دانلود رایگان مقاله انگلیسی اثر بیهوشی دسولفوران – رمی فنتانیل در مقایسه با پروپوفول – رمی فنتانیل بر روی اکسیژن شریانی در طی تهویه یک ریه ای برای جراحی توراکوسکوپی به همراه ترجمه فارسی
عنوان فارسی مقاله | اثر بیهوشی دسولفوران – رمی فنتانیل در مقایسه با پروپوفول – رمی فنتانیل بر روی اکسیژن شریانی در طی تهویه یک ریه ای برای جراحی توراکوسکوپی |
عنوان انگلیسی مقاله | Effect of desflurane-remifentanil vs. Propofol-remifentanil anesthesia on arterial oxygenation during one-lung ventilation for thoracoscopic surgery: a prospective randomized trial |
رشته های مرتبط | پزشکی، بیهوشی، قلب و عروق و هوشبری |
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نشریه | بیهوشی – Anesthesiology |
مجله | BMC |
سال انتشار | 2017 |
کد محصول | F635 |
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فهرست مقاله: مقدمه روشها نتایج بحث نتیجه گیری |
بخشی از ترجمه فارسی مقاله: بحث بر طبق گزارشهای قبلی (21-28)، دادههای ما نشان دهنده کاهش در PaO2 در طی اولین 30 دقیقه OLV و بهبود تدریجی در هر دو گروه میباشد (شکل 2). در طی بیهوشی دسولفوران، PaO2 به طور معنی داری پس از 15 دقیقه OLV در مقایسه با حالت قبل از OLV کاهش یافته و سپس به تدریج به سطوح قبل از OLV در 60 دقیقه بهبود یافت. از سوی دیگر، اکسیژن شریانی در طی بیهوشی پروپوفول در سرتاسر مطالعه، به خوبی حفظ شد. هیچ یک از نقاط زمانی در طی OLV، PaO2 پایین را در مقایسه با حالت قبل از OLV در گروه پروپوفول نشان ندادند. |
بخشی از مقاله انگلیسی: Discussion In this study, oxygenation under desflurane-remifentanil balanced anesthesia was lower than that under propofolremifentanil TIVA during OLV for video-assisted thoracoscopic surgery. This is the first reported clinical trial in which desflurane was shown to impair oxygenation during OLV compared to TIVA in lung cancer patients undergoing thoracoscopic lung surgery. Recently, many surgical procedures have been performed using less-invasive approaches. Large percentages of thoracic operations for lung resection are performed through video-assisted thoracoscopic surgery. Thus, the durations of both the operation and postoperative recovery period have been shortened. Both desflurane and propofol are relatively new anesthetics with short-acting properties characterized by rapid onset and offset due to their low blood gas partition coefficient and low context-sensitive half time, respectively. Therefore, they are highly attractive and offer fast-track anesthesia and earlier recovery for postoperative rehabilitation in minimal invasive thoracic surgery. However, the roles of these modern anesthetics in management of oxygenation during OLV remain unclear in humans. In animal studies, inhalational anesthetics are known to inhibit the protective role of HPV during alveolar hypoxia combined with OLV both in vitro and in vivo [2]. Halothane, enflurane, isoflurane, sevoflurane, and desflurane depressed HPV in a dose-dependent manner in isolated rat or rabbit lung [4, 22, 23]. Isoflurane or desflurane impaired oxygenation during OLV, while intravenous anesthetics, such as propofol or pentobarbital, had no detrimental impact on HPV in animal studies [3, 5, 24, 25]. However, in clinical investigations, results regarding the effects of anesthetics on oxygenation and HPV during OLV have been inconsistent [6–10, 26, 27]. Propofol improved oxygenation and shunt fraction during OLV compared to sevoflurane anesthesia in patients undergoing esophagectomy [6] or thoracotomy pulmonary lobectomy [27]. In other studies, propofol anesthesia did not differ in changes in shunt fraction or oxygenation during OLV for thoracic surgery in comparison with sevoflurane or isoflurane [7–10]. Moreover, arterial oxygenation was not different between propofol-alfentanil vs. isoflurane anesthesia during OLV in patients undergoing thoracoscopic pulmonary surgery or esophageal surgery [26]. Above all, there have been no previous reports comparing the effects of the two commonly used anesthetics, desflurane and propofol, on arterial oxygenation during OLV in thoracic surgical patients. In accordance with previous reports [21, 28], our data demonstrated a decrease in PaO2 during the first 30 min of OLV and gradual improvement thereafter in both groups (Fig. 2). During desflurane anesthesia, PaO2 decreased significantly after 15 min of OLV compared to the pre-OLV state, and then recovered gradually to pre OLV levels at 60 min. On the other hand, arterial oxygenation was relatively well maintained during propofol anesthesia throughout the study. None of the time points during OLV indicated a lower PaO2 compared to pre-OLV state in the propofol group. One explanation for our results is that more vasodilation induced by desflurane anesthesia would have attenuated any protective effect of HPV during alveolar hypoxemia, thus decreased systemic PaO2 in the desflurane group compared to the propofol group. This is partially supported by significantly lower arterial blood pressure despite the lesser use in remifentanil during desflurane anesthesia compared to propofol anesthesia in the present study (Table 2). Significant drop in MAP during desflurane anesthesia compared to propofol anesthesia also has been reported in previous animal study (66 vs. 103 mmHg), in which the effect of anesthetics (desflurane vs. propofol) on arterial oxygenation during OLV was evaluated [3]. Previously, an attempt to inhibit HPV by infusing the potent vasodilator sodium nitroprusside (SNP) during OLV has failed to show significant changes in pulmonary vascular resistance (PVR), shunt fraction, or arterial oxygenation [29]. However, only seven patients were used to evaluate the effect of administering SNP on HPV, by measuring related parameters only once during OLV, before the surgery commenced. Moreover, there was no time window from drug administration to measurement of the variables, or duration of drug infusion to reach the predefined goal (25% decrease in MAP), as presented by the authors. Although vasodilation induced by SNP decreased PVR (166 ± 23–131 ± 22 dynes/s/cm5 ) and PaO2 (285 ± 42–225 ± 47 mmHg) in that study, the decreases were not significant. Therefore, further investigations may be needed. Decreases in PaO2 and use of lung recruitment maneuvers during OLV were observed in three patients that received desflurane, while no cases were observed in the propofol group. During the events, the lowest PaO2 levels under FIO2 of 1.0 were 60, 69, and 87 mmHg, respectively. All episodes occurred after 30 min following initiation of OLV. In the last case, the degree of hypoxemia was not severe; however, the attending anesthesiologist decided to provide rescue treatment and proceed with OLV for the remainder of the surgical procedure. Similar events have been reported in previous animal studies comparing desflurane and propofol during in vivo OLV [3]. In this previous study, 3 of 10 pigs showed oxygen desaturation < 90% during OLV with desflurane anesthesia, while no cases were observed in the group receiving propofol. Although there were no further complications after desaturation in our study, these results suggest that desflurane anesthesia for OLV could result in deterioration of oxygenation especially in subjects with under-reserved pulmonary function. In the current study, blood pressure was managed using adjustment of remifentanil infusion according to the hemodynamic changes during the surgical procedure. We tried to use anesthetic techniques relevant to real clinical practice. It is clearly reflected in the lower use of remifentanil in the desflurane group mainly due to the sustained lower blood pressure in this group compared to the propofol group. In a previous study investigated the effects of different concentrations of remifentanil during OLV, no differences in PaO2 were observed despite the significantly different blood pressures [30]. Therefore, we considered that the observed difference in PaO2 may not the consequence of the difference in remifentanil use between the two groups in this study. Although a significant difference in PaO2 was detected between the groups (170 vs. 202 mmHg at 30 min of OLV in the desflurane vs. propofol group, respectively; p = 0.039), the difference may be clinically irrelevant to the anesthesiologist who is managing oxygenation in patients undergoing OLV. In this trial, we used a FIO2 of 1.0 throughout the OLV period with the expectation that it would better distinguish the difference in oxygenation between the groups [31]. A clinically significant difference in PaO2 may have been found between the two groups if a lower FIO2 had been used. In some studies, desflurane showed relatively conserved vascular resistance compared to sevoflurane [32]. In other studies, desflurane has shown more vasodilatory effect among inhalational anesthetics [11–14]. Although no differences were observed in oxygenation between sevoflurane and propofol anesthesia during OLV in several previous studies [8–10], desflurane, even as balanced anesthesia, showed more impaired oxygenation during OLV compared with propofol anesthesia in the present study. However, we did not compare the two popular inhales, sevoflurane vs. desflurane, in the present trial. Further studies are required for comparison of effects of two commonly used volatile anesthetics. |