Hyperkalemia

Hyperkalemia is defined as a potassium level >5.0. Even when severe, it may present simply as a laboratory abnormality in an asymptomatic patient.

Pathophysiology

  • Hyperkalemia arises through either a shift of potassium out of cells or failure of its excretion (renal). Like hypokalemia, it exerts its adverse effects by disturbing membrane polarization.
  • The most important toxicity of hyperkalemia is cardiac. There may be a progressive series of warning signs on the 12-lead EKG and cardiac monitor, which if left untreated, lead to ventricular dysrhythmia and asystole. Diagnosis and Evaluation
  • Consider coexistent conditions that may require other critical actions in the setting of hyperkalemia:
    ConditionsActions
    Renal failure Evaluate and treat the cause
    If perennial, saline fluid resuscitation
    If post-renal, relieve obstruction (drain urine)
    May require emergent dialysis
    Adrenal insufficiency Administer mineral corticoids IV
    Digitalis toxicityAdminister digoxin specific Fab fragments
    Metabolic acidosisAdminister sodium bicarbonate
    Drug related: 
    - â-blockers
    - ACE Inhibitors
    - heparin
    Consider holding dose/infusion

Laboratory/Studies

  • It is imperative to repeat elevated serum potassium levels as they are frequently falsely elevated due to hemolysis in the specimen. The therapy for elevated levels may itself be dangerous if potassium is not, in fact, elevated—this underscores the importance of the STAT EKG.
  • A STAT 12-lead EKG should be performed looking for the progressive signs of hyperkalemia. These begin with tall, tented T waves and QRS widening. As these changes become more exaggerated and P waves become flattened and disappear, the QRS complexes become difficult to distinguish from T waves. This creates the ominous “sine wave” pattern.
  • The EKG abnormalities of hyperkalemia are a better indication of the degree of cardiac toxicity present than the serum level—hence the EKG findings should be the principal guide for the aggressiveness of therapy.
  • It must be recognized that hyperkalemia can mimic the changes of acute MI on the EKG—its aggressive treatment and careful observation of the EKG will help resolve this dilemma.
  • STAT electrolytes are essential, including Mg, PO4, Ca and albumin. These will need to be repeated frequently (e.g., every hour) when severe derangements of potassium are involved.
  • When an acid-base disturbance is also present, serial measurements of serum pH is also critical during management because of the effect of pH on serum potassium shifts.
  • Measure digitalis level if its use is known or suspected.

ED Management

  • When using RSI, succinylcholine must not be included in the drug regimen if hyperkalemia is known or even a reasonable possibility. This includes rhabdomyolysis, burns or crush injuries after 48-72 h, a history of renal failure, acute urinary retention, tumor lysis syndrome and other causes. Succinylcholine elevates potassium levels and may be fatal in this setting.
  • Patient must be placed on telemetry to monitor for dysrrhythmias.
  • Administration of calcium chloride or gluconate (10 mL of a 10% solution given by slow IV push) is the most time-critical of interventions. It acts within minutes to reverse EKG manifestations and risk of ventricular dysrhythmia. It may be repeated, directing therapy toward the EKG and cardiac monitor. Its effect is only temporary and steps to reduce potassium concentration must occur simultaneously.
  • Potassium may be shifted into cells temporarily using a combination of insulin, glucose and bicarbonate. A typical regimen may include 10 units of insulin IV, 50 g of dextrose (one ampoule of D50) and one ampoule of sodium bicarbonate (use with caution in patients with potential volume overload). Inhaled â agonists, such as albuterol nebulizers, are also effective. These interventions take effect in a 15-45 min time frame.
  • The next step in therapy is to promote excretion of potassium. This is achieved with the use of diuretics (e.g., furosemide 20-80 mg IV push in patients who produce urine) and oral/nasogastric cation exchange resins (e.g., sodium polystyrene sulfonate 25-50 g PO). These are effective in a hour or more after administration.
  • Dialysis is the definitive method of removing excess potassium and may be necessary if the above techniques are ineffective.
       
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