Pulmonary hypertension is characterized by hemodynamic changes (increased pressure or resistance) in the pulmonary circulation which can be caused by various triggers. The result is an increased right ventricular afterload and thus a chronic strain on the right heart. In contrast to the systemic circulation, the pulmonary circulation as a so-called low-pressure system due to its high capacity and large elasticity as well as the small proportion of smooth muscle in small arteries and arterioles primarily has no hypertensive predisposition. However, if the vessel cross-section is reduced by destruction, obliteration or occlusive lesions in the resistance vessels, this leads to an increase in pulmonary vascular resistance and pulmonary arterial pressure. Clinical manifestations, natural course, and reversibility of pulmonary hypertension depend largely on the type of pulmonary lesion and the etiology and severity of the hemodynamic changes.