Introduction
BRASH is an acronym that stands for bradycardia, renal failure, AV (atrioventricular) node block, shock, and hyperkalemia. It describes a syndrome in which severe bradycardia and hyperkalemia occur due to the synergistic effects of AV node blockers and impairment in renal function. It is a less-known complication that is associated with high morbidity. It can result in cardiovascular collapse and multi-organ failure if left untreated.
What Is BRASH Syndrome?
Drugs like Beta blockers and calcium channel blockers are given to treat conditions like coronary artery disease, hypertension, and atrial fibrillation. These medications act on the AV node and result in a decreased heart rate. These medications are given to control the heart rate in narrow complex supraventricular tachyarrhythmias. The BRASH syndrome refers to a condition caused by the synergistic effects of AV blockers with renal impairment in patients taking AV blockers like beta blockers and calcium channel blockers.
The synergistic effects of these medications with renal failure are associated with signs such as (BRASH) bradycardia (reduced heart rate), renal failure, AV node block, shock, and hyperkalemia (high potassium level in the blood). AV node is a small structure located in the heart. It electrically connects the upper and lower chamber of the heart to coordinate beats at the top of the heart. Shock is a condition that occurs when there is a drop in the blood flow through the body. It can be due to trauma, blood loss, allergic reactions, severe burns, or other causes.
What Are the Causes of BRASH Syndrome?
The BRASH syndrome is a distinct condition caused by bradycardia due to the compounding of comorbidities like aging and the use of drugs that target cardiac output. The synergistic effect between AV nodal block and renal failure results in a vicious cycle of bradycardia and hyperkalemia. It is a common condition but remains unrecognized, and therefore it is usually misdiagnosed. It is common in elderly patients with cardiac and renal impairment.
The risk of developing BRASH syndrome increases if the patient is under multiple AV node blockers. ACE (angiotensin-converting enzyme) inhibitors and angiotensin receptor blockers (ARB) can also increase the risk of this syndrome because these medications can develop acute kidney injury and hyperkalemia.
How Does BRASH Syndrome Occur?
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The BRASH syndrome occurs as a synergist effect of hyperkalemia and medications that block the AV node. These medications and hypovolemia promote hyperkalemia or renal impairment. Untreated hyperkalemia and the synergistic effects of AV blockers cause profound bradycardia. Bradycardia decreases cardiac output and leads to hypoperfusion. Hypoperfusion results in worsening renal failure, which further exacerbates hyperkalemia. Hence, a vicious cycle continues, and it may eventually cause multi-organ failure. This cycle is more intense in patients taking beta-blockers because beta blockers are cleared by the kidneys, and renal failure causes the accumulation of beta blockers and accelerates the cycle.
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The BRASH syndrome occurs in the presence of AV node blockers and risk factors that cause renal insufficiency. This syndrome may be triggered by causes responsible for renal failure, hyperkalemia, or increased dose of AV node blockers. ACE inhibitors and ARBs are risk factors for BRASH syndrome because they promote both hyperkalemia and renal function. In some cases, bradycardia and hypertension are more prominent, with mild hyperkalemia. In some cases, severe hyperkalemia is present with moderate bradycardia and preserved hypertension.
Causes of Renal Failure:
Pre-renal
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Shock due to hypovolemia or sepsis.
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Hepatorenal syndrome (development of renal failure in patients with chronic liver disease).
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Hemolytic uremic syndrome (block in the small blood vessels of the kidneys).
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Thrombotic thrombocytopenic purpura (formation of clots in small blood vessels throughout the body).
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Abdominal compartment syndrome (increased pressure in the abdominal cavity).
Intrinsic Renal Failure
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Nephrotoxic medications.
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Acute glomerulonephritis (inflammation of the glomeruli of the kidneys).
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Acute tubulointerstitial nephritis (spaces between the kidney tubules are inflamed).
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Acute tubular necrosis (injury to the cells of the kidney tubules).
Post-renal
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Prostatic obstruction.
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Nephrolithiasis (kidney stones).
Causes of Hyperkalemia:
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Potassium supplements.
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Non-steroidal anti-inflammatory drugs.
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Potassium-sparing diuretics.
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Antibiotics.
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Cyclosporine and Tacrolimus drugs.
What Are the Signs and Symptoms of BRASH Syndrome?
The BRASH syndrome causes symptoms like bradycardia and cardiogenic shock. It presents with decreased renal perfusion due to gastrointestinal illness, dehydration, or medication changes.
What Are the Complications of BRASH Syndrome?
It causes complications like cardiogenic shock and renal failure, which requires hemodialysis. If BRASH syndrome remains untreated, hyperkalemia progresses to cause cardiac arrest.
How Is BRASH Syndrome Diagnosed?
It is challenging to diagnose BRASH syndrome because it presents symptoms that are similar to isolated hyperkalemia and AV node blocker toxicity. The BRASH syndrome usually occurs in individuals taking these medications. The BRASH syndrome can be differentiated from beta-blocker toxicity and calcium-channel blocker toxicity by fingerstick glucose, as beta-blocker toxicity causes hypoglycemia and calcium-channel blocker toxicity causes hyperglycemia.
Hyperkalemia-induced bradycardia is different from bradycardia in BRASH syndrome. Hyperkalemia-induced bradycardia occurs when the serum potassium level exceeds 7 mEq/L (milliequivalents per liter). The electrocardiogram (EKG) shows peaked T waves in the presence of 5.5 to 6.5 mEq/L of potassium and flattened P wave, and prolonged PR wave in the presence of 6.5 to 7 mEq/L of potassium. Bradycardia and QRS wave widening is seen in the electrocardiogram if the potassium level exceeds 7 mEq/L. The progression of EKG findings is seen only in hyperkalemia-induced bradycardia and is not present in BRASH syndrome.
How Is BRASH Syndrome Treated?
The BRASH syndrome presents various symptoms. The dominant symptoms are managed first. Bradycardia and hyperkalemia require immediate treatment because it results in fatal complications. The treatment approaches include the following:
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Patients with multi-organ failure are treated with various intravenous medications like diuretics, bicarbonate, and calcium.
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Calcium counteracts the cardiotoxic effects of hyperkalemia. Hypocalcemia causes an increase in the cardiotoxic effects of hyperkalemia. Intravenous Calcium chloride or Calcium gluconate is given to combat this condition. If bradycardia does not improve, calcium is re-administered.
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Patients with oliguric renal failure present with fluid retention. Diuretics help remove the fluid, thereby reducing the potassium level and re-establishing euvolemia.
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Hypovolemia is managed with fluid resuscitation.
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Kaliuresis is performed to increase the excretion of potassium. It involves volume resuscitation, re-establishment of renal perfusion, and diuretic administration.
Conclusion
The BRASH syndrome occurs as a result of a synergistic effect of AV node blocker and hyperkalemia. It is often unrecognized and misdiagnosed. Proper diagnosis and timely intervention help in managing the condition and also prevent the worsening of the disease and the risk of complications.
