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What are the normal body stores of Potassium?

  • Normal body stores (70 kg adult) are 3000 to 4000 meq K+ (50-55 meq/kg)
  • 98% of K+ is INTRACELLULAR
    • Maintains gradient


What is the intracellular concentration of K+?

140 mEq/L


What is the extracellular concentration of K+?

4-5 mEq/L


What is the average daily intake of K+? What if you are not getting enough?

  • Daily intake averages 40-120 meq
  • If you’re not getting enough K+ in → kidney can reduce K+ excretion to less than 15-25 meq/day


What is the reflected total body deficit if K+ decreased by 1 mEq/L?

(normal serum/plasma K+ 4-5 mEq/L)

200-400 mEq


What is the reflected total body excess if K+ increased by 1 mEq/L?

(normal serum/plasma K+ 4-5 mEq/L)

100-200 mEq


What is the function of K+?

  • Cellular function: role in protein & glycogen synthesis
  • Maintains RMP in muscle cells and neurons
    • via 3:2 Na+/K+ ATPase
  • Determines membrane excitability;
    • allows actions potentials to be generated


What are symptoms of low or high K+?

  • Relates to inability to generate action potentials in muscles
  • Cramps, Muscle weakness/paralysis:  starts in legs
    • Clinical pearl: “My legs are weak” (esp. if CKD) → K+ is high
  • EKG changes & Cardiac Arrhythmias
    • PAC’s, PVC’s, bradycardia, atrial or junctional tachycardia, AV block, v-tach/v-fib
  • Low K+ can look same as high K+


What EKG changes are present in Hypokalemia?

  • PR interval prolongation
  • ST depression
  • Flattened or inverted T waves
  • U-waves
  • QRS widening


What EKG changes are present in Hyperkalemia?

  • PR interval prolongation
  • Elevated T waves
  • Widened QRS interv


How does calcium modify the K+ effects on action potentials?

  • Hypercalcemia increases threshold potential and protects against hyperkalemia
    • which has decreased resting potential
    • “Every time you see the QRS widen, give an amp of calcium” → prevents cardiac arrest (lasts 10-15 min)


How does metabolic acidosis modify the K+ effects on action potentials?

  • Exacerbates hyperkalemia by causing K+ to be released from cells as HCl is buffered into cells
    • Correct with bicarb


How does Potassium effect digoxin levels?

    • HYPOkalemia increases digoxin toxicity 
    • digoxin toxicity causes HYPERkalemia
      • Digoxin disables Na+/K+ ATPase


How is the balance between intracellular and extracellular K+ regulated?

  • Distribution of K+ between cells and extracellular fluid
    • concentration dependent
      • The higher the K+, the more K+ is going to shift into the cells
    • Acid-base status dependent
    • Insulin/catecholamines move K into cells


How does the K+ that you drink in a glass of Orange Juice distribute between the cells and extracellular fluid?

  • Glass of OJ:  40 mEq K+ → 40 meq distributed in 17 L (EC volume of 70 kg male) K+ would increase 2.4 mEq/L
  • K+ distributed rapidly into cells
    • Catecholamines & insulin increase activity of Na+/K+ ATPase → uptake of K+ into skeletal muscle & liver
    • High K+ concentration causes passive movement of K+ into cells


How does potassium shift during states of acidemia and alkalosis?

  • Acidemia:  K+ moves out of cells as H+ is buffered into cells
  • Alkalosis:  K+ moves into cells as H+ is buffered into the extracellular fluid


What determines K+ secretion in the kidney?

  • Plasma K+ concentration
  • Urine flow in distal tubule (permissive)
  • Aldosterone: 
    • causes K+ secretion by principal cells of collecting tubule – outer medulla, cortical & inner medulla


What are the causes of Hypokalemia?

  • Decreased K+ intake (rare)
    • Poverty
    • Hypocaloric liquid protein diet supplements
    • Exacerbated by diuretics for HTN
    • Clay ingestion (a southern phenomenon) 
  • Increased K+ entry into cells
    • Metabolic alkalosis, hyperinsulinemia, increased catecholamines/beta agonists
  • Increased GI losses
    • Nausea/vomiting →exacerbated by metabolic alkalosis & urinary K+ losses
    • Nasogastric (NG) tube suction
    • Diarrhea/intestinal fistulas/tube drainage
  • Increased urinary losses
    • Increased distal flow d/t impaired salt & water reabsorption
      • Diuretics 
      • Salt wasting nephropathies
      • Polydipsia/polyuria
      • Hypercalcemia → increased distal flow
      • Mineralcorticoid excess – aldosterone producing tumor
    • Hypomagnesemia – affects # K channels
  • Increased sweat losses
  • Dialysis


How do you evaluate hypokalemia if the cause is not obvious by history and physical?

  • Determine if loss is GI or renal (GI losses should be obvious, except in cases of anorexia/bulemia/laxative abuse)
  • 24 hour urine K+ when hypokalemic
    • Kidney can decrease urine excretion of K+ to 25-30 meq in 24 hours
    • If urine K is low, then loss is not from kidney
  • Acid/base status: acidosis or alkalosis


What are the possible acid-base etiologies for hypokalemia with low urinary K+?

  • Low urinary K+ (therefore GI losses)
    • Acidosis:  lower GI losses
      • laxatives/villous adenoma
    • Alkalosis: upper GI losses
      • Vomiting


What are the possible acid-base etiologies for hypokalemia with high urinary K+?

  • High urinary K+ (therefore kidney losses)
    • Acidosis = ketoacidosis, type I or II renal tubular acidosis
    • Alkalosis: 
      • Normotensive: vomiting  (GI loss, but high urinary K+ due to urinary bicarb excretion with metabolic alkalosis), diuretics (early), Bartter’s syndrome (Inherited)
      • Hypertension
        • High renin = diuretics, renovascular disease, reninoma, Cushings
        • Low renin – measure aldosterone
        • Low aldosterone = exogenous mineralcorticoid (real licorice)
        • High aldosterone = adrenal adenoma or hyperplasia


What are the major complications of Hypokalemia?

  • Muscle weakness, cramps, cardiac arrhythmias, rhabdomyolysis (K+ < 2.5 mEq/L)
  • Renal dysfunction – common in someone w/ anorexia/bulimia or somebody who is abusing diuretics or Bartter’s
    • Loss of urinary concentrating ability
    • Increase in urinary NH3 and NH4+ production/excretion 
    • Hypokalemic nephropathy/Interstitial fibrosis
  • Hypertension – low K+ diet causes uptake of Na+


What is the treatment for Hypokalemia?

  • Replace K+ → get patient out of danger initially
    • then more gradually replace entire K deficit
  • K+ deficit can only be approximated  
    • 200-400 mEq for each 1 mEq/L drop in K+
    • Below 2, K+ deficit can be much greater due to shifts out of cells to compensate
  • Treat underlying cause of low potassium
  • Potassium replaced orally or IV


What are the three causes of hyperkalemia?

1. Increased Intake:  oral or IV

2. Shift:  Movement from cells into extracellular fluid

3. Decreased urinary excretion


How does the body adapt to increase K+?

  • Normal kidney function – kidneys can adapt to excrete as much as 5x the normal K+ intake (400 meq/day)
  • Chronic Kidney Disease (CKD) = reduced nephron mass, each nephron works harder
    • Increased K+ excretion per nephron as long as distal urine flow is maintained and aldosterone secretion occurs


How can serum K+ be elevated even when total body K+ is normal?

  • Potassium shifts from IC → EC
    • Muscle/tissue breakdown
      • rhabdomyolysis
      • necrotic tissue from gangrene
    • Insulin deficiency with hyperglycemia
    • Metabolic acidosis (K+ moves out of cells)
    • Drugs: 
      • Succinylcholine (paralytic agent)
      • Beta-blockers (anti-catecholamines)
      • Digoxin


What three things cause Hyperkalemia due to decreased urinary excretion?

  • Renal failure: most common cause
  • Effective circulating volume depletion
    • Decreased distal flow
  • Hypoaldosteronism
    • decreased adrenal synthesis (Addison's)
    • decreased RAAS


What is the best way to treat Hyperkalemia?

  • Antagonize K+ effects (seconds/minutes)
    • Calcium IV
  • Shift K+ into cells  (minutes)
    • Glucose & insulin
    • NaHCO3 (make them alkalemic)
    • Beta-agonists:  albuterol nebs
    • 3% NaCl if hyponatremia present
  • Remove excess K+ (hours)
    • Loop diuretics if patient makes urine (Lasix)
    • Cation-exchange resins (kayexalate): avoid rectal use
      • Can cause ischemic bowel
    • Hemodialysis/peritoneal dialysis


When trying to figure out the underlying cause of Hypokalemia/Hyperkalemia, where should you look first?

Look primarily to adrenal glands (mineralcorticoids) and kidneys for causes:  not usually dietary cause


What mechanisms control distal tubule secretion of K+?

  • Principal cells – Luminal membrane:  Na+ & K+ channels; Basolateral membrane:  Na-K ATPase
  • Aldosterone (released in response to 0.1 meq/l increase in K+)
    • Increases # of open Na+ & K+ channels and increases activity of Na-K ATPase
  • K+ concentration in blood – gradient
  • Distal urine flow is permissive to excretion of K+