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Physiological dead space ventilation, disease severity and outcome in ventilated patients with hypoxaemic respiratory failure due to coronavirus disease 2019

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Dear Editor, The severity of acute hypoxemic respiratory failure (AHRF) in Coronavirus Disease 2019 (COVID-19) correlates correlates poorly with lung weight and lung mechanics, leading to the proposal of phenotypes… Click to show full abstract

Dear Editor, The severity of acute hypoxemic respiratory failure (AHRF) in Coronavirus Disease 2019 (COVID-19) correlates correlates poorly with lung weight and lung mechanics, leading to the proposal of phenotypes that may be associated with similar degree of hypoxaemia but different lung volume, weight, and compliance [1]. The alteration of the pulmonary vascular tone and immune thrombosis of the alveolar capillaries [2] may account for these pathophysiological characteristics and for the high physiological dead space observed in these patients. To describe estimated indices of physiological dead space—and their association with respiratory mechanics, severity of hypoxaemia, biomarkers, and outcomes—we performed a retrospective analysis of adult patients with COVID-19 respiratory failure requiring mechanical ventilation in four medical Intensive Care Units (ICU) within Guy’s and St Thomas’ NHS Trust—London, UK (Ethics reference: 10,796). We used the recorded values at the time of worst PaO2/ FiO2 observed on the day of critical care admission. Continuous variables were compared using Mann–Whitney U test. This cohort included 213 patients (73% males), mean (95%CI) age 56 (54–57) years, and PaO2/FiO2 128 (121–135) mmHg. When subdivided in four groups based on cut-off PaO2/FiO2 of 150 mmHg and compliance of 40 mL/cmH2O; 72% (n = 154) had PaO2/ FiO2 < 150 mmHg, of these, 112 (73%, or 53% of the overall cohort) had compliance < 40 mL/cmH2O (eTable 1). The mean (95%CI) estimated physiological dead space fraction [3] was high in the entire cohort at 0.53 (0.51–0.56). ICU outcome was available for 193 patients, where estimated physiological dead space fraction was higher in non-survivors [median (IQR), 0.57 (0.46–0.65) vs. 0.5 (0.4–0.64); p = 0.03]. All estimates of physiological dead space increased with the degree of hypoxaemia, but not with the reduction in lung compliance (Fig. 1). Compared with patients with PaO2/FiO2 > 150 mmHg, patients with PaO2/FiO2 < 150 mmHg had higher estimated physiological dead space fraction [0.55 (0.52–0.57) vs. 0.5 (0.47–0.53); p = 0.036) (Fig. 1A), mean (95%CI) corrected minute volume [4] [9.3(8.8–9.7) vs. 8.2 (7.6–8.8) L/min; p = 0.004] (Fig. 1B), and ventilatory ratio [5] [1.43 (1.37– 1.5) vs. 1.29 (1.2–1.38); p = 0.001] (Fig. 1C). Although patients with compliance < 40 mL/cmH2O had a higher corrected minute volume [4] [9.4 (8.8–10) vs. 8.8 (8.4– 9.3) L/min; p = 0.023] (Fig. 1C), there was no difference in the two compliance groups in estimated physiological dead space fraction [0.55 (0.48–0.56) vs. 0.54 (0.52–0.56); p = 0.72] (Fig. 1A) and ventilatory ratio [5] 1.4 (1.3–1.5) vs. 1.4 (1.33–1.46); p = 0.76) (Fig. 1B). *Correspondence: [email protected] 1 Department of Adult Critical Care, Guy’s and St Thomas’ NHS Foundation Trust, King’s Health Partners, St Thomas’ Hospital, 1st Floor East Wing, Westminster Bridge Road, London SE1 7EH, UK Full author information is available at the end of the article

Keywords: physiological dead; compliance; disease; dead space; pao2 fio2

Journal Title: Intensive Care Medicine
Year Published: 2020

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