We found in the present study that rSO2 increased after the pneumoperitoneum and further increased temporarily after the steep Trendelenburg position, and decreased afterwards. These changes were along with the alteration of MAP and PaCO2. However, the changes did not correlate with the changes of HR, PaO2, or SaO2.
The cerebral perfusion pressure is regarded as MAP minus central venous pressure (or intracranial pressure) . A previous study reported that central venous pressure increased by 2–5 mmHg during the pneumoperitoneum [8, 9]. On the other hand, another previous study reported that MAP did not change after the pneumoperitoneum . Thus, cerebral perfusion pressure should slightly decrease after the pneumoperitoneum. Contrary to the previous study , another study reported that pneumoperitoneum with a consequent increase in intracranial pressure produced systemic hypertension. . Our study concurs with the latter study that MAP increased after the pneumoperitoneum. In patients in this study, cerebral autoregulation should be intact. Owing to the cerebral autoregulation, the cerebral blood flow is maintained constantly within a wide range of cerebral perfusion pressure. It is reasonable to assume that cerebral perfusion pressure remained normal level after the pneumoperitoneum. rSO2 reflects cerebral perfusion . Therefore, we assumed that rSO2 would be unchanged after the pneumoperitoneum. However, rSO2 increased after the pneumoperitoneum in this study. In steady state, cerebral blood flow is maintained constant with static cerebral autoregulation . In acute change in blood pressure, cerebral blood flow is compensatory adjusted by dynamic cerebral autoregulation [12, 13]. However, there is a time lag between the rise in blood pressure and the activation of dynamic cerebral autoregulation . If blood pressure increased suddenly, cerebral blood flow may increase transiently. As a result, rSO2 increased.
After the Trendelenburg position combined with CO2 pneumoperitoneum, rSO2 increased initially. Some studies reported that central venous pressure increased by 10–16 mmHg during the Trendelenburg position combined with CO2 pneumoperitoneum [15,16,17]. On the other hand, blood pressure also increased by 10–15 mmHg during the Trendelenburg position combined with CO2 pneumoperitoneum in the previous studies [2, 15, 17]. In agreement with those studies, we observed that MAP increased by 16–18 mmHg at 5–10 min after the Trendelenburg position combined with CO2 pneumoperitoneum compared with that before the pneumoperitoneum. Change in cerebral perfusion pressure immediately after the Trendelenburg position was 16–18 mmHg (MAP change) minus 10–16 mmHg (assumed CVP change) [15,16,17]. The value was 0–8 mmHg. Whereas change in cerebral perfusion pressure after pneumoperitoneum was 14 mmHg (MAP change) minus 2–5 mmHg (assumed CVP change) [8, 9]. The value was 9–12 mmHg. Therefore, it is assumed that the cerebral perfusion pressure did not increase after the Trendelenburg position compared with that at the CO2 pneumoperitoneum. Cerebral perfusion pressure was not involved in the transient increase in rSO2 just after the Trendelenburg position combined with CO2 pneumoperitoneum. Schramm et al. reported that cerebral autoregulation deteriorated with Trendelenburg position combined with pneumoperitoneum . Garrett et al.  reported that the cerebral blood flow velocity decreased when the posture was changed from the supine to the seated position. Postural change influences cerebral blood flow. Based on those previous studies, cerebral blood flow increased temporarily when the posture was changed from the supine to the Trendelenburg position. Due to transient increase in cerebral blood flow, rSO2 initially increased after the Trendelenburg position combined with CO2 pneumoperitoneum.
Cerebral blood flow varies with PaCO2. We recently reported that changes in rSO2 significantly correlated with changes in PaCO2. . Abdominally insufflated carbon dioxide is absorbed into systemic circulation and is exhaled with ventilation. We attempted to adjust tidal volume and respiratory rate to maintain PaCO2 at 40 ± 5 mmHg. However, PaCO2 increased significantly after the pneumoperitoneum. Thus, rSO2 increased along with the rise in PaCO2. rSO2 gradually decreased after the pneumoperitoneum combined with the Trendelenburg position. Nevertheless, PaCO2 remained high level during the pneumoperitoneum combined with the Trendelenburg position. Although there was a correlation between rSO2 and PaCO2, PaCO2 may be less involved in the change of rSO2. On the other hand, MAP was observed highest at 5 min after the Trendelenburg position (T5 in the Fig. 2a) and it decreased thereafter. Head-down position in combination with a pneumoperitoneum impairs cerebral autoregulation over time . It is likely that rSO2 changes with alterations in mean blood pressure rather than change of PaCO2.
Cerebral oxygenation can be monitored by rSO2 . Cerebral oxygenation may influence the change of rSO2 in this study. According to the manufacturer, rSO2 reflects 25% arterial and 75% venous portion of blood. If cerebral oxygen consumption decreased, venous blood oxygen could be increased. As a result, rSO2 may have increased. However, BIS was unchanged after the induction of anesthesia. There were no factors that involved the decline in cerebral oxygen consumption after the pneumoperitoneum. Furthermore, PaO2 was significantly decreased after pneumoperitoneum. Therefore, oxygenation status was unlikely to participate in the rise of rSO2.
In this study, data before anesthesia were obtained under room air breathing and other data were measured under oxygen inspiration. Therefore, arterial oxygen saturation before anesthesia was significantly lower than that after the induction of anesthesia. However, rSO2 before anesthesia was significantly higher than that after the induction of anesthesia. Mean arterial blood pressure also declined after the induction of anesthesia. In addition, cerebral metabolic rate decreases after the induction of anesthesia that results in decrease in cerebral blood flow . This phenomenon may indicate that rSO2 is firmly affected by MAP and cerebral blood flow rather than arterial oxygenation status in this study situation.
Cerebral autoregulation, which is expected to keep cerebral blood flow constant, mainly depends on cerebral perfusion pressure . If cerebral perfusion pressure were too low (below the lower limit of autoregulation), cerebral blood flow might depend on MAP . When the cerebral perfusion pressure was below the lower limit of autoregulation, cerebral blood flow should have been changed directly with the fluctuation of MAP. In this situation, rSO2 altered along with the change of MAP though decrease in blood pressure below the lower limit of autoregulation was not observed in this study. Nevertheless, individual variation in MAP while anesthetized and the lower limit of autoregulation might make the rSO2-MAP relationship different for different individuals.
In this study, PaO2 decreased after pneumoperitoneum. A previous study suggested that pneumoperitoneum elevated diaphragm that can lead to basilar atelectasis, with resulting right to left shunt formation . Atelectasis caused by pneumoperitoneum may contribute to the decrease of PaO2. After the Trendelenburg position, PaO2 increased. Some studies reported that peak and mean airway pressure increased after the Trendelenburg position [25, 26]. Elevated airway pressure may have contributed to reduce atelectasis. As a result, PaO2 increased.
This study has some limitations. First, we did not measure central venous pressure because central venous catheterization is an invasive method and not always necessary for robotic-assisted endoscopic prostatic surgery. In many studies, central venous pressure was increased after pneumoperitoneum [8, 9] and the Trendelenburg position combined with pneumoperitoneum. [15,16,17] Therefore, the present study was based on an assumption that central venous pressure increased in this study. Second, cerebral blood flow was not measured. Transcranial Doppler can be utilized to assess the cerebral blood flow. However, due to the protection pads that supported the patient during the surgery, there was no space on the patient’s head for the Doppler probe attachment. Third, extracranial contamination affects rSO2. Davie et al. reported that the extracranial contamination potentially affected rSO2 . They also indicated that forehead skin blood made an impact on rSO2 . Trendelenburg position may cause venous stasis, which could result in the increase of venous portion of blood. Therefore, Trendelenburg position may have affected the relative arterial and venous content of the forehead skin blood. Extracranial contamination might have influenced rSO2 in this study.