The Role of Morphological Phenotype in ARDS
The Role of Morphological Phenotype in ARDS
Although most of the information focuses on understanding how the ventilator produces lung
 damage, the pulmonary factors that predispose to ventilator-induced lung injury (VILI) have
 been less studied. Acute respiratory distress syndrome (ARDS) can adopt different
 morphological phenotypes, with its own clinical and mechanical characteristics. This
 morphological phenotypes may favor the development of VILI for same ventilatory strategy
The lung in acute respiratory distress syndrome ARDS) is a heterogeneous viscoelastic system,
 in which areas with different time constants coexist, causing tidal volume to be distributed
 unevenly within an anatomically and functionally reduced lung. The administration of a
 disproportionately high tidal volume for this lung predisposes to the over-distension of the
 better ventilated alveoli and to the injury by tidal opening and closing of the alveoli more
 unstable. In this sense, using low tidal volume and homogenizing the lung by means of the
 prone position have proven beneficial in ARDS.

 Tidal volume, driving pressure, inspiratory flow and respiratory rate have been identified as
 responsible for mechanical ventilation-induced lung injury (VILI). These factors together
 represent the mechanical power, the insulting energy which is repeatedly applied to a
 vulnerable lung parenchyma.

 Although most of the information focuses on understanding how the ventilator produces lung
 damage and/or amplifies the existing one, the pulmonary factors that predispose to VILI have
 been less studied. Acute respiratory distress syndrome can adopt different morphological
 phenotypes, with its own clinical and mechanical characteristics. Understanding how each
 subgroup of ARDS responds to the protective ventilatory strategy could help to personalize
 treatment.

 Objectives: To compare the risk of VILI in two groups of ARDS with different morphological
 phenotypes (focal and non-focal), ventilated with the same protective strategy.

 Design: Patients with ARDS were ventilated under the same conditions of both tidal volume
 (TV) and plateau pressure (PPlat). Positive End Expiratory Pressure (PEEP) was adjusted to
 reach 30 cmH2O of PPlat. A CT was performed in inspiration and expiration. Transpulmonary
 pressures (TP) were measured and lung volumes calculated (Volume Analysis Software,Toshiba,
 Japan). Stress was defined as TP at the end of inspiration (TPinsp) and strain: tidal
 volume/End Expiratory Lung Volume Patients were classified into focal and non-focal according
 to the distribution of aeration loss in CT. Mann - Whitney U test was used to compare
 variables and Pearson correlation coefficient to compare its correlation. Significant: p
 <0.05
Inclusion Criteria:

 Acute respiratory distress syndrome (ARDS).

 Exclusion Criteria:

 Emphysema Asthma Pneumothorax Oxygen saturation ≤ 88% Severe shock Ventricular arrhythmia
 Myocardial ischemia.

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