Hypokalemia

Background

• Potassium (K⁺) < 3.5 mEq/L
• 98% of total body K⁺ is intracellular (majority in muscle cells)
• Goal: prevent life threatening complication (e.g. arrhythmia), replace deficit, elucidate cause
• Insulin and catecholamines (Beta adrenoreceptors) are key drivers of transcellular shifts
• H+ and K⁺ will trade places to maintain electroneutrality

Presentation

• Malaise, weakness, myalgias, decreased gastrointestinal motility
• EKG changes:
  • Mild: ST segment depression, decreased T wave amplitude
  • Severe: U-waves (most commonly seen in precordial leads V2 and V3)
• Severe hypokalemia can lead to rhabdomyolysis

Evaluation

• History: Consider decreased K⁺ intake, increased entry into cells (ex: Increased cell production, elevated beta-adrenergic activity, hypothermia), GI losses, urinary losses (diuretics, hypomagnesemia, RTA, tubular defects, hyperaldosteronism)
• If concomitant metabolic alkalosis: Normal/low BP suggests diuretic use, vomiting or Gitelman/Bartter syndromes
• Hypertension suggests renovascular disease or primary mineralocorticoid excess
• Labs: BMP, CBC, VBG, urine electrolytes, magnesium, POC glucose, CK
• Imaging: Renal US, CT A/P
• Other: aldosterone, renin, cortisol

Management

• Check Mg⁺², replete to 2; Give empirically while waiting for serum Mg⁺²
• K⁺ preparation (route); replete to 4
• Choice of agent:
  • KCl is used for repletion in the hospital
    • • PO tablets for mild asymptomatic hypokalemia
      • IV can be given through peripheral (rate is 10mEq/hr) or central access
  • K⁺ bicarbonate can be dissolved and put through G tube
    • • Useful in pts with hypokalemia and metabolic acidosis
  • K⁺ acetate is given IV, rarely used (often additive to TPN)
• Dose:
  • Normal renal function: 10 mEq K⁺ is expected to raise serum [K⁺] by 0.1 mEq/L
  • Significant CKD or AKI: at risk of overcorrection
    • • Shortcut: multiply the mEq by the Cr = how much K⁺ expected to rise
  • Once K⁺ higher than 5.5, K⁺ increases much faster and rules above do not apply