Hyperkalemia

Last updated: April 19, 2022

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Hyperkalemia (high serum potassium) is a common and potentially life-threatening disorder of potassium balance. The most common cause is decreased kidney function. It can also be caused by acidosis, cell breakdown, endocrinological disturbances (e.g., hypoaldosteronism, hypocortisolism), and drugs such as potassium-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, nonsteroidal antiinflammatory drugs (NSAIDs), and digoxin. Serum potassium (K+) is often falsely elevated due to the method of sampling and levels should be confirmed with repeat testing. To determine the underlying cause of hyperkalemia, it is essential to review the patient's medications, check kidney and endocrine function, and screen for cell lysis (e.g., hemolysis, rhabdomyolysis) and acid-base disorders. Acute increases in serum K+ are very dangerous, as they influence the resting membrane potential and thus the electrical excitability of cells. These changes can lead to life-threatening cardiac arrhythmias. It is, therefore, essential to obtain an ECG to determine the level of cardiotoxicity. Management depends on the severity of the hyperkalemia and includes restriction of dietary K+, as well as medications to bind, shift, or eliminate K+, or to stabilize the cardiac membrane (e.g., calcium gluconate) if necessary. In refractory cases, dialysis may be required. Serum K+ should be monitored closely until it is corrected.

See also “Hypokalemia.”

  • Hyperkalemia: Serum potassium level > 5 mEq/L
  • Acute hyperkalemia: Abnormal ↑ K+ not known to be chronic
  • Chronic hyperkalemia: Recurrent episodic ↑ K+ that require ongoing treatment

References: [1][2]

Errors in blood-drawing technique may lead to red blood cell lysis and a falsely elevated serum potassium concentration (pseudohyperkalemia)!

When K+ shifts out of the cell, it's a BAD LOSS! – Beta blockers, Acidosis, Digoxin, Lysis, hyperOsmolality, high Sugar, Succinylcholine

References:[4][6]

  • Potassium is an important factor in maintaining the resting membrane potential
  • ↑ Extracellular K+concentration → resting membrane potential becomes less negative than -90 mV → ↑ excitability

Particularly acute extracellular changes in concentration influence excitability! Chronic changes lead to intracellular compensation!

Symptoms usually occur if serum potassium levels are > 7.0 mEq/L or they change rapidly.

Hyperkalemia (and hypokalemia) can cause cardiac arrhythmia and lead to ventricular fibrillation!References:[1][7][8][9]

Approach [10]

Laboratory studies [11][12]

An inverse relationship between serum K+ and pH (e.g., pH → ↑ K+) has previously been observed in specific types of metabolic acidosis. However, the underlying mechanisms are complex and this association is inconsistent in clinical practice. [11][15]

ECG findings in hyperkalemia [16][17][18]

There is a weak correlation between serum K+ levels and the severity of ECG changes. Findings are more likely to occur with rapid-onset hyperkalemia.

  • Mild hyperkalemia: 5.5–6.4 mEq/L
  • Moderate hyperkalemia: 6.5–8.0 mEq/L
    • Lengthening of QRS interval (QRS complex widening)
    • Widening and flattening of P wave, which eventually disappears
  • Severe hyperkalemia: > 8.0 mEq/L

Investigation of underlying causes [19][20][21]

Depending on symptoms and risk factors, further testing may be appropriate, particularly if renal function is normal.

Review the patient's medical history and medication list to help identify potential causes of hyperkalemia. [19]

Therapeutic approach to hyperkalemia [2][11][19][23]

  • Determine severity: See “Risk stratification.”
  • Hyperkalemic emergency: Patients require immediate management.
    • Start continuous cardiac monitoring.
    • If there are ECG changes: Stabilize the cardiac membrane first, e.g., with IV calcium gluconate.
    • Initiate treatment to shift potassium intracellularly, e.g.:
      • Short-acting insulin with glucose
      • Consider the addition of inhaled SABAs.
    • Consider nephrology and critical care consults.
    • Admit to hospital for ongoing monitoring and treatment.
    • Repeat serum K+ at minimum 1, 2, 4, 6, and 24 hours after treatment.
  • All patients
    • Identify and treat underlying causes.
    • Review medications and discontinue or modify dosing of medications that may be contributing to hyperkalemia.
      • Decrease dose (or consider discontinuation) of drugs required to treat underlying conditions, e.g., RAAS inhibitors.
      • Avoid nonessential drugs associated with hyperkalemia (e.g., NSAIDs, over-the-counter supplements such as milkweed).
    • Start a low potassium diet and avoid salt substitutes (consider nutrition consult). [12][24]
    • Consider treatment to remove potassium from the body, e.g., cation-exchange resins, diuretics, hemodialysis.
    • Repeat potassium regularly until it is within normal range, e.g., within 1–3 days. [25]

Urgent K+-lowering treatment may be necessary even in the absence of ECG changes.

To remember K+-lowering treatments, think C BIG K Die (if you see a big serum K+, your patient may die!): Calcium salts, Beta-agonists/Bicarbonate, Insulin + Glucose, Kation exchange medication, Dialysis/Diuretics.

The effects of calcium salts, insulin/glucose, and inhaled SABAs on serum K+ are temporary. Repeat doses may be required while waiting for interventions to remove K+ from the body to take effect.

Risk stratification [26]

  • Hyperkalemic emergency is an acute severe elevation that requires urgent lowering and occurs if any of the following are present:
  • Less urgent hyperkalemia (typically chronic elevations that can be lowered more slowly)
    • Patient is asymptomatic
    • Serum K+ is 5.5–6.0 mEq/L
    • Patient has no high-risk comorbidities

Cardiac arrhythmias due to hyperkalemia can cause sudden death.

Cardiac membrane stabilization [23]

Calcium salts reduce cardiac irritability.

Calcium salts should result in normalization of the ECG appearance within 5 minutes; observe the cardiac monitor following initial treatment and repeat the dose if the ECG tracing still appears abnormal.

Calcium salts have no influence on serum K+ levels and therefore should be paired with a K+-lowering agent.

Intracellular potassium shifting [11][26][28]

These drugs should be given in tandem with calcium salts (if calcium is indicated).

Avoid administering calcium carbonate and sodium chloride through the same IV line without extensive flushing in between because of the risk of calcium precipitation. [30]

Enhanced potassium elimination [2][23][28]

  • Not required for all patients; treatment of the underlying cause may be sufficient.
  • The choice of treatment depends on underlying medical conditions and volume status.

Cation-exchange medications [26][31]

  • Mechanism of action: These drugs release Na+ or Ca2+ ions in the gut, which are exchanged for K+, thereby enhancing enteral K+ elimination.
  • Clinical applications: nonurgent lowering of K+ [11]
  • Options
  • Adverse effects
  • Considerations
    • Avoid simultaneous administration with other oral medications, as resins may bind them, reducing absorption.
    • Give with a laxative (avoid sorbitol). [33]

Sodium polystyrene sulfonate carries a risk of intestinal necrosis (especially if combined with the laxative sorbitol) and should be avoided in patients with abnormal bowel function. [33]

Hemodialysis

  • Most effective definitive therapy for refractory hyperkalemia
  • Preferred option in patients with end-stage renal failure ; (particularly if already receiving renal replacement therapy), or oliguria.
  • For all other patients, avoided as a first-line option because of its invasive nature and adverse effects

Loop diuretics [28]

All patients

  • Determine the severity of hyperkalemia.
  • Identify and treat underlying causes.
  • Review medications and discontinue or adjust dosing of medications that may be contributing to hyperkalemia.
  • Consider starting medication to enhance K+ elimination, e.g., cation-exchange medication, diuretics for patients with volume overload.
  • Repeat K+ levels to assess response to treatment.
  • Start a low K+ diet.
  • Consult nephrology for patients with ESRD or refractory hyperkalemia, e.g., for consideration of hemodialysis.

Patients with hyperkalemic emergency

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