Two-Lung and One-Lung Ventilation in Patients - Anesthesia ...

Two-Lung and One-Lung Ventilation in Patients with 

Chronic Obstructive Pulmonary Disease: The Effects of 

Position and FIO 2 

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 

We compared the effects of position and fraction of inspired 

oxygen (Fio 2) on oxygenation during thoracic 

surgery in 24 consenting patients randomly assigned to 

receive an Fio 2 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. Pao 2 decreased during OLV compared with 

TLV in both the supine and lateral positions. In all three 

groups, Pao 2 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 

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 authors wish to dedicate this article to the memory of our 

colleague, Dr. Gizella Bardoczky, who passed away in July, 1998. 

Accepted for publication September 8, 1999. 

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. 

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 Pao 2 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. 

(Anesth Analg 2000;90:35–41) 

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 (Fio 2) 

values during OLV of patients with coronary obstructive 

pulmonary disease (COPD) who are scheduled for lung 

surgery. 

Methods 

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 Fio 2 of 0.4 (Group 0.4 eight patients), 

0.6 (Group 0.6 eight patients), or 1.0 (Group 

©2000 by the International Anesthesia Research Society 

0003-2999/00 Anesth Analg 2000;90:35–41 35

36 CARDIOVASCULAR ANESTHESIA BARDOCZKY ET AL. ANESTH ANALG 

POSITION AND Fio 2 DURING OLV 2000;90:35–41 

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 g 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 CO 2 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 endexpiratory 

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. Pao 2, 

alveolar-arterial oxygen tensions difference [P(A-a)o 2] 

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 Fio 2 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 

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). 

Effects of the Position 

During the period of TLV, the position of the patient 

(supine versus lateral) did not significantly influence 

the variables related to gas exchange in the three 

groups of patients (Tables 2–4). 

In contrast, in the OLV assessment stages, the Pao 2 

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)o 2 

showed similarly significant changes, but in the opposite 

direction (Tables 2–4 and Figure 1). 

While turning the patients from the supine into the 

lateral position, no changes were observed regarding 

the variables related to the mechanical properties of 

the respiratory system (peak inspiratory airway pressure, 

end-inspiratory airway pressure, and intrinsic 

positive end-expiratory pressure), during neither TLV, 

nor OLV (not significant, Wilcoxon matched-pair test). 

Effects of FIO 2 

In the three groups of patients ventilated with different 

Fio 2 values, the differences of Pao 2 values observed 

between the supine and lateral TLV periods 

were not significant. In contrast, the increases of Pao 2

ANESTH ANALG CARDIOVASCULAR ANESTHESIA BARDOCZKY ET AL. 37 

2000;90:35–41 POSITION AND Fio 2 DURING OLV 

Table 1. Demographic Characteristics, Preoperative Pulmonary Function Studies, and Preoperative Arterial Blood Gas 

Values of 24 Patients During Thoracic Surgery 

values observed between the lateral and supine OLV 

were significantly higher when the Fio 2 was higher 

(P 0.02, Kruskall-Wallis test) (Figure 2). 

Pao 2 was decreased and P(A-a)o 2 was increased 

during OLV in comparison with the TLV values in 

both the supine and the lateral positions and at every 

level of Fio 2. However, these changes were more pronounced 

in the supine position (Group 0.4: 61 [17–132] 

vs 19 [5–39]) mm Hg; Group 0.6: 68 [9–150] vs 14 

[4–44] mm Hg; Group 1.0: 107 [5–268] vs 65 [18–205] 

mm Hg; P 0.05, Wilcoxon’s matched pair test). 

When turning the patients from the supine to the 

lateral position, Pao 2 increased significantly when 

comparing the periods of OLV. These Pao 2 increases 

(lateral-supine) were significantly larger when higher 

Fio 2 values were used (Figure 2). 

When comparing the periods of TLV, no significant 

differences in Pao 2 increases (lateral-supine) were 

found, regardless of the Fio 2 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 

Fio 2 

Group 0.4 (n 8) Group 0.6 (n 8) Group 1.0 (n 8) 

Age (yr) 59 (46–62) 60 (24–72) 64 (44–78) 

Height (cm) 175 (169–183) 169 (154–180) 167 (162–184) 

Weight (kg) 75 (51–105) 69 (55–86) 65 (56–98) 

FEV1 (% predicted) 76 (35–81) 79 (51–84) 80 (53–85) 

FRC (% predicted) 152 (122–195) 145 (121–182) 145 (122–181) 

RV (% predicted) 170 (128–177) 156 (131–196) 151 (124–193) 

TLC (% predicted) 115 (99–131) 115 (98–138) 112 (77–135) 

Paco 2 (mm Hg, room air, supine) 37 (31–41) 37 (29–43) 40 (36–47) 

Pao 2 (mm Hg, room air, supine) 78 (66–90) 82 (68–102) 72.5 (64–95) 

Data are median (range). 

Fio 2 fraction of inspired oxygen, FEV1 forced expiratory volume in 1 s, FRC functional residual capacity, RV residual volume, TLC total lung 

capacity. 

Table 2. Respiratory Mechanics and Gas Exchange Data Obtained During TLV and OLV with Patients in the Supine and 

in the Lateral Positions, Fio 2 0.4 (n 8) 

Supine Lateral 

TLV OLV TLV OLV 

Ppeak (cm H 2O) 21 (12–35) 29 (17–40) 20 (12–35) 29 (17–42) 

Pplateau (cm H 2O) 14 (7–23) 18 (9–26) 13 (9–19) 18 (12–24)† 

PEEPi (cm H 2O) 1.5 (0–2) 2.5 (0–6) 1 (0–3) 3 (0–8) 

Paco 2 (mm Hg) 38 (34–47) 39 (32–49) 40.5 (35–47) 38.5 (36–45) 

Pao 2 (mm Hg) 124 (81–240) 63 (57–144) 132 (102–296) 101 (72–201)‡ 

P(A-a)o 2 (mm Hg) 118 (12–170) 181 (94–197) 117 (16–166) 131 (44–177)‡ 


TLV two-lung ventilation, OLV one-lung ventilation, Ppeak peak inspiratory airway pressure, Pplateau end-inspiratory airway pressure, PEEPi 

intrinsic positive end-expiratory pressure, P(A-a)o 2 alveolar-arterial oxygen tension difference. 

* P 0.02, † P 0.05 (OLV versus TLV). 

‡ P 0.02 (lateral versus supine OLV). 

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 Pao 2 and lower 

P(A-a)o 2 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 



Ppeak (cm H 2O) 18 (15–22) 23 (16–35) 19 (12–32) 24 (16–32)† 

Pplateau (cm H 2O) 13 (11–17) 15 (12–23) 14 (9–17) 15 (11–30) 

PEEPi (cm H 2O) 1 (0–4) 2 (0–6) 1.5 (0–4) 3 (0–6) 

Paco 2 (mm Hg) 40 (36–52) 39 (31–46) 38 (35–46) 41 (35–51) 

Pao 2 (mm Hg) 256 (172–391) 155 (114–235)† 289 (225–353) 268 (162–311)‡ 

P(A-a)o 2 (mm Hg) 136 (101–198) 196 (163–254)† 126 (97–213) 151 (123–234)‡ 










Ppeak (cm H 2O) 17 (16–21) 24 (14–32)* 19 (15–24) 24 (17–29)† 

Pplateau (cm H 2O) 15 (8–18) 15 (8–19) 16 (9–19) 18 (11–22) 

PEEPi (cm H 2O) 1.5 (0–3) 2 (0–4) 1.5 (0–4) 2.5 (0–6) 

Paco 2 (mm Hg) 39 (33–48) 38 (36–52) 38 (34–50) 40 (34–51) 

Pao 2 (mm Hg) 472 (232–591) 301 (216–422)† 492 (336–600) 486 (288–563)‡ 

P(A-a)o 2 (mm Hg) 185 (151–382) 267 (212–446)† 173 (144–376) 190 (153–396)‡ 






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. 

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, Pao 2 will 

decrease and P(A-a)o 2 will increase. Indeed, in this 

study, when OLV was initiated in the supine position, 

Pao 2 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)o 2 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



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. 

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 Pao 2 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 Pao 2 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 Pao 2 

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 Fio 2 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 Pao 2 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. Pao 2 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 Fio 2 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 Fio 2 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 closedchest 

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 Pao 2 values 

observed in the second OLV episode. 

Paco 2, especially at high values, influences the level 

HPV response (24). Thus, the Paco 2 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 Pao 2 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 Fio 2 changes cause secondary 

changes in Pao 2, 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 Fio 2 

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 Pao 2 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 

Pao 2 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 

Pao 2 during OLV in the lateral position. The finding of 

significantly lower Pao 2 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 Fio 2 values might 

be used. 

References 

1. Pasque MK, Cooper JD, Kaiser L, et al. Improved technique for 

bilateral lung transplantation: rationale and initial clinical experience. 

Ann Thorac Surg 1990;49:785–91. 

2. Cooper JD, Patterson GA, Sundaresan RS, et al. Results of 150 

consecutive bilateral lung volume reduction procedures in patients 

with severe emphysema. J Thorac Cardiovasc Surg 1996; 

112:1319–30. 

3. Lima O, Ramos L, DiBiasi P, Judice L. Median sternotomy for 

bilateral resection of emphysematous bullae. J Thorac Cardiovasc 

Surg 1981;82:892–7. 

4. Wasnick JD, Acuff T. Anesthesia and minimally invasive thoracoscopically 

assisted coronary artery bypass: a brief clinical 

report. J Cardiothorac Vasc Anesth 1997;11:552–5. 

5. Urschel HC, Razzuk MA. Median sternotomy as a standard 

approach for pulmonary resection. Ann Thorac Surg 1986;41: 

130–4. 

6. Benumof JL. One-lung ventilation and hypoxic pulmonary 

vasoconstriction: implications for anesthetic management. 

Anesth Analg 1985;64:821–33. 

7. Benumof JL. Physiology of the lateral decubitus position, the 

open chest and one-lung ventilation. In: Kaplan JA, ed. Thoracic 

anesthesia. New York: Churchill Livingstone, 1993:193–221. 

8. Arborelius M, Lundin G, Svanberg L, Defares JG. Influence of 

unilateral hypoxia on blood flow through the lungs in man in 

lateral position J Appl Physiol 1960;15:595–7. 

9. Fiser WP, Friday CD, Read RC. Changes in arterial oxygenation 

and pulmonary shunt during thoracotomy with endobronchial 

anesthesia. J Thorac Cardiovasc Surg 1982;83:523–31. 

10. Hannalah MS, Benumof JL, McCarthy PO, et al. Comparison of 

three techniques to inflate the bronchial cuff of left polyvinylchloride 

double-lumen tubes. Anesth Analg 1993;77:990–4. 

11. Deleted in proof. 

12. Rehder K, Wenthe FM, Sessler AD. Function of each lung during 

mechanical ventilation with ZEEP and with PEEP in man 

anesthetized with thiopental-meperidine. Anesthesiology 1973; 

39:597–606. 

13. Gayes JM, Emery RW. The MIDCAB experience: a current look 

at evolving surgical and anesthetic approaches. J Cardiothorac 

Vasc Anesth 1997;11:625–8. 

14. Marshall BE. Hypoxic pulmonary vasoconstriction. Acta Anaesthesiol 

Scand 1990;34:37–41. 

15. Alfery DD, Benumof JL, Trousdale FR. Improving oxygenation 

during one-lung ventilation in dogs: the effects of positive endexpiratory 

pressure and blood-flow restriction to the nonventilated 

lung. Anesthesiology 1981;55:381–5. 

16. Boldt J, Muller M, Uphus D, et al. Cardiorespiratory changes in 

patients undergoing pulmonary resection using different anesthetic 

management techniques. J Cardiothorac Vasc Anesth 

1996;7:854–9. 

17. Rehder K, Knopp TJ, Sessler AD, Didier EP. Ventilationperfusion 

relationship in young healthy awake and 

anesthetized-paralyzed man. J Appl Physiol 1979;47:745–53. 

18. Slinger P, Suissa S, Adam J, Triolet W. Predicting arterial oxygenation 

during one-lung ventilation with continuous positive 

airway pressure to the nonventilated lung. J Cardiothorac 

Anesth, 1990;4:436–40. 

19. Barker SJ, Clarke C, Trivedi N, et al. Anesthesia for thoracoscopic 

laser ablation of bullous emphysema. Anesthesiology 

1993;78:44–50. 

20. Benumof JL. Intermittent hypoxia increases lobar hypoxic pulmonary 

vasoconstriction. Anesthesiology 1983;58:399–404. 

21. Carlsson AJ, Bindslev L, Santesson J, et al. Hypoxic pulmonary 

vasoconstriction in the human lung: the effect of prolonged 

unilateral hypoxic challenge during anaesthesia. Acta Anaesthesiol 

Scand 1985;29:346–51. 

22. Tucker A, Reeves JT. Non-sustained pulmonary vasoconstriction 

during acute hypoxia in anesthetized dogs. Am J Physiol 

1977;42:889–99. 

23. Domino K, Chen L, Alexander C, et al. Time course and responses 

of sustained hypoxic pulmonary vasoconstriction in the 

dog. Anesthesiology 1984;60:562–6. 

24. Benumof JL, Mathers JM, Wahrenbrock EA. Cyclic hypoxic 

pulmonary vasoconstriction induced by concomitant carbon dioxide 

changes. J Appl Physiol 1976;41:466–9. 

25. Benumof JL, Pirlo AF, Johanson I, Trousdale FR. Interaction of 

PVO2 with PAO2 on hypoxic pulmonary vasoconstriction. 

J Appl Physiol 1981;51:871–4.

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