Improving neonatal cardiopulmonary resuscitation hemodynamics: are sustained inflations during compressions the answer?

C hest compressions are rarely needed in newly born infants, with an estimated occurrence of 0.08% for near-term and term deliveries; however, the consequences of a hypoperfused state on the brain and other organ systems can be devastating. 1 Newborns that require prolonged cardiac compressions with no signs of life beyond 10 minutes are at risk for exceptionally poor outcomes, with up to 83% mortality and 77% severe disability noted in survivors. 2 Although initiation of therapeutic hypothermia appears to have some advantage for cardiopulmonary resuscitation (CPR) recipients who survive the delivery room, 3 optimization of the hemodynamics of neo-natal cardiac compressions during CPR remains critical. The infrequent use of cardiac compressions for newborns in the delivery room has impeded the design and completion of rigorous investigations to determine the most effective neona-tal cardiac compression methodologies. 4 The unique physiology of the newborn with initially fluid-filled alveoli, the need to transition from fetal to newborn circulation, the open ductus arteriosus, and the frequent presence of severe asphyxia as the cause of cardiovascular collapse add dimensions that cannot be accurately tested in adult or even pediatric patients or models. Adults most frequently receive CPR for cardiac events, such as ventricular fibrillation. Immediately after cardiac arrest, the aortic oxygen and carbon dioxide concentrations are close to the pre-arrest state. 5 With initiation of CPR, the blood perfusing the coronaries has adequate oxygenation and pH. Thus, the problem in cardiac arrest is primarily the lack of blood flow rather than the content of the blood. For this reason , resuscitation algorithms for cardiac arrest focus predominantly on providing continuous, uninterrupted compressions with much less emphasis on ventilation. Adequate oxygen-ation and ventilation can continue without rescue breathing for several minutes because of chest compression-induced gas exchange and spontaneous gasping during compressions in victims of sudden cardiac arrest. 5–7 This is quite different from resuscitation after asphyxia-induced arrest. Animal models of asphyxia clearly demonstrate that a combination of chest compressions and ventilations generates better outcomes and survival than resuscitation with ventilations or compressions alone, 8,9 particularly during prolonged resuscitation. 10 During asphyxia, blood continues to flow but with ever-increasing hypoxemia, hypercarbia, and acidemia until the heart runs out of energy substrate and becomes severely bradycardic and eventually asystolic. Thus, it is not surprising that ventilation is essential to reversing asphyxial arrest. The recent work by Schmölzer et al 11 appearing in this issue of Circulation …