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CARDIOVASCULAR ANESTHESIA

Sequential Changes of Arterial Oxygen Tension in the Supine Position During One-Lung Ventilation

Department of Anesthesiology, Kurume University School of Medicine, Fukuoka, Japan

Address correspondence and reprint requests to Seiji Watanabe, MD, Department of Anesthesiology, Kurume University School of Medicine, 67 Asahimachi, Kurume, Fukuoka, 830-0011, Japan. Address e-mail to watanabe{at}med.kurume-u.ac.jp

	Abstract

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To investigate how surgical positions affect the severity and progress of hypoxemia during one-lung ventilation (OLV), we studied 33 adult patients undergoing right thoracotomy with left OLV. The patients were divided into three groups according to the positions during surgery as follows: the supine position (SP) group (n = 11), the left semilateral decubitus position (LSD) group (n = 9), and the left lateral decubitus position (LLD) group (n = 13). Analysis of arterial blood gases was sequentially determined every 5 min for 30 min during OLV (fractional ratio of inspiratory oxygen = 1.0) in each position. OLV was promptly terminated and switched to bi-lung ventilation if SpO₂ declined to 90%. PaO₂ progressively decreased with time in all three groups (P < 0.01). The incidence of termination of OLV within 30 min was higher in the SP group (82%), compared with that in the LSD (11%) and LLD (8%) groups (P < 0.01). Final PaO₂ (65 ± 12 mm Hg, mean ± SD, P < 0.01 versus LLD, P < 0.05 versus LSD) and SaO₂ (91% ± 4%, P < 0.01 versus LLD and LSD) at the termination of OLV in the SP group were the lowest. There was no difference between these values in the LSD and LLD groups (128 ± 54 mm Hg, 96% ± 2%, and 167 ± 69 mm Hg, 97% ± 4%, respectively) 30 min after the start of OLV. The time for PaO₂ to decrease to 200 mm Hg calculated from each regression curve was 354 s in the SP group, 583 s in the LSD group, and 798 s in the LLD group. The time for PaO₂ to decline to 100 mm Hg was 794 s in the SP group. In the regression curves of the LSD and LLD groups, the PaO₂ did not decrease to 100 mm Hg. Heart rate was slow at baseline in the SP group (P < 0.05 versus LSD), but other hemodynamic variables did not differ among the three groups throughout this study. The LSD was as effective as the LLD in avoiding life-threatening hypoxemia during OLV.

Implications: Close observation and prompt counteractions including termination of one-lung ventilation (OLV) are crucial for patients under OLV in the supine position, because life-threatening hypoxemia frequently occurs approximately 10 min after starting OLV, even under 100% oxygen inhalation. The left semilateral decubitus position was as effective as the left lateral decubitus position in avoiding life-threatening hypoxemia during OLV.

	Introduction

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Hypoxemia is a common problem of one-lung ventilation (OLV). In general, PaO₂ progressively decreases after the start of OLV toward a plateau value that corresponds to the ratio of ventilation and perfusion in the ventilated lung (1). The surgical posture markedly influences the plateau value and the deterioration speed of PaO₂ after switching to OLV, because gravity controls the distribution of pulmonary perfusion between dependent and nondependent lungs (2). Therefore, the lateral decubitus position is favored for open-chest surgery to maintain high PaO₂ during OLV. Fortunately, few surgeries require OLV in the supine position (SP).

Recently, micro-coagulation therapy with a radio frequency needle electrode was developed for the treatment of hepatic tumors (3). Surgeons request OLV in the SP when there are hepatic tumors in the upper segment facing the diaphragm, because the coagulation needle must be introduced in the center of the tumor through the diaphragm from the site of the chest cavity. Minimally invasive direct coronary bypass grafting also requires OLV in the SP during the time of harvesting the left internal mammalian artery (4). Severe hypoxemia may occur during OLV in SP. However, it is not clear how surgical postures clinically affect the severity and the onset time of hypoxemia during OLV. Therefore, we investigated sequential changes of PaO₂ from the start of OLV in the SP and compared them with the lateral and semilateral decubitus positions.

	Methods

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The protocol was approved by our ethics committee, and informed consent was obtained from all participants before starting the study. The subjects were 33 surgical patients undergoing micro-coagulation therapy (n = 20) and lobectomy or pneumonectomy for lung cancer (n = 13). All subjects were divided into three groups according to the postures during surgery as follows: the SP group (n = 11, 68.9 ± 4.4 yr), the left semilateral decubitus position (LSD) group (n = 9, 61.9 ± 9.2 yr), and the left lateral decubitus position (LLD) group (n = 13, 62.2 ± 13.3 yr). The angle of the line connecting the shoulders ranged from 0° to 10° to the horizontal line in the SP group, from 35° to 55° in the LSD group, and from 80° to 90° in the LLD group. The angle was measured from the cranial side after the positioning of the patients on the surgical table on their back. The 20 patients with hepatic tumors were divided into the SP group and the LSD group, and all 13 patients with lung cancer were enrolled in the LLD group. No patient had a history of respiratory failure or open-chest surgery. Preoperative pulmonary and hepatic functions were within normal limits in all patients. No particular laterality was detected in the lung field with chest roentgenography.

All patients were given IM atropine (0.5 mg) and hydroxydine (50 mg) 30 min before being transferred to the operating room. Anesthesia was induced with IV thiopental (5 mg/kg) and fentanyl (0.2 mg), supplemented by inhaled 1%–2% of sevoflurane in oxygen. A left-sided double-lumen endobronchial tube was placed after the administration of IV vecuronium (6 mg). Proper placement of the endobronchial tube was confirmed by bronchofiberscopy after positioning and at the end of surgery. The radial artery was cannulated for blood pressure monitoring. Subsequent anesthesia was maintained with additional fentanyl (0.2 mg) and inhaled sevoflurane as needed. End-tidal CO₂ and sevoflurane were monitored throughout the study. An epidural catheter was placed for postoperative pain management at the T5–6 or T6–7 vertebral level, but it was not used until the study was completed.

Electrocardiographic findings, radial artery pressure (AP), heart rate (HR), and SpO₂ were also monitored throughout the study. Arterial blood gas was determined as a baseline value under bi-lung ventilation (BLV) after the completion of the positioning but before the commencement of thoracotomy. Then, blood gas analysis was repeated every 5 min after switching to OLV for 30 min. If SpO₂ declined to 90%, arterial blood was sampled to determine the final value and OLV was promptly terminated for the patient’s safety. The times for PaO₂ to decline to 200 mm Hg (T_{200 mm Hg}) and 100 mm Hg (T_{100 mm Hg}) were calculated in each group using the corresponding regression curve (Figure 1). Fractional ratio of inspiratory oxygen (FIO₂) was set at 1.0 from at least 20 min before the start of OLV until completion of the study. Tidal volume was adjusted to 10–12 mL/kg during BLV and to 6–8 mL/kg during OLV. The intratracheal pressure was carefully managed not to exceed 25 cm H₂O during OLV. Respiratory rate was controlled to maintain PaCO₂ at approximately 35 mm Hg.

View larger version (24K): [in this window] [in a new window]   Figure 1. The figure presents sequential changes of PaO2 in the supine position (•, n = 11), left semilateral decubitus position (, n = 9), and left lateral decubitus position (, n = 13) plotted along the elapsed time after starting one-lung ventilation. Final PaO2 indicates the value at the termination of one-lung ventilation in each patient (see text in detail). The numerical values in each group are presented in Table 1. Some of the marks are not filled in the figure because of overlap. Each regression curve is drawn with sigmoidal curve fitting; the solid line represents the supine position, the dashed line represents the left semilateral decubitus position, and the dotted line represents the left lateral decubitus position. The time that elapsed for PaO2 to reach 200 mm Hg or 100 mm Hg was calculated by using the regression curves.

	Results

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SpO₂ decreased to 90% within the 30 min of OLV in 11 of the 33 patients, 9 of 11 in the SP group, 1 of 9 in the LSD group, and 1 of 13 in the LLD group. In these patients, OLV was returned to BLV in the middle of the predetermined period, and subsequent measurements were suspended. The incidence of SpO₂ declining to 90% within the 30 min of OLV was apparently higher in the SP group (82%, P < 0.01), compared with the LSD (11%) and LLD (8%) groups. PaO₂ markedly decreased after switching from BLV to OLV in all groups (P < 0.01). The decrease was rapid for the first 10 min and then slowed (Figure 1). Final PaO₂ was the lowest in the SP group (65 ± 12 mm Hg, P < 0.01 versus LLD, P < 0.05 versus LSD), while there was no difference in the final PaO₂ between the LSD and LLD groups (128 ± 54 and 167 ± 69 mm Hg, respectively). T_{200 mm Hg} obtained from each regression curve was 354 s in the SP group, 583 s in the LSD group, and 798 s in the LLD group. T_{100 mm Hg} was 794 s in the SP group. The regression curve for neither the LSD group nor for the LLD group reached the level of 100 mm Hg for PaO₂ during the 30 min of OLV (Figure 1). Arterial blood pH and PaCO₂ did not change with time in any group and differed among the three groups throughout this study (Table 1). Baseline HR was lower in the SP group than in the other groups (P < 0.05). There was no difference in HR after starting OLV. Systolic AP did not differ among the three groups throughout this study, although systolic AP increased 5 min after the start of OLV in all groups (Table 2). Values of hemoglobin did not differ among the three groups (SP, 11.3 ± 1.6 g/dL; LSD, 11.1 ± 1.6 g/dL; LLD, 11.5 ± 1.3 g/dL, pooled average in each group). End-tidal concentration of sevoflurane was not different among the three groups during the entire study (SP, 2.1% ± 0.8%; LSD, 2.4% ± 0.6%; LLD, 1.9% ± 0.7%, pooled average in each group).

	Discussion

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According to our data of T_{200 mm Hg} and T_{100 mm Hg}, hypoxemia appeared most rapidly in the SP group among the three groups. Pulmonary perfusion in the SP, which was accompanied by little gravity shift to the ventilated lung, would have augmented the dissolution of alveolar oxygen into the blood stream in the nonventilated lung. A rapid decrease in alveolar oxygen pressure leads to the rapid onset of arterial hypoxemia in the SP during OLV. We should be aware of the rapid onset time of hypoxemia during OLV in the SP.

The final PaO₂ is useful to estimate the pulmonary shunt ratio at steady state under OLV in each surgical position. According to the Nunn’s iso-shunt diagram, indicating the theoretical relationship between PaO₂ and FIO₂ (8), pulmonary shunt flow calculated from the each final PaO₂ was markedly higher in the SP group (45%–47%) than in the LSD or LLD groups (25%–28%). Thoracotomy progressively accelerates reduction of the functional residual capacity in the nonventilated lung until complete collapse of the lung. Bindslev et al. (9) reported that, in anesthetized humans, the maximal response of hypoxic pulmonary vasoconstriction (HPV) occurred within 15 minutes under OLV in the SP. HPV is a well known physiological compensation to reduce pulmonary perfusion in the nonventilated lung, leading to an improved ratio of ventilation to perfusion. HPV likely develops, especially in the SP, as a result of the severe hypoxemia.

When the nondependent lung is not ventilated in the LLD, both HPV and gravity would cooperate to reduce pulmonary blood flow in the nondependent lung from 40% to 20% of total blood flow. However, the shift of pulmonary blood flow by gravity is not expected in the SP, because there is no vertical distance between ventilated and nonventilated lungs. HPV may contribute to improve oxygenation much more in the SP than in the LLD or the LSD because of the development of severe hypoxia. However, the estimated shunt flow (45%–47%) under open-chest OLV in the SP was reported to be almost the same as that (45%) under open-chest BLV in the LLD (10). It is likely that the contribution of HPV to redistribute pulmonary perfusion under OLV in the SP is clinically insignificant. The final PaO₂ values indicate that gravity-dependency of pulmonary perfusion is a more dominant factor in the distribution of pulmonary perfusion than HPV in the nonventilated lung.

There is no direct relationship between cardiac output and HPV. However, a critically low level of mixed venous oxygen tension in the SP might secondarily affect the HPV response. HPV is induced by a decrease not only in alveolar oxygen tension, but also in mixed venous oxygen tension (11). Low cardiac output reduces mixed venous oxygen tension. If the reduction of mixed venous oxygen tension is sufficient to evoke a HPV response in the ventilated lung, the shift of pulmonary flow to the nonventilated lung would increase, resulting in severer hypoxemia during OLV. However, hemodynamic changes in our study did not likely contribute to the decrease of PaO₂ during OLV in the SP, because the HR and systolic radial AP did not differ among the three groups during OLV.

An end-tidal concentration of 1%–2% of sevoflurane, which was used for the maintenance of anesthesia, might have suppressed HPV during OLV, leading to exacerbation to hypoxemia. However, a recent study reported that HPV was well preserved at a clinical level of sevoflurane anesthesia and that inhibition of HPV was not a common characteristic in dogs under inhaled anesthesia (12).

We did not use thoracic epidural anesthesia to simplify the interpretation of hypoxemia that developed during OLV. Although thoracic epidural anesthesia was reported not to affect the pulmonary vascular tone primarily during lobar hypoxemia (13), it might activate HPV via hemodynamic changes secondary to the sympathetic block.

Although returning to BLV from OLV is the most effective countermeasure for treating hypoxemia, an expanded lung causes difficulties regarding the continuation of the surgical procedure. Correction of the surgical positioning from the SP to LSD by rotating the table is a simple method used to avoid severe hypoxemia during OLV, if the surgical procedure can be continued.

There are several alternatives to ameliorate hypoxemia during OLV in the SP. Selective blockade of the right middle and inferior lobes with a bronchial balloon blocker is one of the methods used to improve oxygenation during OLV (14). The addition of selective ventilation of the right lung helps to maintain a higher PaO₂ compared with the whole collapse of the right lung. However, pulmonary perfusion tends to distribute to the inferior and middle lobes rather than the upper lobe because of the gravity-dependent shift of pulmonary circulation, even in the SP. Further studies are needed to confirm whether additional upper lobe ventilation improves PaO₂ sufficiently to avoid life-threatening hypoxemia during OLV in the SP.

Artificial restriction of pulmonary blood flow toward the right lung may be useful to increase PaO₂ during OLV in the SP (15). Balloon occlusion of the right pulmonary artery (PA) may help reduce blood flow to the nonventilated lung. The size of the balloon of a standard PA catheter is too small to occlude the right PA, but might be large enough to occlude the inferior and middle pulmonary arteries. A PA catheter introduced blindly is often placed in the right PA. In our clinical experience, transesophageal echocardiography is helpful for the placement of a PA catheter to the targeted PA with visual observation.

Pharmacological interventions have been used to ameliorate hypoxemia encountered during OLV. Scherer et al. (15) showed that prostaglandin F₂ improves oxygenation during OLV in dogs. Moutafis et al. (7) reported that the combination of inhaled nitric oxide (NO) and IV almitrine was effective in avoiding hypoxemia during OLV in a patient in the LLD. Although the exact mechanism is unknown, IV almitrine could augment HPV, and inhaled NO might dilate constricted pulmonary vessels of the ventilated lung. The combination of the effects of inhaled NO and IV almitrine could be attributed to an improvement in the ventilation-perfusion relationships. Pharmacological modulations may improve oxygenation during OLV in the SP, although the effects have not yet been clinically studied.

There is a limitation in our study design. The patients were not fully assigned to each surgical position at random, and all the patients in the LLD group were those with lung cancer. This might affect the present results and our interpretation as a potential bias. However, 20 patients with hepatic tumors were randomly allocated between the SP and the LSD groups.

This study indicated that deterioration of the PaO₂ value during OLV in the SP was rapid and life threatening. Close monitoring of oxygenation and countermeasures to hypoxemia should be prepared for the patient’s safety. Simple rotation of the surgical table toward the LSD is beneficial for the amelioration of hypoxemia during OLV in the SP.

	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