In our previous article, we described how sodium and fluid imbalances affect the clinical status and outcomes of critically ill patients. In this article, we'll look at three more electrolytes involved in the "critical care shuffle," and what you need to know to recognize and correct these electrolyte abnormalities.

Figure. No caption available.

Potassium: Getting pumped

Potassium is the most abundant intracellular (IC) cation, and plays a vital role in many body functions, including a vital role in regulating neuromuscular excitability.1 Potassium balance is largely determined by dietary intake and kidney function. The kidneys are the main source of potassium loss, with 80% to 90% of potassium losses occurring via urine.1 A primary function of potassium familiar to most critical care nurses is its role in regulating the electrical action potential across cell membranes (cardiac, skeletal, and smooth muscle).

Remember that the sodium/potassium-adenosine triphosphate (ATP) pump helps to maintain a higher IC potassium concentration (140 to 150 mEq/L) compared with a lower extracellular (EC) concentration of 3.5 to 5 mEq/L.1,2

Critically ill patients often experience alterations in one or many of the factors that affect the activity of this pump, such as insulin, glucagon, catecholamines, aldosterone, pH, serum osmolality, and IC potassium levels.

Hypokalemia

A serum potassium level of less than 3.5 mEq/L can be caused by excessive losses through the kidneys, gastrointestinal (GI) tract, and skin; redistribution of potassium between the IC and EC spaces; and, less commonly, insufficient intake. Causes of hypokalemia in critically ill patients include underlying conditions or medications, such as diuretics. When the body is experiencing a decrease in potassium, it doesn't initiate any compensatory mechanisms, such as reabsorption, to keep the potassium it has. The kidneys just keep excreting potassium no matter what the patient's serum potassium level. If your patient is hypokalemic, your priority is to quickly identify underlying causes and implement measures to treat the imbalance. Remember these three points:

* A potassium level below 2.5 mEq/L puts the patient at risk for cardiac arrest.

* Patients with hypokalemia may also have decreased magnesium levels; if this is the case, correct the hypomagnesemia first, or the patient may not respond to supplemental potassium administration, because the kidneys can't conserve potassium when magnesium is low.3

* Digoxin, a medication commonly given in CCUs, is contraindicated in patients with hypokalemia because renal changes in hypokalemia increase the risk of digoxin toxicity.4-6

Signs and symptoms of hypokalemia primarily affect the cardiovascular, neuromuscular, GI, and central nervous systems.1

* Mild hypokalemia, defined as a serum potassium level of 3 to 3.4 mEq/L, is characterized by fatigue and minimal muscle weakness.7,8

* Moderate hypokalemia, defined as a serum potassium level of 2.4 to 2.9 mEq/L, is characterized by proximal muscle weakness, nausea and vomiting, paralytic ileus, and diarrhea.

* Severe hypokalemia, defined as a serum potassium level less than 2.4 mEq/L, is characterized by ECG changes, cardiac dysrhythmias, decreased deep tendon reflexes, rhabdomyolysis, myoglobinuria, constipation, hypotension, and respiratory or cardiac arrest.8

Patients with hypokalemia also will have metabolic alkalosis, as indicated by an increased pH due to a primary excess in HCO₃^-.1

Critically ill patients with hypokalemia and underlying heart disease (such as heart failure) are at an increased risk for ventricular dysrhythmias. In contrast, critically ill patients without heart disease rarely experience major cardiac abnormalities due to hypokalemia. Monitor the patient for increased ectopy, which could signal more serious dysrhythmias.9 In these situations, intervene promptly to avoid a medical emergency.

The ECG changes that are commonly associated with hypokalemia include prolonged PR intervals, flattened or inverted T waves, depressed ST segments, or U waves (see ECG changes and electrolytes).7-9 Remember that the presence or absence of ECG changes isn't predictive of hypokalemia or its severity, so critical assessment of the patient and lab findings is always required.8

Treatment goals for a patient with hypokalemia include identifying and correcting the underlying cause, normalizing the serum potassium level, and resolving associated signs and symptoms. Treatment will be based on the severity of the patient's clinical manifestations. One exception is the critically ill patient who's suffered an acute myocardial infarction (MI). Because of the risk of ventricular dysrhythmias, even mild hypokalemia should be treated in these patients, so that the patient's serum potassium level stays above 4.5 mEq/L.8,10

The route and formulation of potassium replacement is patient-specific, and depends on the severity of signs and symptoms and the patient's overall medical status. Increase dietary potassium intake if possible (for example, through orange juice and bananas). Oral potassium preparations, such as potassium chloride, or I.V. potassium chloride may be prescribed.5,8-10

Hyperkalemia

Although less common than hypokalemia, hyperkalemia (defined as a serum potassium level of greater than 5 mEq/L) is potentially more serious.6,8 Hyperkalemia frequently occurs in patients with underlying renal compromise, and can be caused by many conditions experienced by critically ill patients, as well as an extensive list of medications used in critical care.11 Some causes are acute or chronic renal failure, improper use of potassium supplements, pseudohyperkalemia (hemolysis of blood sample), adrenal insufficiency, insulin deficiency and resistance, metabolic acidosis, digoxin overdose, tumor lysis after chemotherapy, tissue damage from rhabdomyolysis, massive blood transfusions, burns, and trauma.5,11

Medications that can cause hyperkalemia include angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, direct rennin inhibitors, cyclosporine, potassium-sparing diuretics such as spironolactone, and NSAIDs. Succinylcholine can, in some patients, trigger potassium release from damaged muscles, resulting in catastrophic hyperkalemia.11

Clinical manifestations of hyperkalemia are largely related to changes in cardiovascular and neuromuscular function. Continuously monitor for ECG abnormalities in patients at risk for or experiencing hyperkalemia. Early ECG changes include tall tented T waves. More severe hyperkalemia can cause prolongation of the PR interval and QRS duration, atrioventricular (AV) conduction delays, loss of P waves, and serious ventricular dysrhythmias.7,8-11

Neuromuscular signs and symptoms include paresthesias, muscle weakness, flaccid paralysis, and hypoventilation if respiratory muscles are affected. GI manifestations include nausea, vomiting, intestinal cramping, and diarrhea.

Treatment for hyperkalemia is aimed at prompt identification and treatment of the underlying causes and includes:

* reducing the body content of potassium by eliminating all sources of exogenous potassium, including dietary sources of potassium and discontinuing medications that cause hyperkalemia (such as potassium-sparing diuretics).

* removing potassium by administering loop or thiazide diuretics, administering a cation exchange resin (sodium polystyrene sulfonate, preferably without sorbitol because of the risk of intestinal necrosis when given with sorbitol), or initiating renal replacement therapy.12

* promoting the movement of potassium from the EC space to the IC space by administering I.V. regular insulin, which works mainly by enhancing the sodium-potassium-ATP pump in skeletal muscle. Glucose is usually given with the insulin to prevent hypoglycemia unless the serum glucose level is equal to or greater than 250 mg/dL. Beta₂ adrenergic agonists, such as albuterol, can also drive potassium into the cells. Sodium bicarbonate may also be used in the acute management of hyperkalemia in the setting of metabolic acidosis.12

* antagonizing the cellular membrane effect of potassium by administering I.V. calcium gluconate.5,7,8,11,13

Calcium: Take two

Most calcium (99%) is found in the bones, with less than 1% present in serum. Forty to 50% of the calcium in serum is bound primary to albumin (plasma protein). Serum calcium is regulated by the parathyroid hormone, vitamin D, and calcitonin.14 Calcium plays a major role in the electrophysiology of the heart and smooth muscles, neuromuscular activity, bone metabolism, coagulation, and platelet adhesion.7 Calcium and phosphate have an inverse relationship; calcium levels fall when phosphorus levels are high and vice versa.15

Calcium can be measured as total serum calcium or ionized serum calcium. Total serum calcium reflects calcium bound to proteins (primarily albumin), and levels are influenced by patient's nutritional status. If the patient's serum albumin level is low (the normal range is 3.5 to 5.5 g/dL), serum calcium levels will also be low. Therefore, in patients with hypoalbuminemia or hyperalbuminemia, the measured serum calcium concentration should be corrected for the albumin abnormality. Serum calcium levels also fluctuate with changes in pH.

Figure. ECG changes and electrolytes

Ionized serum calcium is unbound, and is the biologically active form of calcium. This type of calcium makes up about 50% of calcium in the blood, is regulated by the endocrine system, and plays a crucial role in neuromuscular activity. Levels of ionized serum calcium remain normal even when total serum calcium and serum albumin levels are low. However, ionized calcium levels fall during metabolic alkalosis and rise during metabolic acidosis.4,14

Of the two values, serum ionized calcium is a better marker of the functional status of calcium metabolism, and should be used in critical care areas because of the poor correlation between total serum calcium and serum ionized calcium, especially in critically ill patients with hypoalbuminemia or an acid-base imbalance.14

Hypocalcemia

One of the most frequently seen electrolyte abnormalities, hypocalcemia affects 80% to 90% of critically ill patients, and is defined as a total serum calcium of less than 8.6 mg/dL, or a serum ionized calcium of less than 4.5 mg/dL.11 Causes of hypocalcemia specific to critically ill patients may include hypoalbuminemia, hypomagnesemia, hyperphosphatemia, acute pancreatitis, malabsorption syndromes, surgical or primary hypoparathyroidism, sepsis, and renal insufficiency. Critically ill patients who receive massive blood transfusions or continuous renal replacement therapy also can develop hypocalcemia because of the citrate used in these therapies to prevent coagulation-citrate also prevents calcium ionization.5 Medications such as loop diuretics also put patients at risk for hypocalcemia.

Patients with hypocalcemia will have decreased clotting and prothrombin times, decreased magnesium levels, and increased phosphate levels. Signs and symptoms depend on the severity of hypocalcemia:

* Mild to moderate hypocalcemia is characterized by fatigue, depression, anxiety, confusion, hyperreflexia, muscle cramps, and paresthesias.

* Severe hypocalcemia is characterized by tetany, seizures, laryngospasm, bronchospasm, and stridor, positive Trousseau and Chvostek signs, prolongation of the QT interval, and hypotension.16

* Chronic hypocalcemia is characterized by brittle and grooved nail beds, hair loss, dermatitis, dry skin, eczema, parkinsonism, dementia, subcapsular cataracts, and abnormal dentition.5,7,14,17,18

Pharmacologic management of hypocalcemia usually involves oral (such as calcium carbonate or calcium citrate), or I.V. calcium supplementation (such as calcium gluconate or calcium chloride), along with vitamin D or magnesium supplementation.

Mild to moderate hypocalcemia can be treated with oral calcium supplements or vitamin D, which increases calcium absorption from the GI tract. Calcium acetate, aluminum hydroxide, or calcium carbonate antacids may be used to decrease phosphate levels (more commonly in patients with renal insufficiency). If the patient has concomitant hypomagnesemia, administer magnesium supplements as prescribed to help correct the low calcium levels. A patient with moderate symptomatic hypocalcemia may also need an I.V. calcium salt, preferably I.V. calcium gluconate (which is less likely to cause tissue necrosis if it extravasates, compared with calcium chloride).16

Patients in need of rapid correction or with severe symptomatic hypocalcemia will require an I.V. calcium salt.5,15,18

Hypercalcemia

Elevated calcium levels are less common in critically ill patients, but severe hypercalcemia is associated with a 50% mortality if not treated promptly.7

Mild to moderate hypercalcemia is defined as a total serum calcium between 10.3 mg/dL and 12.9 mg/dL; severe hypercalcemia is a total serum level of 13 mg/dL or greater.

Hypercalcemia is most frequently caused by hyperparathyroidism (which increases calcium release from the bones and increases intestinal and renal absorption of calcium) and malignancy. Another cause is immobility, although this is considered less common. Patients with extensive trauma-related fractures or spinal cord injuries are at an increased risk for developing hypercalcemia. Also, medications such as thiazide diuretics, lithium, and theophylline toxicity can lead to hypercalcemia, as can dehydration.5,7,14

Signs and symptoms of hypercalcemia are proportional to the elevation in calcium level. Initially, the patient may have anorexia, nausea, vomiting, and constipation. As the calcium level increases, the patient may complain of severe bone and abdominal pain, and may develop polyuria and polydipsia.

Severe hypercalcemia is a medical emergency because it can cause acute renal failure, mental status changes, ventricular dysrhythmias, coma, and death if not promptly and appropriately treated. ECG findings indicative of hypercalcemia are shortened QT intervals, bradycardia, and AV block.

* The treatment goals are to identify and treat the underlying cause and normalize the serum calcium level. Typical measures include:

* aggressive I.V. hydration with 0.9% sodium chloride solution to dilute serum calcium and improve renal clearance of calcium)

* I.V. furosemide (after hydration is achieved) to promote diuresis and calcium excretion

hemodialysis, if needed in patients with impaired renal function.5,7,14

Calcitonin may be given via subcutaneous or I.M. injection in patients with heart disease or renal failure, who can't tolerate large sodium loads. Calcitonin decreases bone reabsorption, increases the deposition of calcium and phosphorus in the bones, and increases urinary excretion of calcium and phosphorus. Finally, for patients with malignancy, bisphosphonates may be used because they inhibit osteoclast activity.7

Magnesium: Under investigation

Magnesium is the second most abundant IC cation after potassium, and most of the body's EC magnesium is found in the bones and soft tissues.1 Absorbed in the distal small bowel, magnesium is eliminated by the kidneys, and as with sodium, potassium, and calcium, is needed for neuromuscular and cardiovascular activity. For example, an increased level of magnesium decreases the excitability of the muscle cells, and conversely, a decreased magnesium level increases neuromuscular irritability and contractility. Magnesium also plays a role in protein and carbohydrate metabolism. Remember that a patient with a magnesium deficit will also often have potassium and calcium deficits.

Magnesium is similar to calcium in two respects: the ionized fraction of magnesium is most involved in neuromuscular activity and other pathologic processes, and magnesium levels should be evaluated in conjunction with albumin levels, because 20% to 30% of EC magnesium is protein-bound, typically with albumin.1,7 Scrutinize the patient's lab findings-making these connections is key to implementing appropriate treatment.

Hypomagnesemia

Hypomagnesemia, defined as a serum magnesium level of less than 1.3 mg/dL, is often missed in critically ill patients when it's associated with alcohol abuse or magnesium-deficient enteral or parenteral nutrition formulas. Other causes of hypomagnesemia include starvation, diarrhea, laxatives, intestinal fistulas, nasogastric tube suctioning, vomiting, medications (including diuretics, aminoglycosides, cisplatin, cardiac glycosides, and insulin), diuresis, pancreatitis, burns, infection, acute MI, and heart failure.5,7,9,18

Signs and symptoms of hypomagnesemia include neuromuscular irritability, increased deep tendon reflexes, hypertension, positive Trousseau and Chvostek signs, insomnia, mood changes, anorexia, vomiting, and ECG changes (including dysrhythmias, flat or inverted T waves, prolonged PR or QT intervals, and widened QRS complexes).5,7,9,18

Treatment for hypomagnesemia includes prompt identification and treatment of the underlying cause, as well as administering I.V. magnesium for acute replacement and oral magnesium supplementation for long-term replacement. Monitor the patient's electrolytes closely.

Because hypomagnesemia is a common electrolyte imbalance in critically ill patients, and is associated with increased mortality, keep the patient's serum magnesium level at 1.5 mg/dL. Keep the level at 1.7 mg/dL or greater in patients who've suffered a recent acute MI, to prevent the development of cardiac dysrhythmias.18

Hypermagnesemia

Hypermagnesemia, or a serum magnesium level of greater than 2.3 mg/dL, is most commonly caused by renal failure, excessive intake of magnesium-containing compounds such as laxatives, diabetic ketoacidosis, hypothyroidism, and iatrogenic causes.5,7,9

Signs and symptoms include flushing, hypotension, muscle weakness, drowsiness, hypoactive deep tendon reflexes, depressed respirations, diaphoresis, and ECG changes (such as tachycardia developing into bradycardia; prolonged PR, QRS, and QT intervals; AV block; coma; and cardiac arrest).

Avoid administering magnesium-containing compounds to a patient with hypermagnesemia and renal failure. In extreme cases, patients may need dialysis, or I.V. calcium can be given as a magnesium antagonist.19

The "critical care shuffle" can be challenging, but by understanding these electrolyte and fluid changes, you'll be better-prepared to care for your critically ill patient.

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