Critical Care Management SARS-CoV-2: 

Invasive and noninvasive ventilation strategies

The following data and recommendations have been distilled from published experiences and studies, white paper, manuscripts pending publication, webinars from the American Thoracic society, Society of Critical Care Medicine, ECHO society as well as conference calls with providers in New York and California.  Citations and articles are provided as available.

Pathophysiology

SARS-CoV-2 viral pneumonia and subsequent respiratory failure / ARDS appears to have distinctly different phenotypes.  Patients with more isolated viral pneumonia in the absence of other co-morbid conditions and may often, if not predominantly, present as primarily hypoxic respiratory failure, minimal defects in ventilation (ie relatively normal PCO2s / minimal dead space), and most notably lungs demonstrating normal compliance.  However, these patients also meet the traditional definition of ARDS.  Severe cases of ARDS are often associated with markedly reduced lung compliance, < 20 ml/cm H2O (normal 50-100 ml/H20 in ventilated patients).  Series of 18 ventilated SARS-CoV-2 ARDS patients from Seattle, Washington had a median initial lung compliance of 29 (25-36). Series of 60 ICU patients from Wuhan, China 55% of patients had a mean compliance of 47 ml/cm H2O despite almost identical PaO2/FiO2 ratios compared to 45% of patients with mean compliance 19.  Low lung compliance patients had markedly worse outcomes.   

A significant finding is hypoxic vasoconstriction, explaining the observed severe and sometimes refractory hypoxia and shunt physiology with shunt fractions as high as 50%. In these patients, the major issue is related to perfusion, as lungs are inflated and increasing PEEP does not help. High PEEP (> 15) may compromise right vernicle filling and worsen hemodynamics.  In these normal lung compliance patients, atelectasis is major driver of decompensation and worsening hypoxia.  For a given degree of atelectasis, the amount of subsequent hypoxia is exponentially worse.  Aggressive tactics to combat this need to be employed; moderate uses of PEEP, prone positioning and mobilization.  Post extubation these patients are at greater risk for decompensating due to atelectasis.  Phenotypically these patients just prior to or during decompensation have been described “silently hypoxic” demonstrating minimal distress despite severe hypoxia, again reflective of the relatively minimal defect in ventilation / PCO2.  The cause of the worsening hypoxia in these patients is from atelectasis and the loss of  “good lung”.  Recruitment maneuvers with positive pressure, namely CPAP or high flow nasal cannula (HFNC) at 50 LPM or higher and or prone positioning are often effective and can often lead to the avoidance of intubation and mechanical intubation.  Should be noted the prone positioning these patients is NOT to recruit collapsed sick alveoli but rather improvement in atelectasis and redistribution in blood flow.

More classic ARDS presentations exist in the SARS-CoV-2 population as well.  These patients may represent those with super-infections on top of viral pneumonia or those who may have evolved from the initial atypical ARDS presentation.  Furthermore they may also represent the described “cytokine storm” / high IL-6 population with rapidly progressive respiratory failure and multisystem organ failure.  These patients should be treated with more traditional ARDS ventilation strategies.

Treatment Strategies and Recommendations

* Remember the importance of identifying the clinical characteristics 

Mechanical Ventilation ( high compliance, atypical ARDS ) 

  • Tidal volumes:  start with 8 cc/kg if plateau pressures ≤ 30 

  • Aggressive PEEP up to moderate levels 

    • Rapidly push to 8-12 cmH20 to recruit atelectatic lung segments

    • Continue PEEP of 8 even if during spontaneous breathing trials if PaO2 / FiO2 ratios are marginal ( < 200 ) to combat atelectasis 

    • Only with clear evidence of positive clinical response push PEEP beyond 15; higher PEEP levels can worsen hemodynamics with subsequent increase in pulmonary pressures and decrease in RV function.  Remember, the PEEP is to recruit atelectatic lung

  • Inhaled pulmonary vasodilators for refractory hypoxia: progressively increasing FiO2 requirements or static FiO2 requirements and PaO2 / FiO2 ratios that are not allowing for weaning 

    • Iloprost 20 mcg / 8 cc saline via Aeorogen nebulizer into the ventilator circuit.  Continue therapy until extubated

    • Inhaled nitric oxide starting at 40 ppm.  Wean based on FiO2 when FiO2 down to 60%

  • Manual proning for refractory hypoxia / persistent PaO2 / FiO2 ratios < 150

    • Prone positioning should be considered for recruitment of atelectasis and to facilitate the redistribution of pulmonary blood flow

    • Prone cycle time of 12 hours

Extubation

Post extubation decompensation highly attributable to associated atelectasis and subsequent worsening hypoxia

  • Extubation to positive pressure if there are not contraindications

    • If PaO2/FiO2 ratio ≤ 200, HFNC at 50 LPM

    • If PaO2/FiO2 ratio ≤180, CPAP ≥ 10 cm H2O (barring secretion management)

  • Aggressive post extubation incentive spirometer use and upright positioning

Non-invasive Positive Pressure (high compliance, atypical ARDS) 

*Opportunities in patients often described as “silent hypoxia” demonstrating little distress or increased WOB despite significant oxygen requirement

  • Trial of CPAP (not BiPAP) 12-14 cm H20 

    • Even if oxygen requirement is high on positive pressure (i.e. ≥ 60%); give opportunity to recruit lung that has developed atelectasis.

    • If ventilatory support is required, i.e. there appears to be a need for BiPAP, move to intubation

    • CPAP over BiPAP; given normal lung compliance, protracted use of IPAP leads to larger tidal volumes and subsequent volu-trauma induced lung injury

  • High Flow Nasal Cannula

    • Flow rate ideally ≥ 50 LPM.  Varied data on exactly how much PEEP is provided for a given flow; 40-60 LPM studied.  50 LPM would approximately give 5 cm H2O of PEEP

  • High Flow Nasal Cannula + awake proning

    • PaO2 improves with this strategy; short proning cycles 8 (study demonstrated PaO2 improvement and reduction in intubation in total prone times 1.8 hrs 2 times per day) 

Sources

  • Bhatraju, P; et al. NEJM  2020

  • Peng, Z et al Critical Care & Emergency Medicine. Manuscript, pending review

  • Ding, L; et al. Efficacy and safety of early prone positioning combined with HFNC or NIV in moderate to severe ARDS: a multi-center prospective cohort study. Critical Care (2020) 24:28

  • Spoletini G, Alotaibi M, Blasi F, Hill NS. Heated humidified high-flow nasal oxygen in adults: mechanisms of action and clinical implications. Chest 2015;148:253–261.

  • Adhikari  NK, et al. Inhaled nitric oxide does not reduce mortality in patients with acute respiratory distress syndrome regardless of severity: systematic review and meta-analysis. Crit Care Med 2014;42(2):404–12.

  • Griffiths  MJ, et al. Inhaled nitric oxide therapy in adults. N Engl J Med2005;353(25):2683

  • G Walmrath  D, et al. Aerosolised prostacyclin in adult respiratory distress syndrome. Lancet1993;342(8877):961–62.

  • Kinasewitz, G. Iloprost Improves Gas Exchange in Patients With Pulmonary Hypertension and ARDS. Chest 2013, 144:55-62

  • Haeberle et al. Trials (2020) 21:242

  • British Medical Bulletin 1999,55 (No. 1). 140-164