significant potassium content, and potassium salt infusions Given improvements in blood bank procedure, hyperkalemia is less common with transfusion of red cells Endogenous sources of potassium may result from tissue damage, including burns, trauma, rhabdomyolysis, hemolysis, tumor lysis, and gastrointestinal bleeding with enteral reabsorption Clinical scenarios associated with extracellular shift include metabolic acidosis, hyperosmolarity, insulin deficiency, and the use of β-adrenergic receptor antagonists Reduced renal excretion of potassium may occur in acute or chronic renal insufficiency, hypovolemia, mineralocorticoid deficiency, inherited or acquired renal tubulopathy, and due to the use of certain medications ( Table 100.8 ) Evaluation begins with a thorough history with specific inquiries regarding injuries, muscle pain, history of renal disease, and medications taken Serum potassium should be repeated to rule out pseudohyperkalemia, which results from a hemolyzed specimen due to difficulties in obtaining the specimen Serum sodium, chloride, calcium, phosphorus, bicarbonate levels, and measures of renal function should also be obtained Serum creatinine kinase (CK) should be submitted if there is suspicion for rhabdomyolysis A complete blood count (CBC) should be obtained if there is possibility of hemolysis Urine electrolytes and osmolality should be obtained An ECG should be obtained to monitor for cardiac effect Clinical manifestations The clinical features associated with hyperkalemia are a consequence of altered cellular transmembrane potassium gradient, which reduces the resting membrane potential Initially this increases membrane excitability, which is followed by a sustained reduction in excitability Unless the rise is rapid, symptoms or signs generally not become apparent until the serum potassium concentration exceeds mEq/L Clinical features predominantly involve cardiac conduction and neuromuscular disturbance Cardiac dysrhythmias are the most serious consequence, and toxicity is exacerbated by a rapid rise in potassium concentration, acidosis, hyponatremia, and hypocalcemia Early ECG changes include narrow, peaked T waves with shortened QT interval, which is followed by progressive lengthening of the PR interval and widening of the QRS complex There may be loss of P-wave amplitude and eventual “sine wave” pattern when the QRS merges with the T wave This is typically followed by ventricular fibrillation or standstill Neuromuscular