Predictors for oxygen and carbon dioxide IeveIs during anzesthesia*

Transcription

1 VOL 17 NO 2 ANESTHESIA APRIL 1962 Predictors for oxygen and carbon dioxide IeveIs during anzesthesia* Leverhulme Research Fellow Royal College of Surgeons Postgraduate Medical School University of London The criterion of satisfactory lung function is the maintenance of normal levels of oxygen and carbon dioxide in the arterial blood. In the conscious state, while breathing air, homeostatic mechanisms ensure that blood-gas levels remain close to normal under widely varying circumstances. However, during anasthesia, respiration may be grossly abnormal and values for the arterial carbon dioxide tension (Pco2) have been reported within the range 1@236mm/Hg. This is in marked contrast to the close normal range of 34-44mm/Hg. When a fit person breathes an inspired gas mixture containing 21 per cent oxygen, changes in ventilation cause changes in Pc02 and Po2 which bear a constant relationship to one another. There is, in fact, an established pathway of Pco~/Po~ changes following either under or over-ventilation (TABLE 1). Thus, when breathing air, we Table 1 Common pathway of Pco2/Po2 changes.during under and overventilation when breathing air ALVEOLAR VENTEATION ARTERIAL PCO 2 ARTERIAL PO 2 ARTERIAL -m/hg -m/hg HRMOGLOBIN SATURATION -% Half of normal Normal Double normal may anticipate the Po2 changes associated with a given change in Pco2. However, when the oxygen concentration in the inspired gas is other than 21 per cent, the usual pathway is no longer followed. Thus, *Paper read at the Annual Meeting of the Association of Anzesthetists at Dublin

2 ANESTHESIA 183 if 10 per cent oxygen is inhaled at a normal alveolar ventilation, PCO~ will remain normal, but Po2 will be reduced. Alternatively, underventilation when breathing 30 per cent oxygen may result in a normal P02, but a raised Pc02. It is, of course, quite unusual for anzsthetised patients to breathe 21 per cent oxygen and the range extends from 10 per cent (still used by some for dental anasthesia) to 99 per cent (e.g., closed circuit halothane). Thus, it appears that during anaesthesia there may be, not only gross departures from normal ventilation, but also the patient may stray far from the pathway of Pc02/Po2 changes which is well established for the patient breathing air (TABLE 1). Changes in oxygen and carbon dioxide levels are thus dissociated and must be considered separately. It is easy to say that the maintenance of correct arterial blood gas levels may be accomplished by sampling and analysis. Cooper and Smith1 have assessed the alternatives to arterial blood sampling and there are now a variety of techniques which offer sufficient accuracy for clinical purposes. However, even the simplest apparatus required for this purpose is lacking in most hospitals. Moreover, many anasthetists working single handed are unwilling to accept the distraction of their attention which inevitably results from the use of even the simplest analytical procedures. It is, therefore, customary to rely upon clinical observation for the preservation of gaseous homeostasis. However, even this may be difficult. Many signs of hypercapnia have been described, but cases such as that reported by Schultz et al.2 must dispel the notion that hypercapnia may be reliably diagnosed by clinical observation. Hypoxamia is easier to detect since it is accompanied by cyanosis and, indeed, one may speculate on how difficult and dangerous anasthesia would be if hamoglobin did not change colour on desaturation. Nevertheless, even under the best conditions, cyanosis cannot reliably be detected until the arterial Po2 is reduced to about half the normal value3. The position is still less satisfactory with bad lighting conditions, skin pigmentation or anamia. It should also be noted that, in the lightly cyanosed patient, the arterial point is below the upper bend of the dissociation curve and is poised for a rapid descent in saturation if Po2 should fall any further. There are thus difficulties in assessing arterial blood-gas levels either by analytical methods or by clinical observation. It seems, therefore, that there may be a place for prediction of gas levels from quantities which may be easily measured and in this category may be included the inspired oxygen concentration and the respiratory minute volume. The inspired oxygen concentration may be derived from the rotameters in non-rebreathing circuits (such as the Magill system with adequate fresh gas flow); in rebreathing systems it is more difficult.

3 184 ANBSTHESIA The respiratory minute volume has been difficult to measure in the past, but with the Wright respiratory anemometer4, this measurement is no more difficult than counting the pulse rate. The method is, furthermore, applicable to any gas circuit and has an accuracy considerably in excess of that required for clinical purposes. If the composition of the inspired gas and the respiratory minute volume be known, a great deal can be inferred about the oxygen and carbon dioxide levels of the patient by use of the Bohr and alveolar air equations. These equations are, however, unsuited to mental arithmetic in the operating theatre and this paper describes predictors which have been constructed to solve them quickly and easily. By this means, the composition of the inspired gas and the respiratory minute volume may be used to yield the maximum amount of information to the clinician. Alternatively, predictors may be used to indicate the appropriate inspired gas composition and the respiratory minute volume which is best suited to a particular patient. But perhaps the greatest value of predictors is the development of an appreciation of the quantitative significance of changes in respiratory parameters. CARBON DIOXIDE Principles of prediction Carbon dioxide prediction has already received a good deal of attentions 6. Prediction of arterial PCO~ (Pa,,,) is based upon the following form of Bohr s equation : Of the variables on the right-hand side of the equation, the actual dry barometric pressure - PB (dry) - is replaced by the standard barometric pressure when the carbon dioxide output (VCO~) is converted from its volume measured under standard conditions, to its volume measured under the same conditions as the alveolar ventilation (VA)- body temperature and pressure, saturated with water vapour6. Inhaled carbon dioxide concentration (FI~,J will normally be zero during anaesthesia. The important variables are, therefore, reduced to carbon dioxide output and alveolar ventilation. Carbon dioxide output is probably best predicted from the data of Aub and DuBois7, assuming a respiratory exchange ratio of 0.82, which appears reasonable during anasthesia8. Although it is unlikely that the metabolic respiratory exchange ratio will vary widely from *Symbols used in this paper are listed in the appendix

4 co ML/MI OUTPUT (S.T. I? D.) N 2oo ANESTHESIA , considerable temporary fluctuations will occur during unsteady respiratory states. Aub s data of basal metabolic rate are related to sex, age and body surface area. However, the influence of age throughout adult life is really quite small and for present purposes can be neglected. The use of surface area is inconvenient and body weight is to be preferred for clinical purposes. It is, however, useful to be able to make allowance for changes in metabolic rate - an important factor in anaxthesia and hypothermia. Eighty-five per cent of basal appears to be the mean value during anaesthesia6 8. FIG. 1 shows the values for 3 I I I basal carbon dioxide output which have been used in the preparation of this predictor. The other important variable on the right hand side of equation (i) is the alveolar ventilation. This cannot be measured directly and must be inferred from the minute volume of ventilation. Radford5 made a fixed allowance for the dead space depending upon the body weight of the patient. However, Nunn and Hill9 have shown that, in the fit, intubated, anasthetised patient, the alveolar ventilation approximates more closely to two-thirds of the minute volume. The arterial Pco~, during anasthesia, may thus be predicted with reasonable accuracy from the estimated carbon dioxide output and the minute volume. Construction of the predictor Prediction may be carried out from first principles or by the use of nomograms and charts. If, however, a reasonable number of variables are included, the graphical methods become clumsy and require a number of stages. It therefore appeared that a specially designed slide rule might be more convenient for this purpose. Since all the major steps are either multiplication or division, logarithmic scales can be

5 186 ANESTHESIA used throughout. It is possible to carry out the calculation on a simple slide rule consisting of two moving parts each of which carries a number of scales. The central value is the estimated carbon dioxide production, which is shown as the middle scale on the upper part of FIG. 2. This is CaCONTENT MEg/L I METABOLIC RATE -% OF BASAL - (760 MM Hg. 38.C SAT.) ALVEOLAR VENTILATION- L/MIN 5 6 FIG. 2 Sections of the scales of the PCOZ predictor. The top part moves against the lower part, but the relative position of the various scales on each part is fixed. A cursor is used for reading the parallel scales on the right hand side obtained by setting body weight against estimated metabolic rate : these scales are on the left of FIG. 2. Separate scales for body weight and metabolic rate must be used for male and female patients. The metabolic rate scale and that of the indicated carbon dioxide output are both logarithmic. The body weight scale is irregular since carbon dioxide output is not directly related to body weight. These scales incorporate a factor to convert the carbon dioxide output to the volume measured at body temperature and pressure saturated - the conditions under which the ventilation should be expressed. Equation (i) is solved by the use of three scales - carbon dioxide output, ventilation and Pc02 - all of which are logarithmic. If the alveolar ventilation scale is used, no assumptions are involved which are likely to be seriously in error. The minute volume scale, however, is based on the assumption that the alveolar ventilation is two-thirds of the minute volume, no allowance being made for apparatus dead space. Alongside the Pc02 scale there are additional scales to show ph and plasma carbon dioxide content assuming that there is no metabolic acid-base imbalance : these scales are derived from the carbon dioxide dissociation curve and the Henderson-Hasselbalch equation. The extra scales on the right of FIG. 2 require the use of a cursor. Scope of the Pco2predictor Once set for sex, body weight and metabolic rate, the predictor will indicate the expected PCOZ for any ventilation. Alternatively, it will indicate the ventilation required to produce any required Pc02. It

6 ANESTHESIA 187 affords a graphic demonstration of the effect of changes in ventilation upon Pc02. Limitations of the Pc02predictor The accuracy of prediction of Pc02 during anaesthesia has been discussed elsewhere6. It must be remembered that predictors indicate WHAT YOU MIGHT REASONABLY EXPECT THE Pc02 TO BE and not what it actually is. Thus, under circumstances when the assumptions are invalid, the results may be in error, and if they form the basis for action, they may be dangerous. The most serious sources of error in prediction of Pco 2 are : 1 Incorrect estimation of carbon dioxide output may be due either to an unsteady respiratory state or to a mistaken estimate of the metabolic rate. 2 The relationship : alveolar ventilation=two-thirds minute volume will not apply in patients with appreciable areas of lung which are ventilated but underperfused. A classical example is pulmonary embolus, but of greater practical importance are emphysema, chronic bronchitis, senility10 11 and perhaps prolonged anaesthesia The unexpected presence of carbon dioxide in the inspired gas will elevate the arterial Pc02 in accord with Bohr s equation above. 4 The predictor makes no allowance for apparatus dead space since this wil vary according to the circumstances. This should be added to the predicted tidal volume or subtracted from the measured tidal volume. OXYGEN PREDICTION Prediction of oxygen levels is seldom attempted, although Paskl3 has presented graphs which relate the expected arterial oxygen level to either minute volume (inspired oxygen concentration being held constant), or to inspired oxygen concentration (minute volume being held constant). For the prediction of the arterial Po2 (Pao,) it is first necessary to predict the alveolar Po2 PA^,) on which the arterial Po2 must depend. In the special case when the patient is breathing 100 per cent oxygen and the alveolar gas contains no nitrogen, the alveolar Po2 equals the dry barometric pressure less the alveolar Pc02. However, when gases other than oxygen and carbon dioxide are present, the relationship is considerably more complicated and is most conveniently expressed by the alveolar air equation14, one form of which is as fouows : Principles of prediction... (ii)

7 188 ANZSTHESIA The factor [F] - defined below - is a correction factor required by the difference between the inspired and expired minute volume. It is usually close to unity (the normal value is 0.96) and so it may be omitted if an approximate relationship is adequate. At first sight it is surprising that an equation which yields the alveolar Po2 should contain neither the oxygen consumption (v02) nor the alveolar - two factors which clearly influence the alveolar P02. However: R=- vc02 VO2 (the definition of respiratory exchange ratio) vc02 and PA^^, = Pko, = PB (dry) - VA Substituting in equation (ii), neglecting [F], we find: v02 PA^, = PI^,-- PB (dry)- or VA [from equation (i)] PA^^ = PB (dry) (iii) Equation (iv) yields the alveolar Po2 in terms of the familiar factors which are known to govern its level: PB (dry) the dry barometric pressure FI~, the inspired oxygen concentration v02 the oxygen consumption VA the alveolar ventilation This is probably the most helpful form of the equation for a general understanding of the factors which govern the alveolar P02. However, it is inconvenient for the construction of a predictor for the purely technical reason that it combines subtraction and division of variable factors. This presents difficulties as slide-rules (for multiplication and division) use logarithmic scales, while comparable devices for addition or subtraction require linear scales. Therefore, equation (ii) is pre-

8 ANESTHESIA 189 ferred for the construction of a predictor. Assuming that PB (dry), R and F are all constant, equation (ii) simplifies to :... (v) F where K1 equals the dry barometric pressure and K 2 equals -. R Construction of the predictor It is now simple to construct a slide-rule, with scales incorporating K1 and Kz, which will indicate PA^, from Fb, and PA^^,. Fro, is apparent from the rotameters in non-breathing circuits and PA^^^ (= Pa,,,) FIG. 3 Sections of the scales of the POZ predictor. The top part moves against the lower part, but the relative position of the various scales on each part is fixed. A cursor is used for reading the parallel scales on the right-hand side and is useful for making allowance for the alveolar-to-arterial Po 2 difference may be previously predicted by the method described above. FIG. 3 shows such a device in which: K1 = = 713mm/Hg (saturated water vapour pressure at 38"c is 47mm/Hg) 0.95 andk2 = - = (F is correct for R = 0.8 and Fro, = 0.25) The accuracy of the alveolar Po2 prediction is limited by the validity of these constants. They are dependent upon the following factors : Barometric pressure Variations associated with changes in the weather can be neglected for clinical purposes. Variations resulting from altitude are significant at altitudes above about 4,OOOft. If a

9 190 ANBSTHESIA predictor is used with a fixed factor for barometric pressure (760mml Hg) as in FIG. 3 allowance for an appreciable reduction in pressure may be made by setting the inspired oxygen percentage scale at: actual inspired 0 2 per cent x actual barometric pressure (all pressures being expressed in millimetres of mercury) Thus, for example, when breathing air at 4,OOOft the inspired oxygen scale should be set at: per cent x - 18 per cent Body temperature Small changes in body temperature cause negligible changes in the dry barometric pressure. Even when the body temperature falls to 20 c, the net dry barometric pressure rises only by about 27mm/Hg, which can be ignored for clinical purposes. The major effect of temperature is upon metabolic rate and allowance for this will already have been made in the prediction of Pco2. Respiratory exchange ratio Provided that the same value is assumed for R in the prediction of Po2 as in the prediction of PCOZ, then the error due to an incorrect estimate of R will disappear. Equation (iv) shows that R is not actually a determinant of alveolar Po2 although, for convenience, it is used in equation (ii) on which this prediction is based. The. factor F F= l-f1o2(1 - R) The value of this factor is usually close to unity and when either the respiratory exchange ratio= 1.O, or the inhaled oxygen concentration = 100 per cent, the value of F becomes 1.O. The predictor has been constructed with a value for F of corresponding to an inhaled oxygen concentration of 25 per cent and a respiratory exchange ratio of 0.8. This will be satisfactory for most anaesthetic situations even when 100 per cent oxygen is inhaled. If greater accuracy is required, when R and FI,, differ markedly from the values used in the construction of this predictor, the Pc02 value used for prediction of Po2 should be multiplied by the correction factor indicated in FIG. 4. Relationship of arterial to alveolar Po2 In the case of carbon dioxide, arterial Pc02 approximates very closely to the (ideal) alveolar PCOZ. (This latter quantity should not be confused with alveolar air sampled by the Haldane-Priestly method15.) However, in the case of oxygen, the arterial Po2 is always appreciably

10 ANESTHESIA 191 I R.Q ; I INSPIRED OXYGEN PERCENTAGE FIG. 4 If greater accuracy is required in the prediction of Po2 when the R.Q. and the inspired oxygen concentration differ markedly from the values used in the construction of the predictor, the Pco 2 value used for prediction of Po 2 should be multiplied by the factor indicated in the graph less than the alveolar P02. The difference is due partly to the lower diffusing capacity of oxygen and partly to the admixture of arterial blood with shunted mixed venous blood. Due to the slope of the djssociation curves, the latter has a considerable effect upon P02, whereas the effect on Pc02 is negligible. At very high oxygen tensions the alveolar to arterial (A-a) Po2 difference is due solely to shunts. Around normal values for Pao2 Po2 difference is caused by both shunts and maldistribution (perfusion of relatively underventilated alveoli). At low oxygen tensions (e.g., when breathing 12 per cent oxygen) the shape of the dissociation curve causes the (A-a) Po2 difference due to venous admixture to fall to very low figures. However, within this range, there is an appreciable (A-a) Po2 difference due to the relatively low diffusing capacity of oxygen. For an introduction to this difficult topic the reader is referred to Cornroe16 (page 85 et seq.). In the normal subject Comroe gives the following values for the components of the (A-a) Po2 difference (mm/hg): WHEN THE PATIENT IS BREATHING 12-14%02 Air Venous admixture component % Diffusion component Po difference Estimation of the arterial Po2 in the anzsthetised patient must, therefore, depend on assessment of the magnitude of the (A-a) Po2

11 192 ANBSTHESIA difference under the conditions of anaesthesia. This will depend upon the effect of anaesthesia and surgery on diffusing capacity and venous admixture. Unfortunately, little is known about the (A-a) Po2 difference during anaesthesia. It is difficult to see why an uncomplicated anaesthetic should cause an appreciable change in the diffusing capacity, but there are many possible causes of excessive venous admixture. Of these themost obvious are atelectasis, one-lung intubation and regional airway obstruction. A number of pathological conditions increase the (A-a) Po2 differencelo. The measurement of the (A-a) Po2 difference during anaesthesia is associated with some technical difficulty and few results have been reported. Campbell, Nunn and Peckettl7 studied six anaesthetised, paralysed and intubated patients and, in four patients, found the (A-a) Po2 difference equal to the control value when conscious. In the other two the difference was increased by 20 and 15mm/Hg respectively. Frumin et az.18 reported (A-a) Po2 differences within the normal range in 80 per cent of measurements carried out on forty-five anaesthetised paralysed patients. In the remaining observations, differences as high as 45mm/Hg were observed. Further data are needed and in the meantime caution must be used in estimating the likely arterial Po2 from the predicted alveolar P02. Returning to the predictor (FIG. 3), the arterial Po2 is estimated by moving a cursor back from the indicated alveolar Po2 by adistance equal to the estimated (A-a) Po2 difference. This maneuvre may be facilitated by an (A-a) Po2 difference scale engraved on the cursor. Once the cursor is placed at the estimated arterial P02, it may be arranged to indicate the corresponding haemoglobin saturation on parallel scales. Allowance should be made for the Bohr effect, since wide variations of Pc02 occur during anasthesia. Further changes in the dissociation curve occur in hypothermia and the reader is referred to the Handbook of Respiratory Data19. Scope of the Pozpredictor The oxygen predictor will indicate the likely arterial Po2 for varying combinations of inspired oxygen concentration and Pc02 (inverse of ventilation). Alternatively, it will indicate the inspired oxygen concentration required at varying degrees of respiratory depression (elevation of PCOZ). It will also give some idea of the amount of respiratory depression which will result in hypoxia at varying levels of inspired oxygen concentration. It affords a striking demonstration of the nonlinear relationship between inspired oxygen concentrations, Pco 2 and haemoglobin saturation. Limitations of the Po2 predictor As in the case of Pco2, the predictor will indicate WHAT YOU MIGHT

12 ANESTHESIA 193 REASONABLY EXPECT THE Po2 TO BE and not what it actually is. There should be little difficulty in obtaining a reasonable estimate of the inspired oxygen concentration during anssthesia and an incorrect assessment of the respiratory exchange ratio is unlikely to cause serious error. However, other sources of inaccuracy remain : 1 Errors in the prediction of PCOZ (see above) will be carried forward into the prediction of Po2. 2 Po2 difference may be increased in the following conditions : (a) Decreased diffusing capacity. (b) Abnormally high venous admixture. It has been explained above that an abnormally high venous admixture must be regarded as a relatively frequent complication of anzesthesia and surgery. Provided that the dry barometric pressure, the inspired oxygen concentration, Pc02 and respiratory exchange ratio are known, the prediction of alveolar Po2 is not subject to error. SUMMARY Methods are discussed for the prediction of blood-gas levels from other, more easily measured, respiratory variables. A slide-rule is described which facilitates the calculations. Production of the predictor is being undertaken by British Oxygen Co. Ltd. APPENDIX Symbols are in accord with the recommendation of the committee for the standardisation of definitions and symbols in respiratory physiology 2 0. Pco2 C02 tension or partial pressure Po2 0 2 tension or partial pressure PACO2 Alveolar PCOZ PAOz Alveolar Po 2 P%O, Arterial Pc02 pa02 Arterial Po2 difference = PA,, - Pao, FIC02 Fractional concentration of CO2 in inspired gas FIo, Fractional concentration of 0 2 in inspired gas (note: fractional concentration = % concentration + 100) PB Barometric pressure

13 194 ANESTHESIA PB (dry) Barometric pressure minus water vapour pressure (saturated at body temperature) PIO, Inspired gas Po2 = PB (dry) x F I ~ ~ vcoz coz output VO, 0 2 uptake +co2 R (= R.Q.) Respiratory exchange ratio = - VA Alveolar ventilation F I - Fro, (I - R) References v02 1 COOPER, E. A. and SMITH, H. (1961). Anesthesia, 16,445. *SCHULTZ,E. A.,BUCKLEY, J. J.,OSWALD, A. J. VANBER BERG EN, F. ~.(1960). Anesthesiology, 21,285. ~COMROE, J. H. JR. ~ ~~BOTELHO, s. (1947). Amer. J. med. Sci., 214,l. 4WRIGHT, B. M. (1955). J. Physiol., 127,25P. SRADFORD, E. P. (1955).J. Uppl. Physiol., 7,451. ~NUNN, J. F. (1960). Anesthesia, 15, 123. ~AUB, J. c. and~u~o~s, E. F. (1917). Arch. Int. Med., 19,823. ~NUNN, J. F. andmatthews, R. L. (1959). Brit. J. Anmth., 31, 330. gnunn, J. F. andhill, D. W. (1960).J. Uppl. Physiol., 15,383. IODONALD, K. w., RENZETTI, A., RILEY, R. L. and COURNAND, A. (1952). J. appl. Physiol., 4, COOPER, E. A. Personal communication. ~ZTHORNTON, J. A. (1960). Anesthesia, 15,381. ~~PASK, E. A. (1960). Scientific meeting on Hypoxia, Royal College of Surgeons of England. 14FENN, W. O., RAHN, H. and OTIS, A. B. (1946). Amer.J. Physiol., 146, SHALDANE, J. S. and PRIESTLEY, J. G. (1905).J. Physiol., 32,225. I~COMROE, J. H., FORSTER, R. E., DUBOIS, A. B., BRISCOE, w. A. and CARLSEN, E. (1955). The lung. The Year Book Publishers Inc, Chicago. I CAMPBELL, E. J. M., NU, J. F. andpeckett, B. W. (1958). Brit. J. h@sfh., 30, 166. I~FRUMIN, M. J., BERGMAN, N. A., HOLADAY, D. A., RACKOW, H. and SALANITRE, E. (1959). J. appl. Physiol., 14,694. I~DITTMER, D. s. and GREBE, R. M. (edited by) (1958). Handbook of Respiration, W. B. Saunders Co, Philadelphia. ZOPAPPENHEIMER, J. R., COMROE, J. H., COURNAND, A., FERGUSON, J. K. W., FILLEY, G. F., FOWLER, W. S., GRAY, J. S., HELMHOLTZ, H. F., OTIS, A. B., RAHN, H. and RILEY, R. L. (1950). Fed. Proc., 9,602.