Pulmonary hypertension is defined by mean pulmonary arterial pressure (mPAP) ≥ 25 mmHg. About 1% of adults suffer from pulmonary hypertension. The WHO (World Health Organization) classification categorizes pulmonary hypertension into five groups: pulmonary arterial hypertension, pulmonary hypertension due to left heart disease, pulmonary hypertension due to lung disease and/or hypoxia, chronic thromboembolic pulmonary hypertension and pulmonary hypertension with multifactorial mechanisms. The consequence of chronic and progressive pulmonary hypertension is right ventricular overload, which leads to the right heart failure. Reduced ejection fraction of right ventricle is more important as a prognostic factor for pulmonary hypertension than changes in pulmonary vascular resistance values. The most common symptoms of pulmonary hypertension are progressive dyspnea on exertion, and fatigue. As pulmonary hypertension progresses, signs and symptoms of right heart failure occur, as a result of elevated central venous pressure and decreased cardiac output. The most prominent clinical sign of the right heart failure is peripheral edema. In the late stage of the disease, damage to the function of the kidneys, liver and gastrointestinal tract occurs. The diagnosis of pulmonary hypertension and right heart overload is based on history and physical examination, laboratory and functional tests, non–invasive and invasive diagnostic methods. The most important diagnostic method is echocardiography, which often gives the first suspicion of pulmonary hypertension and right heart overload. The definitive diagnosis is confirmed invasively, by catheterization of the right heart. The care for patients with right heart failure is focused on recognizing the reversible causes of acute right ventricular decompensation and improving function by changing preload, contractility and afterload of the right ventricle. Available pharmacotherapy overcomes the imbalance between vasoconstrictors and vasodilators. It includes endothelin receptor antagonists, phosphodiesterase type 5 inhibitors, stimulators of soluble guanylate cyclase and prostacyclin analogues. If the response to pharmacotherapy is inadequate or disease has progressed, the lung transplantation should be considered.