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CARDIOVASCULAR ANESTHESIA

Two-Lung and One-Lung Ventilation in Patients with Chronic Obstructive Pulmonary Disease: The Effects of Position and FIO₂

Gizella I. Bardoczky, MD, PhD, DABA^*, Laszlo L. Szegedi, MD^*, Alain A. d’Hollander, MD, PhD^*, Jean-Marie Moures, MD^*, Philippe de Francquen, MD, and Jean-Claude Yernault, MD, PhD, FFCP

Departments of *Anesthesiology, Thoracic Surgery, and Chest Medicine, Erasme University Hospital, Free University of Brussels, Brussels, Belgium

Address correspondence and reprint requests to Laszlo L. Szegedi, MD, Department of Anesthesiology, Erasme University Hospital, Free University of Brussels, 808, route de Lennik, 1070 Brussels, Belgium.

	Abstract

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We compared the effects of position and fraction of inspired oxygen (FIO₂) on oxygenation during thoracic surgery in 24 consenting patients randomly assigned to receive an FIO₂ of 0.4 (eight patients, Group 0.4), 0.6 (eight patients, Group 0.6), or 1.0 (eight patients, Group 1.0) during the periods of two-lung (TLV) and one-lung ventilation (OLV) in the supine and lateral positions. TLV and OLV were maintained while the patients were first in the supine and then in the lateral position for 15 min each. Thereafter, respiratory mechanical data were obtained, and arterial blood gas samples were drawn. PaO₂ decreased during OLV compared with TLV in both the supine and lateral positions. In all three groups, PaO₂ was significantly higher during OLV in the lateral than in the supine position: 101 (72–201) vs 63 (57–144) mm Hg in Group 0.4; 268 (162–311) vs 155 (114–235) mm Hg in Group 0.6; and 486 (288–563) vs 301 (216–422) mm Hg in Group 1.0, respectively (P < 0.02, Wilcoxon’s signed rank test). We conclude that, compared with the supine position, gravity augments the redistribution of perfusion as a result of hypoxic pulmonary vasoconstriction, when patients are in the lateral position, which explains the higher PaO₂ during OLV.

Implications: This study compares oxygenation during thoracic surgery during periods of two-lung and one-lung ventilation with patients in the supine and lateral positions when using three different fraction of inspired oxygen values. Arterial oxygen tension was decreased in all three groups during one-lung ventilation in comparison with the two-lung ventilation values, but the decrease was significantly less in the lateral, compared with the supine position.

	Introduction

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As a result of the latest technical developments in cardiothoracic surgery, a variety of thoracic procedures are performed with patients in the supine instead of the traditional lateral position. Double-lung transplantation (1), lung volume reduction surgery (2,3), and minimally invasive coronary artery surgery (4) are routinely performed with patients in the supine position. Median sternotomy has even been recommended for pulmonary resection (5). During these interventions, one-lung ventilation (OLV) is inherently required, generally inducing some degree of hypoxemia. The major protective mechanism against hypoxemia is hypoxic pulmonary vasoconstriction (HPV) (6), but in the lateral position, gravity-induced blood flow redistribution must also be considered (7,8). Data comparing gas exchange in the supine versus lateral position during OLV are lacking (9). The aims of our study were to analyze the role of the position (supine versus lateral) and the effect of varied fraction of inspired oxygen (FIO₂) values during OLV of patients with coronary obstructive pulmonary disease (COPD) who are scheduled for lung surgery.

	Methods

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After approval from the ethics committee of the hospital, informed consent was obtained from 24 consecutive patients scheduled for elective thoracic surgery. All subjects were studied in the supine and lateral positions both during two-lung ventilation (TLV) and OLV, before surgery. Patients were randomly assigned to receive FIO₂ of 0.4 (Group 0.4 = eight patients), 0.6 (Group 0.6 = eight patients), or 1.0 (Group 1.0 = eight patients) throughout the study. The patients had mild pulmonary hyperinflation (functional residual capacity > 120%). All patients were premedicated with midazolam 3 to 5 mg IM, approximately 30 min before the induction of anesthesia. In the operating room, all patients had an epidural catheter inserted around the T7 level, and after the administration of a test dose, an epidural anesthesia was started with 8 mL of 2% lidocaine with 100 µg fentanyl and was maintained with a continuous infusion of epidural bupivacaine 0.5% (2–5 mL/h). The patients were anesthetized with a variable-rate (3–6 mg · kg^-1 · min^-1) continuous infusion of propofol and inhaled isoflurane (0.4%–0.6%) in 40% or 60% oxygen in air or pure oxygen. Muscle relaxation was achieved with pancuronium. In all patients, the bronchus of the dependent lung was intubated with a double-lumen endotracheal tube (DLT) (Broncho-cath^TM; Mallinckrodt Laboratories, Athlone, Ireland) of an appropriate size determined by the height of the patient (10). The correct position of the DLT was determined with fiberoptic bronchoscopy in both the supine and the lateral positions.

The electrocardiogram, heart rate, systemic arterial blood pressure, noninvasive arterial oxygen saturation, and end-tidal CO₂ were continuously monitored. Constant tidal volume of 10 mL/kg was delivered with a Siemens 900C ventilator (Siemens^® Elema^TM, Solna, Sweden) throughout the study. The ventilatory pattern consisted of a volume-controlled, square-wave flow pattern, at a rate of 10 breaths/min. Inspiratory time (T_I/T_TOT) was 0.33 and end-inspiratory pause was 10% of the total respiratory cycle. All measurements were performed with zero applied end-expiratory pressure. Ventilatory variables were kept constant during the study, both during TLV and OLV. This investigation was performed with the chest closed and before the surgical procedure.

After intubation in the supine position and fiberoptic control of the correct DLT position, the two lungs were ventilated with the above-described ventilatory pattern for 15 min. End-inspiratory and end-expiratory occlusions were performed to determine the mechanical characteristics of the respiratory system (peak inspiratory airway pressure, end-inspiratory plateau pressure, and intrinsic positive end-expiratory pressure) and arterial blood gas samples were drawn. Then, the tracheal lumen of the DLT was clamped, and the would-be operated nondependent lung was allowed to deflate to atmospheric pressure. After 15 min of OLV and data collection, TLV was restored with unaltered ventilatory settings, and the patient was turned to the lateral decubitus position. TLV and turning and positioning of the patients generally lasted approximately 30 min. At the end of this period, ventilatory data were recorded, an arterial blood gas sample drawn, and the nondependent lung collapsed again, now with the patient in the lateral decubitus position. After 15 min, respiratory mechanics and gas exchange data were collected again. PaO₂, alveolar-arterial oxygen tensions difference [P(A-a)O₂] were calculated by using standard equations.

Demographic data and preoperative pulmonary functions of the three groups were comparable (Kruskall-Wallis test). The data obtained in the two positions were compared with the Wilcoxon matched pair test. The data caused by FIO₂ differences were analyzed with the Kruskall-Wallis test. Values of P < 0.05 were considered as statistically significant. Data were presented as median (range).

	Results

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Demographic characteristics, preoperative pulmonary function tests, and the values of the preoperative arterial oxygen and carbon dioxide tensions of the 24 patients are shown in Table 1. The differences were not statistically significant among the three groups. Right- and left-sided thoracotomies were comparable in the three groups and among the groups (Kruskall-Wallis test). Initiating OLV with unaltered ventilatory settings increased peak inspiratory pressures significantly in all three groups (Tables 2–4).

In contrast, in the OLV assessment stages, the PaO₂ values in the lateral position were always significantly higher than in the supine position: Group 0.4, 63 (57–144) vs 101(72–201) mm Hg (P < 0.02); Group 0.6, 155 (114–235) vs 268 (162–311) mm Hg (P < 0.02); Group 1.0, 301 (216–422) vs 486 (288–563) mm Hg (P < 0.02) (Wilcoxon’s matched pair test). The values of P(A-a)O₂ showed similarly significant changes, but in the opposite direction (Tables 2–4 and Figure 1).

View larger version (16K): [in this window] [in a new window]   Figure 1. Individual modifications in arterial oxygenation secondary to changes in position in the three groups of patients during thoracic surgery. The bold lines represent the median values.

Effects of FIO₂
In the three groups of patients ventilated with different FIO₂ values, the differences of PaO₂ values observed between the supine and lateral TLV periods were not significant. In contrast, the increases of PaO₂ values observed between the lateral and supine OLV were significantly higher when the FIO₂ was higher (P < 0.02, Kruskall-Wallis test) (Figure 2).

View larger version (18K): [in this window] [in a new window]   Figure 2. Values of arterial oxygen tension increases between lateral and supine positions, during TLV and OLV in the three groups of patients. The bold lines represent the median values. TLV = two-lung ventilation, OLV = one-lung ventilation.

When turning the patients from the supine to the lateral position, PaO₂ increased significantly when comparing the periods of OLV. These PaO₂ increases (lateral-supine) were significantly larger when higher FIO₂ values were used (Figure 2).

When comparing the periods of TLV, no significant differences in PaO₂ increases (lateral-supine) were found, regardless of the FIO₂ values administered (Figure 2).

There were no significant changes in mean arterial pressure or heart rate in any of the patients during the study period.

	Discussion

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In this study, we investigated arterial oxygenation with the patient in the supine and in the lateral positions during TLV and OLV in patients with mild pulmonary hyperinflation scheduled for thoracic surgery. We found significantly higher PaO₂ and lower P(A-a)O₂ when OLV was performed in the lateral position.

Recent developments in thoracic surgery have widened the scale of surgical interventions and changed certain traditions, including the patient positioning. Single-lung transplantation (12) and resection of unilateral emphysematous bullae (3) are performed with the patient in the lateral decubitus position, while double-lung transplantation, lung volume reduction surgery, and minimally invasive coronary artery surgery are performed with the patient placed in the supine position (1,2,13). In both conditions, to facilitate the surgeon’s task, variable periods of OLV are required during these procedures.

To explain the preservation of blood oxygenation in the presence of a large fraction of atelectatic lung, as during OLV, in experimental or clinical conditions, many factors have been mentioned, including principally HPV (8,14), gravity (12), or local mechanical forces (13,15). We have found only one study comparing oxygenation during OLV in the supine and lateral positions (9).

When OLV is performed and one of the lungs is excluded from ventilation, an obligatory right-to-left shunt occurs through the nonventilated lung that is not present during TLV, and arterial oxygenation decreases (7). The pulmonary vessels in that nonventilated, hypoxic area respond by increasing resistance to flow. This reflex HPV of vessels perfusing hypoxic alveoli diverts blood flow from nonventilated lung units (7,14) to ventilated regions and attenuates hypoxemia by actively reducing the perfusion of nonventilated lung tissue.

In the supine position, during anesthesia and controlled mechanical ventilation of both lungs, there are generally no significant differences in the perfusion between the two lungs as both are exposed to the same pressures of gravity (12). Starting OLV will initiate right-to-left shunt, and as a consequence, PaO₂ will decrease and P(A-a)O₂ will increase. Indeed, in this study, when OLV was initiated in the supine position, PaO₂ decreased from 124 (81–240) to 63 (57–144) mm Hg (P < 0.02) in Group 0.4, from 255 (172–391) to 155 (114–235) mm Hg (P < 0.02) in Group 0.6, and from 472 (232–591) to 300.5 (216–422) mm Hg in Group 1.0. Every patient’s P(A-a)O₂ increased significantly during OLV (Tables 2–4).

However, during TLV in the lateral position, the position of the patient reduces perfusion of the upper lung caused by gravitational diversion of blood flow to the dependent lung (7,8). As a result of anesthesia and muscle relaxation, the distribution of ventilation also changes in the lateral position because the applied positive-pressure ventilation displaces the diaphragm preferentially at the nondependent part. Traditionally, this discrepancy is thought to be disadvantageous (7). However, in our patients, the change in position from the supine to lateral decubitus position resulted in a modest change in PaO₂ during TLV (124 [81–240] and 132 [102–296] mm Hg in Group 0.4; 256 [172–391] and 289 [225–353] mm Hg in Group 0.6; and 472 [232–591] and 492 [336–600] mm Hg in Group 1.0, respectively). This is in agreement with the findings of Boldt et al. (16) and Rehder et al. (17), who also reported no difference in PaO₂ between the lateral and the supine positions with TLV.

Inducing OLV when the patient is in the lateral position activates HPV and reduces the further perfusion of the collapsed lung. Hence, we found that PaO₂ was significantly greater when OLV was initiated after turning the patients into the lateral decubitus position (Tables 2–4 and Figures 1 and 2).

Fiser et al. (9) studied the period of OLV in both the supine and the lateral positions and did not find changes in arterial oxygen tension after 10 to 20 minutes of OLV when the patients were turned into the lateral position. However, in the study of Fiser et al. (9), OLV was initiated in the supine position and maintained continuously, even during the period of positioning and turning the patient, with an FIO₂ of 1.0.

The most important mechanism for reducing blood flow of an atelectatic lung is HPV (6,14). When OLV is induced in the lateral position, the blood flow of the nondependent lung is already reduced by gravitational forces, and HPV further reduces blood flow. In contrast, in the supine position, both lungs are equally exposed to an identical gravitational force; thus during OLV, the reduction of blood flow depends solely on the strength of the HPV.

Here, consideration should be given to possible limitations in our experimental methods.

First, concerning the patients included in the study, the presence of chronic airflow obstruction may be associated with better PaO₂ during OLV possibly because of dynamic hyperinflation resulting in an increased functional residual capacity and intrinsic positive end-expiratory pressure in the dependent lung (18). In contrast, in patients with severe COPD, HPV may not be an important protective mechanism, as these patients already have an increased pulmonary arterial pressure and reduced pulmonary vascular bed. The amount of disease in the nondependent lung is also a significant determinant of the amount of blood flow to the nondependent lung. If the nondependent lung is severely diseased, there may be a fixed reduction in blood flow to this lung preoperatively, and the collapse of such a diseased lung may not cause more of an increase in shunt. PaO₂ during TLV may also be a determining factor of oxygenation during OLV (18).

Second, we did not study OLV for long periods (more than two hours) with high FIO₂ values, but according to the study of Barker et al. (19), late hypoxemia occurs (mean OLV time, 170 minutes) when ventilating with 100% oxygen, which may be in part caused by absorption atelectasis. High FIO₂ can lead to arteriovenous shunting in areas of airway closure and, further, cause absent ventilation in lung units with low ventilation/perfusion ratios.

Third, if we consider that the lateral TLV/OLV always followed the supine TLV/OLV sequence, one can argue that a time effect could influence the present results. Concerning the time course of the HPV response, many experimental and clinical studies have been performed, with sometimes contradictory results. Benumof (20) showed that intermittent hypoxic challenges potentiated the hypoxic vasoconstriction in the left lower lobe of open-chest dog lungs, but the preparation and manipulation of the animals required considerable instrumentation and manipulation, which may have interfered with the HPV. Carlsson et al. (21) found maximal HPV response within 15 minutes of hypoxia in a human study, which agrees with observations in animal studies. Tucker and Reeves (22) were unable to maintain HPV during acute hypoxia in anesthetized dogs. During one-lung hypoxia in dogs, Domino et al. (23) studied HPV in closed-chest dogs and found a maximal level from the very first hypoxic challenge. Thus, there is a wide variation in the results obtained concerning the influence of time on HPV. In our study, the experimental procedure was almost identical to the procedure performed by Carlsson et al. (21) or by Domino et al. (23), who concluded that the time factor should not be a hindrance to manipulative studies on the HPV response once a maximal response has been evoked, normally in 10–15 minutes.

Fourth, if we consider that, after the period of supine TLV, we have only declamped the tracheal limb of the DLT and closed it, without sighing the nondependent lung, the 5-mL/kg gas distributed to that lung will not reverse the amount of atelectasis. So, our study may be comparable to the study of Fiser et al. (9), but as significant changes were found in the lateral position, we can argue that if HPV was maximal after the first 15 min of hypoxia, there is another factor, probably gravity, that could contribute to flow redistribution. Nevertheless, in the particular conditions of the present study—patients with mild COPD, closed chest, mixed locoregional/general balanced anesthesia—increased HPV responses in the lateral position cannot be excluded as explanations of PaO₂ values observed in the second OLV episode.

PaCO₂, especially at high values, influences the level HPV response (24). Thus, the PaCO₂ values of the studied patients were always maintained within normal limits in the different periods of blood gas measurements.

Another factor that may influence hypoxia during OLV is the side of the surgery. Left thoracotomy has a better PaO₂ during OLV than right thoracotomy, because the left lung normally receives 10 percent less cardiac output than the right lung (18). In our study, there were no statistical differences concerning the side of surgery in the three groups or among the three groups.

Gravity is a major, pharmacologically and physiopathologically, independent determinant of regional pulmonary blood flow distribution. The extent of blood flow redistribution depends on the local relationship between pulmonary arterial, venous, and airway pressures. In the lateral position, regional blood flow increases from the nondependent to the dependent thoracic wall (8). Unfortunately, the design of our study did not permit us to distinguish between the direct effects of HPV on blood flow and the effects of gravitational redistribution of blood flow.

The differences observed among the three groups of patients supports the hypothesis of Benumof et al. (25), who demonstrated, on a canine left lower lobe preparation, that if FIO₂ changes cause secondary changes in PaO₂, and in the mixed venous oxygen tension, then the mixed venous oxygen tension is a new and important determinant of the magnitude of HPV. This suggests that when one compartment FIO₂ is 1.0 and the other compartment is hypoxic, HPV in the hypoxic compartment is maximal.

The method used to ventilate the dependent lung is an important determinant of the blood flow distribution during OLV. High airway pressures can compress lung vessels, diverting blood flow from ventilated to nonventilated regions. However, hypoventilation of the dependent lung during OLV is associated with lower airway pressure, and the ventilated lung pulmonary vascular resistance may decrease, thus promoting HPV in the nonventilated lung (7). This mechanism of improved PaO₂ was unlikely in the present investigation, as ventilatory settings were kept constant, inspiratory airway pressures were not changed, and the mechanical characteristics of the dependent lung remained unaltered (Tables 2–4) after changing the position. These findings indicate that the improved PaO₂ cannot be attributed to an altered HPV caused by change in ventilatory pattern.

Surgical compression and retraction may also contribute to the passive reduction of nondependent lung blood flow (15). However, in our study, there was no mechanical effect on lung parenchyma, as the data were collected before chest opening. Therefore, surgical manipulation could not influence the amount of shunt occurring.

We conclude that, in addition to HPV, the augmented redistribution of perfusion caused by gravitational forces is probably responsible for the higher PaO₂ during OLV in the lateral position. The finding of significantly lower PaO₂ values occurring when OLV was initiated in the supine position may predict more frequent intraoperative hypoxemia when thoracic surgery requiring OLV is performed with patients in the supine position. If severe hypoxemia occurs during OLV in the lateral position, higher FIO₂ values might be used.

	Footnotes

 
The authors wish to dedicate this article to the memory of our colleague, Dr. Gizella Bardoczky, who passed away in July, 1998.

	References

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999