Fluid, Acid-Base, and Electrolyte Emergencies
Hyperkalemia, Hyponatremia, Acid-Base, and Drug-Induced Disorders
Hyperkalemia Management — Three Sequential Phases
Phase 1 — Immediate
Membrane Stabilization
  • Calcium gluconate IV
  • Raises cardiac threshold potential
  • Does NOT lower serum K
  • Onset: minutes; lasts 30–60 min
  • Buys time for redistribution
Phase 2 — 15–30 min
Redistribution
  • Insulin + dextrose — drives K into cells via Na/K-ATPase
  • Albuterol nebulized (high dose) — beta-2 → Na/K-ATPase
  • Sodium bicarbonate — best in concurrent acidosis
  • Lowers serum K by 0.5–1.5 mEq/L
  • Effect temporary (4–6 hours)
Phase 3 — Definitive
Elimination
  • Loop diuretics — renal K excretion (if urine output present)
  • Patiromer / SZC — GI cation exchangers
  • Avoid sodium polystyrene sulfonate (intestinal necrosis risk)
  • Hemodialysis — most effective; use if refractory or anuric
Drug-Induced Electrolyte Disorders
Feature Amphotericin B Cisplatin Lithium Tenofovir DF
Site Distal tubule Distal tubule + proximal Collecting duct Proximal tubule
Mechanism Membrane pores → ion leak TRPM6 damage → Mg wasting ENaC entry → blocks AQP2 Mitochondrial toxicity
Electrolyte effect Hypokalemia, hypomagnesemia, type 1 RTA Hypomagnesemia, hypokalemia, Fanconi syndrome Nephrogenic diabetes insipidus → hypernatremia Fanconi syndrome — hypophosphatemia, glycosuria
Management Use liposomal formulation IV hydration; aggressive Mg/K repletion Amiloride (blocks ENaC entry) Switch to tenofovir alafenamide
Hyponatremia Safety Rule
Correction Rate Limits
  • Max correction: 6–8 mEq/L in first 24 hours
  • Never exceed 10–12 mEq/L in any 24-hour period
  • Risk if exceeded: osmotic demyelination syndrome (irreversible)
  • Symptomatic (seizure): 3% NaCl rapid infusion → target +2 to 3 mEq/L then slow
  • If overcorrected: give D5W + desmopressin to relow
Metabolic Alkalosis
Urine Cl Diagnostic Pivot
  • Urine Cl <20 mEq/L → chloride-responsive
  • Causes: vomiting, prior diuretics, nasogastric suction
  • Treatment: isotonic saline + K repletion
  • Urine Cl >20 mEq/L → chloride-resistant
  • Causes: hyperaldosteronism, Cushing's, Bartter/Gitelman
  • Volume-overloaded + alkalosis: acetazolamide (ADVOR trial)
Bicarbonate Therapy in High Anion Gap Acidosis — Use With Caution

In lactic acidosis and diabetic ketoacidosis, intravenous bicarbonate generates carbon dioxide that crosses cell membranes and the blood-brain barrier, paradoxically worsening intracellular acidosis. Reserve bicarbonate therapy for pH below 6.9 when cardiac contractility and catecholamine responsiveness are critically impaired. Treating the underlying cause (lactate source, insulin deficiency) is the definitive intervention.