[Pathophysiology of pulmonary hypertension and chronic cor pulmonale].

Abstract

Pulmonary circulation has become possible only by right heart catheterisation. The point of increased pressure in relation to pulmonary capillary wedge pressure is divided into postcapillary (passive), capillary and precapillary (active) pulmonary hypertension (PH). We assume that reduction of alveolar oxygen partial pressure leads to a growth of mast cells not only peribronchially, but also especially perivascularly, causing pulmonary arteriolo-vasoconstriction during release of eicosanoids (mediators). The individual components (vasoconstrictive, obliterative, obstructive, reactive, nutritive, primary, porto-pulmonary) are discussed. Long-term elevated pulmonary artery pressure (increased arterial vasoconstriction) results in right heart hypertrophy, which begins particularly in the right heart ejection tract. Depending on the underlying parenchymal or vascular diseases, we must differentiate between chronic cor pulmonale parenchymal or vascular. Right ventricular catheterisation may be differentiated into compensated or decompensated situation. Timely normalisation of pulmonary artery pressure may even lead to regression of the right ventricular hypertrophy. Right ventricular contractility on hypoxia is basically different in adapted and non-adapted patients (important for therapy and prognosis). Progression of right ventricular muscle mass and constant myocardial vasculature will cause stenocardias; in that case, permanent oxygen insufflation is indicated. Right ventricular hypertrophy affects the left heart, conducting alteration in pulmonary circulation (pulmo cardialis).