Dissolved electrolytes, such as sodium, potassium, calcium, magnesium, and chloride, act as ions within the body and are classified by their ionic charge. Strong anions counter strong cations, resulting in a balance in electrical charge, contributing to acid base balance and promoting proper enzymatic functioning and metabolism.1,2 Within the critical care setting, monitoring and replacement of critical electrolytes ensures optimal cellular functioning while preventing potentially catastrophic events in the form of cardiac dysrhythmias, asystole, or coma.3
As the most abundant intracellular cation, potassium's most important role is to sustain intercellular electrical balance.4 By freely passing through the semi-permeable cell membrane, potassium maintains cellular neutrality, ensuring normal cardiac and neuromuscular functioning and enzyme activation.3,4 Minor elevations can result from beta-adrenergic blockade, but in the critical care environment, acidosis presents a much more significant and global shift, with serum potassium levels rising 0.7 mEq/L for every 0.1 pH unit decrease. Other causes are: burn or crush injuries, tumor lysis syndromes, massive hemolysis, hyperglycemic hyperosmolality, massive blood transfusions or excessive potassium supplement intake. With normal renal function, the kidneys are triggered by aldosterone to increase potassium excretion. Thus kidney disease, hypoaldosteronism, adrenal insufficiency, use of potassium sparing diuretics, and type 1 renal tubular acidosis can all impair serum potassium balance.
Signs and symptoms of both hyperkalemia and hypokalemia result from prolonged suppression of normal cardiac and nerve impulse conduction. Cardiac abnormalities in hyperkalemia include suppressed conduction resulting in tall, peaked T waves (levels 5.5 to 6.0 mEq/L), a prolonged PR interval, and a widened QRS interval (levels 6.0 to 7.0 mEq/L), leading to cardiac arrest from complete heart block at levels greater than 8.0 mEq/L.4 Treatment of hyperkalemia includes identifying and correcting the causative factors and using I.V. calcium to stimulate cardiac conduction and normalize resting membrane potentials. To shift potassium from the serum into the cells, I.V. sodium bicarbonate, beta2-adrenergic agonists (albuterol) or I.V. insulin given with 50% dextrose may be used. With normal kidney function, I.V. loop diuretics can hasten renal excretion and resin binders such as sodium polystyrene sulfonate can bind potassium in the gut.
Diuretic use remains the primary cause of low-serum potassium levels. Hypokalemia can also be caused by renal losses due to diabetes, acute tubular necrosis, hypercalcemia, hypochloremia, or multifactorial polyuria.3 Nonrenal causes include aldosteronism, Cushing's syndrome, excessive fluid resuscitation, postmyocardial infarction, hematological malignancies, nasogastric suctioning, and diarrhea. Resolution of acidosis and use of dopamine (Intropin) or beta-adrenergic agonists (such as albuterol, terbutaline) results in a cellular transfer of potassium from the serum to the cells, lowering serum levels.4
Signs and symptoms of hypokalemia include the muscle and nerve conduction abnormalities listed in Comparison of the signs and symptoms of hyper- and hypokalemia. Flattened or inverted T waves, U waves, depressed ST segments, or increasingly frequent premature ventricular or atrial complexes may signal worsening conduction blockade and impending ventricular tachycardia. Intensive treatment is through the I.V. route with combined oral and I.V. infusion replacement resulting in more effective serum rise. Remember to replace I.V. potassium cautiously, using an infusion pump and a central line when possible. Monitor peripheral I.V. sites closely, as chemical phlebitis and discomfort are a frequent result of I.V. replacement.
Magnesium: Intracellular cation
As the second most abundant intracellular cation, magnesium is 30% protein bound and another 15% loosely coupled to phosphate and other anions.5,6 The low serum albumin levels of critically ill patients reduces the amount of protein-bound magnesium, and hypomagnesium continues to be considered a factor in hypertension.5,7 Magnesium forms complexes with adenosine triphosphate to serve as an essential cofactor for enzymes, transporters, and nucleic acids in cellular replication, and protein and carbohydrate metabolism.3,6
Since normal kidneys can excrete large amounts of magnesium, hypermagnesemia is rarely seen in the absence of renal insufficiency. Massive exogenous magnesium exposures are usually through the gastrointestinal (GI) tract, as with prolonged retention of magnesium agents in patients with intestinal ileus, obstruction, or perforation. Magnesium release can also occur with extensive soft tissue injury or necrosis as with trauma, shock, sepsis, cardiac arrest, or severe burns.6
At levels greater than 4 mEq/L, the most prominent clinical manifestation of hypermagnesemia is vasodilatation refractory to vasopressors or volume expansion. At levels greater than 8 mEq/L, nausea, lethargy, and weakness may progress to respiratory failure, hypoactive tendon reflexes, paralysis, and coma. Other findings of hypermagnesemia include paradoxical bradycardia, prolongation of cardiac conduction and, with levels approaching 20 mEq/L, asystole may occur.6 Magnesium also potentiates the effects of neuromuscular blockade from agents such as cisatracurium (Nimbex), but doesn't alter the patient's hemodynamic stability, and low levels are common with chronic or acute asthmatic patients.7,8
Treatment of hypermagnesemia involves identifying and interrupting the source of magnesium. With sources from the GI tract, use magnesium-free cathartics or enemas to increase clearance. In the hypovolemic patient with normal renal function, use aggressive I.V. hydration to equalize serum ion concentrations. For patients with significant renal insufficiency, hemodialysis may be required.6
Causes of hypomagnesemia include alcohol abuse; errors in intestinal absorption as with protracted vomiting, diarrhea, or intestinal drainage; and defective reabsorption as with renal tubular dysfunction. Recovery from diabetic ketoacidosis, starvation, or respiratory acidosis can cause serum magnesium to shift into cellular spaces. Large amounts of magnesium may be lost with acute pancreatitis, extensive burns, during pregnancy, and lactation.
Signs and symptoms of hypomagnesemia result from altered vascular tone and include altered neuromuscular manifestations such as tetany, tremors, seizures, muscle weakness, ataxia, nystagmus, vertigo, apathy, depression, irritability, delirium, and psychosis.8 Raising levels to normal postmyocardial infarction limits submyocardial injury, reducing mortality and improving ventricular function.3,5 Patients with levels greater than 1 mEq/L are asymptomatic, but sensitivity to digoxin toxicity may be enhanced. Both hypercalcemia and hypokalemia may be refractory to correction until the magnesium level is normalized. The most common cardiac dysrhythmias include supraventricular tachycardias, including sinus tachycardia and ventricular dysrhythmias. PR or QT intervals may be prolonged and T waves flattened or inverted.
With normal renal function, I.V. magnesium chloride supplements are administered as a continuous infusion.
As the major extracellular anion, chloride functions to maintain serum acid-base balance. The relationship between chloride and bicarbonate serves as an important acid-base diagnostic indicator, and speculation about the role of chloride in hypertension continues.10 A high chloride level with a normal sodium level indicates acidosis, while a simultaneous increase in chloride and sodium levels indicate dehydration.3 A normal anion gap with a high chloride level also indicates acidosis, resulting from diarrhea or renal tubular acidosis which causes preferential loss of bicarbonate and retention of chloride. A low anion gap and low chloride level indicates alkalosis and hypochloremia from vomiting, nasogastric suctioning, and diuretics.4
Low serum chloride levels can result from Cushing's syndrome, excessive aldosterone secretion, hypokalemia, massive blood transfusions, over administration of I.V. solutions containing bicarbonate, excessive ingestion of bicarbonate containing antacids, or large volume nasogastric losses without proton pump blockade. High serum chloride levels are almost exclusively a result of iatrogenically induced hyperchloremic metabolic acidosis, stemming from excessive administration of chloride relative to sodium, most commonly as 0.9% normal saline solution, 0.45% normal saline solution or lactated ringer's solution, all of which result in a nongap metabolic acidosis. Hyperchloremia causes a decrease in renal blood flow and glomerular filtration rate and is associated with impaired coagulation. Hyperchloremic metabolic acidosis often contributes to patient morbidity and increased utilization of intensive care resources.
Careful monitoring of electrolyte levels is essential in critical care nursing to preserve the patient's optimal ability to perform cellular functions.