new pilot study from the Icahn School of Medicine at Mount Sinai suggests that COVID-19 is causing significant dilation of the blood vessels of the lung, specifically the capillaries. This vasodilation is contributing to the very low oxygen levels seen in COVID-19 respiratory failure and also helps explain why the disease behaves differently than classic acute respiratory distress syndrome (ARDS). The study was published in the American Journal of Respiratory and Critical Care Medicine.
In classical ARDS, pulmonary inflammation leads to leaky pulmonary blood vessels that flood the lungs with fluid, making the lungs stiff and impairing oxygenation. Many patients with COVID-19 pneumonia demonstrate severe hypoxemia that is markedly out of proportion to the degree of lung stiffness. This disconnect between gas exchange and lung mechanics in COVID-19 pneumonia has raised the question of whether the mechanisms of hypoxemia in COVID-19 differ from those in classical ARDS.
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American Journal of Respiratory and Critical Care Medicine (PDF file):
