THE PULMONARY CAPILLARY BED IN MITRAL VALVE DISEASE

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Abstract
The disturbancesln the physiological behavior of the pulmonary capillary bed have been investigated in 40 patients with mitral valve disease. Measurements of carbon monoxide absorption were used to calculate the pulmonary capillary volume (Vc), and the membrane component of gas transfer (DM), an estimate of the changes in the alveolar-capillary membrane. Seventeen patients with serious mitral stenosis and 12 patients with serious mitral stenosis associated with moderate mitral incompetence were studied. Similar changes were found in these 2 groups of patients: the capillary volume (Vc) was increased in 38% and the membrane component (DM) was reduced in 41%. These changes are consistent with the histological evidence of an increase in the size and nun ber of the pulmonary capillaries and thickening of the alveolar walls in mitral stenosis. Four patients with severe mitral incompetence had serious impairment of the membrane component (DM) but normal capillary volumes (Vc). Seven patients with mild mitral valve disease showed no consistent abnormality. Cardiac catheterization was performed in 21 patients. The findings suggest that the capillary volume (Vc) depends on both pulmonary venous pressure and pulmonary blood flow. Variations in capillary volume would be expected to affect the membrane component (DM) by altering the area available for diffusion. Changes of this type in response to an increase in pulmonary venous pressure are probably masked by the associated increase in thickness of the alveolar-capillary membrane and by the effects of uneven distribution of ventilation and blood flow in the lung. However, there is a relation between the membrane component (DM) and pulmonary blood flow, and the serious impairment of the membrane component (DM) in severe mitral incompetence is probably related to the low cardiac output in these patients. The increase in capillary volume (Vc) tends to counteract the effects of the reduction in the membrane component (DM), so that measurements of the whole process of transfer of gas from the alveoli to the red cells, i. e. "diffusing capacity" (DL ), are often normal in mitral valve disease. In spite of the histological findings of an increase in the thickness of the alveolar-capillary membrane, the changes in gas transfer demonstrated here are not sufficient to reduce the arterial O2 saturation. When this occurs uneven distribution of ventilation and blood flow in the lungs are probably responsible.