Background: Circulatory failure in neonates is often secondary to asphyxia. Ventilation (PPV) during neonatal resuscitation, improves gas exchange, enhances cerebral, pulmonary, and cardiac blood flow. Chest compressions (CC) are indicated in neonatal bradycardia (heart rate-HR<60 bpm) after 30 sec of effective PPV. The effect of CC asynchronous with the patient's own cardiac activity on perfusion to vital organs is not known.
Objective: In an ovine model of perinatal asphyxia, we compared the effect of CC during bradycardia (HR<60 but >0 bpm) and complete cardiac arrest (HR=0) on coronary, cerebral, and pulmonary hemodynamics. We hypothesized that the coronary, carotid, and pulmonary blood flows will be higher when CC is initiated during bradycardia compared to after complete cardiac and circulatory arrest.
Design/Methods: Near-term fetal lambs were asphyxiated by umbilical cord occlusion until they were a) persistently bradycardic (HR<60 bpm) or b) until complete arrest. The resuscitation was initiated with PPV, followed by CC and intravenous epinephrine (EPI) until the return of spontaneous circulation (ROSC) or until 20 min. In the bradycardia model, the resuscitation was initiated immediately after target HR <60bpm was achieved. While in the cardiac arrest model, resuscitation was initiated after 2 min of no detectable HR to ensure complete circulatory arrest.
Results: Six out of the 7 lambs with cardiac arrest and 5 out of 6 lambs with bradycardia achieved ROSC (fig 1/table 1). The time to ROSC was significantly longer with cardiac arrest (fig 1/table 1). The changes in flow during resuscitation are shown in fig 2. Compared to PPV alone, CC did not enhance coronary, carotid or cerebral flow in the bradycardia model. Blood flows achieved during CC were similar between the two models (fig 3). In the bradycardia model, we observed a loss of innate cardiac activity during CC in 5/6 lambs (fig 4). Epinephrine use was similar in both models.
Conclusions: Chest compressions increased flow to vital organs in complete circulatory arrest but time to ROSC was longer compared to bradycardia. There was no difference in hemodynamics during CC in both models. The initiation of CC during bradycardia did not enhance flow to vital organs but led to the loss of innate activity before recovery. More translational studies are needed to study the optimal cut-off (HRs of 60 vs. 30) for initiation of CC and its effect on the cerebral and cardiac injury during resuscitation in a bradycardia model of perinatal asphyxia.
