Definition
- 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.
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TABLE 16 " “67Normal Range for PotassiumView LargeTABLE 16 " “67Normal Range for Potassium From Age Reference Range (mmol/L) Critical Range (mmol/L) 0 " “4 mo 4.0 " “6.2 <2.6 >7.5 4 mo " “1 y 3.7 " “5.6 <2.6 >7.5 >1 y 3.5 " “5.3 <3.0 >6.2
Use
- 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
Interpretation
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
- Drugs (e.g., spironolactone, triamterene, amiloride)
- Hyperkalemic type of distal RTA (e.g., sickle cell disease, obstructive uropathy)
- 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
Limitations
- 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.