Management of acid–base disturbances requires an understanding of the four simple acid–base disorders (metabolic alkalosis, metabolic acidosis, respiratory alkalosis, and respiratory acidosis) as well as combinations of more complex disturbances.

1. Overview of Acid–Base Equilibrium. Conventionally, acid–base equilibrium is described using the Henderson-Hasselbalch equation (Fig. 14-1: Henderson-Hasselbalch equation). Because the concentration of bicarbonate is largely regulated by the kidneys and CO₂ is controlled by the lungs, acid–base interpretation has emphasized examining disorders in terms of metabolic disturbances (bicarbonate primarily increased or decreased) and respiratory disturbances (PaCO₂ primarily increased or decreased).
   1. The negative logarithm of the hydrogen ion concentration is described as the pH. A pH of 7.4 corresponds to a hydrogen ion concentration of 40 nmol/L.
   2. From a pH of 7.2 to 7.5, the curve of hydrogen ion concentration is relatively linear, and for each change of 0.01 pH unit from 7.4, the hydrogen ion concentration can be estimated to increase (pH >7.4) or decrease (pH >7.4) by 1 nmol/L.
2. Metabolic alkalosis (pH >7.45 and bicarbonate >27 mEq/L) is the most common acid–base abnormality in critically ill patients (Table 14-1: Generation of Metabolic Alkalosis and Table 14-2: Factors that Maintain Metabolic Alkalosis).
   1. Metabolic alkalosis exerts multiple physiologic effects (Table 14-3: Physiologic Effects Produced by Metabolic Alkalosis).
   2. Recognition of hyperbicarbonatemia justifies arterial blood gas (ABG) analysis and should alert the anesthesiologist to the possibility that the patient has hypovolemia or hypokalemia.
   3. Treatment of metabolic alkalosis (Table 14-4: Treatment of Metabolic Alkalosis).
3. Metabolic Acidosis (pH <7.35 and bicarbonate <21 mEq/L)
   1. Two types of metabolic acidosis occur based on whether the calculated anion gap is normal or increased (Table 14-5: Differential Diagnosis of Metabolic Acidosis). The commonly measured cation (sodium) usually exceeds the total concentration of anions (chloride, bicarbonate) by 9 to 13 mEq/L.
   2. Metabolic acidosis exerts multiple physiologic effects (Table 14-6: Physiologic Effects Produced by Metabolic Acidosis).
   3. Anesthetic implications of metabolic acidosis are proportional to the severity of the underlying process (Table 14-7: Anesthetic Implications of Metabolic Acidosis).
   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: Calculation of Sodium Bicarbonate Dose). 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.
4. 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: Causes of Respiratory Alkalosis).
   2. Respiratory alkalosis exerts multiple physiologic effects (Table 14-10: Physiologic Effects Produced by Respiratory Alkalosis).
   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.
5. 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: Causes of Respiratory Acidosis).
   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).
      1. Administration of opioids and sedatives, even in low doses, may cause hazardous depression of ventilation.
      2. 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.
6. 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.

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