Poster 1022: Beyond Traditional CPR: eCPR as a Rescue Strategy in Refractory Shock with Systemic Lupus Erythematosus & Antiphospholipid Syndrome

Background: A 33-year-old female with ESRD, SLE, and APS presented with a thrombosed AV fistula and hyperkalemia. Post-declotting, she suffered cardiovascular collapse due to acute hyperkalemia and pulmonary emboli. Despite prolonged CPR, definitive ROSC was only achieved after 40 minutes using VA-ECMO, highlighting eCPR as a rescue strategy in refractory shock.

Methods: The patient underwent a declotting procedure with tissue plasminogen activator for a thrombosed AV fistula. Following the procedure, she experienced sudden cardiovascular collapse due to hyperkalemia (7.6 mEq/L), telemetry showed bradycardia progressing to sine wave and pulseless electrical activity. Despite aggressive resuscitation, and achieving transient ROSC multiple times, definitive ROSC was only attained with eCPR after initiating VA-ECMO. CT angiography post-ROSC revealed multiple pulmonary emboli, likely due to systemic embolization from thrombolysis. Echocardiogram showed McConnell's Sign, consistent with acute PE and RV strain and dysfunction. The combination of APS, SLE, and endothelial injury likely triggered immunothrombosis, exacerbating pulmonary vascular resistance and systemic inflammation. Residual electrolyte imbalances and intravascular volume shifts post-dialysis further sensitized the patient to procedural insults. ECMO provided immediate circulatory support, enabling aggressive potassium correction with CRRT. The patient was transitioned to VAV-ECMO as left ventricular function improved, allowing the heart to function within physiological parameters. With further improvement in pulmonary pressures and stabilization of LV function, the patient was transitioned to VV ECMO for ongoing respiratory support. ECMO allowed myocardial rest, reduced oxygen demand, and facilitated recovery. ECMO integration with CRRT provided hemodynamic stabilization and organ perfusion, addressing refractory cardiogenic and obstructive shock.

Outcome: The patient was successfully weaned off ECMO by day 12 and extubated shortly thereafter. Neurological assessment revealed complete cognitive and motor recovery, a remarkable outcome given the prolonged CPR duration. ECMO played a critical role in stabilizing hemodynamics, correcting hyperkalemia, and supporting organ perfusion during prolonged resuscitation. The transition from VA-ECMO to VAV-ECMO and later to VV-ECMO allowed gradual cardiac and pulmonary recovery. CT angiography confirmed multiple pulmonary emboli, likely resulting from systemic embolization during thrombolysis. The combination of APS, SLE, and endothelial injury likely contributed to immunothrombosis, further complicating the clinical picture. ECMO, by reducing myocardial workload and oxygen demand, created an environment conducive to cardiac recovery. The integration of ECMO with CRRT addressed refractory hyperkalemia and provided a viable rescue strategy in this complex case. Preventive strategies, such as pre-procedural optimization of electrolyte levels, especially in this vulnerable population where a potassium level of < 4 might be appropriate prior to interventions involving thrombolysis, and vigilant intraoperative monitoring are essential to mitigate hyperkalemia-induced cardiac events. This case underscores the value of eCPR and ECMO in managing refractory shock, particularly in patients with complex comorbidities like SLE and APS.

Conclusion: eCPR, particularly VA-ECMO, proved pivotal in achieving definitive ROSC and hemodynamic stabilization in refractory shock. ECMO reduced myocardial workload, facilitated cardiac recovery, and enabled aggressive potassium correction. This case highlights ECMO’s role in prolonged resuscitation and underscores the importance of preventive strategies in high-risk populations.