Mechanical ventilation in COVID-19: A physiological perspective

Abstract

New findings: What is the topic of this review? This review presents the fundamental concepts of respiratory physiology and pathophysiology, with particular reference to lung mechanics and the pulmonary phenotype associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and subsequent coronavirus disease 2019 (COVID-19) pneumonia. What advances does it highlight? The review provides a critical summary of the main physiological aspects to be considered for safe and effective mechanical ventilation in patients with severe COVID-19 in the intensive care unit.

Abstract: Severe respiratory failure from coronavirus disease 2019 (COVID-19) pneumonia not responding to non-invasive respiratory support requires mechanical ventilation. Although ventilation can be a life-saving therapy, it can cause further lung injury if airway pressure and flow and their timing are not tailored to the respiratory system mechanics of the individual patient. The pathophysiology of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to a pattern of lung injury in patients with severe COVID-19 pneumonia typically associated with two distinct phenotypes, along a temporal and pathophysiological continuum, characterized by different levels of elastance, ventilation-to-perfusion ratio, right-to-left shunt, lung weight and recruitability. Understanding the underlying pathophysiology, duration of symptoms, radiological characteristics and lung mechanics at the individual patient level is crucial for the appropriate choice of mechanical ventilation settings to optimize gas exchange and prevent further lung injury. By critical analysis of the literature, we propose fundamental physiological and mechanical criteria for the selection of ventilation settings for COVID-19 patients in intensive care units. In particular, the choice of tidal volume should be based on obtaining a driving pressure < 14 cmH₂ O, ensuring the avoidance of hypoventilation in patients with preserved compliance and of excessive strain in patients with smaller lung volumes and lower lung compliance. The level of positive end-expiratory pressure (PEEP) should be informed by the measurement of the potential for lung recruitability, where patients with greater recruitability potential may benefit from higher PEEP levels. Prone positioning is often beneficial and should be considered early. The rationale for the proposed mechanical ventilation settings criteria is presented and discussed.

Keywords: COVID-19; SARS-CoV-2; artificial; critical care; physiology; respiration; respiratory; respiratory distress syndrome.

FIGURE 1

Computed tomography (CT) scans showing different degrees of lung consolidation associated with similar levels of arterial oxygenation in patients with coronavirus disease 2019 (COVID‐19). (a) The CT scan was acquired during spontaneous breathing and associated with low Hounsfield unit values, indicating well‐aerated compartments. (b) The CT scan was acquired during controlled mechanical ventilation, with positive end‐expiratory pressure at 5 cmH₂O, and associated with a marked proportion of high Hounsfield unit values, indicating non‐aerated compartments. Abbreviations: $F_{\mathrm{I},{\mathrm{O}}_2}$, fraction of inspired oxygen; $P_{\mathrm{a}{\mathrm{O}}_2}$, arterial partial pressure of oxygen. Reproduced with permission from Gattinoni, Chiumello, Caironi, et al. (2020)

FIGURE 2

The interalveolar septa of a 78‐year‐old male patient who died from coronavirus disease 2019 (COVID‐19), showing slightly expanded alveolar walls and multiple fibrinous microthrombi (arrowheads) in the alveolar capillaries. Scale bar: 50 μm. Reproduced with permission from Ackermann, Verleden, et al. (2020), Copyright Massachusetts Medical Society

FIGURE 3

Diagram summarizing pathophysiological features associated with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection and the proposed management of mechanical ventilation for patients with severe coronavirus disease 2019 (COVID‐19) in the intensive care unit. The figure shows the main known pathophysiological mechanisms that can lead to hypoxaemia, with paired CT images (top row) and iodine perfusion maps (bottom row) indicative of the main phases. Initially, hypoxaemia is related to increased shunt (arrows) and dead space ventilation (asterisks), with minimal lung parenchymal pathology at risk of ventilator‐induced lung injury. Lung gas volume can decrease over time because of oedema and atelectasis, which may be reversible with prone positioning or higher PEEP. Eventually, dense consolidation and/or fibrosis can make the condition less responsive to both proning and PEEP (low PLR). Macrothrombosis is also present, with pulmonary emboli causing large areas of reduced or absent perfusion. Abbreviations: CT, computed tomography; DP, driving pressure (plateau pressure minus PEEP); PEEP, positive end‐expiratory pressure; PLR, potential for lung recruitment or recruitability (ability to open previously gasless lung regions with an increase in transpulmonary pressure); VT, tidal volume. Left‐hand images are from Santamarina, Boisier Riscal, et al. (2020) and right‐hand images from Ridge et al. (2020), with permission