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Hypokalemia is characterized by a serum K concentration of less than 3.5 mEq/L. Ninety-eight percent of K is intracellular.
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 low potassium, potasium
Nonrenal Potassium Loss
Gastrointestinal loss can be caused by diarrhea, laxative abuse, villous adenoma, biliary drainage, enteric fistula, clay ingestion, potassium binding resin ingestion, or nasogastric suction.
Sweating, prolonged low potassium ingestion, hemodialysis and peritoneal dialysis may also cause nonrenal potassium loss.
Renal Potassium Loss
Hypertensive High Renin States. Malignant hypertension, renal artery stenosis, renin-producing tumors.
Hypertensive Low Renin, High Aldosterone States. Primary hyperaldosteronism (adenoma or hyperplasia).
Hypertensive Low Renin, Low Aldosterone States. Congenital adrenal hyperplasia (11 or 17 hydroxylase deficiency), Cushing's syndrome or Hypokalemia, Low Potassium disease, exogenous mineralocorticoids (Florinef, licorice, chewing tobacco), Liddle's syndrome.
Normotensive States
Metabolic acidosis. Renal tubular acidosis Hypokalemia, Low Potassium Hypokalemia, Low Potassium(type I or II)
Metabolic alkalosis (urine chloride <10 mEq/day). Vomiting
Metabolic alkalosis (urine chloride >10 mEq/day). Bartter's syndrome, diuretics, magnesium depletion, normotensive hyperaldosteronism
Drugs associated with potassium loss include amphotericin Hypokalemia, Low Potassium Hypokalemia, Low Potassium B, ticarcillin, piperacillin, and loop diuretics.
Clinical Effects of Hypokalemia
Cardiac Effects
The most lethal consequence of hypokalemia is cardiac Hypokalemia, Low Potassium Hypokalemia, Low Potassium arrhythmias.
Electrocardiographic Effects. U waves >1 mm in height, T waves in the same lead; ST segment depression; T wave flattening, followed by inversion.
Atrial and ventricular ectopy, including ectopic atrial tachycardia, atrioventricular blocks, premature ventricular contractions, ventricular tachycardia and fibrillation.
Musculoskeletal Effects. The initial manifestation of K depletion is muscle weakness which can lead to paralysis. In severe cases, respiratory muscle paralysis may occur.
Gastrointestinal Effects. Nausea, vomiting, constipation, and
Diagnostic Evaluation
The 24-hour urinary potassium excretion should be measured.
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.
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.
If hypertension is absent and patient is acidotic, renal tubular acidosis should be considered.
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
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 abnormalitiesconsistent with severe K depletion, myocardial infarction, hypoxia, digitalis intoxication, marked muscle weakness, or respiratory muscle paralysis.
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 hypokalemia, low potassium replacement is 30 mEq/hour. The K concentration of IV fluids should be 40 mEq/L or less if hypokalemia, low potassium given via a peripheral vein. Frequent monitoring of serum K and constant hypokalemia, low potassium electrocardiographic monitoring are required when potassium is
Non-Emergent Treatment of hypokalemia, low potassium Hypokalemia
A. Attempts should be made to hypokalemia, low potassium normalize K levels if <3.5 mEq/L.
B. Oral supplementation is hypokalemia, low potassium significantly safer than IV. Micro-encapsulated and sustained-release forms of KCL are hypokalemia, low potassium less likely to induce gastrointestinal disturbances than are wax-matrix tablets or liquid hypokalemia, low potassium preparations.
1. KCL elixir, 1-3 tablespoon q