Department of Anaesthesiology, Mizonokuchi Hospital Teikyo University School of Medicine, Kanagawa, Japan.
PLoS One. 2021 Oct 13;16(10):e0258504. doi: 10.1371/journal.pone.0258504. eCollection 2021.
We previously reported that there were no differences between the lung-protective actions of pressure-controlled inverse ratio ventilation and volume control ventilation based on the changes in serum cytokine levels. Dead space represents a ventilation-perfusion mismatch, and can enable us to understand the heterogeneity and elapsed time changes in ventilation-perfusion mismatch.
This study was a secondary analysis of a randomized controlled trial of patients who underwent robot-assisted laparoscopic radical prostatectomy. The inspiratory to expiratory ratio was adjusted individually by observing the expiratory flow-time wave in the pressure-controlled inverse ratio ventilation group (n = 14) and was set to 1:2 in the volume-control ventilation group (n = 13). Using volumetric capnography, the physiological dead space was divided into three dead space components: airway, alveolar, and shunt dead space. The influence of pressure-controlled inverse ratio ventilation and time factor on the changes in each dead space component rate was analyzed using the Mann-Whitney U test and Wilcoxon's signed rank test.
The physiological dead space and shunt dead space rate were decreased in the pressure-controlled inverse ratio ventilation group compared with those in the volume control ventilation group (p < 0.001 and p = 0.003, respectively), and both dead space rates increased with time in both groups. The airway dead space rate increased with time, but the difference between the groups was not significant. There were no significant changes in the alveolar dead space rate.
Pressure-controlled inverse ratio ventilation reduced the physiological dead space rate, suggesting an improvement in the total ventilation/perfusion mismatch due to improved inflation of the alveoli affected by heterogeneous expansion disorder without hyperinflation of the normal alveoli. However, the shunt dead space rate increased with time, suggesting that atelectasis developed with time in both groups.
我们之前的报告表明，基于血清细胞因子水平的变化，压力控制反比通气与容量控制通气的肺保护作用没有差异。死腔代表通气-灌注不匹配，能让我们了解通气-灌注不匹配的异质性和时间变化。
这是一项机器人辅助腹腔镜前列腺根治术患者的随机对照试验的二次分析。在压力控制反比通气组（n = 14）中通过观察呼气流量-时间波来单独调整吸呼比，将其设置为 1:2，在容量控制通气组（n = 13）中则设置为 1:2。使用容量测二氧化碳图法，将生理死腔分为三个死腔成分：气道、肺泡和分流死腔。采用 Mann-Whitney U 检验和 Wilcoxon 符号秩检验分析压力控制反比通气和时间因素对各死腔成分率变化的影响。
与容量控制通气组相比，压力控制反比通气组的生理死腔和分流血腔率降低（p < 0.001 和 p = 0.003），两组的死腔率均随时间增加而增加。气道死腔率随时间增加，但两组间差异无统计学意义。肺泡死腔率无明显变化。
压力控制反比通气降低了生理死腔率，提示由于不均匀扩张障碍导致的肺泡充气改善，总通气-灌注不匹配得到改善，而正常肺泡没有过度充气。然而，分流血腔率随时间增加，提示两组均随时间发生肺不张。
