Sudden infant death syndrome--a defect in circulatory control?

The majority of Sudden Infant Death Syndrome (SIDS) infants die during sleep and especially during the overnight sleep period. Recent evidence from SIDS cases, which occurred while on a cardiorespiratory monitor at home, has suggested that the mechanism of death involves circulatory failure, with the development of a shock like state, associated with a progressive bradycardia in the presence of continued breathing movements. In this paper we explore the circulatory effects of sleep and in particular the down regulation of the baroreceptor reflex, associated with a reduction in vasomotor tone and a fall in central venous return, cardiac output and blood pressure. This sequence of events would be exacerbated by many of the known SIDS risk factors, namely the prone sleeping position, overheating and co-sleeping. Poor central venous return,with diminished cardic distension could induce a progressive bradycardia as occurs in adults with neuro-cardiogenic syncope. Alternatively a reduced cardiac output could result in the rapid onset of severe hypoxia through poor lung perfusion. The effects of sleep on circulatory control deserve further study in infants.