Potassium PearlsO Potassium is the major intracellular cation.O A healthy adult has roughly 50 mEq/Kg of K+ in his/her body. O 70 Kg man = 70x50 = 3500 mEq in bodyO Only 2% is found outside the cells and of this only 0.4% of your K+ is found in the plasma. O Thus serum K+ measurements have limitations at reflecting TOTAL body K+ stores.O A 1 mEq/L drop in K+ reflects between 200-400 mEq total body K+ deficit O 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!
HypokalemiaO Clinical consequences of hypokalemia usually goes unnoticed.O Common findings include weakness, fatigue, constipation, ileus, and respiratory muscle dysfunction.O Symptoms seldom occur unless plasma K+ is less than 3.0 mmol/L.
ECG changesO ST depressions with prominent U waves and prolonged repolarization
Hypokalemia - CausesO Spurious - i.e. K+ is falsely lowO Diminished intakeO Redistribution – i.e. movement into cellsO Extrarenal loss – usually associated with preservation of renal K+O Renal loss – often associated with acid- base disturbances.
Spurious HypokalemiaO 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.O Insulin given just prior to blood draw allows a small amount (about 0.3 mEq) to shift into cells in the blood tube.
Redistribution HypokalemiaO Transcellular shiftO 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.O 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 HypokalemiaO Other causes of hypokalemia due to cell entry include risperidone, quetiapine, and cesium, hypothermia, barium intoxication, chloroquine intoxication.
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 more than total body deficit of 300 mEq.O Villous adenoma at rectosigmoid
Renal K+ LossUrine K+ >20 mEq/24 hours or spot urine K+ of > 30O Renal hypokalemia with metabolic acidosis O RTA type I (distal) and type II (proximal) O DKA O Carbonic anhydrase inhibitor therapy O ureterosigmoidostomy
Renal K+ LossUrine K+ >20 mEq/24 hours or spot urine K+ of > 30O Renal hypokalemia with metabolic alkalosis: 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.
Renal K+ LossUrine K+ >20 mEq/24 hours or spot urine K+ of > 30O Renal hypokalemia with no acid-base disorder: 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
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 : > 4 Extra renal loss : < 4
TreatmentO Therapeutic goals O Prevent life-threatening complications (arrhythmias, respiratory failure, hepatic encephalopathy) O Correct the K+ deficit O Minimize ongoing losses O Treat the underlying cause
TreatmentO K+ deficit O (4 – Actual K+) x 300 2 O (4 – 2.5) x 300 = 225 meqs 2O 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
TreatmentO Oral therapy O Generally safer O Degree of K+ depletion does not correlate well with the plasma K+ O KCl is usually the preparation of choice O Kalium durule: 1 durule = 10 meqs KCl O KCl syrup: 1meq/mL O Ie. Kalium durule 750mg TID PO x 2-3days or KCl syrup 15-30cc TID
TreatmentO IV therapy O For severe hypokalemia or those who are unable to take anything by mouth O Maximum rate at which potassium is infused into peripheral veins is usually 10 meq/hr O Central – 20 meq/hr O Rate of infusion should not exceed 20 meq/hour unless paralysis or malignant ventricular arrhythmias are present O Ie. 40 meqs KCl in 230cc PNSS x 5meq/hr (32cc/hr) OR 20 meqs KCl in 100cc PNSS x 1hr
HyperkalemiaO Remember that total body K+ is roughly 50 mEq/kg and only a small fraction if found outside the cells.O 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.O To get a serum K+ rise by 1 meq/L you only need to give 100-200 meq of extra K+.
HyperkalemiaO The most serious effect of hyperkalemia is cardiac toxicityO 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
Hyperkalemia - CausesO Increased K+ intake O Rarely the sole cause O Iatrogenic hyperkalemia may result from overzealous parenteral K+ replacement or in patients with renal insufficiencyO Pseudohyperkalemia O Artificially elevated plasma K+ due to K+ movement out of the cells immediately before or following venipuncture
Hyperkalemia - CausesO Transcellular shift O Tumor lysis syndrome and rhabdomyolysis lead to K+ release from cells O Metabolic acidosis can be associated with mild hyperkalemia resulting from intracellular buffering of H+ O Insulin deficiency and hypertonicity promote K+ shift from the ICF to the ECF
HYPERKALEMIAPSEUDOHYPERK K RETENTION REDISTRIBUTION GFR < 20 ml/min GFR > 20 ml/minHemolysis Renal failure AcidosisThrombocytosis Insulin deficiency/DKALeukocytosis Beta blockersMononucleosis Aldosterone Tubular hyperK Periodic paralysis deficiency Acquired Digitalis intoxication Addison’s disease SLE Succinylcholine RTA Type 4 Obstr. Uro. Exercise Drugs Amyloidosis Tissue damage Heparin AIDS NSAIDs TID ACE inhibitors Drugs Cyclosporine Trimethoprim K sparers
EKG ChangesNote the ―tented‖ or ―pinched‖ shape to Twaves
Acute TreatmentO Calcium Gluconate 10 ml of 10% solution (1gram) IV slowly over 5-10 min. O Decreases membrane excitability O Temporarily (1 hour) antagonizes cardiac effects of hyperkalemia while more definitive 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 not improve.
Acute TreatmentO Glucose/Insulin – 100 ml of 25% glucose solution with 10 units of Regular insulin. Infuse over 15-30 minutes. O Insulin stimulates cellular uptake of K+ by activating Na+K+ATPase ( decreasing plasma K+ ) O Temporarily translocates K+ into cells. O Effect occurs w/in 30-60 min and lasts about 1 hr. O May induce hyperglycemia, thus if already hyperglycemic just use insulin.
Acute TreatmentO Beta 2 agonists (Albuterol) - 10-20 mg over 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 and the effect lasts for 2-4 hours O Potentially dangerous in patients with coronary artery disease!
Acute TreatmentO Lasix – 40 to 80 mg IV. O Especially helpful in aldosterone deficiency states and renal failure.O NaHCO3 – 1 standard amp (50mEq) IV over 5-10 min. O Can shift K+ into the cells. O Mostly used with acidemic states. O Will precipitate with Calcium!!!! Thus don’t give while using calcium gluconate.
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 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. O Each gram may remove 1 mEq K+ in exchange for 1-2 mEq Na+ thus may cause ECF volume overload.
TREATMENT OF HYPERKALEMIAMEDICATION MECHANISM OF DOSAGE PEAK EFFECT ACTIONCalcium Antagonism of 10-30 ml of 10% 5 minutesgluconate membrane solution IV over actions 10 minutesInsulin and Increased K entry 10 units insulin 30-60 min.glucose to cells plus 50 ml D20Sodium Increased K entry 50 meq IV over 5 30-60 min.bicarbonate to cells minutesAlbuterol Increased K entry 10-20 mg IV or 30-60 min. to cells nebulized