Background: 69 Yo female was activated for a rapid response for a sustained HR in the 40’s. EKG shows non specific T wave changes. Potassium 5.8. Pt a has decreased urine output the last few hours with signs of shock. Lactate is elevated and her POCUS revealed collapsible IVC, normodynamic heart, absent Blines.
History shows chronic atrial fibrillation on calcium channel blocker with recent hospitalization for UTI.
Pathophysiology, Key points to remember.
BRASH syndrome is: Bradycardia, Renal Failure, AV nodal blockade, Shock, and Hyperkalemia.
There us a higher prevalence in elderly individuals with both underlying cardiac and renal impairment. The risk of developing this complication increases further when the patient is on multiple AV nodal blockers and ACE (angiotensin-converting enzyme) inhibitors. Angiotensin receptor blockers also increase the risk as these medications increase the likelihood of developing an acute kidney injury as well as hyperkalemia.
Synergistic effect of AV nodal blockade and hyperkalemia resulting in severe bradycardia. The resulting reduction in cardiac output, in turn, leads to poor renal perfusion, therefore, worsening the acute kidney injury as well as the degree of hyperkalemia. It is well documented that severe hyperkalemia alone can cause bradycardia. However, due to this synergistic effect, profound bradycardia can occur even in the setting of mild hyperkalemia. Renally cleared AV nodal blockers, such as metoprolol and amlodipine, impose a greater risk as the renal tubules’ concentrations inversely increase as the GFR decreases.
***In isolated hyperkalemia, as the serum potassium levels elevate, the T waves begin to peak with PR interval prolongation followed by QRS widening and subsequent bradycardia; however, these morphologies are commonly absent in BRASH syndrome patients.
Treatment
Correct underlying shock.
Hypocalcemia increases the cardiotoxic effects of hyperkalemia; therefore, prompt intravenous administration of either calcium chloride or calcium gluconate is warranted.
If calcium fails to improve the bradycardia within five minutes, it can be re administered. If bradycardia persists, epinephrine can be used, which will increase the heart rate and increase the systemic vascular resistance and shift potassium back into the cells. This can be accomplished with a push dose pressor of 10 to 20 mcg.
Kaliuresis.
***Atropine may not work as this bradycardia is not vagally-mediated.
Names, dates, and personal identifying details have been changed throughout this website to comply with the Health Insurance Portability and Accountability Act (HIPAA). **
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