Hyperkalemia

What is hyperkalemia?

too much Potassium in the blood

What are the causes of hyperkalemia?

↑Dietary K+ intake

↓Renal K+ excretion

Renal tubular unresponsive to aldosterone

Pseudohyperkalemia: Re-distribution of K+ to extracellular space(appears higher than what it is)

Rhabdomyolysis

Burn injuries

Drugs

Symptoms of hyperkalemia

Frequently asymptomatic

Palpitations

Serum K+ > 5.5mEq/L

ECG changes

at what concentrations do we see Peaked T-waves?

6-7mEq/L; this is indicative if early ECG changes

What factors lead to hyperkalemia

Acid/Base Imbalance, Metabolic Acidosis:

• When metabolic acidosis occurs, potassium levels in the blood rise.

• For every 0.1 unit decrease in pH, potassium concentration increases by 0.6–0.8 mEq/L.

  • This is because, during acidosis, hydrogen ions (H⁺) move into cells, pushing potassium (K⁺) out of cells and into the bloodstream.

Hyperosmolality:

• For every 10 mOsm/kg increase in osmolality, potassium concentration increases.

  • Osmolality shifts water out of cells, increasing potassium in the extracellular space.

Cell Lysis / Cell Destruction:

• release potassium stored in cells into the bloodstream, raising blood potassium.

Renal Failure:

• Potassium levels increase particularly when there is acute kidney injury (AKI) or if potassium supplements are given.

• Since the kidneys help regulate potassium, impaired function can lead to elevated levels.

Drugs

What drugs lead to hypoaldosteronism?

ACEi/ARB/ Direct renin inhibitors

What drugs impair cellular uptake?

beta adergenic blockers

What drugs inhibit Na/K/ATPase pump?

digoxin

What drugs block aldosterone effects?

Aldosterone antagonists(spironolactone)

What drugs block aldosterone production?

Heparin

What drugs impair K secretion?

Cyclosporine/ Tacrolimus

NSAIDs

What factors lead to hyperkalemia(shift K+ to serum)

acidosis, hyperglycemia, B2 adergenic antagonists, increase in osmolality, exercise

What happens in CKD patients with hyperkalemia?

hyperkalemia is not seen until there is a severe reduction in GFR (CKD4 and 5)

• remaining nephrons adapt to excrete more potassium and maintain normokalemia

  • stimulates Aldosterone activity

• Reduced capacity for K excretion – struggle with large potassium loads

• Increase in fecal K excretion can maintain normokalemia

What is the normal potassium excretion per day?

50- 100mEq/day

Renal 90-95%;

GI 5-10%

What is the acute goal for hypperkalemia?

prevent arrhythmias, reversal of symptoms, K <5.5mEq/L within minutes

What is the chronic goal for hyperkalemia?

Maintain K 4-5mEq/L, prevent symptoms and arrhythmias

What is emergent hyperkalemia?

K>7mEq/L or K 5.5-6.9mEq/L with ECG changes

Step by step for hyperkalemic emergency

How to treat chronic hyperkalemia

Avoid drugs that cause hyperkalemia

Encourage a low potassium diet

Avoid salt substitutes

Drugs to administer:

• Intermittent Sodium Polystyrene Sulfonate

• Patiromer(Veltassa)

• Sodium zirconium cyclosilicate(Lokelma)

Calcium Gluconate or Chloride as treatment for hyperkalemia

(Dose, ROA, Onset/DOA, Acuity and MOA)

• Dose: 1 g

• Route of Administration: IV over 5-10 minutes

• Onset/Duration: 1-2 min / 10-30 min

• Acuity: Acute

• Mechanism of Action: Raises cardiac threshold potential

• Expected Result: Reverses electrocardiographic effects

Furosemide as treatment for hyperkalemia

(Dose, ROA, Onset/DOA, Acuity and MOA)

• Dose: 20-40 mg

• Route of Administration: IV

• Onset/Duration: 5-15 min / 4-6 h

• Acuity: Acute

• Mechanism of Action: Inhibits renal Na⁺ reabsorption

• Expected Result: Increased urinary K⁺ loss

Regular Insulin as treatment for hyperkalemia

(Dose, ROA, Onset/DOA, Acuity and MOA)

• Dose: 5-10 units

• Route of Administration: IV or subcut

• Onset/Duration: 30 min / 2-6 h

• Acuity: Acute

• Mechanism of Action: Stimulates intracellular K⁺ uptake

• Expected Result: Intracellular K⁺ redistribution

Dextrose 10% as treatment for hyperkalemia

(Dose, ROA, Onset/DOA, Acuity and MOA)

• Dose: 1,000 mL (100 g)

• Route of Administration: IV over 1-2 hours

• Onset/Duration: 30 min / 2-6 h

• Acuity: Acute

• Mechanism of Action: Stimulates insulin release

• Expected Result: Intracellular K⁺ redistribution

Dextrose 50% as treatment for hyperkalemia

(Dose, ROA, Onset/DOA, Acuity and MOA)

• Dose: 50 mL (25 g)

• Route of Administration: IV over 5 minutes

• Onset/Duration: 30 min / 2-6 h

• Acuity: Acute

• Mechanism of Action: Stimulates insulin release

• Expected Result: Intracellular K⁺ redistribution

Sodium Bicarbonate as treatment for hyperkalemia

(Dose, ROA, Onset/DOA, Acuity, and MOA)

• Dose: 50-100 mEq (50-100 mmol)

• Route of Administration: IV over 2-5 minutes

• Onset/Duration: 30 min / 2-6 h

• Acuity: Acute

• Mechanism of Action: Raises serum pH

• Expected Result: Intracellular K⁺ redistribution

Albuterol as treatment for hyperkalemia

(Dose, ROA, Onset/DOA, Acuity, and MOA)

• Dose: 10-20 mg

• Route of Administration: Nebulized over 10 minutes

• Onset/Duration: 30 min / 1-2 h

• Acuity: Acute

• Mechanism of Action: Stimulates intracellular K⁺ uptake

• Expected Result: Intracellular K⁺ redistribution

Hemodialysis as treatment for hyperkalemia

(Dose, ROA, DOA, Acuity, and MOA)

4 hours

• Route of Administration: N/A

• Onset/Duration: Immediate / variable

• Acuity: Acute

• Mechanism of Action: Removal from serum

• Expected Result: Increased K⁺ elimination

Sodium Polystyrene Sulfonate as treatment for hyperkalemia

(Dose, ROA, Onset/DOA, Acuity, and MOA)

• Dose: 15-60 g

• Route of Administration: Oral or rectal

• Onset/Duration: 1 h / variable

• Acuity: Nonacute

• Mechanism of Action: Resin exchanges Na⁺ for K⁺

• Expected Result: Increased K⁺ elimination

Patiromer as treatment for hyperkalemia

(Dose, ROA, Onset/DOA, Acuity and MOA)

Veltassa

• Dose: 8.4-25.2 g

• Route of Administration: Oral

• Onset/Duration: Hours / variable

• Acuity: Nonacute

• Mechanism of Action: Resin exchanges Ca²⁺ for K⁺

• Expected Result: Increased K⁺ elimination

Drug Interactions: separate administration of other medications by 3 hours before and after

• Ciprofloxacin, levothyroxine, metformin

Side effects: (>5%): GI, hypomagnesemia

Sodium Zirconium Cyclosilicate as treatment for hyperkalemia

(Dose, ROA, Onset/DOA, Acuity and MOA)

• Dose: 5-15 g

• Route of Administration: Oral

• Onset/Duration: 1 h / variable

• Acuity: Nonacute

• Mechanism of Action: Resin exchanges Na⁺ for K⁺

• Expected Result: Increased K⁺ elimination

What foods are low in potassium?

Apples, berries, grapes, pears, peaches, pineapple

Asparagus, corn, green beans, peppers, eggplant,

Rice, pasta

White bread

Coffee, tea

What are the adverse effects of sodium polystyrene sulfonate

GI:

• constipation, nausea/vomiting, anorexia

Electrolyte disturbances:

• decrease in Potassium, Calcium, Magnesium

• increase in Sodium

Intestinal necrosis→ this is CI in those with bowel dysfunction or recent GI surgery

What is there to know about Patiromer

Brand name: veltassa

• Potassium binder in exchange for Ca (sodium-free)

• DELAYED effect – not for acute use

• Dosing: 8.4g PO once daily titrated to 25.2g/day

• Drug Interactions: separate administration of other medications by 3 hours before and after

  • Ciprofloxacin, levothyroxine, metformin

• Side effects: (>5%): GI, hypomagnesemia

What is there to know about Sodium Zicronium Cyclosilicate?

Brand name: Lokelma

• Inorganic cation exchanger, highly specific for K+

  • Contains sodium

• More rapid correction of hyperkalemia

• Dosing: 10g PO TID x 48 hours, then 10g once daily

• Interactions: Separate administration from other medications by at least 2 hours:

  • Clopidogrel, dabigatran, warfarin

• Side Effects: Edema