Abstract
Physio-logical dead space was measured by simultaneous and continuous measurement of vol. flow and N2 content of gas expired following the change from breathing air to breathing 99.6% O2. In normal subjects the effect of nonuniform alveolar gas on dead space measurements can largely be eliminated. The avg. vol. of the physiol. dead space in 45 healthy males at rest was 156 cc; the avg. expired vol. required to wash out the dead space was 325 cc. The physiol. dead space/tidal vol. fraction averaged 25.9%, but varied widely in different individuals. The vol. of the physiol. dead space is affected by: (a) Anatomical vol. of the bronchial tree. Maximal variations of inspiratory lung vol. changed dead space by about 100 cc. Voluntary hyperventilation and post-exercise hyperpnea increased physiol. dead space equally, the increase being 100 cc. or less. (b) Gas diffusion between terminal bronchioles and alveolar spaces. Prolongation of inspiratory time by 2 to 3 sec. significantly reduced the vol. of the physiol. dead space, and breath-holding, during inspiration (20 sec.), caused reductions of 44-82 cc. In slow deep breathing the anatomical vol. increase is counteracted by diffusion occurring during the prolonged inspiratory time. Variations in the rate of inspiratory vol. flow did not affect the vol. of the physiol. dead space. Clinical applns. of the method are suggested.