Discusses the physiological basis and terminology for using carbon monoxide to assess the pulmonary capillary bed in mitral valve disease.
Provides physiological rationale for carbon monoxide uptake in mitral valve disease; leaves open prospective validation before clinical adoption.
Disturbances in the exchange of gases between the alveolar air and the blood in the pulmonary capillaries can be used to estimate the effects of disease on the pulmonary capillary bed. These techniques have been applied to the investigation of the effects of sustained elevation of the pul-monary venous pressure in mitral valve disease. Carbon monoxide is used as a test substance to assess abnormalities in gas absorption as it behaves in the same way as oxygen, combining avidly with the hemoglobin in the pulmonary capillary red cells. Measurement of the factors affecting carbon monoxide uptake is much simpler than in the case of oxygen. The rate of absorption of these gases, expressed in relation to the difference in partial pressure of the gas between the alveoli and the capillaries (i.e. in ml./mm. Hg/min.), has usually been described as the " diffusing capacity " (DL) on the hypothesis that diffusion was the only process involved. However, it has been shown (Roughton and Forster, 1957) that the chemical reaction between the respiratory gases and hemoglobin is relatively slow and accounts for much of the resistance to absorption of these gases. In view of this, Cotes (1963) has suggested the non-committal term "gas transfer factor " to describe these measurements. The competition between carbon monoxide
No takes yet. Share an insight, caveat, or question.
John Hamer (1965) studied this question.
Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context: