INTRODUCTION
Pediatric acute respiratory distress syndrome (PARDS) has a high morbidity and mortality rate. While mortality rates are decreasing over time and vary across regions, overall mortality continues to be between 15-20%1-3 with multi-organ dysfunction syndrome and refractory shock accounting for up to 60% of mortality4,5. Right ventricular (RV) systolic dysfunction and pulmonary hypertension (PH) have been independently associated with worse outcomes in PARDS, presumably by further impairing oxygenation and increasing the risk of multiple organ dysfunction syndrome6,7. Early detection and treatment of RV dysfunction and/or PH in PARDS may improve patient outcomes.
The lung physiologic dead space ratio (VD/VT) can be estimated through the Enghoff modification of the Bohr formula8. This is also known as the alveolar dead space fraction (AVDSf) and is a measure of ventilation-perfusion mismatch that represents the proportion of inhaled air not participating in gas exchange. It is an easily obtained clinical variable at the bedside, requiring only measurement of end-tidal carbon dioxide (PetCO2) and arterial partial pressure of CO2 (PaCO2). AVDSf is low in healthy children and increases in the setting of pulmonary injury and low cardiac output9. Higher AVDSf at the onset of PARDS is associated with mortality10,11. As it is affected by perfusion abnormalities from intrinsic pulmonary vascular disease, AVDSf may be a marker for risk of developing RV systolic dysfunction or acute cor pulmonale in adults12. However, the prognostic utility of AVDSf in PARDS may also be due to lung overdistension, iatrogenic generation of dead space, or reflect the risks associated with unsafe ventilator pressures. Whether AVDSf is primarily a marker of decreased pulmonary blood flow in the setting of RV dysfunction or PH or is primarily a marker of pulmonary overdistension in children with PARDS is unknown.
The primary objective of this study was to determine the association between AVDSf at PARDS onset with evidence of RV systolic dysfunction by 2D speckle tracking echocardiography. Our hypothesis was that higher AVDSf at PARDS onset would be associated with evidence of RV systolic dysfunction as measured by RV global longitudinal strain on clinically obtained echocardiograms within 24 hours of PARDS onset.