Long-term oxygen therapy (LTOT) is a cornerstone of management for chronic hypoxemic respiratory diseases, such as chronic obstructive pulmonary disease, yet its physiological impact as a potent modulator of cardiovascular function remains a subject of ongoing investigation. While oxygen is primarily prescribed to correct arterial desaturation, its role as a regulator of vascular tone and cellular metabolism suggests it can exert significant, and sometimes contrasting, effects on the heart and systemic circulation. This review evaluates the evidence for LTOT in heart failure and pulmonary hypertension, 2 conditions where oxygen is frequently utilized despite varying levels of baseline hypoxemia. In heart failure, LTOT has not been shown to improve key hemodynamic variables and relevant endpoints, such as exercise capacity, in normoxemic patients. Some studies suggest that supplemental oxygen may even impose hemodynamic strain in this population by increasing systemic vascular resistance and reducing cardiac output. On the other hand, LTOT shows promise in improving relevant hemodynamic variables in pulmonary hypertension, such as mean pulmonary arterial pressure, as well as exercise capacity and other clinical measures across various baseline oxygen saturation levels. These findings suggest that the cardiovascular response to LTOT is highly dependent on the specific underlying pathology.
Kusayev et al. (Wed,) studied this question.