EXTRACELLULAR FLUID POTASSIUM CONCENTRATION

• Extracellular fluid potassium concentration is normally maintained at about 4.2 mEq/L.
• Potassium concentration usually changes by no more than ±0.3 mEq/L.
• Precise potassium regulation is essential because many cell functions depend on it.
• Even a small increase in plasma potassium can affect the heart.
• An increase of only 3–4 mEq/L may cause cardiac arrhythmias.
• Severe hyperkalemia can cause cardiac arrest or ventricular fibrillation.
• Less than 2% of total body potassium is present in the extracellular fluid.
• More than 98% of total body potassium is located inside cells.
• Therefore, extracellular potassium concentration can change rapidly if potassium moves between compartments.
• A typical meal may contain about 50 mEq of potassium.
• Daily potassium intake usually ranges from 50–200 mEq/day.
• Failure to rapidly remove excess potassium from extracellular fluid can cause life-threatening hyperkalemia.
• Small losses of extracellular potassium can cause severe hypokalemia if not corrected quickly.
• Potassium balance depends mainly on the kidneys.
• Only a small amount of potassium is excreted in the feces.
• The kidneys must rapidly adjust potassium excretion according to intake.
• Precise renal regulation is essential for maintaining normal potassium balance.
• Potassium distribution between extracellular and intracellular compartments is a major part of potassium homeostasis.
• Cells act as a storage site for excess extracellular potassium during hyperkalemia.
• Cells can release potassium during hypokalemia.
• Potassium shifting between cells and extracellular fluid provides the first line of defense against changes in plasma potassium concentration.
• Skeletal muscle is the body’s largest potassium reservoir.
• Skeletal muscles normally contain 60–75% of total body potassium.
• Muscle potassium storage depends on factors such as sex, age, and physical activity.

KEY CONCEPT

• Potassium is tightly regulated because small changes can cause serious cardiac problems.
• More than 98% of body potassium is intracellular.
• Cells provide the first line of defense by rapidly shifting potassium between compartments.
• Kidneys provide long-term potassium balance by adjusting potassium excretion.
• Skeletal muscle is the major storage site for body potassium.

REGULATION OF INTERNAL POTASSIUM DISTRIBUTION

• After a potassium-rich meal, potassium must rapidly move into cells to prevent dangerous hyperkalemia.
• If ingested potassium remained in the extracellular fluid, plasma potassium concentration would rise significantly.
• Most absorbed potassium quickly shifts into cells until the kidneys remove the excess.
• Between meals, cells release potassium to replace the potassium excreted by the kidneys.
• Internal potassium redistribution helps maintain a nearly constant plasma potassium concentration.
• Extracellular potassium concentration is tightly regulated around 4.2 mEq/L.
• Small changes in extracellular potassium can significantly affect cell function.
• Even a modest increase in plasma potassium can cause cardiac arrhythmias.
• Severe hyperkalemia may cause cardiac arrest or ventricular fibrillation.
• More than 98% of body potassium is located inside cells.
• Less than 2% is present in extracellular fluid.
• Because extracellular potassium is very small, even minor potassium shifts can greatly alter plasma potassium concentration.
• Potassium balance depends mainly on renal excretion.
• The kidneys must rapidly adjust potassium excretion according to intake.
• Cellular potassium shifts and renal excretion work together to maintain potassium homeostasis.
• Cells serve as a reservoir for potassium.
• During hyperkalemia, cells take up excess extracellular potassium.
• During hypokalemia, cells release potassium into the extracellular fluid.
• Potassium redistribution between cells and extracellular fluid provides the first line of defense against potassium imbalance.

FACTORS AFFECTING INTERNAL POTASSIUM DISTRIBUTION

INSULIN

• Insulin stimulates potassium uptake into cells.
• Insulin increases Na⁺-K⁺ ATPase activity.
• After a meal, insulin helps move potassium from extracellular fluid into cells.
• Insulin deficiency causes a greater rise in plasma potassium after eating.
• Insulin administration can correct hyperkalemia.
• Excess insulin may cause hypokalemia.

ALDOSTERONE

• Aldosterone increases potassium uptake into cells.
• Aldosterone stimulates Na⁺-K⁺ ATPase activity.
• Aldosterone also increases renal potassium secretion.
• Insulin and aldosterone work together to promote cellular potassium uptake after a potassium-rich meal.
• Excess aldosterone (Conn syndrome) commonly causes hypokalemia.
• Aldosterone deficiency (Addison disease) commonly causes hyperkalemia.

β-ADRENERGIC STIMULATION

• Epinephrine promotes movement of potassium into cells.
• This effect occurs through stimulation of β₂-adrenergic receptors.
• β₂ stimulation increases Na⁺-K⁺ ATPase activity.
• β-blockers reduce cellular potassium uptake.
• β-blockers increase the tendency toward hyperkalemia.

ACID–BASE DISTURBANCES

• Metabolic acidosis causes potassium to move out of cells.
• Acidosis increases extracellular potassium concentration.
• Acidosis reduces Na⁺-K⁺ ATPase activity.
• Reduced cellular potassium uptake contributes to hyperkalemia.
• Metabolic alkalosis causes potassium to move into cells.
• Alkalosis decreases extracellular potassium concentration.
• Alkalosis can contribute to hypokalemia.

CELL LYSIS

• Cell destruction releases large amounts of intracellular potassium.
• Potassium released from damaged cells increases extracellular potassium concentration.
• Severe tissue injury can cause significant hyperkalemia.
• Red blood cell destruction can also cause hyperkalemia.

STRENUOUS EXERCISE

• Exercise causes potassium release from skeletal muscle.
• This release may increase extracellular potassium concentration.
• Hyperkalemia after exercise is usually mild.
• Intense exercise can occasionally cause clinically significant hyperkalemia.
• The risk is greater in patients with insulin deficiency or those taking β-blockers.
• Severe exercise-induced hyperkalemia may cause cardiac toxicity.

DEHYDRATION AND INCREASED EXTRACELLULAR OSMOLARITY

• Increased extracellular osmolarity causes water to move out of cells.
• Cellular dehydration increases intracellular potassium concentration.
• Increased intracellular potassium promotes potassium diffusion out of cells.
• This process raises extracellular potassium concentration.
• Decreased extracellular osmolarity has the opposite effect.
• Potassium moves into cells when extracellular osmolarity falls.

KEY CONCEPT

• Internal potassium redistribution provides the first line of defense against changes in plasma potassium concentration.
• Insulin, aldosterone, and β₂-adrenergic stimulation shift potassium into cells.
• Acidosis, cell lysis, strenuous exercise, and dehydration shift potassium out of cells.
• More than 98% of body potassium is intracellular, making cells the major potassium reservoir.
• Kidneys provide long-term potassium balance, while cellular shifts provide rapid short-term regulation.