There were no statistical differences between the two groups in PaCO (2), PvO2, SvCO2, mean airway pressure, HR, CaO2, or CvO2 in the three measurements conducted (Table 2).
In starting OLV, there was a significant decrease in PaO2, CaO2, and CvO2, and an increase in the Qs/Qt% in the two groups of patients. However, there were no significant changes when comparing the values of OLV + 15 with those of OLV + 30.
There were significant differences between the two groups with respect to Qs/Qt% in OLV + 15 and OLV + 30 (Table 2). The two groups presented values of Qs/Qt% similar to each other during the TLV. However, with OLV, there was an increase of these values in both groups: the intrapulmonary shunt increased to 32.1% in the GA group, and the TEA group showed a shunt of 37.4%. When comparing these values between the two groups in OLV + 15 and OLV + 30, there were significant differences (P < 0.05).
Two patients in the GA group and five in the TEA group had a peak Qs/Qt% >or=to40% during OLV. The shunt increased by 76% in the GA group and by 115% in the other group during the OLV (P < 0.05). In analyzing the Qs/Qt% of the patients, depending on the operated side, we observed that during OLV, in the GA group, we obtained values of 29.9% and 34.2% in the operations on the left side and right side, respectively. In the TEA group, these values were 36.7% and 38.3% for the left operated side and right operated side, respectively, during OLV.
There were no complications associated with the TEA technique (epidural hematoma, neurological damage, etc.). In 15 patients, there was a significant decrease in systemic arterial blood pressure with the administration of local anesthetics in the epidural space, which was treated by administering a dose of 10 mg of IV ephedrine. In all these cases, this drug was administered before the start of OLV. In the GA group, ephedrine administration was not required at any time.
OLV creates an obligatory transpulmonary shunt through the atelectatic lung. Passive (gravity and surgical interferences) and active (HPV) mechanisms minimize the diversion of blood flow to the atelectatic lung and prevent the PaO2 from decreasing; however, the most significant diversion of blood flow to the dependent lung is caused by HPV .
We demonstrated that when comparing both anesthetic techniques, using combined anesthesia (GA plus TEA with local anesthetics) for thoracic surgery produces a larger decrease in the PaO2 and a larger increase in the intrapulmonary shunt during OLV than does IV GA.
In a preliminary study, the effects of TEA and GA on PaO2 and intrapulmonary shunt were compared. The values for PaO2 were decreased by adding local anesthetics by means of a thoracic epidural catheter; however, with so few patients in the group (n = 8), it is impossible to extract any definite conclusions for statistic purposes .
The reason for the decrease PaO2 is uncertain: the pulmonary vasculature is innervated by the autonomic nervous system. Stimulation of sympathetic nerves to the lung causes an increase in PVR produced by activation of alpha-receptors in the pulmonary vascular bed. The mediator released from sympathetic nerve endings is norepinephrine . Blockade of the sympathetic nervous system with alpha-adrenergic antagonists or beta-adrenergic agonists attenuates HPV, whereas the beta-adrenergic antagonists increase this response.
Perhaps block of the activity of the thoracic sympathetic over the vascular pulmonary response is a factor. In these studies, TEA did not affect the primary pulmonary vascular tone during OLV, but it slightly enhanced the diversion of blood flow from the hypoxic lobe to the other well oxygenated areas of the lung . However, Kazemi et al.  reported a reduction in the hypoxic response of the lung after sympathectomy. The problem is that most these studies were not performed under the same conditions as those in the present study (e.g., anesthetized patients, lateral decubitus position, and atelectatic lung).
Other factors that could decrease PaO2 are the cardiovascular and hemodynamic effects of TEA: decrease in HR, MAP, stroke volume, and cardiac output (CO) due to blockade of the sympathetic nervous system. Furthermore, the systemic effects of the absorption of the local anesthetics can contribute to circulatory changes, such as a decrease in CO [4,10]. We do not believe that the best oxygenation during OLV in the GA group could be due to a decrease in CO, because this mechanism fundamentally affects the HPV through variations in the SvO2 and PvO2. In our patients, we observed values very similar in the SvCO2 and PvO2 in the two groups of patients during the study. However, there were significant differences in the values of PaO2 and the Qs/Qt% in OLV + 15 and OLV + 30.
When the nondependent lung is ventilated in lateral decubitus position, it receives approximately 40% pulmonary blood flow . Our patients (both groups together) had an average shunt of 18.8% during TLV with the patient in the lateral decubitus position. If this shunt was equally distributed between the nondependent and dependent lungs and if blood flow to the atelectatic nondependent lung was not acutely decreased, then the shunt during OLV would have been 49.4% (18.8/2% + 40%) for all our patients (because the same number of right- and left-side lung operations were performed). However, in the GA group, the shunt was 31%, versus 39.5% in the TEA group. The most likely mechanism of the acute decrease in blood flow to the atelectasic nondependent lung is HPV . If so, HPV was better conserved in the GA group. In the TEA group, the lower PaO2 and higher shunt values during OLV are consistent with a greater depression of HPV, probably due to sympathectomy and/or systemic absorption of local anesthetics.
Another unlikely possible mechanism for acute decrease in nondependent lung blood flow during clinical OLV could be surgical interference. However, we had the cooperation of our surgeons to ensure that no manipulation, retraction, or clamping of the other lung occurred during the measurements. We felt that the PaCO2 was well controlled. The patients from the TEA group showed values slightly greater than those of the GA group, although not statistically significant. Yet, we know that hypercapnia during OLV seems to act as a vasoconstrictor by selectively increasing ventilated lung pulmonary vascular resistance (enhanced directly regional HPV) . High airway pressures in the dependent lung may counteract HPV in the non-dependent lung by diverting blood flow away from the ventilated lung, thereby increasing the pulmonary shunt fraction . However, the average values of airway pressures in both groups are similar.
HPV is a primary regulator of blood flow distribution in the atelectatic lung, of which the alveolar oxygen tension is the primary stimulus, but with atelectasis, the oxygen tension of most lung tissue approaches the mixed venous oxygen tension. Domino et al.  showed that when PvO2 was normal (46 +/- 2 mm Hg) or lower, HPV occurred, and approximately 50% of the blood flow was diverted away from the atelectatic lung; however, when PvO2 was high (i.e., 100-140 mm Hg), HPV was inhibited. For ethical reasons, venous samples were drawn from the right atrium in this study to obviate the need for pulmonary artery catheterization. Antman et al.  indicated that the average difference between pulmonary artery and right atrial oxygen concentration was 0.34% +/- 2.5 SD. Berridge et al.  suggest that ScvO2 is a good estimate of SvO2, even when the exact position of the central venous catheter is unknown. In our patients, the values of PvO2, as well as those of SvCO2, stayed in a similar range in the two groups of patients, thereby leading us to think that this could not be the cause of the poor oxygenation and higher shunt of the TEA group. Finally, the administration of ephedrine was only necessary in the TEA group. This explains the similarity of the compared values of HR and MAP in the two groups, but it does not explain poorer oxygenation, because ephedrine seems to produce an increase in PaO2 without altering the intrapulmonary shunt in OLV during thoracic surgery .
We conclude that vasodilation by sympathetic blockade counteracts HPV and thereby produces a larger shunt and a decrease in oxygenation during the OLV. Although TEA likely facilitates early extubation of patients undergoing thoracic surgery, we cannot confirm this conclusion. The anesthesiologist who extubated the trachea knew which anesthetic technique was used, which could cause bias.
In summary, TEA during OLV with the patient in the lateral decubitus position increases the intrapulmonary shunt and decreases the PaO2. We conclude that TEA cannot be recommended in patients undergoing OLV.
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