Hyperkalemia Michael Levin, D.O. Medical Resident PGY II P.C.O.M.

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Presentation transcript:

Hyperkalemia Michael Levin, D.O. Medical Resident PGY II P.C.O.M

Daily Requirements 1 meq/kg/day 1 meq of K + per inch of banana If the average person weighs 70 kg then to fulfill your necessary daily requirements you need to eat a 6 foot banana

Definition Normal serum potassium mEq/L Hyperkalemia is a serum potassium greater than 5.5 mEq/L

What to Do?? Is the value accurate?? Are there EKG changes?? Is there evidence of Hemolysis on lab specimen?? Recheck blood

EKG Changes Peaked T Waves

EKG Changes Widening of QRS Complex

EKG Changes Ventricular Tach/Torsades

Treatment 1- Stabilize myocardial membrane 2- Drive extracellular potassium into the cells 3- Removal of Potassium from the body

Treatment Stabilize the Myocardial Membrane Elevations in the extracellular potassium concentration will result in a decrease in membrane excitability that may be manifested clinically by impaired cardiac conduction and/or muscle weakness or paralysis Calcium antagonizes the cellular effects of Hyperkalemia

Treatment Stabilize the Myocardial Membrane Types of Calcium Calcium Gluconate  can be given central or peripherally Calcium Chloride  can only be given via central line – Has higher concentration of calcium and if given peripherally will cause local sclerosis and gangrene

Treatment Drive Extracellular Potassium Into the Cells 1-  2 Agonists (albuterol) – Drives K 2+ intracellular by increasing Na-K ATPase in skeletal muscle Usual dose for asthma 0.5 cc/3cc NSS Dose for hyperkalemia 5cc over 10 min – 10X more potent Effects occur in min ADR-palpitations/arrhythmia

Treatment Drive Extracellular Potassium Into the Cells 2- Insulin and Glucose – Drives K 2+ intracellular by increasing Na-K ATPase in skeletal muscle 1 amp D50 with 5-10 units of regular insulin IV Effects seen in 30 min with peak in 60 min Duration several hours ADRs: hypoglycemia

Treatment Drive Extracellular Potassium Into the Cells 3- Sodium Bicarbonate (NaHCO 3 ) – Causes an alkalosis leading to potassium wasting – Only works if hyperkalemia 2 o to ongoing severe metabolic acidosis Onset few minutes but effects are not long lasting

Treatment Removal of Potassium From the Body 1- Loop Diuretic – Leads to loss of K + in urine by inhibiting NA-K-2CL transporter in Loop of Henle – Need renal function and volume to get filtrate to Loop of Henle

Treatment Removal of Potassium From the Body 2- Sodium Polystyrene Sulfonate (Kayexalate ) – Exchanges Na + for K + and binds it in gut, primarily in large intestine, decreasing total body potassium – K removed from body 8-12 hours after administration in stool Given PO/PR ADRs: intestinal necrosis/gangrene DO NOT GIVE INDISCRIMINATLY

Treatment Removal of Potassium From the Body Hemodialysis Peritoneal Dialysis

Causes Pseudohypokalemia Transcellular shift Endogenous Medications Excessive intake

Causes Pseudohypokalemia Prolonged use of tourniquet Hemolysis (in vitro) Delay in processing of blood Severe leukocytosis Severe thrombocytosis

Causes Endogenous Rhabdomyolysis Hemolysis Tumor lysis syndrome Severe exercise

Causes Transcellular Shift  Blockers, Digoxin Insulin deficient states Hyperglycemia/hypert onic-severe Metabolic acidosis Ischemic gut – NSAID!!! Sepsis- inc catecholamine states Adrenal insufficiency Hyporenin/Hypoaldo states – Type 4 RTA, sickle cell, intestinal nephritis, obstructive uropathy

Causes Transcellular Shift (cont) Renal failure – With dec. renal perfusion from hypovolemia there may not be adequate distal flow to allow distal principle cell Na and K exchange – If ATN with tubule damage the also no NA K exchange – Azotemia may cause metabolic acidosis

Causes Medications  Blockers Bactrim K sparing diuretics Digoxin Succinycholine NSAIDS – Dec GFR Inhibit Aldosterone Ace I/ARBS Spironolactone Heparin/Lovenox NSAID’s