Potassium (K)


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Subject: Potassium (K)

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  • Potassium is a primary intracellular ion; <2% is extracellular. High intracellular concentrations are maintained by the Na–K ATPase pump, which continuously transports potassium into the cell against a concentration gradient. This pump is a critical factor in maintaining and adjusting the ionic gradients, on which nerve impulse transmission and contractility of cardiac and skeletal muscle depends. In acidemia, potassium moves out of cells; in alkalemia, potassium moves into cells. Hypokalemia inhibits aldosterone production; hyperkalemia stimulates aldosterone production. Plasma sodium and potassium control potassium reabsorption. Each 1 mmol/L decrease of serum potassium reflects a total deficit of <200–400 mmol; a serum potassium <2 mmol/L may reflect a total deficit >1,000 mmol.

  • Normal range: see Table 16.67.

TABLE 16–67
Normal Range for Potassium


  • Evaluation of electrolyte balance, cardiac arrhythmia, muscular weakness, hepatic encephalopathy, and renal failure

  • Diagnosis and monitoring hyperkalemia and hypokalemia in various conditions (e.g., treatment of diabetic coma, renal failure, severe fluid and electrolyte loss, effect of certain drugs)

  • Diagnosis of familial hyperkalemic periodic paralysis and hypokalemic paralysis


Increased In

  • Potassium retention

    • GFR <3–5 mL/minute

      • Oliguria caused by any condition (e.g., renal failure)

      • Chronic nonoliguric renal failure associated with dehydration, obstruction, trauma, or excess potassium

      • Drugs

      • Renal toxicity (e.g., amphotericin B, methicillin, tetracycline)

    • GFR >20 mL/minute

      • Decreased (aldosterone) mineralocorticoid activity

      • Addison disease

      • Hypofunction of the renin–angiotensin–aldosterone system

      • Hyporeninemic hypoaldosteronism with renal insufficiency (GFR, 25–75 mL/minute)

      • Various drugs (e.g., NSAIDs, ACE inhibitors, cyclosporine, pentamidine)

      • Decreased aldosterone production

      • Pseudohypoaldosteronism

      • Aldosterone antagonist drugs (e.g., spironolactone, captopril, heparin)

    • Inhibition of tubular secretion of potassium

    • Mineralocorticoid-resistant syndromes

      • Primary tubular disorders

      • Hereditary

      • Acquired (e.g., SLE, amyloidosis, sickle cell nephropathy, obstructive uropathy, renal allograft transplant, chloride shift)

  • Potassium redistribution

    • Familial hyperkalemic periodic paralysis (Gamstorp disease, adynamia episodica hereditaria)

    • Acute acidosis (especially hyperchloremic metabolic acidosis; less with respiratory; little with metabolic acidosis due to organic acids) (e.g., diabetic ketoacidosis, lactic acidosis, acute renal failure, acute respiratory acidosis)

      • Decreased insulin

      • Beta-adrenergic blockade

      • Drugs (e.g., succinylcholine, great excess of Digitalis, arginine infusion)

      • Use of hypertonic solutions (e.g., saline, mannitol)

      • Intravascular hemolysis (e.g., transfusion reaction, hemolytic anemia), rhabdomyolysis

      • Rapid cellular release (e.g., crush injury, chemotherapy for leukemia or lymphoma, burns, major surgery)

  • Urinary diversion

    • Ureteral implants into jejunum

    • In neonates—dehydration, hemolysis (e.g., cephalohematoma, intracranial hemorrhage, bruising, exchange transfusion), acute renal failure, CAH, adrenocortical insufficiency

Decreased In

  • Excess renal excretion (in patients with hypokalemia, urine potassium, >25 mmol in 24 hours or >15 mmol/L implies at least a renal component)

    • Osmotic diuresis of hyperglycemia (e.g., uncontrolled diabetes)

    • Nephropathies

      • Renal tubular acidosis (proximal and especially distal)

      • Bartter syndrome

      • Liddle syndrome

      • Magnesium depletion due to any cause

      • Renal vascular disease, malignant hypertension, vasculitis

      • Renin-secreting tumors

    • Endocrine

      • Hyperaldosteronism (primary, secondary)

      • Cushing syndrome especially caused by ectopic ACTH production

      • CAH

      • Hyperthyroidism (especially in Asian persons)

    • Drugs

      • Diuretics (e.g., thiazides, ethacrynic acid, furosemide); assay for diuretics should be done if urine chloride >40 mmol/L

      • Mineralocorticoids (e.g., fluorocortisone)

      • High-dose glucocorticoids

      • High-dose antibiotics (e.g., penicillin, nafcillin, ampicillin, carbenicillin)

      • Substances with mineralocorticoid effect (e.g., glycyrrhizic acid [licorice], carbenoxolone, gossypol)

      • Drugs associated with magnesium depletion (e.g., aminoglycosides, cisplatin, amphotericin B, foscarnet)

    • Acute myelogenous, monomyeloblastic, or lymphoblastic leukemia

  • Nonrenal causes of excess potassium loss

    • In patients with hypokalemia, urine potassium levels should be <25 mmol/24 hours. If levels drops to <15 mmol/L it implies extrarenal loss.

    • GI

      • Vomiting

      • Diarrhea (e.g., infections, malabsorption, radiation)

      • Drugs (e.g., laxatives [phenolphthalein], enemas, cancer therapy)

      • Neoplasms (e.g., villous adenoma of the colon, pancreatic VIPoma that produces VIP >200 pg/mL, Zollinger-Ellison syndrome)

      • Excessive spitting (sustained expectoration of all saliva in neurotic persons and to induce weight loss in professional wrestlers)

    • Skin

      • Excessive sweating

      • CF

      • Extensive burns

      • Draining wounds

    • Cellular shifts

      • Respiratory alkalosis

      • Classic periodic paralysis

      • Insulin

      • Drugs (e.g., bronchodilators, decongestants)

      • Accidental ingestion of barium compounds

      • Treatment of severe megaloblastic anemia with vitamin B12 or folic acid

      • Physiologic (e.g., highly trained athletes)

    • Diet

      • Severe eating disorders (e.g., anorexia nervosa, bulimia)

      • Dietary deficiency

    • Delirium tremens

    • In neonates—asphyxia, alkalosis, renal tubular acidosis, iatrogenic (glucose and insulin), diuretics

  • Major causes of hypokalemia with hypertension:

    • Diuretic drugs (e.g., thiazides)

    • Primary aldosteronism

    • Secondary aldosteronism (renovascular disease, renin-producing tumors)

    • Cushing syndrome

    • Malignant hypertension

    • Renal tubular acidosis


  • Laboratory artifacts

    • Hemolysis during venipuncture, conditions associated with thrombocytosis or leukocytosis, incomplete separation of serum and clot, double spinning (respinning) of blood collection tubes

    • Arm in upward position while collecting blood

    • Betadine application

    • Laboratory order of draw (lavender top tubes drawn before serum chemistry tubes)

    • Drawing above IV site

    • Vigorously mixed tubes

    • Collection techniques

    • Traumatic draw

    • Pneumatic tube system issues: speed too high, unpadded canisters, excessive agitation

    • Delay in processing

    • Centrifuging at too high G force

    • Increased heat exposure in centrifuge

    • Chilling whole blood beyond 2 hours

    • Prolonged tourniquet use and hand exercise when drawing blood

  • Potassium value can be elevated approximately 15% in slight hemolysis (Hb ≤50 mg/dL) and elevated approximately 30–50% in moderate hemolysis (Hb >100 mg/dL). Therefore, potassium status can be assessed in those with slight hemolysis but not in those with moderate hemolysis.

  • Excess dietary intake or rapid potassium infusion.

  • Drugs with high potassium content (e.g., 1 million units of penicillin G potassium contains 1.7 mmol of potassium).

  • Transfusion of old blood.