Fluid & Electrolyte Imbalances

Electrolytes are minerals that carry an electric charge when dissolved in body fluids. They regulate how much water the body holds and where it sits, acid–base balance, nutrient transport into and waste out of cells, and the function of nerves, muscle, the heart, and the brain. The clinically dominant ones are sodium, potassium, calcium, and magnesium — and the master rule of the whole chapter is that water follows solute across compartments.

That rule is why IV fluid tonicity matters. Isotonic fluid (0.9% normal saline, lactated Ringer’s) stays in the intravascular space and raises blood pressure — the choice for fluid volume deficit. Hypotonic fluid (0.45% saline) shifts water into cells to treat cellular dehydration such as hypernatremia — but excess risks cerebral edema. Hypertonic 3% saline pulls water out of cells and is reserved for one job only: severe symptomatic hyponatremia — it is never a hypernatremia treatment.

Volume problems come in two directions. Fluid volume deficit (hypovolemia) is fluid loss exceeding intake — diarrhea, vomiting, sweating, fever, bleeding, poor intake, diuretics — and the body compensates exactly as it would for hemorrhage: sympathetic activation raises heart rate and constricts vessels, the RAAS retains sodium and water, and ADH conserves free water. Fluid volume excess (hypervolemia) is fluid retained in the intravascular compartment — heart failure, kidney failure, cirrhosis, pregnancy — and hydrostatic pressure pushes it out as pitting edema, ascites, and crackles that appear first in the lower posterior lung fields.

Potassium maintains the resting membrane potential of every excitable cell — nerve, skeletal muscle, smooth muscle, and above all cardiac myocytes. That is why derangement in either direction is a cardiac emergency: the normal band is narrow (3.5–5.0 mEq/L), and the ECG deteriorates in a predictable, testable sequence on each side of it.

Hypokalemia (K⁺ below 3.5) flattens T waves, depresses the ST segment, produces a U wave, and prolongs the QT — severe cases end in torsades de pointes or VT/VF. It is often silent until below 3.0, then shows as weakness, cramps, fatigue, palpitations, and constipation (smooth-muscle hypoactivity). Hyperkalemia climbs a ladder by level: tall peaked T waves (5.5–6.5) → flattened or lost P waves (6.5–7.5) → widening QRS (7–8) → sine wave and asystole (8–10). Mild elevation is usually asymptomatic — the first manifestation can be a lethal arrhythmia.

The potassium safety rules are absolute. IV potassium is never given IV push — it can immediately stop the heart. Potassium is always diluted and infused — rates above 10 mmol/h cause pain and phlebitis, rates above 20 mmol/h risk rebound hyperkalemia, and rates above 10 mEq/h require continuous cardiac monitoring (central access preferred for higher concentrations).

Sodium disorders are really water disorders, and the organ that pays is the brain. In hyponatremia (Na⁺ below 135 mEq/L; severe below 125) water shifts into brain cells — cerebral edema — worst when the drop is acute, before brain cells can adapt. Symptoms progress from fatigue, weakness, and gait abnormality through cramps, nausea, and drowsiness to seizures, falling consciousness, and cardiorespiratory collapse. Sorting it by volume status points to the cause: hypovolemic (GI losses, diuretics), hypervolemic (heart failure, cirrhosis, renal failure — water gained in excess of sodium), or euvolemic (SIADH, a diagnosis of exclusion where vasopressin is secreted despite normal volume).

In hypernatremia (Na⁺ above 145 mEq/L) water shifts out of cells — intracellular dehydration. It happens to people who lose water and cannot replace it: unreplaced GI, insensible, or renal losses, diabetes insipidus, and above all impaired thirst or no independent water access — infants, older adults, the neurologically impaired. Findings run from irritability and agitation to lethargy, twitching, seizures, and coma, with a "doughy" skin feel; shrinking brain cells can even tear bridging veins and hemorrhage, the highest risk in infants.

Both directions carry the same exam hook: correct slowly. Raising sodium faster than about 10–12 mEq/L in 24 hours (target 4–6/day in severe symptomatic cases) causes osmotic demyelination syndrome — delayed, often permanent neurologic injury up to locked-in syndrome. Lowering sodium faster than 12 mEq/L in 24 hours (about 0.5 mEq/L/h, corrected over 48–72 hours with serum checks every 2–4 hours) causes cerebral edema as water rushes back into adapted brain cells. Severe symptomatic hyponatremia gets 3% saline in 100-mL boluses over 10 minutes (up to 3); chronic euvolemic/SIADH cases get fluid restriction below 1 L/day first; hypernatremia gets oral or enteral water when possible, hypotonic IV fluids when not.

Calcium stabilizes excitable membranes, so hypocalcemia (total Ca²⁺ below about 8.6 mg/dL) produces neuromuscular irritability: perioral and fingertip paresthesias, cramps, tetany, and the two classic bedside signs — Trousseau (carpal spasm when a BP cuff is inflated above systolic for 2–3 minutes) and Chvostek (facial twitch on tapping the facial nerve in front of the ear). Severe cases threaten laryngospasm, seizures, and a prolonged QT that predisposes to torsades — airway and cardiac emergencies. Always check albumin first: total calcium falls about 0.8 mg/dL for every 1 g/dL drop in albumin while ionized calcium stays normal. Hypercalcemia (about 90% from hyperparathyroidism or malignancy) is the mirror image — "stones, bones, groans, and psychiatric overtones": renal stones, bone pain, constipation, polyuria, weakness, confusion, with a shortened QT; a level of 14 mg/dL or more is hypercalcemic crisis, treated first with aggressive 0.9% saline.

Magnesium is the gatekeeper electrolyte: hypomagnesemia causes refractory hypokalemia in about 60% of cases and impairs PTH secretion, producing secondary hypocalcemia — neither potassium nor calcium corrects until magnesium is replaced. Low magnesium looks like low calcium (tremor, hyperreflexia, fasciculations, positive Trousseau and Chvostek, seizures) and adds ventricular arrhythmias including torsades de pointes — for which magnesium itself is the treatment. Its causes cluster around losses: diarrhea and malabsorption, loop and thiazide diuretics, proton pump inhibitors, and alcohol use disorder (about 30% prevalence).

Hypermagnesemia is above all a renal-failure problem: the kidney can no longer excrete magnesium once creatinine clearance falls below about 20 mL/min, so magnesium-containing antacids, laxatives, and bowel preps become dangerous in renal disease — and obstetric magnesium sulfate infusions run levels deliberately high. It sedates the neuromuscular system in stages: flushing and hypotension, then loss of deep tendon reflexes with bradycardia and drowsiness (7–12 mg/dL), then flaccid paralysis, respiratory depression, and conduction delays (above 12), then coma and cardiac arrest (above 15). The magnesium-infusion safety triad follows directly: stop the infusion for urine output below 80 mL in 4 hours, absent deep tendon reflexes, or a respiratory rate below 12/min. IV calcium gluconate directly antagonizes magnesium at the heart and neuromuscular junction; dialysis removes it definitively in renal failure.