electrolytes 2 - hyperkalemia (↑K+)

what causes hyperkalemia through trans cellular movement of K⁺?

• digitalis

• acidosis* (also through impaired renal excretion of K⁺)

what causes hyperkalemia through increased intake of K⁺?

oral or IV K⁺

what causes hyperkalemia through impaired renal excretion of K⁺?

• chronic kidney disease

• acute kidney injury

• ACE inhibitors

• ARBs

• acidosis* (also through trans cellular movement of K+)

primary causes of hyperkalemia

1. increased potassium intake

2. impaired potassium excretion

   • AKI or stage 4 to 5 CKD

   • drug induced hyperkalemia:

     • ACEIs, ARBs, NSAIDs, direct renin inhibitors, potassium-sparing diuretics

   • tubular unresponsiveness to aldosterone

3. redistribution of potassium into the extracellular space

   • metabolic acidosis, diabetes mellitus, or lactic acidosis

   • drug induced redistribution of potassium: β-blockers

clinical pitfall of hyperkalemia

hemolysis can cause an erroneously elevated potassium

signs and symptoms of mild hyperkalemia

• 5.1 - 5.9 mEq/L

• may be asymptomatic

• muscle twitching, cramping, weakness

signs and symptoms of moderate and severe hyperkalemia

• moderate = 6.0 - 7.0 mEq/L

• severe = > 7.0 mEq/L

• arrhythmias

• death

general principles of hyperkalemia treatment

1. determine if pt needs chronic vs acute hyperkalemia

   • ECG, symptoms, etiology of hyperkalemia

2. treat underlying causes of hyperkalmeia:

   • renal insufficiency (e.g. CKD)

     • missing dialysis appointments —> acute hyperkalemia

     • acute kidney injury (AKI) —> acute hyperkalemia

   • metabolic acidosis (pH ↓, K⁺↑)

     • for every 0.1 decrease of arterial pH, K⁺ increase by 0.6 mEq/L

   • medications that increase K⁺ —> chronic or acute

     • K⁺ spring diuretics, ACEIs, ARBs

methods to manage chronic hyperkalemia (CKD)

promote physical removal of potassium

• cation-exchangers (aka “potassium binders”)

• dialysis (if already on dialysis)

methods to manage acute hyperkalemia

• shift potassium intracellularly

  • insulin regular, sodium bicarbonate, beta-2 agonists

• increase potassium excretion

  • diuretics

• promote physical removal of potassium

  • dialysis

K+ binders

there are 3 potassium binders:

• Sodium polystyrene sulfonate [SPS] (Kayexalate)

• Patiromer (Veltassa)

• Sodium zirconium cyclosilicate [SZC] (Lokelma)

general MOA: binds to and increases fecal K+ excretion

• non-absorbed cation exchange polymer that binds to K+ in exchange for a cation in the colon

• efficacy variable

Sodium polystyrene sulfonate [SPS]

brand: Kionex, Kayexalate

MOA: non-absorbed cation exchange polymers that binds to K+ in exchange for Na+ in the colon (efficacy variable)

dose:

• oral suspension 15 NG/PO 1-4 times daily (up to 60 g/day)

• rectal suspension: 30-50 g PR q6h

administration:

• suspend each dose in water/syrup (3-4 mL per g of resin)

• give at least 3 hours before or after other medications

onset: 1 hour

• sometimes given as an adjunct in acute hyperkalemia

AE: N/V, constipation, fecal impaction, hypoCa²⁺, hypoK⁺

• serious: GI obstruction, necrosis (FDA warning)

patiromer

brand: Veltassa

MOA: non-absorbed cation exchange polymers that binds to K+ in exchange for Ca2+ in the distal colon

dose: 8.4 g PO once daily, titrate by 8.4 g at 1-wk intervals (max 25.2 g/day)

administer:

• measure 1/3 cup of water —> pour ½ glass, mix drug, add other ½ (mixture will look cloudy — powder does NOT dissolve)

• give at least 3 hours before or after oral medications

• do NOT heat or add to heated foods/liquids

onset: 7 hours (peak K+ lowering in 48h)

• NOT used for acute hyperkalemia (only chronic)

AE: constipation, hypomagnesemia

sodium zirconium cyclosilicate

brand: Lokelma

MOA: non-absorbed cation exchange polymer (zirconium silicate) that binds to K+ in exchange for H+ and Na+ in the distal colon

dose: 10 g PO TID for up to 48 hrs; then 10 g PO daily

administer:

• add powder to at least 3 tablespoons water

• give at least 2 hours before or after oral medications

onset: 1 hour

• sometimes given as an adjunct in acute hyperkalemia

AE: edema

acute hyperkalemia management

“C a BIG (K) (Drop)”

• calcium

• albuterol

• bicarbonate

• insulin

• (glucose)

• (K⁺ binders)

• (dialysis)

first step in treating acute hyperkalemia

first step for acute hyperkalemia to stabilize cardiac membrane

• calcium does NOT decrease serum [K⁺]

• purpose: raise the depolarization threshold

calcium IV products

calcium chloride (CaCl₃)

• administer 1 g as a slow IVP via central line

• available as a vial or prefilled syringe (1g/10mL)

• 3x more elemental calcium than gluconate

• can cause tissue necrosis so central line is preferred UNLESS in a cardiac arrest/code blue (emergency) situation

calcium gluconate

• administer 1 g IVPB over 10 minutes or slow IVP

• available as a vial (1g/10mL)

second step in treating acute hyperkalemia

shift K+ into cells using:

• albuterol

• bicarbonate

• insulin

• (glucose)

first line for intracellularly shifting K+

1st line: insulin regular 5-10 units IVP

• if BG (blood glucose) < 250 mg/dL, then also give 25-50g (50-100 mL) D50W to prevent hypoglycemia

• check BG q30min for ≥2 hrs; monitor potassium

other methods to intracellularly shifting K+

sodium bicarbonate 50-100 mEq slow IVP

• minimal K+ lowering

• onset: 30 min

• duration 2-6 hrs

• adjunct to insulin, use if pt has metabolic acidosis or hyperkalemia due to a toxicological etiology

nebulizer albuterol 10-20 mg nebulized over 10 mins

• onset: 30 minutes

• duration: 1-2 hours

• adjunct to insulin; commonly used on ambulance for hyperK

third step in treating acute hyperkalemia

remove K+ from body:

• (Kayexalate)

• (Dialysis)

potassium removal in acute hyperkalemia

potassium binders

• sodium polystyrene sulfonate or sodium zirconium cyclosilicate may be used as an adjunct if pt has acute on chronic hyperkalemia

furosemide 20-40 mg IV

• onset 5-15 min

• duration 4-6 hrs

• adjunct; only use if pt has good renal function

dialysis:

• NOT used in all cases

• use if pt is already on dialysis

• use if pt having severe arrhythmias or need dialysis for toxin removal (overdose situations)

primary causes of hyperkalemia (concept map)

• increased potassium intake

• decrease potassium excretion

• tubular unresponsiveness to aldosterone

• redistribution of potassium into the ECF

drug-induced hyperkalemia (concept map)

• ACEIs

• ARBs

• direct renin inhibitors

• K⁺ sparing diuretics

• NSAIDs

• beta blockers

what affects the kidneys and causes hypokalemia and hyperkalemia? (concept map)

aldosterone activation —> hypokalemia (↓)

• loop and thiazide diuretic

aldosteron inhibition —> hyperkalemia (↑)

• ACEIs

• ARBs

• direct renin inhibitors

• potassium-sparing diuretics

• NSAIDs

what affects both the cell membrane AND the kidneys and causes hypokalemia and hyperkalemia? (concept map)

alkalosis —> hypokalemia (↓)

acidosis —> hyperkalemia (↑)

what affects the cell membrane and causes hypokalemia and hyperkalemia? (concept map)

redistribution between ICF and ECF; NO loss of K+ from TBW

Na⁺-K⁺-ATPase activation —> hypokalemia (↓)

• beta2 agonists, insulin overdose

Na⁺-K⁺-ATPase inhibition —> hyperkalemia (↑)

• beta blockers