Pathophysiology of coronavirus-19 disease acute lung injury

Abstract

Purpose of review More than 230 million people have tested positive for severe acute respiratory syndrome-coronavirus-2 infection globally by September 2021. The infection affects primarily the function of the respiratory system, where ∼20% of infected individuals develop coronavirus-19 disease (COVID-19) pneumonia. This review provides an update on the pathophysiology of the COVID-19 acute lung injury. Recent findings In patients with COVID-19 pneumonia admitted to the intensive care unit, the PaO 2 /FiO 2 ratio is typically <26.7 kPa (200 mmHg), whereas lung volume appears relatively unchanged. This hypoxaemia is likely determined by a heterogeneous mismatch of pulmonary ventilation and perfusion, mainly associated with immunothrombosis, endothelialitis and neovascularisation. During the disease, lung weight, elastance and dead space can increase, affecting respiratory drive, effort and dyspnoea. In some severe cases, COVID-19 pneumonia may lead to irreversible pulmonary fibrosis. Summary This review summarises the fundamental pathophysiological features of COVID-19 in the context of the respiratory system. It provides an overview of the key clinical manifestations of COVID-19 pneumonia, including gas exchange impairment, altered pulmonary mechanics and implications of abnormal chemical and mechanical stimuli. It also critically discusses the clinical implications for mechanical ventilation therapy.

Diagnosis and management of covid-19 in pregnancy

“…Interaction between the increased cardiac output, which occurs later in pregnancy, and the alterations in ventilation/perfusion distribution characteristic of covid-19, make pregnant women more likely to develop more severe hypoxemia than non-pregnant patients with the same degree of lung involvement. This means that, given the same degree of lung consolidation, the higher cardiac output increases the functional pulmonary shunt, leading to worse hypoxemia, particularly in covid-19, where the pathophysiology of hypoxemia is initially and primarily due to an increased functional and anatomical (through neovascularization) shunting of affected lung regions 6667. In addition, the reduction in lung volumes owing to the pregnant uterus may increase lung strain for the same inspiratory volume and may increase the risk of lung injury (eg, pneumomediastinum) when the inspiratory effort is high and not controlled by non-invasive or invasive ventilation.…”

Interferon-γ Preferentially Promotes Necroptosis of Lung Epithelial Cells by Upregulating MLKL

“…Globally, ARDS affects approximately 3 million patients annually and accounts for 10% of intensive care unit admissions [3]. Due to the ongoing coronavirus disease 2019 (COVID-19) pandemic, the number of patients diagnosed with ARDS/ALI increased substantially [4,5]. Clinically, ALI/ARDS manifests as hypoxemia, lung edema, decreased lung compliance and diffuse pulmonary infiltrates [1,2,4].…”

SARS-CoV-2 and COVID-19: A Narrative Review

“…As the dominant clinical features of COVID-19 are pneumonia, pneumonitis, and ARDS, a potential severe long-term consequence is the clinically-recognised interstitial lung disease (ILD) ( 158 ). Post-infection imaging often reveals pulmonary fibrosis, characterised by excessive deposition of extracellular matrix material by fibroblast secondary to the inflammation, whilst other methods point to microvascular damage and microthrombi ( 159 , 160 ), leading to (at least) COPD and emphysema.…”