Respiratory management of adult patients with acute respiratory distress syndrome due to COVID‐19

In late 2019, a novel coronavirus later named severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) was identified as a cause of pneumonia in Wuhan, China. The World Health Organization named the disease coronavirus disease 2019 (COVID-19) and, on 11 March 2020, characterized COVID-19 as a pandemic. As of late July 2020, over 15 million confirmed cases have been reported globally with a case fatality rate of 4%. In the United States, as of July 23, there are nearly 4 million confirmed cases with over 140 000 deaths. This commentary focuses on the respiratory management of adults with COVID-19-associated hypoxaemic respiratory failure and acute respiratory distress syndrome (ARDS). The pathophysiological mechanisms in COVID-19 include airflow obstruction, ARDS and ‘cytokine storm’. Gattinoni et al. described two phenotypes of ARDS: type L (low elastance, high compliance and patchy ground-glass opacities on chest imaging) and type H (high elastance, low compliance, diffuse and bilateral infiltrates on chest imaging). Histological examination shows diffuse alveolar damage, hyaline membrane formation, type 2 pneumocyte hyperplasia, multinucleated giant cells and platelet-fibrin thrombi in small vessels and capillaries of the lung. The most common symptoms are fever, cough and shortness of breath. The disease course is variable with an incubation period of up to 14 days (median: 5 days). Diagnosis of COVID-19 is made by the detection of SARS-CoV-2 via reverse transcription polymerase chain reaction testing of a nasal or nasopharyngeal swab. Laboratory findings in the acute phase include lymphopenia, elevated C-reactive protein, ferritin, D-dimer, fibrinogen and lactate dehydrogenase, and normal or low procalcitonin. The hypoxaemic respiratory failure and ARDS observed in COVID-19 range from mild to severe. Basic management principles may be applied based on the type L or H phenotype. Type L patients respond to an increase in fraction of inspired oxygen (FiO2) with nasal cannula, high-flow nasal oxygen (HFNO) or noninvasive ventilation (NIV). Type H patients who require mechanical ventilation should be managed following the traditional ARDSnet ventilator protocol. Hospitalized patients with mild symptomatic respiratory insufficiency require supplemental oxygen via nasal canula (up to 6 L) to maintain arterial O2 saturation greater than 90%. Bronchodilators, if needed, should be administered via metred dose inhalers instead of nebulizers to prevent aerosolization of the virus. Patients with moderate hypoxaemic respiratory failure are those requiring HFNO, non-rebreather masks or NIV. Controversy exists regarding the safety of bilevel positive pressure ventilation (BiPAP), continuous positive airway pressure ventilation (CPAP) and HFNO, given the risk of aerosolization with these devices to healthcare providers. Professional societies recommend their use with airborne precautions and appropriate personal protective equipment (PPE), preferably in a negative pressure room. CPAP has a theoretical benefit of being able to provide the highest mean airway pressures, thus helping with alveolar recruitment. The National Health Service (United Kingdom) recommends the use of NIV with a non-vented mask, an exhalation port and a bacterial/viral filter between the mask and oxygen, over HFNO given the lower risk of aerosolization. Another strategy in patients with mild to moderate respiratory failure is awake proning. Proning facilitates oxygenation by improving ventilation/perfusion mismatch with increased perfusion to the healthier alveoli in the anterior lung, improved secretion management and alveolar recruitment in the posterior lung. Larger epidemiological studies have reported rates of invasive mechanical ventilation ranging from 2.3% to 33.1% of hospitalized COVID-19 patients and 29.1% to 89.9% among patients admitted to the intensive care unit (ICU). Risk factors of ARDS and need for ICU admission include age >60 years, male gender and comorbidities such as heart disease, diabetes mellitus, chronic lung disease, immunocompromised state and malignancy. Given that COVID-19 may cause hypoxia with minimal respiratory distress (‘silent hypoxia’), the threshold for intubation should be lower particularly for those patients with persistent hypoxia despite escalation to HFNO and exhibiting shortness of breath. When needed, rapid sequence intubation technique without bagging should be used. Intubation should be performed by the most experienced clinician under strict airborne precautions. Other considerations include use of dry ventilator circuits, heat moisture exchangers and bacterial/viral filters at exhalation ports. The approach to mechanical ventilation in COVID19 patients should adhere to evidence-based practices utilized in the general population with ARDS. Ventilatory strategies to implement are low tidal volume ventilation (tidal volume 6 mL/kg of predicted body weight) and targeting plateau pressures of <30 cm H2O. There are no studies of high versus low positive end-expiratory pressure (PEEP) in patients