(52 - Friday) Understanding the Hemodynamic Response to Blood Transfusions Utilizing High-Fidelity Realtime Telemetry after the Arterial Switch Operation
Assistant Professor, Pediatrics UT Austin Dell Childrens Austin, Texas, United States
Abstract:
Introduction: Pediatric congenital heart disease patients are at risk of organ dysfunction due to disease burden, surgical repair state, and exposure to interventions with unintended hemodynamic consequence, including packed red blood cell transfusions (pRBCTx). Our current understanding of the hemodynamic response to pRBCTx in this population is limited to retrospective reviews of binary data points, despite the high frequency of exposure. With a high-fidelity telemetry monitoring platform, we can analyze second-to-second changes in hemodynamic variables to better understand the effect of pRBCTx.
Methods: This is a single-center, retrospective review of patients with dextro-transposition of the great arteries who received a pRBCTx after the arterial switch operation (ASO) from 7/1/2020-7/1/2021. Pre- and post-pRBCTx laboratory variables were collected and analyzed using paired Wilcoxon signed-rank tests. Bedside telemetry monitor data were measured from up to 6 hours before to 6 hours after pRBCTx with “time zero” being pRBCTx initiation. Pre-pRBCTx baselines for mean arterial pressure (MAP) and heart rate (HR) were interpreted as their average values prior to time zero. A non-overlapping five-minute moving average was applied to MAP and HR time series to filter out monitor “noise”. MAP and HR were converted into percent change relative to baseline. An aggregate comparison of baseline HR and MAP 1 hour prior to pRBCTx to HR and MAP 6 hours after pRBCTx was performed with paired Wilcoxon signed-rank test.
Results: Six patients underwent ASO at median age 8.5 [IQR:5-21.75] days and weight 3.1 [IQR:2.8-3.2] kg, encompassing 10 pRBCTx. One patient had prior pulmonary artery band surgery. Median pRBCTx prescriptions were 10 [IQR:7.5-20] ml/kg, over 169 [IQR:89.5-189] minutes at median time of post-operative hour 36 [IQR:8.5-40]. There was an increase in median hemoglobin from before to after pRBCTx (10.4 [IQR:9-11] to 12 [IQR:11.6-12.3], p=0.021), but no change in pH, pCO2, PaO2, HCO3-, or lactate. Overall, pRBCTx demonstrated a 6.0% [95% CI:0.01%-12.1%] increase in MAP from baseline and 3.1% [95% CI:-8.6%-2.2%] decrease in HR from baseline (Figure). When examining specific time points, at 3 hours post-pRBCTx there was a 6.7% (standard error=1.3%) increase in MAP compared to baseline (p=0.004) that was no longer significant at six hours post-pRBCTx (6.1% (standard error=2.6%), p=0.055).
Conclusions: pRBCTx given after the ASO was associated with an increase in MAP and decrease in HR. The increase in MAP seen at hour 3 after pRBCTx was no longer seen at hour 6 in this relatively homogeneous population. To our knowledge, this is the first attempt to describe the hemodynamic response of pRBCTx in the CHD population utilizing a high-fidelity, real-time telemetry monitoring platform.