The Effect of Intermittent Positive Pressure Breathing and Voluntary Hyperventilation upon the Distribution of Ventilation and Pulmonary Blood Flow to the Lung in Chronic Obstructive Lung Disease*

Journal/Book: Journal of Clinital Investigation Vol. 45 1966 No. 7 S.1221-1233. 1966;

Abstract: (From the Cardiopulmonary Laboratory and Chest Service Columbia University Division Bellevue Hospital New York and the Department of Medicine State University of New York Downstate Medical Center Brooklyn N. Y.) * Submitted for publication April 14 1965; accepted April 13 1966. This study was supported in part by research grants HE 02001-10 and HE 5757 from the National Institutes of Health and U-1067 and U-1361 from the Health Research Council of the City of New York. Address requests for reprints to Dr. George E. Emmanuel State University of New York Downstate Medical Center Brooklyn N. Y. 11203. Summary Studies were made an 14 patients with chronic obstructive disease of the lungs at rest during intermittent positive pressure breathing and during voluntary hyperventilation. Changes in arterial blond gases measured during air breathing are correlated with changes in nitrogen washout curves measured during oxygen breathing. Both intermittent positive pressure breathing and voluntary hyperventilation had the same effect an arterial blond gases raising arterial oxygen saturation to a normal value and lowering arterial carbon dioxide tension to a subnormal value. During both procedures there was an increase in oxygen consumption that was about four times as much per liter of added ventilation during voluntary hyperventilation as it was during intermittent positive pressure breathing. During intermittent positive pressure breathing about one-tenth of the extra ventilation was directed into the slow space. This was enough to account for the observed rise in arterial oxygen saturation. During voluntary hyperventilation the increase in the ventilation of the slow space was less than one-tenth and was not enough to account for the rise in arterial oxygen saturation. This suggests that during voluntary hyperventilation the rise in arteriai oxygen saturation was partly due to a reduced fractional perfusion of the slow space.

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