Haemodynamic changes during prone versus supine position in patients with COVID-19 acute respiratory distress syndrome.

BACKGROUND: Prone positioning improves oxygenation in patients with acute respiratory distress syndrome (ARDS) secondary to COVID-19. However, its haemodynamic effects are poorly understood. OBJECTIVES: The objective of this study was to investigate the acute haemodynamic changes associated with prone position in mechanically ventilated patients with COVID-19 ARDS. The primary objective was to describe changes in cardiac index with prone position. The secondary objectives were to describe changes in mean arterial pressure, FiO2, PaO2/FiO2 ratio, and oxygen delivery (DO2) with prone position. METHODS: We performed this cohort-embedded study in an Australian intensive care unit, between September and November 2021. We included adult patients with severe COVID-19 ARDS, requiring mechanical ventilation and prone positioning for respiratory failure. We placed patients in the prone position for 16 h per session. Using pulse contour technology, we collected haemodynamic data every 5 min for 2 h in the supine position and for 2 h in the prone position consecutively. RESULTS: We studied 18 patients. Cardiac index, stroke volume index, and mean arterial pressure increased significantly in the prone position compared to supine position. The mean cardiac index was higher in the prone group than in the supine group by 0.44 L/min/m2 (95% confidence interval, 0.24 to 0.63) (P < 0.001). FiO2 requirement decreased significantly in the prone position (P < 0.001), with a significant increase in PaO2/FiO2 ratio (P < 0.001). DO2 also increased significantly in the prone position, from a median DO2 of 597 mls O2/min (interquartile range, 504 to 931) in the supine position to 743 mls O2/min (interquartile range, 604 to 1075) in the prone position (P < 0.001). CONCLUSION: Prone position increased the cardiac index, mean arterial pressure, and DO2 in invasively ventilated patients with COVID-19 ARDS. These changes may contribute to improved tissue oxygenation and improved outcomes observed in trials of prone positioning.

ricu: R's interface to intensive care data.

OBJECTIVE: To develop a unified framework for analyzing data from 5 large publicly available intensive care unit (ICU) datasets. FINDINGS: Using 3 American (Medical Information Mart for Intensive Care III, Medical Information Mart for Intensive Care IV, electronic ICU) and 2 European (Amsterdam University Medical Center Database, High Time Resolution ICU Dataset) databases, we constructed a mapping for each database to a set of clinically relevant concepts, which are grounded in the Observational Medical Outcomes Partnership Vocabulary wherever possible. Furthermore, we performed synchronization in the units of measurement and data type representation. On top of this, we built functionality, which allows the user to download, set up, and load data from all of the 5 databases, through a unified Application Programming Interface. The resulting ricu R-package represents the computational infrastructure for handling publicly available ICU datasets, and its latest release allows the user to load 119 existing clinical concepts from the 5 data sources. CONCLUSION: The ricu R-package (available on GitHub and CRAN) is the first tool that enables users to analyze publicly available ICU datasets simultaneously (datasets are available upon request from respective owners). Such an interface saves researchers time when analyzing ICU data and helps reproducibility. We hope that ricu can become a community-wide effort, so that data harmonization is not repeated by each research group separately. One current limitation is that concepts were added on a case-to-case basis, and therefore the resulting dictionary of concepts is not comprehensive. Further work is needed to make the dictionary comprehensive.

Vasopressin in Vasodilatory Shock.

Vasodilatory shock is the final common pathway for all forms of severe shock, with sepsis the most common primary etiology and the leading cause of critical illness-related mortality. The pathophysiology of this condition remains incompletely elucidated. Deficiency of the neuropeptide hormone vasopressin seems to play a significant role. The physiology of vasopressin and its interaction with the pathophysiology of vasodilatory shock are described in this review. A brief review of the major randomized controlled trials assessing the efficacy and safety of vasopressin and its analogs in this complex patient cohort is also provided.