Blood gas analysis is often performed in the initial diagnosis of acute pulmonary embolism (APE), and it is recognized that hypoxemia (H) strengthen its suspicion. However, the diagnostic power of hypoxemia is very week. Hypoxemia, usually deep, occurs in almost all patients with massive APE whereas moderate hypoxemia occurs in about 75% of unselected normotensive APE population without co-morbitides. H occurs also in most patients with chronic thromboembolic pulmonary hypertension (CTEPH). The patomechanism of H in pulmonary embolism is not completely known and is associated mainly with obstruction of pulmonary vasculature, pulmonary hypertension, and with co-morbitides. However, the secondary failure of ventilation followed by alveolar hypoxia can not be excluded in many cases of chronic pulmonary embolism. Hypoxemia seems to have moderate value in prognosis in APE and in CTEPH. H in massive APE requires oxygen therapy, and it can be speculated, whether long term oxygenation should be added to the anticoagulation in nonoperated, hypoxemic patients with CTEPH.