Clinical Evidence of Ventilator-Induced Lung Injury Vortex in Patients with SARS-CoV-2

Author(s): Néstor Pistillo, Pablo Castelluccio, Ricardo Ciano, Eduardo Palermo, Sergio Lage, Edgar Amundarain, Osvaldo H Fariña

The concept of ventilator-induced lung injury vortex (VILI vortex) has recently been proposed as a progressive lung injury mechanism in which the alveolar stress/strain increases as the ventilable lung “shrinks”.

Research Question
The objective of this study is to evaluate the incidence of the VILI vortex in patients with SARS-CoV-2.

Study design and methods
Patients were ventilated with low tidal volume (Vt: 6 ±1 ml/kg/PBW) and limited plateau pressure (PPlat <30 cmH2O). FiO2 and respiratory frequency were adjusted to obtain SaO2: 92 to 96% and pH >7.20, respectively. PEEP was scored based on best compliance of respiratory system. Data were registered for 14 days. VILI vortex was defined as a progressive and sustained increase in driving pressure (ΔP) in the context of constant or decreasing tidal volume.

Sixty-five patients were admitted and fifteen of them (23%) progressed to VILI vortex. This phenomenon started subtly but developed fast (ΔP: day 0: 13.1 ±3.6 cmH2O, day 7: 15.6 ±3.6 vs. ΔP day 14: 24.1 ±7.8 cmH2O, p 0.0007). Initially, mechanical impairment was not accompanied by worsening in oxygenation [PaO2/FiO2 day 0: 150 ±73 vs. day 14: 160 ±75), p= NS], thus the PaO2/FiO2 ratio was not sensitive enough for its early detection. Finally, almost all patients with VILI vortex died of refractory hypoxemia (14/15). Negative factors such as delay in invasive mechanical ventilation [14 (11-15) vs. 7.5 (5-11) days, p= 0.0005], fluid overload [965 (501-1280) vs. 471 (206-.730), ml/day, p= 0.002], presence of bacteremia (60 vs. 20%, p 0.002), persistent fever (46.6 vs. 20%, p: 0.03) and need for noradrenaline >0.1 γ/kg/min (80 vs. 34%, p= 0.001) prevailed in VILI vortex group.

VILI vortex

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