474 - Hemorrhagic, hypovolemic neonatal cardiac arrest and response to epinephrine
Saturday, April 23, 2022
3:30 PM – 6:00 PM US MT
Poster Number: 474 Publication Number: 474.230
Rebecca Valdez, University of California, Davis, School of Medicine, Brentwood, CA, United States; Amy Lesneski, University of California, Davis, School of Medicine, Davis, CA, United States; Evan Giusto, University of California Davis Children's Hospital, Sacramento, CA, United States; Houssam M. Joudi, University of California, Torrance, CA, United States; Morgan Hardie, University of California, Davis, School of Medicine, Davis, CA, United States; Victoria Hammitt, University of California, Davis, School of Medicine, Sacramento, CA, United States; Kirstie Shulman, UC Davis, Dixon, CA, United States; Emily Lane, University of California Davis Children's Hospital, Sacramento, CA, United States; Lida I. Zeinali, University of California, Davis, School of Medicine, Sacramento, CA, United States; Payam Vali, University of California Davis Children's Hospital, Sacramento, CA, United States; Satyan Lakshminrusimha, University of California Davis Children's Hospital, Sacramento, CA, United States; Deepika Sankaran, University of California Davis Children's Hospital, Sacramento, CA, United States
Trainee University of California, Davis Davis, California, United States
Background: Hypovolemia is a common cause of lack of response to epinephrine. The severity of hypovolemia associated with impaired response to epinephrine during neonatal resuscitation is not known.
Objective: To compare the hemodynamics during euvolemic and hypovolemic (moderate and severe) cardiac arrest in the fetal lamb, time to return of spontaneous circulation (ROSC) and response to epinephrine.
Design/Methods: Asphyxial arrest was induced in 4 fetal lambs by cord occlusion. Exsanguination (blood draw of 30-mL/kg in 4 lambs, and 45-mL/kg in 5 lambs) was followed by cord occlusion in fetal lambs to induce moderate and severe hypovolemia respectively with cardiac arrest. Following 5 minutes of asystole, term lambs were resuscitated per neonatal resuscitation program guidelines and intravenous epinephrine was administered every 3 minutes until ROSC for a maximum of 4 doses. Hemodynamics and blood gases were monitored.
Results: The carotid arterial blood flow decreased significantly during exsanguination in both 30-ml/kg and 45-ml/kg groups prior to cord occlusion and was very low after cord occlusion when compared lambs in asphyxial arrest by cord occlusion alone (Figure 1, p< 0.01). All lambs achieved ROSC (Table 1). Median (IQR) time to ROSC after epinephrine dose was delayed with 45-mL/kg exsanguination (75 (70-80) sec – often due to need for volume resuscitation) compared to cord occlusion only (48 (34-64) sec) and 30-mL/kg exsanguination (30 (26-37) sec, p= 0.03). Figure 2 shows changes in heart rate and mean blood pressures during exsanguination, cardiac arrest and after ROSC in the 3 groups. Mean left carotid arterial blood flows and mean blood pressures were lower with 45-mL/kg group after ROSC (Figures 1 and 2).Conclusion(s): Response to epinephrine is delayed in severe hypovolemic asphyxial arrest, but not in moderate hypovolemia. Post-ROSC hemodynamics are significantly compromised in severe hypovolemic arrest. Response to epinephrine does not rule out significant hypovolemia and careful attention to hemodynamic status is important in the post-ROSC period. Rebecca Valdez CVRebecca Valdez CV 1-6-22.pdf Figure 2: Comparison of heart rate and mean blood pressures during exsanguination, cardiac arrest and after return of spontaneous circulation in the study groups.Data presented as mean (standard error of mean. * p < 0.05 by ANOVA repeated measures. CPR: cardiopulmonary resuscitation. ROSC: return of spontaneous circulation.