Martínez Guerra M L, Fernández Bonetti P, Sandoval Zárate J, Lupi Herrera E
Arch Inst Cardiol Mex. 1981 Jul-Aug;51(4):365-70.
Thirty-five patients with an average overweight of 67.1% were studied. Pulmonary restriction of a variable degree was found in 68.6/; in 60% due to reduction of respiratory reserve volume. Bronchial obstruction was detected in 57% as measured by forced midexpiratory flow (25-75%). In addition, 14% showed a decrease of 75-85% in forced expiratory flow, which suggested that the pathology was located in the small respiratory airways. The PaO2 while breathing room air and in a resting state was of 52.6 +/- 9.42 mmHg, and after breathing it increased to 69.07 +/- 11.01 mmHg. The PaO2 breathing inspiratory fractions of 99.6% O2 in a resting condition was 309.34 +/- 70.07 mmHg, and after deep breathing it rose to 354.0 +/- 64.27 mmHg. The mechanisms which produce hypoxemia in the obese were analysed and it was concluded that they were due fundamentally to alterations of the ventilation perfusion ratio and to an increase of the venous-arterial shunt. In some cases, alveolar hypoventilation contributed (Pickwick syndrome). By increasing the pulmonary volume with deep breathing, the ventilation perfusion ratio improves or becomes normal, likewise, the venous-arterial shunt can improve or persist as the only cause of hypoxemia.
对35名平均超重67.1%的患者进行了研究。发现68.6%的患者存在不同程度的肺限制;其中60%是由于呼吸储备量减少所致。通过用力呼气中期流速(25%-75%)测量,57%的患者存在支气管阻塞。此外,14%的患者用力呼气流量下降75%-85%,这表明病变位于小呼吸道。静息状态下呼吸室内空气时的动脉血氧分压(PaO2)为52.6±9.42 mmHg,呼吸后升至69.07±11.01 mmHg。静息状态下呼吸含99.6%氧气的吸入气时的PaO2为309.34±70.07 mmHg,深呼吸后升至354.0±64.27 mmHg。分析了肥胖患者产生低氧血症的机制,得出结论认为其主要是由于通气-灌注比例改变和静脉-动脉分流增加所致。在某些情况下,肺泡通气不足也起作用(匹克威克综合征)。通过深呼吸增加肺容量,通气-灌注比例可改善或恢复正常,同样,静脉-动脉分流可改善或持续存在,成为低氧血症的唯一原因。