Hypokalemia¶
Peter Thorne and Patrick Steadman
Background¶
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Potassium (K+) \< 3.5 mEq/L
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98% of total body K+ is intracellular (majority in muscle cells)
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Goal: prevent life threatening complication (e.g. arrhythmia), replace deficit, elucidate cause
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Insulin and catecholamines (Beta adrenoreceptors) are key drivers of transcellular shifts
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H+ and K+ will trade places to maintain electroneutrality
Presentation¶
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Malaise, weakness, myalgias, decreased gastrointestinal motility
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EKG changes:
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Mild: ST segment depression, decreased T wave amplitude
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Severe: U-waves (most commonly seen in precordial leads V2 and V3)
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Severe hypokalemia can lead to rhabdomyolysis
Evaluation¶
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History: decreased K+ intake, increased entry into cells (ex: elevated beta-adrenergic activity, hypothermia), GI losses, urinary losses (diuretics, hypomagnesemia, RTA, tubular defects, hyperaldosteronism)
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If concomitant metabolic alkalosis: Normal/low BP suggests diuretic use, vomiting or Gitelman/Bartter syndromes
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Hypertension suggests renovascular disease or primary mineralocorticoid excess
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Labs: BMP, CBC, VBG, urine electrolytes, magnesium, POC glucose, CK. Possibly aldosterone, renin, cortisol pending clinical context
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Imaging: Renal US, CT AP
Management¶
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Check Mg+2, replete to 2; Give empirically while waiting for serum Mg+2
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K+ preparation (route); replete to 4
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Choice of agent:
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KCl is used for repletion in the hospital
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PO tablets for mild asymptomatic hypokalemia
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IV can be given through peripheral (rate is 10mEq/hr, may have burning sensation) or central access
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K+ bicarbonate can be dissolved and put through G tube
- Useful in pts with hypokalemia and metabolic acidosis
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Dose:
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Normal renal function: 10 mEq K+ is expected to raise serum [K+] by 0.1 mEq/L
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Significant CKD or AKI: at risk of overcorrection
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Shortcut: multiply the mEq by the Cr = how much K+ expected to rise
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Once K+ higher than 5.5, K+ increases much faster and rules above do not apply
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