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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.
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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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.
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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 (T200 mm Hg) and 100 mm Hg (T100 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.
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, 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
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Analyses were performed with a statistical package (SPSS Ver 7.5.2J; SPSS, Chicago, IL). Frequency ratio of decreasing into hypoxemia (determined when SpO2 declined to 90%) was examined among the groups by Pearson’s
2 analysis. Difference in the variable at each point of measurement was also tested among groups by using multiple comparison with Bonferroni’s correction. Sequential changes of each variable with time in each group were confirmed by using multiple comparison using a general linear model (type IV sums of squares) with the Dunnett test. Differences were considered significant at P < 0.05. All data were expressed as mean ± SD. |
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). T200 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. T100 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).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Life-threatening hypoxemia (SpO2 < 90%) frequently develops approximately 10 minutes after the start of OLV in the SP, although the value of the final PaO2 did not decrease to the life-threatening level in most cases in the LSD and LLD groups. PaO2 values during OLV varied widely in previous investigations, probably as a result of differences in surgical posture, anesthetic management, and ventilation techniques (5,6). The time of the PaO2 measurements after the start of OLV is also responsible for the indefinite PaO2 after the start of OLV, because PaO2 decreases progressively with time toward a steady value (7). We allowed at least 20 minutes between completion of surgical positioning and the start of OLV. Shift of pulmonary perfusion by gravity would have been completed at the start of measurement in our study.
According to our data of T200 mm Hg and T100 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.
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References |
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- 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, 1991:193–221.
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Hakim TS, Dean GW, Lisbona R. Effect of body posture on spatial distribution of pulmonary blood flow. Appl Physiol 1988;64:1160–70.
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Rossi S, Buscarini E, Garbagnati F, et al. Percutaneous treatment of small hepatic tumors by an expandable RF needle electrode. AJR 1998;170:1015–22.
[Abstract/Free Full Text] - Greenspun HG, Adourian UA, Fonger JD, et al. Minimally invasive direct coronary artery bypass (MIDCAB): surgical techniques and anesthetic considerations. J Thorac Cardiovasc Anesth 1996;4:507–9.
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Abe K, Shimizu T, Takashina M, et al. The effects of propofol, isoflurane, and sevoflurane on oxygenation and shunt fraction during one-lung ventilation. Anesth Analg 1998;87:1164–9.
[Abstract/Free Full Text] - Katz Y, Zisman E, Isserles SA, et al. Left, but not right, one-lung ventilation causes hypoxemia during endoscopic transthoracic sympathectomy. J Cardiothoracic Vasc Anesth 1996;10:207–9.[Web of Science][Medline]
- Moutafis M, Lie N, Dalibon N, et al. The effects of inhaled nitric oxide and its combination with intravenous Almitrine on PaO2 during one-lung ventilation in patients undergoing thoracoscopic procedures. Anesth Analg 1997;85:1130–5.[Abstract]
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Lawler PGP, Nunn JF. A reassessment of the validity of the iso-shunt graph. Br J Anaesth 1984;56:1325–35.
[Abstract/Free Full Text] - Bindslev L, Jolin Å, Hedenstierna G, et al. Hypoxic pulmonary vasoconstriction in the human lung: effect of repeated hypoxic challenges during anesthesia. Anesthesiology 1985;62:621–5.[Web of Science][Medline]
- Marshall B, Marshall C. Continuity of response to hypoxic pulmonary vasoconstriction. Physiol 1980;49:189–96.
- Domino KB, Wetstein L, Glassor SA, et al. Influence of mixed venous oxygen tension (PVO2) on blood flow to atelectatic lung. Anesthesiology 1983;59:428–34.[Web of Science][Medline]
- Lesitsky M, Davis S, Murry PA. Preservation of hypoxic pulmonary vasoconstriction during sevoflurane and desflurane anesthesia compared to the conscious state in chronically instrumented dogs. Anesthesiology 1998;89:1501–8.[Web of Science][Medline]
- Ishibe Y, Shiokawa Y, Umeda T, et al. The effect of thoracic epidural anesthesia on hypoxic pulmonary vasoconstriction in dogs: an analysis of the pressure-flow curve. Analg 1996;82:1049–55.[Abstract]
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Scherer R, Vigfusson G, Lawin P. Pulmonary blood flow reduction by prostaglandin F2 and pulmonary artery balloon manipulation during one-lung ventilation. Scand 1986;30:2–6.
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