圍手術期單雙肺通氣策略

1、“圍術期單肺與雙肺通氣的肺保護策略 — ASA 2015 知識更新“讀書報告,Perioperative Lung Protection Strategiesin One-lung and Two-lung Ventilation Peter Slinger, MD, FRCPC Department of Anesthesia University of Toronto and Toronto General Hospita

2、l Toronto, Ontario, Canada,,提綱,1.COPD :呼吸驅動力、肺大泡、氣流受限、auto-peep2、機械通氣:ALI、VILI(呼吸機相關肺損傷)3、圍術期管理：外科相關因素、揮發(fā)性麻醉藥在肺保護中的作用、超保護性肺通氣(Ultraprotective Lung Ventilation)、液體和細胞外被、其它肺保護治療4、總結,,COPD,所有3期（FEV1 30～49%預期值）及4期（FEV1<

3、;30%預期值）COPD患者都需要進行動脈血氣分析檢查←通常的病史采集、體格檢查以及肺功能檢查難以將這類“CO2潴留”與其他非潴留情況相鑒別。此類患者術后必須補充給氧，以預防與術后不可避免的功能殘氣量減少有關的低氧血癥發(fā)生，同時要預料到可能會伴隨有PaCO2升高，密切監(jiān)測PaCO2變化。,,2.Parot S, Saunier C, Gauthier H, Milic-Emile J, Sadoul P: Breathing patt

4、ern and hypercapnia in patients with obstructive pulmonary disease. Am Rev Respir Dis 1980; 121:985–91.Perioperative Lung Protection Strategiesin One-lung and Two-lung Ventilation Peter Slinger, MD, FRCPC Department o

5、f Anesthesia University of Toronto and Toronto General Hospital Toronto, Ontario, Canada,呼吸驅動力COPD患者瀕臨呼衰時，予高濃度氧氣誘發(fā)高碳酸血癥性昏迷?,之前的理論認為，慢性高碳酸血癥的患者有賴于低氧刺激以保證呼吸驅動，而對PaCO2敏感性降低。,,3.Aubier M, Murciano D, Milic-Emili J, et al.:

6、Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure. Am Rev Respir Dis 1980; 122:747–54. 4.Simpson SQ: Oxygen-induc

7、ed acute hypercapnia in chronic obstructive pulmonary disease: What’s the problem? Crit Care Med 2002; 30:258–60.5.Hanson CW. III, Marshall BE, Frasch HF, Marshall C: Causes of hypercarbia in patients with chronic obstr

8、uctive pulmonary disease. Crit Care Med 1996; 24:23–8.,肺大泡,正壓通氣→破裂、張力性氣胸、支氣管胸膜瘺在維持低氣道壓力的情況下，肺大泡患者可以安全地應用正壓通氣；但應保證配備合適的專業(yè)人員和設備，以便必要時可以及時置入胸腔引流管和進行肺隔離。,Perioperative Lung Protection Strategiesin One-lung and Two-lung Ven

9、tilation Peter Slinger, MD, FRCPC Department of Anesthesia University of Toronto and Toronto General Hospital Toronto, Ontario, Canada,氣流受限,由于肺的動力性高度膨脹，嚴重氣流受限的患者接受正壓通氣時存在血流動力學崩潰的風險：他們吸入阻力沒有增加，但是存在明顯的呼氣阻塞，所以面罩手動通氣時即使輕微的正壓

10、通氣也可引起患者出現(xiàn)低血壓。“Lazarus拉撒路綜合征”搶救措施和正壓通氣停止后，心跳驟停的患者卻復蘇過來的現(xiàn)象的原因。,9.Ben-David B, Stonebraker VC, Hershman R, Frost CL,Williams HK: Survival after failed intraoperative resuscitation: A case of ‘‘Lazarus syndrome’’. Anesth

11、Analg 2001; 92:690–4.,Auto-PEEP,,10. Slinger P, Hickey D: The interaction between applied PEEP and auto- PEEP during one-lung ventilation. J Cardiothorac Vasc Anesth 1998; 12:133–7.11. Caramez MP, Borges JB, Tucci MR, e

12、t al.: Paradoxical responses to positive end-expiratory pressure in patients with airway obstruction during controlled ventilation. Crit Care Med 2005; 33:1519–28.12. Slinger P, Kruger M, McRae K, Winton T: The relation

13、 of the static compliance curve and positive end-expiratory pressure to oxygenation during one-lung ventilation. Anesthesiology 2002; 95: 1096–102.,機械通氣,大潮氣量的應用是無急性肺損傷（ALI）患者發(fā)生肺損傷的主要危險因素?！?5】Gajic等一項前瞻性研究發(fā)現(xiàn)：潮氣量＞700ml以及氣

14、道峰壓＞30cmH2O是ARDS形成的獨立危險因素?！?6】食道手術,“單肺/雙肺通氣中使用vt9ml/kg不加用PEEP VS 單肺通氣5ml/kg或雙肺通氣9ml/kg全程加用5cmH2O PEEP” 小潮氣量合并PEEP組血漿炎癥因子（IL-1ß、IL-6、IL-8）水平明顯更低；且患者具有更好的單肺通氣中和單肺通氣后即刻氧合水平（限于術后18小時）?！?7】Olivera等,隨機分組并按預測體重分別以

15、10-12ml/kg+5cmH2O的PEEP VS 6-8ml/kg+5cmH2O的PEEP進行通氣,兩組患者都逐級調(diào)整吸入氧濃度以保持SpO2>90% 12小時后，大潮氣量組患者的支氣管肺泡灌洗液炎癥因子（TNFα和 IL-8）顯著升高.【18】Choi等比較了12ml/kg無PEEP VS 6ml/kg加用10cmH2O PEEP兩種通氣策略 5小

16、時機械通氣后，大潮氣量組灌洗液顯示促凝性改變。【19】一項納入了150例無ALI危重患者隨機對照研究將按預測體重給予10ml/kg VS 6ml/kg兩種潮氣量的效果進行了對比 常規(guī)通氣量組患者的血漿炎性因子顯著升高。【20】,15. Gajic O, Dara SI, Mendez JL, et al.: Ventilator-associated lung injury in patients without acute

17、 lung injury at the onset of mechanical ventilation. Crit Care Med 2004; 32:1817–24.16. Gajic O, Frutos-Vivar F, Esteban A, Hubmayr RD, Anzueto A: Ventilator settings as a risk factor for acute respiratory distress synd

18、rome in mechanically ventilated atients. ntensive Care Med 2005; 31:922–26.17. Michelet P, D’Journo X-B, Roch A, et al.: Protective ventilation influences systemic inflammation after esophagectomy: A randomized contro

19、lled study. Anesthesiology 2006; 105:911–19.18. Pinheiro de Oliveira R, Hetzel MP, Silva M, Dallegrave D, Friedman G: Mechanical ventilation with high tidal volume induces inflammation in patients without lung disease.

20、Crit Care 2010; 14:R39.19. Choi G, Wolthuis EK, Bresser P, et al.: Mechanical ventilation with lower tidal volumes and positive end-expiratory pressure prevents alveolar coagulation in patients without lung injury. Anes

21、thesiology 2006; 105:689–95.20. Determann R, Royakkers A, Wolthuis EK, et al.: Ventilation with lower tidal volumes as compared with conventional tidal volumes for patients without acute lung injury: A preventive andom

22、ized controlled trial. Crit Care 2010; 14:R1.,,,,,,,,非傷害性或所謂保護性的通氣設定仍可能使原本健康的肺形成肺損傷,小鼠 “單次打擊”所致VILI模型進行的動物研究顯示：即使是最小的傷害性肺通氣設置仍可引起符合肺損傷的生化和組織病理學改變?！?1】對嚙齒動物模型進行機械通氣的另一項研究顯示：僅僅90分鐘的保護性通氣后就會出現(xiàn)顯著的基因表達（包括參與免疫和炎癥反應的基因）。這些改變是否

23、對臨床轉歸有影響，目前還不確定?！?2】ALI是術后發(fā)生呼吸衰竭最常見的病因且與降低的術后生存率有關?！?3】,21. Wolthuis EK, Vlaar APJ, Choi G, et al.: Mechanical ventilation using non-injurious ventilation settings causes lung injury in the absence of pre-existing lung

24、 injury in healthy mice. Crit Care 2009; 13:R1.22. Ng CSH, Song Wan Ho AMH, Underwood MJ: Gene expression changes with a ‘‘non-injurious’’ ventilation strategy. Crit Care 2009; 13:403–10.23. Fernandez-Perez ER, Sprung

25、J, Alessa B, et al.: Intraoperative ventilator settings and acute lung injury after elective surgery: A nested case control study. Thorax 2009; 64:121–27.,圍術期肺損傷,圍術期肺損傷,,Q:ALI的主要危險因素？,Fernandez-Perez等，4000名患者，前瞻性病例對照研究，

26、觀察術中呼吸機設定與擇期手術后發(fā)生ALI的情況。研究顯示：高危擇期手術后ALI的發(fā)生率為3%。與對照組相比，發(fā)生ALI的患者術后生存率明顯降低且住院時間延長。 有趣的是，ALI的發(fā)生與術中氣道峰壓有關，而與潮氣量、PEEP或吸入氧濃度無關。一項特別觀察危重患者發(fā)生ARDS的術中危險因素的回顧性隊列研究發(fā)現(xiàn)：術中接受液體復蘇大于20ml/kg/h的患者比接受液體復蘇小于10ml/kg/h的患者發(fā)生ARDS的可能性高3倍（OR 3

27、.1, 95% CI = 1.0–9.9, P = 0.05）。 在此項研究中，潮氣量和血制品輸注量與ARDS的發(fā)生無相關性，且大多數(shù)患者按理想體重設置潮氣量為8-10ml/kg的通氣，術中PEEP為0?！?4】,,①氣道峰壓？②潮氣量？③PEEP？④吸入氧濃度？⑤液體量？⑦輸血？⑥其他？,24.Hughes C, Weavind L, Banerjee A, et al.: Intraoperative risk factors

28、 for acute respiratory distress syndrome in critically ill patients Anesth Analg 2010; 111:464–67.,SO:?,,Recent studies have identified the use of large tidal volumes as a major risk factor for development of lung injury

29、 in mechanicallyventilated patients without ALI. Gajic et al.15reported that 25% of patients with normal lungs ventilated in an intensive care unit setting for 2 days or longer developed ALI or ARDS. The main risk fact

30、ors for ALI were use of large tidal volumes, restrictive lung disease, and blood product transfusion. A prospective study from the same group found that tidal volumes higher than 700mL and peak airway pressures above 30

31、cm H2O were independently associated with the development of ARDS.16,Gajic等報道，約25%肺部正常的患者在ICU經(jīng)歷2天或更久的機械通氣后發(fā)生了ALI或ARDS?！?5】ALI的主要危險因素包括：使用大潮氣量、存在限制性肺部疾病以及輸注血液制品。同一研究小組的一項前瞻性研究發(fā)現(xiàn)：潮氣量＞700ml以及氣道峰壓＞30cmH2O是ARDS形成的獨立危險因素。[16],

32、VILI,,25. Lionetti V, Recchia FA, Ranieri VM: Overview of ventilator-induced lung injury mechanisms. Curr Opin Crit Care 2005; 11:82–6.,解釋ALI/ARDS中見到的遠隔器官發(fā)生功能障礙，優(yōu)化通氣策略在改善這種情況中的意義：,VILI至生物學創(chuàng)傷 持續(xù)加重肺損傷，

33、 遠隔器官發(fā)生功能障礙一項探討VILI引起遠隔器官損傷新機制的研究顯示：機械通氣可引起腎臟及小腸的內(nèi)皮細胞凋亡，并且同時伴有器官功能障礙的生化改變?！?6】對小鼠進行的損傷性機械通氣發(fā)現(xiàn)：肺泡牽拉誘發(fā)的粘性分子不只見于肺部，也可見于肝臟和腎臟。此外，機械通氣后肺、肝、腎中細胞因子和趨化因子的表達伴隨著粒細胞聚集的增加?！?7】,,,26. Imai Y, Parodo J, Kajikawa O, et al.:

34、Injurious mechanical ventilation and end-organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome. JAMA 2003; 280:2104–112.27. Hegeman MA, Henmus MP, Heijnen

35、CJ, et al.: Ventilator-induced endothelial activation and inflammation in the lung and distal organs. Crit Care 2009; 13:R182.,術中呼吸機相關性肺損傷1、ARDS患者應用的肺保護性通氣策略【28】是否適用于肺部健康患者的術中階段？,一篇針對該問題的論文指出：目前仍缺少關于術中最佳潮氣量、PEEP和肺復張應用的隨

36、機對照研究?！?9】盡管關于轉歸方面的研究不足，但基于我們對機械通氣作用的認知，圍術期目標性應用保護性肺通氣策略似乎是合理的。三項【30-32】在腹部大手術患者中的隨機對照研究顯示了相互矛盾的結果。這些結果仍有待大規(guī)模研究來確認。,29. Beck-Schimmer B, Schimmer RC: Perioperative tidal volume and intraoperative open lung strategy in he

37、althy lungs: Where are we going? Best Pract Res Clin Anaesthesiol 2010; 24:199–210.30. Treschan TA, KaisersW, Schafer MS, et al.: Ventilation with low tidal volumes during upper abdominal surgery does not improve posto

38、perative lung function. Br J Anaesth 2012; 109:263–71.31. Futier E, Constantin J-M, Paugam-Burtz C, et al.: A trial of intraoperative low tidal-volume in abdominal surgery. N Engl J Med 2013; 369:428–36.32. Severgnini

39、P, Selmo G, Lanza C, et al.: Protective mechanical ventilation during general anesthesia for open abdominal surgery improves postoperative pulmonary function. Anesthesiology 2013; 118:1254–7.,2、單肺？雙肺？,,一項在微創(chuàng)食管切除術中進行單肺通氣的

40、研究也發(fā)現(xiàn)：小潮氣量和PEEP可改善肺部轉歸?！?4】單肺通氣本身對通氣側和非通氣側肺均可造成損傷，【35】且這種損傷取決于單肺通氣的時間長短?！?6】因此最好要避免傳統(tǒng)的單肺通氣模式，而盡可能對非通氣肺應用連續(xù)氣道正壓（CPAP）?！?7】這在不涉及肺的微創(chuàng)胸內(nèi)手術（如心血管、食道手術）中是一個特別值得注意的選擇。,34. Shen Y, Zhong M, Wu W, et al.: The impact of tidal volum

41、e on pulmonary complications following minimally invasive esophagectomy. J Thorac Cardiovasc Surg 2013; 146:1267–73.35. Kozian A, Schilling T, Freden F, et al.: One-lung ventilation induces hyperperfusion and alveolar d

42、amage in the ventilated lung. Br J Anaesth 2008; 00:549–59.36. Tekinbas C, Ulusoy H, Yulug E, et al.: One-lung ventilation: For how long? J Cardiothorac Vasc Surg 2007; 134:405–10. 37. Verhage RJ, Boone J, Rijkers GT,

43、 et al.: Reduced local immune response with continuous positive airway pressure during one-lung ventilation for sophagectomy. Br J Anaesth 2014; 112: 920–8.,3、過量補液？大潮氣量？,傳統(tǒng)觀點經(jīng)常把肺切除后肺損傷的發(fā)生歸咎于手術中麻醉醫(yī)師的過量補液?，F(xiàn)有證據(jù)表明：相比過量補液，AL

44、I可能與單肺通氣中過度應用大潮氣量更具相關性。【38】目前尚缺少在人身上應用小VT/大VT進行單肺通氣的具有說服力的前瞻性研究，但已有大型動物研究。,,38. Slinger P: Postpneumonectomy pulmonary edema: Good news, bad news. Anesthesiology 2006; 105:2–5.39. Kuzkov V, Subarov E, Kirov M, et al.: E

45、xtravascular lung water after pneumonectomy and one-lung ventilation in sheep. Crit Care Med 2007; 35:1550–9.,圍術期管理1、外科相關因素,手術部位是肺部發(fā)生并發(fā)癥的一個重要預測指標，其中上腹部、胸部切口（任何接近靠近膈肌的切口）影響最大?！?0】與開放式手術相比，大型體腔手術時如果使用微創(chuàng)技術可減少肺部并發(fā)癥的發(fā)生。【41-4

46、2】肺不張作為一種可引起肺損傷的病理狀態(tài)，經(jīng)常發(fā)生于開放手術后及高達90%的全麻患者中。【43】存在爭議，回顧【45，46】與前瞻性【47】研究均顯示合適的胸段硬膜外鎮(zhèn)痛能減少腹部大手術及胸部手術后呼吸并發(fā)癥（肺不張、肺炎以及呼衰）的發(fā)生。硬膜外鎮(zhèn)痛的獲益程度似乎與患者潛在肺部疾病的嚴重程度直接成正比，如合并COPD的患者看起來是從硬膜外鎮(zhèn)痛中獲益最多的?！?8】尚未對高?；颊哌M行特別的研究，但是通過對胸外科手術患者應用椎旁阻滯和硬

47、膜外鎮(zhèn)痛進行比較顯示：椎旁阻滯與硬膜外鎮(zhèn)痛效果相當，而椎旁阻滯副作用和并發(fā)癥更少?！?9，50】對于腹部大手術后出現(xiàn)早期氧飽和度下降的患者，術后階段積極進行物理治療并結合應用CPAP可降低嚴重呼吸并發(fā)癥的發(fā)生?！?1】,,40. Smetana GW: Postoperative pulmonary complications: An update on risk assessment and reduction. Cleve Cli

48、n J Med 2009; 76: S60–5.41. Weller WE, Rosati C: Comparing outcomes of laparoscopic versus open bariatric surgery. Ann Surg 2008; 248:10–15.42. Ramivohan SM, Kaman L, Jindal R, Singh R, Jindal SK: Postoperative pulmona

49、ry function in laparoscopic versus open cholecystectomy: Prospective, comparative study. Indian J Gastroenterol 2005; 24:6–8.43. Duggan M, Kavanagh B: Pulmonary atelectasis: A pathogenic perioperative entity. Anesthesio

50、logy 2005; 102:834–54.44. Tusman G, Bohm SH, Suarez-Shipman F: Alveolar recruitment improves ventilatory efficiency of the lungs during anesthesia. Can J Anaesth 2004; 51:723–7.45. Ballantyne JC, Carr DB, de Ferranti S

51、: The comparative effects of postoperative analgesic therapies on pulmonary outcome: Cumulative meta-analysis of randomized, controlled trials. Anesth Analg 1998; 86:598–612.46. Liu SS, Wu CL: Effect of postoperative an

52、algesia on major postoperative complications: A systematic update of the evidence. Anesth Analg 2007; 3:689–702.47. Rigg J, Jamrozik K, Myles P, et al.: Epidural anaesthesia and analgesia and outcome after major surgery

53、: A randomized trial. Lancet 2002; 359:1276–82.48. Licker MJ, Widikker I, Robert J, et al.: Operative mortality and respiratory complications after lung resection for cancer: Impact of chronic obstructive pulmonary dis

54、ease and time trends. Ann Thorac Surg 2006; 81:1830–8.49. Scarci M, Joshi A, Attia R: In patients undergoing thoracic surgery is paravertebral block as effective as epidural analgesia for pain management. Interact Cardi

55、ovasc Thorac Surg 2010; 10:92–6.50. Davies RG, Myles PS, Graham JM: A comparison of the analgesic efficacy and side effects of paravertebral vs. epidural blockade for thoracotomy—A systematic review and meta-analysis of

56、 randomized trials. Br J Anaesth 2006; 96:418–26.51. Squadrone V, Coha M, Cerutti E, et al.: Continuous positive airway pressure for the treatment of postoperative hypoxemia: A randomized controlled trial. JAMA 2005; 29

57、3:589–95.,2、揮發(fā)性麻醉藥在肺保護中的作用,揮發(fā)性麻醉藥具有免疫調(diào)節(jié)功能。近期對單肺通氣中ALI模型及肺缺血再灌注損傷病例的研究顯示：揮發(fā)性麻醉藥可以作為預處理或后處理藥物通過抑制促炎調(diào)節(jié)因子的表達來實現(xiàn)肺保護作用【52】。對內(nèi)毒素介導的動物ALI模型進行異氟醚預處理，多型核白細胞集聚及微血管蛋白漏出的減少證明預處理產(chǎn)生了保護作用。【53】對活體大鼠ALI模型進行七氟醚后處理減輕了肺損傷的程度并保護了肺功能?！?4】在一項前瞻

58、性研究中，應用單肺通氣接受胸外科手術的患者被隨機分為丙泊酚組和七氟醚組。通過比較非通氣側的肺部炎癥標志物水平，研究者發(fā)現(xiàn)七氟醚組患者具有較輕的炎癥反應?！?5】值得注意的是，七氟醚組患者有更好的臨床轉歸且總體不良事件發(fā)生率明顯更低。【56】一項比較了單肺通氣中分別應用地氟醚和丙泊酚麻醉并檢測了通氣側肺部炎癥反應的研究表明：地氟醚組患者的炎癥標志物如IL-8, IL-10, PMN elastase和TNFα均明顯更低。 現(xiàn)有結果確實

59、已經(jīng)指明：無論是在損傷前、損傷中、還是損傷后應用，揮發(fā)性麻醉藥都具有減輕發(fā)生在肺部和受損器官的促炎癥反應的作用。,,52. Fujinaga T, Nakamura T, Fukuse T, et al.: Isoflurane inhalation after circulatory arrest protects against warm ischemia reperfusion injury of the lungs. Trans

60、plantation 2006; 82:1168–74.53. Reutershan J, Chang D, Hayes JK, Ley K: Protective effects of isoflurane pretreatment in endotoxin-induced lung injury. Anesthesiology 2006; 104:511–7.54. Voigtsberger S, Lachmann RA, Le

61、utert AC, et al.: Sevoflurane ameliorates gas exchange and attenuates lung damage in experimental lipopolysaccharide-induced lung injury. Anesthesiology 2009; 111:1238–48.55. De Conno E, Steurer MP, Wittlinger M, et al

62、.: Anesthetic-induced improvement of the inflammatory response to one-lung ventilation. Anesthesiology 2009; 110:1316–26.56. Schilling T, Kozian A, KretzschmarM, et al.: Effects of propofol and desflurane anaesthesia on

63、 the alveolar inflammatory response to onelung ventilation. Br J Anaesth 2007; 99:368–75.,3、超保護性肺通氣(Ultraprotective Lung Ventilation),概念：由ALI/ARDS中的保護性肺通氣發(fā)展而來，應用體外肺支持裝置以及近似靜止通氣（near-static ventilation）策略。[57]ARDSNet及動物研

64、究數(shù)據(jù)顯示更小的潮氣量（3ml/kg，相比6-12ml/kg）可顯著減輕內(nèi)皮細胞和上皮細胞損傷。[58,59]換言之，“保護性”潮氣量仍可誘發(fā)VILI，而應用更小潮氣量時，存在二氧化碳清除和氧合的問題。Novalung:一種無泵裝置，可在顯著減少分鐘通氣量的同時糾正PaCO2和pH。一項使用Novalung（潮氣量2.2ml/kg，呼吸頻率每分鐘6次）進行通氣的肺切除后ARDS的動物模型研究顯示：與傳統(tǒng)的肺保護性通氣策略相比，Nova

65、lung可明顯改善患者的轉歸。[60]一系列不同病情的人類病例報道結果：Novalung使潮氣量不高于3 mL/kg、低吸氣平臺壓、高PEEP以及低呼吸頻率通氣都成為可能，這減少了VILI和繼發(fā)性遠隔器官衰竭的發(fā)生。[61]一項對嚴重ARDS患者進行的隨機研究顯示：與應用常規(guī)通氣策略的患者生存率（47%）相比，應用有泵的ECMO結合保護性肺通氣可明顯增加患者的生存率（達63%）。[62],,57. The Cardiothoracic

66、 Surgery Network website. Available at: www.CTSNet.org. Accessed January 30, 2015.58. Hager DN, Krishnan JA, Hayden DL, Brower RG. ARDS Clinical Trials Network. Tidal volume reduction in patients with acute lung injury

67、when plateau pressures are not high. Am J Respir Crit Care Med 2005; 10:1241–5.59. Frank JA, Gutierrez JA, Jones KD, et al.: Low tidal volume reduces epithelial and endothelial injury in acid-injured rat lungs. AmJ Resp

68、ir Crit Care Med 2002; 165:242–9.60. Iglesias M, Jungebluth P, Petit C, et al.: Extracorporeal lung membrane provides better lung protection than conventional treatment for severe stpneumonectomy noncardiogenic acute r

69、espiratory distress syndrome. J Thorac Cardiovasc Surg 2008; 6:1362–71.61. Mallick A, Elliot S, McKinlay J, BodenhamA: Extracorporeal carbon dioxide removal using the Novalung in a patient with intracranial bleeding. An

70、aesthesia 2007; 62:72–4.62. Peek GJ, Mugford M, Tiruvoipati R, et al.: Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure