Causes of Hyperkalemia
Hyperkalemia results from increased intake, decreased excretion, or transcellular shift out of cells. **Decreased excretion** (most common): CKD/AKI (#1 overall cause), ACE inhibitors/ARBs (block aldosterone effect → reduced renal K⁺ secretion), potassium-sparing diuretics (spironolactone, eplerenone, amiloride, triamterene), NSAIDs (reduce renal blood flow and aldosterone), Addison's disease (adrenal insufficiency → aldosterone deficiency), hypoaldosteronism (Type IV RTA — common in DM with hyporeninemia). **Transcellular shift** (out of cells): acidosis (each 0.1 pH unit decrease → K⁺ rises ~0.5–0.6 mEq/L — H⁺ shifts into cells, K⁺ shifts out), insulin deficiency (DKA), beta-blockers (block beta-2 adrenergic mediated K⁺ uptake), succinylcholine (depolarizing NMB → K⁺ release from skeletal muscle — dangerous in burns, crush injuries, denervation, rhabdomyolysis). **Increased intake**: rare cause; usually combined with impaired excretion. **Pseudohyperkalemia**: hemolysis during blood draw (most common), thrombocytosis (>1 million platelets), severe leukocytosis → repeat with plasma K⁺ or careful hemolysis-free sample.
ECG Changes: Progression with Rising K⁺
ECG changes correlate roughly with K⁺ level (though individual variability is significant — ECG, not just the K⁺ value, guides urgency): **K⁺ 5.5–6.5 mEq/L**: Peaked T waves (tall, narrow, symmetric — 'tented' — in precordial leads; contrasts with the asymmetric T-wave of ischemia). **K⁺ 6.5–7.0**: Prolonged PR interval, widened QRS. **K⁺ 7.0–8.0**: Absent P waves (atrial standstill), very wide QRS (>160 ms). **K⁺ >8.0**: Sine wave pattern (QRS merges with T wave), fatal arrhythmias (VF, asystole). Peaked T waves are the FIRST ECG change. Never wait for symptoms before treating — ECG drives urgency. Hypocalcemia and acidosis exacerbate cardiac toxicity at a given K⁺ level.
Treatment: C-BIG-K-D Mnemonic
**C** — **Calcium** (calcium gluconate 1 g IV over 2–3 min): stabilizes cardiac membrane, does not lower K⁺. Acts within minutes, lasts 30–60 min. Use when K⁺ >6.5 or ECG changes present. Calcium chloride has 3× more elemental calcium but is caustic to veins (use central line or for cardiac arrest). **B** — **Bicarb** (sodium bicarbonate 50 mEq IV): temporarily shifts K⁺ into cells via Na⁺-H⁺ exchange. Most effective in metabolic acidosis; less effective in ESRD or normal pH. **I** — **Insulin** (regular insulin 10 units IV) + **Glucose** (50 mL of D50W to prevent hypoglycemia if not hyperglycemic): shifts K⁺ into cells via Na⁺-K⁺-ATPase. Most reliable cellular shift. Check glucose q1h. **G** — the 'G' in BIGKD is sometimes grouped with insulin/glucose above. **K** — this 'K' reminds you the above only shifts K⁺ — must now REMOVE it. **D** — **Dialysis** (hemodialysis — fastest K⁺ removal; indicated for severe symptomatic hyperkalemia with AKI/ESRD), **Diuretics** (furosemide — increases urinary K⁺ excretion in patients with intact renal function), **Kayexalate** (sodium polystyrene sulfonate) or patiromer or sodium zirconium cyclosilicate (cation exchange resins — GI K⁺ removal, delayed effect, use for non-emergent). **Albuterol** (beta-2 agonist nebulizer) is also a rapid cellular shift agent (10–20 mg nebulized) — useful adjunct.