Potential protective effects of continuous anterior chest compression in the acute respiratory distress syndrome: physiology of an illustrative case

• Published in: Critical care (London, England) Vol. 25; no. 1; pp. 1 - 4
• Main Authors: Carteaux, Guillaume, Tuffet, Samuel, Mekontso Dessap, Armand
• Format: Journal Article
• Language: English
• Published: London BioMed Central 01.06.2021; BioMed Central Ltd; BMC
• Subjects: Acute respiratory distress syndrome; Care and treatment; Case studies; CPR (First aid); Critical care; Critical Care Medicine; Emergency Medicine; Esophagus; Intensive; Life Sciences; Medicine; Medicine & Public Health; Patients; Physiology; Regions; Research Letter; Respiratory distress syndrome; Respiratory system; Severe acute respiratory syndrome coronavirus 2; Tomography; Ventilators; France
• ISSN: 1364-8535; 1466-609X; 1364-8535; 1366-609X; 1466-609X
• DOI: 10.1186/s13054-021-03619-0

To the Editor, Continuous anterior chest compression (CACC) may have protective effects in patients with the Acute Respiratory Distress Syndrome (ARDS) by decreasing the anterior chest wall compliance, thus decreasing the anterior transpulmonary pressure and the resulting risk of overdistension [1] along with promoting redistribution of ventilation through the dependent regions. Regional effects of CACC were the followings: * A decrease in anterior (ventral) lung regions distension: the positive stress index pattern disappeared, the end-inspiratory transpulmonary pressure decreased and the regional lung compliance in the anterior half increased. * A recruitment of the posterior (dorsal) lung regions: the number of pixels showing positive ∆Z in the posterior half of EIT matrix increased by 10% and the regional lung compliance in the posterior half increased. * A homogenization of tidal ventilation: the ratio between ventilation distributions of the anterior and posterior halves went from 60%/40% to 50%/50%. Discussion The dramatic increase in respiratory system compliance during CACC in this ARDS patient may result from several combined mechanisms: 1-In the part of the lung already aerated but subject to intra-tidal overdistension, the noticeable decrease in the end expiratory lung volume resulted in a leftward shift of the pressure–volume curve below the upper inflexion point [3], 2-the concomitant recruitment in the posterior regions resulted in an increase in the number of aerated lung units [4].