Hyperkalemia Crisis Protocol: Acute Management Playbook and the Calcium Conundrum in High-Stakes Hospital Medicine

In this episode of Hospital Medicine Unplugged, we power through hyperkalemia—confirm fast, monitor the heart, stabilize the membrane, shift K⁺ in, and remove K⁺ out—while fixing the cause and keeping RAASi on board when safe.

We open with the do-firsts: repeat K⁺ to exclude pseudohyperkalemia; 12-lead ECG + telemetry; hunt triggers (AKI/CKD, meds, acidosis, tissue breakdown). Remember: no ECG changes ≠ safe—severe hyperkalemia can be silent.

Call it when serum K⁺ >5.0 mmol/L (often severe ≥6.0). High-risk hosts: CKD, HF, diabetes, RAASi/K-sparing diuretics, hospitalized/critically ill. Why it matters: arrhythmias & sudden death—risk climbs with rapid rises and higher K⁺.

Treatment—build the three-part stack:

• A. Stabilize the myocardium (now if ECG changes or K⁺ ≥6.5): Calcium gluconate 10% 10 mL IV over 2–5 min (repeat if QRS doesn’t narrow). In arrest/central line, calcium chloride is acceptable. Calcium doesn’t lower K⁺—it buys time.

• B. Shift K⁺ into cells (on board within minutes): Insulin 10 U IV + dextrose 25 g (consider 50 g or dextrose infusion in CKD; q30–60 min glucose checks—hypoglycemia is common). Albuterol 10–20 mg nebulized (additive; watch for tachyarrhythmia/ischemia). Sodium bicarb only if metabolic acidosis or TLS/DKA physiology—limited effect otherwise.

• C. Remove K⁺ (definitive): Loop diuretic if making urine. Potassium binders: prioritize patiromer or sodium zirconium cyclosilicate for non-emergent/bridging and RAASi maintenance; avoid routine SPS (variable efficacy; GI injury risk). Hemodialysis = fastest & most reliable for severe/refractory, ESRD/AKI, TLS/rhabdo, or life-threatening ECG changes.

Etiology plays (treat the cause): • Decreased excretion: AKI/CKD, hypoaldosteronism, low distal Na⁺ delivery. • Meds: ACEi/ARB/ARNI, spironolactone/eplerenone, amiloride/triamterene, NSAIDs, heparin, calcineurin inhibitors, trimethoprim, non-selective β-blockers. • Redistribution: acidosis, insulin deficiency (DKA), β-blockade, succinylcholine, tissue breakdown (TLS, rhabdo). • Increased intake: supplements, salt substitutes, PRBCs/TPN. • Pseudohyperkalemia: hemolysis, thrombocytosis, leukocytosis—repeat plasma K⁺ before you treat aggressively.

Monitoring & safety that sticks: trend K⁺ q1–2 h after temporizers (watch rebound), then q4–6 h as stable; continuous telemetry for severe cases; point-of-care glucose after insulin; reassess ECG after calcium/each step. Document timing—time-to-therapy saves myocardium.

Special situations: • ESRD/AKI: skip diuretics if anuric—dialyze early. • TLS/rhabdo: simultaneous aggressive K⁺ control + underlying-cause therapy. • DKA: insulin alone will fall K⁺—replace K⁺ once <5.0 and urine flows. • Pregnancy: avoid SPS; binder choice and dialysis per severity. • Digoxin toxicity: avoid IV calcium in classic “stone heart” concern—prioritize digoxin-specific Fab and temporizers.

Recurrence prevention: • Medication audit (de-risk combos, stop non-essentials), correct metabolic acidosis, tailor diet (focus on processed/animal K⁺; don’t over-restrict plant-based foods), and use patiromer/SZC to maintain RAASi in HF/proteinuric CKD. • Build a monitoring plan for CKD/HF/diabetes or prior hyperkalemia (e.g., check K⁺ within 3–7 days after RAASi/diuretic changes, then space out).

Controversies & pitfalls you don’t want to meet: • Under-dosing insulin or skipping glucose checks → hypoglycemia. • Overreliance on ECG—normal ECG doesn’t rule out danger. • Reflex SPS use despite GI risk and uncertain benefit. • Stopping RAASi permanently after a single episode—use binders/monitoring to preserve cardio-renal benefit when feasible. • Missing pseudohyperkalemia—treat the patient + lab context, not a single hemolyzed value.

We close with the system moves: a hyperkalemia bundle that (1) auto-repeats K⁺ if hemolysis suspected; (2) routes to telemetry for severe cases; (3) fires a calcium-insulin-albuterol pathway with glucose checks; (4) preloads dialysis for ESRD/AKI or ECG danger; (5) flags culprit meds and suggests safer alternatives; (6) offers patiromer/SZC order sets to keep RAASi on board; (7) embeds follow-up K⁺ monitoring and patient education.

Confirm fast, protect the heart, shift now, remove for keeps, fix the cause—and keep the kidneys & heart therapies rolling when you can.