Fast Five Quiz: Electrolyte Disorders

Vecihi Batuman, MD


March 23, 2021

Decreased potassium excretion is the most common cause of hyperkalemia. Excessive potassium intake and a shift of potassium from the intracellular to the extracellular space are also potential pathophysiologic mechanisms.

Many individuals with hyperkalemia are asymptomatic. When present, the symptoms of hyperkalemia are nonspecific and predominantly related to muscular or cardiac function. The most common symptoms are weakness and fatigue. Occasionally, a patient may have frank muscle paralysis or shortness of breath. Patients also may have palpitations or chest pain. Patients may report nausea, vomiting, and paresthesia. The history is most valuable in identifying conditions that may predispose to hyperkalemia.

Ask about the use of medications that impair renal potassium excretion, as follows:

  • Potassium-sparing diuretics, which are especially used in the treatment of cirrhosis and chronic heart failure

  • NSAIDs

  • ACE inhibitors

  • The combination of spironolactone and ACE inhibitors

  • ARBs

  • Direct renin inhibitors (eg, aliskiren)

  • Calcineurin inhibitors (eg, cyclosporine, tacrolimus)

  • Antibiotics (eg, pentamidine and trimethoprim-sulfamethoxazole)

  • Epsilon-aminocaproic acid

  • Oral contraceptive agents, such as drospirenone

Ascertain whether the elevated potassium level is real or factitious. In a patient who does not have a predisposition to hyperkalemia, blood testing should be repeated before taking any actions to bring down the potassium level, unless changes are present on ECG. Renal function testing is important. If the patient has renal failure, the serum calcium level should be checked because hypocalcemia can exacerbate cardiac rhythm disturbances. Other tests include:

  • ECG

  • Urine potassium, sodium, and osmolality

  • Complete blood cell count

  • Metabolic profile

Measurement of the TTKG remains widely used to assess whether decreased renal excretion of potassium is contributing to hyperkalemia. Despite its initial promise, some research has called its accuracy into question. Some experts recommend that TTKG measurement be abandoned.

The aggressiveness of therapy for hyperkalemia is directly related to the rapidity with which the condition has developed, the absolute level of serum potassium, and the evidence of toxicity. The faster the rise in the potassium level, the higher it will be, and the greater the evidence of cardiotoxicity, the more aggressive therapy should be. If the patient has only a moderate elevation in potassium level and no ECG abnormalities, excretion can be increased by using a cation exchange resin or diuretics, and the source of excess potassium (eg, increased intake or inhibited excretion) can be corrected.

In patients with severe hyperkalemia, treatment focuses on immediate stabilization of the myocardial cell membrane, rapid shifting of potassium to the intracellular space, and total body potassium elimination. In addition, all sources of exogenous potassium should be immediately discontinued; including intravenous and oral potassium supplementation, total parenteral nutrition, and any blood product transfusion. Drugs associated with hyperkalemia should also be discontinued.

Definitive therapy is hemodialysis in patients with renal failure or when pharmacologic therapy is not sufficient. Any patient with significantly elevated potassium levels should undergo dialysis; pharmacologic therapy alone is not likely to bring about adequate reduction of potassium levels in a timely fashion.

Read more about hyperkalemia.


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