Bronchiolitis and Potential Pathophysiological Implications in Coronavirus Disease 2019 ARDS Patients With Near-Normal Respiratory Compliance

To the Editor:

We read with enthusiasm the study by Mauri et al (1) using electrical impedance tomography to assess recruitment potential in patients with acute respiratory distress syndrome (ARDS) from coronavirus disease 2019 (COVID-19). The authors reported large variability in recruitability, reiterating individualized mechanical ventilation (MV) treatment.

The discrepancy between hypoxemia severity and radiology/respiratory mechanics in COVID-19 ARDS patients has been attributed to loss of hypoxic pulmonary vasoconstriction. This “Type L/1 phenotype” is purported to have low recruitability (2). Our experience supports what Mauri et al (1) reported. In addition, we opine in recruitment-response COVID-19 ARDS patients: 1) bronchiolitis, in a histologic context, is a plausible pathophysiological mechanism and 2) a simple bedside physiologic test could potentially determine recruitment potential in resource-limited settings.

Chest CT scans are regulated due to infection control reasons at our center. Chest radiographs, we observed, often failed to reflect the degree of hypoxemia. Ground-glass opacities, especially milder ones are frequently radiolucent. Similarly, small airway disease cannot be readily appreciated on radiographs—which engendered our bronchiolitis postulation and bedside study. We define bronchiolitis as inflammation of noncartilaginous airways immediately proximal to the pulmonary acinus. In first half of April 2020, four among five severe COVID-19 ARDS patients had radiologic-physiologic mismatch and received protocolized MV below.

1. Measure postintubation lung mechanics without spontaneous breathing.

2. Assist pressure control ventilation; tidal volume (V_T) ≤ 8 mL/kg ideal body weight.

3. Optimize positive end-expiratory pressure (PEEP); incremental approach from 8 cm H₂o.

4. Lower Fio₂ promptly (target Spo₂ ≥ 90%); avoid hyperoxia to not exacerbate cytokine release syndrome.

Median preintubation Pao₂/Fio₂ (PF) ratio was 125.4 (range 92.9–160.0) on venturi mask 50%/nonrebreather mask. Respiratory static compliance values were ≥ 40 mL/cmH₂o. In all patients, Spo₂ ≥ 90% was achieved while lowering Fio₂ (range 0.3–0.5) and increasing PEEP (range 10–14 cmH₂o). Twenty-four hours later, median PF ratio was 220 (range 176.5–265.0). None required paralysis/prone positioning.

Pathophysiology

Alveolar pattern and bronchiolitis are well-accepted pathology in many acute viral bronchiolitis. In COVID-19, bronchiolitis as true viral-related pathology is gaining traction (3, 4). Physiologic-wise, bronchiolitis remains compatible with our findings suggesting positive recruitment potential, and we elucidate this, aided by physiologic changes observed in our 61-year-old female patient.

Bronchiolitis could be likened to age-related lung elasticity loss. Both lead to small airway closure, increased ventilation/perfusion (VQ) mismatch, and hypoxemia, which PEEP counters by increasing end-expiratory lung volume past the elevated “diseased” closing capacity. Exploiting Enghoff modification of Bohr’s equation’s drawback in physiologic dead space (V_D) calculation, that is, V_D disproportionately affected by VQ mismatch compared with shunt/diffusion limitation (5), expected physiologic effects on volume–control ventilation are:

1. reduced V_D, V_D/V_T,

2. increased alveolar ventilation, and

3. reduced global VQ heterogeneity; improved oxygenation.

Lung mechanics, arterial blood gas, and end-tidal Co₂ were repeated 10 minutes apart on unchanged MV settings/min ventilation except PEEP (5 and 14 cmH₂O). The results—reduction in V_D/V_T (0.27–0.11) and alveolar–arterial gradient (165.3–147.5), improvement in V_A (246.2–321.6 mL), and PF ratio (163.5–218.3)—lend strength to our postulation.