Hypokalemia 1

Hypokalemia

Hypokalemia is characterized by a serum K concentration of less than 3.5 mEq/L.

Ninety-eight percent of K is intracellular.
I. Pathophysiology of Hypokalemia

A. Cellular Redistribution of Potassium. Hypokalemia may result from the

intracellular shift of potassium by insulin, beta-2 agonist drugs, stress

induced catecholamine release, thyrotoxic periodic paralysis, and

alkalosis-induced shift (metabolic or respiratory).

B. Nonrenal Potassium Loss

1. Gastrointestinal loss can be caused by diarrhea, laxative abuse, villous

adenoma, biliary drainage, enteric fistula, clay ingestion, potassium

binding resin ingestion, or nasogastric suction.

2. Sweating, prolonged low potassium ingestion, hemodialysis and

peritoneal dialysis may also cause nonrenal potassium loss.

C. Renal Potassium Loss

1. Hypertensive High Renin States. Malignant hypertension, renal artery

stenosis, renin-producing tumors.

2. Hypertensive Low Renin, High Aldosterone States. Primary

hyperaldosteronism (adenoma or hyperplasia).

3. Hypertensive Low Renin, Low Aldosterone States. Congenital

adrenal hyperplasia (11 or 17 hydroxylase deficiency), Cushing's

syndrome or disease, exogenous mineralocorticoids (Florinef, licorice,

chewing tobacco), Liddle's syndrome.

4. Normotensive States

a. Metabolic acidosis. Renal tubular acidosis (type I or II)

b. Metabolic alkalosis (urine chloride <10 mEq/day). Vomiting

c. Metabolic alkalosis (urine chloride >10 mEq/day). Bartter's

syndrome, diuretics, magnesium depletion, normotensive

hyperaldosteronism
5. Drugs associated with potassium loss include amphotericin B,
2 Hypokalemia

ticarcillin, piperacillin, and loop diuretics.

II. Clinical Effects of Hypokalemia

A. Cardiac Effects. The most lethal consequence of hypokalemia is cardiac

arrhythmias. Electrocardiographic effects include depressed ST seg-

ments, decreased T-wave amplitude, U waves, and a prolonged QT-U
interval.

B. Musculoskeletal Effects. The initial manifestation of K depletion is

muscle weakness, which can lead to paralysis. In severe cases,

respiratory muscle paralysis may occur.

C. Gastrointestinal Effects. Nausea, vomiting, constipation, and paralytic

ileus may develop.

III. Diagnostic Evaluation

A. The 24-hour urinary potassium excretion should be measured.

B. If >20 mEq/day, excessive urinary K loss is the cause. If <20 mEq/d, low

K intake, or non-urinary K loss is the cause.

C. In patients with excessive renal K loss and hypertension, plasma renin

and aldosterone should be measured to differentiate adrenal from non-

adrenal causes of hyperaldosteronism.

D. If hypertension is absent and patient is acidotic, renal tubular acidosis

should be considered.

E. If hypertension is absent and serum pH is normal to alkalotic, a high urine

chloride (>10 mEq/d) suggests hypokalemia secondary to diuretics or

Bartter's syndrome. A low urine chloride (<10 mEq/d) suggests vomiting.

IV. Emergency Treatment of Hypokalemia

A. Estimated Potassium Deficit

1. At a serum K <3 mEq/L, there is a K deficit of more than 300 mEq

2. At a serum K <2 mEq/L, there is a K deficit of more than 700 mEq

B. Indications for Urgent Replacement. Electrocardiographic abnormalities

consistent with severe K depletion, myocardial infarction, hypoxia, digitalis

intoxication, marked muscle weakness, or respiratory muscle paralysis.
 Hypokalemia 3

C. Intravenous Potassium Therapy

1. Intravenous KCL is usually used unless concomitant

hypophosphatemia is present (diabetic ketoacidosis), where potassium
phosphate is indicated.
2. The maximal rate of intravenous K replacement is 30 mEq/hour. The
K concentration of IV fluids should be 40 mEq/L or less if given via a
peripheral vein. Frequent monitoring of serum K and constant
electrocardiographic monitoring are required when potassium is being

infused.

V. Non-Emergent Treatment of Hypokalemia

A. Attempts should be made to normalize K levels if <3.5 mEq/L.

B. Oral supplementation is significantly safer than IV. Micro-encapsulated

and sustained-release forms of KCL are less likely to induce

gastrointestinal disturbances than are wax-matrix tablets or liquid

preparations.

1. KCL elixir, 1-3 tablespoon qd-tid PO after meals (20 mEq/Tbsp 10%

sin).
2. Micro-K, 10 mEq tabs, 2-3 tabs tid PO after meals (40-100 mEq/d). §