COVID-19 pneumonia: pathophysiology and management

Abstract

Coronavirus disease 2019 (COVID-19) pneumonia is an evolving disease. We will focus on the development of its pathophysiologic characteristics over time, and how these time-related changes determine modifications in treatment. In the emergency department: the peculiar characteristic is the coexistence, in a significant fraction of patients, of severe hypoxaemia, near-normal lung computed tomography imaging, lung gas volume and respiratory mechanics. Despite high respiratory drive, dyspnoea and respiratory rate are often normal. The underlying mechanism is primarily altered lung perfusion. The anatomical prerequisites for PEEP (positive end-expiratory pressure) to work (lung oedema, atelectasis, and therefore recruitability) are lacking. In the high-dependency unit: the disease starts to worsen either because of its natural evolution or additional patient self-inflicted lung injury (P-SILI). Oedema and atelectasis may develop, increasing recruitability. Noninvasive supports are indicated if they result in a reversal of hypoxaemia and a decreased inspiratory effort. Otherwise, mechanical ventilation should be considered to avert P-SILI. In the intensive care unit: the primary characteristic of the advance of unresolved COVID-19 disease is a progressive shift from oedema or atelectasis to less reversible structural lung alterations to lung fibrosis. These later characteristics are associated with notable impairment of respiratory mechanics, increased arterial carbon dioxide tension (P _aCO2 ), decreased recruitability and lack of response to PEEP and prone positioning.

FIGURE 1

A representative flow of patients with COVID-19 from the emergency department through the high-dependency unit to intensive care from an unspecified number of infected individuals. Data from Martinelli et al. [5], from 281 461 patients. Post-COVID-19 data not available. ED: emergency department; HDU: high-dependency unit; ICU: intensive care unit; PH: prehospital.

FIGURE 2

COVID-19 representative computed tomography scans. a) Emergency department: Lung weight=1197.5 g; Gas volume=3937.6 mL; Fraction of non-aerated tissue=0.054; P_aO2/F_IO2 ratio=146. b) High-dependency unit: Lung weight=1088.6 g; Gas volume=1569.9 mL; Fraction of non-aerated tissue=0.168; P_aO2/F_IO2 ratio=210. c) Intensive care unit: Lung weight=1399.2 g; Gas volume=1257.5 mL; Fraction of non-aerated tissue=0.389; P_aO2/F_IO2 ratio=112. F_IO2: inspiratory oxygen fraction; P_aO2: arterial oxygen tension.

FIGURE 3

Summary of COVID-19 pathophysiology time course of patients who fail to improve. Atelectasis/recruitability progressively increase during the disease course until a later phase, characterised by fibrosis development. These anatomical changes are associated with a progressive decrease of respiratory system compliance, same or higher ventilation and a decreased P_aCO2. Note that oxygenation does not change remarkably during the disease course, although, the mechanisms of hypoxaemia are likely to shift from V′_A/Q′ misdistribution to true shunt. ED: emergency department; HDU: high-dependency unit; ICU: intensive care unit; P_aCO2: arterial carbon dioxide tension; V′_A/Q′: ventilation/perfusion ratio.