Restoring electrolyte balance
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Restoring electrolyte balance
CE credit is no longer available for this article. (Expired May 2007)
Originally posted May 2005
By Sonia M. Astle, RN, MS, CCRN
Sonia Astle is a critical care clinical specialist at Inova Fairfax Hospital in Falls Church, VA, and a member of the RN editorial board. The author has no financial relationships to disclose.
A shift up. A shift down. Either way, an imbalance in electrolytes spells trouble for your patients. Averting a crisis hinges on your clinical skills. This review will help you sharpen them.
Electrolytes, or ions, are the charged particles in body fluids that help transmit electrical impulses for proper nerve, heart, and muscle function.1,2 The number of positive ions, called cations, and negative ions, called anions, is supposed to be equal. Anything that upsets this balance can have life-threatening consequences.
There's a long list of conditions that lead to electrolyte imbalances, including dehydration, diabetic ketoacidosis, cancer, and even head injury. But renal disease is at the top of the list.1-3 It's the kidneys' job to control fluid, electrolyte, and acid-base balance.
Because too much or too little of any one of the electrolytes quickly becomes a major problem of its own, doing everything possible to maintain the proper balance is a vital component of patient care. Therefore, monitoring electrolytes and checking for signs of an imbalance should be an integral part of your nursing assessment.
Here, then, is a review of the role each electrolyte plays, the causes of imbalances, and the corrective measures required.
Understanding sodium's effect on water balance
Sodium (Na), the most abundant cation in extracellular fluid, plays a key role in transmitting nerve impulses. It also helps maintain serum concentration, or osmolality.1
Water follows salt in the body, so a gain or loss in sodium results in a gain or loss in water. For instance, when you eat too much salt, the rise in serum osmolality triggers thirst and the release of antidiuretic hormone (ADH) from the pituitary gland. Thirst leads you to drink, while ADH signals the kidneys to hang onto water.1,2
The opposite is also true: Low serum osmolality from too little salt stops thirst and inhibits ADH release, allowing more water to be excreted by the kidneys.2
Hypernatremia occurs when either too much water is lost or too much salt is taken in. (You'll find a list of normal values and causes of electrolyte imbalances in the box on page 37). The elderly are particularly at risk for hypernatremia following surgery or a fever because of volume depletion, and because of a diminished thirst mechanism.4 All patients on fluid restrictions and those receiving diuretic therapy, hypertonic IV solutions, or tube feedings are at risk, as well.1,4 So, too, are patients with diabetes, because of dehydration related to their hyperglycemia.3
Regardless of the cause, patients with hypernatremia may appear thirsty, tachycardic, and lethargic.1,2 As their cells become more dehydrated, patients may develop disorientation, weakness, irritability, and muscle twitching. Urine output is generally low as the body tries to compensate by hanging onto water. The exception is untreated diabetes insipidus, where a lack of ADH results in a high urine output—possibly as much as 20 liters in 24 hours.1,2 Regardless, though, of whether urine output is high or low, seizures, coma, or death may result if hypernatremia is left untreated.1,2
Correcting the situation requires that you focus on the underlying cause. That may be as simple as replacing volume orally or by the IV administration of isotonic solutions such as normal saline.5 Or it may be as complex as putting the patient on dialysis. Part of your routine nursing care for the hypernatremic patient will involve monitoring serum sodium and osmolality and administering fluids based on the results.5 You'll also carefully monitor intake and output, and avoid overhydration.
The flip side of the sodium equation is hyponatremia, which usually occurs when the body loses more sodium than water or when excess water dilutes the normal sodium concentration.1,2 Dilutional hyponatremia can be caused by excess fluid intake, and conditions such as congestive heart failure or syndrome of inappropriate antidiuretic hormone secretion (SIADH).2
The neurological symptoms of hyponatremia are similar to those of hypernatremia—lethargy and confusion—with the possible addition of nausea and vomiting resulting from cerebral edema.2 Other signs and symptoms depend upon the cause. Patients who've lost sodium through diarrhea, certain diuretics, suctioning, or laxatives, for example, may show signs of dehydration, including tachycardia and hypotension. Those with dilutional hyponatremia may show signs of fluid overload, such as hypertension and difficulty breathing.
Treatment depends upon both the degree of sodium deficiency and the cause. In cases of mild hyponatremia, an increased intake of dietary sodium may be ordered, while patients who are both hyponatremic and hypovolemic may receive IV fluid replacement using solutions containing normal saline.6 Those with mild dilutional hyponatremia from overadministration of free water may need nothing more than the restriction of fluid intake. This approach is also appropriate for patients with hyponatremia caused by SIADH.2,5,6
Severe hyponatremia, however, is a medical emergency: Permanent neurological damage can occur when serum sodium falls below 110 mEq/L.2 Giving hypertonic saline (3% NaCl) solution is the treatment of choice, but must be done with caution: A rapid increase in serum sodium can cause fluid overload and cardiac failure, as well as cerebral osmotic demyelination syndrome—a condition caused by osmotic injury to myelinated nerve fibers that leads to paralysis and death.2,5
Other imbalances to watch for
Potassium (K), magnesium (Mg), calcium (Ca), and phosphorus (PO4) imbalances can also alter the electrical equilibrium of the cells. The end result? Serious changes in cardiac conduction that can quickly turn lethal.1,2 Let's look at each of these electrolytes and the implications that an imbalance will have on your care.
Potassium. This electrolyte is the major intracellular cation. The 2% that's found in extracellular fluid is crucial to neuromuscular and cardiac function.2 Normally, elevated serum potassium stimulates the release of aldosterone, a hormone produced by the adrenal gland. In the kidneys, aldosterone triggers the excretion of potassium and the retention of sodium until serum potassium levels return to normal.2
But when the kidneys aren't functioning properly, that correction doesn't take place. Not surprisingly, renal disease is the most common cause of hyperkalemia, but acidosis, aldosterone deficiency, sodium depletion, and excess oral intake of potassium supplements are among a number of other possible causes. Signs and symptoms of hyperkalemia include abdominal cramping, fatigue, lethargy, and muscle weakness or paralysis.
Severe hyperkalemia will slow cardiac impulse conduction, producing classic changes on EKG:1,2 Tall, peaked T waves are often seen first, followed by a prolonged PR interval and widened QRS complex, signifying delayed conduction, and a shortened QT interval. Left untreated, the excess potassium will continue to suppress conduction until cardiac arrest occurs.1
Severe hyperkalemia requires rapid action: Stop any potassium administration, and give IV calcium chloride or calcium gluconate, as ordered, to stimulate conduction.5 The doctor may also order IV sodium bicarbonate, insulin and 50% dextrose, or albuterol to try to shift potassium out of the bloodstream and back into the cells.5
Depending upon their kidney function, patients with hyperkalemia that is not severe may be given IV diuretics to promote potassium excretion by the kidneys or a resin such as sodium polystyrene sulfonate (Kayexalate) that will bind potassium in the gut. But if these efforts fail, hemodialysis may be required in addition to treating the underlying cause.2,5
When it comes to hypokalemia, diuretic therapy with inadequate potassium replacement is the most common cause, but patients who lose large amounts of potassium through nasogastric suctioning and diarrhea, for instance, are also at risk.1,2 Interestingly, so, too, are patients who were recently hyperkalemic—especially when acidosis is the cause or they're given too much of a drug that brings the potassium down. In acidosis, as pH returns to normal, potassium returns to the cells, lowering serum potassium and increasing the risk of hypokalemia.1,2
Symptoms of hypokalemia include muscle weakness or tenderness, leg cramps, drowsiness, confusion, loss of appetite, abdominal distention, and abnormal cardiac conduction.
Look for flattened or inverted T waves and a depressed ST segment on an EKG tracing. The lack of potassium makes cardiac muscle irritable, increasing the risk of premature atrial and/or ventricular contractions that can trigger ventricular tachycardia, which can progress to fibrillation and death.2
Initial treatment of hypokalemia, especially when it is accompanied by cardiac symptoms, focuses on replacing potassium.2,5 But this requires great care: Given too rapidly, IV potassium can cause cardiac arrest, so never administer it by IV push.5 Follow your institution's protocol, using a pump, if possible, to regulate the infusion so that it runs in over at least an hour when 15 - 20 mEqs are mixed in 100 mls of solution.
Because potassium is very irritating to tissues, administration through a central line is recommended.5 For the same reason, you should give oral preparations with food to reduce gastric irritation and abdominal discomfort. Report continued complaints of abdominal pain or distention to the physician. This could be a sign of upper GI ulcers caused by potassium.1,4
Magnesium. This cation is found primarily in the cells and is responsible for reactions that involve muscle function, energy production, and carbohydrate and protein metabolism.7 Renal failure is the major cause of hypermagnesemia.1,7 Other causes include excessive intake of magnesium-containing antacids and laxatives and conditions that produce acidosis such as diabetic ketoacidosis.3
Signs of hypermagnesemia include lethargy, altered mental status that can progress to coma, respiratory depression, and muscle weakness. Impaired cardiac conduction and contractility produce bradycardia and hypotension and can progress to a full cardiac arrest.1,3,7 EKG changes include a prolonged PR interval, widened QRS complex, and lengthened QT interval.7
If a patient's renal function is normal, treatment may include diuretics to promote magnesium loss. Calcium gluconate given intravenously can help counteract muscle weakness and improve cardiac function.5,7 Patients with severe hypermagnesemia and renal failure may need hemodialysis.
The other side of the magnesium equation is hypomagnesemia. It's common in critically ill patients and is associated with high mortality rates.7 Diuretic therapy, chronic alcoholism, cirrhosis, pancreatitis, and preeclampsia can all cause excessive magnesium loss, as can losses from the GI tract through nasogastric suctioning, fistula drainage, and diarrhea.
Signs and symptoms of hypomagnesemia include muscle weakness or tremors, anorexia, nausea, and dizziness, as well as neurologic changes including lethargy, confusion, and coma.7 Like hypokalemia, hypomagnesemia increases cardiac muscle irritability and the potential for ventricular dysrhythmias, especially in patients with a recent MI.2
EKG changes associated with low serum magnesium are similar to those seen in hypokalemia: a flat or inverted T wave and ST segment depression. There is also a shortened QT interval.7
Treatment focuses on giving the patient magnesium—either in IV or oral form—as ordered to return levels to normal.5,7 This is especially important in patients recovering from an acute MI. Research has shown that maintaining adequate serum magnesium levels in these patients can significantly improve ventricular function and reduce mortality rates.7
Calcium and phosphorus. These two electrolytes are inversely related in the blood: When calcium levels are high, phosphorus levels are low, and vice versa.1,2
Calcium is a cation with multiple functions, including transmitting nerve impulses, maintaining cell wall permeability, and activating the body's clotting mechanism.1 It's also involved in contracting cardiac and smooth muscle, generating cardiac impulses, mediating cardiac pacemaker function, and forming bones and teeth.
Phosphorus, the major intracellular anion, also plays a major role in bone formation.1 It's necessary for energy production in the cells and for carbohydrate, protein, and fat metabolism, as well.1,2 Phosphorous also helps maintain acid-base balance by buffering hydrogen ions.1,2
Parathyroid hormone (PTH) is responsible for regulating calcium and phosphorus. When calcium levels are low, PTH increases calcium reabsorption, and blocks phosphorus from being reabsorbed.
Hypocalcemia can result from diarrhea, diuretics, or acute pancreatitis. It can also be caused by malignancies that steal calcium for abnormal bone formation, conditions that affect the parathyroid gland and thus interfere with PTH production, and disorders that interfere with the availability of calcitrol, such as vitamin D deficiency and malabsorption syndromes.1,2
The drop in calcium that occurs in the presence of these disorders triggers a concomitant rise in phosphorus. But there are primary triggers for hyperphosphatemia to watch for, as well. Hyperphosphatemia can occur in patients with normal renal function if they abuse laxatives that are high in phosphorus or have too much of the mineral in their diet.
Both hypocalcemia and hyperphosphatemia can cause lethargy, fatigue, bone or joint pain, and sudden seizures. Low calcium levels also produce neuromuscular symptoms, including tremors, cramps, and numbness or tingling in the extremities and around the mouth. Patients may also complain of nausea, abdominal distention, vomiting, or constipation and develop cardiac symptoms, including life-threatening ventricular dysrhythmias.
EKG tracings will show prolonged ST segments and QT intervals.1,2 Decreased cardiac output and vascular smooth muscle relaxation produce decreases in BP that can progress to circulatory collapse.
Treatment focuses on increasing calcium and lowering phosphorus.5 Give IV calcium gluconate or calcium chloride or oral preparations, as ordered. Aluminum hydroxide gels that bind to phosphorus are given to increase elimination through the bowel.5 Patients with normal renal function may also receive the diuretic acetazolamide (Diamox) to promote renal excretion of phosphorus.2,5 When necessary, hemodialysis is used to quickly correct hyperphosphatemia.
Now let's take a look at the clinical picture for hypercalemia and hypophosphatemia. Causes of hypercalcemia include excessive use of dietary supplements containing calcium and vitamin D, which increase calcium reabsorption, and hyperparathyroidism. A primary cause of low serum phosphorus is chronic alcoholism.
Symptoms of hypercalcemia and hypophosphatemia include lethargy, fatigue, changes in mental status, anorexia, nausea, diminished bowel sounds, and constipation. Patients may also complain of bone pain; flank and thigh pain is associated with stones formed by excess calcium in the kidneys. Cardiovascular effects include hypertension and conduction abnormalities, seen as AV blocks on EKG, that can progress to cardiac arrest.1,2
IV saline infusions and diuretics are given to lower serum calcium through increased renal excretion.2,5 Steroids may also be administered to decrease intestinal reabsorption of calcium and mithramycin (Mithracin) is given to stimulate calcium deposits in bones.5 Phosphorus replacements can be given orally or by IV infusion.
Acid-base balance must be maintained
Chloride (Cl) and bicarbonate (HCO3) are the major extracellular anions. While both play an important role in maintaining acid-base balance, bicarbonate is by far the star of the show.1,2 Bicarbonate is the body's major buffer system. It helps keep the ratio between acids and bases in a tight range that's numerically expressed as the pH (normal pH is 7.35 - 7.45).1 A rise in pH above normal (alkalosis) or below normal (acidosis) causes cellular damage and can eventually lead to a patient's death.
For its part, chloride exists in an inverse relationship with bicarbonate.1 When there's too little chloride, bicarbonate builds up, and metabolic alkalosis results. The flip side of this—too much chloride—is a bit more complicated. If chloride is high and sodium is normal, the patient may be acidotic.1,2 If chloride is high and the sodium is also high, the patient is likely to be dehydrated.
One way to determine the cause of an acid-base imbalance is by calculating the anion gap.2,5 To calculate this gap, you need to take your patient's lab results and add the chloride and bicarbonate values. Then, subtract the sum of the two from the value for sodium. The normal anion gap range is 8 - 12.5
A high anion gap (>12) is indicative of conditions such as diabetic- or alcohol-induced ketoacidosis.5 A high anion gap may also be your first indication of lactic acidosis in patients with shock or sepsis. A normal anion gap with elevated chloride levels should also raise a flag for acidosis. That's because in cases of diarrhea and renal tubular acidosis, bicarbonate is lost, and chloride is retained to maintain electrical neutrality.1 Either way, interventions focus on treating the underlying cause of the acidosis.5
A low anion gap indicates alkalosis and hypochloremia from vomiting, nasogastric suctioning, or diuretic therapy.2,5 But other causes of alkalosis include Cushing's syndrome, excessive aldosterone secretion, and hypokalemia. Massive blood transfusions, over-administration of IV fluids containing bicarbonate, and excessive intake of antacids containing sodium bicarbonate can also cause bicarbonate levels to rise.
Again, treatment focuses on resolving the underlying cause. Patients with alkalosis may receive acetazolamide.5 The drug lowers bicarbonate levels by increasing its excretion in the urine and prevents the formation of new bicarbonate.2,5 Prolonged use can lead to acidosis, however, so watch bicarbonate levels closely.5
Your careful attention to bicarbonate, chloride, and the other electrolytes mentioned here, can have a tremendous impact on your patient's well-being. Understanding what the lab values mean in relation to changes in a patient's condition can be a challenge. But getting a firm handle on things will ensure that you take the necessary steps to correct imbalances before the situation becomes dire.
1. Kee, J., Paulanka, B., & Purnell, L. (2004). Fluids and electrolytes with clinical applications: A programmed approach (7th ed.). Clifton Park, NY: Delmar Learning.
2. Smeltzer, S. C., & Bare, B. G. (2004). Brunner and Suddarth's textbook of medical-surgical nursing (10th ed.). Philadelphia: Lippincott, Williams and Wilkins.
3. Chiasson, J. L., Aris-Jilwan, N., et al. (2003). Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. CMAJ, 168(7), 159.
4. Luckey, A. E., & Parsa, C. J. (2003). Fluid and electrolytes in the aged. Arch Surg, 138(10), 1055.
5. Metheny, N. M. (2000). Fluid and electrolyte balance nursing considerations (4th ed.). Philadelphia: Lippincott.
6. Johnson, A. L., & Criddle, L. M. (2004). Pass the salt. Crit Care Nurse, 24(5), 36.
7. Dacey, M. J. (2001). Hypomagnesemic disorders. Crit Care Clin, 17(1), 155.
Electrolyte values: What's behind that shift?
While renal disease is a key cause of imbalance, a wide range of disorders may be responsible for shifts in electrolyte levels. Here's a listing of some other causes to consider when values exceed or fall below the normal range:
Sources: 1. Kee, J., Paulanka, B., & Purnell, L. (2004). Fluids and electrolytes with clinical applications: A programmed approach (7th ed.). Clifton Park, NY: Delmar Learning. 2. Springate, J. "Cerebral salt wasting." November 7, 2003. www.medicine.com/ped/topic354.htm (14 Feb. 2005).