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Potassium Management

Potassium Management. Courtney Nelson DO HOIII UNMC Family Med. Potassium Pearls. A healthy adult has roughly 50 mEq/Kg of K+ in his/her body. 70 Kg man = 70x50 = 3500 mEq in body Only 2% is found outside the cells and of this only 0.4% of your K+ is found in the plasma.

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Potassium Management

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  1. Potassium Management Courtney Nelson DO HOIII UNMC Family Med.

  2. Potassium Pearls • A healthy adult has roughly 50 mEq/Kg of K+ in his/her body. • 70 Kg man = 70x50 = 3500 mEq in body • Only 2% is found outside the cells and of this only 0.4% of your K+ is found in the plasma. • Thus as you can see serum K+ measurements have limitations at reflecting TOTAL body K+ stores. • A 1 mEq/L drop in K+ reflects between 200-400 mEq total body K+ deficit • Example: a K+ of 2.5 means that someone is roughly 300 mEq in the negative. This would require 7 boluses of 40 mEQ of K+ to make up for this!

  3. Hypokalemia • Clinical consequences of hypokalemia usually goes unnoticed. Common findings include weakness, fatigue, constipation, ileus, and respiratory muscle dysfunction. • Thus, most of the time K+ gets replaced out of habit or to please the consultants. (e.g. Cardiology likes a K+ of 4.0 or above in MI patients.)

  4. Don’t Forget about EKG • ST depressions with prominent U waves and prolonged repolarization

  5. Hypokalemia - Causes • Do you need to go through a large workup every time the K+ is less than 3.5? NO • Usually the reason can be easily obtained from the history as there are a lot of reasons to have hypokalemia in the hospital. (NG tubes, vomitting, lasix…) Thus, most of the time we just treat the low potassium. • Having said that let us discuss the causes because in cases of severe or recurrent hypokalemia having a good approach to find the cause is helpful.

  6. Hypokalemia - Causes • Spurious - i.e. K+ is falsely low • Redistribution – i.e. movement into cells • Extrarenal loss – usually associated with preservation of renal K+ • Renal loss – often associated with acid-base disturbances.

  7. Spurious Hypokalemia • Marked leukocytosis and blood tube that has been sitting at room temp too long gives time for K+ to enter the white blood cells and thus falsely lower K+ value. • Insulin given just prior to blood draw allows a small amount (about 0.3 mEq) to shift into cells in the blood tube.

  8. Redistribution Hypokalemia • Alkalosis (response H+ out K+ in) – a key point is that alkalosis disorders are usually involved in depletion of total body K+ in addition to redistribution. • Increased B adrenergic effect – increases Na/K ATPase activity. Think of both medications or increased sympathetic tone like MI, head trauma, DTs, and theophylline toxicity.

  9. Redistribution Hypokalemia • Familial hypokalemic periodic paralysis (autosomal dominant) – causes recurrent episodes of flaccid paralysis in childhood. often precipitated by rest after exercise, stress, or a carbohydrate meal, events that are often associated with increased release of epinephrine or insulin • Hypokalemic periodic paralysis of thyrotoxicosis. Complication of excess T4/T3. Similar sx as above.

  10. Redistribution Hypokalemia • Other causes of hypokalemia due to cell entry include risperidone, quetiapine, and cesium hypothermia, barium intoxication, chloroquine intoxication.

  11. Extrarenal K+ Loss Urine K+ < 20 mEq/24 hours or spot urine K+ of < 30 • Diarrhea – causes loss of HCO3 and K+ thus you get metabolic acidosis + hypokalemia. • Chronic Laxative Abuse • Sweat – 9 mEq/L of K+ in sweat. • Fasting/inadequate diet – usually no more than total body deficit of 300 mEq. • Villous adenoma at rectosigmoid

  12. Renal K+ LossUrine K+ >20 mEq/24 hours or spot urine K+ of > 30 • Renal hypokalemia with metabolic acidosis • RTA type I (distal) and type II (proximal • DKA • Carbonic anhydrase inhibitor therapy • ureterosigmoidostomy

  13. Renal K+ LossUrine K+ >20 mEq/24 hours or spot urine K+ of > 30 • Renal hypokalemia with metabolic alkalosis: • Almost always occurs with hypokalemia because virtually every cause of metabolic alkalosis also causes hypokalemia. • The excess HCO3 acts as a poorly reabsorbable anion and carries more Na+ to the collecting tubules leading to increased Na-K exchange and urinary K loss.

  14. Renal K+ LossUrine K+ >20 mEq/24 hours or spot urine K+ of > 30 • Renal hypokalemia with no acid-base disorder: • Recovery from ARF, postobstructive diuresis, and osmotic diuresis, PCNs all increase Na delivery to collecting tubules resulting in increased K excretion. • Low magnesium- think of with resistant cases. Hypomagnesemia is present in up to 40% of patients with hypokalemia

  15. Treatment • If a person is eating do we need to give K+ in our fluids? No • Is IV the best route for replacement? No • If a person’s K+ level is 2.5 and they are 300 meq down, you will have to run 7 bags of ½ NS with 40 meq/L of KCL to approach this deficit! (assuming no ongoing losses)

  16. Treatment • In otherwise stable patients: the preferred method is oral replacement with divided doses over several days with frequent determinations of K+. • KCL most commonly used. • Thus, 20 mEq KCL bid or tid for K+ of 3.0-3.5. • And, 40 mEq KCL bid or tid for K+ of 2.5-3.0.

  17. Treatment • If not able to take PO or severe hypokelemia: then have K+ added to the NS or ½ NS. • KCL comes in ampules of concentrated solution (1-2 mEq/ml of K+) that are added to a dilutent (NS or ½ NS). • You can order 10 mEq of K+ to be added to 100 ml of NS or ½ NS and you with have highly concentrated solution of potassium (100 meq/L). • Any concentration of 30 meq/L is irritating to the veins. (note: but sometimes necessary)

  18. Treatment • Rule: Do not infuse more than 10 meq of K+ per hour! • So, if you have your bag of 10 meq K+ in 100 ml NS you could run this over an hour. • If you put 40 meq of K+ in 400 ml of NS you could run this in over 4 hours.

  19. Hyperkalemia • Remember that total body K+ is roughly 50 mEq/kg and only a small fraction if found outside the cells. • Contrary to struggling to try to replae a low K+ with mEq after mEq and watching it slowly climb into the normal range; only a small shift if intracellular K+ to the extracellular space or a small amount of K+ given to a person with a bad kidneq can cause quick problems. • To get a serum K+ rise by 1 meq/L you only need to give 100-200 meq of extra K+.

  20. Code Blue

  21. EKG Changes Note the “tented” or “pinched” shape to Twaves

  22. Acute Treatment • Calcium Gluconate 10 ml of 10% solution (1gram) IV slowly over 5-10 min. • Temporarily (1 hour) antagonizes cardiac effects of hyperkalemia while more definitive therapy is begun. • Warning: may induce Digitalis toxicity! • May precipitate if given with NaHCO3. • May repeat after 5 min. if ECG does not improve.

  23. Digoxin interacts heavily with K+, Na+ and Ca2+

  24. Acute Treatment • Glucose/Insulin – 100 ml of 25% glucose solution with 10 units of Regular insulin. Infuse over 15-30 minutes. • Temporarily translocates K+ into cells. • Effect occurs w/in 30-60 min and lasts about 1 hr. • May induce hyperglycemia, thus if already hyperglycemic just use insulin.

  25. Acute Treatment • Beta 2 agonists (Albuterol) - 10-20 mg over 15 minutes via nebulizer. • Potentially dangerous in patients with coronary artery disease! • Onset 30 minutes.

  26. Acute Treatment • Lasix – 40 to 80 mg IV. • Especially helpful in aldosterone deficiency states and renal failure. • NaHCO3 – 1 standard amp (50mEq) IV over 5-10 min. • Mostly used with acidemic states. • Will precipitate with Calcium!!!! Thus don’t give while using calcium gluconate.

  27. Acute Treatment • Kayexalate (Sodium Polystyrene Sulfonate) – 15 g ORALLY 1 to 4 times daily as a slurry in water or syrup. • Onset 2-24 hours with duration of 4-6 hours. • Effect—In the intestine (mostly the large intestine), Na ions are released and are replaced by K+ and other cations before the resin is passed from the body. • Each gram may remove 1 mEq K+ in exchange for 1-2 mEq Na+ thus may cause ECF volume overload.

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