Continuous long-term wireless measurement of right ventricular pressures and estimated diastolic pulmonary artery pressure in patients with severe COVID-19 acute respiratory distress syndrome

对重症 COVID-19 急性呼吸窘迫综合征患者进行右心室压力和估计舒张期肺动脉压的连续长期无线测量

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Abstract

AIMS: We continuously monitored right ventricular pressures and the estimated diastolic pulmonary artery pressure (ePAD) for up to 30 days in mechanically ventilated patients with severe COVID-19 acute respiratory distress syndrome in order to detect and treat right ventricular and pulmonary artery hypertension. METHODS AND RESULTS: We retrospectively evaluated right ventricular pressures and the ePAD measured in 30 invasively ventilated COVID-19 acute respiratory distress syndrome patients between 1 October 2020 and 31 March 2021. We divided the patients into two groups, survivors and non-survivors based on their 60 day mortality. Primary outcome variables were the values of right ventricular pressures and the ePAD over time after insertion of the right ventricular probe. Right ventricular systolic pressure [RVSP, (IQR; 25th to 75th percentile)] was significantly lower on the first and the last measurement day in the survivors compared with the non-survivors [Day 1: 38 (27-45) vs. 46 (44-49), P = 0.036; last day: 36 (27-44) vs. 51 (40-57) mmHg, P = 0.006]. 16/22 survivors and 7/8 non-survivors received sildenafil orally, one survivor received additionally inhaled nitric oxide and one survivor and one non-survivor each inhaled iloprost. On the last measurement day, both right ventricular pressure amplitude [31 (26-37) vs. 38 (35-47) mmHg, P = 0.027] and ePAD [22 (16-26) vs. 31 (23-34) mmHg, P = 0.043] were significantly lower in the survivors compared with the non-survivors. Four patients in the survivor group developed excessive high RVSP in the course of their disease (peak: 57/61/78/105 mmHg). After sildenafil 20 mg every 8 h, additional inhaled nitric oxide (20 ppm) in one and additional inhaled iloprost 20 μg every 4 h in another patient RVSP consecutively decreased substantially in all four patients until the end of the measurement period (47/23/42/47 mmHg). CONCLUSIONS: The RVSP and right ventricular pressure amplitude both were significantly lower in the survivors compared with those in the non-survivors with a significant decrease in RVSP over time in the survivors suggesting successful lowering by pulmonary vasodilators. The ePAD as an indicator of left heart failure was significantly higher in non-survivors compared to the surviving patients.

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