The strategy adopted during the earliest phase of support is crucial to curtailing cumulative exposure to high-stress cycles and improving eventual outcome. My first priority is to reduce vulnerability to VILI and the body’s needs for ventilation, oxygenation, and blood flow. For example, when spontaneous breathing is vigorous, deep sedation and/or paralytics minimize
transpulmonary pressures, ventilatory demand, and the work of breathing. Estimating lung capacity serves to assess both disease severity and heterogeneity. Severely affected patients, judged either by criteria of refractory or worsening hypoxemia, or very low compliance, are proned [
12]. Prone positioning usually recruits airspaces and helps even the distributions of transpulmonary pressures and tissue stresses [
13]. Simultaneously, improved O
2 exchanging efficiency typically allows reduction of FIO
2. Fever and agitation are also suppressed to lessen ventilation demand. Successfully addressing the underlying cause of respiratory distress shortens the duration of ventilator support.
Once demands and co-contributors to vulnerability are minimized, ventilator settings assume top priority. In descending order of importance, those settings are as follows: (1) DP and PEEP, (2) V
E, and (3) inspiration to expiration (I:E) ratio and flow profile. Whether during noninvasive or invasive ventilation, I attend first to both
transpulmonary plateau pressure and
transpulmonary driving pressure, and then to ventilating frequency and V
E. I monitor the latter as a key component of power and helpful indicator of ventilating efficiency. Allowing hypercapnea (to PaCO
2 ≤ ≈60 mmHg) promotes reductions of the frequency, V
E, and ventilating power. I do not target a “fully open lung” but use stepwise recruiting maneuvers and “decremental” approach to find the least PEEP that achieves an effective balance between recruitment and overdistention. Assuming passive inflation and a normal chest wall, I regulate tidal volume so as to keep DP ≤ 15 cmH2O
and plateau pressure ≤ 27 cmH
2O. With tidal pressures and frequency set, I next modulate inspiratory flow, keeping the I:E ratio adjusted between 1:1.5 and 1:1. When the patient is passive, a controlled constant flow profile is preferred to the decelerating flow profile of pressure control [
11,
14]. Because excessive power may be central to VILI risk, I assess and try to downregulate each of power’s determinants, as indicated. I do
not set a specific upper limit for ventilating power itself, however, nor feel confident about using power criteria alone for initiating extracorporeal CO
2 removal, as injury thresholds vary and numerical guidance from high-quality clinical studies is not currently available. (A deteriorating clinical trajectory is my primary criterion.) Finally, to minimize cumulative power exposure and VILI risk, I frequently re-evaluate my assumptions regarding needs and levels of ongoing respiratory supports.