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lunes, 15 de febrero de 2016

BRASH syndrome

Resultado de imagen de PulmCrit (Em crit)
PulmCrit - February 15, 2016 - By Josh Farkas
Introduction
This is one of my favorite diagnoses. When first encountered, it may seem bewildering and difficult to treat. Indeed, standard ACLS algorithms may fail with these patients. However, once understood, this disorder is easily treated and patients typically improve rapidly.
Pathophysiology & definition
BRASH syndrome is defined as a combination of the following:
  • Bradycardia
  • Renal failure
  • AV node blocker: beta-blocker, verapamil, or diltiazem (2)
  • Shock
  • Hyperkalemia
This syndrome is due to a vicious cycle in the setting of medications, hyperkalemia, and renal failure (shown below). Renal failure causes hyperkalemia and may cause the accumulation of some AV node blockers (e.g. atenolol, nadolol). Hyperkalemia synergizes with AV node blockers to cause bradycardia and hypo perfusion. Hypoperfusion, in turn, causes worsening of the renal failure.
The pathophysiologic key of BRASH syndrome is the ability of hyperkalemia to synergize with AV node blockers to cause bradycardia. This has been proven using a canine model

Summary: The Bullet
  • BRASH syndrome refers to a vicious cycle which may occur when a patient taking AV node blockers develops renal failure and hyperkalemia. This leads to a spiral of worsening hyperkalemia, renal failure, and bradycardic shock.
  • BRASH syndrome can be triggered by dehydration, medication up-titration, or any cause of hypoperfusion or renal dysfunction.
  • The treatment of BRASH syndrome centers around aggressive therapy for hyperkalemia. Additionally, many patients require a catecholamine infusion to support their perfusion.