Buehler Sarah, Lozano-Zahonero Sara, Wirth Steffen, Runck Hanna, Gamerdinger Katharina, Förster Katharina, Haberstroh Jörg, Guttmann Josef, Schumann Stefan
1Division of Experimental Anesthesiology, Department of Anesthesiology and Intensive Care Medicine, University Medical Center, Freiburg, Germany. 2Department of Cardiovascular Surgery, Heart Center, University of Freiburg, Freiburg, Germany. 3Experimental Surgery, CEMT-FR, University Medical Center Freiburg, Freiburg, Germany.
Crit Care Med. 2016 Jul;44(7):e502-8. doi: 10.1097/CCM.0000000000001474.
In mechanical ventilation, normoventilation in terms of PCO2 can be achieved by titration of the respiratory rate and/or tidal volume. Although a linear relationship has been found between changes in respiratory rate and resulting changes in end-tidal cO2 (△PetCO2) as well as between changes in respiratory rate and equilibration time (teq) for mechanically ventilated patients without lung injury, it is unclear whether a similar relationship holds for acute lung injury or altered hemodynamics.
We performed a prospective randomized controlled animal study of the change in PetCO2 with changes in respiratory rate in a lung-healthy, lung-injury, lung-healthy + altered hemodynamics, and lung-injury + altered hemodynamics pig model.
University research laboratory.
Twenty mechanically ventilated pigs.
Moderate lung injury was induced by injection of oleic acid in 10 randomly assigned pigs, and after the first round of measurements, cardiac output was increased by approximately 30% by constant administration of noradrenalin in both groups.
We systematically increased and decreased changes in respiratory rate according to a set protocol: +2, -4, +6, -8, +10, -12, +14 breaths/min and awaited equilibration of Petco2. We found a linear relationship between changes in respiratory rate and △PetCO2 as well as between changes in respiratory rate and teq. A two-sample t test resulted in no significant differences between the lung injury and healthy control group before or after hemodynamic intervention. Furthermore, exponential extrapolation allowed prediction of the new PetCO2 equilibrium and teq after 5.7 ± 5.6 min.
The transition between PetCO2 equilibria after changes in respiratory rate might not be dependent on moderate lung injury or cardiac output but on the metabolic production or capacity of cO2 stores. Linear relationships previously found for lung-healthy patients and early prediction of PetCO2 equilibration could therefore also be used for the titration of respiratory rate on the PetCO2 for a wider range of pathologies by the physician or an automated ventilation system.
在机械通气中,通过调整呼吸频率和/或潮气量可实现二氧化碳分压方面的正常通气。尽管在无肺损伤的机械通气患者中,已发现呼吸频率变化与呼出末二氧化碳变化量(△PetCO2)以及呼吸频率变化与平衡时间(teq)之间存在线性关系,但尚不清楚急性肺损伤或血流动力学改变时是否也存在类似关系。
我们在肺健康、肺损伤、肺健康+血流动力学改变以及肺损伤+血流动力学改变的猪模型中,对呼吸频率变化时PetCO2的变化进行了一项前瞻性随机对照动物研究。
大学研究实验室。
20只机械通气猪。
随机选取10只猪注射油酸诱导中度肺损伤,在第一轮测量后,两组均通过持续给予去甲肾上腺素使心输出量增加约30%。
我们按照既定方案系统地增加和减少呼吸频率变化:+2、-4、+6、-8、+10、-12、+14次/分钟,并等待Petco2达到平衡。我们发现呼吸频率变化与△PetCO2以及呼吸频率变化与teq之间存在线性关系。双样本t检验结果显示,血流动力学干预前后,肺损伤组与健康对照组之间无显著差异。此外,指数外推法可预测5.7±5.6分钟后的新PetCO2平衡和teq。
呼吸频率变化后PetCO2平衡之间的转变可能不依赖于中度肺损伤或心输出量,而是取决于二氧化碳的代谢产生或储存能力。因此,先前在肺健康患者中发现的线性关系以及PetCO2平衡的早期预测,也可用于医生或自动通气系统针对更广泛病症,根据PetCO2滴定呼吸频率。