Rapid intravenous infusion of 20 ml/kg saline does not impair resting pulmonary gas exchange in the healthy human lung.
Rapid intravenous infusion of 20 ml/kg saline does not impair resting pulmonary gas exchange in the healthy human lung.
复制标题
快速静脉输注 20 ml/kg 生理盐水不会损害健康人肺的静息肺气体交换。
DOI：
10.1152/japplphysiol.00787.2009
复制
发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Hopkins,SusanR
中科院分区：
文献类型：
--
作者：
Prisk,GKim;Olfert,IMark;Arai,TatsuyaJ;Wagner,PeterD;Hopkins,SusanR
静脉内快速输注生理盐水是一种肺间质水肿模型，可改变肺灌注的分布，增加肺毛细血管血容量，并增加人体支气管壁厚度。我们假设输液会通过增加通气/灌注（V̇a/Q̇）不平等来扰乱肺部气体交换，而不是氧交换的弥散性损害。 7 名男性（26 ± 3 岁；FEV1：110 ± 16% 预测值）进行了肺活量测定，并使用多重惰性气体消除技术测量了 V̇a/Q̇ 不匹配，在 30 分钟内静脉注射 20 ml/kg 生理盐水之前和之后。输注使经胸阻抗的胸液含量增加了 12%（P<0.0001），FVC 保持不变，但呼气流量减少（FEF25-75 从 5.1±0.4 下降到 4.2±0.4l/s，P<0.05）。然而，通过通气 (LogSDV̇) 和灌注 (LogSDQ̇) 分布的对数标准差测量的 V̇a/Q̇ 不匹配保持不变； LogSDV̇：前 0.40 ± 0.03，后 0.38 ± 0.04，NS； LogSDQ̇：前 0.38 ± 0.03，后 0.37 ± 0.03，NS。动脉Po2无显着变化（术前99±2mmHg，术后99±3mmHg，NS），但动脉Pco2降低（术前38.7±0.6，术后36.8±1.2mmHg，P<0.05）。因此，输液压迫小气道并引起轻度过度通气。没有证据表明 O2 交换存在弥散性限制，在 FiO2= 0.125（术前 4.3 ± 1.0，术后 5.2 ± 1.0，NS）时，测量预测的肺泡动脉氧分压差未因输注而改变。输注后，当受试者呼吸高氧气体混合物时，流向 V̇a/Q̇ < 1 区域的灌注分数增加 [0.72 ± 0.06 (FiO2= 0.21), 0.80 ± 0.06 (FiO2= 0.30),P< 0.05]，在 V̇a 和 Q̇ 不变的情况下，对通气的影响相似。这些结果表明，在空气呼吸期间，可以主动控制流向通气减少区域的血流，从而最大限度地减少气体交换的后果。
Rapid infusion of intravenous saline, a model of pulmonary interstitial edema, alters the distribution of pulmonary perfusion, raises pulmonary capillary blood volume, and increases bronchial wall thickness in humans. We hypothesized that infusion would disrupt pulmonary gas exchange by increasing ventilation/perfusion (V̇a/Q̇) inequality as opposed to a diffusive impairment in O2exchange. Seven males (26 ± 3 yr; FEV1: 110 ± 16% predicted.) performed spirometry and had V̇a/Q̇ mismatch measured using the multiple inert gas elimination technique, before and after 20 ml/kg iv of normal saline delivered in ∼30 min. Infusion increased thoracic fluid content from transthoracic impedance by 12% (P< 0.0001) and left FVC unchanged but reduced expiratory flows (FEF25–75falling from 5.1 ± 0.4 to 4.2 ± 0.4 l/s,P< 0.05). However, V̇a/Q̇ mismatch as measured by the log standard deviation of the ventilation (LogSDV̇) and perfusion (LogSDQ̇) distributions remained unchanged; LogSDV̇: 0.40 ± 0.03 pre, 0.38 ± 0.04 post, NS; LogSDQ̇: 0.38 ± 0.03 pre, 0.37 ± 0.03 post, NS. There was no significant change in arterial Po2(99 ± 2 pre, 99 ± 3 mmHg post, NS) but arterial Pco2was decreased (38.7 ± 0.6 pre, 36.8 ± 1.2 mmHg post,P< 0.05). Thus, infusion compressed small airways and caused a mild degree of hyperventilation. There was no evidence for a diffusive limitation to O2exchange, with the measured-predicted alveolar-arterial oxygen partial pressure difference being unaltered by infusion at FiO2= 0.125 (4.3 ± 1.0 pre, 5.2 ± 1.0 post, NS). After infusion, the fraction of perfusion going to areas with V̇a/Q̇ < 1 was increased when a subject breathed a hyperoxic gas mixture [0.72 ± 0.06 (FiO2= 0.21), 0.80 ± 0.06 (FiO2= 0.30),P< 0.05] with similar effects on ventilation in the face of unchanged V̇aand Q̇. These results suggest active control of blood flow to regions of decreased ventilation during air breathing, thus minimizing the gas exchange consequences.