Intrapulmonary Shunting during Induced Hypotension
Intrapulmonary Shunting during Induced Hypotension
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诱发低血压期间的肺内分流
DOI：
10.1097/00132586-198212000-00001
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发表时间：
1982
影响因子：
5.7
通讯作者：
E. Lear
中科院分区：
文献类型：
--
作者：
P. Casthely;S. Lear;J. Cottrell;E. Lear
在全麻下观察硝普钠和硝酸甘油对14例成人肺分流的影响，其中9例肺功能正常，5例慢性阻塞性肺疾病。肺功能正常者应用硝普钠后，肺血管阻力从147.75达因秒/厘米~5降至147.75达因秒/厘米~5(p>；0.025)，肺动脉压由18.5降至8托(p>；0.005)，P>；t由5.19%升至8.81%。在这些患者中，硝酸甘油使t从5.13%增加到6.19%(p>；0.005)，平均动脉压从18分降至10分(p>；0.005)，Pvr从237分/分降至162.6达因秒/分(p>；0.025)。在COPD患者中，SNP和TNG对&OV0422；S/&OV0422；T、PAP和PVR无显著影响。两组患者的心输出量均保持不变。解释这些结果的各种机制是可以假设的。当肺功能正常的患者发生低血压时，PAP下降，重力作用使更多的血液通过大多数分流单位所在的依赖区域。在COPD患者中，破坏性的血管改变会增加PAP，从而阻止血管扩张剂降低PVR。此外，SNP和TNG对缺氧性肺血管收缩(如果存在)的扩张作用不依赖于上述两种机制。这些结果为SNP和TNG诱导的低血压可能导致肺功能正常患者的肺气体交换明显受损提供了证据。在COPD患者中，SNP或TNG故意降压后，肺气体交换不受影响。
The effect of sodium nitroprusside (SNP) and nitroglycerin (TNG) on pulmonary shunting (&OV0422;s/&OV0422;t) in 14 consenting adults [nine with normal lung function and five with chronic obstructive pulmonary disease (COPD)] was studied under general anesthesia. &OV0422;s/&OV0422;t significantly increased (p > 0.005) from 5.19% to 8.81%, whereas pulmonary arterial pressure (PAP) decreased from 18.5 to 8 torr (p > 0.005) and pulmonary vascular resistance (PVR) decreased from 235 to 147.75 dynes sec/cm5 (p > 0.025) when SNP was administered to patients with normal lung function. Nitroglycerin increased &OV0422;s/&OV0422;t from 5.13% to 6.19% (p > 0.005), whereas PAP decreased from 18 to 10 torr (p > 0.005) and PVR decreased from 237 to 162.6 dynes sec/cm5 (p > 0.025) in these patients. In patients with COPD, SNP and TNG produced no significant changes in &OV0422;s/&OV0422;t, PAP, or PVR. Cardiac output remained unchanged in both groups of patients. Various mechanisms to explain these results can be postulated. When hypotension is induced in patients with normal pulmonary function, PAP decreases and the effect of gravity puts more blood through dependent areas where most of the shunt units are. In patients with COPD, destructive vascular changes increase PAP, preventing vasodilators from decreasing PVR. In addition, dilation of hypoxic pulmonary vasoconstriction (if present) by SNP and TNG will occur independent of the two previously mentioned mechanisms. These results provide evidence that SNP-and TNG-induced hypotension may cause significant impairment in pulmonary gas exchange in patients with normal lung function. In patients with COPD pulmonary gas exchange is not affected after deliberate hypotension with SNP or TNG.