potassium management

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  • 1. Potassium Management Marica A. Lazo, MD

2. Potassium PearlsO Potassium is the major intracellular cation.O A healthy adult has roughly 50 mEq/Kg of K+ inhis/her body. O 70 Kg man = 70x50 = 3500 mEq in bodyO Only 2% is found outside the cells and of this only0.4% of your K+ is found in the plasma. O Thus serum K+ measurements have limitations atreflecting TOTAL body K+ stores.O A 1 mEq/L drop in K+ reflects between 200-400 mEqtotal body K+ deficit O Example: a K+ of 2.5 means that someone isroughly 300 mEq in the negative. This wouldrequire 7 boluses of 40 mEQ of K+ to make up forthis! 3. HypokalemiaO Clinical consequences of hypokalemiausually goes unnoticed.O Common findings include weakness,fatigue, constipation, ileus, and respiratorymuscle dysfunction.O Symptoms seldom occur unless plasmaK+ is less than 3.0 mmol/L. 4. ECG changesO ST depressions with prominent U waves and prolonged repolarization 5. ECG changes 6. Hypokalemia - CausesO Spurious - i.e. K+ is falsely lowO Diminished intakeO Redistribution i.e. movement into cellsO Extrarenal loss usually associated withpreservation of renal K+O Renal loss often associated with acid-base disturbances. 7. Spurious HypokalemiaO Marked leukocytosis and blood tube thathas been sitting at room temp too longgives time for K+ to enter the white bloodcells and thus falsely lower K+ value.O Insulin given just prior to blood drawallows a small amount (about 0.3 mEq) toshift into cells in the blood tube. 8. Redistribution HypokalemiaO Transcellular shiftO Alkalosis (response H+ out K+ in) a keypoint is that alkalosis disorders are usuallyinvolved in depletion of total body K+ inaddition to redistribution.O Increased B adrenergic effect increasesNa/K ATPase activity. Think of bothmedications or increased sympathetictone like MI, head trauma, DTs, andtheophylline toxicity. 9. Redistribution HypokalemiaO Other causes of hypokalemia due to cell entry include risperidone, quetiapine, and cesium, hypothermia, barium intoxication, chloroquine intoxication. 10. Extrarenal K+ LossUrine K+ < 20 mEq/24 hours or spot urine K+ of < 30O Diarrhea causes loss of HCO3 and K+thus you get metabolic acidosis +hypokalemia.O Chronic Laxative AbuseO Sweat 9 mEq/L of K+ in sweat.O Fasting/inadequate diet usually no morethan total body deficit of 300 mEq.O Villous adenoma at rectosigmoid 11. Renal K+ LossUrine K+ >20 mEq/24 hours or spot urine K+ of > 30O Renal hypokalemia with metabolicacidosis O RTA type I (distal) and type II (proximal) O DKA O Carbonic anhydrase inhibitor therapy O ureterosigmoidostomy 12. Renal K+ LossUrine K+ >20 mEq/24 hours or spot urine K+ of > 30O Renal hypokalemia with metabolicalkalosis: O Almost always occurs with hypokalemia because virtually every cause of metabolic alkalosis also causes hypokalemia. O 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. 13. Renal K+ LossUrine K+ >20 mEq/24 hours or spot urine K+ of > 30O Renal hypokalemia with no acid-basedisorder: O Recovery from ARF, postobstructive diuresis, and osmotic diuresis, PCNs all increase Na delivery to collecting tubules resulting in increased K excretion. O Low magnesium- think of with resistant cases. Hypomagnesemia is present in up to 40% of patients with hypokalemia 14. Renal Vs Extra renal loss 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 : > 4Extra renal loss : < 4 15. TreatmentO Therapeutic goalsO Prevent life-threatening complications(arrhythmias, respiratory failure, hepaticencephalopathy)O Correct the K+ deficitO Minimize ongoing lossesO Treat the underlying cause 16. TreatmentO K+ deficit O (4 Actual K+) x 300 2 O (4 2.5) x 300 =225 meqs2O Estimation of K+ deficit O 3.0 meq/L= total body K+ deficit of 200-400 meq/70kg O 2.5 meq/L = 500 meq/70kg O 2.0 meq/L = 700 meq/70kg 17. TreatmentO Oral therapyO Generally saferO Degree of K+ depletion does not correlatewell with the plasma K+O KCl is usually the preparation of choiceO Kalium durule: 1 durule = 10 meqs KClO KCl syrup: 1meq/mLO Ie. Kalium durule 750mg TID PO x 2-3days or KCl syrup 15-30cc TID 18. TreatmentO IV therapyO For severe hypokalemia or those who areunable to take anything by mouthO Maximum rate at which potassium is infusedinto peripheral veins is usually 10 meq/hrO Central 20 meq/hrO Rate of infusion should not exceed 20meq/hour unless paralysis or malignantventricular arrhythmias are presentO Ie. 40 meqs KCl in 230cc PNSS x 5meq/hr(32cc/hr) OR 20 meqs KCl in 100cc PNSS x1hr 19. HyperkalemiaO Remember that total body K+ is roughly50 mEq/kg and only a small fraction iffound outside the cells.O Contrary to struggling to try to replace alow K+ with mEq after mEq and watchingit slowly climb into the normal range; onlya small shift of intracellular K+ to theextracellular space or a small amount ofK+ given to a person with a bad kidneycan cause quick problems.O To get a serum K+ rise by 1 meq/L youonly need to give 100-200 meq of extraK+. 20. HyperkalemiaO The most serious effect of hyperkalemia iscardiac toxicityO Hyperkalemia partially depolarizes the cellmembrane, which impairs membraneexcitability and is manifest as weaknessthat may progress to flaccid paralysis andhypoventilation if the respiratory musclesare involved 21. Hyperkalemia - CausesO Increased K+ intakeO Rarely the sole causeO Iatrogenic hyperkalemia may result fromoverzealous parenteral K+ replacement orin patients with renal insufficiencyO PseudohyperkalemiaO Artificially elevated plasma K+ due to K+movement out of the cells immediatelybefore or following venipuncture 22. Hyperkalemia - CausesO Transcellular shiftO Tumor lysis syndrome and rhabdomyolysislead to K+ release from cellsO Metabolic acidosis can be associated withmild hyperkalemia resulting fromintracellular buffering of H+O Insulin deficiency and hypertonicitypromote K+ shift from the ICF to the ECF 23. HYPERKALEMIAPSEUDOHYPERKK RETENTIONREDISTRIBUTIONGFR < 20 ml/min GFR > 20 ml/minHemolysisRenal failure AcidosisThrombocytosis Insulin deficiency/DKALeukocytosis Beta blockersMononucleosis Aldosterone Tubular hyperK Periodic paralysis deficiencyAcquiredDigitalis intoxicationAddisons diseaseSLE SuccinylcholineRTA Type 4 Obstr. Uro. ExerciseDrugsAmyloidosis Tissue damage Heparin AIDS NSAIDsTID ACE inhibitorsDrugs Cyclosporine TrimethoprimK sparers 24. EKG ChangesNote the tented or pinched shape to Twaves 25. Acute TreatmentO Calcium Gluconate 10 ml of 10% solution (1gram) IV slowly over 5-10 min.O Decreases membrane excitabilityO Temporarily (1 hour) antagonizes cardiaceffects of hyperkalemia while moredefinitive therapy is begun.O Warning: may induce Digitalis toxicity!O May precipitate if given with NaHCO3.O May repeat after 5 min. if ECG does notimprove. 26. Acute TreatmentO Glucose/Insulin 100 ml of 25% glucosesolution with 10 units of Regular insulin.Infuse over 15-30 minutes.O Insulin stimulates cellular uptake of K+ byactivating Na+K+ATPase ( decreasing plasmaK+ )O Temporarily translocates K+ into cells.O Effect occurs w/in 30-60 min and lasts about 1hr.O May induce hyperglycemia, thus if alreadyhyperglycemic just use insulin. 27. Acute TreatmentO Beta 2 agonists (Albuterol) - 10-20 mgover 15 minutes via nebulizer.O Promotes cellular uptake of K+O Onset 30 minutes.O Lowers plasma K+ by 0.5-1.5 mmol/L andthe effect lasts for 2-4 hoursO Potentially dangerous in patients withcoronary artery disease! 28. Acute TreatmentO Lasix 40 to 80 mg IV.O Especially helpful in aldosterone deficiencystates and renal failure.O NaHCO3 1 standard amp (50mEq) IVover 5-10 min.O Can shift K+ into the cells.O Mostly used with acidemic states.O Will precipitate with Calcium!!!! Thus dontgive while using calcium gluconate. 29. Acute TreatmentO Kayexalate (Sodium Polystyrene Sulfonate) 15 g ORALLY 1 to 4 times daily as a slurry in water or syrup.O Onset 1-2 hours with duration of 4-6 hours.O EffectIn the intestine (mostly the largeintestine), Na ions are released and arereplaced by K+ and other cations beforethe resin is passed from the body.O Each gram may remove 1 mEq K+ inexchange for 1-2 mEq Na+ thus maycause ECF volume overload. 30. TREATMENT OF HYPERKALEMIAMEDICATIONMECHANISM OF DOSAGE PEAK EFFECTACTIONCalcium Antagonism of10-30 ml of 10%5 minutesgluconate membrane solution IV overactions10 minutesInsulin and Increased K entry 10 units insulin30-60 min.glucose to cellsplus 50 ml D20SodiumIncreased K entry 50 meq IV over 5 30-60 min.bicarbonate to cellsminutesAlbuterol Increased K entry 10-20 mg IV or30-60 min.to cellsnebulized

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