Hypotension following the return of spontaneous circulation (ROSC) occurs frequently and correlates with poorer patient outcomes, yet the immediate circulatory reaction to prehospital adrenaline administration remains inadequately characterized. This study investigated minute-by-minute blood pressure pathways surrounding the recorded commencement of adrenaline infusions in patients with out-of-hospital cardiac arrest (OHCA) who attained stable ROSC and retained a palpable pulse upon emergency department arrival. We conducted a retrospective linked cohort investigation utilizing data from adult patients treated by emergency medical services for out-of-hospital cardiac arrest in Victoria, Australia, between 2019 and 2023. Eligible cases achieved stable ROSC, possessed linked ZOLL® monitor-defibrillator records, and presented with a pulse at hospital handover. The study sample was limited to individuals initiated on a prehospital adrenaline infusion within 60 min of achieving ROSC. Segmented mixed-effects models, controlled for initial pre-infusion values and pre-infusion trajectories, were applied to assess minute-level trends in mean arterial pressure (MAP) and systolic blood pressure (SBP) from 10 min before 20 min following infusion initiation. Among 3655 eligible adult ROSC cases with complete monitor integration and a pulse at hospital presentation, 1920 individuals received a prehospital adrenaline infusion within 60 min post-ROSC. Blood pressure values typically decreased during the 10 min preceding the infusion, reaching their lowest point concurrently with or immediately after infusion onset, then increased over the subsequent 20 min. In primary adjusted models, MAP decreased by 1.64 mmHg/min pre-infusion and increased by 1.15 mmHg/min post-infusion, representing a trajectory reversal of 2.79 mmHg/min (95% CI = 2.48–3.09). SBP decreased by 2.25 mmHg/min before infusion and increased by 1.71 mmHg/min afterward, demonstrating a trajectory change of 3.96 mmHg/min (95% CI = 3.55–4.38). These adjustments indicated a pronounced inversion in blood pressure trends at the onset of infusion. Descriptively, mean MAP rose from 81.2 mmHg at 5 min post-infusion to 95.4 mmHg at 20 min, whereas mean SBP climbed from 107.9 to 128.4 mmHg over the same period. The recorded initiation of an adrenaline infusion coincided with the termination of a declining blood pressure trend. It prompted a steady elevation in both MAP and SBP across the subsequent 20 min. These observations help characterize the arterial pressure responsiveness to adrenaline during prehospital post-ROSC care and provide data to inform future investigations regarding vasopressor timing, hemodynamic targets, and clinical trial methodologies.
