Fiser W P, Friday C D, Read R C
J Thorac Cardiovasc Surg. 1982 Apr;83(4):523-31.
Eight-five veterans underwent thoracic operations, mainly for carcinoma of the lung, with the aid of endobronchial anesthesia. Changes in arterial oxygenation (PaO2) and pulmonary shunt (Qs/Qt) were determined sequentially. Mean PaO2 after both lungs were ventilated for 20 minutes, supine, with 100% oxygen was 433 +/- 8 mm Hg. Selective ventilation of one bronchus dropped this value significantly (p less than 0.01) to 247 +/- 13 mm Hg. PaO2 did not change appreciably when the patient was turned to the lateral position; however, following pleurotomy there was a significant (p less than 0.01) decline in mean PaO2 to a nadir of 178 +/- 17 mm Hg at 90 minutes. Transient hypoxemia (PaO2 less than 60 mm Hg) occurred in 11 of 85 patients, most frequently (7/11) during positioning. Preoperative PaO2 PaCO2, forced expiratory volume in 1 second, forced vital capacity, or medical status did not predict hypoxemia. Qs/Qt increased significantly (p less than 0.01) at the onset of atelectasis from 18% +/- 0.9% to 25.4% +/- 0.9% but did not change with turning. The maximal mean Qs/Qt (30.3% +/- 1.1%) occurred immediately after opening the pleura and then decreased significantly (p less than 0.05), despite the fall in PaO2. Blood loss greater than 1,000 cc (n = 10), especially with hypotension, resulted in a significant increase (p less than 0.05) in Qs/Qt and a fall in PaO2. Thus pulmonary vascular adaptation to acute atelectasis has been demonstrated in man, and this, as in animal models, fails with hemorrhage.
85例退伍军人接受了胸科手术，主要是肺癌手术，采用支气管内麻醉。连续测定动脉血氧合（PaO₂）和肺分流（Qs/Qt）的变化。双肺以100%氧气仰卧通气20分钟后的平均PaO₂为433±8mmHg。选择性单支气管通气使该值显著下降（p<0.01）至247±13mmHg。患者转为侧卧位时PaO₂无明显变化；然而，胸膜切开术后平均PaO₂显著下降（p<0.01），在90分钟时降至最低点178±17mmHg。85例患者中有11例出现短暂性低氧血症（PaO₂<60mmHg），最常见于体位摆放时（7/11）。术前的PaO₂、PaCO₂、第1秒用力呼气量、用力肺活量或身体状况均不能预测低氧血症。肺不张开始时Qs/Qt显著增加（p<0.01），从18%±0.9%增至25.4%±0.9%，但体位变动时未改变。胸膜打开后立即出现最大平均Qs/Qt（30.3%±1.1%），然后显著下降（p<0.05），尽管PaO₂下降。失血超过1000cc（n=10），尤其是伴有低血压时，导致Qs/Qt显著增加（p<0.05）和PaO₂下降。因此，在人体已证实肺血管对急性肺不张有适应性，并且与动物模型一样，出血会破坏这种适应性。
