The body fluids are maintained in an isotonic state with regulation of the concentration of sodium and its most abundant anion, chloride. Concentrations of sodium and chloride in the fluids are maintained primarily via loss or retention of water. Loss of salt is accompanied by loss of water and retention of salt by retention of water. Water moves into areas where salt is in higher concentration, which is why patients are often placed on a low-salt diet in an effort to reduce fluid overload on the heart and other major organs. However, patients who receive magnesium sulfate can also have impaired fluid excretion.

Of particular interest to the perianesthesia nurse are patients who have undergone urologic surgery and have been or are currently receiving irrigation fluids in the bladder. These patients are at risk of developing hyponatremia. The most common surgical procedure associated with this complication is a transurethral resection of the prostate. Irrigation fluids typically consist of sorbitol and mannitol or glycine in distilled water. The irrigants are isotonic. The amount of irrigation solution absorbed through the venous sinuses in the bladder averages 10 to 30 mL per minute of resection time. For this reason, the resection time should ideally be limited to 1 hour or less. The absorption of the irrigating fluid results in the fluid entering the vascular system; this can lead to volume overload and ultimately to dilutional hyponatremia.

The resulting lowered serum sodium concentrations can cause serious cardiac and neurologic consequences. Concentrations of sodium at 140 mEq/L are usually associated with the development of cardiac dysrhythmias that can lead to cardiac arrest. Progressive neurologic symptoms include restlessness, confusion, nausea, vomiting, coma, and convulsions.

Hypernatremia is most often caused by a loss of body fluids resulting in excess sodium. Elective surgery should be postponed until sodium levels greater than 150 mEq/L are corrected. Correction of water deficit should take place over 48 hours with hypotonic solutions. Rapid correction can result in seizures, cerebral edema, and coma.³

Potassium depletion can be accompanied by changes in plasma potassium concentration. True depletion develops only with a net loss of potassium, whereas a decrease in plasma potassium, hypokalemia, can occur with a shift of potassium from the ECF to the ICF. Decreased intake can cause a mild deficit because the mechanisms for potassium conservation are not as efficient as those for sodium. Severe depletion results from abnormal losses rather than decreased intake. The most common causes of severe potassium loss are usually associated with diuretics (see Chapter 13), vomiting, acute blood loss, gastrointestinal surgery, and nasogastric suctioning. Cardiac arrhythmias, polyuria, confusion, and weakness of skeletal muscle are commonly observed in mild hypokalemia. Hallucinations, diminished reflexes, ST-segment depression, widened QRS, flattened T waves, and cardiac arrest could result from severe depletion. Oral replacement with potassium chloride is in the range of 60 to 80 mEq/day. Peripheral intravenous (IV) potassium should not exceed 8 mEq/h so as not to irritate veins. Central IV potassium can be infused at 10 to 20 mEq/h. The administration of 0.5 mEq/kg of potassium chloride usually raises the serum potassium concentration by 0.6 mEq/L. If the patient is receiving catecholamine drugs, the increase is approximately 0.1 mEq/L; if the patient is receiving beta-adrenergic antagonists, the serum concentration increases by approximately 0.9 mEq/L. It is important to note that correction of hypomagnesemia may be needed to avoid the increased loss of potassium by the kidneys.

Hyperkalemia is often associated with situations in which cells are injured or destroyed. Examples include chronic and acute renal failure, crush injuries, burn victims, and newborns who receive relatively large transfusions. The administration of succinylcholine, a depolarizing skeletal muscle relaxant, can also produce hyperkalemia (discussed in Chapter 23). Accidental lethal doses of supplemental IV potassium have been administered to patients with rapid intravenous infusion in the PACU. Cases have been recorded in which death occurred within 5 minutes of the rapid injection of just 25 mEq of potassium; therefore, under no circumstance should potassium chloride be given via IV push.³

Hypocalcemia can result from any number of causes such as hypoparathyroidism, pancreatitis, renal failure, or decreased serum albumin levels. In hypocalcemia, the nervous system becomes progressively more irritable as the membrane becomes increasingly permeable to sodium. At a certain critical level of calcium, the nerve fibers become so irritable that they begin to fire spontaneously. Impulses pass to skeletal muscles and can cause skeletal muscle spasm including laryngospasm. Severe tetanic spasms are called tetany. Hypocalcemia occurs when the serum calcium concentration is lower than approximately 8 mg/dL. Neuromuscular function becomes increasingly impaired with decreased myocardial contractility, increased central venous pressure, and hypotension. Because of skeletal muscle spasm and potential laryngospasm, when caring for patients with hypocalcemia, the perianesthesia nurse should have appropriate airway equipment readily available for resuscitation (Fig. 14.2).⁴

An increased secretion of parathyroid hormone, most commonly caused by a parathyroid tumor, can cause hypercalcemia. In this situation, nervous system depression results in reduced reflex activity, and depression of muscle contractility results in skeletal muscle weakness, constipation, and loss of appetite. Because some calcium is excreted in the urine, a mild hypercalcemia can induce kidney stones as the calcium combines with phosphate or other anions and precipitates.

Hypomagnesemia is frequently overlooked as an electrolyte deficiency. Patients with alcoholism, poor diets or starvation, total parenteral nutrition without supplementation, nasogastric suctioning, or protracted vomiting or diarrhea can have this syndrome. Patients who have undergone cardiopulmonary bypass surgery are susceptible because of the dilutional effects of the pump-priming solutions. Symptoms of acute hypomagnesemia can include Chvostek and Trousseau signs as with hypocalcemia, stridor, skeletal muscle weakness, seizures, and coma. In the perianesthesia period, ventricular dysrhythmias are usually the most common symptom of hypomagnesemia. Treatment for this syndrome is magnesium 1 to 2 g IV over 15 to 60 minutes or a continuous infusion of magnesium at 0.5 to 1.0 g/h. With severe life-threatening hypomagnesemia, an infusion of magnesium of 10 to 20 mg/kg is usually administered over 10 to 20 minutes.

Hypermagnesemia is a rare clinical phenomenon. The most common cause of hypermagnesemia is the parenteral administration of magnesium as a treatment for pregnancy-induced hypertension. Symptoms of hypermagnesemia include sedation, myocardial depression, relaxed skeletal muscles and, when severe, paralysis of the muscles of ventilation. Treatment of the life-threatening hypermagnesemia is with calcium gluconate (1 g) given intravenously followed by a loop diuretic and increased fluid loading to produce diuresis in an effort to enhance the excretion of excess magnesium. Monitoring for vasodilation and negative inotropic effects is critical.²