Compressions given during cardiopulmonary resuscitation generate small, ineffective passive ventilations through oscillating waves. Positive end-expiratory pressure increases the volume of these passive ventilations; however, its effect on passive ventilation is unknown. Our objective was to determine if increasing positive end-expiratory pressure during cardiopulmonary resuscitation increases passive ventilation generated by compressions to a clinically significant point. This study was conducted on 13 Landrace-Yorkshire pigs. After inducing cardiac arrest with bupivacaine, cardiopulmonary resuscitation was performed with a LUCAS 3.1. During cardiopulmonary resuscitation, pigs were ventilated at a positive end-expiratory pressure of 0, 5, 10, 15, 20 cmH2O (randomly determined) for 9 min. Using the NM3 respiratory monitoring device, expired minute ventilation and volumetric capnography were measured. Arterial blood gas was obtained for each positive end-expiratory pressure level to compare the effects of positive end-expiratory pressure on carbon dioxide. Increasing positive end-expiratory pressure from 0 to 20 cmH2O increased the mean (SEM) expired minute ventilation from 6.33 (0.04) to 7.33 (0.04) mL/min. With the 5-cmH2O incremental increases in positive end-expiratory pressure from 0 to 20 cmH2O, volumetric capnography increased from a mean (SEM) of 94.19 (0.78) to 115.18 (0.8) mL/min, except for 15 cmH2O, which showed greater carbon dioxide exhalation with volumetric capnography compared with 20 cmH2O. PCO2 declined significantly as positive end-expiratory pressure was increased from 0 to 20 cmH2O. When increasing positive end-expiratory pressure from 0 to 20, the contribution to overall ventilation from gas oscillations generated by the compressions became more significant, and may even lead to hypocapnia, especially when using positive end-expiratory pressures between 15 and 20.

中文翻译：

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在猪模型中呼气末正压对 CPR 按压产生的额外被动通气的影响

心肺复苏期间进行的按压会通过振荡波产生小而无效的被动通气。呼气末正压会增加这些被动通气量；然而，它对被动通气的影响尚不清楚。我们的目标是确定在心肺复苏期间增加呼气末正压是否会将按压产生的被动通气增加到具有临床意义的程度。这项研究是在 13 头长白-约克郡猪身上进行的。用布比卡因诱导心脏骤停后，用 LUCAS 3.1 进行心肺复苏。在心肺复苏期间，猪以 0、5、10、15、20 cmH2O（随机确定）的呼气末正压通气 9 分钟。使用NM3呼吸监测装置，测量呼出分钟通气量和容积二氧化碳图。获取每个呼气末正压水平的动脉血气，以比较呼气末正压对二氧化碳的影响。将呼气末正压从 0 增加到 20 cmH2O，使平均 (SEM) 每分钟呼气通气量从 6.33 (0.04) 增加到 7.33 (0.04) mL/min。随着呼气末正压从 0 到 20 cmH2O 增加 5 cmH2O，容积二氧化碳图从平均值 (SEM) 的 94.19 (0.78) 增加到 115.18 (0.8) mL/min，除了 15 cmH2O，显示更大与 20 cmH2O 相比，容积式二氧化碳描记法呼出二氧化碳。随着呼气末正压从 0 增加到 20 cmH2O，PCO2 显着下降。当呼气末正压从 0 增加到 20 时，