Respiratory restriction and elevated pleural and esophageal pressures in morbid obesity

Respiratory restriction and elevated pleural and esophageal pressures in morbid obesity
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DOI:
10.1152/japplphysiol.91356.2008
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发表时间:
2010-01-01
影响因子:
3.3
通讯作者:
Loring, Stephen H.
Loring, Stephen H.
中科院分区:
医学2区
文献类型:
--
作者:
Behazin, Negin;Jones, Stephanie B.;Loring, Stephen H.

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Behazin N、Jones SB、Cohen RI、Loring SH。病态肥胖症的呼吸限制和胸膜压和食管压升高。 J Appl Physiol 108: 212-218, 2010。首次发表于 2009 年 11 月 12 日; doi:10.1152/japplphyol.91356.2008.-为了探索严重肥胖患者限制性呼吸生理学和高胸膜压 (P-Pl) 的机制,我们研究了 51 名肥胖受试者(体重指数 = 38-80.7 kg/m(2))和 10 名非肥胖受试者,两组均没有肺部疾病,均进行麻醉和瘫痪以进行手术。我们使用球囊导管测量食管和胃压力(P-Es、P-Ga)、气道压力(P-AO)、流量和容量。我们将 P-E 与基于 P-AO 和流量的 P-Pl 估计值进行了比较。推理到 P-AO 超过肺泡压和胸膜压 (P-AO > P-Alv > P-Pl) 之前肺部不会充气,我们将受试者与呼吸机断开 10-15 秒,让他们达到舒张量 (V-Rel),然后缓慢升高 P-AO 直到肺容积增加 10 毫升,指示充气的“阈值 P-AO”(PAO-Thr),我们将其视为估计值在 V-Rel 的胸部中找到的最低 P-Alv 或 P-Pl 的值。肥胖受试者的 PAO-Thr 范围为 0.6 至 14.0 cmH(2)O,对照受试者的 PAO-Thr 范围为 0.2 至 0.9 cmH(2)O。肥胖受试者的 V-Rel 的 P-E 高于对照受试者(12.5 +/- 3.9 与 6.9 +/- 3.1 cmH(2)O,平均值 +/- SD;P = 0.0002),并且与 PAO-Thr 相关(R-2 = 0.16,P = 0.0015)。肥胖者的呼吸系统顺应性 (C-RS) 低于对照组(0.032 +/- 0.008 与 0.053 +/- 0.007 l/cmH(2)O),主要是由于肺顺应性较低(0.043 +/- 0.016 与 0.084 +/- 0.029 l/cmH(2)O),而不是胸壁顺应性(肥胖 0.195) +/- 0.109,对照 0.223 +/- 0.132 l/cmH(2)O)。我们得出的结论是,许多严重肥胖的仰卧受试者在放松量下整个胸部的 P-pl 呈阳性。高 P-Es 表明此类个体的高 P-Pl。由于呼吸时肺容量异常低,肺和呼吸系统的顺应性较低。
Behazin N, Jones SB, Cohen RI, Loring SH. Respiratory restriction and elevated pleural and esophageal pressures in morbid obesity. J Appl Physiol 108: 212-218, 2010. First published November 12, 2009; doi:10.1152/japplphysiol.91356.2008.-To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P-Pl) in severe obesity, we studied 51 obese subjects (body mass index = 38-80.7 kg/m(2)) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (P-Es, P-Ga) using a balloon-catheter, airway pressure (P-AO), flow, and volume. We compared P-Es to another estimate of P-Pl based on P-AO and flow. Reasoning that the lungs would not inflate until P-AO exceeded alveolar and pleural pressures (P-AO > P-Alv > P-Pl), we disconnected subjects from the ventilator for 10-15 s to allow them to reach relaxation volume (V-Rel) and then slowly raised P-AO until lung volume increased by 10 ml, indicating the "threshold P-AO" (PAO-Thr) for inflation, which we took to be an estimate of the lowest P-Alv or P-Pl to be found in the chest at V-Rel. PAO-Thr ranged from 0.6 to 14.0 cmH(2)O in obese and 0.2 to 0.9 cmH(2)O in control subjects. P-Es at V-Rel was higher in obese than control subjects (12.5 +/- 3.9 vs. 6.9 +/- 3.1 cmH(2)O, means +/- SD; P = 0.0002) and correlated with PAO-Thr (R-2 = 0.16, P = 0.0015). Respiratory system compliance (C-RS) was lower in obese than control (0.032 +/- 0.008 vs. 0.053 +/- 0.007 l/cmH(2)O) due principally to lower lung compliance (0.043 +/- 0.016 vs. 0.084 +/- 0.029 l/cmH(2)O) rather than chest wall compliance (obese 0.195 +/- 0.109, control 0.223 +/- 0.132 l/cmH(2)O). We conclude that many severely obese supine subjects at relaxation volume have positive P-pl throughout the chest. High P-Es suggests high P-Pl in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes.