Electrolyte Abnormalities

Severity: - Mild: 5.5–6.5 mEq/L - Moderate: 6.6–7.5 - Severe: > 7.5

Causes: - Renal disease (esp. GFR < 15) - Drugs: ACEi/ARBs, NSAIDs, K-sparing diuretics, digoxin, β-blockers - Acidosis, hyponatremia, hypocalcemia - Hemolysis, transfusion (esp. old pRBCs — K of 50+ in the bag!) - Succinylcholine acute ↑ 0.5–1 mEq/L (greater in susceptible patients) - Tourniquet, trauma, rhabdo, MH - Do not give verapamil with dantrolene

EKG progression: 1. Tall peaked T waves (precordial leads) 2. Long PR, low P-wave amplitude 3. Wide QRS → sine wave → VF / asystole - K > 7: ascending flaccid paralysis, inability to phonate, respiratory arrest

Stabilize membrane (acts fast, brief duration): - Calcium gluconate 10% 10 cc IV over 5 min (peripheral OK) - Calcium chloride 10% 5 cc IV (central line preferred) - Avoid Ca in digitalis toxicity → "stone heart"

Shift K intracellular (temporary): - NaHCO₃ 50–100 mEq IV over 5–10 min - Regular insulin 10 units IV + D50 25 g (50 mL) - Albuterol nebulized

Remove K from body (definitive): - Loop or thiazide diuretics - Kayexalate (sodium polystyrene sulfonate): PO 30 g in sorbitol, PR 50 g in sorbitol - Dialysis

Anesthetic considerations: - Cancel elective cases if K > 5.5 - Avoid succinylcholine - EKG monitoring - Avoid hypoventilation (worsens acidosis → K shift) - Treat acidosis - Monitor for ↑ sensitivity to NMBA - Choose non-NS fluids if hyperchloremic acidosis is worsening K

Severity: - Mild: 3.1–3.5 - Moderate: < 3 with PACs - Severe: < 3 with PVCs

Causes: - GI losses (NGT, N/V, diarrhea) - Lasix, renal tubular acidosis - Mg deficiency - Alkalosis (intracellular shift) - Insulin - Hypothermia

Signs: - PACs, PVCs, SVT (afib/flutter) - EKG: flattened/inverted T, U waves, ST depression - Metabolic alkalosis - Weakness, ↓ DTRs, ileus - Digoxin toxicity - ↑ sensitivity to NMBAs

Treatment: - Acute = cellular shift → reverse cause (e.g., hyperventilation) - Chronic = total body depletion (1 mEq/L deficit = 175–350 mEq total) - Peripheral IV: 10 mEq/h - Central: 10–20 mEq/h - Life-threatening: 5–6 mEq bolus

Consider cancelling elective surgery if K < 3–3.5 (chronicity matters). Reduce NMBA by 25–50%. Avoid respiratory alkalosis.

Causes: hyperparathyroidism, malignancy (lung, ENT, GU, GYN, multiple myeloma), immobilization, AKI, thiazides, lithium.

Signs: EKG short QT, HTN, polyuria, "stones, bones, abdominal groans, psychic moans."

Treatment: crystalloid bolus + loop diuretic; bisphosphonates; dialysis if severe.

Anesthetic considerations: maintain hydration; consider invasive monitoring if Ca > 14; expect resistance to NMBAs.

Causes: hypoparathyroidism (post-thyroid/parathyroid surgery), vitamin D deficiency, CKD, pancreatitis, massive transfusion (citrate), sepsis, alkalosis (binds ionized Ca).

Signs: Chvostek (facial twitch with facial nerve tap), Trousseau (carpal spasm with BP cuff), perioral numbness, tetany, laryngospasm. EKG: prolonged QT.

Treatment: CaCl₂ 1 g IV (central) or Ca gluconate 1–2 g IV (peripheral). Replace Mg.

Anesthetic considerations: monitor for QT prolongation, dysrhythmias; expect ↑ sensitivity to NMBAs.

Categorize by volume status: - Hypovolemic: GI/renal losses, diuretics - Euvolemic: SIADH, hypothyroid, glucocorticoid deficiency, TURP syndrome - Hypervolemic: CHF, cirrhosis, nephrotic syndrome

Acute (< 48 h) correction can be faster (cerebral edema risk dominates). Chronic must be corrected slowly to avoid central pontine myelinolysis: - ≤ 10–12 mEq/L in 24 h - ≤ 18 mEq/L in 48 h

Severe symptomatic (seizure, coma): 3% saline 100 mL bolus, may repeat × 2.

Anesthetic considerations: elective surgery generally deferred if Na < 130. ↓ MAC. Risk of cerebral edema with overcorrection.