Bishop M J, Cheney F W
Anesthesiology. 1983 Feb;58(2):130-5. doi: 10.1097/00000542-198302000-00005.
The authors investigated whether the increases in venous admixture and intrapulmonary shunt which occur with increases in cardiac output (Qt) results from an effect mediated by mixed venous PO2 (PVO2) or an effect mediated by the increase in pulmonary blood flow. Using a veno-venous bypass system thay were able to alter PVO2 independent of variations in Qt and vice versa. During room air ventilation of dogs with normal lungs at constant Qt, an increase in PVO2 from 33 +/- 7 (mean +/- SD) to 54 +/- 9 mmHg (P less than 0.05) resulted in a decrease in venous admixture from 22 +/- 11 to 13 +/- 4% (P less than 0.05). During room air ventilation of normal dogs at a constant PVO2, raising Qt from 2.16 +/- .53 to 3.49 +/- 0.91 l/min (P less than 0.05) increased venous admixture from 10 +/- 5 to 16 +/- 5% (P less than 0.05). During oxygen ventilation in these two groups of dogs, changes in PVO2 and Qt had no effect on shunt. During oxygen ventilation of dogs with significant shunts from oleic-acid-induced pulmonary edema, independent increases in either PVO2 or pulmonary blood flow resulted in increased shunt. At constant Ot, an increase in PVO2 from 30 +/- 8 to 52 +/- 3 mmHg (P less than 0.05) resulted in an increase in shunt from 39 +/- 12 to 43 +/- 12% (P less than 0.05). When PVO2 remained constant, increasing Qt from 1.97 pm 0.42 to 3.61 +/- 0.50 l/min (P less than 0.05) resulted in an increase in shunt from 47 +/- 17 to 53 +/- 15% (P less than 0.05). The authors conclude that during oxygen ventilation, normal dogs have shunts which are unaffected by changes in blood flow or PVO2. Increases in pulmonary blood flow increase venous admixture during room air ventilation, while increases in PVO2 decrease venous admixture during air ventilation. In edematous lungs, increases in either PVO2 or pulmonary blood flow increase shunt.
作者们研究了随着心输出量(Qt)增加而出现的静脉混合血和肺内分流增加,是由混合静脉血氧分压(PVO2)介导的效应还是由肺血流量增加介导的效应引起的。通过使用静脉 - 静脉旁路系统,他们能够独立于Qt的变化来改变PVO2,反之亦然。在正常肺的犬类进行室内空气通气且Qt恒定的情况下,PVO2从33±7(平均值±标准差)增加到54±9 mmHg(P<0.05),导致静脉混合血从22±11%降至13±4%(P<0.05)。在正常犬类进行室内空气通气且PVO2恒定的情况下,将Qt从2.16±0.53升高至3.49±0.91 l/min(P<0.05),静脉混合血从10±5%增加到16±5%(P<0.05)。在这两组犬类进行氧气通气期间,PVO2和Qt的变化对分流无影响。在油酸诱导的肺水肿导致显著分流的犬类进行氧气通气期间,PVO2或肺血流量的独立增加均导致分流增加。在Qt恒定的情况下,PVO2从30±8增加到52±3 mmHg(P<0.05),导致分流从39±12%增加到43±12%(P<0.05)。当PVO2保持恒定时,将Qt从1.97±0.42增加到3.61±0.50 l/min(P<0.05),导致分流从47±17%增加到53±15%(P<0.05)。作者得出结论,在氧气通气期间,正常犬类存在不受血流或PVO2变化影响的分流。在室内空气通气期间,肺血流量增加会增加静脉混合血,而PVO2增加会在空气通气期间减少静脉混合血。在水肿肺中,PVO2或肺血流量增加都会增加分流。