Document Type

Conference Proceeding

Publication Date


Publication Title

J Gen Intern Med


CASE: A 58-year-old African American male with a past medical history of chronic diastolic heart failure, chronic kidney disease stage IV, and poorly controlled hypertension who presented following persistent bradycardia, and hypotensive readings at home. His antihypertensive regimen prior to arrival included Lisinopril, Nifedipine, Hydralazine, Isosorbid Mononitrate, and Carvedilol daily. On arrival, he was hemodynamically labile with a systolic blood pressure in the 90's, heart rate in the low 50's, and hypothermic to 33.8 degree Celsius. Initial lab work showed a creatinine of 3.56 (baseline of 2.80) and potassium of 6.4. A rapid EKG demonstrated sinus bradycardia, and CXR consistent with pulmonary edema. He was transferred to the MICU after initial management with calcium gluconate, Insulin, D50, Lokelma, and warming measures with a bear hugger. On arrival to the MICU, he required 4L via nasal cannula due to pulmonary edema and was aggressively diuresed with resolution of potassium disturbance. However, he was found to rebound and became increasingly hypertensive to 200s systolic without evidence of end organ damage. His blood pressure was medically managed on the floors and within 24 hours his kidney function neared baseline. He was discharged on a new regimen of antihypertensives, specifically with discontinuation of his beta blocker. IMPACT/DISCUSSION: The combination of bradycardia, renal failure, av nodal blockade, shock, and hyperkalemia creates a condition known as BRASH syndrome. Unfortunately, this is a cycle where one complication begets another in patients who take av nodal blocking agents and anti-hypertensives that cause hyperkalemia. There are different thoughts on whether it is renal failure or the combination of beta blockers and hyperkalemia that stimulates the cascade. Nonetheless, these components are interrelated and the cycle will continue if it's not identified and treated immediately, ultimately leading to multiorgan failure. What is unique to this case is the rare complication of hypertensive urgency as a result of sympathetic overdrive in response bradycardia causing reduced cardiac output. Furthermore, what is controversial is whether or not to restart medications that demonstrate improved mortality in patients with heart failure, yet may be the cause of this disease process. CONCLUSION: BRASH syndrome is unique because it's a continuum of a single disease, and therapy includes correction of hyperkalemia, fluid management, and vasopressor support when required. There is not enough data that shows if re-introducing these medications following resolution of BRASH syndrome is necessary and whether recurrence rates are significant in those who are restarted on these medications. Additionally, a rare complication that physicians should be aware of is the sympathetic drive that can lead to hypertensive urgency as a result of bradycardia causing reduced cardiac cardiac output.




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