Effects of breathing liquid fluorocarbons on regional differences in pleural pressures and other physiological parameters

D. J. Sass, E. H. Wood, J. F. Greenleaf

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A water immersion respirator and liquid oxygenator assembly of special design was used to control respiratory rate and tidal and residual lung volumes in dogs breathing first air or oxygen, and then, either liquid fluorocarbon FC 80 or silicone oil DC 200. In separate studies in 30 animals the following conclusions were reached: Arterial hypoxemia due to dependent pulmonary arteriovenous shunting caused by transverse acceleration was not minimized by water immersion alone, but liquid breathing combined with water immersion did prevent dependent pulmonary arteriovenous shunting and downward displacement of the heart due to transverse acceleration. Blood flow velocity in the ascending aorta was recorded by a chronically implanted electromagnetic flowmeter, and the beat to beat stroke volume was computed by an on line CDC 3300 digital computer. Phasic changes in left ventricular stroke volume were caused by variations in intrathoracic, airway, and other internal body pressures produced by the respirator to maintain adequate respiratory gas exchange with liquid fluorocarbon. The spatial distribution of pulmonary blood flow was determined by a radioactive embolization technique. Up to 4 injections of differentially labeled microspheres were made into the right ventricle, and the distribution of microspheres from each injection, representative of pulmonary blood flow at the time of each injection, was determined throughout the entire lung by a high resolution computer controlled scintiscanning technique. When dogs breathed the heavier than blood fluorocarbon, blood flow was increased in the superior regions of the lung during exposures to transverse acceleration; blood flow decreased when they breathed the lighter than blood silicone oil. Blood PCO2 could be controlled at normal or hypocapnic levels in normothermic dogs breathing oxygenated fluorocarbon for 4 to 8 hr. The possibility is discussed that oxygen toxicity and/or escape of fluorocarbon from the airways into the circulatory system contributed to the death of these animals 24 to 30 hr after cessation of liquid breathing. On line digital computer processing of multiple physiological variables used in these studies is described.

Original languageEnglish (US)
JournalAeromedical Reviews
StatePublished - 1972

ASJC Scopus subject areas

  • General Medicine


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