Damiani L Felipe, Basoalto Roque, Oviedo Vanessa, Alegria Leyla, Soto Dagoberto, Bachmann M Consuelo, Jalil Yorschua, Santis Cesar, Carpio David, Ulloa Rodrigo, Valenzuela Daniel, Vera Magdalena, Schultz Marcus J, Retamal Jaime, Bruhn Alejandro, Bugedo Guillermo
Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Diagonal Paraguay 362, 6º Piso, P.O. Box 114D, Santiago, Chile.
Departamento de Kinesiología, Facultad de Medicina, Escuela de Ciencias de la Salud, Pontificia Universidad Católica de Chile, Santiago, Chile.
Intensive Care Med Exp. 2025 Jul 9;13(1):69. doi: 10.1186/s40635-025-00782-4.
The respiratory rate (RR) is a key determinant of the mechanical power of ventilation (MP). The effect of reducing the RR on MP and its potential to mitigate ventilator-induced lung injury remains unclear.
To compare invasive ventilation using a lower versus a higher RR with respect to MP and plasma biomarkers of lung injury in COVID-19 ARDS patients.
In a randomized cross-over clinical study in COVID-19 ARDS patients, we compared ventilation using a lower versus a higher RR in time blocks of 12 h. Patients were ventilated with tidal volumes of 6 ml/kg predicted body weight, and positive-end-expiratory pressure and fraction of inspired oxygen according to an ARDS network table. Respiratory mechanics and hemodynamics were assessed at the end of each period, and blood samples were drawn for measurements of inflammatory cytokines, epithelial and endothelial lung injury markers. In a subgroup of patients, we performed echocardiography and esophageal pressure measurements.
We enrolled a total of 32 patients (26 males [81%], aged 52 [44-64] years). The median respiratory rate during ventilation with a lower and a higher RR was 20 [16-22] vs. 30 [26-32] breaths/min (p < 0.001), associated with a lower median minute ventilation (7.3 [6.5-8.5] vs. 11.6 [10-13] L/min [p < 0.001]) and a lower median MP (15 [11-18] vs. 25 [21-32] J/min [p < 0.001]). No differences were observed in any inflammatory (IL-6, IL-8, and TNF-R1), epithelial (s-RAGE and SP-D), endothelial (Angiopoietin-2), or pro-fibrotic activity (TGF-ß) marker between high or low RR. Cardiac function by echocardiography, and respiratory mechanics using esophageal pressure measurements were also not different.
Reducing the respiratory rate decreases mechanical power in COVID-19 ARDS patients but does not reduce plasma lung injury biomarkers levels in this cross-over study. Study registration This study is registered at clinicaltrials.gov (study identifier NCT04641897).
呼吸频率（RR）是通气机械功率（MP）的关键决定因素。降低RR对MP的影响及其减轻呼吸机诱发肺损伤的潜力尚不清楚。
比较新型冠状病毒肺炎（COVID-19）急性呼吸窘迫综合征（ARDS）患者采用较低RR与较高RR进行有创通气时的MP及肺损伤血浆生物标志物。
在一项针对COVID-19 ARDS患者的随机交叉临床研究中，我们在12小时时间段内比较了采用较低RR与较高RR的通气情况。患者采用6 ml/kg预测体重的潮气量进行通气，并根据急性呼吸窘迫综合征网络表格设置呼气末正压和吸入氧分数。在每个时间段结束时评估呼吸力学和血流动力学，并采集血样以测量炎症细胞因子、肺上皮和内皮损伤标志物。在一个亚组患者中，我们进行了超声心动图检查和食管压力测量。
我们共纳入32例患者（26例男性[81%]，年龄52[44 - 64]岁）。较低RR和较高RR通气期间的中位呼吸频率分别为20[16 - 22]次/分钟和30[26 - 32]次/分钟（p < 0.001），相应的中位分钟通气量较低（7.3[6.5 - 8.5]L/分钟 vs. 11.6[10 - 13]L/分钟[p < 0.001]），中位MP也较低（15[11 - 18]焦耳/分钟 vs. 25[21 - 32]焦耳/分钟[p < 0.001]）。在高RR或低RR之间，任何炎症（白细胞介素-6、白细胞介素-8和肿瘤坏死因子受体1）、上皮（可溶性晚期糖基化终末产物受体和表面活性蛋白-D）、内皮（血管生成素-2）或促纤维化活性（转化生长因子-β）标志物均未观察到差异。超声心动图评估的心脏功能以及食管压力测量的呼吸力学也无差异。
在这项交叉研究中，降低COVID-19 ARDS患者的呼吸频率可降低机械功率，但不会降低血浆肺损伤生物标志物水平。研究注册 本研究已在clinicaltrials.gov注册（研究标识符NCT04641897）。
