Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, and The University of Sydney, Australia.
Compr Physiol. 2011 Apr;1(2):663-97. doi: 10.1002/cphy.c090012.
Ventilation-perfusion (VA/Q) inequality is the underlying abnormality determining hypoxemia and hypercapnia in lung diseases. Hypoxemia in asthma is characterized by the presence of low VA/Q units, which persist despite improvement in airway function after an attack. This hypoxemia is generally attenuated by compensatory redistribution of blood flow mediated by hypoxic vasoconstriction and changes in cardiac output, however, mediator release and bronchodilator therapy may cause deterioration. Patients with chronic obstructive pulmonary disease have more complex patterns of VA/Q inequality, which appear more fixed, and changes in blood flow and ventilation have less benefit in improving gas exchange efficiency. The inability of ventilation to match increasing cardiac output limits exercise capacity as the disease progresses. Deteriorating hypoxemia during exacerbations reflects the falling mixed venous oxygen tension from increased respiratory muscle activity, which is not compensated by any redistribution of VA/Q ratios. Shunt is not a feature of any of these diseases. Patients with cystic fibrosis (CF) have no substantial shunt when managed according to modern treatment regimens. Interstitial lung diseases demonstrate impaired oxygen diffusion across the alveolar-capillary barrier, particularly during exercise, although VA/Q inequality still accounts for most of the gas exchange abnormality. Hypoxemia may limit exercise capacity in these diseases and in CF. Persistent hypercapnic respiratory failure is a feature of advancing chronic obstructive pulmonary disease and CF, closely associated with sleep disordered breathing, which is not a prominent feature of the other diseases. Better understanding of the mechanisms of hypercapnic respiratory failure, and of the detailed mechanisms controlling the distribution of ventilation and blood flow in the lung, are high priorities for future research.
通气-灌注（VA/Q）失衡是导致肺部疾病低氧血症和高碳酸血症的根本异常。哮喘中的低氧血症的特征是存在低 VA/Q 单位，尽管气道功能在发作后得到改善，但这些单位仍然存在。这种低氧血症通常通过缺氧性血管收缩和心输出量变化介导的血液重新分布得到缓解，然而，介质释放和支气管扩张剂治疗可能会导致恶化。慢性阻塞性肺疾病患者的 VA/Q 失衡模式更为复杂，表现为更为固定，血液和通气的变化对改善气体交换效率的益处较小。随着疾病的进展，通气无法匹配增加的心输出量，从而限制了运动能力。在恶化期间，低氧血症的恶化反映了呼吸肌活动增加导致混合静脉血氧分压下降，而这种下降无法通过任何 VA/Q 比值的重新分布来补偿。分流不是这些疾病的特征。按照现代治疗方案管理的囊性纤维化（CF）患者没有实质性的分流。间质性肺疾病表现为肺泡毛细血管屏障的氧气扩散受损，特别是在运动期间，尽管 VA/Q 失衡仍然是气体交换异常的主要原因。低氧血症可能会限制这些疾病和 CF 中的运动能力。持续性高碳酸血症呼吸衰竭是慢性阻塞性肺疾病和 CF 进展的特征，与睡眠呼吸障碍密切相关，而睡眠呼吸障碍不是其他疾病的突出特征。更好地了解高碳酸血症呼吸衰竭的机制，以及控制肺部通气和血流分布的详细机制，是未来研究的重中之重。
