1. Physiologic Role of Electrolytes (Table 14-19: Physiologic Role of Electrolytes)
2. Sodium. Disorders of sodium concentration (hyponatremia, hypernatremia) usually result from relative excesses or deficits of water. Regulation of the quantity and concentration of electrolytes is accomplished primarily by the endocrine and renal systems.
   1. Hyponatremia (<130 mEq/L) is the most common electrolyte disturbance in hospitalized patients (postoperative, acute intracranial disease) and is usually caused by excess total body water.
      1. Signs and symptoms of hyponatremia depend on the rate at which the plasma sodium concentration decreases and the severity of the decrease (Table 14-20: Signs and Symptoms of Hyponatremia).
      2. The cerebral salt-wasting syndrome appears to be mediated by brain natriuretic peptide; the secretion of antidiuretic hormone is appropriate.
      3. Many patients develop hyponatremia as a result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The cornerstone of SIADH management is free water restriction and elimination of precipitating causes (Table 14-21: Precipitating Causes of Inappropriate Antidiuretic Hormone Secretion).
      4. Inappropriately rapid correction of hyponatremia may result in abrupt brain dehydration. (Osmotic demyelination syndrome is most likely when hyponatremia has persisted >48 hours.)
      5. For patients who require long-term pharmacologic therapy of hyponatremia, vasopressin receptor antagonists may be useful.
   2. Hypernatremia (>150 mEq/L) is usually the result of decreased total body water.
      1. Signs and symptoms of hypernatremia most likely reflect the effect of dehydration on neurons and the presence of hypoperfusion caused by hypovolemia (Table 14-22: Signs and Symptoms of Hypernatremia). When hypernatremia develops abruptly, the associated sudden brain shrinkage may stretch and disrupt cerebral vessels, leading to subdural hematoma, subarachnoid hemorrhage, and venous thrombosis.
      2. Postoperative neurosurgical patients who have undergone pituitary surgery are at particular risk of developing transient or prolonged diabetes insipidus, leading to hypernatremia.
      3. Treatment of hypernatremia is influenced by the clinical assessment of ECF volume (Table 14-23: Treatment of Hypernatremia).
3. Potassium
   1. Hypokalemia (<3.0 mEq/L) may result from acute redistribution of potassium from the extracellular to the ICF (total body potassium concentration is normal) or from chronic depletion of total body potassium. With chronic potassium loss, the ratio of intracellular to extracellular potassium remains relatively constant, but acute redistribution of potassium substantially changes the resting potential difference across cell membranes.
      1. Plasma potassium concentration poorly reflects total body potassium, and hypokalemia may occur with high, normal, or low total body potassium. The plasma potassium concentration (98% of potassium is intracellular) correlates poorly with total body potassium stores. Total body potassium approximates 50 to 55 mEq/kg. As a guideline, a chronic decrease in serum potassium of 1 mEq/L corresponds to a total body deficit of about 200 to 300 mEq.
      2. Signs and symptoms of hypokalemia reflect the diffuse effects of potassium on cell membranes and excitable tissues (Table 14-24: Signs and Symptoms of Hypokalemia).
      3. Cardiac rhythm disturbances are among the most dangerous complications of hypokalemia. Although no clear threshold has been defined for a level of hypokalemia below which safe conduct of anesthesia is compromised, serum potassium concentrations below 3.5 mEq/L may be associated with an increased incidence of perioperative dysrhythmias (atrial fibrillation or flutter in cardiac surgical patients).
      4. Potassium depletion may induce defects in renal concentrating ability, resulting in polyuria.
      5. Hypokalemia causes skeletal muscle weakness and, when severe, may even cause paralysis.
      6. Treatment of hypokalemia consists of potassium repletion, correction of alkalosis, and discontinuation of offending drugs (diuretics, aminoglycosides) (Table 14-25: Treatment of Hypokalemia). Hypokalemia secondary only to acute redistribution may not require treatment. Oral potassium chloride (chloride deficiency may limit the ability of the kidneys to conserve potassium) is preferable to IV replacement if total body potassium stores are decreased. IV potassium replacement at a rate >20 mEq/hr should be continuously monitored with electrocardiography (ECG).
   2. Hyperkalemia (>5 mEq/L) is most often caused by renal insufficiency or drugs that limit potassium excretion (nonsteroidal antiinflammatory drugs, angiotensin-converting enzyme inhibitors, cyclosporine, potassium-sparing diuretics). The most lethal manifestations of hyperkalemia involve the cardiac conducting system (Fig. 14-2: Electrocardiographic (ECG) changes that may accompany progressive increases in serum potassium concentrations). Overall, ECG is an insensitive and nonspecific method of detecting hyperkalemia.
      1. Signs and symptoms of hyperkalemia primarily involve the central nervous and cardiovascular systems (Table 14-26: Signs and Symptoms of Hyperkalemia).
      2. Treatment of hyperkalemia is designed to eliminate the cause, reverse membrane hyperexcitability, and remove potassium from the body (Fig. 14-3: Treatment of hyperkalemia and Table 14-27: Treatment of Severe Hyperkalemia).
4. Calcium
   1. Hypocalcemia (ionized calcium <4.0 mg/dL) occurs as a result of parathyroid hormone deficiency (surgical parathyroid gland damage or removal, burns, sepsis) or because of calcium chelation or precipitation (hyperphosphatemia, as from cell lysis secondary to chemotherapy).
      1. The hallmark of hypocalcemia is increased neuronal membrane irritability and tetany (Table 14-28: Signs and Symptoms of Hypocalcemia).
      2. Decreased total serum calcium concentration occurs in as many as 80% of critically ill and postsurgical patients, but few patients develop ionized hypocalcemia (multiple traumas, after cardiopulmonary bypass, massive transfusion [citrate]).
      3. Treatment of hypocalcemia (Table 14-29: Treatment of Hypocalcemia).
   2. Hypercalcemia (ionized calcium >5.2 mg/dL) occurs when calcium enters the ECF more rapidly than the kidneys can excrete the excess. Clinically, hypercalcemia most commonly results from an excess of bone resorption over bone formation, usually secondary to malignant disease, hyperparathyroidism, or immobilization.
      1. Signs and symptoms are listed in Table 14-30: Signs and Symptoms of Hypercalcemia.
      2. Treatment of hypercalcemia in the perioperative period includes saline infusion and administration of furosemide to enhance calcium excretion (urine output should be maintained at 200–300 mL/hr).
5. Magnesium is principally intracellular and is necessary for enzymatic reactions.
   1. Hypomagnesemia (<1.8 mg/dL) is common in critically ill patients, most likely reflecting nasogastric suctioning and an inability of the renal tubules to conserve magnesium. Hypomagnesemia can aggravate digoxin toxicity and congestive heart failure.
      1. Signs and symptoms are listed in Table 14-31: Signs and Symptoms of Hypomagnesemia.
      2. Treatment of hypomagnesemia (Table 14-32: Treatment of Hypomagnesemia). During magnesium repletion, the patellar reflexes should be monitored frequently and magnesium withheld if the reflexes become suppressed. During IV infusion of magnesium, it is important to continuously monitor the ECG to detect cardiotoxicity.
   2. Hypermagnesemia (>2.5 mg/dL) is usually iatrogenic (e.g., treatment of pregnancy-induced hypertension or premature labor).
      1. Signs and symptoms are listed in Table 14-33: Signs and Symptoms of Hypermagnesemia.
      2. Hypermagnesemia antagonizes the release and effect of acetylcholine at the neuromuscular junction, manifesting as potentiation of the action of nondepolarizing muscle relaxants.
      3. Treatment of neuromuscular and cardiac toxicity produced by hypermagnesemia can be promptly but transiently antagonized by 5 to 10 mEq IV of calcium. Urinary excretion of magnesium can be increased by expanding the ECF volume and inducing diuresis with a combination of furosemide and saline. In emergency situations and in patients with renal failure, magnesium may be removed by dialysis.

Fluids, Electrolytes, and Acid–Base Physiology

1. Acid–Base Interpretation and Treatment
2. Practical Approach to Acid–Base Interpretation
3. Physiology of Fluid Management
4. Fluid Replacement Therapy
5. Colloids, Crystalloid, and Hypertonic Solutions
6. Fluid Status: Assessment and Monitoring
7. Electrolytes