Chapter 18 Hyperkalemia
Definition and Epidemiology
Hyperkalemia is typically defined as a serum potassium concentration exceeding 5.0 to 5.5 mEq/L. Hyperkalemia occurs in up to 10% of hospitalized patients and can lead to life-threatening cardiac arrhythmias. Medications have been cited as a primary or contributing cause of up to 75% of inpatient hyperkalemia.
True Hyperkalemia (Box 18-1)
Excessive Potassium Intake
Excessive potassium intake will rarely cause hyperkalemia in healthy individuals with normal renal function and no other contributing factors, because the kidney can excrete hundreds of milli-equivalents of potassium daily. However, excessive potassium intake can exceed excretion in patients with comorbidities predisposing to hyperkalemia, such as renal failure. Therefore, as a general rule of thumb, potassium sliding scales should not be used if the serum creatinine concentration is ≥ 2 mg/dL or if serum creatinine has increased by ≥ 0.5 mg/dL within 24 hours. Elderly patients with low muscle mass may have profound renal insufficiency with lower serum creatinine measurements. In these settings, and in patients receiving intravenous potassium (maximum infusion rate is 10 mEq/hr through a peripheral line and 20 mEq/hr through a central line), we do not administer more than 40 mEq potassium at any one time. In these patients, we obtain serum potassium measurements 2 hours after potassium supplementation to assess the adequacy of repletion and re-dose potassium, if necessary. Profound hypokalemia may require more aggressive treatment, including placement of a central venous catheter to administer potassium at a faster rate.
Intracellular to Extracellular Shift
Most potassium is located within cells, actively transported against a concentration gradient by the ubiquitous membrane-bound sodium–potassium–ATPase (Na–K–ATPase) pump. Therefore, medications that inhibit the Na–K–ATPase (digitalis, cyclosporine, tacrolimus, beta-blockers) will reduce potassium movement from the extracellular to intracellular compartment and may cause hyperkalemia (Table 18-1).
Table 18-1 Common Drugs that Cause Hyperkalemia
| Medication | Mechanisms |
|---|---|
| Angiotensin converting enzyme (ACE) inhibitors | Reduces aldosterone production |
| Angiotensin II receptor blocker (ARB) | Decreases renal blood flow |
| Nonsteroidal anti-inflammatory drugs | |
| Mineralocorticoid receptor antagonists (Spironolactone, eplerenone) | Reduces aldosterone action |
| Potassium-sparing diuretics (triamterene, amiloride) | Reduces sodium reabsorption in the principal cell of the kidney |
| Trimethoprim (high-dose) | |
| Pentamidine | |
| Potassium supplements | Excessive intake exceeding excretion |
| Cyclosporine | Decreases aldosterone synthesis |
| Tacrolimus (FK-506) | Reduces Na-K-ATPase activity |
| Heparin | Inhibits aldosterone production |
| Digitalis toxicity | Inhibits Na-K-ATPase |
| Beta-blockers | Inhibits renin secretion |
| Reduces Na-K-ATPase activity | |
| Inhibits potassium channels in principle cells | |
| Succinylcholine | Depolarizes cell membranes |
| Medicine salts (penicillin G) | High salt content |
| Insulin deficiency | Potassium redistribution from the intracellular space |
Reprinted from Perazella MA, Drug-induced hyperkalemia: old culprits and new offenders, Am J Med. 109:307,2000, with permission from Excerpta Medica, Inc.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
