Clinical trial NCT04157946: The Role of Morphological Phenotype in ARDS
Official title: Risk Assessment of Ventilator-induced Lung Injury in Patients With Acute Respiratory Distress Syndrome: The Role of Morphological Phenotype in ARDS
Study type: OBSERVATIONAL
Overall status: COMPLETED
Conditions: Respiratory Distress Syndrome, Adult
Keywords: Respiratory Insufficiency
Ventilator-Induced Lung Injury
Ventilators, Mechanical
Lead sponsor: Hospital El Cruce
Sponsor class: OTHER
First posted: 2019-11-08
Enrollment: 12
Sex: ALL
Minimum age (years): 18
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: no
Observational model: COHORT
Time perspective: PROSPECTIVE
Sampling method: NON_PROBABILITY_SAMPLE
Study population: Patients with moderate to severe ARDS diagnosis were studied according to the Berlin definition. The AECC defined ARDS as the acute onset of hypoxemia (arterial partial pressure of oxygen to fraction of inspired oxygen \[PaO2/FIO2\] ≤ 200 mm Hg) with bilateral infiltrates on frontal chest radiograph, with no evidence of left atrial hypertension.

Brief summary: 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

Detailed description: 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

Eligibility criteria: 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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Primary outcomes:
measure: Measuring the level of pulmonary stress caused by mechanical ventilation
timeFrame: One year
measure: Measurement of pulmonary strain caused by mechanical ventilation
timeFrame: One year
measure: Measurement of injury due to cyclic opening and closing of the most unstable caused by mechanical ventilation .
timeFrame: One year
Secondary outcomes:
measure: Measurement of pulmonary hyperinflation caused by mechanical ventilation
timeFrame: One year
Other outcomes:
Locations:
city: Florencio Varela
country: Argentina
facility: Hospital El Cruce
state: Buenos Aires
Study officials:
affiliation: Hospital El Cruce
name: Nestor Pistillo, MD
role: PRINCIPAL_INVESTIGATOR
References:
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