[The lung in heart diseases]

The effects of "hypocirculation" and "hypercirculation" of the lungs are small. Hypocirculation has an influence of the ventilation/perfusion ratio, and can thus contribute to hypocapnia. In the early stages, hypercirculation--in particular via a left-to-right shung, leads to an increase in diffusion capacity; after a course of many years, a "counter-situation" occurs. Progressive pulmonary hypertension, as is exemplified for mitral stenosis, leads to measurable restrictive and obstructive impairment of function, and possible to unspecific hyper-reaction, as also, over the long-term, to a diminishement in membrane diffusion capacity. Chronic left heart failure is characterised by interstitial oedema at the level of the alveolar and bronchial capillary beds. The results are measurable restrictions in the static volumes, and in particular of the obstruction parameters and the closing volume that involve the small airways. In the individual case, no statement as to the extent of left heart failure is possible. In the passive pulmonary hypertension phase, diffusion capacity increases; in the further course of the disease, with development of interstitial and alveolar oedema, it decreases again. In acute left heart failure, the persistance and/or extent of pulmonary oedema is not determined solely by the magnitude of the pulmonary venous pressure. Permeability oedema--brought about by mediators--would appear to be significant on the basis of animal experiments. Not infrequently, left cardiac failure leads to small pleural effusions which occur in combination with substantial atelectasia, the aetiology of which is unclear. Interpretation difficulties are caused by the clinical findings and function-analytical data obtained in patients with a combination of chronic lung disease and reducted volume storage capacity of the pulmonary circulation and of the left heart failure, a common situation in the elderly patient. Diminished pulmonary function parameters that fail to adequate respond to bronchodilators may be an expression of left ventricular failure.