Hypokalemia¶

Peter Thorne and Patrick Steadman

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

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

History: decreased K+ intake, increased entry into cells (ex: 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. Possibly aldosterone, renin, cortisol pending clinical context
Imaging: Renal US, CT AP

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, may have burning sensation) or central access
- K+ bicarbonate can be dissolved and put through G tube
  - Useful in pts with hypokalemia and metabolic acidosis
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