A56-14 Vasopressin Use and Outcomes in Post-cardiac Arrest Syndrome: A Prospective Observational Study

Rationale Post-cardiac arrest syndrome (PCAS) is a complex phenomenon that occurs after resuscitation following cardiac arrest. PCAS encompasses post-cardiac arrest brain injury, myocardial dysfunction, and systemic inflammatory response due to reperfusion injury. [1]. Shock develops in the immediate and early phases and is typically managed with vasopressors. While vasopressin has been studied in cardiac arrest resuscitation [2], evidence on its role as a continuous infusion adjunct in PCAS remains limited. This study aimed to evaluate the impact of vasopressin on clinical outcomes, including mortality, length of stay (LOS), and end-organ dysfunction, in patients with PCAS. Methods This multicenter prospective observational cohort study enrolled adults (>18 years) with PCAS. Demographics, comorbidities, arrest details, and baseline variables (pH, lactate, sequential organ failure assessment (SOFA) score, vasopressor requirements) were recorded. Vasopressin timing was documented, (immediate <20 min, early <12 h, intermediate 12-72 h) and response (mean arterial pressure increase >10 mmHg or vasopressor reduction). Serial measures (SOFA, lactate at 0, 24, 48, 72 h) and outcomes (hospital LOS, vasopressor/mechanical ventilation/renal replacement therapy duration, neurological outcome, mortality) were collected. Statistical analyses included descriptive statistics, univariate comparisons, and multivariable logistic regression adjusting for age, SOFA, lactate, and arrest duration. Results Of 59 patients, 14 (24%) received vasopressin. The vasopressin group had higher baseline severity: SOFA 11.4 (±2.8) vs 7.6 (±3.5) (p = 0.0004), lactate 10.0 (±5.1) vs 5.2 (±3.7) mmol/L (p = 0.0009), arrest duration 23.6 (±18.2) vs 14.8 (±14.5) min (p = 0.09). Crude mortality was higher (86% vs 51%, p = 0.03), with shorter LOS (7.0±9.4 vs 8.7±6.5 days, p = 0.09) and longer vasopressor time (30.7±28.2 vs 18.1±36.4 h, p = 0.006). In multivariable logistic regression, vasopressin was not independently associated with mortality (OR 1.54, p = 0.47). Mixed models showed persistently higher SOFA (p < 0.001) and lactate (p < 0.001) in patients receiving vasopressin. Among patients who received vasopressin, responders (n = 6) had shorter arrest duration (12.0±6.4 vs 30.3±19.8 min, p = 0.01) but similar outcomes. Conclusions In this dataset from a prospective PCAS cohort, patients who received vasopressin had greater baseline illness severity and higher crude mortality. No benefits in organ dysfunction trajectories or other outcomes were observed. Among patients receiving vasopressin, responders had shorter arrest duration, but similar outcomes. These unpublished findings suggest vasopressin may allow for vasopressor dose reduction and improvement in MAP in patients with short arrest time; however, it may not improve PCAS prognosis. Patients continue to be recruited to this study, which remains underpowered, and there is a need for randomized trials to clarify its role. This abstract is funded by: None