Schwartges Ingo, Schwarte Lothar A, Fournell Artur, Scheeren Thomas W L, Picker Olaf
Department of Anaesthesiology, University Hospital Duesseldorf, Moorenstrasse 5, 40225 Duesseldorf, Germany.
Intensive Care Med. 2008 Oct;34(10):1898-906. doi: 10.1007/s00134-008-1183-8. Epub 2008 Jun 25.
To clarify the effects of hypercapnia (increased PaCO2) on gastric mucosal oxygenation during anaesthesia in dogs.
Prospective, controlled animal study.
Experimental research laboratory of an university hospital.
Six chronically instrumented dogs.
Dogs were anaesthetized (sevoflurane 1.5 MAC), mechanically ventilated (etCO2 = 35 mmHg) and randomly assigned to the following protocols: in a first series, ventilation was adjusted to increase etCO(2) to 45, 55, 65 and 70 mmHg. In a second series, animals were ventilated to achieve 70 mmHg of etCO2, which was maintained for 120 min to test if effects are transient or prolonged and to achieve a similar time course in both protocols.
Gastric mucosal oxygenation (microHbO2) was assessed continuously by tissue reflectance spectrophotometry. Mean arterial blood pressure (MAP) and cardiac output (CO) were continuously measured. Blood was sampled for blood gas analysis and lactate concentration. Hypercapnia increased gastric mucosal oxygenation concentration dependently from 48 +/- 6% (35 mmHg etCO2) to 51 +/- 4, 54 +/- 5, 56 +/- 5 and 59 +/- 3% (etCO2 45, 55, 65 and 70 mmHg, respectively). This reflected changes in CO (68 +/- 16, 74 +/- 16, 82 +/- 12, 91 +/- 11 and 97 +/- 16 ml kg(-1) min(-1), respectively) and systemic oxygen delivery (10 +/- 2, 11 +/- 3, 13 +/- 2, 14 +/- 2 and 14 +/- 2 ml kg(-1) min(-1), respectively). These effects persisted for 2 h (microHbO2 53 +/- 6 vs. 64 +/- 4%, CO 73 +/- 16 vs. 92 +/- 15 ml kg(-1) min(-1), DO2 12 +/- 4 vs. 14 +/- 3 ml kg(-1) min(-1), etCO2 35 and 70 mmHg, respectively).
Hypercapnia increased systemic and regional oxygenation. If this experimental finding may be transferred to the clinical setting, permissive hypercapnia might be used to augment the oxygenation of the splanchnic region, e.g. gastrointestinal mucosa.
阐明高碳酸血症(动脉血二氧化碳分压升高)对犬麻醉期间胃黏膜氧合的影响。
前瞻性对照动物研究。
某大学医院的实验研究实验室。
6只长期植入仪器的犬。
犬麻醉(七氟醚1.5MAC),机械通气(呼气末二氧化碳分压 = 35mmHg),并随机分为以下方案:在第一个系列中,调整通气使呼气末二氧化碳分压升高至45、55、65和70mmHg。在第二个系列中,使动物通气以达到70mmHg的呼气末二氧化碳分压,并维持120分钟,以测试效应是短暂的还是持久的,并使两个方案具有相似的时间进程。
通过组织反射分光光度法连续评估胃黏膜氧合(微血红蛋白氧含量)。连续测量平均动脉血压(MAP)和心输出量(CO)。采集血样进行血气分析和乳酸浓度测定。高碳酸血症使胃黏膜氧合浓度依赖性增加,从48±6%(呼气末二氧化碳分压35mmHg)分别增至51±4%、54±5%、56±5%和59±3%(呼气末二氧化碳分压45、55、65和70mmHg)。这反映了心输出量(分别为68±16、74±16、82±12、91±11和97±16ml·kg⁻¹·min⁻¹)以及全身氧输送(分别为10±2、11±3、13±2、14±2和14±2ml·kg⁻¹·min⁻¹)的变化。这些效应持续2小时(微血红蛋白氧含量分别为53±6%和64±4%,心输出量分别为73±16和92±15ml·kg⁻¹·min⁻¹,氧输送分别为12±4和14±3ml·kg⁻¹·min⁻¹,呼气末二氧化碳分压分别为35和70mmHg)。
高碳酸血症增加全身和局部氧合。如果这一实验结果可应用于临床情况,允许性高碳酸血症可用于增强内脏区域(如胃肠道黏膜)的氧合。