Lu Q, Capderou A, Cluzel P, Mourgeon E, Abdennour L, Law-Koune J D, Straus C, Grenier P, Zelter M, Rouby J J
Surgical Intensive Care Unit Pierre Viars and Departments of Anesthesiology, Physiology, and Radiology, La Pitié-Salpêtrière Hospital, University of Paris, Paris, France.
Am J Respir Crit Care Med. 2000 Nov;162(5):1898-904. doi: 10.1164/ajrccm.162.5.2003105.
This study was directed at assessing changes in bronchial cross-sectional surface areas (BCSA) and in respiratory resistance induced by endotracheal suctioning in nine anesthetized sheep. Cardiorespiratory parameters (Swan-Ganz catheter), respiratory resistance (inspiratory occlusion technique), BCSA, and lung aeration (computed tomography) were studied at baseline, during endotracheal suctioning, and after 20 consecutive hyperinflations. Measurements performed initially at an inspired oxygen fraction (FI(O(2))) of 0.3 were repeated at an FI(O(2)) of 1.0. At an FI(O(2)) of 0.3, endotracheal suctioning resulted in atelectasis, a reduction in BCSA of 29 +/- 23% (mean +/- SD), a decrease in arterial oxygen saturation from 95 +/- 3% to 87 +/- 12% (p = 0.02), an increase in venous admixture from 19 +/- 10% to 31 +/- 19% (p = 0. 006), and an increase in lung tissue resistance (DR(rs)) (p = 0. 0003). At an FI(O(2)) of 1.0, despite an extension of atelectasis and an increase in pulmonary shunt from 19 +/- 5% to 36 +/- 2% (p < 0.0001), arterial O(2) desaturation was prevented and BCSA decreased by only 7 +/- 32%. A recruitment maneuver after endotracheal suctioning entirely reversed the suctioning-induced increase in DR(rs) and atelectasis. In three lidocaine-pretreated sheep, the endotracheal suctioning-induced reduction of BCSA was entirely prevented. These data suggest that the endotracheal suctioning-induced decrease in BCSA is related to atelectasis and bronchoconstriction. Both effects can be reversed by hyperoxygenation maneuver before suctioning in combination with recruitment maneuver after suctioning.
本研究旨在评估九只麻醉绵羊经气管内吸引后支气管横截面积(BCSA)和呼吸阻力的变化。在基线、气管内吸引期间以及连续20次过度充气后,研究了心肺参数(Swan-Ganz导管)、呼吸阻力(吸气阻断技术)、BCSA和肺通气(计算机断层扫描)。最初在吸入氧分数(FI(O₂))为0.3时进行的测量在FI(O₂)为1.0时重复进行。在FI(O₂)为0.3时,气管内吸引导致肺不张,BCSA减少29±23%(平均值±标准差),动脉血氧饱和度从95±3%降至87±12%(p = 0.02),静脉混合血增加从19±10%至31±19%(p = 0.006),肺组织阻力(DR(rs))增加(p = 0.0003)。在FI(O₂)为1.0时,尽管肺不张范围扩大且肺内分流从19±5%增加至36±2%(p < 0.0001),但动脉血氧饱和度未降低,BCSA仅减少7±32%。气管内吸引后进行的复张手法完全逆转了吸引引起的DR(rs)增加和肺不张。在三只利多卡因预处理的绵羊中,气管内吸引引起的BCSA减少被完全预防。这些数据表明,气管内吸引引起的BCSA降低与肺不张和支气管收缩有关。在吸引前进行高氧手法并结合吸引后进行复张手法可逆转这两种效应。