Causes of a high physiological dead space in critically ill patients

Since around 1950, physiological dead space – the difference between arterial and mixed expired pCO(2 )(partial pressure of carbon dioxide) divided by the arterial pCO(2 )– has been a useful clinical parameter of pulmonary gas exchange. In the previous issue of Critical Care, Niklason and colleagues remind us that physiological dead space, while easily measured, consolidates potentially very complex physiological derangements into a single number. The authors show how shunts raise arterial pCO(2), thereby increasing dead space, and how changes in other variables such as cardiac output and acid/base state further modify it. A solid understanding of respiratory physiology is required to properly interpret physiological dead space in the critically ill.