Cardiopulmonary effects of pulmonary venous hypertension with special reference to pulmonary lymphatic flow.

Abstract

Acute elevation of left atrial pressure could be precisely controlled at any desired level up to a mean of 60 mm. Hg in dogs with an intact thorax. The following observations were made in a series of 15 dogs. Right lymphatic duct flow did not increase at acutely elevated left atrial mean pressure below 25 mm. Hg, whereas flow increased 3- to 4-fold at mean pressure above 25 mm. Hg. The total amount of lymph at maximum flow, however, was only 0.3 ml./min. Lymph flow remained elevated for as long as 1 hour after left atrial pressure was restored to normal. Elevation of left atrial pressure did not affect lymph flow in the thoracic duct. Pulmonary edema did not occur readily at left atrial mean pressure elevated only slightly above plasma oncotic pressure. The production of pulmonary edema was observed only after a considerable elevation of left atrial pressure above plasma oncotic pressure was maintained for a period of one half hour or more in an otherwise normal dog. The hematocrit increased significantly after a 10-minute period of high left atrial pressure. Pulmonary vascular resistance decreased sharply as left atrial mean pressure was raised from 0 to 15 mm. Hg. The resistance gradually rose as left atrial pressure was raised to between 15 and 30 mm. Hg. Pulmonary arterial pressure uniformly rose and cardiac output uniformly declined with increasing left atrial pressure. Chronic elevation of left atrial pressure was achieved in 15 dogs. Left atrial mean pressure varied from 10 to 23 mm. Hg. These dogs were followed up to 10 months and the following observations were made. Right lymphatic duct flow did not increase at chronically elevated left atrial mean pressure below 25 mm. Hg. Flow was not studied at higher pressures since we were unable to sustain left atrial mean pressure above 25 mm. Hg in any dog in our chronic group. The animals that were brought to left atrial mean pressure between 30 and 40 mm. Hg and in whom these high levels were presumably maintained were found dead in their cages with pulmonary edema 1 to 2 days after tightening the snare. Many of the usual functional and structural changes often found in lungs of patients with mitral stenosis, except for hemosiderosis, were not observed in our experimental animals although the extent of the supravalvular stenosis produced was marked. Pulmonary arterial pressure rose slightly and cardiac output declined slightly. No change was noted in pulmonary vascular resistance. Ascites and other signs of right sided failure were not encountered.