Effects of sevoflurane and propofol on pulmonary shunt fraction during one-lung ventilation for thoracic surgery

D. H. Beck, U. R. Doepfmer, C. Sinemus, A. Bloch, M. R. Schenk and W. J. Kox

Universitätsklinik Charité, Abteilung für Anaesthesiologie und operative Intensivmedizin, Schumannstrasse 20-21, D-10117 Berlin, Germany*Corresponding author

Accepted for publication: August 29, 2000


    Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Forty patients requiring one-lung ventilation (OLV) for thoracic surgery were randomly assigned to receive propofol (4-6 mg kg–1 h–1) or sevoflurane (1 MAC) for maintenance of anaesthesia. Three sets of measurements were taken: (i) after 30 min of two-lung ventilation (TLV), (ii) after 30 min of one-lung ventilation (OLV-1) in the supine position and (iii) during OLV in the lateral position (OLV-2) with the chest open and before surgical manipulation of the lung. There were no differences between groups in patient characteristics or preoperative condition. Increases in shunt fraction during OLV-1 were 17.4% and 17.2% (P=0.94), those during OLV-2 were 18.3% and 16.5% (P=0.59) for the propofol and sevoflurane group, respectively. Cardiac index and other haemodynamic and respiratory variables were similar for the two groups. We conclude that inhibition of hypoxic pulmonary vasoconstriction by sevoflurane may only account for small increases in shunt fraction and that much of the overall shunt fraction during OLV has other causes.

Br J Anaesth 2001; 86: 38–43

Keywords: lung, hypoxic pulmonary vasoconstriction; anaesthetics i.v., propofol; anaesthetics volatile, sevoflurane; lung, pulmonary shunt fraction; surgery, thoracic


    Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Hypoxic pulmonary vasoconstriction (HPV) is a mechanism that diverts pulmonary blood flow away from lung regions with low alveolar oxygen tensions to better ventilated areas of the lung, thus reducing venous admixture. Intravenous anaesthetic agents do not seem to affect HPV, whereas in animal experiments, inhalational agents inhibit HPV in a dose-dependent manner, increase intrapulmonary shunt fraction and reduce arterial oxygen tension.1 In vitro, dose-related inhibition of HPV by sevoflurane is comparable to that observed with isoflurane.2

Clinical investigations in patients undergoing one-lung ventilation (OLV) have been less conclusive. Two studies failed to detect significant differences in arterial oxygenation between propofol and isoflurane3 or between isoflurane and sevoflurane anaesthesia.4 In contrast, Kellow and colleagues5 found significantly greater shunt fractions during isoflurane anaesthesia than during propofol anaesthesia.

Sevoflurane has useful effects during thoracic surgery. It is a potent bronchodilatator and its low blood–gas partition coefficient allows rapid adjustment of the depth of anaesthesia. Rapid emergence from anaesthesia allows rapid return of spontaneous respiration and avoids the risks of postoperative mechanical ventilation. We compared the effects of sevoflurane and propofol on pulmonary shunt fraction in patients requiring OLV for thoracic surgery.


    Patients and methods
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
After approval by the institutional ethics committee and written informed consent one day before surgery, 40 patients requiring OLV for thoracic surgery were randomized to receive inhalational anaesthesia with sevoflurane (n=20) or intravenous anaesthesia with propofol (n=20).

All patients were premedicated with oral midazolam 0.1 mg kg–1 in the ward. In the operating theatre, a radial artery catheter was placed under local anaesthesia. Etomidate 0.2 mg kg–1 and fentanyl 0.1–0.2 mg were used to induce anaesthesia. Neuromuscular block was achieved with cisatracurium 0.15 mg kg–1, followed by endobronchial intubation with a left-sided double-lumen tube (Broncho-Cath, Mallinckrodt Medical, Athlone, Ireland) in all patients. The correct position of the tube was initially confirmed by auscultation and the absence of a leak from the lumen connecting to the non-ventilated lung, and by direct observation of the atelectatic, non-ventilated lung after thoracotomy. After induction of anaesthesia, a central vein was cannulated and a flow-directed thermodilution catheter (Arrow International, Reading, PA, USA) was placed in the pulmonary artery.

Propofol was infused continuously at an initial rate of 9 mg kg–1 h–1 which was reduced to 6 mg kg–1 h–1 after 10 min. Sevoflurane was given to maintain an end-expiratory concentration of 1.8 vol%. Arterial pressure was maintained within 20% of baseline values by administration of crystalloids and fentanyl. Increments of cisatracurium were given to maintain suppression of the second twitch using a train-of-four stimulation.

We used a mixture of oxygen and air to avoid increased venous admixture from absorption atelectasis. The fractional inspired concentration of oxygen was initially set at 0.5 and adjusted to maintain arterial haemoglobin saturation above 91%, measured by pulse oximetry. During two-lung ventilation (TLV) and OLV, tidal volumes of 10 ml kg–1 were used with the ventilatory rate adjusted to maintain end-tidal PCO2 at 35–40 mm Hg. After blood gas analysis, the rate was adjusted to obtain an arterial PCO2 of 35–45 mm Hg. During OLV, the lumen of the non-ventilated lung remained open to atmosphere; tidal volumes were decreased if peak airway pressure exceeded 35 cm of water. Positive end-expiratory pressure was not applied. The ratio of inspiratory to expiratory time was 1:2.

At the time of measurement, inspiratory and expiratory gas concentrations had been stable for >=15 min and were not allowed to change by >10%. All measurements were performed before surgical manipulation of the lung. Cardiac output was measured and mixed-venous and arterial blood gas analysis done (i) after 30 min of TLV with the patient in the supine position; (ii) after 30 min of stable OLV in the supine position (OLV-1); and (iii) after opening of the pleura in the lateral decubitus position and before surgical manipulation of the lung (OLV-2). In patients undergoing thoracoscopy, trocars were left open to atmosphere at the time of measurement (OLV-2). Mixed venous and arterial blood samples were collected in duplicate. Mixed venous blood was drawn over >=30 s to avoid inadvertent arterialization. The samples were analysed immediately using a blood gas analyser (ABL 505; Radiometer, Copenhagen, Denmark), which was calibrated daily according to the manufacturer’s instructions. The mean of two measurements was recorded. Thermodilution cardiac output was measured by forcible injection of 10 ml of normal saline at room temperature. Measurements were repeated until the difference between three successive readings was <10%. The mean of the readings was recorded as cardiac index. At the same time, haemodynamic variables were recorded, including heart rate, mean arterial and pulmonary artery pressure, pulmonary artery occlusion and central venous pressure (Marquette Electronics, Milwaukee, WI, USA). Inaccuracies in cardiac output measurements could have occurred, because the position of the pulmonary artery catheters was not verified by imaging techniques.

Calculation of shunt fraction
The shunt fraction was computed using a standard formula based on the three-compartment model proposed by Riley and colleagues:6

Qs/Qt=(Cc'O2CaO2)/(Cc'O2CvO2)

where Qs=shunt flow, Qt=cardiac output and Cc'O2, CaO2 and CvO2 represent the oxygen content of pulmonary end-capillary, arterial and mixed venous blood, respectively. Arterial and mixed venous oxygen content were calculated according to the formula

CO2=PO2x0.0031+(Hbx1.34SO2/100)

where PO2 and SO2 represent the partial pressure (mm Hg) and oxyhaemoglobin saturation in the arterial (CaO2) or mixed venous (CvO2) blood. Arterial and mixed venous PO2 and SO2 can be directly measured. In the case of Cc'O2 the relevant partial pressure and saturation have to be derived from the alveolar oxygen tension (PAO2):

PAO2=FIO2x(PBPH2O)–(PaCO2/R)

where FIO2 is the fractional inspired oxygen concentration, PB is barometric pressure, PH2O is the saturated vapour pressure of water (47 mm Hg) at body temperature, PaCO2 is arterial carbon dioxide partial pressure and R is the respiratory quotient (assumed to be 0.8). Therefore, Cc'O2=PAO2x0.0031+(1.34Hb). The actual barometric pressure was recorded before each measurement. PACO2 tension was assumed to equal PaCO2 and an assumption was made that the haemoglobin would be 100% saturated.

The sample size was estimated using the data of a previous investigation.16 A difference of 8.5% in the mean increase of shunt fraction between the groups and a standard deviation of 9.3% were used for the calculation. Forty patients would be required to give 80% probability (power) of demonstrating this difference at the 5% significance level.

Statistical analysis
One-way analysis of variance (ANOVA) was used to test the difference between the means of normally distributed data. Simple linear regression was used to analyse the relationship between cardiac index (predictor variable) and shunt fraction (dependent variable). We applied best subsets linear regression analysis to assess the association between five predictor variables and the dependent variable (shunt fraction). This technique allows a systematic search of the different combinations of predictor veriables, selecting those subsets that best contribute to the variation of the dependent variable. We tested five variables: cardiac index, mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), PvO2) and PaCO2. We decided not to test derived variables such as pulmonary and systemic arterial resistance, since their calculation uses haemodynamic variables included in the analysis (cardiac output, MAP and MPAP). We finally did a post hoc power analysis to assess the sensitivity of the study to detect a true difference between the groups.


    Results
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Forty patients were enrolled in the study. Two patients, one from each group, were excluded from analysis because hypotensive episodes during induction of anaesthesia required vasoactive drugs to be given. Patient details, preoperative lung function tests and blood gas values were similar in the two treatment groups (Table 1). Twenty patients had thoracotomy, nine in the propofol and 11 in the sevoflurane group; nine right-sided and 11 left-sided thoracotomies were performed. Eighteen patients, 10 in the propofol group and eight in the sevoflurane group, had video-assisted thoracoscopic procedures, of which 11 involved the left and seven the right hemithorax (Table 2). Seven patients in the propofol group and eight in the sevoflurane group required FIO2 concentrations of >0.5 to keep arterial oxygen saturation above 91%.


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Table 1 Patient details, lung function tests and preoperative laboratory investigations; values are mean±SD, except for age (mean and range). BMI=body mass index, FEV1=forced expiratory vital capacity, FVC=forced vital capacity
 

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Table 2 Type and side of surgical procedures; VA refers to video-assisted thoracoscopic operations
 
Compared with the baseline measurements (TLV), average shunt fractions during OLV-1 increased by 17.4% and 17.2% (P=0.94), and those during OLV-2 by 18.3% and 16.5% (P=0.59) for the propofol and sevoflurane group, respectively (Figure 1). There were no significant differences in haemodynamic and respiratory variables between the groups (Table 3). In particular, those variables known to influence HPV directly, such as cardiac index, mixed-venous oxygen tension and arterial carbon dioxide partial pressure, did not differ significantly between the treatment groups. Thus, possible effects on calculated shunt fraction resulting from these confounding variables can be assumed to have been of similar magnitude for both groups. For the range of values of cardiac output and shunt fraction observed in our study population, simple linear regression analysis showed a positive trend, but no significant correlation between cardiac index and shunt fraction. This is described by the regression equation y=19.775+2.95x (P=0.06; correlation coefficient r=0.230). Best subsets regression analysis showed that only two variables contributed significantly to the variation in shunt fraction, namely cardiac index (P=0.02) and PaCO2 (P=0.04). PvO2 (P=0.09) and the other haemodynamic variables tested did not explain changes in shunt fraction (MAP, P=0.43; MPAP, P=0.45).



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Fig 1 Measurements of shunt at the three measurement times. TLV=two-lung ventilation; OLV-1, one-lung ventilation, supine; OLV-2, one-lung ventilation, lateral. Error bars represent SEM.

 

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Table 3 Haemodynamic measurements, PvO2, PaO2 and shunt fraction; values are mean (SD). TLV=two-lung ventilation; OLV-1=one-lung ventilation, supine position; OLV-2=one-lung ventilation, lateral position; HR=heart rate; MAP=mean arterial pressure (mm Hg); CVP=central venous pressure (cm H2O); PCOP=pulmonary capillary occlusion pressure (mm Hg), MPAP=mean pulmonary artery pressure (mm Hg); SVRI and PVRI=systemic and pulmonary vascular resistance index (dyn s cm–5 m2); CI=cardiac index (litres min–1 m2); PaCO2=arterial carbon dioxide tension (mm Hg); PvO2 and PaO2 =mixed venous and arterial oxygen tension (mm Hg)
 
The results of the post hoc power analysis using the data from our study showed that there was an 80% probability (power) of detecting an 8.5% difference in the mean increase of shunt fractions (TLV to OLV-2) between the groups. The probability of demonstrating a 10.5% difference was 90%. Both calculations were performed using a standard deviation of 9.1% and a significance level of 5%.


    Discussion
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Compared with propofol, the administration of sevoflurane resulted in similar increases in shunt fraction during OLV. Small increases in shunt fraction by direct inhibition of the HPV response by sevoflurane could have been opposed by improved ventilation–perfusion (V/Q) matching during OLV and, consequently, reduced venous admixture.

Inhibition of the HPV response by inhalational anaesthetics is well established in animals. Depression of HPV has a typical sigmoid dose–response curve with an effective dose (ED50) slightly less than twice the minimal alveolar concentration (MAC) and an ED90 of 3 MAC. There is no major difference between the volatile anaesthetics.1 7 During inhalational anaesthesia at 1 MAC (1.8 vol%) of sevoflurane, the HPV response would be reduced by approximately 25%.2

Cardiac output, mixed venous PO2 and lung perfusion
There are several reasons for the failure to reproduce these findings in the clinical context. The conflicting results obtained from human studies comparing intravenous and volatile anaesthetic agents in patients undergoing OLV have been widely attributed to haemodynamic changes, particularly the reduction of cardiac output, which may be more pronounced especially with the older volatile agents. The efficacy of HPV is inversely related to the cardiac output,8 but interactions between several physiological variables can obscure the effects of cardiac output on HPV and shunt fraction in the clinical setting. A reduction in cardiac output will decrease PvO2 and increase pulmonary vasoconstriction. Volatile agents inhibit HPV by direct action, but at the same time augmentation of the HPV response occurs from decreasing cardiac output. Consequently, pulmonary shunt fraction and, by inference, HPV will appear to be unaffected.9

The HPV response is a function of both mixed venous and alveolar oxygen tension (PAO2).10 During OLV, the PAO2 of the non-ventilated, atelectatic lung can be assumed to equilibrate with the PvO2. In animal experiments, low and normal PvO2 values between 25 and 46 mm Hg (3.2–6.1 kPa) cause maximal diversion of the blood flow (40–50%) away from the collapsed lung.11 Hambraeus-Jonzon and colleagues,12 however, showed that during unilateral hypoxic ventilation (FIO2=0.05) and hyperoxic ventilation of the other lung (FIO2 =1.0) in humans, the moderate decrease in PvO2 made only a minor contribution to blood flow diversion compared with the reduction in alveolar PO2.

Variations in cardiac output not only influence PvO2 but also affect pulmonary perfusion. Domino and colleagues13 demonstrated that marked increases in cardiac output will increase pulmonary perfusion and worsen ventilation–perfusion mismatch; a 50% increase in pulmonary blood flow increased V/Q heterogeneity by 25%. On the other hand, low cardiac output can cause inhomogeneous distribution of blood flow in the ventilated lung with similar consequences for the ventilation–perfusion ratio. The effects of changes in cardiac output and subsequent alterations in PvO2 and lung perfusionare difficult to separate during OLV, but PvO2 values are usually within the range at which maximal stimulation of the HPV response occurs. Only dramatic changes in cardiac output and pulmonary perfusion will attenuate this response. In the present study, cardiac index and PvO2 values were similar for both treatment groups and are therefore unlikely to cause differences in shunt fractions between the groups.

V/Q scatter and bronchodilation
The method we used to derive shunt fraction does not allow distinction between venous admixture resulting from perfusion of non-ventilated lung regions (‘true shunt’) with ventilation–perfusion ratios of zero (V/Q=0) and lung regions that are perfused, but poorly ventilated and therefore have low, but not zero, V/Q ratios. Ventilation–perfusion mismatch is often present in patients undergoing lung resection surgery. Sevoflurane may have caused more uniform distribution of ventilation to the dependent lung during OLV, thereby decreasing shunt fraction. This could have opposed or even overcome the increase in venous admixture from inhibition of the HPV response.

The increase in shunt fraction by direct inhibition of HPV by inhalational anaesthetics administered in concentrations of 1 MAC can be expected to be rather small.1 Despite maximal stimulation of the HPV response, there will be an obligatory shunt fraction of 25% during OLV.12 14 Attenuation of the maximal HPV response by 25% would increase shunt fraction from 25% to 30% in the presence of 1 MAC sevoflurane, provided other confounding variables remain unchanged. Thus, direct inhibition of HPV could cause a 5% increase in shunt fraction.

Shunt fraction in clinical investigations
Propofol in doses of 6–12 mg kg–1 h–1 had no significant effect on PaO2 or shunt fraction.15 Reports comparing propofol with volatile agents overestimated the effects of direct inhibition of HPV by volatile agents, since shunt fractions increased more than expected from animal data. Shunt fractions during OLV were greater in patients who had received enflurane16 (1 MAC) and isoflurane5 (1 MAC). In both studies, shunt fractions were derived from oxygenation indices in a similiar manner to the present study.

Carlsson and colleagues17 18 applied multiple inert gas elimination techniques to investigate the influence of isoflurane and enflurane on HPV in human lungs. This complex method allows accurate measurement of the ‘true’ shunt fraction. The authors found a 2–3% increase in shunt fraction after administration of 1.5 vol% isoflurane, which corresponded to an attenuation of the HPV response by 20%. They found that effects on hypoxia-induced pulmonary vasoconstriction were almost immeasurable when isoflurane was administered in clinically used concentrations. Similarly, up to 2 MAC of enflurane caused no significant change in shunt or arterial oxygenation.

Abe and colleagues19 investigated the effects of propofol, sevoflurane and isoflurane in patients undergoing oesophageal surgery and concluded that the administration of propofol was associated with significantly improved oxygenation and lower shunt fractions. However, the experimental sequence was such that the volatile agents always preceded propofol. The reduction in shunt fraction may be because propofol was always given at a later stage of surgery and after a longer period of OLV.

The timing of the measurements and their relation to the stage of the surgical procedure is important since surgical trauma can temporarily inhibit HPV.20 We made measurements before surgical manipulation of the non-ventilated lung. Beside the direct effects of surgical trauma to lung tissues, the efficacy of HPV response may vary with the duration of OLV. Rees and colleagues found a maximal increase in shunt fraction after 30 min of OLV during enflurane anaesthesia.21 In patients who required prolonged OLV for oesophageal surgery, oxygenation improved significantly over time. Minimal PaO2 values occurred after 30 min and reached a maximum after 90 min of OLV.22 23

For our patients, simple linear regression showed a positive trend, but no significant correlation, between cardiac index and shunt fraction during OLV, consistent with the postulated inverse relationship between cardiac output and HPV response.8 Other investigators,24 however, reported improved arterial oxygenation with increasing cardiac output. Best subsets regression analysis showed that only cardiac index and PaCO2 contributed significantly to the variations in shunt fraction. Mixed venous oxygen tension, which is also thought to affect the HPV response, did not explain changes in shunt fraction. This supports the view that the attenuation of the HPV response occurs at much lower PvO2 values than those usually achieved during OLV.

In summary, sevoflurane administered in clinical concentrations of 1 MAC resulted in similar changes in shunt fraction as did propofol. Cardiac index, mixed PvO2 and PaCO2 did not differ between the groups. Much of the overall shunt fraction during OLV may result from sources other than the attenuation of the HPV response. Haemodynamic stability and appropriate ventilatory manoeuvres are probably far more important for achieving optimal arterial oxygenation during OLV than is the choice of the anaesthetic agent.


    References
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
1 Marshall C, Lindgren L, Marshall BE. Effects of halothane, enflurane, and isoflurane on hypoxic pulmonary vasoconstriction in rat lungs. Anesthesiology 1984; 60: 304–8[ISI][Medline]

2 Ishibe Y, Gui X, Uno H, Shiokawa J, Umeda T, Suekane K. Effects of sevoflurane on hypoxic pulmonary vasoconstriction in the perfused rabbit lung. Anesthesiology 1993; 79: 1348–53[ISI][Medline]

3 Reid CW, Slinger PD, Lenis S. A comparison of the effects of propofol–alfentanil versus isoflurane anesthesia on arterial oxygenation during one-lung ventilation. J Cardiothorac Anesth 1996; 10: 860–63[ISI]

4 Wang JYY, Russell GN, Page RD, Jackson M, Pennefather SH. Comparison of isoflurane and sevoflurane on arterial oxygenation during one lung ventilation. Br J Anaesth 1998; 81: 850–53[Abstract/Free Full Text]

5 Kellow NH, Scott AD, White SA, Fenech RO. Comparison of the effects of propofol and isoflurane anaesthesia on right ventricular function and shunt fraction during thoracic surgery. Br J Anaesth 1995; 75: 578–82[Abstract/Free Full Text]

6 Riley RL, Lilienthal JL, Proemmel DD, Franke RE. On the determination of the physiologically effective pressures of oxygen and carbon dioxide in alveolar air. Am J Physiol 1946; 147: 191[ISI]

7 Domino KB, Borowec L, Alexander CM et al. Influence of isoflurane on hypoxic pulmonary vasoconstriction in dogs. Anesthesiology 1986; 64: 423–29[ISI][Medline]

8 Eisenkraft JB. Effects of anaesthetics on the pulmonary circulation. Br J Anaesth 1990; 65: 63–78[ISI][Medline]

9 Nunn JF. Nunn’s Applied Respiratory Physiology, 4th Edn. Oxford: Butterworth–Heinemann, 1993; 414

10 Marshall C, Marshall BE. Site and sensitivity for hypoxic pulmonary vasoconstriction. J Appl Physiol 1983; 55: 711–16[Abstract/Free Full Text]

11 Domino KB, Wetstein L, Glasser SA et al. Influence of mixed-venous oxygen tension (PvO2) on blood flow to atelectatic lung. Anesthesiology 1983; 59: 428–34[ISI][Medline]

12 Hambraeus-Jonzon K, Bindslev L, Mellgard AJ, Hedenstierna G. Hypoxic pulmonary vasoconstriction in human lungs: a stimulus–response study. Anesthesiology 1997; 86: 308–15[ISI][Medline]

13 Domino KB, Eisenstein BL, Tran T, Hlastala MP. Increased pulmonary perfusion worsens ventilation–perfusion mismatch. Anesthesiology 1993; 79: 817–21

14 Marshall BE, Marshall C, Benumof J, Saidman LR. Hypoxic pulmonary vasoconstriction: effects of lung segment size and alveolar oxygen tension. J Appl Physiol 1981; 38: 846–50

15 Kerr LV, Aken HV, Vandermeersch E, Vermaut G, Lerut T. Propofol does not inhibit hypoxic pulmonary vasoconstriction in humans. J Clin Anesth 1989; 1: 284–8[Medline]

16 Spies C, Zaune U, Pauli MHF, Boeden G, Martin E. Comparison of enflurane and propofol during thoracic surgery. Anaesthesist 1991; 40: 14–18[ISI][Medline]

17 Carlsson AJ, Hedenstierna G, Bindslev L. Hypoxic-induced pulmonary vasoconstriction in human lungs exposed to enflurane anaesthesia. Acta Anaesthesiol Scand 1987; 31: 57–62[Medline]

18 Carlsson AJ, Bindslev L, Hedenstierna G. Hypoxia-induced pulmonary vasoconstriction in the human lung: the effect of isoflurane anesthesia. Anesthesiology 1987; 66: 312–16[ISI][Medline]

19 Abe K, Shimizu T, Takashina M, Yoshiya I. The effects of propofol, isoflurane and sevoflurane on oxygenation and shunt fraction during one-lung ventilation. Anesth Analg 1998; 87: 1164–9[Abstract]

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22 Ishikawa S, Makita K, Nakazawa K, Amaha K. Continuous intraarterial blood gas monitoring during oesophagectomy. Can J Anaesth 1998; 45: 273–6[Abstract]

23 Ishikawa S. Oxygenation may improve with time during one lung ventilation. Anesth Analg 1999; 89: 258

24 Slinger P, Scott WAC. Arterial oxygenation during one-lung anesthesia: a comparison of isoflurane and enflurane. Anesthesiology 1996; 82: 940–46[ISI]





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