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肺气肿的病理生理学

Pathophysiology of emphysema.

作者信息

Robins A G

出版信息

Clin Chest Med. 1983 Sep;4(3):413-20.

PMID:6357602
Abstract

The pathophysiology of emphysema is best explained on the basis of decreased pulmonary elastic recoil. At any pleural pressure, the lung volume is higher than normal. Additionally, the altered relation between pleural and alveolar pressure facilitates expiratory dynamic compression of airways. Such compression limits airflow during forced expiration and, in severe instances, during tidal expiration. Another factor contributing to airflow limitation is disease of the airways, both large and small. In general, patients with relatively pure emphysema maintain blood gases in or near the normal range until very late in their course. PaO2 is maintained because of the preserved matching of ventilation and perfusion as alveolar walls are destroyed. PaCO2 is maintained because the ventilatory response to CO2 is not usually impaired. It is not clear why patients who are categorized clinically as "chronic bronchitics" are more likely to respond to an increased flow-resistive work of breathing by hypoventilating. Physical findings in emphysema are not specific. Radiologic changes are insensitive and are of less value than physiologic measurements.

摘要

肺气肿的病理生理学最好基于肺弹性回缩力降低来解释。在任何胸膜腔内压下,肺容积均高于正常。此外,胸膜腔与肺泡压力之间关系的改变促进了气道的呼气动态压缩。这种压缩在用力呼气时限制气流,在严重情况下,在潮气量呼气时也会限制气流。导致气流受限的另一个因素是大小气道疾病。一般来说,相对单纯性肺气肿患者在病程晚期之前,其血气维持在正常范围或接近正常范围。由于肺泡壁破坏时通气与灌注仍保持匹配,所以PaO2得以维持。PaCO2得以维持是因为对CO2的通气反应通常未受损。目前尚不清楚临床上归类为“慢性支气管炎患者”为何更有可能通过通气不足来应对呼吸气流阻力增加的情况。肺气肿的体格检查结果并不具有特异性。放射学改变不敏感,其价值低于生理学测量。

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