• Hyperkalemia is defined as a serum potassium >5.5 mEq/L. If it goes unrecognized or there is a delay in treatment, it can lead to cardiac and respiratory arrest.
• Potassium is predominantly an intracellular cation and is important in electrophysiological functions. The body has several regulatory mechanisms to maintain the potassium concentration within narrow levels; to avoid hyperkalemia, the cation is shifted intracellularly and/or excretion is enhanced.
• Hyperkalemia may present preoperatively or develop intraoperatively. The anesthesia provider must be vigilant in the identification and treatment of this potentially life-threatening electrolyte abnormality.

• Altered internal balance: Acidosis, insulin deficiency, renal failure, decreased aldosterone levels, increased tissue breakdown.
• Altered external balance: Blood transfusions, drugs that affect renal excretion or internal balance.
• Pseudohyperkalemia: Thrombocytosis, leucocytosis, hemolyzed sample, increased release from abnormal cells.

• Nearly 98% of total body potassium is intracellular; the remaining 2% is extracellular. The total potassium load in the body is ~50 mEq/kg (average 70 kg human has ~3500 mEq). Serum potassium is usually maintained from 3.5 to 5.0 mEq/L.
• Na⁺/K⁺ ATPase is located in the cell membrane. It is a counter-exchange mechanism that pumps Na⁺ extracellularly and K⁺ intracellularly in a 3:2 ratio. The pump functions to maintain the resting cell membrane potential, cell volume, and intracellular calcium concentration. It is further regulated by insulin, acidosis, drugs, and catecholamines.
• Hyperkalemia from intracellular to extracellular shifting:
  • Insulin directly stimulates the Na⁺/K⁺ ATPase pump in the liver, skeletal muscle, and fat cells. It promotes intracellular uptake of potassium. Insulin deficiency can hence impair the transcellular uptake of glucose as well as the Na⁺/K⁺ ATPase pump.
  • Excessive tissue breakdown or increased cellular catabolism can result in a release of excessive amounts of potassium to the extracellular environment. Examples include malignant hyperthermia, rhabdomyolysis, massive hemolysis, and tumor lysis syndrome.
  • Beta-2 adrenergic agonists promote intracellular uptake of potassium by stimulating the Na⁺/K⁺ ATPase pump. Conversely, non-selective beta-blockers may decrease uptake.
  • Metabolic acidosis promotes potassium efflux via hydrogen ion exchange. for every 0.1 mmol/L decrease in pH, there is a 0.6 mmol/L increase in serum potassium. The Na⁺ -H⁺ ion exchanger allows for the cells to function as a buffer against alkalemia or acidemia. In acidemia, H⁺ ions move intracellularly, in exchange for Na⁺ moving extracellularly. This reduces intracellular shifting of K⁺ via the Na⁺ -K⁺–ATPase. The opposite occurs in alkalemic states.
  • Hypertonicity leads to a loss of intracellular water and concentrates the intracellular potassium concentration. This creates a driving force that favors potassium movement out of the cell.
  • Medications, including NSAIDS and digoxin, impair the movement of potassium into the cell by inhibiting the Na⁺/K⁺ ATPase pump in the cell membrane.
  • Succinylcholine causes rapid transient hyperkalemia from "cellular leak."
• Hyperkalemia from impaired excretion occurs primarily from renal and gastrointestinal derangements. In the kidneys, excretion occurs mainly at the cortical collecting duct and aldosterone is a hormonal regulator of serum K⁺. Approximately 60–75% of filtered potassium in the glomerulus is reabsorbed in the proximal tubule and 15–20% in the thick ascending limb of the loop of Henle. Hyperkalemia stimulates aldosterone production with resultant renal tubular elimination of K⁺ and reabsorption of Na⁺ and water.
  • In patients with a glomerular filtration rate (GFR) of 5–10 mL/min, potassium excretion is impaired at the distal collecting duct as a result of a decrease in sodium and water delivery. Conditions like severe heart failure, dehydration, or hypovolemia also limit the sodium and water delivery to the distal collecting ducts.
  • Mineralocorticoid deficiency (aldosterone) can decrease excretion at the cortical collecting duct.
  • Medications such as potassium sparing diuretics (amiloride, triamterene) and antibiotics (trimethoprim-sulfamethoxazole, pentamidine) can decrease urinary potassium excretion by inhibiting the sodium channels in the kidney.
  • Aging results in decreased renal mass, renal blood flow, GFR, and loss of tubular transport function. This predisposes elderly patients to hyperkalemia. Additionally, elderly patients are more likely to take NSAIDS, ACE inhibitors, beta-blockers, digitalis, and potassium sparring diuretics.
• Hyperkalemia from increased intake
  • In patients with intact renal function, a supranormal intake is needed to cause hyperkalemia. In patients with impaired renal function (GFR <15 mL/min/1.73 m²), only a slight increase in potassium intake can cause severe hyperkalemia.
• Electrophysiologic effects of hyperkalemia in heart muscles:
  • Hyperkalemia leads to an increased resting membrane potential (less negative; e.g., –90 mV to –80 mV) secondary to a decrease in the transmembrane potassium gradient. This result manifests as a shortening in the duration of the action potential in all cardiac cells.
  • Phase 0. When the membrane is partially depolarized, there are fewer sodium channels in the resting state that are ready for opening and ion conductance. This results in a decrease in the Vmax (phase 0), slowing of the impulse conduction, and prolongation of membrane depolarization. On the EKG, this is manifested by a prolonged P wave, PR interval, and QRS complex.
  • Phase 2 and 3. The potassium current in the myocyte membrane is responsible for the potassium efflux during these phases. Potassium currents increase during hyperkalemic states, via unknown mechanisms, leading to acceleration of repolarization. On the EKG, this is manifested by a peaked T wave.
  • Atrial tissue is more sensitive to hyperkalemia than the ventricles and nodal cells. At a potassium level of 8–9 mEq/L, the SA node may stimulate the ventricle without evidence of atrial activity, producing a sinoventricular rhythm. On the EKG, this is manifested as an absent P wave with a wide QRS complex.
  • As hyperkalemia worsens, SA node conduction ceases, and the passive junctional pacemaker becomes the primary electrical stimulation for myocardium. On the EKG, this is manifested as a QRS complex that continues to widen, blends with the T wave, and produces the classic sine wave pattern. At this point, ventricular fibrillation and asystole is imminent.
• Pseudohyperkalemia is defined as a [K⁺] increase of at least 0.5 mEq/L and results from difficult phlebotomy, excessive alcohol swabbing of the skin, or clenching of the fist. When the value is excessive or does not fit the clinical picture, the lab draw should be repeated to confirm true hyperkalemia.

• Additional care and strict monitoring of serum potassium is needed for patients with impaired renal function or heart failure who are on spironolactone and ACE inhibitor.
• Serial measurement of serum potassium coupled with EKG monitoring and management of the patient's overall clinical condition can prevent fatal cardiac arrhythmia.
• In patients with normal renal function, temporarily shifting potassium intracellularly can be therapeutic. In patients with poor renal function, shifting potassium intracellularly may need to be combined with hemodialysis.

Pseudohyperkalemia

• Hypokalemia
• Acid-Base Physiology
• Diabetic Ketoacidosis

276.7 Hyperpotassemia

E87.5 Hyperkalemia

Michael S. Green , DO

Poovendran Saththasivam , MD