Fluids, Electrolytes, and Acid–Base Physiology

As a consequence of underlying diseases and therapeutic manipulations, surgical patients may develop potentially harmful disorders of acid–base equilibrium, intravascular and extravascular volume, and serum electrolytes (Prough DS, Funston JS, Svensen CH, Wolf SW. Fluids, electrolytes, and acid-base physiology. In: Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Ortega R, Stock MC, eds. Clinical Anesthesia. Philadelphia: Lippincott Williams & Wilkins; 2013: 327–361). Precise management of acid–base status, fluids, and electrolytes may limit perioperative morbidity and mortality.

I. Acid–Base Interpretation and Treatment

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.

Overview of Acid–Base Equilibrium. Conventionally, acid–base equilibrium is described using the Henderson-Hasselbalch equation (Fig. 14-1). 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).
- 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.
- 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.
Metabolic alkalosis (pH >7.45 and bicarbonate >27 mEq/L) is the most common acid–base abnormality in critically ill patients (Tables 14-1 and 14-2).
- Metabolic alkalosis exerts multiple physiologic effects (Table 14-3).
- Recognition of hyperbicarbonatemia justifies arterial blood gas (ABG) analysis and should alert the anesthesiologist to the possibility that the patient has hypovolemia or hypokalemia.
- Treatment of metabolic alkalosis (Table 14-4).
Metabolic Acidosis (pH <7.35 and bicarbonate <21 mEq/L)
- Two types of metabolic acidosis occur based on whether the calculated anion gap is normal or increased (Table 14-5). The commonly measured cation (sodium) usually exceeds the total concentration of anions (chloride, bicarbonate) by 9 to 13 mEq/L.
- Metabolic acidosis exerts multiple physiologic effects (Table 14-6).
- Anesthetic implications of metabolic acidosis are proportional to the severity of the underlying process (Table 14-7).
- 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.
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.
- The development of spontaneous respiratory alkalosis in a previously normocarbic patient requires prompt evaluation (Table 14-9).
- Respiratory alkalosis exerts multiple physiologic effects (Table 14-10).
- 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).
- Preoperative recognition of chronic hyperventilation necessitates intraoperative maintenance of a similar PaCO₂.
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.
- Respiratory acidosis may be acute (absence of renal bicarbonate retention) or chronic (renal retention of bicarbonate returns the pH to near normal).
- Respiratory acidosis occurs because of a decrease in minute ventilation or an increase in CO₂ production (Table 14-11).
- 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).
  - Administration of opioids and sedatives, even in low doses, may cause hazardous depression of ventilation.
  - 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.)
- 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.
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.

pH = 6.1 + log [HCO₃]/0.03 × PaCO₂

Figure 14-1. Henderson-Hasselbalch equation.

Table 14-1 Generation of Metabolic Alkalosis

Generation	Examples
Loss of Acid from the Extracellular Space
Loss of gastric fluid (HCl)	Vomiting
Acid loss in urine; increased distal sodium delivery in the presence of hyperaldosteronism	Primary aldosteronism plus diuretic
Acid shifts into cells	Potassium deficiency
Loss of acid into stool	Congenital chloride-losing diarrhea
Excessive Bicarbonate Loads
Absolute
Oral or parenteral bicarbonate	Milk alkali syndrome
Metabolic conversion of the salts of organic acids to bicarbonate	Lactate, acetate, or citrate administration
Relative	Sodium bicarbonate dialysis
Posthypercapnic states	Correction (mechanical ventilatory support) of chronic hypercapnia

Table 14-2 Factors that Maintain Metabolic Alkalosis

Factor	Proposed Mechanism
Decreased GFR	Increases fractional bicarbonate reabsorption and prevents elevated plasma bicarbonate concentrations from exceeding Tm
Volume contraction	Stimulates proximal tubular bicarbonate reabsorption
Hypokalemia	Decreases GFR and increases proximal tubular bicarbonate reabsorption Stimulates sodium-independent, potassium-dependent (low) secretion in cortical collecting tubules
Hypochloremia*	Increases renin Decreases distal chloride delivery
Passive backflux of bicarbonate	Creates a favorable concentration gradient for passive bicarbonate movement from proximal tubular lumen to blood
Aldosterone	Increases sodium-dependent proton secretion in cortical collecting tubules and sodium-independent proton secretion in cortical collecting tubules and medullary collecting tubules
*Animal models. GFR = glomerular filtrate rate; Tm.

Table 14-3 Physiologic Effects Produced by Metabolic Alkalosis

Hypokalemia (potentiates effects of digoxin; evokes ventricular cardiac dysrhythmias)
Decreased serum ionized calcium concentration
Compensatory hypoventilation (may be exaggerated in patients with COPD or those who have received opioids; compensatory hypoventilation rarely results in PaCO₂ > 55 mm Hg)
Arterial hypoxemia (reflects effect of compensatory hypoventilation)
Increased bronchial tone (may contribute to atelectasis)
Leftward shift of oxyhemoglobin dissociation curve (oxygen less available to tissues)
Decreased cardiac output
Cardiovascular depression and cardiac dysrhythmias (result of inadvertent iatrogenic respiratory alkalosis to pre-existing metabolic alkalosis during anesthetic management)

COPD = chronic obstructive pulmonary disease.

Table 14-4 Treatment of Metabolic Alkalosis

Etiologic Therapy
Expand intravascular fluid volume (intraoperative fluid management with 0.9% saline; lactated Ringer’s solution provides an additional substrate for generation of bicarbonate).
Administer potassium.
Avoid iatrogenic hyperventilation of the patient’s lungs.

Nonetiologic Therapy
Administer acetazolamide (causes renal bicarbonate wasting).
Administer hydrogen (ammonium chloride, arginine hydrochloride, hydrochloric acid [must be injected into a central vein]).

Table 14-5 Differential Diagnosis of Metabolic Acidosis

Normal Anion Gap
Renal tubular acidosis
Diarrhea
Carbonic anhydrase administration
Early renal failure
Saline administration

Elevated Anion Gap (> 13 mEq/L)
Uremia
Ketoacidosis
Lactic acidosis
Toxins (methanol, ethylene glycol, salicylates)

Table 14-6 Physiologic Effects Produced by Metabolic Acidosis

Decreased myocardial contractility
Increased pulmonary vascular resistance
Decreased systemic vascular resistance
Impaired response of the cardiovascular system to endogenous and exogenous catecholamines
Compensatory hyperventilation

Table 14-7 Anesthetic Implications of Metabolic Acidosis

Monitor arterial blood gases and pH.
Check for possible exaggerated hypotensive responses to drugs and positive-pressure ventilation of the patient’s lungs (reflects hypovolemia).
Consider monitoring with an intra-arterial catheter and pulmonary artery catheter.
Maintain previous degree of compensatory hyperventilation.

Table 14-8 Calculation of Sodium Bicarbonate Dose

Sodium bicarbonate (mEq/L) = Weight (kg) × 0.3 × (24 mEq/L [actual bicarbonate])/2

Table 14-9 Causes of Respiratory Alkalosis

Hyperventilation syndrome (diagnosis of exclusion; most often encountered in the emergency department)
Iatrogenic hyperventilation
Pain
Anxiety
Arterial hypoxemia
Central nervous system disease
Systemic sepsis

Table 14-10 Physiologic Effects Produced by Respiratory Alkalosis

Hypokalemia (potentiates toxicity of digoxin)
Hypocalcemia
Cardiac dysrhythmias
Bronchoconstriction
Hypotension
Decreased cerebral blood flow (returns to normal over 8–24 hours corresponding to the return of cerebrospinal fluid pH to normal)

Table 14-11 Causes of Respiratory Acidosis

Decreased Alveolar Ventilation
Central nervous system depression (opioids, general anesthetics)
Peripheral skeletal muscle weakness (neuromuscular blockers, myasthenia gravis)
Chronic obstructive pulmonary disease
Acute respiratory failure

Increased Carbon Dioxide Production
Hypermetabolic states
Sepsis
Fever
Multiple trauma
Malignant hyperthermia
Hyperalimentation

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).

The pH status usually indicates the primary process (acidosis or alkalosis).
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.)
If neither an acute nor a chronic respiratory change could have resulted in the ABG measurements, then a metabolic disturbance must be present.
Compensation in response to metabolic disturbances is prompt via changes in PaCO₂, but renal compensation for respiratory disturbances is slower.
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.