Hyperkalemia

Causes: K>5.0mM

Potassium Excess

  • Acute/Chronic kidney disease
  • Decreased ECV
  • Decreased aldosterone: type 4 RTA, adrenal insufficiency, ACEI/ARBs
  • K+ sparing diuretics

Redistribution

  • Diabetes, beta-blockers, metabolic/ respiratory acidosis
  • Insulin deficiency, beta-adrenergic blockade, metabolic or respiratory acidosis

Lab error (Pseudohyperkalemia)

  • Hemolysis
  • Prolonged tourniquet use

EKG

Hyperkalemia can present with various EKG changes which may not necessarily follow a textbook sequence. It can mimic many pathologies such as STEMI and various bundle/conduction blocks. Severe hyperkalemia (Potassium >7 mM) might even occur without notable EKG changes

  • Peaked T-waves: Narrow, pointy, and prominent T-waves. Often, this is the most visible finding on the EKG
  • Ventricular tachycardia mimic: In this case, the QRS wave widens and P-waves might disappear, making it look like ventricular tachycardia. The T-waves could be sharper than usual, and the heart rate may be slower than expected for ventricular tachycardia
  • Profound widening of QRS complex and peaked T-waves mimicking a sine wave
  • Bradycardia

Textbook EKG progression in hyperkalemia (although this is rarely the case in real life)

    Symptoms

    Many patients with hyperkalemia are asymptomatic. However, if left untreated, hyperkalemia may cause: Neuromuscular weakness, bradycardia, ventricular tachycardia/fibrillation, or sudden cardiac death.

    Severity & Risk Stratification

    Potassium level: Levels greater than 6.5-7 mM are more worrisome

    Chronicity: Chronic hyperkalemia is better tolerated than acute hyperkalemia

    EKG changes: Bradycardia, QRS widening, or junctional rhythm are particularly worrisome

    Ongoing potassium release: Conditions like tumor lysis syndrome or rhabdomyolysis increase the likelihood of deterioration

    Causes

    Critically ill patients often develop hyperkalemia due to a combination of several factors such as hypovolemia, renal dysfunction, and the use of medications like ACE inhibitors. Successful treatment may require addressing many of these problems simultaneously

    Treatment

    • IV calcium to stabilize the myocardium (3g IV calcium gluconate peripherally over 10 minutes or 1g IV calcium chloride centrally over 10 minutes)
    • IV insulin plus dextrose to shift potassium into cells (5 units IV insulin and 2 ampules of D50W, adjusted based on blood glucose level)
    • Beta-2 agonists such as albuterol (10-20 mg nebulized-->4-8 standard nebs back-to-back)
    • IV epinephrine (phenomenal for hyperkalemia-induced bradycardia, because it simultaneously treats both the hyperkalemia and the bradycardia)
    • Promote excretion: Using diuretics such as IV furosemide 60-160 mg IV or thiazide (500-1,000 mg IV chlorothiazide, or 5-10 mg metolazone) among patients able to produce urine
    • Volume expansion if hypovolemic
      • Bicarb < 22 mM use isotonic bicarbonate
      • Bicarb > 22 mM use lactated Ringers
    • GI binders: Lokelma (10 g TID for 48 hours) or patiromer (8.4 g, repeated daily as needed, less effective than Lokelma)
      • Kayexalate is no longer recommended at it has proven to be ineffective and can cause bowel necrosis
    • Discontinue any nephrotoxins, establish a state of euvolemia with adequate perfusion, and consider a renal diet with limited potassium intake
    • Dialysis: In patients with severe kidney function impairment. Hemodialysis is preferred since the rate of potassium removal is many times faster than with peritoneal dialysis