Prematurity is an important risk factor for life-threatening apnea in infants undergoing general anesthesia. The risk of postanesthetic respiratory depression is inversely related to gestational age and postconceptual age (PCA) at the time of anesthesia. It has been stated that infants may be at risk up to 60 weeks after conception.
NEONATAL GAS EXCHANGE AND BREATHING
The reduced PaO2 of neonates is compensated by a greater oxygen-carrying capacity due to increased hemoglobin concentrations, which decline during the first several weeks of life.
At birth, the hemoglobin content of the blood is made up of 50% fetal hemoglobin, which has an in vivo oxygen–dissociation curve that is shifted to the left in comparison with normal adult hemoglobin. The shift in position of the oxygen–dissociation curve depends on the ratio of adult to fetal hemoglobin. It shifts to the right during the course of the first week of life, reflecting a switch from fetal to adult hemoglobin formation. Normal PaCO2 and pH are somewhat lower in the neonatal period than in later infancy.
In neonates, the primary variables which control pulmonary ventilation are the PaO2, PaCO2, and pH. The PaO2 acts mainly through peripheral chemoreceptors in the carotid and aortic bodies while the PaCO2 and pH act on central chemoreceptors in the medulla. Unlike an adult, an infant’s response to hypercapnia is not potentiated by hypoxia. In fact, hypoxia may depress the hypercapnic ventilatory response in term and preterm infants. High concentrations of oxygen depress the neonate’s respirations, whereas low concentrations stimulate it. The hypoxic response is not sustained. However, sustained hypoxia leads first to a return to baseline ventilation and then to ventilatory depression. This pattern of response persists in normal term infants for the first week of life, after which the response to sustained hypoxia is replaced by a sustained increase in ventilation. This pattern also persists longer in preterm infants.
Apnea is defined as cessation of breathing with implicit pathophysiology. Most alarms on infant breathing monitors are set to alert after detecting a respiratory pause greater than 20 seconds. In a preterm infant, this time period is the equivalent of 17 missed breaths. Apnea is likely to be better defined by associated consequence than by pause duration alone in this age group; however, the degree of change in heart rate or oxygen saturation that defines a respiratory pause as pathological is yet to be defined.
Normal periodic breathing in a neonate occurs when breathing ceases for roughly 5–10 seconds and respiratory effort and air movement is absent, but desaturation and bradycardia does not occur. In contrast, there are three types of neonatal apnea:
Apnea of central origin results from immaturity or depression of the respiratory drive. It may be caused by the ...