Potassium Management

1. Potassium Management Marica A. Lazo , MD

2. Potassium Pearls Potassium is the major intracellular cation . 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 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. Symptoms seldom occur unless plasma K+ is less than 3.0 mmol /L.

4. ECG changes ST depressions with prominent U waves and prolonged repolarization

5. ECG changes

6. Hypokalemia - Causes Spurious - i.e. K+ is falsely low Diminished intake 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 Transcellular shift 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+ 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

13. 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 Na-K exchange and urinary K loss.

14. 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

15. HYPOKALEMIA Consider poor intake (Urine K < 10 meq /L) Consider shift (alkalosis, Beta 2 agonists, insulin, HPP) Serum HCO 3 < 24 meq /L > 24 meq /L

16. Serum HCO 3 < 24 meq /L HYPOKALEMIA

17. Serum HCO 3 > 24 meq /L HYPOKALEMIA 2 Hyperaldo 1 Hyperaldo

18. Urinary K+: > 20 mEq /L – Renal loss Urinary K + : < 20 mEq /L – Extrarenal loss TTKG : Transtubular Potassium Gradient ( Urine K+ / Plasma K+ ) ( Urine Osm / Plasma Osm ) TTKG : Renal loss : > 4 Extra renal loss : < 4 Renal Vs Extra renal loss

19. Treatment Therapeutic goals Prevent life-threatening complications (arrhythmias, respiratory failure, hepatic encephalopathy) Correct the K+ deficit Minimize ongoing losses Treat the underlying cause

20. Treatment K+ deficit (4 – Actual K+) x 300 2 (4 – 2.5) x 300 = 225 meqs 2 Estimation of K+ deficit 3.0 meq /L= total body K+ deficit of 200-400 meq /70kg 2.5 meq /L = 500 meq /70kg 2.0 meq /L = 700 meq /70kg

21. Treatment Oral therapy Generally safer Degree of K+ depletion does not correlate well with the plasma K+ KCl is usually the preparation of choice Kalium durule : 1 durule = 10 meqs KCl KCl syrup: 1meq/mL Ie . Kalium durule 750mg TID PO x 2-3days or KCl syrup 15-30cc TID

22. Treatment IV therapy For severe hypokalemia or those who are unable to take anything by mouth Maximum rate at which potassium is infused into peripheral veins is usually 10 meq / hr Central – 20 meq / hr Rate of infusion should not exceed 20 meq /hour unless paralysis or malignant ventricular arrhythmias are present Ie . 40 meqs KCl in 230cc PNSS x 5meq/ hr (32cc/ hr ) OR 20 meqs KCl in 100cc PNSS x 1hr

23. Case #1 43 yo male, with no comorbids , came in at the ER due to 3 day history of vomiting. He claimed to have eaten seafoods at a party 4 days ago. PE: Laboratories: CBC Na 130 K 2.7

24. 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)

25. 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.

26. 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)

27. 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.

28. 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 replace a low K+ with mEq after mEq and watching it slowly climb into the normal range; only a small shift of intracellular K+ to the extracellular space or a small amount of K+ given to a person with a bad kidney 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+.

29. Hyperkalemia The most serious effect of hyperkalemia is cardiac toxicity Hyperkalemia partially depolarizes the cell membrane, which impairs membrane excitability and is manifest as weakness that may progress to flaccid paralysis and hypoventilation if the respiratory muscles are involved

30. Hyperkalemia - Causes Increased K+ intake Rarely the sole cause Iatrogenic hyperkalemia may result from overzealous parenteral K+ replacement or in patients with renal insufficiency Pseudohyperkalemia Artificially elevated plasma K+ due to K+ movement out of the cells immediately before or following venipuncture

31. Hyperkalemia - Causes Transcellular shift Tumor lysis syndrome and rhabdomyolysis lead to K+ release from cells Metabolic acidosis can be associated with mild hyperkalemia resulting from intracellular buffering of H+ Insulin deficiency and hypertonicity promote K + shift from the ICF to the ECF

32. HYPERKALEMIA PSEUDOHYPERK K RETENTION REDISTRIBUTION GFR < 20 ml/min GFR > 20 ml/min