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.