![]() We hypothesised that in early COVID-19 pneumonitis, hypoxaemia is associated with both increased intrapulmonary shunt and increased alveolar dead space. Pulmonary vessel microembolism reduces capillary blood flow, thus generating areas of high V′ A/ Q′ and promoting increased alveolar dead space. However, pathology reports from COVID-19 infected lungs also frequently demonstrate pulmonary vasculature involvement, including severe endothelial injury, widespread thrombosis with microangiopathy and new vessel growth. The hypoxaemia is likely related to ventilation/perfusion ( V′ A/ Q′) mismatch and in particular to increased intrapulmonary shunt arising from alveolar filling with fluid or cellular debris. Patients with early COVID-19 respiratory failure present with hypoxaemia and hyperventilation. Worldwide there have been more than 6 million deaths. Many have required hospitalisation, with 10–20% of those requiring intensive care, mainly due to respiratory compromise. Some apparatus dead space may actually reduce total dead space, as an ETT bypasses the majority of anatomical dead space of the patient (nasopharynx).ĭead space from the patient.Since the beginning of 2020, over half a billion people have been diagnosed with coronavirus disease 2019 (COVID-19), a disease caused by infection with the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Types of Dead Spaceĭead space from equipment, such as tubes ventilator circuitry. ![]() Glomerular Filtration and Tubular Functionĭead space is the proportion of minute ventilation which does not participate in gas exchange. Functional Anatomy and Control of Blood Flow ![]()
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