Department of Emergency Medicine, University of Minnesota, Minneapolis, MN, USA.
Resuscitation. 2013 Apr;84(4):450-3. doi: 10.1016/j.resuscitation.2012.07.036. Epub 2012 Aug 17.
Intrathoracic pressure regulation (IPR) is a novel, noninvasive therapy intended to increase cardiac output and blood pressure in hypotensive states by generating a negative end expiratory pressure of -12 cm H2O between positive pressure ventilations. In this first feasibility case-series, we tested the hypothesis that IPR improves End tidal (ET) CO2 during cardiopulmonary resuscitation (CPR). ETCO2 was used as a surrogate measure for circulation.
All patients were treated initially with manual CPR and an impedance threshold device (ITD). When IPR-trained medics arrived on scene the ITD was removed and an IPR device (CirQLATOR™) was attached to the patient's advanced airway (intervention group). The IPR device lowered airway pressures to -9 mmHg after each positive pressure ventilation for the duration of the expiratory phase. ETCO2, was measured using a capnometer incorporated into the defibrillator system (LifePak™). Values are expressed as mean ± SEM. Results were compared using paired and unpaired Student's t test. p values of <0.05 were considered statistically significant.
ETCO2 values in 11 patients in the case series were compared pre and during IPR therapy and also compared to 74 patients in the control group not treated with the new IPR device. ETCO2 values increased from an average of 21 ± 1 mmHg immediately before IPR application to an average value of 32 ± 5 mmHg and to a maximum value of 45 ± 5mmHg during IPR treatment (p<0.001). In the control group ETCO2 values did not change significantly. Return of spontaneous circulation (ROSC) rates were 46% (34/74) with standard CPR and ITD versus 73% (8/11) with standard CPR and the IPR device (p<0.001).
ETCO2 levels and ROSC rates were significantly higher in the study intervention group. These findings demonstrate that during CPR circulation may be significantly augmented by generation of a negative end expiratory pressure between each breath.
胸腔内压调节（IPR）是一种新型的非侵入性治疗方法，旨在通过在正压通气之间产生-12cmH2O 的呼气末负压来增加低血压状态下的心输出量和血压。在这项首次可行性病例系列研究中，我们检验了 IPR 可提高心肺复苏（CPR）期间潮气末（ET）CO2 的假设。ETCO2 被用作循环的替代测量指标。
所有患者最初均接受手动 CPR 和阻抗阈值设备（ITD）治疗。当接受过 IPR 培训的医护人员到达现场时，将 ITD 移除，并将 IPR 设备（CirQLATOR™）连接到患者的高级气道（干预组）。在呼气阶段，IPR 设备在每次正压通气后将气道压力降低至-9mmHg。使用整合在除颤器系统（LifePak™）中的二氧化碳描记器测量 ETCO2。数值表示为平均值±SEM。使用配对和非配对学生 t 检验比较结果。p 值<0.05 被认为具有统计学意义。
在病例系列中的 11 名患者中，比较了 IPR 治疗前后的 ETCO2 值，并与未接受新 IPR 设备治疗的 74 名对照组患者进行了比较。ETCO2 值从 IPR 应用前的平均 21±1mmHg 增加到 IPR 治疗期间的平均 32±5mmHg 和最大值 45±5mmHg（p<0.001）。在对照组中，ETCO2 值没有显著变化。ROSC 率在接受标准 CPR 和 ITD 的患者中为 46%（34/74），而在接受标准 CPR 和 IPR 设备的患者中为 73%（8/11）（p<0.001）。
在研究干预组中，ETCO2 水平和 ROSC 率显著更高。这些发现表明，在 CPR 期间，通过在每次呼吸之间产生呼气末负压，循环可能会得到显著增强。
