Ventilation/perfusion mismatch is not the sole reason for hypoxaemia in COVID-19 patients.

What is it about?

Our article explains the inadequacy of the existing theory of hypoxemia in the COVID-19 patient. This theory that dominates to this day, indicates that in the initial phase of hypoxemia in the patient with COVID-19 it is due to the imbalance of ventilation (V) and perfusion (Q) in the pulmonary alveoli, that is, V/Q < 1. According to the new articles, there is such a high difference between the partial pressure of arterial carbon dioxide (PaCO2) and the partial pressure of exhaled carbon dioxide (PetCO2) in the initial phase of hypoxemia in the patient with COVID-19 that at It sometimes exceeds this difference in severely ill patients with adult respiratory distress syndrome (ARDS). The theory based on V/Q mismatch cannot explain the high PaCO2 - PetCO2 difference, because we do not have a shunt in the initial phase of hypoxemia. By the laws of physics, although V/Q mismatch can cause hypoxemia, but it cannot induce a difference in PaCO2 and PetCO2 values ​​(in this case both values ​​rise, but not difference, because CO2 quickly equilibrates on two sides of the alveolar wall). Our concept explains the phenomenon described by the laws of biochemistry: the pulmonary microcirculation in the patient with COVID-19 is converted to the peripheral circulation type as in other organs, that is, the hemoglobin is able to release more oxygen and maintain a lot of CO2. As a consequence of this, the hemoglobin passing through the affected pulmonary capillaries is not able to become 100% saturated with oxygen and transfers a lot of CO2 to the arteries, causing a high difference in PaCO2 and PetCO2

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Why is it important?

It is important to take into account for treatment of COVID-19 patients, the Hb’s oxygen affinity and the presence of the biochemical shunt in the alveolar-capillary bed.

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