Domino K B, Lu Y, Eisenstein B L, Hlastala M P
University of Washington Medical School, Seattle.
Anesthesiology. 1993 Jan;78(1):91-9. doi: 10.1097/00000542-199301000-00014.
Hyperventilation frequently is employed to reduce carbon dioxide partial pressure in patients in the operating room and intensive care unit. However the effect of hypocapnia on oxygenation is complex and may result in worsening in patients with preexisting intrapulmonary shunt. To better define the interplay between hypocapnia and oxygenation, the effects of hypocapnia and hypercapnia on the matching of ventilation (VA) and perfusion (Q) were studied in dogs with oleic acid-induced pulmonary edema, using the multiple inert gas elimination technique.
Eight pentobarbital-anesthetized, closed-chested dogs were administered 0.06 ml/kg of oleic acid at least 150 min prior to study. Ventilation was set with an FIO2 of 0.90, a tidal volume of 20 ml/kg, and a respiratory rate of 35 breaths/min. The arterial carbon dioxide tension (PaCO2) was varied in a randomized order to three levels (26, 38, and 50 mmHg) by altering the amount of CO2 in the inspired gas mixture. Gas exchange was assessed by true shunt, dead space, the log standard deviation of the perfusion (log SDQ) and the ventilation (log SDV) distributions, and the tracer inert gas arterial-alveolar difference ([a-A]D) area.
Cardiac output (4.1 +/- 0.4 L/min), mean pulmonary artery pressure (25 +/- 1 mmHg), inert gas shunt (22 +/- 3%), and dead space (38 +/- 4%) during normocapnia were not different from that during hypocapnia and hypercapnia. Hypocapnia increased (P < .05) the alveolar-arterial oxygen tension difference (P[A-a]O2) and decreased (P < .05) the arterial blood oxygen tension (PaO2, 181 +/- 33 mmHg vs. 221 +/- 35 mmHg with normocapnia). P[A-a]O2 and PaO2 were unaffected by hypercapnia. During hypocapnia, VA/Q inequality increased, demonstrated by an increase (P < .05) in log SDQ (1.60 +/- 0.15 vs. 1.35 +/- 0.19 with normocapnia) and in the [a-A]D area (0.63 +/- 0.09 vs. 0.50 +/- 0.09 with normocapnia) indexes of VA/Q heterogeneity. During hypercapnia, the [a-A]D area (0.63 +/- 0.11) and log SDV (1.13 +/- 0.10 compared to 0.97 +/- 0.12 with normocapnia) also were increased (P < .05). With hypocapnia, there was a small but insignificant increase in blood flow to shunt and low VA/Q areas (29 +/- 4% compared to 26 +/- 4% with normocapnia). In the presence of a high FIO2, this small increase in shunt and low VA/Q may result in a significant decrease in PaO2.
Both hypocapnia and hypercapnia were associated with an increased VA/Q inequality. However, PaO2 decreased and P[A-a]O2 increased with only hypocapnia. These results suggest that hyperventilation to reduce PaCO2 may be detrimental to arterial PO2 in some patients with lung disease.
在手术室和重症监护病房中，常采用过度通气来降低患者的二氧化碳分压。然而，低碳酸血症对氧合的影响较为复杂，可能会使已有肺内分流的患者病情恶化。为了更好地明确低碳酸血症与氧合之间的相互作用，我们采用多惰性气体消除技术，研究了低碳酸血症和高碳酸血症对油酸诱导的肺水肿犬通气（VA）与灌注（Q）匹配的影响。
在研究前至少150分钟，给8只戊巴比妥麻醉、开胸的犬静脉注射0.06 ml/kg的油酸。通气设置为吸入氧分数（FIO2）为0.90、潮气量为20 ml/kg、呼吸频率为35次/分钟。通过改变吸入气体混合物中的二氧化碳量，将动脉二氧化碳分压（PaCO2）随机调整为三个水平（26、38和50 mmHg）。通过真性分流、死腔、灌注（log SDQ）和通气（log SDV）分布的对数标准差以及示踪惰性气体动脉 - 肺泡差值（[a - A]D）面积来评估气体交换。
正常碳酸血症时的心输出量（4.1±0.4 L/分钟）、平均肺动脉压（25±1 mmHg）、惰性气体分流（22±3%）和死腔（38±4%）与低碳酸血症和高碳酸血症时相比无差异。低碳酸血症使肺泡 - 动脉氧分压差（P[A - a]O2）升高（P < 0.05），动脉血氧分压（PaO2）降低（P < 0.05）（正常碳酸血症时PaO2为221±35 mmHg，低碳酸血症时为181±33 mmHg）。高碳酸血症对P[A - a]O2和PaO2无影响。低碳酸血症时，VA/Q不均一性增加，表现为log SDQ升高（P < 0.05）（正常碳酸血症时为1.35±0.19，低碳酸血症时为1.60±0.15）以及[a - A]D面积增加（P < 0.05）（正常碳酸血症时为0.50±0.09，低碳酸血症时为0.63±0.09），这两个指标均反映了VA/Q的异质性。高碳酸血症时，[a - A]D面积（0.63±0.11）和log SDV（正常碳酸血症时为0.97±0.12，高碳酸血症时为1.13±0.10）也升高（P < 0.05）。低碳酸血症时，分流和低VA/Q区域的血流有小幅但不显著的增加（正常碳酸血症时为26±4%，低碳酸血症时为29±4%）。在高FIO2情况下，分流和低VA/Q的这种小幅增加可能导致PaO2显著降低。
低碳酸血症和高碳酸血症均与VA/Q不均一性增加有关。然而，只有低碳酸血症时PaO2降低且P[A - a]O2升高。这些结果表明，对于一些肺部疾病患者，过度通气以降低PaCO2可能对动脉血氧分压有害。
