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A 76-year-old man presented to the emergency department with lethargy and a reduced level of awareness after a period of experiencing a very low heart rate. The patient said he did not feel faint or dizzy, nor had he experienced chest pains or heart palpitations.

On hospital admission, findings from a physical examination showed that his heart rate was 26 beats per minute; his blood pressure was 80/40 mm Hg, with a mean arterial pressure of 53 mm Hg; his body temperature was 35.6° C; and his respiratory rate was 18 breaths per minute, with 95% peripheral oxygen saturation without supplementary oxygen. Results were otherwise normal.

His medical history included psoriasis, stage 4 chronic kidney disease (creatinine clearance of 29 mL/min/1.73 m²), and essential hypertension. He was taking amlodipine 5 mg twice daily and atenolol 25 mg twice daily; he noted that he takes these regularly, as prescribed.

Notable findings from lab tests included:

• White blood cell count of 5.450 cells/μL
• Creatinine level of 3.7 mg/dL
• Serum potassium level of 7.3 mg/dL
• Thyroid-stimulating hormone level of 4.92 μUI/mL
• C-reactive protein level of 48.9 mg/dL

Chest x-ray and transthoracic echocardiography results were normal, with no evidence of systolic or diastolic dysfunction, and no notable heart valve changes (left ventricular dimension 46 mm; interventricular septum 9 mm; posterior wall 9 mm; ejection fraction 64%). An ECG performed at the time of admission revealed sinus bradycardia with junctional escape rhythm. Based on these findings, clinicians suspected that the patient may have BRASH syndrome (bradycardia, renal failure, atrioventricular blockade, shock, and hyperkalemia).

The patient was started on an IV bolus of 20 mL/kg of sodium chloride 0.9% and discontinued his previous medications. He also received four doses of IV atropine 0.5 mg, glucagon 5 mg, 20 mL of 10% calcium gluconate, hydrocortisone 100 mg, 70 mL of sodium bicarbonate, and a solution of 250 mL dextrose 20% with 10 units of regular insulin.

However, the patient's blood pressure remained very low, at <65 mm Hg, so he was started on a continuous infusion of IV epinephrine, up to a dose of 10 μg/kg/min. When the bradycardia continued to be a concern after his elevated potassium levels began to respond to treatment, the team implanted a temporary transvenous pacemaker and he was admitted to the intensive care unit (ICU) for further care.

On the patient's first day in the ICU, his potassium level returned to normal, and his creatinine level gradually returned to baseline values. Four days later, clinicians stopped the IV epinephrine. On his fifth day in the ICU, they removed the temporary pacemaker, since he was maintaining a sinus rhythm with a heart rate of 60 to 70 beats per minute.

The patient was discharged 8 days after hospital admission. Clinicians advised him to avoid beta-blockers, and referred him for an outpatient cardiology follow-up. ECG showed normal sinus rhythm; his serum creatinine level was 2.36 mg/dL, and his potassium level was 4.9 mg/dL.

Discussion

The authors reporting this rare of BRASH syndrome suggested that this patient's elevated potassium levels and the ensuing spiral of events may have been related to his treatment with the beta-blocker atenolol, 40% of which is excreted in the urine.

The group noted that while the pathophysiological process of BRASH syndrome is not well understood, it is thought to be the result of a synergistic effect between AV nodal block and hyperkalemia, resulting in severe bradycardia. This slowed heart rate in turn leads to a "reduction in cardiac output with consequent reduced renal perfusion and acute kidney injury, as well as worsening hyperkalemia," they wrote. Those who develop BRASH syndrome tend to adhere closely to use of their medications as prescribed, and thus rarely present with excessively elevated blood levels of AV nodal-blocking agents, they added.

The authors explained that the "vicious cycle" seen in BRASH syndrome patients is often initially triggered by hypovolemia or AV nodal-blocking medications. If diagnosis is not timely, the condition can progress, resulting in shock and multiple organ failure requiring transvenous pacing and hemodialysis.

To complicate diagnosis, BRASH syndrome has a wide range of presentations, from asymptomatic bradycardia to cardiac arrest, the authors noted. In this patient's case, they explained that they suspected BRASH syndrome based on the presence of the five clinical signs referred to by the acronym, combined with the absence of other potentially contributing conditions, such as sepsis or acute heart disease.

While it is well known that hyperkalemia alone can cause bradycardia, this is not usually seen unless potassium levels exceed 7 mg/dL. ECG changes associated with potassium levels of 5.5 to 6.5 mg/dL include peaked T waves, while moderate hyperkalemia is associated with a flattening of P waves and PR prolongation, noted a . It is not until potassium levels exceed 7 mg/dL that there are QRS widening and bradycardia, a progression of ECG findings often seen in hyperkalemia-induced bradycardia, but often absent in BRASH syndrome.

The case authors outlined treatment goals, which included correcting hyperkalemia; providing hemodynamic support for bradycardia and hypotension; and addressing any triggering events, such as hypovolemia or AV nodal-blocking medication.

Another suggested that initial management of BRASH syndrome requires IV treatment with insulin, glucose, and calcium for membrane stabilization. This is also the standard treatment for severe hyperkalemia. These authors noted that because the Advanced Cardiac Life Support (ACLS) algorithm for bradycardia does not include IV calcium, it does not appropriately address BRASH syndrome and may lead to unnecessary use of transvenous pacing in patients who could have responded to medical treatment.

The patient in the current case had chronic renal failure and had been taking a beta-blocker, conditions known to be associated with an increased risk of developing BRASH syndrome, the authors pointed out. In addition, elevated potassium levels have been implicated in the development of bradyarrhythmias. However, in contrast to previously reported cases of BRASH syndrome, "our patient's ECG findings showed significant bradycardia without the classic stigmata of hyperkalemia (e.g., peaked T waves, sine waves)," they wrote.

The rapid response with "hemodynamic support, correction of hyperkalemia, and beta-blocker withdrawal was essential to progressive recovery ... without need for renal replacement therapy," they added. Because his bradycardia persisted after his potassium levels were corrected and he had received epinephrine, "we decided on temporary use of a transvenous pacemaker," they explained.

BRASH syndrome is a "poorly recognized and potentially lethal clinical entity," in which AV nodal-blocking agents and hyperkalemia may play a role, the authors concluded. "Early recognition and treatment of this entity can prevent the development of multiple-organ failure and death."

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