Bradycardia, Renal Failure, Atrioventricular Node Blockers, Shock, and Hyperkalemia Syndrome: A Tale of Hyperkalemia Bradyarrhythmia and Block

Ravi Ranjan¹ https://orcid.org/0000-0003-2736-179X, Nikesh K Roshan² https://orcid.org/0000-0002-4187-1529, Priya³ https://orcid.org/0009-0009-3298-3228, Sneha Verma⁴ https://orcid.org/0009-0002-9549-106X

^1,2,4Department of Critical Care Medicine, Big Apollo Spectra Hospital, Patna, Bihar, India

³Department of Pathology, Patna Medical College and Hospital, Patna, Bihar, India

Corresponding Author: Ravi Ranjan, Department of Critical Care Medicine, Big Apollo Spectra Hospital, Patna, Bihar, India, Phone: +91 7985391158, e-mail: rranjan819@gmail.com

Received: 10 December 2024; Accepted: 24 January 2025; Published on: 25 February 2025

ABSTRACT

Aim and background: Bradycardia, renal failure, atrioventricular node blockers, shock, and hyperkalemia (BRASH) syndrome, a pentad of bradycardia, renal failure, atrioventricular (AV) block, shock, and hyperkalemia, was first coined in 2016 by Dr Josh Farkas. It represents a complex interplay between AV nodal block and hyperkalemia, leading to severe bradycardia and shock, often affecting older patients with limited renal reserve. However, it is still underrecognized, as even though there is a history of AV nodal blocker intake, it is not given the same importance as hyperkalemia due to its less ”fear factor.”

Case description: We present the management of one such case: a 70-year-old female on amlodipine and atenolol. Her initial potassium level was 5.8 mEq/L and she was in a state of cardiogenic shock.

Conclusion: With early intervention, the bradyarrhythmia in BRASH syndrome is reversible. The aim of this case report is to raise awareness of BRASH syndrome, as timely intervention will improve patient outcomes, and the offending agent can be withdrawn.

Keywords: Atrioventricular block, BRASH syndrome, Case report, Hyperkalemia, Renal injury

How to cite this article: Ranjan R, Roshan NK, Priya, et al. Bradycardia, Renal Failure, Atrioventricular Node Blockers, Shock, and Hyperkalemia Syndrome: A Tale of Hyperkalemia Bradyarrhythmia and Block. Indian J Crit Care Case Rep 2025;4(2):47–49.

Source of support: Nil

Conflict of interest: None

Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.

INTRODUCTION

Severe hyperkalemia affects cardiac myocytes by suppressing impulse generation and reducing the conduction of generated impulses, causing bradycardia and conduction blocks that can lead to cardiac arrest. Such a life-threatening condition can be seen even in mildly elevated potassium when amalgamated with certain medications such as atrioventricular (AV) node blockers in the presence of certain trigger events. This condition is termed as bradycardia, renal failure, atrioventricular node blockers, shock, and hyperkalemia (BRASH) syndrome. It is still an underrecognized clinical entity, as even though there is a history of intake of AV nodal blockers and trigger events such as poor oral intake, they don’t carry the same impact as raised potassium or bradycardia due to its less ”fear factor.” We present the management of one case where the initial potassium level was 5.8 mEq/L.

CASE DESCRIPTION

A 70-year-old female presented with the complaint of difficulty in breathing for 6 hours, altered sensorium for 1 day, and abdominal pain for 3 days. She was known to be hypertensive on amlodipine 10 mg and atenolol 50 mg. The patient was normal when, three days before her admission, she complained of diffuse, nonradiating abdominal pain. Her oral intake decreased, leading to decreased urine output. One day before her arrival, her sensorium was also reduced. There was a history of the passage of stool. There was a negative history of associated fever, rigors, chest pain, generalized body swelling, or other underlying disease.

Hemodynamic variables at the time of admission were a pulse rate of 42 beats per minute, mean blood pressure of 55 mm Hg, respiratory rate of 29/minute, and Glasgow Coma Scale (GCS) was 8/15. Significant lab results were potassium of 5.8 mEq/L and creatinine of 2 mg/dL. Her random blood sugar level, complete blood count panel, and endocrine panel were normal. Blood and urine ketones were negative. In the ECG, there were variable P waves with wide, bizarre QRS complexes (Fig. 1). Cardiac enzymes were also not raised. Bedside echocardiography didn’t show any apparent regional wall motion abnormality; the ejection fraction was 45%. Lung ultrasound showed bilateral and diffuse B lines with effusion.

Fig. 1: ECG

The patient’s son initially denied consent for intensive care unit (ICU) care and intubation, as he believed that she had a similar episode 3 years back and she responded with management in the emergency department. So, in the emergency department, her resuscitation was started along with antihyperkalemic measures. One hour later, the patient was intubated and shifted to the ICU postconsent from the patient’s son.

Given cardiogenic shock due to conduction block, she was given atropine, but her heart rate did not improve, so she was started on an adrenaline infusion. For hyperkalemia, she was medically managed with 10% calcium gluconate, infusion of regular insulin dextrose, sodium bicarbonate, and nebulization with salbutamol. Approximately, 1 hour post these measures, potassium levels decreased to 4.9 mEq/L, and the rhythm also converted to sinus. Her hemodynamic parameters, GCS, and urine output improved, and she was extubated on day 2 of hospitalization. To prevent further recurrence, the offending drugs were removed, and the patient’s family was educated about the trigger events and warning signs. She was discharged on day 5 of hospitalization.

DISCUSSION

BRASH syndrome is a pathological state due to the synergistic effect of AV nodal blockers, hyperkalemia, and renal failure, ending in bradycardia and shock. Elderly patients on AV-nodal blocking medications are at an increased risk of developing BRASH syndrome. AV nodal-blocking medications, hyperkalemia, and decreased renal perfusion cultivate a collegial atmosphere for refractory bradycardia and shock.

Diagnosis is tangled, as symptoms are vague, and our differential diagnoses spectrum ranged from subacute intestinal obstruction, sepsis, prerenal acute kidney injury (AKI), endocrinal emergencies, cardiogenic shock, and even acute coronary syndrome. Computerized tomography of the abdomen ruled out obstruction, perforation, or pancreatitis. Infectious etiology was ruled out from history, physical examination, and normal blood and urine workup. The cause of AKI was poor oral intake leading to decreased renal perfusion. Electrocardiogram (ECG) without any ischemic changes, normal cardiac enzyme levels, and echocardiography ruled out a myocardial ischemic event.

AV nodal blocker toxicity was another differential; however, the patient’s son’s assertion regarding medication compliance ruled out this scenario. So, either it was raised potassium or its collaboration with AV nodal blockers (BRASH syndrome) that was likely to be the cause. Persistence of shock despite potassium coming down to normal values directed the spotlight towards BRASH syndrome. The likely trigger event was poor oral intake that led to decreased renal perfusion, causing kidney injury and subsequently resulting in decreased clearance of antihypertensive medications, thereby potentiating their effect on myocytes, leading to cardiogenic shock (Fig. 2).

Fig. 2: Pathophysiology of BARSH syndrome

The treatment of BRASH syndrome concentrates on the removal of the offending drug, treatment of the trigger events, and hemodynamic stabilization through correcting hyperkalemia and fluid resuscitation. Hyperkalemia can be managed medically by membrane stabilizers, moving potassium intracellularly, or through hemodialysis. Epinephrine is a sound option for BRASH patients with refractory bradycardia and shock, as its low dose recruits the beta-adrenergic receptors, leading to (1) increased chronotropy and inotropy through beta-1 and (2) intracellular potassium shift by effect on the beta-2 receptor. Fluid resuscitation needs to be individualized.¹ Fortunately, the patient recovered without the need for more aggressive therapies such as hemodialysis, lipid emulsions, glucagon, and cardiac pacing.¹

CONCLUSION

BRASH syndrome is a vicious interaction between AV nodal blocking agents, renal injury, and hyperkalemia, terminating in bradycardia and shock. Patient education and judicious use of beta and calcium channel blockers, especially in elderly patients, should be done. Once identified, the management of BRASH syndrome focuses on hemodynamic support involving a multidisciplinary approach in a critical care setting.

ORCID

Ravi Ranjan https://orcid.org/0000-0003-2736-179X

Nikesh K Roshan https://orcid.org/0000-0002-4187-1529

Priya https://orcid.org/0009-0009-3298-3228

Sneha Verma https://orcid.org/0009-0002-9549-106X

REFERENCES

1. Farkas J. BRASH syndrome: Bradycardia, renal failure, AV blocker, shock, hyperkalemia. Pulmcrit (Emcrit); 2016.

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