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. 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!

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.)

Dont Forget about EKG

ST depressions with prominent U waves and prolonged repolarization

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.

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.

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.

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.

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.

Redistribution Hypokalemia

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

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

Renal K+ Loss
Urine 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

Renal K+ Loss
Urine 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 NaK exchange and urinary K loss.

Renal K+ Loss
Urine 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

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 persons K+ level is 2.5 and they are 300 meq down, you will have to run 7 bags of NS with 40 meq/L of KCL to approach this deficit! (assuming no ongoing losses)

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.

Treatment

If not able to take PO or severe hypokelemia: then have K+ added to the NS or NS.

KCL comes in ampules of concentrated solution (1-2 mEq/ml of K+) that are added to a dilutent (NS or NS). You can order 10 mEq of K+ to be added to 100 ml of NS or 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)

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.

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+.

Code Blue

EKG Changes
Note the tented or pinched shape to Twaves

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.

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

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.

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.

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 dont give while using calcium gluconate.

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. EffectIn 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.