According to a new pilot study by the researchers of Icahn School of Medicine reported that COVID-19 is causing dilation of the blood vessels in the lung, especially the capillaries. Further, this vasodilation is results in very low oxygen levels, which is observed in COVID-19 patients having respiratory failure and it also enlightens why it behaves inversely, in comparison to acute respiratory distress syndrome (ARDS).
Researchers explained that in the case of acute respiratory distress syndrome, pulmonary inflammation results in leaky pulmonary blood vessels, which fill the lungs with fluid, causing the lung to stiff and hampers oxygenation. It has been observed that several patients with COVID-19 pneumonia reported about severe hypoxemia which depends on the degree of lung stiffness. This discontinuation between gas exchange and lung mechanics in COVID-19 pneumonia raised questions on the mechanisms of hypoxemia in COVID-19 and how does it differ from ARDS.
Researchers in the initial stage concentrated on assessing cerebral blood flow in mechanically ventilated COVID-19 patients and focused on abnormalities consistent with stroke. Researchers utilized a robotic transcranial Doppler (TCD), to perform non-invasive and painless ultrasound technique called ‘bubble study’. This diagnostic machine provided insights into the pathophysiology of a pulmonary disease and its automated monitoring allowed researchers to assess cerebral blood flow while reducing the potential for exposure to COVID-19.
In this research study, 18 severe COVID-19 pneumonia patients who were ventilated mechanically underwent TCD with bubble study. The researchers observed that 15 patients (83%) patients exhibited microbubbles, which indicated the presence of abnormally dilated pulmonary blood vessels. The number of microbubbles detected by the TCD interrelated with the acuteness of hypoxemia, signifying that the pulmonary vasodilations might explain the inconsistent hypoxemia observed in patients with COVID-19 pneumonia.