HyperkalemiaEdit

Hyperkalemia is an electrolyte disorder defined by an elevated level of potassium in the bloodstream. Potassium homeostasis is essential for the normal function of nerves, muscles, and particularly the heart. When serum potassium rises, the risk of dangerous cardiac conduction disturbances and muscle weakness increases. In clinical practice, thresholds commonly cited place hyperkalemia above about 5.0 mEq/L, with greater risk as levels rise toward 6.0–6.5 mEq/L or higher, especially if there are accompanying disorders or ECG changes. The condition often reflects an imbalance between potassium intake, release from cells, and renal or colonic excretion, and it can emerge acutely or chronically. See Potassium regulation and Electrolyte disorders for broader context.

Hyperkalemia occurs most frequently in people with impaired kidney function, including those with chronic kidney disease or acute kidney injury, because the kidneys are the primary route for potassium elimination. It also arises when there is a shift of potassium from inside cells to outside, such as during tissue breakdown or severe acidosis, or when medications reduce potassium excretion or increase intake. Common contributing factors include the use of certain prescription drugs, dietary patterns, and acute illnesses. See Renal failure and Acidosis for related mechanisms and conditions.

Pathophysiology

Potassium balance is maintained by renal excretion, transcellular shifts between intracellular and extracellular compartments, and, to a lesser extent, gastrointestinal losses. In the heart and skeletal muscle, extracellular potassium levels influence membrane potential and excitability. Small increases in potassium can alter conduction and repolarization, which is why timely recognition and treatment are critical. See Potassium homeostasis and Cardiac electrophysiology for additional detail.

Causes and risk factors

Decreased potassium excretion: largely due to kidney disease, including chronic kidney disease and acute kidney injury.
Transcellular shifts: conditions such as severe acidosis, insulin deficiency, cell lysis (e.g., rhabdomyolysis or massive tissue injury), or certain medications that affect cellular uptake of potassium.
Increased potassium intake or intake in the setting of reduced excretion: ingestion of potassium-rich foods or supplements, and drug effects.
Drugs that raise potassium or impair its excretion: including ACE inhibitors and ARBs, certain potassium-sparing diuretics such as spironolactone and eplerenone, potassium supplements, and some nonsteroidal anti-inflammatory drugs. See Potassium-sparing diuretics for more.

Clinical features and diagnosis

Symptoms can be nonspecific, including fatigue, weakness, paresthesias, and in severe cases, numbness or paralysis. The most feared complication is a life-threatening effect on heart rhythm, which can present as palpitations, syncope, or sudden cardiac arrest. Diagnosis rests on a blood test measuring serum potassium and is interpreted in the context of the patient’s renal function, acid-base status, and medications. An electrocardiogram (ECG or electrocardiography) is often used to identify conduction abnormalities that accompany higher potassium levels, such as peaked T waves, widened QRS complexes, or other evolving patterns. It is also important to consider pseudohyperkalemia—apparent elevations caused by sample handling rather than true systemic excess.

Evaluation and management

Initial assessment and stabilization

Severe hyperkalemia or hyperkalemia with ECG changes requires rapid stabilization of the myocardium. This is typically achieved with intravenous calcium, most commonly calcium gluconate, to protect the heart while other interventions lower potassium. See Calcium gluconate for details.

Shifting potassium into cells

Insulin with glucose: Insulin drives potassium into cells; glucose is given to prevent hypoglycemia. See Insulin therapy.
Beta-adrenergic agonists: Inhaled albuterol (a beta-2 agonist) can promote cellular uptake of potassium.
Sodium bicarbonate: In patients with metabolic acidosis, bicarbonate can help shift potassium, though its use is case-dependent. See Alkalosis and Metabolic acidosis.

Removing potassium from the body

Diuretics: Loop diuretics such as furosemide can increase potassium excretion in patients with sufficient kidney function.
Potassium binders: Historically, sodium polystyrene sulfonate (Kayexalate) has been used, but concerns about efficacy and safety have led to increased use of newer agents such as patiromer (brand name Veltassa) and sodium zirconium cyclosilicate (brand name Lokelma). See Potassium binders for overview.
Dialysis: In patients with advanced kidney failure or life-threatening hyperkalemia not responsive to other measures, dialysis is a definitive method to remove potassium from the bloodstream. See Hemodialysis and Peritoneal dialysis.

Chronic management and prevention

Prevention focuses on addressing the underlying cause, optimizing medications, and, where appropriate, using potassium binders to enable continuation of beneficial therapies (for example, RAAS inhibitors in patients with heart or kidney disease) while maintaining safe potassium levels. Dietary potassium management may be individualized, balancing nutritional needs with cardiovascular and renal risk. See Dietary potassium and Chronic kidney disease management.

Controversies and policy considerations

In many medical systems, debates center on how aggressively to treat mild or asymptomatic hyperkalemia, how to balance cost with patient outcomes, and how to integrate newer therapies into standard practice. Some points of discussion from a practical, policy-aware perspective include:

Use of newer potassium binders in chronic management: Patiromer and sodium zirconium cyclosilicate offer the ability to continue therapies that improve outcomes in cardiovascular or renal disease (for example, RAAS inhibitors), but their higher cost compared with older approaches prompts discussions about cost-effectiveness, insurance coverage, and patient access. See Cost-effectiveness in hyperkalemia and Clinical guidelines on treatment strategies.
Dietary restrictions versus nutrition: Overly aggressive potassium restriction can impact nutrition, especially in older adults or those with multiple health conditions. The prudent approach emphasizes individualized assessment and shared decision-making rather than blanket limits. See Dietary management and Nutrition in chronic disease.
Role of dialysis in chronic hyperkalemia: For patients with advanced kidney disease, dialysis is a life-saving intervention, but its timing and frequency involve complex considerations of quality of life, healthcare resources, and patient preference. See Hemodialysis.
Access and equity: In healthcare systems with variable access, disparities in timely recognition and treatment of hyperkalemia can affect outcomes. This is especially relevant for patients with limited access to primary care, emergency services, or renal specialty care.

From a framing that emphasizes personal responsibility and efficient use of medical resources, proponents argue for evidence-based, cost-conscious approaches that prioritize treatments with proven benefit, while also leveraging newer therapies when they meaningfully improve outcomes and preserve important medications. Critics of overly cautious or paternalistic approaches contend that well-supported, patient-centered choices—including appropriate use of binders and continuation of beneficial therapies—benefit patients without unnecessary restrictions. See Health economics and Evidence-based medicine for broader context.