Pathophysiology:

Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L. Ranges are as follows:

• 5.5 - 6.0 mEq/L - Mild condition
• 6.1 - 7.0 mEq/L - Moderate condition
• 7.0 mEq/L and greater - Severe condition

Hyperkalemia results from the following:

• Decreased or impaired potassium excretion - As observed with acute or chronic renal failure (most common), potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, and systemic lupus erythematosus (SLE)
• Additions of potassium into extracellular space - As observed with potassium supplements (e.g.: PO/IV potassium, salt substitutes), rhabdomyolysis, and hemolysis (e.g.: venipuncture, blood transfusions, burns, tumor lysis)
• Transmembrane shifts (i.e.: shifting potassium from the intracellular to extracellular space) - As observed with acidosis and medication effects (e.g.: acute digitalis toxicity, beta-blockers, succinylcholine)
• Factitious or pseudohyperkalemia - As observed with improper blood collection (e.g.: ischemic blood draw from venipuncture technique), laboratory error, leukocytosis, and thrombocytosis

Frequency:

History:

Physical:

Causes:

Lab Studies:

• BUN and creatinine - For evaluation of renal status
• Calcium level - If patient has renal failure (because hypocalcemia can exacerbate cardiac rhythm disturbances)
• Glucose level - In patient with diabetes mellitus
• Digoxin level - If patient is on a digitalis medication
• ABGs - If acidosis is suspected
• Urinalysis - If signs of renal insufficiency are present (to look for evidence of glomerulonephritis)

Other Tests include: continuous cardiac monitoring - Indicated for evaluation of rhythm disturbances, ECG is essential and may be instrumental in diagnosing hyperkalemia in the appropriate clinical setting. ECG changes have a sequential progression of effects, which roughly correlate with the potassium level. ECG findings may be observed as follows: early changes of hyperkalemia include peaked T waves, shortened QT interval, and ST segment depression. These changes are followed by bundle branch blocks causing a widening of the QRS complex, increases in the PR interval, and decreased amplitude of the P wave. Without treatment, the P wave eventually disappears and the QRS morphology widens to resemble a sine wave. Ventricular fibrillation or asystole follows, and the patient has a cardiac arrest. ECG findings generally correlate with the potassium level, but potentially life-threatening arrhythmias can occur without warning at almost any level of hyperkalemia.

Treatment:

• Perform continuous ECG monitoring with frequent vital sign checks when hyperkalemia is suspected or when laboratory values indicative of hyperkalemia are received.
• Initial management includes assessment of the ABCs and prompt evaluation of the patient's cardiac status with an ECG.
• Discontinue any potassium-sparing drugs or dietary potassium.
• If the hyperkalemia is severe (potassium >7.0 mEq/L) or the patient is symptomatic, begin treatment before diagnostic investigation of the underlying cause.

The goal of treatment is to stabilize the myocardium, shift potassium from the extracellular environment to the intracellular compartment, and to promote the renal excretion and GI loss of potassium. The treatment of hyperkalemia is somewhat complex. Suffice it to say that the medications listed are each appropriate under different circumstances. The medications include electrolyte supplements such as calcium that reduce the risk of ventricular fibrillation. Glucose, insulin and bicarbonate function by driving extracellular potassium into the cell thereby reducing serum potassium. Kayexalate exchanges sodium for potassium by binding it in the gut, thereby decreasing total body stores of potassium. Lasix increases the secretion of potassium. Magnesium suppresses arrythmias caused by high levels of potassium.

Medical/Legal Concerns:

Liability also can result from a delay in instituting definitive therapy after initial successful stabilization of the patient's condition. Medications such as calcium, insulin, glucose, and sodium bicarbonate are temporizing measures. Definitive loss of excess potassium can be achieved only with resin- binding agents, dialysis, or increased renal excretion. Begin administration of a resin-binding agent (like Kayexalate) soon after the other drugs have been administered.

Another potential pitfall is overcorrection of the potassium level. Liability may result from failure to adjust therapy for concurrent conditions. For example, in diabetic ketoacidosis (DKA) and in many other types of metabolic acidosis, the extracellular potassium level is elevated, yet the patient may have a total body deficit of potassium. Once the clinician initiates therapy for DKA, the extracellular potassium level decreases spontaneously and sometimes precipitously with catastrophic outcomes.