Liu Ling, Wu Ai-Ping, Yang Yi, Liu Song-Qiao, Huang Ying-Zi, Xie Jian-Feng, Pan Chun, Yang Cong-Shan, Qiu Hai-Bo
Department of Critical Care Medicine, School of Medicine, Nanjing Zhongda Hospital, Southeast University, Nanjing, Jiangsu 210009, China.
Chin Med J (Engl). 2017 May 20;130(10):1155-1160. doi: 10.4103/0366-6999.205864.
Propofol is increasingly used during partial support mechanical ventilation such as pressure support ventilation (PSV) in postoperative patients. However, breathing pattern, respiratory drive, and patient-ventilator synchrony are affected by the sedative used and the sedation depth. The present study aimed to evaluate the physiologic effects of varying depths of propofol sedation on respiratory drive and patient-ventilator synchrony during PSV in postoperative patients.
Eight postoperative patients receiving PSV for <24 h were enrolled. Propofol was administered to achieve and maintain a Ramsay score of 4, and the inspiratory pressure support was titrated to obtain a tidal volume (VT) of 6-8 ml/kg. Then, the propofol dose was reduced to achieve and maintain a Ramsay score of 3 and then 2. At each Ramsay level, the patient underwent 30-min trials of PSV. We measured the electrical activity of the diaphragm, flow, airway pressure, neuro-ventilatory efficiency (NVE), and patient-ventilator synchrony.
Increasing the depth of sedation reduced the peak and mean electrical activity of the diaphragm, which suggested a decrease in respiratory drive, while VT remained unchanged. The NVE increased with an increase in the depth of sedation. Minute ventilation and inspiratory duty cycle decreased with an increase in the depth of sedation, but this only achieved statistical significance between Ramsay 2 and both Ramsay 4 and 3 (P < 0.05). The ineffective triggering index increased with increasing sedation depth (9.5 ± 4.0%, 6.7 ± 2.0%, and 4.2 ± 2.1% for Ramsay 4, 3, and 2, respectively) and achieved statistical significance between each pair of depth of sedation (P < 0.05). The depth of sedation did not affect gas exchange.
Propofol inhibits respiratory drive and deteriorates patient-ventilator synchrony to the extent that varies with the depth of sedation. Propofol has less effect on breathing pattern and has no effect on VT and gas exchange in postoperative patients with PSV.
丙泊酚在术后患者的部分支持机械通气(如压力支持通气[PSV])过程中使用越来越频繁。然而,呼吸模式、呼吸驱动及患者-呼吸机同步性会受到所用镇静剂及镇静深度的影响。本研究旨在评估不同深度丙泊酚镇静对术后患者PSV期间呼吸驱动及患者-呼吸机同步性的生理影响。
纳入8例接受PSV时间<24小时的术后患者。给予丙泊酚以达到并维持 Ramsay 评分4分,吸气压力支持进行滴定以获得6-8 ml/kg的潮气量(VT)。然后,降低丙泊酚剂量以达到并维持 Ramsay 评分3分,随后为2分。在每个 Ramsay 水平,患者接受30分钟的PSV试验。我们测量了膈肌电活动、流量、气道压力、神经通气效率(NVE)及患者-呼吸机同步性。
镇静深度增加使膈肌的峰值和平均电活动降低,这表明呼吸驱动下降,而VT保持不变。NVE随镇静深度增加而增加。分钟通气量和吸气占空比随镇静深度增加而降低,但仅在Ramsay 2分与Ramsay 4分和3分之间达到统计学意义(P<0.05)。无效触发指数随镇静深度增加而增加(Ramsay 4分、3分和2分分别为9.5±4.0%、6.7±2.0%和4.2±2.1%),且在每对镇静深度之间达到统计学意义(P<0.05)。镇静深度不影响气体交换。
丙泊酚抑制呼吸驱动并使患者-呼吸机同步性恶化,其程度随镇静深度而异。丙泊酚对呼吸模式影响较小,对接受PSV的术后患者的VT和气体交换无影响。