air, and during oxygen therapy from 24, 28 and 35% venturi masks. Pao ... oxygen therapy did not correspond to predictions based on an iso-shunt lung model.
Br.J. Anaesth. (1977), 49, 789
OXYGEN THERAPY AFTER ABDOMINAL SURGERY G. B. DRUMMOND AND D. J. WRIGHT SUMMARY Arterial blood was sampled from 10 patients, on the day after upper abdominal surgery, breathing air, and during oxygen therapy from 24, 28 and 35% venturi masks. Pao, during breathing each concentration of oxygen correlated with PaQt during air breathing. The difference between pulmonary end-capillary and arterial oxygen content was used as an index of the impairment of oxygen transfer in the lung. This difference was reduced by oxygen therapy. The response to oxygen therapy did not correspond to predictions based on an iso-shunt lung model. These findings suggest that hypoxaemia in these patients is predominantly caused by ventilation/perfusion mismatching.
Upper abdominal surgery is followed by an impairment of arterial oxygenation. The decrease in efficiency of arterial oxygenation by the lungs is considered commonly to be caused in two possible ways: the shunting of blood flow through areas of collapsed lung tissue, and an increase in the range of ventilation to perfusion ratios [V\Q ratios) throughout the lung. Impairment of gas exchange of both types has been studied by means of mathematical lung models, and the influence of oxygen therapy in either circumstance can be predicted. Comparison of these predictions with the observed effects of oxygen therapy on patients after operation should indicate the manner in which lung function is disturbed. The first type of abnormality is simulated by the use of the concept of physiological shunt. This is a means of expressing the impaired oxygen transfer as if the cardiac output (Qi) of arterial blood (with an oxygen content Ca02) were composed of a mixture of blood that has passed through the lungs (endcapillary blood) and of blood that has not undergone gas exchange (£)s), and which therefore has an oxygen content identical to that of mixed venous blood (CvOa). The oxygen content of the endcapillary blood (Cc'O2) is calculated on the assumption that it has become fully equilibrated with "ideal" alveolar gas. Because the amount of oxygen carried in the arterial blood is the sum of the oxygen carried in these two portions of the cardiac output, then Cv'O2 G.
B.
DRUMMOND,
M.A.,
F.F.A.R.C.S.;
D.
J.
(1)
WRIGHT,
F.F.A.R.C.S. ; Department of Anaesthetics, Royal Infirmary, Edinburgh EH3 9YW.
Thus, impaired oxygen transfer is expressed "as if" a proportion of the cardiac output, ()s/gt, were acting as shunt. The model is based on the assumption that this proportion remains constant. "Oxygen therapy" in this model will result in an increase in arterial oxygen content, but if the arteriovenous oxygen content difference is considered to remain unchanged then the content difference between endcapillary and arterial blood should be unaltered. This can be shown by rearranging the above equation to yield the expression: - 0s).(Ca O2 -Cv O2 ) (2) Benatar, Hewlett and Nunn (1973) calculated the effects of oxygen therapy on the basis of these assumptions (iso-shunt predictions). The second type of abnormality is modelled by assuming that the defect is the result of a scatter of ventilation to perfusion ratios in a log-normal distribution. If the arteriovenous oxygen content difference is kept constant, an increase in alveolar Po 2 (.PA02) causes a progressive reduction in the value of the expression {Cc'0%—CaOs), although the relationship is not simple (Kerr, 1975). This reduction in (Cc'Oa—Ca02) as P A 0 2 increases is more marked when P A 0 2 is small, because the effect of F/() imbalance is greatest when alveolar tensions of oxygen are least. Drummond (1975) studied patients who received 35% oxygen after upper abdominal surgery. He showed that the effect on arterial oxygen tension resembled the response of patients with other forms of lung disease (Mithoefer, Keighley and Karetzky, 1971), and suggested that this response was the result
790
BRITISH JOURNAL OF ANAESTHESIA
of an increase in areas of lung with low VjQ ratios after operation. The response of such patients to three concentrations of oxygen has been studied to test this hypothesis and to assess the predictability of the response to oxygen in the clinical situation. METHODS
Patients about to undergo elective upper abdominal surgery for either peptic ulcer or biliary tract disease gave written consent for the study after a full explanation of the extent and nature of the procedures involved. Forced expiratory volume in I s (FEVJ and forced vital capacity (FVC) were measured with the patients standing, using a dry wedge-type spirometer (Vitalograph). The age, height and weight of the patient were noted, along with any history or symptoms of chest or heart disease. Premedication and anaesthetic agents were not standard, but chosen by the anaesthetist. Anaesthesia was with nitrous oxide, oxygen and neuromuscular blockade, with either halothane or opiate supplement. Papaveretum was used for analgesia for all patients after the operation, given i.m. "on demand" in a dose appropriate to the size and age of the patient, between 10 and 20 mg. Measurements were made on the morning after the operation, within 2 h of an injection of papaveretum. The patient was studied in bed, in a standard semi-recumbent position, with the head and trunk supported at about 50° to the horizontal. The operation, site of incision and type of abdominal drain, if present, were recorded. A venous blood sample was taken for measurement of haemoglobin and the oral temperature noted. Allen's test (Allen, 1929) was performed to check that an adequate ulnar arterial supply to the hand was present. The subcutaneous tissues and tissues around the radial artery on that side were infiltrated with 1% lignocaine, a cannula inserted (Everett Venflon 0.6 mm i.d.) and closed with a tap. The cannula was flushed intermittently with heparin in saline (0.9% saline 2 units/ml). After the cannula had been fixed in place the patient was allowed to rest for 5 min and then a 6-ml sample of blood was taken from the cannula over a period of about 1 min. The sample was taken anaerobically into a glass syringe with the deadspace filled with heparin, and immediately stoppered and shaken. The patient was then given oxygen for 20 min from a 24% venturi-type mask (Blease mix-o-mask) supplied with oxygen at a flow of 4 litre.min" 1 ,
and a further sample of blood was taken. The venturi portion of the mask was then rapidly changed to a 28% type supplied with oxygen at 6 litre. min" 1 . The next arterial sample was taken 20 min later, the venturi was changed for a 35% type supplied with oxygen at 8 litre. min" 1 , and a final arterial sample was taken after a further 20-min period. The cannula was then removed. The same venturi devices and flowmeter were used for the entire study. The oxygen concentrations produced were checked using a paramagnetic oxygen analyser (Servomex OA 101) at the start and end of the study, and were found to be unchanged. The values are given in table I. TABLE I. Mean oxygen concentration delivered by each venturi system (%). {Mean of six observations) Nominal concentration (%)
Delivered concentration (%)
24 28 35
24.52 27.93 35.07
SEM 0.22 0.11 0.32
The samples were analysed for oxygen and carbon dioxide tension and pH, using a standard IL 213 electrode system kept at 37 °C. The oxygen electrode was calibrated with water equilibrated with room air at 37 °C. With this system, the standard deviation for 20 duplicate analyses for oxygen tension was 0.24 kPa, over a range 5-15 kPa. Comparison with a Radiometer electrode gave a standard error of 0.04 kPa for the differences of duplicate analyses, over a range 4-40 kPa. The results were corrected for the difference in temperature between the patient and the electrode, using Kelman's computer routine (Kelman and Nunn, 1966). Ideal alveolar Po2 was computed from the alveolar air equation:
where PB = barometric pressure PS20 = saturated vapour pressure of water at the patient's temperature FiOi was taken to be the concentration delivered by the mask and it was assumed that PAQQ. = P&cos> and R = 0.9 (Drummond, 1975). Oxygen saturation of the arterial and pulmonary end-capillary blood was computed using the routine described by
791
OXYGEN THERAPY AFTER ABDOMINAL SURGERY Kelman (1966) and oxygen contents were calculated using these values, the measured haemoglobin concentration, assuming an oxygen solubility in plasma of 0.022 ml. dl" 1 . kPa - 1 and an oxygencarrying capacity for haemoglobin of 1.34ml.g" 1 . Predictions were made for the arterial oxygen tension that would result in each patient if (Cc'Oa— CaOa) during air breathing were to have remained unchanged during oxygen therapy. This was done by first deriving the arterial oxygen content: O2 (on oxygen) =
C c 'o 2 (on oxygen) "(C^'o^Ckoz) (air) and then computing the appropriate Pa 02 using an iterative technique to the nearest 0.13 kPa. Paired samples were tested statistically using Students' t test. RESULTS
Details of the patients, their operations and postoperative details are given in tables II and III. Their weights are expressed as a percentage of the
average for a subject of the same age, sex and height (Documenta Geigy Scientific Tables). Two patients were obese, with weights that were 141% and 131% of average. FVC and FEVa are expressed as a percentage of the predicted value (Cotes, 1975). Four patients smoked, and two of these had chronic bronchitis, according to the MRC criteria (Medical Research Council, 1965). All the surgical incisions were in the upper abdomen. The drains, if present, were placed into the peritoneal cavity, and classified as vacuum, for example Steritex, Redivac; or plain, for example corrugated or tube type. None of the patients had any form of surgical complication, such as haemorrhage, either before or at the time of study. The blood-gas results are shown in tables IV and V. One arterial sample was unsuitable for analysis for technical reasons. Table IV gives individual and mean Pa C02 values for the patients breathing air and during oxygen therapy. The mean Pa c 0 2 value for the air-breathing period was very slightly less than the mean values for the oxygen therapy periods,
TABLE II. Details of patients studied
Patient
Sex
1 2 3 4 5 6 7 8 9 10
M F M
M F F F F F F
Weight
FEV!
FVC
Age (yr)
Height (m)
predicted)
predicted)
predicted)
25 21 68 62 48 41 51 54 37 63
1.78 1.57 1.75 1.57 1.71 1.50 1.50 1.76 1.80 1.65
100 88 85 97 141 105 115 105 131 95
100 97 73 90 68 119 84 127 101 68
100 91 33 96 70 94 76 121 83 87
Smoking (cigarettes daily) — 15 — 20 20
— yes
15 —
— —
yes
TABLE III. Operative and postoperative details Patient 1 2 3 4 5 6 7 8 9 10
Operation
Incision
vagotomy and pyloroplasty cholecystectomy partial gastrectomy cholecystectomy cholecystectomy cholecystectomy cholecystectomy cholecystectomy cholecystectomy cholecystectomy
paramedian subcostal midline subcostal subcostal subcostal subcostal subcostal subcostal subcostal
Haemoglobin (g/dl)
Temp.
none
14.5
37.8
plain plain plain plain plain + vacuum plain plain plain plain
13.2 11.6 12.8 13.6 11.6 10.7 12.8 12.1 10.3
37.4 37.4 36.5 37.2 37.0 37.5 37.2 38.0 37.8
Drain
Bronchitis
BRITISH JOURNAL OF ANAESTHESIA
792
TABLE V. Oxygen tension and content data
TABLE IV. Pa^o, (JtPa) for patients breathing air and oxygen at progressively increasing concentrations
too. Patient 1 2 3 4
5 6 7 8 9 10
Mean SEM
Patient
0.21
0.24
0.28
0.35
5.9 5.3 5.4 5.3 5.1 4.9 5.4 5.5 4.7 5.2
6.1 5.1 6.1 5.5 5.2 — 5.6 5.5 5.4 5.0
5.9 5.7 4.9 5.5 5.2 5.1 5.4 6.0 5.6 5.0
6.5 5.7 5.7 5.5 5.4 5.3 5.4 6.0 5.7 5.0
5.27 0.33
5.50 0.39
5.43 0.38
5.53 0.28
but there was no statistically significant difference between any of the periods. Arterial oxygen tensions, and calculated values for the alveolar tensions, and end-capillary and arterial oxygen contents, are shown in table V. Figure 1 illustrates the response of Pa 02 in each patient to oxygen therapy. Patients with more severe hypoxaemia showed less response to oxygen therapy. The relationship between Pa 02 breathing oxygen and Pa 02 breathing air for each patient is shown in figures 2, 3 and 4, for each concentration of oxygen, with the linear regression line and 95% confidence limits. All these relationships are highly significant (P< 0.0001).
20
10
18
f
0.21 0.24 0.28 0.35 0.21 0.24 0.28 0.35 0.21 0.24 0.28 0.35 0.21 0.24 0.28 0.35 0.21 0.24 0.28 0.35 0.21 0.28 0.35 0.21 0.24 0.28 0.35 0.21 0.24 0.28 0.35 0.21 0.24 0.28 0.35 0.21 0.24 0.28 0.35
* *HJj
*-"- U,
* aOt
*-jaOa
(kPa)
(ml/dl)
(kPa)
(ml/dl)
13.1 15.8 19.7 26.5 14.1 17.1 20.3 27.0 13.9 16.0 21.0 26.9 14.1 16.8 20.6 27.2 14.2 16.9 20.7 27.2 14.8 21.4 27.9 13.9 16.6 20.6 27.2 13.7 16.5 19.7 26.3 14.4 16.4 20.0 26.4 14.2 17.3 21.2 27.8
19.8 20.1 20.3 20.6 18.2 18.4 18.6 18.8 16.0 16.1 16.4 16.6 17.7 17.9 18.1 18.3 18.8 19.0 19.2 19.4 18.8 19.2 19.4 14.8 15.0 15.2 15.4 17.6 17.9 18.0 18.3 16.7 16.9 17.1 17.3 14.3 14.5 14.6 14.9
10.9 13.6 16.5 19.9 10.6 13.3 13.8 17.1
19.4 19.8 20.1 20.3 17.7 18.2 18.2 18.4 14.0 15.0 15.2 15.6 15.9 16.4 16.6 17.2 17.6 17.9 18.1 18.5 17.2 18.3 18.7 13.2 14.0 14.1 14.6 17.1 17.6 17.6 17.8 16.2 16.4 16.7 16.9 13.5 13.9 14.1 14.2
7.5 9.0 9.5
11.3 7.2 7.8 8.2
10.2 8.6 9.3
10.0 11.7 8.4
11.0 13.4 7.6 9.1 9.6
11.9 10.4 13.0 13.3 16.4 10.2 11.7 13.4 16.3 9.0
10.7 11.7 13.1
16 U 12 10 8 020
025
030
035
F\, FIG. 1. Relationship of />aot and FIQ, in the 10 patients.
In figure 5, (Cc' O2 -Ca O2 ) is plotted against PA 0 2 for each patient. The relationship is markedly nonlinear, and 24% oxygen caused a reduction in (Cc'O2 — Ca02) in all the patients. In the five patients with the greatest oxygen content differences, when breathing air, this difference was reduced even more by 35% oxygen. In the less hypoxaemic patients, 35% oxygen caused either no change or a slight increase in the value of (Cc'Oa—CaOa). The differences between the Pa 02 values observed during oxygen therapy and those predicted if the hypoxaemia were the result of a shunt-like effect
OXYGEN THERAPY AFTER ABDOMINAL SURGERY 20
793
20
0-24
X
IB
8
16
breatiling
°en 6
§
J512
F\Ol 035
U 12 10
o
8
9
10
8
11
8
Pa 0 ! (kPa) breathing air
9
10
11
dLQ2 (kPa) breathing air
FIG. 2. Relationship of Pao, breathing air with Pag, breathing 24% oxygen for nine patients, with the linear regression line and its 95% confidence limits: r = 0.97, P < 0.0001, slope = 1.44, standard error of slope 0.13.
FIG. 4. Relationship of Pao, breathing air with Pao, breathing 35% oxygen for 10 patients, with the linear regression line and its 95 % confidence limits: r = 0.95, P < 0.0001, slope = 2.13, standard error of slope 0.24. 2Q
20
aj 18
028
•a
1-6 U
o 16
1 12
en u
§
Z "o 2! 12
o
teri
o
08
o
10
0-6 k OX
p.ll
Q_
6
a
8
a. 9 10 breathing air
11
FIG. 3. Relationship of Pao, breathing air with Pao, breathing 28% oxygen for 10 patients, with the linear regression line and its 95% confidence limits: r = 0.95, P < 0.0001, slope = 1.72, standard error of slope 0.19.
alone are shown in table VI. In eight of the patients, this difference increased progressively with increasing FiOi!. DISCUSSION
The pattern of change of (Cc'Os—CaOj) with changing PAO2 may have been influenced by several factors, 63
10
02
LU
"10
12
V. 16 18 20 22 2i 26 28 Alveolar oxygen tension (kPa)
FIG. 5. Relationship between PAO, and the pulmonary end-capillary to arterial oxygen content difference in 10 patients.
both in the method and in the response of the patient. Oxygen tensions were not corrected for any change that occurred in the time between sampling and analysis, However, as all the samples were analysed within 5 min of collection and the arterial tension values, in general, were not great, any
BRITISH JOURNAL OF ANAESTHESIA
794 TABLE V I . Differences between observed and predicted values (kPa)
Patient 1 2 3 4 5 6 7 8 9 10
Mean SEM
0.24
0.28
0.35
1.4 1.7 1.4 0.5 0.2 — 1.4 1.7 0.7 1.2
2.5 1.1 1.7 0.7 0.3 2.4 1.6 0.6 1.5
1.1 0.5
1.4 0.7
2.7 1.7 3.0 2.4 1.3 4.1 3.3 1.2 2.3 1.8 1.9 1.0
16
change in oxygen tension in these circumstances would be small (Eldridge and Fretwell, 1965). Although the change of oxygen tension would be greater in samples in which the original oxygen tension was great, the change in the calculated content would be similar whatever the original tension. The gas exchange ratio (/?) was assumed to be 0.9 on the basis of previous measurements in similar patients (Drummond, 1975). However, in the present study, samples were taken from a cannula whereas the previous study involved intermittent arterial puncture. It is likely that the patients would have been less apprehensive about sampling from a cannula, and that they might not have hyperventilated or had an increased gas exchange ratio. Consequently, the alveolar oxygen tensions were calculated also for an R value of 0.8 to assess the effect of this assumption. As might be expected, there was no change in the general pattern of the observed relationship between (Cc'Oa—CaOj) and PAO 2 , or in the discrepancies between observed Pa Os values during oxygen therapy and the PaOl! values predicted on the assumption that the hypoxaemia was caused by the same degree of shunt. The patients breathed each concentration of oxygen for 20 min before samples were taken. Complete equilibration of all lung regions, particularly those with small V/Q ratios, was unlikely to have occurred within this time, but it was felt on ethical grounds that the investigation should not be prolonged unduly. The concentrations of oxygen were given in increasing order so that any lack of equilibration would cause only a small difference between actual and final oxygen concentrations in
the lung. If equilibration did not occur, this would result in the oxygen therapy having less effect than observed. As the effect was greater than expected on the basis of shunting alone, incomplete equilibration does not seem to explain this effect. The oxygen masks used may not have delivered the correct oxygen concentration to the patient. Gibson and co-workers (1976) demonstrated that tracheal oxygen concentrations in subjects breathing from venturi oxygen masks were less than the concentrations that the masks were said to deliver. The maximum concentration in the trachea was between 2 and 5% less than the stated concentration for 24, 28 and 35% oxygen masks during simulated "quiet" and "normal" breathing (peak inspiratory flows of 21 and 37 litre. min- 1 ). However, samples from this site would be diluted with water vapour added to the inspired gas from the upper airways. This would reduce the concentration of 35% oxygen to about 33% if the humidification was complete. This dilution effect is accounted for in the alveolar gas equation, and would not be a source of error in the calculation of PAOi- Another factor that would reduce the inspired oxygen concentration would be the entraining of air in addition to the delivered mixture. This is more likely with the 35% mask as the total flow of the mixture is least, about 32 litre. min" 1 which could be less than the peak inspiratory flow of the patient. Leigh (1970) showed that the 35% ventimask had a less predictable performance than the 28% ventimask, and Campbell and Minty (1976) suggested that small volume venturi masks (such as the Mix-o-mask) have to produce a total flow of 50 litre. min- 1 to give consistent results, although 30 litre. min- 1 is sufficient for quiet breathing. If the inspired oxygen concentration is less than the stated value, then the calculated PA O 2 and hence Cc'O2 would be greater than the actual values, and the calculated value for (Cc'O2—CaOa) would also be greater than the actual value. Such an overestimate of (Cc'O2—Ca02) may be responsible for the increase noted with 35% oxygen therapy in three of the patients. However, a dilution of the inspired oxygen concentration cannot be responsible for the reduction of (Cc' O2 -Ca O2 ) noted with 24% oxygen. If oxygen therapy caused a change in the arteriovenous oxygen content difference, then it is clear from equation (2) that this would result in a change in (Cc'Oa —Ca02), if the shunt fraction were to remain constant. Such a change would occur if cardiac output were to increase, if oxygen consumption
OXYGEN THERAPY AFTER ABDOMINAL SURGERY were to decrease, or both. The change in arteriovenous content difference would have to be by more than 30% to account for the change noted in three of the patients studied. Administration of oxygen in similar concentrations has been shown not to change arteriovenous oxygen content difference both in normal subjects and in patients after abdominal operations (Troell, 1952; Karetzky, Keighley and Mithoefer, 1971). The relationship of (Cc'Os, — Ca02) to PA OZ for each patient resembles closely the predicted effect on patients with differing degrees of severity of VjQ scatter. Even moderate oxygen concentrations result in a marked improvement in oxygenating efficiency. It is difficult to detect if there is also an additional component of the (Cc'O2—Ca02) that is the result of blood flow through unventilated alveoli, because the Vj@ ratios of the lung responsible for a persistent (Cc'O2—Ca02) at these alveolar tensions will be very small (West, 1969). Estimation of the nitrogen tension difference between arterial blood and alveolar gas at Fi02 0.35 would be valuable in the demonstration of impaired oxygen transfer caused by V\() scatter (Markello, Winter and Olszowka, 1972). A third effect influencing the relationship noted in this study could also be present but cannot be detected with certainty. This is the decrease in oxygenating efficiency demonstrated in patients ventilated with high concentrations of oxygen (Kerr, 1975; Suter, Fairley and Schlobohm, 1975). This effect has been attributed to the loss of the normal reflex regulation of blood flow to lung units by the alveolar gas tensions within the units (Bergofsky, 1974; Grant et al., 1976). However, this loss does not seem to occur in normal subjects spontaneously breathing high oxygen concentrations (Cole and Bishop, 1967). The ages, weights and respiratory function of the patients studied varied considerably. Although all the incisions were upper abdominal, the type of incision was not constant. The patients could not be studied at a standard time after the administration of analgesia. However, some of these differences are unlikely to be important. For example, Vaughan, Engelhardt and Wise (1974) showed that although hypoxaemia after abdominal operation in obese patients was more severe if the incision was vertical rather than transverse, this difference was not apparent on the first day after operation. Also, Alexander, Parikh and Spence (1973) demonstrated that considerable differences in the amount of narcotic analgesic given
795
to men after gastric surgery caused only marginal differences in lung function. Residual pneumoperitoneum predisposes to lung complications after upper abdominal surgery (Sergievskiy, 1947; Bevan, 1961), but all the patients in the present study would be likely to have a pneumoperitoneum, as none had a vacuum drain only. Factors present before operation appear to be important in determining the degree of hypoxaemia after the operation. PaOl! breathing air after operation could be correlated with age, height, weight, FEVX and FVC using a multiple regression equation with a correlation coefficient of 0.92. This suggests that these factors are more important than factors such as the type of incision, drain or analgesia. Heller, Watson and Imredy (1965) noted that patients in most need of oxygen therapy after operation were those who showed the least improvement in arterial tension when this therapy was given. The present study substantiates this finding, but shows that even modest oxygen concentrations improved the efficiency of arterial oxygenation, particularly in those patients with most impairment. Although V/Q imbalance appears to play a significant part in impaired gas exchange on the first day after upper abdominal surgery, it is possible that subsequent changes in the lung, for example, airway obstruction and atelectasis, can subsequently change the nature of the defect, to one of blood flow through unventilated lung tissue. Siler and others (1974) suggested that venous admixture was the major factor causing hypoxaemia after upper abdominal surgery, and that this effect was more pronounced in patients with atelectasis. In their investigation, venous admixture was estimated from PaOa after breathing 100% oxygen for 10 min. This time might not be long enough to obtain complete washout of nitrogen from regions of low V\() (Haab, Piiper and Rahn, 1960). ACKNOWLEDGEMENTS
We would like to thank Messrs A. C. B. Dean. A. J. Duff, I. B. MacLeod, J. W. W. Thomson and T. J. McNair for permission to study patients in their care. We would also like to thank Professor G. R. Kelman for advice on interpretation of the data, Dr P. Wagner for a copy of Dr J. B. West's computer model and Mr A. McKinnon for his meticulous analysis of all the specimens involved. REFERENCES
Alexander, J. I., Parikh, R. K., and Spence A. A. (1973). Postoperative analgesia and lung function; a comparison of analgesic regimens. Br. J. Anaeuh., 45, 346.
796 Allen, E. V. (1929). Thromboangiitis obliterans; methods of diagnosis of chronic occlusive arterial lesions distal to the wrist with illustrative cases. Am. J. Med. Set., 178, 237. Benatar, S. R., Hewlett, A. M., and Nunn, J. F. (1973). The use of iso-shunt lines for control of oxygen therapy. Br.J. Anaesth., 4S, 711. Bergofsky, E. H. (1974). Mechanisms underlying vasomotor regulation of regional pulmonary blood flow in normal and disease states. Am. J. Med., 57, 378. Bevan, P. G. (1961). Postoperative pneumoperitoneum and pulmonary collapse. Br. Med. J., 2, 609. Campbell, E. J. M., and Minty, K. B. (1976). Controlled oxygen therapy at 60% concentration. Lancet, 1, 1199. Cole, R. B., and Bishop, J. M. (1967). Variation in A - a O 2 tension differences at high levels of alveolar O2 tension. J. Appl. PhysioL, 22, 685. Cotes, J. E. (1975) Lung Function, 3rd edn, p. 380. Oxford: Blackwell Scientific Publications. Drummond, G. B. (1975). Postoperative hypoxaemia and oxygen therapy. Br. J. Anaesth., 47, 491. Eldridge, F., and Fretwell, L. K. (1965). Change in oxygen tension of shed blood at various temperatures. J. Appl. PhysioL, 20, 790. Gibson, R. L., Comer, P. B., Beckham, R. W., and McGraw, C. P. (1976). Actual tracheal oxygen concentrations with commonly used oxygen equipment. Anesthesiology, 44,71. Grant, B. J. B., Davies, E. E., Jones, H. A., and Hughes, J. M. B. (1976). Local regulation of pulmonary blood flow and ventilation-perfusion ratios in the coatimundi. J. Appl. PhysioL, 40, 216. Haab, P., Piiper, J., and Rahn, H. (1960). Attempt to demonstrate the distribution component of the alveolararterial oxygen pressure difference. J. Appl. PhysioL, 15, 235. Heller, M. L., Watson, T. R., and Imredy, D. S. (1965). Postoperative hypoxaemia and its treatment with nasal oxygen; polarographic study. Surgery, 58, 819. Karetzky, M. S., Keighley, J. F., and Mithoefer, J. C. (1971). The effect of oxygen administration on gas exchange and cardiopulmonary function in normal subjects. Respir. PhysioL, 12, 361. Kelman, G. R. (1966). Digital computer subroutine for the conversion of oxygen tension into saturation. J. Appl. PhysioL, 12, 1375. Nunn, J. F. (1966). Nomograms for correction of blood Po 2 , Pcot, pH and base excess for time and temperature. J. Appl. PhysioL, 21, 1484. Kerr, J. H. (1975). Pulmonary oxygen transfer during IPPV in man. Br.J. Anaesth., 47, 695. Leigh, J. M. (1970). Variation in performance of oxygen therapy devices. Anaesthesia, 25, 210. Markello, R., Winter, P., and Olszowka, A. (1972). Assessment of ventilation-perfusion inequalities by arterialalveolar nitrogen differences in intensive care patients. Anesthesiology, 37, 4. Medical Research Council (1965). Definition and classification of chronic bronchitis for clinical and epidemiological purposes. Lancet, 1, 448. Mithoefer, J. C , Keighley, J. F., and Karetzky, M. S. (1971). Response of the arterial Po, to oxygen administration in chronic pulmonary disease. Ann. Intern. Med., 74, 328.
BRITISH JOURNAL OF ANAESTHESIA Sergievskiy, S. A. (1947). Postoperative pneumoperitoneum and its influence on the development of pulmonary complications. Vestn. Khir., 67, 23. Siler, J. N., Rosenberg, H., Mull, T. D., Kaplan, J. A., Bardin, H., and Marshall, B. E. (1974). Hypoxemia after upper abdominal surgery: comparison of venous admixture and ventilation/perfusion inequality components, using a digital computer./lnH. Surg., 179, 149. Suter, P. M., Fairley, H. B., and Schlobohm, R. M. (1975). Shunt, lung volume and perfusion during short periods of ventilation with oxygen. Anesthesiology, 43, 617. Troell, L. (1952). Postoperative changes in circulation and the effects of oxygen therapy. Acta Chir. Scand., 102, 203. Vaughan, R. W., Engelhardt, R. C , and Wise, L. (1974). Postoperative alveolar-arterial oxygen tension difference; its relation to the operative incision in obese patients. Anesth. Analg. (fileve.), 54, 433. West, J. B. (1969). Ventilation-perfusion inequality and overall gas exchange in computer models of the lung. Respir. PhysioL, 7, 88. OXYGENOTHERAPIE APRES CHIRURGIE ABDOMINALE RESUME
On a pr£leve des 6chantillons de sang arteriel sur 10 malades, le lendemain d'une intervention chirurgicale a la partie sup£rieure de l'abdomen, alors qu'ils respiraient de l'air et aussi pendant oxygenoth6rapie a l'aide de masques a venturi a 24, 28 et 35%. La Pao, obtenue pendant la respiration de chaque concentration d'oxygene a correspondu a la Pao, obtenue pendant la respiration d'air. La difference entre le teneur en oxygene des capillaires pulmonaires d'extremit£ et la teneur en oxygene arteriel a 6t6 utilisee comme indice de l'alteration du transfert d'oxygene dans les poumons: cette difference a 6te diminue'e par l'oxygtoothSrapie. La reaction a l'oxygenotherapie n'a pas correspondu aux provisions basees sur une maquette de poumon isoshunt. Ces observations permettent de penser que, sur ces malades, Phypox&nie est surtout caus£e par une mauvaise harmonisation de la ventilation et de la perfusion. SAUERSTOFFTHERAPIE NACH UNTERLEIBSOPERATIONEN ZUSAMMENFASSUNG
Arterielle Blutproben wurden von 10 Patienten entnommen, und zwar am Tage nach dem Unterleibseingriff, bei Luftatmung und wahrend Sauerstofftherapie mit Venturimasken von 24, 28 und 35%. Der Wert fur .Pao, beim Atmen der jeweiligen Sauerstoffkonzentrationen entsprach dem Pao, wahrend Luftatmung. Der Unterschied zwischen dem Sauerstoffgehalt der Endkapillar-Lungengefasse und der Arterien wurde als Index fur die Beeintrachtigung der Sauerstoffzufuhr in der Lunge verwendet. Dieser Unterschied wurde durch die Sauerstofftherapie verringert. Die Reaktion auf die Sauerstofftherapie entsprach nicht den auf einem Iso-Shunt-Lungenmodell basierende Vorhersagen. Diese Ergebnisse lassen erkennen, dass Hypoxamie bei diesen Patienten hauptsachlich durch ein Missverhalmis von Beluftung und Durchblutungsdruck verursacht wird.
OXYGEN THERAPY AFTER ABDOMINAL SURGERY OXIGENOTERAPIA CONSECUTIVA A CIRUGIA ABDOMINAL SUMARIO
Se tomaron muestras de sangre arterial a 10 pacientes al dia siguiente de una intervention abdominal alta, respirando aire, y durante oxigenoterapia de mascarillas Venturij de 24%, 28% y 35%. Pa 0 , durante la inhalation de cada concentration de oxigeno se correspondio con el P&ot
797
durante la respiration de aire. La diferentia entre el contenido de oxigeno arterial y capilar final pulmonar se utilizo como indice de la disminucion de transferencia de oxigeno en el pulmon. Esta diferencia fue aminorada mediante oxigenoterapia. La respuesta obtenida no correspondio con las predictiones basadas en un modelo de pulmon iso-derivacion. Estos hallazgos sugieren que la hipoxemia en estos pacientes esta causada predominantemente por la falta de correlation entre ventilaci6n/perfusi6n.
