Objective: To avoid ventilator induced lung injury, tidal volume should be low in acute lung injury (ALI). Reducing dead space may be useful for example by using a pattern of inspiration that prolongs the time available for gas distribution and diffusion within the respiratory zone, the mean distribution time (MDT). A study was conducted to investigate how MDT affects CO 2 elimination in pigs at health and after ALI.Design and setting: Randomised crossover study in the animal laboratory of Lund University Biomedical Center. Subjects and intervention:Healthy pigs and pigs with ALI, caused by surfactant perturbation and lungdamaging ventilation were ventilated with a computer-controlled ventilator. With this device each breath could be tailored with respect to insufflation time and pause time (T I and T P ) as well as flow shape (square, increasing or decreasing flow). Measurements and results:The single-breath test for CO 2 allowed analysis of the volume of expired CO 2 and the volume of CO 2 re-inspired from Y-piece and tubes. With a long MDT caused by long T I or T P , the expired volume of CO 2 increased markedly in accordance with the MDT concept in both healthy and ALI pigs. High initial inspiratory flow caused by a short T I or decreasing flow increased the re-inspired volume of CO 2 . Arterial CO 2 increased during a longer period of short MDT and decreased again when MDT was prolonged.Conclusions: CO 2 elimination can be enhanced by a pattern of ventilation that prolongs MDT. Positive effects of prolonged MDT caused by short T I and decreasing flow were attenuated by high initial inspiratory flow.

Although dead space is often increased in disease, it is not frequently measured in the clinic. This may reflect that an adequate method as well as reference values are missing. Healthy males and females, n=38, age 20-61 yrs, were connected to a pneumotachograph and a fast CO2 analyser after radial artery catheterization. The physiological dead space was partitioned into airway and alveolar dead space using a delineation principle denoted the pre-interface expirate. Physiological dead space was 201+/-41 mL in males and 150+/-34 mL in females. Dead space values were depending upon parameters reflecting lung size (predicted total lung capacity), breathing pattern and age. After multiple correlation the variation decreased and differences between males and females disappeared. The residual SD was then for physiological dead space 18.9 mL. The clinical use of the new method for determination of dead space can be based upon reference values, with a more narrow range than previous data.