The alveolar ventilation is defined as the respiratory rate times (tidal volume – dead space volume). No lung volume or frequency changes, parasympatholytic or sympathomimetic drugs, or altered patterns of breathing simulated the late delivery of dead space seen in age and some obstructive syndromes.Based on the recently published paper “Impact of Respiratory Rate and Dead Space in the Current Era of Lung Protective Mechanical Ventilation”, we will discuss here briefly the different part of the dead space and how it can be reduced, as well as the relations with respiratory rate, tidal volume and alveolar ventilation (part 2). Although an increase in VD(F) occurred with frequency, this was significantly less than that seen by VD(O), i.e., VD(F) did not see the progressive increase in phase I volume with frequency. An increase in VD(O) occurred with increasing respiratory frequency that was explained by the increase in volume of phase I. Physiological dead space (VD(p)) however, did not change significantly with lung volume, showing 'alveolar' dead space to diminish as a result. Both measures increased with lung volume, the increase being entirely due to an increase in the volume of phase I. VD(O) was appreciably larger than VD(F) in our normal subjects. VD(O) is known to increase with age and is enlarged in some obstructive syndromes. It may also be measured from an inert gas washout (VD(O)) that describes both volume and the delivery of VD(O) throughout the expiration. The 'anatomical' dead space is commonly measured by sampling an inert gas (N2) and volume in the exhalation following a large breath of oxygen (VD(F)).

Lung dead space volume