RT Journal Article
SR Electronic
T1 Dead space: the physiology of wasted ventilation
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 1704
OP 1716
DO 10.1183/09031936.00137614
VO 45
IS 6
A1 H. Thomas Robertson
YR 2015
UL http://erj.ersjournals.com/content/45/6/1704.abstract
AB An elevated physiological dead space, calculated from measurements of arterial CO2 and mixed expired CO2, has proven to be a useful clinical marker of prognosis both for patients with acute respiratory distress syndrome and for patients with severe heart failure. Although a frequently cited explanation for an elevated dead space measurement has been the development of alveolar regions receiving no perfusion, evidence for this mechanism is lacking in both of these disease settings. For the range of physiological abnormalities associated with an increased physiological dead space measurement, increased alveolar ventilation/perfusion ratio (V′A/Q′) heterogeneity has been the most important pathophysiological mechanism. Depending on the disease condition, additional mechanisms that can contribute to an elevated physiological dead space measurement include shunt, a substantial increase in overall V′A/Q′ ratio, diffusion impairment, and ventilation delivered to unperfused alveolar spaces.A review of current understanding of factors accounting for abnormal physiological dead space measurements in disease http://ow.ly/Dnyw1