Relation of valvular lesions and of exercise to auricular pressure, work tolerance, and to development of chronic, congestive failure in dogs.

T HE PATHOGENESIS of congestive failure is still uncertain. In 1910 Bolton and Starling (I) wrote that the analysis of the factors involved in the production of the disease was rendered difficult by the impossibility of accurately reproducing these states in animals. Since that time numerous methods have been tried to precipitate congestive failure in dogs. The attempts have met with limited success despite severe injury to the myocardium by coronary ligation (2), injection of silver nitrate (3), implantation of radon seeds (4), or burning of the myocardium (5). Single valvular lesions rarely led to congestive failure (6, 7). The cardiac reserve is apparently so great that nearly lethal injury to the heart must be produced before clear evidence of congestive failure appears in the resting dog. Landis et al. (8) have suggested the importance of exercise in the pathogenesis of congestive failure, and have shown in acute experiments on dogs that minor decreases in cardiac competence, which are not apparent at rest, may lead to elevation of central venous pressure during exercise. They have postulated that these transient elevations of venous pressure during muscular activity may play an important role in the development of the signs and symptoms of congestive failure. Our purpose was I) to study the effects of valvular lesions and of exercise on auricular pressure and work tolerance of’unanesthetized dogs, and 2) to attempt to determine which lesions could produce chronic, congestive failure in the dog. The valvular lesions, limited to the right side of the heart, were: a) insufficiency of the pulmonary valve, b) stenosis of the pulmonary artery, c) the combination of pulmonary stenosis and pulmonary insufficiency, d) insufficiency of the tricuspid valve and e) combined tricuspid insufficiency and pulmonary stenosis. Pulmonary insufficiencv had little effect on auricular pressure or work tolerance over a period of months. Pulmonary stenosis, or pulmonary stenosis plus pulmonary insufficiency, which elevated resting auricular pressure little or none at all, did lead to a significant rise of central venous pressure during exercise. Exercise tolerance was normal (one exception). Tricuspid insufficiency elevated resting auricular pressure moderately. Exercise further increased central venous pressure, but work capacity was normal. The combined insufficiency of the tricuspid valve and pulmonary stenosis led to a syndrome similar to right-sided congestive failure as seen in man.