Hickling K G, Joyce C
Department of Intensive Care, Christchurch Hospital, New Zealand.
Acta Anaesthesiol Scand Suppl. 1995;107:201-8. doi: 10.1111/j.1399-6576.1995.tb04359.x.
Many experimental studies have shown that mechanical ventilation with high tidal volumes (Vt) or with a low end-expiratory volume allowing repeated end-expiratory collapse, can result in acute parenchymal lung injury and probably an inflammatory response. Low volume ventilation with permissive hypercapnia has been used in an attempt to avoid such injury in ARDS. Such management can affect oxygenation in many complex ways. The right-shift of the haemoglobin-oxygen dissociation curve during acute respiratory acidosis may increase venous oxygen tension (PvO2) which could allow increased O2 uptake in ischaemic tissues. Acidosis may reduce intrapulmonary shunt (Qs/Qt) by potentiating hypoxic pulmonary vasoconstriction, and there may also be direct and autonomically mediated effects of hypercapnia both on the lung vasculature and on the airways. Cardiac output usually increases as a consequence of hypercapnia and perhaps as a result of reduced intrathoracic pressure, further increasing PvO2 and CvO2, but the increase in cardiac output (CO) may tend to increase Qs/Qt as flow increases preferentially in unventilated lung. The reduction of mean airway pressure may directly increase Qs/Qt. Hypercapnia may affect the distribution of systemic blood flow both within organs and between organs. Limited clinical studies suggest that tissue oxygenation is usually unchanged or improved during permissive hypercapnia with increased CO, reduced arterio-venous O2 content difference and reduced blood lactate concentration. However, acute hypercapnia per se can reduce lactate production. Further studies are required of this complex issue.
许多实验研究表明，采用高潮气量（Vt）机械通气或采用允许反复呼气末肺萎陷的低呼气末容积机械通气，可导致急性肺实质损伤，并可能引发炎症反应。为避免急性呼吸窘迫综合征（ARDS）出现此类损伤，人们采用了允许性高碳酸血症的小潮气量通气。这种管理方式会以多种复杂方式影响氧合。急性呼吸性酸中毒期间血红蛋白-氧解离曲线右移可能会增加静脉血氧张力（PvO2），这可能会使缺血组织的氧摄取增加。酸中毒可通过增强缺氧性肺血管收缩来减少肺内分流（Qs/Qt），高碳酸血症对肺血管系统和气道可能也有直接及自主神经介导的作用。高碳酸血症通常会使心输出量增加，可能是由于胸内压降低所致，这会进一步增加PvO2和CvO2，但心输出量（CO）增加可能会使Qs/Qt增加，因为未通气肺中的血流优先增加。平均气道压降低可能会直接增加Qs/Qt。高碳酸血症可能会影响全身血流在器官内和器官间的分布。有限的临床研究表明，在允许性高碳酸血症期间，组织氧合通常保持不变或得到改善，同时伴有CO增加、动静脉氧含量差减小和血乳酸浓度降低。然而，急性高碳酸血症本身可减少乳酸生成。对于这个复杂问题还需要进一步研究。
