Step 2 CK · Emergency & Critical Care

Acid-Base, Electrolyte & Metabolic Emergencies

Name: Acid-Base, Electrolyte & Metabolic Emergencies
Creator: Veli Bakalov, MD

The ICU one-liners that must be reflexive

Emergency & Critical Care·Critical Care·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Hyperkalemia with ECG changes (peaked T → PR prolongation and flat P → wide QRS → sine wave) or K >6.5: give IV calcium gluconate first to stabilize the myocardium; it does not lower K.
After calcium, shift K into cells (insulin + glucose, albuterol, bicarbonate if acidotic) and remove it (loop diuretic, patiromer or sodium zirconium cyclosilicate, dialysis as definitive therapy).
DKA = glucose ≥200 or known diabetes, β-hydroxybutyrate ≥3.0 mmol/L, pH <7.3 and/or HCO3 <18 (2024 consensus); HHS = glucose ≥600, effective osmolality >300 (or total >320), pH ≥7.3, HCO3 ≥15, β-hydroxybutyrate <3.0, higher mortality.
DKA: fluids first, IV insulin, replace K when ≤5.0, hold insulin if K <3.5, add dextrose when glucose <200, and continue insulin until the anion gap closes.
Correct chronic hyponatremia by <8 mEq/L per 24 h (3% saline only for severe symptoms) to avoid osmotic demyelination; lower hypernatremia by no more than 10–12 mEq/L per 24 h to avoid cerebral edema.
Thyroid storm: propranolol → PTU → iodine at least 1 hour after the thionamide → glucocorticoids.
Myxedema coma: IV hydrocortisone with or before IV levothyroxine; adrenal crisis: IV hydrocortisone 100 mg plus dextrose-saline immediately, never delayed for testing.
Rhabdomyolysis: CK at least 5x normal, heme-positive dipstick without RBCs, hyperkalemia, hyperphosphatemia, hypocalcemia → aggressive isotonic fluids.
Malignant hyperthermia (RYR1; volatile anesthetics or succinylcholine): rising end-tidal CO2 is the earliest sign, then rigidity and hyperthermia → stop the trigger and give dantrolene.

Hyperkalemia

Peaked T waves warn of arrest. Hyperkalemia is K >5.5 mEq/L. The ECG evolves from peaked (tented) T waves to PR prolongation with flattened or absent P waves, then a widened QRS, and finally a sine wave that precedes VF or asystole. Any ECG change, or K >6.5, is an emergency. A high K with a normal ECG warrants a repeat sample, because hemolysis during the draw causes pseudohyperkalemia.

StabilizeIV calcium gluconate protects the myocardium within minutes; it does NOT lower K.
ShiftInsulin with glucose, inhaled albuterol, and bicarbonate if acidotic move K into cells.
RemoveLoop diuretics and binders (patiromer, sodium zirconium cyclosilicate).
DefinitiveHemodialysis, especially in kidney failure.

Emergency hyperkalemia: stabilize, shift, remove

Calcium buys minutes but removes nothing; shifting agents wear off in hours, so potassium must still be eliminated. Calcium chloride delivers more calcium but is a vesicant best given through a central line.

DKA and HHS

Glucose, gap, ketones make DKA. Diabetic ketoacidosis (usually type 1) requires glucose ≥200 mg/dL or known diabetes (2024 consensus), a high anion gap metabolic acidosis (pH <7.3 and/or HCO₃⁻ <18), and ketonemia (β-hydroxybutyrate ≥3.0 mmol/L). Precipitants include infection, insulin nonadherence, and MI; SGLT2 inhibitors can cause euglycemic DKA. Look for Kussmaul breathing, fruity breath, abdominal pain, and vomiting.

HHS: sky-high glucose, minimal ketones. The hyperosmolar hyperglycemic state (type 2) brings glucose ≥600 mg/dL (may exceed 1000), effective serum osmolality >300 mOsm/kg (or total >320), profound dehydration, and altered mental status, with minimal ketosis and no significant acidosis (pH ≥7.3, HCO₃⁻ ≥15, β-hydroxybutyrate <3.0 mmol/L). Enough insulin remains to block ketogenesis. Mortality is higher than in DKA, and fluids are the mainstay.

DKA vs HHS

Feature	DKA	HHS
Typical patient	Type 1 diabetes (absolute insulin deficiency)	Older adult with type 2 diabetes
Glucose	≥200 mg/dL or known diabetes	≥600 mg/dL, may exceed 1000
Acid-base	pH <7.3, HCO₃⁻ <18, high anion gap	pH ≥7.3, HCO₃⁻ ≥15, little or no acidosis
Ketones	Marked (β-hydroxybutyrate ≥3.0 mmol/L)	Minimal (β-hydroxybutyrate <3.0)
Osmolality, mental status	Variable; mentation often preserved	Effective >300 (total >320); altered mental status
Mortality	Lower	Higher

Fluids, insulin, and mind the potassium. Give aggressive isotonic IV fluids first, then a continuous IV regular insulin infusion, and replete potassium. Total-body K is depleted despite a normal or high serum K, so add potassium when K is 5.0 or lower and HOLD insulin if K is <3.5 until it is repleted. Add dextrose when glucose falls below 200 and continue insulin until the anion gap closes; treat the gap, not just the glucose. Overlap subcutaneous basal insulin before stopping the drip. Bicarbonate is reserved for severe acidemia (pH <6.9).

Insulin drives K into cells; starting it when K is low can precipitate fatal hypokalemia and arrhythmia. In children, overly rapid correction risks cerebral edema.

Sodium disorders

Correct sodium slowly or the pons dies. Severe symptomatic hyponatremia (seizures, coma) is treated with 3% hypertonic saline, given as small boluses aiming for a quick rise of a few mEq/L to stop symptoms. Chronic hyponatremia must be corrected SLOWLY, under 8 mEq/L per 24 hours; overcorrection causes osmotic demyelination syndrome (central pontine myelinolysis) with quadriparesis and dysarthria days later. Alcohol use disorder, malnutrition, hypokalemia, and liver disease raise the risk. If the limit is exceeded, re-lower the sodium with free water and desmopressin.

Hypernatremia: replace water, but not fast. Hypernatremia (Na >145) reflects a free-water deficit: diabetes insipidus, insensible or GI water losses, or poor intake in patients without access to water. Free-water deficit = total body water × (Na/140 − 1). Replace water and lower Na by no more than about 10–12 mEq/L per 24 hours, because rapid correction causes cerebral edema.

<8 mEq/L per 24 hRaising chronic hyponatremia: "low to high, the pons will die"

≤10–12 mEq/L per 24 hLowering hypernatremia: "high to low, the brain will blow"

Thyroid and adrenal crises

Thyroid storm presents with fever, tachyarrhythmia, and agitation or delirium, often after infection, surgery, or an iodine load. Treat in order:

β-blockerPropranolol controls adrenergic symptoms and blocks T4 → T3 conversion.
ThionamidePTU preferred; it also blocks peripheral conversion.
IodineAt least 1 hour AFTER the thionamide; high-dose iodine blocks hormone release and, via the Wolff-Chaikoff effect, synthesis.
GlucocorticoidsFurther reduce conversion and cover relative adrenal insufficiency.

Thyroid storm sequence

Given before a thionamide, iodine becomes substrate for new hormone synthesis and worsens the storm (Jod-Basedow effect). Use acetaminophen rather than aspirin for fever, because aspirin displaces thyroid hormone from binding proteins.

Myxedema coma is severe hypothyroidism with hypothermia, bradycardia, hypotension, hyponatremia, hypoventilation, and altered mentation, often triggered by infection, cold, or sedatives. Treat with IV levothyroxine (T4) plus IV hydrocortisone, giving the glucocorticoid first or concurrently to cover possible coexisting adrenal insufficiency, along with ventilatory support and passive rewarming.

Adrenal (Addisonian) crisis causes hypotension refractory to fluids and pressors, hyponatremia, hyperkalemia, and hypoglycemia, often after stress or abrupt steroid withdrawal. Give IV hydrocortisone 100 mg plus saline with dextrose immediately; draw cortisol and ACTH if it causes no delay, but never delay steroids for confirmatory testing. Hyperkalemia points to primary adrenal failure, because aldosterone is lost as well.

Waterhouse-Friderichsen syndrome: adrenal hemorrhage from meningococcemia causing acute adrenal crisis.

Rhabdomyolysis and malignant hyperthermia

Rhabdomyolysis is muscle breakdown from crush injury, prolonged immobilization, extreme exertion, seizures, drugs (statins, cocaine), or hyperthermic syndromes. CK is at least 5 times normal and often >5000 U/L. Myoglobinuria makes the urine dipstick positive for blood with no RBCs on microscopy. Expect hyperkalemia, hyperphosphatemia, early hypocalcemia, and acute kidney injury. Treat with aggressive isotonic IV fluids targeting a high urine output to prevent AKI; do not treat asymptomatic hypocalcemia, which reverses as calcium leaves the damaged muscle.

Malignant hyperthermia is an autosomal dominant RYR1 (ryanodine receptor) mutation unmasked by volatile anesthetics (sevoflurane, halothane, isoflurane) and succinylcholine. A rising end-tidal CO₂ is the earliest sign, followed by masseter or generalized rigidity, tachycardia, hyperthermia, acidosis, and hyperkalemia. Stop the trigger and give dantrolene, which blocks calcium release through the ryanodine receptor; add 100% oxygen, active cooling, and treatment of hyperkalemia.