Causes of a high physiological dead space in critically ill patients

Abstract

Since around 1950, physiological dead space - the difference between arterial and mixed expired pCO2 (partial pressure of carbon dioxide) divided by the arterial pCO2 - 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 pCO2, 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.

Figure 1

Comparison of effects of shunt (top) and ventilation/perfusion ratio (${\dot{\text{V}}}_{\text{A}}/\dot{\text{Q}}$) inequality (bottom) on calculated physiological dead space. In general, ${\dot{\text{V}}}_{\text{A}}/\dot{\text{Q}}$ inequality leads to greater dead space than shunt does. Log SDQ, second moment (dispersion) of the ventilation/perfusion distribution on a log scale.