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.