Mild Hypokalemia (3 to 3.5 mEq/L)

Patients without significant comorbid conditions tolerate mild hypokalemia very well. Muscular symptoms are generally absent, although occasionally patients experience mild cramping or early muscle fatigue. Hypokalemia may affect smooth muscle function in the gastrointestinal tract with resultant constipation or abdominal cramping, or both. Cardiac and neurologic symptoms are absent.

Moderate Hypokalemia (2.5 to 2.9 mEq/L)

Muscular symptoms become more pronounced as the degree of hypokalemia worsens; the weakness is generalized, but proximal and lower extremity muscle groups are typically affected to a greater degree.² Cardiac manifestations may include palpitations, non–life-threatening dysrhythmias (premature atrial contractions, premature ventricular contractions), and atrial fibrillation. Electrocardiographic (ECG) changes occur but do not correlate with the degree of hypokalemia (Box 165.2; Fig. 165.3).

Fig. 165.3 Electrocardiographic findings in hypokalemia.

A, Normal. B, Mild T-wave flattening (the earliest change). C, U wave associated with T-wave flattening. D, Slight ST depression and a “pseudo–P pulmonale” pattern. E, ST depression is more noticeable, and the U wave increases in amplitude. F, The U wave overtakes the T wave—“QU” prolongation.

Hypokalemia may precipitate or worsen encephalopathy in patients with severe liver disease. Potassium depletion increases renal production of ammonia, which readily crosses the blood-brain barrier in the setting of alkalosis.² Hypokalemia also inhibits the release of insulin and may cause hyperglycemia in patients with preexisting glucose intolerance or non–insulin-dependent diabetes mellitus. The renal complications of moderate hypokalemia reflect vasopressin resistance to the tubular reabsorption of water; symptoms include nocturia, polydipsia, and polyuria.²

Severe Hypokalemia (<2.5 mEq/L)

Alcoholics have the greatest risk for severe hypokalemia. Musculoskeletal symptoms include pronounced fasciculations, tetany, and rhabdomyolysis. Myolysis may cause a transient release of intracellular potassium that can mask the inciting hypokalemic state. In rare cases, life-threatening ascending paralysis and loss of deep tendon reflexes can result in quadriplegia.²

Cardiac manifestations of severe hypokalemia worsen the previously mentioned ECG abnormalities. Of great concern is the development of potentially life-threatening ventricular arrhythmias in patients with preexisting cardiac disease. Ventricular ectopy ranges from premature ventricular contractions to couplets, bigeminy, trigeminy, and episodes of ventricular tachycardia, torsades de pointes, and ventricular fibrillation. In the setting of myocardial infarction or digitalis toxicity, hypokalemia-induced ventricular dysrhythmias are directly proportional to the degree of potassium depletion.²

Mild Hyperkalemia (5 to 6 mEq/L)

Mild hyperkalemia is generally asymptomatic. Patients with underlying cardiac disease occasionally report palpitations or other well-tolerated disturbances in rhythm.

Moderate Hyperkalemia (6.1 to 7 mEq/L)

Patients with moderate hyperkalemia may exhibit ECG abnormalities, including peaked T waves and prolongation of the PR interval and QRS complex⁴ (Figs. 165.4 to 165.7; Box 165.3).

Fig. 165.4 Electrocardiographic findings in hyperkalemia.

(Adapted from Gennari FJ. Disorders of potassium homeostasis: hypokalemia and hyperkalemia. Crit Care Clin 2002;18:273–88.)

Fig. 165.5 Baseline electrocardiogram in a patient 1 month before emergency department evaluation (K⁺ = 4.3 mmol/L).

Fig. 165.6 Patient with severe hyperkalemia on arrival at the emergency department (K⁺ = 8.3 mmol/L).

Fig. 165.7 Patient during treatment of severe hyperkalemia, now with mild to moderate hyperkalemia (K⁺ = 6.3 mmol/L).

Neuromuscular symptoms similar to those seen with hypokalemia can occur. Muscle cramps and weakness are the most commonly reported complaints.

Severe Hyperkalemia (>7 mEq/L)

Progressively worsening hyperkalemia can result in significant conduction abnormalities, heart block, potentially life-threatening arrhythmias, and asystole. Symptoms such as palpitations, syncope, chest pain, and dyspnea (from left-sided heart failure) may be present. Ascending paralysis and tetany may result.

Patients with Cardiovascular Disease

Optimal goals for serum potassium repletion are predicated on the underlying pathology. Patients with a history of congestive heart failure, coronary artery disease, or dysrhythmias and hypertensive patients being treated with diuretic medications should have a serum potassium level of at least 4 mEq/L. These patients require oral supplementation for even mild, asymptomatic hypokalemia with potassium chloride tablets (20 to 40 mEq daily).⁵ If the patient is taking a potassium-sparing diuretic, the dose should be decreased.

Table 165.1 Treatment of Hypokalemia

Adapted from Zull DN. Disorders of potassium metabolism. Emerg Med Clin North Am 1989;7:771–94; and Schaefer TJ, Wolford RW. Disorders of potassium. Emerg Med Clin North Am 2005;23:723–47.

Asymptomatic Mild Hypokalemia

Healthy patients with asymptomatic, mild hypokalemia (3 to 3.5 mEq/L) do not require pharmacologic potassium supplementation. Treatment should be focused on minimizing further potassium loss and increasing oral intake. Patients should be encouraged to eat a diet rich in potassium (Box 165.4). Potassium-wasting diuretics should be decreased or eliminated, as blood pressure allows. Use of substances that contain glycyrrhizic acid (e.g., licorice, chewing tobacco, laxatives) should be avoided.^1,6

Symptomatic Mild and Moderate Hypokalemia

Potassium supplementation is required for patients with symptomatic mild or moderate (<3 mEq/L) hypokalemia. Potassium supplements are available in several forms: potassium chloride, potassium phosphate, potassium citrate, potassium acetate, potassium gluconate, and potassium bicarbonate. Potassium chloride is the preferred formulation for most ED cases of hypokalemia. Potassium phosphate may be beneficial in certain cases of diabetic ketoacidosis.⁶ Oral potassium supplements are available as tablets, powder, or elixir.

Dosing ranges from 20 to 80 mEq/day; doses greater than 40 mEq should be divided and given either two or three times per day. Oral therapy should be monitored daily because serum potassium levels will rise within 48 to 72 hours.⁶ Healthy patients who require daily oral supplementation can be discharged from the ED safely if repeated serum potassium measurements can be monitored by the primary care physician for 1 to 2 days. Patients who are elderly, have significant comorbid conditions, or have poor access to follow-up should be admitted to the hospital for a 24-hour observation period.

Magnesium deficiency should be suspected in patients who fail to respond to oral potassium therapy within 96 hours. Magnesium promotes activity of the Na⁺,K⁺-ATPase pump, which will replenish intracellular fluid concentrations in the first days of potassium supplementation.⁶

Severe Hypokalemia

Intravenous (IV) potassium replacement is indicated for patients with severe hypokalemia (<2.5 mEq/L) or moderate hypokalemia accompanied by cardiac arrhythmias, familial periodic paralysis, or severe myopathy.⁶

Replacement consists of 100 mEq of potassium chloride in 1 L of normal saline (or 5% dextrose in water [D₅W]) infused at a rate of 100 to 200 mL/hr (10 to 20 mEq/hr). If the patient has any form of heart block or renal insufficiency, the initial infusion rate should be reduced to 50 mL/hr (5 mEq/hr).

In rare instances of extreme hypokalemia or life-threatening clinical findings, potassium may be infused at a rate of 40 to 60 mEq/hr (400 to 600 mEq/L of normal saline at 100 mL/hr) for a short period (10 to 20 minutes). Therapy should be monitored with great caution. Serum potassium levels should be rechecked after every 40 to 60 mEq infused.

IV potassium supplementation can cause excruciating phlebitis and cardiac arrest if directly injected into a vessel—potassium should never be administered as an IV push. Peripheral IV lines can be used for rates of 10 to 20 mEq/hr or less. In cases of moderate hypokalemia, potassium infusions should remain at 10 mEq/hr. To minimize the risk for phlebitis, a central line is necessary for infusion rates greater than 20 mEq/hr (see earlier indications). There is a theoretic concern for cardiac arrest when potassium is administered via central venous access—splitting the potassium infusion rate over two peripheral lines may be preferable.²

In general, patients receiving IV potassium supplementation require telemetry monitoring and frequent repeated potassium measurements (up to every 1 to 3 hours after the initial infusion begins). Significant potassium depletion may take days to correct. As serum potassium levels approach 3.5 mEq/L, patients should be converted to oral therapy if possible. IV potassium supplementation should be discontinued if any ECG signs of hyperkalemia are noted or if a single potassium measurement is higher than 3.5 mEq/L.

Unstable ventricular arrhythmias resulting from severe hypokalemia should be managed according to standard practice guidelines. Severe neuromuscular manifestations may endanger adequate respiratory effort and therefore mandate aggressive airway stabilization. Any volume depletion should be corrected, and coexisting medical conditions that may exacerbate the effects of hypokalemia should be addressed.¹

Transcellular Shift: Insulin and Albuterol

Potassium can be temporarily shifted from the extracellular to the intracellular compartment through stimulation of the Na⁺,K⁺-ATPase pump by insulin or a β₂-agonist such as albuterol. Although either of these agents can temporize moderate hyperkalemia when given alone, studies suggest that combination therapy with both agents may be more efficacious.

Insulin forces a transcellular shift of potassium into liver and muscle cells. Regular (short-acting) insulin administered as a 10-unit IV bolus will begin to lower serum potassium concentrations within 10 to 20 minutes, and the clinical effect lasts several hours. An ampule of D₅₀W should be given concurrently to prevent hypoglycemia; patients who are already hyperglycemic (>250 mg/dL) do not require supplemental dextrose. Blood glucose should be rechecked 1 hour after insulin administration because hypoglycemia may develop despite initial supplementation with dextrose.

Albuterol is the most readily available β₂-agonist used to treat hyperkalemia in the ED. Nebulized albuterol in 10- to 20-mg continuous treatments will decrease serum potassium by 1 mEq/L over a 1- to 2-hour period.⁸ Though not approved for use in the United States, IV administration of albuterol shifts potassium into the intracellular fluid compartment even more rapidly. Once routinely used for treatment of hyperkalemia, the use of sodium bicarbonate has been challenged. Recent studies have demonstrated that sodium bicarbonate may only enhance urinary elimination of potassium and does not function at a cellular level. It may especially have a deleterious effect on anuric patients and worsen the degree of intracellular acidosis.⁹

Elimination: Resin Exchange (Kayexalate) and Dialysis

Definitive treatment of hyperkalemia is elimination of potassium. For patients with renal insufficiency, resin exchange (Kayexalate) and dialysis are the mainstays of therapy. Potassium-wasting diuretics (thiazides, loop diuretics) may be taken by patients with normal renal function and mild asymptomatic hyperkalemia. Sodium bicarbonate infusion may also promote renal secretion of potassium but is no longer considered a first-line agent in the treatment of hyperkalemia.

Sodium polystyrene sulfonate (Kayexalate) is an inert resin that exchanges sodium for potassium in the intestinal tract. One gram of Kayexalate removes approximately 0.5 to 1 mEq of potassium in exchange for 2 to 3 mEq of sodium.⁸ The usual dose of Kayexalate is 30 to 60 g given orally or rectally. Oral Kayexalate begins to reduce total body potassium within several hours of administration, and the clinical effect lasts 4 to 6 hours. Rectal Kayexalate has a shorter time to onset than the oral formulation but is less efficacious.

Emerging literature questions the efficacy and safety of Kayexalate. Although Kayexalate reliably decreases serum potassium when administered over a period of several days, recent literature reviews suggest that the acute effects of the resin may not be as significant as once thought.¹⁰ Colonic necrosis, ischemic colitis, colonic bleeding, and perforation have been reported when Kayexalate is combined with 70% sorbitol.⁹ Kayexalate is often premixed with 33% sorbitol to prevent resin-induced constipation, and there is little evidence to suggest that Kayexalate with 33% sorbitol causes significant colonic pathology at standard doses.¹¹ Very rare instances of colonic injury have been observed when 33% sorbitol is coadministered with Kayexalate as an enema to patients after recent colon surgery.^10,11 High-dose Kayexalate precipitates pulmonary edema by increasing extracellular sodium in fluid-overloaded patients.

Hemodialysis is the most rapid method of potassium elimination in patients with persistent, symptomatic, or severe hyperkalemia. If a potassium-free dialysate is used, serum potassium may decrease as much as 1.5 mEq/L/hr. Stable patients may be transferred to an inpatient hemodialysis unit for therapy under strict cardiac monitoring. Patients with ECG abnormalities, hypotension, significant volume overload, or respiratory distress should undergo dialysis in the ED or intensive care unit. Cell membrane stabilization with IV calcium, IV insulin or glucose, and inhalational albuterol is necessary to prevent arrhythmia while awaiting emergency hemodialysis.