A Protocol for O2 Escalation (goal sat low 90s, unless end stage lung disease):
1. up to 6L nc (40% FiO2). Treat pleuritic pain to prevent splinting.
2. 12-15L facemask (50-60% FiO2)
3. HFNC if available. Use ROX index to determine failure.
Who to definitely intubate? End organ injury/hypoperfusion (ex elevated lactate), AMS, hypotension, respiratory acidosis/hypercapnea (w/o hx of CHF or COPD)
CPAP failure: PEEP >8? and 100% FiO2, not cooperative
Use ROX Index to determine failure of HFNC:
ROX = (SpO2/FiO2) / RR
ROX < 4.88 – intubate
failure with trial of HFNC @2h: ROX < 2.85, @6h: ROX < 3.47, @12h: ROX < 3.85
Note that PF ratio is meant for intubated pts (FiO2 is most accurate on vented pt).
-NIV may be useful in preventing ETI if concomitant COPD or CHF – NIV shown to work for hypercapnea
-the vast majority of pts with hypoxemic respiratory failure with previously normal lungs (ie PNA, ARDS) fail NIV and need mechanical ventilation. The risk of a trial of NIV is delaying needed intubation, worsening end-organ damage (mechanical ventilation reduces energy expenditure on respiration), and possibly worsening volume-induced lung trauma for ARDS pts.
-some studies suggest mortality benefit to NIV and reduced need for intubation for early hypoxemic respiratory failure as compared to Venturi or NRB mask in carefully selected pts: no shock or end-organ dysfunction (including arrhythmia), can clear secretions, and are cooperative.
–however, evidence from different RCTs on both mortality and need for intubation is conflicting!
–if pursue, use CPAP only as tachypneic pts can pull excessive tidal volumes on BIPAP and further damage ARDS lungs
–if no clinical improvement after 1 hour, consider it a failure of NIV
In ARDS patients, it has been shown that the use of noninvasive inspiratory pressure support can decrease the inspiratory effort compared with no inspiratory assistance only if sufficient pressure support
is added [69
]. Of concern, the tidal volume can also be significantly higher during NIV, especially when substantial inspiratory pressure is delivered, and further exacerbated by the high inspiratory demand seen in patients with acute hypoxic respiratory failure [70
]. Therefore, the total pressure dissipated to inflate the lungs can be excessive during NIV. Such large transpulmonary pressures and the resulting large tidal volumes may exacerbate lung injury if prolonged
over time. It is possible, although not proven, that NIV is especially useful in patients who do not substantially increase their tidal volume, but further work is needed in this area
Invasive ventilation for hypoxaemic respiratory failure clearly reduces work of breathing and permits paralysis if total control of breathing is desired, effects that can redistribute blood flow from the respiratory muscles to other organs in patients with shock and hence help to treat shock itself
]. The ability of NIV to achieve optimal pressures to reduce the work of breathing reliably in acute hypoxaemic respiratory failure is challenging because the high pressures often required increase air leaks, gastric insufflation and patient intolerance [69
]. Thus, the ability to use lung protective ventilator strategies (such as maintaining a low tidal volume of 6 mL·kg−1
of predicted body weight) may be more difficult with NIV than with invasive ventilation [73
]. Some evidence even supports the idea that spontaneous ventilation can induce harm similar to ventilator-induced lung injury in situations of severe lung injury [75
], which raises a note of caution when using NIV that combines spontaneous effort with ventilator support
NIV has also been studied as an alternative to intubation, with occasional reports showing benefit . Positive studies on hypoxaemic, nonhypercapnic respiratory failure, mainly caused by community- or hospital-acquired pneumonia, have enrolled carefully selected patients who are cooperative with no associated major organ dysfunction, cardiac ischaemia or arrhythmias, and with no limitations in clearing secretions [29, 60, 85–87], which may explain the benefits seen.
Until recently, almost all studies on NIV for de novo ARF compared it with oxygen delivered with standard air entrainment (Venturi masks) or reservoir masks. Recently, high-flow nasal cannula therapy has been shown to offer several advantages compared with NIV, including better tolerance and dead space reduction . One recent RCT reported a survival benefit of high-flow nasal cannula over standard oxygen therapy and bilevel NIV, although the primary end-point of intubation was not significantly different .
The main risk of NIV for the indication of de novo ARF is to delay a needed intubation . Early predictors of NIV failure include higher severity score, older age, ARDS or pneumonia as the aetiology for respiratory failure, or a failure to improve after 1 h of treatment . Although the reasons for a poorer outcome are not completely understood, patients with NIV failure have higher tidal volumes before intubation  and develop more complications after intubation . Studies have shown that NIV failure is an independent risk factor for mortality specifically in this population, although careful patient selection seems to reduce this risk [91, 92].
In summary: evidence of NIV on mortality and need for intubation is conflicting.
—Definite no’s: pts with shock, end-organ damage (including arrhythmias), poor cooperation, or poor secretion clearance
—Maybe: pts with concomitant hypercapneic failure from CHF or COPD, very early hypoxemic failure without other organ dysfunction, and pts not pulling large tidal volumes
Success rates in critically ill COVID-19-patients are limited, delayed intubation is associated with poor outcome and the treatment as well as a possibly necessary emergency intubation in cases of treatment failure increase the risk for transmission to staff [8
]; however, in situations with an imbalanced resources-needs ratio, this approach could help bridge the time until decision-making and intubation, or it could also be a therapeutic option in cases of lacking ventilatory capacities.