Hemodynamic characteristics of COVID-19 patients with acute respiratory distress syndrome requiring mechanical ventilation. An invasive assessment using right heart catheterization.

AIMS: Interstitial pneumonia due to 2019 coronavirus disease (COVID-19) is often complicated by severe respiratory failure. In addition to reduced lung compliance and ventilation/perfusion mismatch, a blunted hypoxic pulmonary vasoconstriction has been hypothesized, that could explain part of the peculiar pathophysiology of the COVID-19 cardio-respiratory syndrome. However, no invasive hemodynamic characterization of COVID-19 patients has been reported so far. METHODS AND RESULTS: Twenty-one mechanically-ventilated COVID-19 patients underwent right heart catheterization. Their data were compared both with those obtained from non-mechanically-ventilated paired control subjects matched for age, sex and body mass index, and with pooled data of 1937 patients with "typical" acute respiratory distress syndrome (ARDS) from a systematic literature review. Cardiac index was higher in COVID-19 patients than in controls (3.8 [2.7-4.5] vs 2.4 [2.1-2.8] L/min/m2 , p<0.001), but slightly lower than in ARDS (p=0.024). Intrapulmonary shunt and lung compliance were inversely related in COVID-19 (r=-0.57, p=0.011) and did not differ from ARDS. Despite this, pulmonary vascular resistance of COVID-19 was normal, similar to that of control subjects (1.6 [1.1-2.5] vs 1.6 [0.9-2.0] WU, p=0.343), and lower than reported in ARDS (p<0.01). Pulmonary hypertension was present in 76% of COVID-19 and in 19% of control subjects (p<0.001), and it was always post-capillary. Pulmonary artery wedge pressure was higher in COVID-19 than in ARDS, and inversely related to lung compliance (r=-0.46, p=0.038). CONCLUSIONS: The hemodynamic profile of COVID-19 patients needing mechanical ventilation is characterized by combined cardio-pulmonary alterations. Low pulmonary vascular resistance, coherent with a blunted hypoxic vasoconstriction is associated with high cardiac output and post-capillary pulmonary hypertension, that could eventually contribute to lung stiffness, and promote a vicious circle between the lung and the heart. This article is protected by copyright. All rights reserved.