Obstructive sleep apnea (OSA) is characterized by repetitive episodes of complete or partial obstruction of the upper airway during sleep that lead to an increase in airway resistance and respiratory effort. This may produce oxygen desaturation, hypercapnia and central nervous system arousal that restore airflow. OSA is associated with hemodynamic changes that are related to alterations in the activity of the autonomic nervous system. During the course of an apnea, the heart rate may slow down, increase or remain stable. The blood pressure decreases at the start of the apnea and increases at its terminal portion. When ventilation resumes, heart rate, blood pressure and ventilation reach a peak accompanied by an abrupt reduction in left ventricular stroke volume. During the early phase of apnea, sympathetic nerve activity (SNA) is suppressed; it then increases constantly and reaches a peak at the end of apnea and on arousal. As soon as ventilation resumes, there is an abrupt inhibition of SNA in the peripheral blood vessels. The resumption of ventilation occurs in the context of peripheral vasoconstriction and increased peripheral resistance. This situation persists for several seconds after the SNA has ceased, due to the kinetics of norepinephrine uptake, release and washout at the neurovascular junction. Hypoxemia, hypercapnia, lung inflation and blood pressure are important factors that may modulate these autonomic changes. The alterations in the autonomic nervous system are carried over into wakefulness and may contribute to the development of the cardiovascular disorders associated with OSA, including sympathovagal imbalance accompanied with changes in the baroreflex and chemoreflex. The hemodynamic and autonomic dysfunction associated with OSA is improved following treatment with continuous positive airway pressure.