Primary pulmonary hypertension is a progressive disease. Most affected patients are young and middle-aged women. Etiology is unknown, although a familial and genetic factor is present in up to 6% of cases. Endothelial dysfunction and abnormalities in calcium channels of smooth muscle fibers are the present pathogenetics theories. Diagnostic tests try to exclude secondary causes of pulmonary hypertension and to evaluate its severity. Acute vasodilatory test is vital in the selection of treatment. Oral anticoagulation is indicated in all patients. Lung transplant is performed when medical treatment is unsuccessful. Atrial septostomy is an alternative and palliative treatment for selected cases. Chronic thromboembolic pulmonary hypertension is a special form of secondary pulmonary hypertension, clinically undistinguishable from primary primary hypertension, is of mandatory diagnosis because it can be cured with thromboembolectomy. Pulmonary embolism is common in hospitalised patients. The mortality rate for pulmonary embolism continues to be high: up to 30% in untreated patients. The accurate detection of pulmonary embolism remains difficult, as pulmonary embolism can accompany as well as mimic other cardiopulmonary illnesses. Non-invasive diagnostic tests have poor specificity and sensitivity. The D-dimer level and the spiral CT angiography have also been employed as new alternatives and important tools for precise diagnosis of suspected pulmonary embolism. The standard therapy of pulmonary embolism is intravenous heparin for 5 to 10 days in conjunction with oral anticoagulants posteriorly for 3 to 6 months. The incidence of deep venous thrombosis, pulmonary embolism and death due to pulmonary embolism, can be reduced significantly and shown clear benefits only by adoption of a prophylactic strategy with low-molecular-weight-heparins or dextrans in patients at risk.