Domino K B, Hlastala M P
University of Washington School of Medicine, Seattle.
Anesthesiology. 1994 Dec;81(6):1445-53. doi: 10.1097/00000542-199412000-00020.
Hyperventilation has been recommended to increase blood pH during metabolic acidosis. However, hypocapnia may adversely affect arterial blood oxygenation, especially in the presence of lung disease. We therefore studied the effects of metabolic acidosis, with and without normalization of pH by hyperventilation, on pulmonary gas exchange in dogs with permeability pulmonary edema.
Six pentobarbital-anesthetized dogs were administered 0.06 ml/kg of oleic acid at least 150 min before study. Ventilation was set with an inspired O2 fraction of 0.90 and a tidal volume of 18 ml/kg, and the respiratory rate was adjusted to alter the arterial CO2 tension (PaCO2) per the experimental protocol. The protocol in random order was (1) normal pH (7.36 +/- 0.01)/normal PaCO2 (39 +/- 1 mmHg); (2) low pH 7.20 +/- 0.01)/normal PaCO2 (40 +/- 1 mmHg); (3) low pH (7.18 +/- 0.01)/hyperventilation with inspired CO2 (PaCO2 = 40 +/- 1 mmHg); and (4) normal pH (7.35 +/- 0.01)/hyperventilation with low PaCO2 (24 +/- 1 mmHg). In phases 2-4, the pH was slowly reduced by intravenous infusion of 2 N hydrochloric acid. The pH was normalized in phase 1 where necessary by infusion of sodium bicarbonate. The pH in phase 4 was normalized by reducing the PaCO2 by increasing the respiratory rate. Gas exchange was assessed by the multiple inert-gas elimination technique.
The hemodynamic measurements remained constant throughout the protocol. Arterial O2 tension increased from 244 +/- 55 to 293 +/- 49 mmHg in the presence of metabolic acidosis (P < 0.05). Hyperventilation to normalize the pH during metabolic acidosis (phase 4), increased arterial O2 tension (313 +/- 44 mmHg, P < 0.05), and reduced shunt (from 20 +/- 5% to 12 +/- 3%, P < 0.05) compared with normal acid-base conditions (phase 1). No change in shunt was observed with hyperventilation compared with metabolic acidosis alone (phase 2). The decrease in pulmonary shunt was not attributable to the direct effects of hyperventilation, because shunt was increased (20 +/- 5%) when PaCO2 was normalized during hyperventilation by inspiration of CO2 (phase 3).
Hyperventilation to normalize blood pH during hydrochloric acid-induced metabolic acidosis did not adversely affect pulmonary gas exchange in dogs with permeability pulmonary edema.
在代谢性酸中毒期间，建议进行过度通气以提高血液pH值。然而，低碳酸血症可能会对动脉血氧合产生不利影响，尤其是在存在肺部疾病的情况下。因此，我们研究了代谢性酸中毒（无论是否通过过度通气使pH值正常化）对渗透性肺水肿犬肺气体交换的影响。
在研究前至少150分钟，给6只戊巴比妥麻醉的犬静脉注射0.06 ml/kg油酸。通气设置为吸入氧分数0.90，潮气量18 ml/kg，并根据实验方案调整呼吸频率以改变动脉二氧化碳分压（PaCO2）。实验方案按随机顺序进行：（1）正常pH值（7.36±0.01）/正常PaCO2（39±1 mmHg）；（2）低pH值（7.20±0.01）/正常PaCO2（40±1 mmHg）；（3）低pH值（7.18±0.01）/吸入二氧化碳进行过度通气（PaCO2 = 40±1 mmHg）；（4）正常pH值（7.35±0.01）/低PaCO2（24±1 mmHg）进行过度通气。在第2 - 4阶段，通过静脉输注2 N盐酸使pH值缓慢降低。在必要时，第1阶段通过输注碳酸氢钠使pH值正常化。第4阶段通过增加呼吸频率降低PaCO2使pH值正常化。采用多惰性气体排除技术评估气体交换。
在整个实验过程中，血流动力学测量值保持恒定。在代谢性酸中毒情况下，动脉血氧分压从244±55 mmHg升至293±49 mmHg（P < 0.05）。与正常酸碱状态（第1阶段）相比，在代谢性酸中毒期间过度通气使pH值正常化（第4阶段），可提高动脉血氧分压（313±44 mmHg，P < 0.05），并减少分流（从20±5%降至12±3%，P < 0.05）。与单纯代谢性酸中毒（第2阶段）相比，过度通气时未观察到分流变化。肺分流的减少并非归因于过度通气的直接作用，因为在过度通气期间通过吸入二氧化碳使PaCO2正常化时，分流增加（20±5%）（第3阶段）。
在盐酸诱导的代谢性酸中毒期间，过度通气使血液pH值正常化对渗透性肺水肿犬的肺气体交换没有不利影响。
