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:
Conditions | Actions |
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 toxicity | Administer digoxin specific Fab fragments |
Metabolic acidosis | Administer 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.
|
|