Hypokalemia in the Hospitalized Patient: The 0.05 Rule, IV Safety Protocols, and Why You Must Check the Mag

In this episode of Hospital Medicine Unplugged, we sprint through hypokalemia—define fast, find the source, replete safely, prevent rebounds.

We open with the do-firsts: confirm K+ <3.5 mmol/L (<3.0 severe), review meds (loop/thiazide diuretics, insulin, steroids), check GI losses, volume/BP, and get serum/urine electrolytes + acid–base. ECG if symptomatic or K+ ≤3.0. Distinguish renal vs extrarenal losses early with urine K+ (spot or 24-hr) and chloride.

Call the diagnosis and risk: hypokalemia is common in the hospital (>20%) and not benign—arrhythmias, weakness/paralysis, ileus, and death. Even mild deficits raise morbidity/mortality, especially in heart failure, CKD, and digoxin users. Rapid drops are riskier.

Pathophys plays (why K+ falls): • External balance: diet in, kidney/colon out; aldosterone drives distal secretion. • Internal shifts: insulin, β-agonists, alkalosis push K+ into cells. • Usual culprits: diuretics, vomiting/diarrhea or NG suction, renal tubulopathies, surreptitious laxatives/vomiting, hypomagnesemia.

Diagnostic road map: • Urine K+: <20 mmol/L → extrarenal/poor intake; ≥20 → renal wasting. UK/Cr, FEK, or TTKG help if needed. • If metabolic alkalosis + HTN, think mineralocorticoid excess (check renin/aldo). If alkalosis + normal/low BP, think diuretics or tubulopathies. • Always pair with Mg, acid–base, and medication review.

Treatment—build the repletion core: • Oral first for mild–moderate and intact GI: typically 20–40 mmol/day (mild) or 40–100 mmol/day in divided doses (moderate). • IV KCl for severe (<2.5), symptoms/ECG changes, or no PO: 10–20 mmol/hr (central line for higher rates; max 40 mmol/hr in ICU with continuous ECG). Avoid dextrose-containing fluids. • Expect variability: the classic “10 mEq → +0.1 mmol/L” often overestimates; median response ~+0.05 mmol/L per 10 mEq, and loop diuretics blunt the rise—dose accordingly. • Choose the salt wisely: KCl is default; use K-bicarb/citrate with metabolic acidosis or K-phosphate when phosphate is low.

If the backbone buckles: • Fix Mg first/with K+—hypomagnesemia makes hypokalemia refractory. • Ongoing renal K+ wasting? Add K-sparing diuretics (e.g., spironolactone, amiloride) and reduce offending diuretics if possible. • Persistent GI loss? Replace chloride and treat the cause.

Risk-stratify & admit when any: K+ <2.5, symptoms (weakness, paralysis), ECG changes/arrhythmia, rapid fall, digoxin use, significant comorbidity (HF/CKD), or inability to take PO. In-house: telemetry if severe or IV rates >10 mmol/hr, frequent labs, and address etiology.

Monitoring that sticks: • Mild (3.0–3.5, asymptomatic): recheck within 24 h. • Moderate (2.5–2.9) or symptoms/ECG: q4–6 h during active repletion. • Severe (<2.5) or IV infusion: q2–4 h with continuous ECG for higher rates. • Track renal function and Mg, avoid overshoot—iatrogenic hyperkalemia is real, especially in CKD or with large cumulative doses.

Complications & pitfalls you don’t want to meet: • Overcorrection → hyperkalemia/arrhythmias—titrate and trend. • Slow-release K+ tabs can cause GI irritation; favor microencapsulated forms. • Dextrose-containing IVs worsen hypokalemia via insulin surge. • Failure to document and recheck leads to missed targets and harm.

Research horizon: • Better dose–response tools under real-world meds (esp. loops). • Oral vs IV comparative outcomes across HF/CKD. • Role of dietary K+ in restoring and maintaining normokalemia in chronic care.

Fast, physiology-led, and safety-first—fix the cause, replete smart (PO when you can, IV when you must), correct Mg, and monitor like it matters.