Hyperkalemia is characterized by an elevated serum potassium level greater than 5.5 mmol/L and is classified as an electrolyte abnormality. [1]  Acute hyperkalemia is often preceded by issues such as illness, dehydration, or introduction of medications that affect potassium levels. [2] 


Approximately 1 to 10 percent of hospital patients are affected by hyperkalemia.  [2]

The mortality rate for patients with hyperkalemia is approximately 1 in 1000. [1]

Patients with hyperkalemia tend to be older than the general hospital population. 

There appears to be correlation between gender and development of hyperkalemia. [3]

In children with chronic kidney disease, the prevalence of hyperkalemia is approximately 1.6 percent.[4]

Characteristics/Clinical Presentation

Hyperkalemia most commonly occurs in patients with chronic renal failure and is also correlated with diabetes. [2] [5]

Signs and Symptoms

  1. muscular weakness
  2. flaccid paralysis
  3. ileus
  4. ECG changes[2]
  5. nausea
  6. slow, weak or irregular pulse
  7. sudden collapse (heart rate too slow or stops)[6]
  8. paraestesias
  9. fatigue
  10. palpitations

Potassium is regulated through excretion via the renal system. When this system's function declines, the extracellular potassium concentration increases and can lead to membrane excitability.  Some signs and symptoms listed above are a result of the impaired nerve conduction and muscle contraction dysfunction.  Muscular dysfunction includes the cardiac system and can lead to life threatening ventricular arrhythmias.  Electrocardiogram (ECG) dysfunction is more common in patients with acute hyperkalemia.[1]

Associated Co-morbidities

                                                     Table 1

                                Disorders Causing Hyperkalemia

Disorders leading to hyperkalemia caused by impaired renal excretion of potassium Disorders leading to hyperkalemia caused by shift of potassium into the extracellular space
acquired hyporeninemic hypoaldosteronism acidosis
Addison's disease damage to tissue from rhabdomyolysis, burns, or trauma
congenital adrenal hyperplasia (recessive or autosomal dominant) familial hyperkalemic periodic paralysis
mineralocorticoid deficiency hyperosmolar states (uncontrolled diabetes, glucose infusions)
primary hypoaldosteronism or hyporeninemia tumor lysis syndrome
pseudohypoaldosteronism insulin deficiency or resistance
renal insufficiency or failure
systemic lupus erythematosus
type IV renal tubular acidosis



Medications Used in Acute Treatment of Hyperkalemia
Medication Dosage Onset Length of Effect Mechanism of Action Cautions
Calcium gluconate 10 to 20 mL of 10 percent solution IV over two to three minutes immediate 30 minutes Protects myocardium from toxic effects of calcium; no effect on serum potassium level Can worsen digoxin toxicity
 Insulin Regular insulin 10 units IV with 50 mL of 50 percent glucose 15 to 30 minutes two to six hours Shifts potassium out of the vascular space and into the cells; no effect on total body potassium Consider 5 percent dextrose solution infusion at 100 mL per hour to prevent hypoglycemia with repeated doses. Glucose unnecessary if blood sugar elevated above 250 mg per dL (13.9 mmol per L)

Beta agonists:

Albuterol (Ventolin)

10 to 20 mg by nebulizer over 10 minutes (use concentrated form, 5 mg per mL) 15 to 30 minutes two to three hours Shifts potassium into the cells, additive to the effect of insulin; no effect on total body potassium May cause a brief initial rise in serum potassium


Furosemide (Lasix)

20 to 40 mg IV, give with saline if volume depletion is a concern 15 minutes to one hour four hours Increases renal excretion of potassium Only effective if adequate renal response to loop diuretic

Potassium binding resins: 

Sodium polystyrene sulfonate (Kayexalate)

Oral: 50 g in 30 mL of sorbitol solution Rectal: 50 g in a retention enema one to two hours (rectal route is faster) four to six hours Removes potassium from the gut in exchange for sodium Sorbitol may be associated with bowel necrosis. May lead to sodium retention

IV = intravenously

--Medications listed from most to least urgent.[2]

Diagnostic Tests/Lab Tests/Lab Values

Initial diagnosis is initiated with patient history, medication review, and physical examination. 

Laboratory tests include:

  1. serum electrolytes (especially potassium and glucose [1])
  2. creatinine
  3. blood urea nitrogen (BUN)
  4. spot urine test (potassium, creatinine, and osmoles)
  5. transtubular potassium gradient (assessment of renal potassium handling)
  6. trial of oral fludrocortisone (Florinef)[2]

Patients will likely not present with symptoms of hyperkalemia until potassium levels have exceeded 7 mmol/L.  However, immediate medical attention is required when potassium level exceed 6.5 mmol/L or exceed 6.0 mmol/L with ECG changes consistent with hyperkalemia.[1]

ECG is monitored in patients with hyperkalemia:

Ecg thing.gif



Hyperkalemia is typically caused when the kidneys can no longer excrete potassium, when the body is unable to effectively distribute potassium between the extracellular and intracellular space, or the effects of medications (including increased potassium intake).  For hyperkalemia caused by decreased excretion of potassium, there is an insufficient delivery of sodium and water in the kidney and the presence of aldosterone.  For medication induced hyperkalemia, a combination of ACE inhibitors and spironolactone or the use of NSAIDs in patients with impaired kidney function or diabetes can predispose the patient.  An interesting fact about spironolactone is its involvement with the onset of renal failure and hyperkalemia.  The article by Tamirisa et al. reported that spironolactone had to be discontinued due to induced hyperkalemia and renal failure in 7.6% of patients rather than the 2% prevalence reported in previous research[5].  Adrenal insufficiency is another potential cause, particularly when the patient also presents with hyponatremia and muscular weakness.  Congenital factors that can produce hyperkalemia include pseudohypoaldosteronism and aldosterone synthesis abnormalities.[2]

Many factors influence the aforementioned causes of hyperkalemia:

Table 1. Causes of Hyperkalemia [1]

Factitious hyperkalemia (laboratory value higher than serum value)

- hemolysis due to specimen handling or collection error

- laboratory error

Increased intake of potassium

- potassium supplements

- penicillin G potassium

- nutritional supplements 

Increased shift of potassium from intracellular space

- exercise

- tissue destruction (e.g., tumour lysis syndrome, rhabdomyolysis, trauma)

- normal anion gap acidosis

- lack of insulin

- hyperosmolality

- hyperkalemic periodic paralysis

- medications (succinylcholine, beta blockers, digitoxin intoxication, intravenous amino acids)

Impaired renal potassium excretion

- decreased flow (e.g. from decreased effective circulating volume, chronic or acute renal failure, nonsteroidal anti-inflammatories)

- hypoaldosterone

- primary adrenal insufficiency

- medications (e.g. spironolactone, triamterene, amiloride, ACE inhibitors, ARBs, trimethoprim, pentamidine, cyclosporine, tacrolimus, heparin)

- primary renin insufficiency

- pseudohypoaldosteronism

- distal renal tubular acidosis

- congenital adrenal hyperplasia

- interstitial renal disease

Unknown mechanism

- herbal medicine (e.g. alfalfa, dandelion, noni juice, horsetail, milkweed, thistle)

ACE = angiotensin-converting enzyme

ARB = angiotensin receptor blocker

  Systemic Involvement  

Table 5-10 Clinical Features of Various Electrolyte Imbalances[7]

Potassium Imbalance (hyperkalemia) System Dysfunction
Cardiovascular tachycardia and later bradycardia, ECG changes, cardiac arrest (with levels .7.0 mEq/L)
GI nausea, diarrhea, abdominal cramps
Musculoskeletal muscle weakness, flaccid paralysis
Genitourinary oliguria, anuria
Central nervous system areflexia progressing to weakness, numbness, tingling, and flaccid paralysis
Acid-base balance metabolic acidosis

Medical Management (current best evidence)

The presence of ECG changes, a rapid rise of serum potassium, indications of decreased kidney function, or significant acidosis require immediate medical treatment for hyperkalemia.  Although ECG changes are common indicators for severe hyperkalemia, the patient may still have life threatening hyperkalemia even if ECG readings are normal.  The intent of immediate medical intervention is to stabilize the myocardium to prevent arrhythmias.  In addition to the medications listed in Table 5, total body potassium levels can be lowered through kidney excretion, gastrointestinal (GI) elimination, or dialysis.  Lowering via kidney excretion is achieved by the use of diuretics, while lowering via GI elimination occurs with the use of Kayexalate, both of which are explained in greater detail in Table 5.  Long term management is focused on addressing the underlying cause, which can be achieved by discontinuing medications or consuming low potassium diets.[2]


Figure 2:  Algorithm for the management of hyperkalemia.[2]

Foods high in potassium can also be implicated in the development of hyperkalemia. 

Table 2. High-potassium foods[1]

(National Kidney foundation, 2010)

- salt substitutes and salt free broth

- yogurt, milk

- molasses

- seaweed

- chocolate

- bran cereal, wheat germ, granola

- vegetables (acorn squash, artichoke, bamboo shoots, beets, broccoli, brussel sprouts, chinese cabbage, carrots, greens (except kale), kohlrabi, mushrooms (canned), parsnips, potatoes, pumpkin, rutabagas, spinach, tomatoes, vegetable juices)

- dried fruit (apricot, dates, figs, raisins, prunes)

- nuts and seeds, (peanut butter)

- dried peas and beans (lima beans, black beans, refried beans, lentils, legumes)

- fruit and juice (apricot, avocado, banana, cantaloupe, grapefruit, honeydew, kiwi fruit, mango, nectarine, orange, papaya, pomegranate, prune)

Physical Therapy Management (current best evidence)

Potassium levels < 3.2 mEq/L or > 5.1 mEq/L are contraindicated for physical therapy intervention due to the potential for arrhythmia and tetany.  When potassium levels are not within the normal range (3.5-5.0 mEq/L) exercise is not effective due to decreased muscle pH and action potentials as well as inhibition of motor neurons.  With a patient who has marginal potassium levels, vital signs (including pulse rhythm) and any signs of dizziness, muscle weakness or cramping, numbness or tingling, and changes in balance should be closely monitored.  At this time, no research addresses the change in potassium level that occurs with exercise.  However, it is known that patients with hyperkalemia are at risk for ventricular arrhythmias which can result in reduced exercise tolerance.[7]

Hyperkalemia is a disorder that is not managed primarily by a physical therapist, however physical therapists should be aware of signs and symptoms of this disorder and should refer the patient to a medical doctor when indicated.

Differential Diagnosis

Pseudohyperkalemia occurs when lab reports indicate elevated serum potassium levels but the patient does not actually have elevated serum potassium.  This phenomenon occurs most commonly with destruction of red blood cells with collection of blood specimen.[2]

In patients with renal failure, digoxin toxicity can commonly be mistaken for hyperkalemia. [8]

Case Reports/ Case Studies

Case Study 1

Colonic ulceration in a patient with renal disease and hyperkalemia [9]

51 year old male who developed large GI ulcer following pharmacological management of hyperkalemia

Case Study 2

Beating the odds--surviving extreme hyperkalemia [10]

58 year old woman who survived severe hyperkalemia (> 10 mmol/L)


High Potassium (Hyperkalemia)--Mayo Clinic

High Potassium Levels--Medline Plus

Hyperkalemia--University of Maryland Medical Center


see adding references tutorial.

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Raymond C, Sood A, Wazny L. Treatment of hyperkalemia in patients with chronic kidney disease--a focus on medications. CANNT Journal [serial on the Internet]. (2010, July), [cited March 22, 2013]; 20(3): 49-54. Available from: CINAHL with Full Text. http://search.ebscohost.com/login.aspx?direct=true&db=c8h&AN=2010782358&site=ehost-live (accessed 22 Mar 2013)
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Hollander-Rodriguez JC, Calvert, Jr. JF. Hyperkalemia. American Family Physician 2006; 73(2):283-290. Available from: PubMed. http://www.ncbi.nlm.nih.gov/pubmed/16445274 )22 March 2013)
  3. Stevens MS, Dunlay RW. Hyperkalemia in hospitalized patients. International Urology and Nephrology 2000; 32(2):177-180. Available from: SpringerLink. http://link.springer.com/article/10.1023/A%3A1007135517950#page-1 (4 Apr 2013)
  4. Wong H, Mylrea K, Feber J, Drukker A, Filler G. Prevalence of complications in children with chronic kidney disease according to KDOQI. Kidney International [serial on the Internet]. (2006, Aug), [cited April 4, 2013]; 70(3): 585-590. Available from: Academic Search Premier.
  5. 5.0 5.1 Tamirisa KP, Aaronson KD, Koelling TM. Spironolactone-induced renal insufficiency and hyperkalemia in patients with heart failure, American Heart J 2004; 148(6):971-978. Available from: Europe Pubmed Central. http://www.sciencedirect.com/science/article/pii/S0002870304007501 (Accessed 4 April 2013)
  6. Dugdale DC, Zieve D. MedlinePlus. [homepage on the Internet]. 2011 [cited 2013 Mar 22]. Available from: U.S. National Library of Medicine, National Institutes of Health Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001179.htm
  7. 7.0 7.1 Goodman CC & Fuller KS. In K Falk editor. Pathology: Implications for the Physical Therapist. St. Louis: Saunders Elsevier; 2009. pp.150, 157, 187-189, 480, 558, 927, 1243, 1640-1641
  8. Papadakis MA, Wexman MP, Fraser C. Hyperkalemia complicating digoxin toxicity in a patient with renal failure. Am J Kidney Dis. 1985; 5(1):64-66. Available from: PubMed. http://www.ncbi.nlm.nih.gov/pubmed/3966471 (Accessed 4 Apr 2013)
  9. Chelcum JL, Sable RA, Friedman K. Colonic ulceration in a patient with renal disease and hyperkalemia, J of American Academy of Physician Assistants 2012; 25(10):34-38. Available from: ProQuest. http://search.proquest.com/docview/1288361388/fulltextPDF?accountid=6741 (Accessed 22 Mar 2013)
  10. Muck PM, Letterer S, Lindner U, et al. Beating the odds-surviving extreme hyperkalemia. The American J of Emergency Medicine 2012; 30:250.e1 - 250.e4. Available from: ProQuest. http://search.proquest.com/docview/1030946274/fulltext/13D368764547F8F25FD/1?accountid=6741 (Accessed 22 Mar 2013)