What question did this study set out to answer?

This case aims to illustrate the challenges of diagnosing BRASH syndrome in critically ill patients with respiratory failure and other comorbidities.

May 20, 2026

B51-20 Brash Syndrome Presenting as Acute on Chronic Respiratory Failure in a Patient With COPD and Heart Failure

Key Points

This case aims to illustrate the challenges of diagnosing BRASH syndrome in critically ill patients with respiratory failure and other comorbidities.
Case report of a 73-year-old male with COPD and heart failure presenting to the ICU.
Diagnosis and management of severe dyspnea, bradycardia, hyperkalemia, and respiratory failure.
Multidisciplinary approach involving nephrology and pharmacological interventions.
Patient presented with bradycardia (HR 45 bpm), hyperkalemia (potassium 6.5 mmol/L), and acute kidney injury (creatinine 2.91 mg/dL).
Despite treatment, initial response to glucagon for beta-blocker toxicity was inadequate, but potassium and renal function improvement resolved bradycardia and shock.
The patient's clinical course included hypertensive crisis and critical illness myopathy, ultimately stabilizing on high-flow oxygen.

Abstract

Abstract BRASH Syndrome Presenting as Acute on Chronic Respiratory Failure in a Patient with COPD and Heart Failure Background Beta-blockers are essential in the treatment of heart failure and hypertension, however in the setting of renal dysfunction and electrolyte imbalance, they can trigger BRASH syndrome, a dangerous cycle of Bradycardia, Renal failure, AV-nodal blockade, Shock, and Hyperkalemia. Its presentation may mimic other common ICU conditions, making diagnosis challenging, especially when respiratory failure or sepsis are also suspected. Case Presentation We present the case of a 73-year-old man with a history of pulmonary disease not on home oxygen, heart failure with reduced ejection fraction, kidney disease, and hypertension who presented with severe dyspnea and altered mental status. On arrival, he was profoundly bradycardic with a heart rate of 45 bpm, blood pressure 112/64 mmHg, potassium 6.5 mmol/L, creatinine 2.91 mg/dL, BUN 43 mg/dL, arterial pH 7.19, pCO2 79 mmHg, pO2 60 mmHg, and bicarbonate 20 mmol/L. He was in acute kidney injury while taking both metoprolol and carvedilol. Soon after the presentation, he lapsed into respiratory failure and required intubation, vasopressor support, and aggressive potassium correction. He was admitted to the Intensive Care Unit (ICU) for respiratory failure and septic shock, and broad-spectrum antibiotics were started for suspected pneumonia. Nephrology was also consulted. Beta-blocker toxicity was also suspected, and he was treated with glucagon without significant improvement. As his potassium and renal function were treated and improved, bradycardia and shock also resolved. He was successfully extubated to BiPAP then transitioned to high-flow oxygen. Clinical course was complicated by hypertensive crisis with flash pulmonary edema, managed with antihypertensives and diuretics, as well as critical illness myopathy managed with physical therapy. He was ultimately stabilized on high-flow oxygen and was transferred to a long-term acute care facility. Discussion This case illustrates how BRASH syndrome can be hidden by other more commonly seen conditions in the ICU, such as septic shock. Treating isolated components such as beta-blocker toxicity or hyperkalemia are insufficient unless the BRASH cycle is recognized. Prompt withdrawal of AV-nodal blockers, correction of hyperkalemia, and supportive therapy must happen in conjunction with a successful outcome. Overall, this case emphasizes the importance of careful medication reconciliation and multidisciplinary management in critically ill patients, for the recognition of less commonly seen conditions such as BRASH syndrome. This abstract is funded by: self

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