Primary central sleep apnea of infancy is a well-recognized, though oftentimes forgotten entity in infancy. There is a predominance of central events; however, mixed and obstructive apnea may be present. Sleep apnea during infancy results from the interplay of three important mechanisms. First, in normal breathing, an increase in upper airway muscle tone is required prior to diaphragmatic contraction for unobstructed inspiration to occur. In newborn infants, this sequence of events may be altered, leading to upper airway collapse and airway obstruction during inspiration. Next, immaturity of respiratory control results in overcompensation for changes in CO2 and oxygen levels through a mechanism known as “loop gain,” which refers to the magnitude of ventilatory response for a given gas exchange disturbance. Those with high loop gain are prone to respiratory instability, whereas those with low loop gain are quite resistant to periodic breathing. Loop gain is affected by many components, including the central respiratory controller, the efficiency of CO2 excretion, and the delays imposed by hemoglobin binding and the circulation. Any of these various “gains” can serve to elevate the overall loop gain and create a propensity for breathing instability. Finally, a lower functional residual capacity in infants leaves less available oxygen stores. This, accompanied by a high loop gain, predisposes infants to respiratory instability.