Several reflexes are initiated in the fetus and newborn when hypochloremic or strongly acidic solutions contact the epithelium that surrounds the entrance to the laryngeal airway. These reflexes, known collectively as the laryngeal chemoreflex (LCR), include startle, rapid swallowing, apnea, laryngeal constriction, hypertension, and bradycardia. Many studies have shown that prolonged apnea associated with the LCR may be life threatening and might conceivably be a cause of sudden infant death syndrome. This certainly may be true, but the concept of a lethal LCR paradoxically contrasts with the view that these several reflexes have an important airway-protective role.

As the infant matures, rapid swallowing and apnea become much less pronounced, whereas cough and possibly laryngeal constriction become more prominent. This transformation is primarily related to central neural processing rather than to changes in the airway mucosal “water receptors” that initiate the reflex. The LCR develops in the fetus, in an all-aqueous environment, during a period in which aspiration of amniotic fluid poses a serious threat to life. This and other considerations suggest that the transformation in LCR responses from fetal to adult life can be viewed as functionally appropriate to their primary role in defending the airway from aspiration. The laryngeal “water receptors” that initiate the LCR in infants and adults alike appear to be the primary sensory mechanism for defending the airway from aspiration of liquids.