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" (1). This positive feedback inexorably leads to the acceleration of lung damage, with potentially irreversible results. Little is known about the clinical aspects of this condition. Understanding its behavior could contribute to changing its potential devastating impact. The objective of this study is to evaluate the incidence of VILI vortex in patients with acute respiratory syndrome (ARDS) secondary to COVID-19, to establish a connection between this phenomenon and mortality, and to identify the factors that have an impact on its development.
Mechanical ventilation is an essential tool for the treatment of patients with acute respiratory distress syndrome (ARDS). However, as with other strategies, it is not free of complications. Inadequate ventilation may have a negative impact on pulmonary and systemic hemodynamics, and it could both cause structural damage to pulmonary parenchyma and activate inflammation (2). This process is known as ventilator-induced lung injury (VILI) and may promote the development of multiple organ failure and, eventually, death. VILI results from the interaction between the mechanical load applied to the ventilable lung and its capacity to tolerate it. Factors such as tidal volume (Vt), driving pressure (ΔP), inspiratory flow rate (VI), respiratory rate (RR), excessive inspiratory effort, high levels of FiO2 and, in some cases, PEEP, have been involved in damage mechanism. In that sense, the concept of mechanical power (MP) tries to encompass most of these factors within a measurable unit (3). Furthermore, the decrease in ventilable lung volume (baby lung concept), the heterogeneous lung compromise in ARDS), and the presence of cofactors that have a negative impact on the lung (fluid overload, presence of sepsis or shock) could increase its susceptibility to damage (4-5). Due to the fact that the mechanical conditions of the lung change dynamically with the progression of the disease, the ventilatory strategy needs constant adjustments in order to maintain a balance between the load and the size of the ventilable lung (concept of ergonomic ventilation). In fact, a protective ventilatory strategy of low tidal volume (Vt: 6 ml/kg/PBW) and limited plateau pressure (PPlat \<30 cmH2O) may cause damage if the functional residual capacity (FRC) decreases significantly, thus making a lower number of alveoli (including capillaries) withstand a higher mechanical load per unit. The concept of VILI vortex has recently been proposed as a progressive lung injury mechanism in which the alveolar stress/strain increases as the ventilable lung "shrinks". This positive feedback inexorably leads to the acceleration of lung damage, with potentially irreversible results (1). Little is known about the clinical aspects of this condition. Understanding its behavior could contribute to changing its potential devastating impact. The objective of this study is to evaluate the incidence of VILI vortex in patients with ARDS secondary to COVID-19, to establish a connection between this phenomenon and mortality, and to identify the factors that have an impact on its development.
Mechanical variables and PaO2/FiO2 were registered daily for 14 days or until initiating assisted ventilation. These data were obtained in passive mechanical conditions. Ventilator-induced lung injury vortex was defined as a progressive increase in driving pressure (ΔP) as Vt remained constant or even decreased. Refractory hypoxemia was defined as PaO2/FiO2 \<100 despite the optimization of mechanical ventilation and prone positioning.
Avellaneda, Buenos Aires, Argentina