublesome when the central optical clear zone is small) isespecially disabling in conditions such as night driving,which some patients have to discontinue after radial

keratotomy.Although the initial postoperative instability of refraction

and acuity appears to settle in most patients at about 3-6months, a proportion of eyes show a persistent reduction inmyopia (or increase in hypermetropia): in 27% refractionchanged by 1 D or more between 6 months and 4 years aftersurgery. Diurnal fluctuations in refraction also occur insome eyes. This fluctuation is greatest at about 2 weeks

postoperatively (up to 4 D change from morning to

evening), reducing to 1-5-2 D at 6 months.4 37% haddiurnal variation of 05 D or more at 35 years,s associatedwith diurnal variation in uncorrected acuity of 2 or moreSnellen lines in 21%. It was not possible to identify thefactors responsible for the unpredictability and instability ofpostoperative refraction, except to confirm earlierindications that those whose initial myopia was lowergenerally do better.The reported complications of refractive corneal surgery

occur early in the postoperative course, and include

perforation, endophthalmitis," keratitis,7,8 persistent cornealepitheliopathy,9 ptosis,l° and cystoid macular oedema."Experience of long-term complications or tolerance of latersurgery (eg, for cataract or glaucoma) is not yet available.

Radial keratotomy is an irreversible surgical procedurecarried out on the healthy cornea of a healthy eye to avoid theneed to wear glasses. This aim was achieved in the PERKstudy in 64% of patients, while 36% had to continue to wearoptical correction. At 1 year less than half (48%) the patientswho had undergone keratotomy were "very satisfied" withthe result, 42% were "moderately satisfied", and 10% weredissatisfied.l2 The "desire to see unaided may transcend

reason",13 and patients contemplating refractive surgerymust be fully informed of the risks of ocular and visualcomplications, as well as of the real possibility that they maystill need glasses after surgery. Those with a compellingneed for good unaided distance acuity, who are genuinelyintolerant of contact lenses and are prepared to risk surgicaland refractive complications, may entertain the procedure.In most low to moderate myopes, for whom the desire to dowithout glasses is largely a question of convenience orcosmesis, it would seem safer to keep them or to perseverewith contact lenses rather than to choose a risky operationthat offers only small gains.

1. Fyodorov SN, Durnev VV. Operation of dosaged dissection of thecorneal circular ligament in cases of myopia of mild degree. AnnOphthalmol 1979; 11: 1885-90.

2. Santos VR, Waring GO, Lynn MJ, et al. Relationship between refractive