A prospective study of 179 patients in whom pulmonary dead space was measured within 24 hours of ARDS onset indicated that dead space was markedly elevated in the early phase of ARDS and was associated with higher mortality [ 4].
Previous studies, computing the pulmonary dead space by measuring the expired carbon dioxide and the Enghoff equation, found that the dead space fraction was significantly higher in the non-survivors; it was even an independent risk of death.
We found no increase in pulmonary dead space fraction.
As a result, neutrophils migrate into the pulmonary interstitial space releasing inflammatory mediators.
Pulmonary dead space, ratio of right over left ventricular stroke work, PaO2/FiO2 ratio, and oxygenation index are proven to be independent predictors of mortality.
Elevated pulmonary dead space fraction likely reflects the extent of pulmonary microvascular thrombosis and injury or frank destruction of the pulmonary vascular bed, providing an important index of the severity of acute lung injury.
Several subsequent studies have also reported that an elevated ratio of pulmonary dead space to tidal volume (VD /VT) within 24 h of onset of ARDS was associated with higher mortality [24, 25].
During inspiration the metameric rows of gastralia likely stiffened the ventral body wall, helping to prevent it from moving inwards and encroaching on pulmonary air space [35].
Thus, any changes in intrapulmonary shunting, ventilation/perfusion ratio, or CO2 solubility (Haldane effect) can affect the pulmonary dead space.
However, there was a moderate correlation between BNP levels and pulmonary dead space fraction (r = 0.39, p = 0.01).
The pulmonary dead space increase, which is due primarily to an alteration in pulmonary blood flow distribution, is largely responsible for carbon dioxide retention.
