Howell H B, Parker J, Benumof J L, Harders D
Department of Anesthesia, University of California, San Diego School of Medicine, La Jolla 92093.
J Cardiothorac Anesth. 1989 Oct;3(5):558-63. doi: 10.1016/0888-6296(89)90152-x.
It has previously been reported that continuous insufflation of either supracarinal or subcarinal oxygen in addition to intermittent positive-pressure ventilation (IPPV) in patients under general anesthesia, and in critically ill patients in the intensive care unit, causes increased proximal airway pressure, decreased systemic blood pressure, and decreased cardiac output. The investigators hypothesized that these deleterious hemodynamic effects were due to intrapulmonary air trapping, resulting in an increased distal intrapulmonary pressure and volume. The purpose of this study was to test this hypothesis in an appropriate mechanical lung model. The study determined end-inspiratory and end-expiratory lung pressures and volumes during eight experimental sequences: (1) IPPV alone; (2) insufflation of oxygen alone at 2.5, 5.0, and 10.0 L/min (O2-2.5, 5.0, 10.0); (3, 4, and 5) IPPV plus insufflation of oxygen (IPPV + O2-0.0, 2.5, 5.0, 10.0) through a supracarinal catheter (sequence 3), subcarinal catheters (sequence 4), and through a CO2 sampling port of an endotrachael tube (sequence 5); (6 and 7) IPPV + O2-5.0 with increased expiratory time caused by an increased inspiratory flow rate (sequence 6) and a decreased respiratory rate (sequence 7); (8) IPPV + O2-5.0 with increased airway diameter. Experimental sequences 1 and 2 resulted in no increases or minimal ones in lung pressure and volume, respectively. With each insufflation catheter system (sequences 3, 4, and 5), each incremental increase in insufflation flow rate resulted in significant increases in lung pressure and volume. Increasing expiratory times (sequences 6 and 7 compared with 3, 4, and 5) decreased lung pressure and volume. Increasing the airway diameter (sequence 8) had only slight effect on lung pressure and volume.(ABSTRACT TRUNCATED AT 250 WORDS)
此前有报道称，在全身麻醉患者以及重症监护病房的危重症患者中，除间歇性正压通气（IPPV）外，持续经隆突上或隆突下吹入氧气会导致近端气道压力升高、体循环血压降低以及心输出量减少。研究人员推测，这些有害的血流动力学效应是由于肺内气体潴留，导致肺内远端压力和容积增加。本研究的目的是在合适的机械肺模型中验证这一假设。该研究在八个实验序列中测定了吸气末和呼气末的肺压力和容积：（1）仅IPPV；（2）分别以2.5、5.0和10.0 L/min的流速单独吹入氧气（O2 - 2.5、5.0、10.0）；（3、4和5）通过隆突上导管（序列3）、隆突下导管（序列4）以及通过气管内导管的二氧化碳采样口（序列5）进行IPPV加吹入氧气（IPPV + O2 - 0.0、2.5、5.0、10.0）；（6和7）通过增加吸气流量（序列6）和降低呼吸频率（序列7）来延长呼气时间的IPPV + O2 - 5.0；（8）增加气道直径的IPPV + O2 - 5.0。实验序列1和2分别导致肺压力和容积无增加或仅有极小增加。对于每个吹入导管系统（序列3、4和5），吹入流速的每次增量增加都会导致肺压力和容积显著增加。延长呼气时间（序列6和7与3、4和5相比）会降低肺压力和容积。增加气道直径（序列8）对肺压力和容积仅有轻微影响。（摘要截选至250字）
