Pfeiffer B, Hachenberg T, Feyerherd F, Wendt M
Klinik und Poliklinik für Anästhesiologie und Intensivmedizin, Ernst-Moritz-Arndt-Universität Greifswald.
Anasthesiol Intensivmed Notfallmed Schmerzther. 1998 Jun;33(6):367-72. doi: 10.1055/s-2007-994265.
Low volume pressure-limited ventilation with permissive hypercapnia (PH) may decrease the mechanical stress of the lung in acute respiratory insufficiency. Alveolar PCO2 is a determinant of regional ventilation, whereas increased mixed-venous and arterial PCO2 may affect systemic and pulmonary haemodynamics. The aim of this study was to analyse the ventilation-perfusion (VA/Q) distribution during controlled ventilation with permissive hypercapnia.
The study was approved by the ethical committee of the Ernst-Moritz-Arndt University of Greifswald. Eleven patients with severe ARDS (lung injury severity score 2.77 +/- 0.47) were studied. Intrapulmonary shunt (QS/QT, % of QT), lung areas with 0.005 < or = VA/Q < or = 0.1 ("low" VA/Q, % of QT), lung areas with 10 < or = VA/Q < or = 100 ("high" VA/Q, % of VE), dead space ventilation (VD/VT = VA/Q > 100, % of VE) and the mean distribution of ventilation (Vmean VA/Q) and perfusion (Qmean VA/Q) were determined by the multiple inert gas elimination technique during normocapnic (NC) and hypercapnic (HC) mechanical ventilation. In addition, systemic mean arterial and pulmonary arterial pressure, cardiac output (CO) and arterial and mixed venous partial pressures for oxygen (PaO2, PvO2) and carbondioxide (PaCO2, PvCO2) were assessed.
Low-volume pressure-limited ventilation was associated with moderate hypercapnia (PaCO2 = 61 +/- 12 mmHg vs. 39 +/- 6 mmHg, p < 0.01). QS/QT increased (28 +/- 16% [NC] vs. 36 +/- 17% [HC], p < 0.05), whereas Qmean VA/Q decreased from 1.01 +/- 0.37 (NC) to 0.65 +/- 0.49 (HC), (p < 0.01) and Vmean VA/Q decreased from 1.54 +/- 0.58 (NC) to 1.12 +/- 0.93 (HC) (p < 0.05). Hypercapnia induced mild systemic hypotension and pulmonary hypertension. CO increased from 10.8 +/- 2.3 l/min to 11.6 +/- 2.6 l/min (p < 0.05). PaO2 was almost unchanged, but PvO2 increased significantly from 40 +/- 4 mmHg (NC) to 49 +/- 7 mmHg (HC) (p < 0.01).
The mechanical ventilation with permissive hypercapnia may increase shunt due to alveolar derecruitement and an impaired hypoxic pulmonary vasoconstriction. PaO2 was unchanged due to an increased CO, PvO2 and--to a lesser extent--shift of the oxyhaemoglobin dissociation curve.
采用允许性高碳酸血症（PH）的小潮气量压力限制通气可能会降低急性呼吸功能不全时肺的机械应力。肺泡二氧化碳分压（PCO2）是区域通气的决定因素，而混合静脉血和动脉血PCO2升高可能会影响全身和肺的血流动力学。本研究的目的是分析允许性高碳酸血症控制通气期间的通气-灌注（VA/Q）分布。
本研究经格赖夫斯瓦尔德恩斯特-莫里茨-阿恩特大学伦理委员会批准。对11例重度急性呼吸窘迫综合征患者（肺损伤严重程度评分2.77±0.47）进行了研究。在正常碳酸血症（NC）和高碳酸血症（HC）机械通气期间，采用多惰性气体消除技术测定肺内分流（QS/QT，占心输出量QT的百分比）、0.005≤VA/Q≤0.1的肺区域（“低”VA/Q，占QT的百分比）、10≤VA/Q≤100的肺区域（“高”VA/Q，占每分钟通气量VE的百分比）、死腔通气（VD/VT = VA/Q＞100，占VE的百分比）以及通气（Vmean VA/Q）和灌注（Qmean VA/Q）的平均分布。此外，还评估了全身平均动脉压和肺动脉压、心输出量（CO）以及动脉血和混合静脉血的氧分压（PaO2、PvO2）和二氧化碳分压（PaCO2、PvCO2）。
小潮气量压力限制通气与中度高碳酸血症相关（PaCO2 = 61±12 mmHg对39±6 mmHg，p＜0.01）。QS/QT增加（28±16%[NC]对36±17%[HC]，p＜0.05），而Qmean VA/Q从1.01±0.37（NC）降至0.65±0.49（HC），（p＜0.01），Vmean VA/Q从1.54±0.58（NC）降至1.12±0.93（HC）（p＜0.05）。高碳酸血症导致轻度全身低血压和肺动脉高压。CO从10.8±2.3升/分钟增加至11.6±2.6升/分钟（p＜0.05）。PaO2几乎未变，但PvO2从40±4 mmHg（NC）显著增加至49±7 mmHg（HC）（p＜0.01）。
允许性高碳酸血症机械通气可能因肺泡萎陷和缺氧性肺血管收缩受损而增加分流。由于CO增加、PvO2增加以及氧合血红蛋白解离曲线较小程度的偏移，PaO2未发生变化。
