3. Anesthetic implications of metabolic acidosis are proportional to the severity of the underlying process (Table 14-7).

4. Treatment of metabolic acidosis consists of the treatment of the primary pathophysiologic process (hypoperfusion, arterial hypoxemia) and, if pH is severely depressed, administration of sodium bicarbonate (Table 14-8). Current opinion is that sodium bicarbonate should rarely be used to treat acidemia induced by metabolic acidosis because it does not improve the cardiovascular response to catecholamines and does decrease plasma-ionized calcium.

D. Respiratory alkalosis (pH > 7.45 and PaCO₂ < 35 mm Hg) results from an increase in minute ventilation that is greater than that required to excrete metabolic CO₂ production.

1. The development of spontaneous respiratory alkalosis in a previously normocarbic patient requires prompt evaluation (Table 14-9).

2. Respiratory alkalosis exerts multiple physiologic effects (Table 14-10).

3. Treatment of respiratory alkalosis per se is often not required. The most important steps are recognition and treatment of the underlying cause (e.g., arterial hypoxemia, hypoperfusion-induced lactic acidosis).

4. Preoperative recognition of chronic hyperventilation necessitates intraoperative maintenance of a similar PaCO₂.

E. Respiratory acidosis (pH, 7.35; PaCO₂ > 45 mm Hg) occurs because of a decrease in minute ventilation and or an increase in production of metabolic CO₂.

1. Respiratory acidosis may be acute (absence of renal bicarbonate retention) or chronic (renal retention of bicarbonate returns the pH to near normal).

2. Respiratory acidosis occurs because of a decrease in minute ventilation or an increase in CO₂ production (Table 14-11).

3. Patients with chronic hypercarbia caused by intrinsic pulmonary disease require careful preoperative evaluation (ABG and pH determinations), anesthetic management (direct arterial blood pressure monitoring and frequent ABG measurements), and postoperative care (pain control, often with neuraxial opioids, and mechanical support of ventilation).

a. Administration of opioids and sedatives, even in low doses, may cause hazardous depression of ventilation.

b. Intraoperatively, a patient with chronic hypercapnia should be ventilated to maintain a normal pH. (An abrupt increase in alveolar ventilation may produce profound alkalemia because renal excretion of bicarbonate is slow.)

4. Treatment of acute respiratory acidosis is elimination of the causative factor (opioids, muscle relaxants) and mechanical support of ventilation as needed. Chronic respiratory acidosis is rarely managed with mechanical ventilation but rather with efforts to improve pulmonary function to permit more effective elimination of CO₂.

F. In patients requiring mechanical ventilation for respiratory failure, ventilation with a lung-protective strategy may result in hypercapnia, which in turn can be managed with alkalinization.

II. PRACTICAL APPROACH TO ACID–BASE INTERPRETATION. Rapid interpretation of a patient’s acid–base status involves integration of data provided by ABG, pH, and electrolyte measurements and history. After obtaining these data, a stepwise approach facilitates interpretation (Table 14-12).

A. The pH status usually indicates the primary process (acidosis or alkalosis).

B. If the PaCO₂ and the pH change reciprocally but the magnitude of the pH and bicarbonate changes is not consistent with a simple acute respiratory disturbance, a chronic respiratory or metabolic problem (>24 hours) should be considered. (pH becomes nearly normal as the body compensates.)

C. If neither an acute nor a chronic respiratory change could have resulted in the ABG measurements, then a metabolic disturbance must be present.

D. Compensation in response to metabolic disturbances is prompt via changes in PaCO₂, but renal compensation for respiratory disturbances is slower.

E. Failure to consider the presence or absence of an increased anion gap results in an erroneous diagnosis and failure to initiate appropriate treatment. Correct assessment of the anion gap requires correction for hypoalbuminemia.

III. PHYSIOLOGY OF FLUID MANAGEMENT

A. Body Fluid Compartments. Accurate replacement of fluid deficits necessitates an understanding of the distribution spaces of water, sodium, and colloid. Total body water approximates 60% of total body weight (42 L in a 70-kg adult). Total body water consists of intracellular fluid (ICF; 28 L) and extracellular fluid (ECF; 14 L). Plasma volume is about 3 L, and red blood cell volume is about 2 L. Whereas sodium is present principally in the ECF (140 mEq/L), potassium is present principally in the ICF (150 mEq/L). Albumin is the most important oncotically active constituent of ECF (4 g/dL).

B. Distribution of Infused Fluids. Conventionally, clinical prediction of plasma volume expansion after fluid infusion assumes that body fluid spaces are static. However, infused fluid does not simply equilibrate throughout an assumed distribution volume but is added to a highly regulated system that attempts to maintain intravascular, interstitial, and intracellular volume. Kinetic models of intravenous (IV) fluid therapy allow clinicians to more accurately predict the time course of volume changes produced by infusions of fluids of various compositions.

C. Regulation of ECF volume is influenced by aldosterone (enhances sodium reabsorption), antidiuretic hormone (enhances water reabsorption), and atrial natriuretic peptide (enhances sodium and water excretion).

IV. FLUID REPLACEMENT THERAPY

A. Maintenance Requirements for Water, Sodium, and Potassium. In healthy adults, sufficient water is required to balance gastrointestinal losses (100–200 mL/day), insensible losses (500–1,000 mL/day representing respiratory and cutaneous losses), and urinary losses (1,000 mL/day)

1. Water maintenance requirements are often calculated on the basis of body weight. For a 70-kg adult, the daily water maintenance requirement is about 2,500 mL (Table 14-13).

2. Renal sodium conservation is highly efficient, such that the average daily maintenance requirement in an adult is about 75 mEq.

3. The average daily maintenance requirement of potassium is about 40 mEq. Physiologic diuresis induces an obligate potassium loss of at least 10 mEq for every 1,000 mL of urine.

4. Electrolytes such as chloride, calcium, and magnesium do not require short-term replacement, although they must be supplied during chronic IV fluid maintenance.

B. Dextrose. Addition of glucose to maintenance fluid solutions is indicated only in patients considered to be at risk for developing hypoglycemia (infants, patients on insulin therapy). Otherwise, the normal hyperglycemic response to surgical stress is sufficient to prevent hypoglycemia.

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