Hyperkalemia

Starters

Potassium is largely an intracellular electrolyte
Intracellular potassium is regulated through the Na⁺/K⁺ ATPase channel
Normal serum K⁺ levels: 3.5 – 5.0 mEq/L
Consider repeating lab draw: False hyperkalemic readings may results from drawing from an IV with a potassium-rich fluid running through it. Also, prolonged tourniquet constriction of arm during blood draw can cause localized cell lysis and false readings of hyperkalemia

Etiologies

High intake
- Lactated Ringer’s
- Penicillin G
- Total parenteral nutrition (TPN)

Low output (90% of serum K⁺ is excreted through the kidney ₁)
- Acute Kidney Injury (AKI)
- Type 4 Renal Tubular Acidosis (Hypoaldosteronism)
- Medications (Most of these share the end effect of decreasing the level of aldosterone in the body)
  - ACE Inhibitors (ACEI): Lisinopril, captopril, etc.
  - Angiotensin-Receptor Blockers (ARBs): Losartan, valsartan, etc.
  - Aldosterone-Receptor Antagonists: Spironolactone, eplerenone
  - Epithelial Na⁺ channel (ENaC) inhibitors: Amiloride, triamterene
  - NSAIDs
  - Ketoconazole (inhibits aldosterone synthase)

K⁺ shifting from intracellular to extracellular
- Acidemia: Stimulates H⁺/K⁺ exchange channels, shifting H⁺ inside the cell and K⁺ out of the cell
- Hypertonicity: Causes water to flow out of cell, potassium moves with it
- Cell Lysis
  - Tumor Lysis Syndrome
  - Rhabdomyolysis
  - Trauma
  - Hemolysis

EKG changes

Management

Stabilize the cardiac membrane
- Calcium gluconate
  - Indications: Conduction abnormalities on EKG or significantly elevated potassium level (generally > 6.5 mEq/L)
  - Physiology: The Nernst equation tells us that in hyperkalemia, the resting membrane potential is shifted to a less negative value. Therefore, a lower stimulation is necessary to generate an action potential. However, after repeated depolarizations, sodium channels in the membrane become inactivated. This leads to a decreased ability of the cardiac muscle to generate action potentials ₍₂₎. Administration of calcium shifts the threshold potential of the membrane to a less negative value, so that the difference between the resting membrane potential and the threshold potential remains ~15 mV ₍₃₎
  - Effect lasts ~30 minutes, so repeated administration is necessary if still indicated

Decrease serum potassium levels
- Quick, temporary
  - IV Regular Insulin
    - Stimulates Na⁺/K⁺ ATPase
    - Give D50W at the same time to avoid hypoglycemia
  - IV Sodium Bicarbonate
    - Increases serum pH, causing cell membrane H⁺/K⁺ exchange channels to activate, shifting H⁺ outside the cell and K⁺ into the cell
  - β-2 agonist (e.g. albuterol)
    - Stimulates Na⁺/K⁺ ATPase
- Slow, permanent
  - Loop diuretics (e.g. furosemide)
    - Increase renal excretion of potassium
  - Sodium polystyrene
    - Increases GI excretion of potassium (but, as above, ~90% of potassium is excreted through kidneys)

Dialysis
- Indicated if:
  - Symptomatic (weakness/paralysis)
  - Conduction abnormalities on EKG
  - Hyperkalemia refractory to above therapies
  - Severe renal dysfunction
  - Significantly elevated potassium level (generally > 6.5 mEq/L)

References

Nohara‐Shitama, Y., Yume Nohara‐Shitama Division of Cardio‐Vascular Medicine, Adachi, H., Hisashi Adachi Division of Cardio‐Vascular Medicine, Enomoto, M., Mika Enomoto Division of Cardio‐Vascular Medicine, . . . Adachi, *. (2018, January 04). Twenty‐four‐Hour Urinary Potassium Excretion, But Not Sodium Excretion, Is Associated With All‐Cause Mortality in a General Population. Retrieved January 12, 2021, from https://www.ahajournals.org/doi/full/10.1161/jaha.117.007369
RM, B., & MN, L. (1981). Cardiovascular Physiology, 4th edition. St. Louis, MO: Mosby.
Parham, W., Mehdirad, A., Biermann, K., & Fredman, C. (2006). Hyperkalemia revisited. Retrieved January 12, 2021, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/