Department of Internal Medicine V-Pneumology, Allergology and Critical Care Medicine, 39072University Hospital of Saarland and Saarland University, Homburg/Saar, Germany.
Interdisciplinary COVID-19-Center, 39072University Hospital of Saarland, Saarland University, Homburg/Saar, Germany.
J Intensive Care Med. 2021 Jun;36(6):655-663. doi: 10.1177/0885066621995386. Epub 2021 Mar 8.
It has been suggested that COVID-19-associated severe respiratory failure (CARDS) might differ from usual acute respiratory distress syndrome (ARDS) due to failing autoregulation of pulmonary vessels and higher shunt. We sought to investigate pulmonary hemodynamics and ventilation properties in patients with CARDS compared to patients with ARDS of pulmonary origin.
This was a retrospective analysis of prospectively collected data from consecutive adults with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 patients treated in our ICU in 04/2020 and a comparison of the data to matched controls with ARDS due to respiratory infections treated in our ICU from 01/2014 to 08/2019 for whom pulmonary artery catheter data were available.
CARDS patients (n = 10) had ventilation characteristics similar to those of ARDS (n = 10) patients. Nevertheless, mechanical power applied by ventilation was significantly higher in CARDS patients (23.4 ± 8.9 J/min) than in ARDS (15.9 ± 4.3 J/min; < 0.05). COVID-19 patients had similar pulmonary artery pressure but significantly lower pulmonary vascular resistance, as cardiac output was higher in CARDS vs. ARDS patients ( < 0.05). Shunt fraction and dead space were similar in CARDS compared to ARDS ( > 0.05) and were correlated with hypoxemia in both groups. The arteriovenous pCO difference (▵pCO) was elevated (CARDS 5.5 ± 2.8 mmHg vs. ARDS 4.7 ± 1.1 mmHg; > 0.05), as was the PCO/CO ratio (CARDS mean 2.2 ± 1.5 vs. ARDS 1.7 ± 0.8; > 0.05).
Respiratory failure in COVID-19 patients seems to differ only slightly from ARDS regarding ventilation characteristics and pulmonary hemodynamics. Our data indicate microcirculatory dysfunction. More data need to be collected to assure these findings and gain more pathophysiological insights into COVID-19 and respiratory failure.
有人提出,COVID-19 相关的严重呼吸衰竭(CARDS)可能与常见的急性呼吸窘迫综合征(ARDS)不同,因为肺血管的自身调节失败和分流增加。我们试图研究与由呼吸道感染引起的 ARDS 患者相比,CARDS 患者的肺血管动力学和通气特性。
这是对 2020 年 4 月在我们的 ICU 接受治疗的实验室确诊的严重急性呼吸综合征冠状病毒 2 患者的前瞻性数据进行的回顾性分析,并将这些数据与从 2014 年 1 月至 2019 年 8 月在我们的 ICU 接受治疗且有肺动脉导管数据的由呼吸道感染引起的 ARDS 患者的匹配对照组进行比较。
CARDS 患者(n = 10)的通气特征与 ARDS 患者(n = 10)相似。然而,CARDS 患者的通气机械功率明显高于 ARDS 患者(23.4 ± 8.9 J/min)(23.4 ± 8.9 J/min)(<0.05)。COVID-19 患者的肺动脉压相似,但肺血管阻力明显较低,因为 CARDS 患者的心输出量高于 ARDS 患者(<0.05)。CARDS 患者的分流量和死腔量与 ARDS 患者相似(>0.05),并且与两组的低氧血症相关。动静脉 pCO 差(△pCO)升高(CARDS 5.5 ± 2.8 mmHg 比 ARDS 4.7 ± 1.1 mmHg;>0.05),PCO/CO 比值(CARDS 平均 2.2 ± 1.5 比 ARDS 1.7 ± 0.8;>0.05)升高。
COVID-19 患者的呼吸衰竭在通气特征和肺血管动力学方面与 ARDS 仅略有不同。我们的数据表明存在微循环功能障碍。需要收集更多的数据来证实这些发现,并对 COVID-19 和呼吸衰竭的病理生理学有更深入的了解。