As a consequence of the rapid pandemic spread of the novel coronavirus (SARS-CoV2), and the exponential rising of patients with coronavirus disease 2019 (COVID-19), health systems of affected countries are facing an increasing number of patients presenting to Emergency Departments with hypoxemic respiratory failure. The demand of mechanical support and endotracheal intubation (ETI) is higher than normal and often exceeds available resources, with the need to rapidly expand the medical resources available.
SARS-CoV2, similar to SARS-CoV [1], causes a range of heterogeneous clinical pictures in human going from common cold to severe respiratory failure. Due to its respiratory system tropism, it can lead to diffuse alveolar damage with cellular fibro myxoid exudates, desquamation of pneumocytes, and hyaline membrane formation [2]. Emerging evidence suggests an exuberant “cytokine storm” reaction of the host with features similar to bacterial sepsis, and reports high inflammatory markers like elevated C-reactive protein, d-dimer, and ferritin being able to relate to disease severity and mortality [3]. Severe disease might result in acute and progressive respiratory failure due to massive alveolar damage, till Acute Respiratory Distress Syndrome (ARDS) develops [4].
A high rate of COVID-19 patients presents with severe hypoxic respiratory failure, 19% in first data coming from China with 5% requiring mechanical ventilation and intensive-care unit (ICU) [5]. Therefore, immediately supplemental oxygen therapy is mandatory when SpO2 levels are low (< 90%), with the aim to increase SpO2 and maintain it no higher than 96% [6]. Evidence showed that a liberal oxygen strategy is associated with increased risk of hospital mortality in acutely ill patients [7].
They have usually a fairly normal pulmonary compliance, especially in the first phases of the disease. That indicates well-preserved lung gas volume and relatively low work of breathing prior to intubation in sharp contrast to expectations for severe ARDS. The loss of lung perfusion regulation and hypoxic vasoconstriction might play an important role in generating their severe hypoxemia. Due to preserved compliance, COVID-19 patients do not have excessively increased work of breathing and may develop “silent hypoxemia” with the risk of a rapid decline without severe symptoms complaint.
Due to progressive alveolar damage and infiltrates, progressive alveolar collapse can develop, with a gradual distortion of lung architecture promoting collapsing of neighboring alveoli and development of atelectasic areas.
The application of a positive end expiratory pressure (PEEP) is useful for lung recruitment and to improve ventilation perfusion mismatch.
Evidence on non-invasive positive pressure ventilation (NIPPV) in acute respiratory failure (ARF) due to viral pneumonia is lacking and its use is still of uncertain benefit [8, 9]. Data from observational studies on the use of NIPPV in Influenza A (H1N1) viral pneumonia showed a variable successful rate between 40.7 and 48% [10,11,12]. Some studies reported an increased ICU mortality in patients who failed NIPPV trial compared with early invasive mechanical ventilation, whereas NIPPV success resulted in shorter hospital stay. NIPPV failure was associated with higher SOFA scores and lower P/F levels [10, 11, 13]. A high rate of NIPPV failure (92.4%) was reported in critically ill patients with the Middle East Respiratory Syndrome (MERS) [14].
Due to the lack of Randomized-Controlled Trials, no recommendations are offered on NIPPV use in these patients, but according to data from observational studies, a cautious NIPPV trial in selected patients in a protected environment and experienced centers can be tried. An NIPPV trial could be attempted for 60 min, being aware that a prolonged NIPPV treatment can be harmful delaying intubation and provoking large tidal volumes, injurious transpulmonary pressures, and increasing the risk of patient self-inflicted lung injury [15].
Because COVID-19 patients have often a tolerable work of breathing, they may not need much mechanical inspiratory support, but can benefit from a simply continuous positive airways pressure (CPAP). CPAP is able to deliver PEEP and to provide alveolar recruitments, avoiding excessive harmful tidal volumes, and reducing patient’s high negative intrathoracic pressure swings which can increase lung injury. Due to its potential negative effects, the lowest useful PEEP should be find to avoid severe hemodynamic impairment, fluid retention, gastric insufflation, and aspiration. CPAP delivered by head helmet has been shown as safe and effective as CPAP delivered by face mask, and better tolerated for prolonged ventilation periods [16]. Moreover, with the use of a closed system and viral filters, the helmet can be reasonably safe regarding viral transmission [17].