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TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: BRASH Syndrome is a phenomenon characterized by bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia. Literature on this syndrome is limited given its under-recognition. CASE PRESENTATION: A 77-year-old female with a past medical history of atrial fibrillation, coronary artery disease, diastolic heart failure, and chronic kidney disease (CKD) III presented with dyspnea. Her home medications included furosemide, metoprolol, spironolactone, warfarin, and rosuvastatin. Comprehensive metabolic panel was significant for an elevated creatinine from baseline. Cardiac BNP was elevated, chest X-ray demonstrated cardiomegaly, and physical exam was significant for jugular venous distention. Electrocardiogram (EKG) revealed atrial fibrillation with rapid ventricular response (Image 1). Diltiazem was added for rate control however the patient was ultimately electrically cardioverted. Post procedure EKG revealed a junctional rhythm (Image 2). Hypotension persisted however. The patient soon developed oliguric renal failure and hyperkalemia, prompting upgrade to the medical intensive care unit (ICU) for shock. The patient had persistent bradycardia with heart rates as low as 32 beats per minute (bpm). Hemodialysis was initiated the following morning and the patient's shock, bradycardia, and hyperkalemia resolved. DISCUSSION: Transient abnormal rhythms have been reported post cardioversion, however the persistence of bradycardia with our patient's other abnormal lab findings raised concerns for different etiologies. BRASH syndrome is an under recognized pathophysiological phenomenon. Patients with congestive heart failure and CKD are at risk when in an inpatient setting. Different triggers are noted in recent reports, including medications such as Ranolazine and Bactrim, anaphylaxis, and even COVID-19. These cases varied in clinical severity, ranging from asymptomatic bradycardia to multiorgan failure. The hallmark mechanism of BRASH syndrome is a synergistic effect of AV nodal blocking medications and hyperkalemia promoting bradycardia. This, in conjunction with renal injury, produces the cycle of objective findings that define BRASH syndrome. Acute kidney injury caused by renal hypoperfusion can exacerbate the effects of AV nodal blocking medications as well as worsen hyperkalemia. Profound hyperkalemia and AV nodal blockade will in turn synergistically promote and prolong bradycardia. Bradycardia can depress cardiac output and further worsen renal hypoperfusion, continuing this viscous cycle. CONCLUSIONS: We believe electrical cardioversion into a junctional rhythm caused BRASH syndrome in our patient. Treatment is tailored to correcting the individual abnormalities. Many of these case reports had favorable outcomes. This case suggests that BRASH syndrome can often go undiagnosed yet still successfully be managed with supportive care. REFERENCE #1: Farkas, J., Long, B., Koyfman, A., et al. BRASH SYNDROME: BRADYCARDIA, RENAL FAILURE, AV BLOCKADE, SHOCK, AND HYPERKALEMIA. The Journal of Emergency Medicine, 59(2):216-223, pp. 1–8, 2020. DOI: 10.1016/j.jemermed.2020.05.001 REFERENCE #2: Cakulev, I., Efimov, I., Waldo, A., et al. Cardioversion: Past, Present, and Future. Circulation. Oct 20;120(16):1623-32. 2009. DOI:10.1161/circulationaha.109.865535 REFERENCE #3: Flores, S., Anaphylaxis induced bradycardia, renal failure, AV-nodal blockade, shock, and hyperkalemia: A-BRASH in the emergency department, American Journal of Emergency Medicine 38(9), P1987.E1-1987.E3. 2020. DOI: 10.1016/j.ajem.2020.05.033 DISCLOSURES: No relevant relationships by John Madara, source=Web Response No relevant relationships by Nathaniel Rosal, source=Web Response No relevant relationships by Franklin Thelmo, source=Web Response No relevant relationships by Stephanie Tzarnas, source=Web Response