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Pain Medicine  |   December 2001
Isoflurane and Sevoflurane Anesthesia in Pigs with a Preexistent Gas Exchange Defect
Author Affiliations & Notes
  • Axel Kleinsasser, M.D.
    *
  • Karl H. Lindner, M.D.
  • Christoph Hoermann, M.D.
  • Andreas Schaefer, M.S.
    §
  • Christian Keller, M.D.
  • Alexander Loeckinger, M.D.
    *
  • * Resident, † Professor and Chair, ‡ Assistant Professor, § Medical Student and Research Fellow.
  • Received from the Department of Anesthesiology and Critical Care Medicine, The Leopold-Franzens University, Innsbruck, Austria.
Article Information
Pain Medicine
Pain Medicine   |   December 2001
Isoflurane and Sevoflurane Anesthesia in Pigs with a Preexistent Gas Exchange Defect
Anesthesiology 12 2001, Vol.95, 1422-1426. doi:
Anesthesiology 12 2001, Vol.95, 1422-1426. doi:
VOLATILE anesthetics are known to decrease the arterial partial pressure of oxygen (Pao2). 1 One recognized mechanism behind this phenomenon is the inhibition of hypoxic pulmonary vasoconstriction (HPV). 1,2 HPV represents an autonomic regulatory mechanism of the pulmonary circulation whose primary function is to divert blood flow away from poorly aerated lung areas, thereby improving ventilation/perfusion (V̇A/Q̇) matching. HPV is a function of both decreased alveolar partial pressure of oxygen (PAo2) and decreased mixed venous partial pressure of oxygen (PV̇o2). 3 Inhibition of this local vasoconstriction may modify the distribution of blood flow in the lung. Considerable research was performed regarding the effect of halothane on HPV, pulmonary gas exchange, and Pao2. Besides the proven influence of halothane on the HPV, 4 halothane alters the distribution of pulmonary ventilation and blood flow, 5 major determinants of pulmonary V̇A/Q̇ matching and thus of Pao2. In the latter study, Dueck et al.  5 showed that halothane anesthesia redistributes pulmonary blood flow toward lung areas with low and zero V̇A/Q̇ ratios in patients with chronic obstructive lung disease. Meanwhile, halothane has been widely replaced by isoflurane and sevoflurane as standard anesthetics. Contrasting with halothane, the effects of these newer anesthetics on the distribution of pulmonary blood flow and ventilation remain uncertain. In patients with reactive airway disease and chronic obstructive pulmonary disease, however, volatile anesthetics are favored, but further increases of V̇A/Q̇ mismatch during inhalational anesthesia are undesirable in these patients. Isoflurane and sevoflurane might be contraindicated when gas exchange defects are present. In the current study, we sought to examine how isoflurane and sevoflurane affect pulmonary gas exchange in a porcine model with preexisting right-to-left shunt. We hypothesized that sevoflurane resulted in significantly more gas exchange disturbances in comparison with isoflurane or control.
Methods
Animal Preparation
After approval of the Federal Animal Investigational Committee of Vienna, Austria, this study was performed in 21 healthy, 16- to 18-week-old pigs weighing 40–45 kg. Animals were fasted overnight but had free access to water. Already in the stable, pigs were premedicated with azaperone (4 mg/kg intramuscular) and atropine (0.01 mg/kg intramuscular) 1 h before surgery. Anesthesia was induced using propofol (2–4 mg/kg intravenous). After intubating the trachea, the lungs were ventilated in a volume-controlled mode (SA-2, semi-open circle; Dräger, Lübeck, Germany) at an inspiratory fraction of oxygen of 0.3 (oxygen enriched air), a tidal volume of 10 ml/kg, and 17 breaths/min. Positive end-expiratory pressure was set to 5 cm H2O. Respiratory rate was then adjusted to achieve an arterial partial pressure of carbon dioxide (Paco2) between 35 and 40 mmHg. Respirator settings were not changed thereafter. Until the baseline measurement, anesthesia was maintained using propofol (6 mg · kg1· h1) and piritramide (30 mg). Ringer’s solution (6 ml · kg1· h1) and a 3% gelatin solution (4 ml · kg1· h1) were administered throughout the study period. A standard lead II electrocardiograph was used to monitor cardiac rhythm. If cardiovascular variables indicated a reduced depth of anesthesia during the preparatory phase, additional propofol and piritramide were administered. Body temperature was maintained between 38 and 39°C using an electric heating blanket.
Generating a Standardized Pulmonary Gas Exchange Defect
In the current study, the pigs’ peritoneal cavities were insufflated with purified air at a pressure of 15 cm H2O because pneumoperitoneum results in a reproducible redistribution of pulmonary blood flow to lung areas with a V̇A/Q̇ ratio of zero (shunt). 6 The intraperitoneal pressure was then continuously monitored and maintained at 15 cm H2O using a manometer (VBM Kontroll Inflator; VBM Medizintechnik, Sulz, Germany). 6 
Hemodynamic Measurements and Calculations
A 7-French catheter was advanced into the aorta for withdrawal of arterial blood and measurement of mean arterial blood pressure. A 7-French pulmonary artery catheter was advanced into a pulmonary artery to measure mean pulmonary artery pressure, pulmonary capillary wedge pressure, and cardiac output (thermodilution technique) and to withdraw mixed venous blood. All catheters were saline-filled and connected to standard pressure transducers that had been zeroed to ambient pressure at the level of the right atrium. Pulmonary vascular resistance index (dyn · s · cm5· kg1) was then calculated according to the standard formula.
Blood Gas and Inert Gas Measurements
Arterial and mixed venous blood gases were measured with a blood gas analyzer (Chiron, East Walpol, MA). V̇A/Q̇ distributions were determined using the multiple inert gas elimination technique as previously described. 7–9 Briefly, a mixture of six inert gases, including sulfur hexafluoride, ethan, cyclopropane, halothane, ether, and acetone dissolved in saline, was infused via  an auricular vein at a rate of 3 ml · kg1· h1. This infusion was started 1 h before the first set of measurements. Ten-milliliter mixed venous and arterial blood samples were collected in duplicate into heparinized matched-barrel glass syringes. Mixed expired gas samples of 30 ml were collected from a heated mixing chamber. All samples were kept at a temperature of 38.5°C and then analyzed. Gas extraction was performed as described by Wagner et al.  7 Concentrations of inert gases were measured using gas chromatography (HP-5890, Series II; Hewlett-Packard, Wilmington, DE). V̇A/Q̇ distributions were determined from inert gas data by using the 50-compartment model of Wagner et al.  7–9 Calculation of V̇A/Q̇ distributions in subjects anesthetized with volatile anesthetics requires a different approach to obtain the retention–solubility relation of the inert gases because the chromatographic peaks of isoflurane and sevoflurane superpose the halothane peak, one of the six inert tracer gases. Because halothane could not be measured chromatographically from samples taken during isoflurane or sevoflurane anesthesia, calculation of the retention–solubility curve was performed using five inert gases in all measurements after baseline. In measurements taken at baseline, six tracer gases were used for calculation. Measures to obtain the isolated chromatographic halothane peak during isoflurane or sevoflurane anesthesia, such as increasing the gas chromatograph’s oven temperature during the experimental runs, 10 were dropped for two reasons. First, the chromatogram of sevoflurane has an extremely wide basis at the standard temperature of the method, which could only be narrowed using much higher oven temperatures or increased carrier gas flow rates. This in turn results in decreased or lost discrimination of less-soluble tracer gases. Furthermore, for isolation of sevoflurane’s chromatographic peak, temperatures above the allowed maximum temperature (180°C) for packed columns used are needed. Second, halothane represents one point in the unbowed section of the retention–solubility curve. Calculation of the distribution using five gases omitting halothane results only in a negligible deviation from the calculation with six gases.
Distributions of V̇Aand Q̇ are presented as:
  • 1. blood flow to unventilated lung units, shunt flow  (V̇A/Q̇ < 0.005)
  • 2. blood flow to poorly ventilated lung units, low  A/Q̇  (low V̇A/Q̇ > 0.005–0.1)
  • 3. blood flow to normally ventilated lung units, normal  A/Q̇  (V̇A/Q̇ > 0.1–10)
  • 4. blood flow to poorly perfused lung units, high  A/Q̇  (V̇A/Q̇ > 10–100)
  • 5. ventilation of nonperfused lung units, alveolar dead space  (V̇A/Q̇ > 100)
The residual sum of squares was used as an indicator of fit of the data to this 50-compartment model. 9 
Experimental Protocol
Between completed animal preparation and baseline measurement, 30 min were allowed for corrections of body temperature and corrections of the fluid status (targeted by central venous pressure and pulmonary capillary wedge pressure) in all animals. Pigs were randomly assigned to three groups. After generating an air pneumoperitoneum 30 min before the baseline measurement, all groups received propofol until the baseline measurement, which included hemodynamic, blood gas, and inert gas measurements. Isoflurane (n = 7), sevoflurane (n = 7), or propofol (n = 7, control) anesthesia was continued for 30 min, and then a second set of measurements was performed. Isoflurane and sevoflurane were administered at 1 human MAC end-tidal concentration (1.15% and 2.0%, 11 respectively). Control group animals received propofol at 6 mg · kg1· h1.
Statistical Analysis
Repeated-measures two-way analysis of variance was used to determine statistical intergroup and intragroup significance. Two-sided tests were used. Nonparametric tests were additionally used in the analysis of the amount of blood flow to lung areas with a low V̇A/Q̇ ratio. Significant results were analyzed post hoc  using the Newman–Keuls test. P  < 0.05 was considered significant. Data are presented as mean ± SD. Sample size (n = 7) was based on data from a pilot study performed in three animals for a type I error of 0.05 and a power of 0.9.
Results
Comparing baseline values, no significant intergroup difference was found in any parameter.
Respiratory Data
Respiratory minute volume remained stable. Values are shown in table 1.
Table 1. Respiratory, Inert Gas, and Acid–Base Status Variables
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Table 1. Respiratory, Inert Gas, and Acid–Base Status Variables
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Hemodynamic Findings and Calculations
Data are presented in table 2. Except for an increase in heart rate during sevoflurane anesthesia, no significant differences were detected. Other measured or calculated variables, including mean pulmonary artery pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance index, and cardiac index, remained unchanged during the study period.
Table 2. Hemodynamic and Blood Gas Variables and Calculations
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Table 2. Hemodynamic and Blood Gas Variables and Calculations
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Blood Gas and Inert Gas Measurements and Calculations
Data are presented in tables 1 and 2and figure 1. Inert gas shunt was significantly increased in animals treated with sevoflurane, whereas isoflurane had no influence on this variable. Blood flow to lung areas with a normal V̇A/Q̇ ratio and a normal Pao2were significantly depressed in animals treated with sevoflurane. Residual sums of squares were comparable throughout the measurements. Considering all measurements performed, 88% of the sums of squares were less than 5.3, and 97.6% were less than 10.6. At the second measurement calculated using five inert gases, 90.4% of the residual sums of squares were less than 5.3, and 95.2% were less than 10.6. Other inert gas or blood gas variables remained statistically unchanged throughout the measurements. Venous admixture in percent of cardiac output was calculated using the standard formula corrected for an inspiratory fraction of oxygen of 0.3. At baseline, venous admixtures were 18 ± 4% (control group), 18 ± 3% (isoflurane group), and 17 ± 5% (sevoflurane group). At the second measurement, venous admixtures were 18 ± 2% (control group), 20 ± 7% (isoflurane group), and 23 ± 6% (sevoflurane group).
Fig. 1. (Left  ) At baseline, all animals were anesthetized using propofol. (Right  ) Values after 30 min of inhalational anesthesia or control. Shunt = blood flow to lung areas with zero ventilation; low V̇A/Q̇= blood flow to lung areas with a low ventilation/perfusion ratio; normal V̇A/Q̇= blood flow to lung areas with a normal ventilation/perfusion ratio; Pao2= arterial partial pressure of oxygen. Data are mean ± SD; error bars indicate SD;P  values refer to intergroup comparison. Numeric data at the second measurement were as follows: shunt: control (9 ± 1%) versus  isoflurane (11 ± 2%), P  = 0.2; control versus  sevoflurane (15 ± 3%), P  = 0.02. Low V̇A/Q̇: control (1.1 ± 1.2%) versus  isoflurane (2.5 ± 2.3%), P  = 0.8; control versus  sevoflurane (1.3 ± 2.8%), P  = 0.5. Normal V̇A/Q̇: control (89 ± 1%) versus  isoflurane (86 ± 3%), P  = 0.2; control versus  sevoflurane (83 ± 5%) , P  = 0.04. Pao2: control (102 ± 15 mmHg) versus  isoflurane (102 ± 12 mmHg), P  = 0.9; control versus  sevoflurane (88 ± 11 mmHg) , P  = 0.04.
Fig. 1. (Left 
	) At baseline, all animals were anesthetized using propofol. (Right 
	) Values after 30 min of inhalational anesthesia or control. Shunt = blood flow to lung areas with zero ventilation; low V̇A/Q̇= blood flow to lung areas with a low ventilation/perfusion ratio; normal V̇A/Q̇= blood flow to lung areas with a normal ventilation/perfusion ratio; Pao2= arterial partial pressure of oxygen. Data are mean ± SD; error bars indicate SD;P 
	values refer to intergroup comparison. Numeric data at the second measurement were as follows: shunt: control (9 ± 1%) versus 
	isoflurane (11 ± 2%), P 
	= 0.2; control versus 
	sevoflurane (15 ± 3%), P 
	= 0.02. Low V̇A/Q̇: control (1.1 ± 1.2%) versus 
	isoflurane (2.5 ± 2.3%), P 
	= 0.8; control versus 
	sevoflurane (1.3 ± 2.8%), P 
	= 0.5. Normal V̇A/Q̇: control (89 ± 1%) versus 
	isoflurane (86 ± 3%), P 
	= 0.2; control versus 
	sevoflurane (83 ± 5%) , P 
	= 0.04. Pao2: control (102 ± 15 mmHg) versus 
	isoflurane (102 ± 12 mmHg), P 
	= 0.9; control versus 
	sevoflurane (88 ± 11 mmHg) , P 
	= 0.04.
Fig. 1. (Left  ) At baseline, all animals were anesthetized using propofol. (Right  ) Values after 30 min of inhalational anesthesia or control. Shunt = blood flow to lung areas with zero ventilation; low V̇A/Q̇= blood flow to lung areas with a low ventilation/perfusion ratio; normal V̇A/Q̇= blood flow to lung areas with a normal ventilation/perfusion ratio; Pao2= arterial partial pressure of oxygen. Data are mean ± SD; error bars indicate SD;P  values refer to intergroup comparison. Numeric data at the second measurement were as follows: shunt: control (9 ± 1%) versus  isoflurane (11 ± 2%), P  = 0.2; control versus  sevoflurane (15 ± 3%), P  = 0.02. Low V̇A/Q̇: control (1.1 ± 1.2%) versus  isoflurane (2.5 ± 2.3%), P  = 0.8; control versus  sevoflurane (1.3 ± 2.8%), P  = 0.5. Normal V̇A/Q̇: control (89 ± 1%) versus  isoflurane (86 ± 3%), P  = 0.2; control versus  sevoflurane (83 ± 5%) , P  = 0.04. Pao2: control (102 ± 15 mmHg) versus  isoflurane (102 ± 12 mmHg), P  = 0.9; control versus  sevoflurane (88 ± 11 mmHg) , P  = 0.04.
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Discussion
In the current study, we examined the influence of isoflurane and sevoflurane on pulmonary gas exchange. In comparison with a control group anesthetized with propofol, sevoflurane but not isoflurane further impaired gas exchange in a pig model with a preexisting gas exchange defect. Propofol was selected for the control group because it is not known to alter Pao2. 12 Multiple inert gas elimination technique analysis showed that during sevoflurane anesthesia, blood flow to lung areas with a V̇A/Q̇ ratio of zero (shunt) was increased, whereas blood flow to lung areas with a normal V̇A/Q̇ ratio was reduced. Pao2was correspondingly decreased. Calculating the pulmonary vascular resistance index, no reduction indicating inhibition of HPV was observed during inhalational anesthesia. The influence of inhalational anesthetics on HPV seems to be ambivalent. Based on a number of studies, Nunn 13 concluded that inhalational anesthetics inhibit HPV by direct action, whereas they may intensify HPV by reducing mixed venous Po2(Pvo2) as a result of decreasing cardiac output. In our experiment, neither isoflurane nor sevoflurane at 1 MAC had any effect on cardiac output or Pvo2. Comparing our results with those Dueck et al.  10 found in humans shows that the effects of sevoflurane are comparable to those of halothane. Both drugs apparently redistribute pulmonary blood flow away from lung areas with a normal V̇A/Q̇ ratio toward lung areas with a lower V̇A/Q̇ ratio or shunt. Why sevoflurane but not isoflurane exerts this influence on pulmonary blood flow cannot be determined from our data. Possible reasons include the different inspiratory concentrations applied and the different physical properties of the examined volatile anesthetics. Also, methodologic reasons should be considered. However, gas exchange was not affected by acid–base status disturbances because the corresponding variables remained stable.
Three limitations of this study should be mentioned. First, pulmonary data obtained in a porcine model cannot be fully transposed to humans because pigs lack collateral ventilation. Second, the animals we used were examined while in the supine position, which is not a physiologic position for a pig but allowed unrestricted thoracic movements, resulting in normal respiratory mechanics. Third, inhibition of HPV is possibly very subtle at a hyperoxic inspiratory fraction of oxygen of 0.3.
We conclude that sevoflurane but not isoflurane further impairs pulmonary gas exchange in a porcine model with a previously existing gas exchange defect. Further studies in humans are warranted to determine the effect of inhalational anesthetics on pulmonary gas exchange in patients presenting with pulmonary disease.
References
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Bjertnaes LJ, Hauge A, Torgrimsen T: The pulmonary vasoconstrictor response to hypoxia: The hypoxia-sensitive site studied with a volatile inhibitor. Acta Physiol Scand 1980; 109: 447–62Bjertnaes, LJ Hauge, A Torgrimsen, T
Marshall C, Marshall B: Site and sensitivity for stimulation of hypoxic pulmonary vasoconstriction. J Appl Physiol 1983; 55: 711–6Marshall, C Marshall, B
Johnson D, Mayers I, To T: The effects of halothane in hypoxic pulmonary vasoconstriction. A nesthesiology 1990; 72: 125–33Johnson, D Mayers, I To, T
Dueck R, Young I, Clausen J, Wagner PD: Altered distribution of pulmonary ventilation and blood flow following induction of inhalation anesthesia. A nesthesiology 1980; 52: 113—25Dueck, R Young, I Clausen, J Wagner, PD
Loeckinger A, Kleinsasser A, Hoermann C, Gassner M, Keller C, Lindner KH: Inert gas exchange during pneumoperitoneum at incremental values of positive end-expiratory pressure. Anesth Analg 2000; 90: 466–71Loeckinger, A Kleinsasser, A Hoermann, C Gassner, M Keller, C Lindner, KH
Wagner PD, Saltzman JA, West JB: Measurement of continuous distributions of ventilation-perfusion ratios: Theory. J Appl Physiol 1974; 36: 588–99Wagner, PD Saltzman, JA West, JB
Wagner PD, Naumann PF, Laravuso RB: Simultaneous measurement of eight foreign gases in blood by gas chromatography. J Appl Physiol 1974; 36: 600–5Wagner, PD Naumann, PF Laravuso, RB
Evans JW, Wagner PD Limits on VA/Q distributions from analysis of experimental inert gas elimination. J Appl Physiol 1977; 42: 889–98Evans, JW Wagner, PD
Dueck R, Rathbun M, Wagner PD: Chromatographic analysis of multiple tracer inert gases in the presence of anesthetic gases. A nesthesiology 1978; 49: 31–6Dueck, R Rathbun, M Wagner, PD
Ozaki M, Sessler DI, Suzuki H, Ozaki K, Tsunoda C, Atarashi K: Nitrous oxide decreases the threshold for vasoconstriction less than sevoflurane or isoflurane. Anesth Analg 1995; 80: 1212–6Ozaki, M Sessler, DI Suzuki, H Ozaki, K Tsunoda, C Atarashi, K
Mendoza CU, Suarez M, Castaneda R, Hernandez A, Sanchez R: Comparative study between the effects of total intravenous anesthesia with propofol and balanced anesthesia with halothane on the alveolar-arterial oxygen tension difference and on the pulmonary shunt. Arch Med Res 1992; 23: 139–42Mendoza, CU Suarez, M Castaneda, R Hernandez, A Sanchez, R
Nunn JF: Respiratory aspects of anaesthesia, Nunn’s Applied Respiratory Physiology, 4th edition. Edited by Nunn JF. Oxford, Butterworth-Heinemann, 1997, pp 384–417
Fig. 1. (Left  ) At baseline, all animals were anesthetized using propofol. (Right  ) Values after 30 min of inhalational anesthesia or control. Shunt = blood flow to lung areas with zero ventilation; low V̇A/Q̇= blood flow to lung areas with a low ventilation/perfusion ratio; normal V̇A/Q̇= blood flow to lung areas with a normal ventilation/perfusion ratio; Pao2= arterial partial pressure of oxygen. Data are mean ± SD; error bars indicate SD;P  values refer to intergroup comparison. Numeric data at the second measurement were as follows: shunt: control (9 ± 1%) versus  isoflurane (11 ± 2%), P  = 0.2; control versus  sevoflurane (15 ± 3%), P  = 0.02. Low V̇A/Q̇: control (1.1 ± 1.2%) versus  isoflurane (2.5 ± 2.3%), P  = 0.8; control versus  sevoflurane (1.3 ± 2.8%), P  = 0.5. Normal V̇A/Q̇: control (89 ± 1%) versus  isoflurane (86 ± 3%), P  = 0.2; control versus  sevoflurane (83 ± 5%) , P  = 0.04. Pao2: control (102 ± 15 mmHg) versus  isoflurane (102 ± 12 mmHg), P  = 0.9; control versus  sevoflurane (88 ± 11 mmHg) , P  = 0.04.
Fig. 1. (Left 
	) At baseline, all animals were anesthetized using propofol. (Right 
	) Values after 30 min of inhalational anesthesia or control. Shunt = blood flow to lung areas with zero ventilation; low V̇A/Q̇= blood flow to lung areas with a low ventilation/perfusion ratio; normal V̇A/Q̇= blood flow to lung areas with a normal ventilation/perfusion ratio; Pao2= arterial partial pressure of oxygen. Data are mean ± SD; error bars indicate SD;P 
	values refer to intergroup comparison. Numeric data at the second measurement were as follows: shunt: control (9 ± 1%) versus 
	isoflurane (11 ± 2%), P 
	= 0.2; control versus 
	sevoflurane (15 ± 3%), P 
	= 0.02. Low V̇A/Q̇: control (1.1 ± 1.2%) versus 
	isoflurane (2.5 ± 2.3%), P 
	= 0.8; control versus 
	sevoflurane (1.3 ± 2.8%), P 
	= 0.5. Normal V̇A/Q̇: control (89 ± 1%) versus 
	isoflurane (86 ± 3%), P 
	= 0.2; control versus 
	sevoflurane (83 ± 5%) , P 
	= 0.04. Pao2: control (102 ± 15 mmHg) versus 
	isoflurane (102 ± 12 mmHg), P 
	= 0.9; control versus 
	sevoflurane (88 ± 11 mmHg) , P 
	= 0.04.
Fig. 1. (Left  ) At baseline, all animals were anesthetized using propofol. (Right  ) Values after 30 min of inhalational anesthesia or control. Shunt = blood flow to lung areas with zero ventilation; low V̇A/Q̇= blood flow to lung areas with a low ventilation/perfusion ratio; normal V̇A/Q̇= blood flow to lung areas with a normal ventilation/perfusion ratio; Pao2= arterial partial pressure of oxygen. Data are mean ± SD; error bars indicate SD;P  values refer to intergroup comparison. Numeric data at the second measurement were as follows: shunt: control (9 ± 1%) versus  isoflurane (11 ± 2%), P  = 0.2; control versus  sevoflurane (15 ± 3%), P  = 0.02. Low V̇A/Q̇: control (1.1 ± 1.2%) versus  isoflurane (2.5 ± 2.3%), P  = 0.8; control versus  sevoflurane (1.3 ± 2.8%), P  = 0.5. Normal V̇A/Q̇: control (89 ± 1%) versus  isoflurane (86 ± 3%), P  = 0.2; control versus  sevoflurane (83 ± 5%) , P  = 0.04. Pao2: control (102 ± 15 mmHg) versus  isoflurane (102 ± 12 mmHg), P  = 0.9; control versus  sevoflurane (88 ± 11 mmHg) , P  = 0.04.
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Table 1. Respiratory, Inert Gas, and Acid–Base Status Variables
Image not available
Table 1. Respiratory, Inert Gas, and Acid–Base Status Variables
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Table 2. Hemodynamic and Blood Gas Variables and Calculations
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Table 2. Hemodynamic and Blood Gas Variables and Calculations
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