Cardiac Asystole at Birth Re-Visited: Effects of Acute Hypovolemic Shock

Abstract

Births involving shoulder dystocia or tight nuchal cords can deteriorate rapidly. The fetus may have had a reassuring tracing just before birth yet may be born without any heartbeat (asystole). Since the publication of our first article on cardiac asystole with two cases, five similar cases have been published. We suggest that these infants shift blood to the placenta due to the tight squeeze of the birth canal during the second stage which compresses the cord. The squeeze transfers blood to the placenta via the firm-walled arteries but prevents blood returning to the infant via the soft-walled umbilical vein. These infants may then be born severely hypovolemic resulting in asystole secondary to the loss of blood. Immediate cord clamping (ICC) prevents the newborn’s access to this blood after birth. Even if the infant is resuscitated, loss of this large amount of blood volume may initiate an inflammatory response that can enhance neuropathologic processes including seizures, hypoxic–ischemic encephalopathy (HIE), and death. We present the role of the autonomic nervous system in the development of asystole and suggest an alternative algorithm to address the need to provide these infants intact cord resuscitation. Leaving the cord intact (allowing for return of the umbilical cord circulation) for several minutes after birth may allow most of the sequestered blood to return to the infant. Umbilical cord milking may return enough of the blood volume to restart the heart but there are likely reparative functions that are carried out by the placenta during the continued neonatal–placental circulation allowed by an intact cord.