Neurocardiogenic syncope: a model for SIDS

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Abstract
A 5½ month old male infant who had suffered three acute life threatening episodes was admitted for overnight sleep studies but was found dead after their completion while still in hospital. A necropsy classified the cause of death as sudden infant death syndrome (SIDS). The sleep studies had shown no periods of apnoea (> 20 seconds) or bradycardia (< 90 beats/min), and a rapid response to nasal occlusion (5 seconds). However, autonomic function during sleep was poor, with reduced heart rate variability (6 beats/minv control 24 beats/min, SD 6.2) and postural hypotension (a 12–14% fall in resting systolic blood pressure) associated with a fall in heart rate when tilted to a vertical position. Postural hypotension with bradycardia occurs in adults with unexplained syncopal episodes and is called a neurocardiac reflex. It involves poor vasomotor tone with peripheral pooling of blood, a consequent reduction in central venous return and cardiac distension, and in some individuals a neurally mediated bradycardia, as seen in this infant, rather than the expected tachycardia. A progressive bradycardia is the predominant mechanism of death seen in SIDS infants dying on cardiorespiratory monitors at home. This case suggests that a neurocardiac reflex occurs in infants, may have been involved in this infant’s death, and deserves further study in the context of SIDS.