Abstract

One of the most interesting unanticipated findings by André Cournand and Dickinson Richards in their groundbreaking studies of cardiac catheterization was the very low pressure in the normal pulmonary circulation. At the time, in the 1940s, the significance of this was not appreciated. For example, in their speeches at the Nobel Prize ceremony, neither of these laureates referred to the low pressure, although they did discuss other features of the pulmonary circulation. It was up to the cardiologist, William Dock, to point out that these low pressures implied a very uneven distribution of blood flow in the lung, and in particular that in the normal upright lung, the blood flow to the apex would be extremely small. Dock went on to argue that this low blood flow at the top of the lung was responsible for the characteristic apical distribution of adult pulmonary tuberculosis. Since that time, it has been recognized that the low pressures in the pulmonary circulation have many implications in pulmonary pathophysiology. For example, if the vascular pressure is further reduced, such as in hemorrhagic shock, gas exchange is seriously affected because of the development of a large alveolar dead space. Furthermore, if humans are subjected to increased acceleration, such as in a high-performance aircraft, the distribution of blood flow becomes extremely abnormal, with much of the lung being completely unperfused. There are also diseases where distribution in the lung is affected by the uneven distribution of blood flow. These include alpha-1 antitrypsin deficiency and metastatic calcification of the lung.

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