Handbook of Clinical Anesthesia

Chapter 14

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: Acid-base, fluids and electrolytes. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 290–325). Precise management of acid–base status, fluids, and electrolytes may limit perioperative morbidity and mortality.

  1. 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.

  1. 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 but 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).
  2. 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.
  3. 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.


Figure 14-1. Henderson-Hasselbalch equation.

  1. 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).
  2. Metabolic alkalosis exerts multiple physiologic effects (Table 14-3).
  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.
  4. Treatment of metabolic alkalosis (Table 14-4).
  5. Metabolic Acidosis(pH <7.35 and bicarbonate <21 mEq/L)
  6. 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.

Table 14-1 Generation of Metabolic Alkalosis



Loss of Acid from the Extracellular Space

Loss of gastric fluid (HCl)


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



Oral or parenteral bicarbonate

Milk alkali syndrome

Metabolic conversion of the salts of organic acids to bicarbonate

Lactate, acetate, or citrate administration


Sodium bicarbonate dialysis

Posthypercapnic States

Correction (mechanical ventilatory support) of chronic hypercapnia

Table 14-2 Factors that Maintain Metabolic Alkalosis


Proposed Mechanism

Decreased GFR

Increases fractional bicarbonate reabsorption and prevents elevated plasma bicarbonate concentrations from exceeding Tm

Volume contraction

Stimulates proximal tubular bicarbonate reabsorption


Decreases GFR and increases proximal tubular bicarbonate reabsorption
Stimulates sodium-independent/potassium-dependent (low) secretion in cortical collecting tubules


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


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.

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 chronic obstructive pulmonary disease 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)


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]).

  1. Metabolic acidosis exerts multiple physiologic effects (Table 14-6).
  2. Anesthetic implications of metabolic acidosis are proportional to the severity of the underlying process (Table 14-7).
  3. Treatment of metabolic acidosis consists of the treatment of the primary pathophysiologic process (hypo-perfusion, 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.

Table 14-5 Differential Diagnosis of Metabolic Acidosis

Normal Anion Gap
Renal tubular acidosis
Carbonic anhydrase administration
Early renal failure
Saline administration
Elevated Anion Gap(>13 mEq/L)
Lactic acidosis
Toxins (methanol, ethylene glycol, salicylates)

  1. P.156

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

  1. 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.
  2. The development of spontaneous respiratory alkalosis in a previously normocarbic patient requires prompt evaluation (Table 14-9).
  3. Respiratory alkalosis exerts multiple physiologic effects (Table 14-10).
  4. 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).
  5. Preoperative recognition of chronic hyperventilation necessitates intraoperative maintenance of a similar PaCO2.
  6. 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.
  7. Respiratory acidosis may be acute (absence of renal bicarbonate retention) or chronic (renal retention of bicarbonate returns the pH to near normal).
  8. Respiratory acidosis occurs because of a decrease in minute ventilation or an increase in CO2production (Table 14-11).

Table 14-7 Anesthetic Implications of Metabolic Acidosis

Monitor arterial blood gases and pH
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

  1. P.157

Table 14-8 Calculation of Sodium Bicarbonate Dose

Table 14-9 Causes of Respiratory Alkalosis

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

Table 14-10 Physiologic Effects Produced by Respiratory Alkalosis

Hypokalemia (potentiates toxicity of digoxin)
Cardiac dysrhythmias
Decreased cerebral blood flow (returns to normal over 8 to 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
Multiple trauma
Malignant hyperthermia

  1. P.158
  2. 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).
  3. Administration of opioids and sedatives, even in low doses, may cause hazardous depression of ventilation.
  4. 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.)
  5. 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 in order 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.
  7. 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).

  1. The pH status usually indicates the primary process (acidosis or alkalosis).
  2. If the PaCO2and 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 hr) should be considered. (pH becomes nearly normal as the body compensates.)
  3. If neither an acute nor chronic respiratory change could have resulted in the ABG measurements, then a metabolic disturbance must be present.


Table 14-12 Sequential Approach to Acid–Base Interpretation

Is the pH life threatening, requiring immediate intervention?
Does the pH reflect a primary acidosis or alkalosis?
Could the arterial blood gas and pH readings represent an acute change in PaCO2?
If there is no evidence of an acute change in PaCO2, is there evidence of a chronic respiratory disturbance or of an acute metabolic disturbance?
Are appropriate compensatory changes present?
Is an anion gap present?
Do the clinical data fit the acid–base picture?

  1. Whereas compensation in response to metabolic disturbances is prompt via changes in PaCO2, renal compensation for respiratory disturbances is slower.
  2. 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

  1. 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).
  2. 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 modes 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.

  1. Regulation of ECF volumeis influenced by aldosterone (enhances sodium reabsorption), antidiuretic hormone (enhances water reabsorption), and atrial natriuretic peptide (enhances sodium and water excretion).
  2. Fluid Replacement Therapy
  3. Maintenance Requirements for Water, Sodium, and Potassium.In healthy adults, sufficient water is required to balance gastrointestinal losses (100–200 mL/day), insensible losses (500–1000 mL/day representing respiratory and cutaneous losses), and urinary losses (1000 mL/day)
  4. Water maintenance requirements are often calculated on the basis of body weight. For a 70-kg adult, the daily water maintenance requirement is about 2500 mL (Table 14-13).
  5. Renal sodium conservation is highly efficient, such that the average daily maintenance requirement in an adult is about 75 mEq.
  6. 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 1000 mL of urine.
  7. Electrolytes such as chloride, calcium, and magnesium do not require short-term replacement, although they must be supplied during chronic IV fluid maintenance.
  8. 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. Iatrogenic hyperglycemia can limit the effectiveness of fluid resuscitation by inducing an osmotic diuresis.

Table 14-13 Maintenance Water Requirements




1–10 kg



11–20 kg



>20 kg




  1. Surgical Fluid Requirements
  2. Water and Electrolyte Composition of Fluid Losses.Surgical patients require replacement of plasma volume and ECF secondary to hemorrhage and tissue manipulation (third-space loss). Lactated Ringer's solution is often selected for replacement of third-space losses as well as for gastrointestinal secretions.
  3. Influence of Perioperative Fluid Infusion Rates on Clinical Outcomes.Conventionally, intraoperative fluid management included replacement of fluids assumed to accumulate extravascularly in surgically manipulated tissues. Until recently, perioperative clinical practice included, in addition to maintenance fluids and blood loss, 4 to 6 mL/kg/hr for procedures involving minimal tissue trauma, 6 to 8 mL/kg/hr for those involving moderate trauma, and 8 to 12 mL/kg/hr for those involving extreme trauma. Yet perioperative fluid management may be linked to minor and major morbidity.
  4. Fluid restriction appears to be less well tolerated than liberal fluid administration in patients undergoing surgery of a limited scope (e.g., knee arthroscopy).
  5. In patients undergoing major intraabdominal surgery, restrictive fluid administration is associated with combinations of positive and negative effects.
  6. Critically ill patients with acute lung injury may benefit from conservative fluid replacement without an increased incidence of renal failure.
  7. Colloids, Crystalloid, and Hypertonic Solutions
  8. Physiology and Pharmacology.IV fluids vary in oncotic pressure, osmolarity, and tonicity. When the capillary membrane is intact, fluids containing colloid, such as albumin or hydroxyethyl starch, preferentially expand plasma volume rather than ICF volume.
  9. Clinical Implications of Choices between Alternative Fluids. Despite the relative advantages and disadvantages, no evidence supports the superiority of either colloid-containing or crystalloid-containing solutions (Table 14-14).


Table 14-14 Possible Advantages and Disadvantages of Colloid versus Crystalloid Intravenous Fluids





Smaller volume infused
Prolonged increase in plasma volume
Greater peripheral edema
Less cerebral edema

Greater cost
Coagulopathy (dextran > hetastarch)
Pulmonary edema (capillary leak states)
Decreased glomerular filtration rate
Osmotic diuresis (low-molecular-weight dextran)


Lower cost
Greater urinary flow
Replaces interstitial fluid

Transient hemodynamic improvement
Peripheral edema (protein dilution)
Pulmonary edema (protein dilution plus high pulmonary artery occlusion pressure)

  1. Despite a commonly held opinion, the risk of pulmonary edema seems to be independent of the selection of a crystalloid- or colloid-containing solution.
  2. Colloid-induced expansion of the plasma volume redistributes slowly, such that diuretic therapy is often required if pulmonary edema develops.
  3. There appears to be no important clinical difference in pulmonary function after administration of crystalloid or colloid solutions in the absence of hypervolemia.
  4. Implications of Crystalloid and Colloid Infusions on Intracranial Pressure.Despite a clinical notion, the risk of increased intracranial pressure seems to be independent of the selection of a crystalloid- or colloid-containing solution.
  5. Clinical Implications of Hypertonic Fluid Administration.Hypertonic and hyperoncotic fluids seem most likely to be effective in the treatment of hypovolemic patients who have decreased intracranial compliance.


Table 14-15 Conditions Associated With Deficits in Blood Volume and Extracellular Fluid Volume

Bowel obstruction
Chronic systemic hypertension
Chronic diuretic use
Prolonged gastrointestinal losses

  1. Fluid Status: Assessment and Monitoring
  2. Conventional Clinical Assessment.The preoperative clinical assessment of blood volume and ECF volume begins with the recognition of conditions in which deficits are likely to occur (Table 14-15).
  3. Physical signs of hypovolemia are insensitive and nonspecific (Table 14-16). A normal blood pressure reading may represent relative hypotension in an elderly or chronically hypertensive patient. Conversely, substantial hypovolemia may occur despite an apparently normal blood pressure and heart rate.
  4. Elderly patients may demonstrate orthostatic hypotension despite a normal blood volume.
  5. Young, healthy subjects can tolerate an acute blood loss equivalent to 20% of their blood volume while exhibiting only postural tachycardia and variable postural hypotension.
  6. Orthostatic changes in central venous pressure, coupled with assessment of the response to fluid infusion, may represent a useful test of the adequacy of blood volume.

Table 14-16 Signs and Symptoms of Hypovolemia

Oliguria (rule out renal failure, stress-induced endocrine response)
Hypotension in the supine position (implies blood volume deficit >30%)
Positive tilt test result (increase in heart rate [>20 bpm] and decrease in systolic blood pressure [>20 mm Hg] when patient assumes the standing position)

  1. P.164

Table 14-17 Laboratory Evidence of Hypovolemia

Hemoconcentration (hematocrit is a poor indicator of blood volume)
Azotemia (may be influenced by events unrelated to blood volume)
Low urine sodium concentration (<20 mEq for every 1000 mL of urine)
Metabolic alkalosis
Metabolic acidosis (reflects organ hypoperfusion)

  1. Laboratory data may suggest hypovolemia or ECF volume depletion (Table 14-17).
  2. Hematocrit is a poor indicator of blood volume because it is influenced by the time elapsed since hemorrhage and the volume of asanguineous fluid replacement. Hematocrit is virtually unchanged by acute hemorrhage; later, hemodilution occurs as fluids are administered or as fluid shifts from the interstitial to the intravascular space. If the intravascular fluid volume has been restored, hematocrit measurement will more accurately reflect red blood cell mass and can be used to guide transfusion.
  3. Blood urea nitrogen and serum creatinine levels may be increased if hypovolemia is sufficiently prolonged. (Both measurements may also be influenced by events unrelated to blood volume.) Although hypovolemia does not cause metabolic alkalosis, ECF volume depletion is a potent stimulus for the maintenance of metabolic alkalosis.
  4. Intraoperative Clinical Assessment.Visual estimation, as seen on operative sponges and drapes, is the simplest technique for quantifying intraoperative blood loss.
  5. Adequacy of intraoperative blood volume replacement cannot be ascertained by any single modality (Table 14-18).

Table 14-18 Clinical Indicators of the Adequacy of Intraoperative Blood Volume Replacement

Heart rate (tachycardia is insensitive and nonspecific)
Blood pressure
Central venous pressure
Urinary output
Arterial oxygenation and pH

  1. P.165
  2. Preservation of the blood pressure accompanied by a central venous pressure of 6 to 12 mm Hg in the presence of a volatile anesthetic suggests an adequate blood volume.
  3. During profound hypovolemia, indirect measurement of blood pressure may significantly underestimate true blood pressure, emphasizing the potential value of direct blood pressure measurements in selected patients.
  4. An additional advantage of direct arterial pressure monitoring may be recognition of increased systolic blood pressure variation accompanying positive pressure ventilation in the presence of hypovolemia.
  5. Urinary output usually decreases precipitously (<0.5 mL/kg/hr) in the presence of moderate to severe hypovolemia.
  6. Oxygen Delivery as a Goal of Management.No intraoperative monitor is sufficiently sensitive or specific to detect hypoperfusion in all patients. In high-risk surgical patients, systemic oxygen delivery of 600 mL/m2/min or above (equivalent to a cardiac index of 3 L/m2/min and a hemoglobin concentration equivalent to 14 g/dL) may result in improved outcome.

VII. Electrolytes

  1. Physiologic Role of Electrolytes(Table 14-19).
  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.
  3. 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.
  4. 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).
  5. The cerebral salt-wasting syndrome appears to be mediated by brain natriuretic peptide; the secretion of antidiuretic hormone is appropriate.
  6. 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).

Table 14-19 Physiologic Role of Electrolytes


Physiologic Role


Extracellular fluid volume
Action potential


Transmembrane potential
Action potential


Enzyme function
Cardiac pacemaker activity
Cardiac action potential
Bone structure


Stores energy (adenosine triphosphate)
Component of second messengers (cyclic adenosine monophosphate)
Component of cell membranes (phospholipids)


Enzyme cofactor (sodium-potassium pump)
Controls potassium movement into cells
Membrane excitability
Bone structure

  1. Inappropriately rapid correction of hyponatremia may result in abrupt brain dehydration (osmotic demyelination syndrome is most likely when hyponatremia has persisted >48 hours).

Table 14-20 Signs and Symptoms of Hyponatremia

Altered consciousness (sedation to coma)
Cerebral edema
Loss of appetite
Nausea and vomiting

  1. P.167

Table 14-21 Precipitating Causes of Inappropriate Antidiuretic Hormone Secretion

Pulmonary disease
Central nervous system trauma
Endocrine dysfunction
Drugs that mimic antidiuretic hormone

  1. Hypernatremia(>150 mEq/L) is usually the result of decreased total body water.
  2. 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). When hypernatremia develops abruptly, the associated sudden brain shrinkage may stretch and disrupt cerebral vessels, leading to subdural hematoma, subarachnoid hemorrhage, and venous thrombosis.
  3. Postoperative neurosurgical patients who have undergone pituitary surgery are at particular risk of developing transient or prolonged diabetes insipidus, leading to hypernatremia.
  4. Treatmentof hypernatremia is influenced by the clinical assessment of ECF volume (Table 14-23).
  5. Potassium
  6. 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.

Table 14-22 Signs and Symptoms of Hypernatremia

Intracranial hemorrhage
Polyuria or oliguria
Renal insufficiency

  1. P.168

Table 14-23 Treatment of Hypernatremia

Sodium Depletion (Hypovolemia)
Correct hypovolemia (0.9% saline).
Correct hypernatremia (hypotonic fluids).
Sodium Overload (Hypervolemia)
Enhance sodium removal (loop diuretics, dialysis).
Replace water deficit (hypotonic fluids).
Normal Total Body Sodium (Euvolemia)
Replace water deficit (hypotonic fluids).
Control diabetes insipidus (desmopressin, vasopressin, chlorpropamide).
Control nephrogenic diabetes insipidus (restrict sodium and water intake, thiazide diuretics).

  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).
  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).


Table 14-24 Signs and Symptoms of Hypokalemia

Cardiac dysrhythmias (premature ventricular contractions)
ECG changes (widened QRS segment, S-T segment depression, first-degree AV heart block)
Potentiates digitalis toxicity
Postural hypotension
Skeletal muscle weakness (hypoventilation)
Concentrating defect
Glucose intolerance
Potentiation of hypercalcemia and hypomagnesemia

AV = atrioventricular; ECG = electrocardiograph.

  1. Potassium depletion may induce defects in renal concentrating ability, resulting in polyuria.
  2. Hypokalemia causes skeletal muscle weakness and, when severe, may even cause paralysis.
  3. Treatment of hypokalemia consists of potassium repletion, correction of alkalosis, and discontinuation of offending drugs (diuretics, aminoglycosides) (Table 14-25). 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 of greater than 20 mEq/hr should be continuously monitored with electrocardiography (ECG).

Figure 14-2. Electrocardiographic (ECG) changes that may accompany progressive increases in serum potassium concentrations.

Table 14-25 Treatment of Hypokalemia

Correct Precipitating Factors(alkalosis, hypomagnesemia, drugs)
Mild Hypokalemia (>2.0 mEq/L)
Infuse potassium chloride ≤10 mEq/hr IV.
Severe Hypokalemia (<2.0 mEq/L, ECG changes, intense skeletal muscle weakness)
Infuse potassium chloride ≤40 mEq/hr IV.
Continuously monitor the ECG.

ECG = electrocardiograph; IV = intravenous.

  1. P.170
  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). Overall, ECG is an insensitive and nonspecific method of detecting hyperkalemia.
  3. Signs and symptoms of hyperkalemia primarily involve the central nervous and cardiovascular systems (Table 14-26).

Figure 14-3. Treatment of hyperkalemia. ECF = extracellular fluid; ECG = electrocardiogram; ICF = intracellular fluid; IV = intravenous.

Table 14-26 Signs and Symptoms of Hyperkalemia

Cardiac dysrhythmias (heart block)
ECG changes (widened QRS segment, tall peaked T waves, atrial asystole, prolongation of P-R interval)
Skeletal muscle weakness

ECG = electrocardiograph.

  1. P.171
  2. Treatment of hyperkalemia is designed to eliminate the cause, reverse membrane hyperexcitability, and remove potassium from the body (Fig. 14-3 and Table 14-27).


Table 14-27 Treatment of Severe Hyperkalemia*

Reverse Membrane Effects
Calcium (10% calcium chloride IV over 10 min)
Transfer Potassium Into Cells
Glucose (D10W) and regular insulin (5–10 U regular insulin for every 25–50 g of glucose)
Sodium bicarbonate (50–100 mEq over 5 to 10)
β-2 agonists
Remove Potassium from Body
Diuretics (proximal or loop)
Potassium-exchange resins
Hemodialysis (removes 25–50 mEq/hr)

*>7 mEq/L, ECG changes.
ECG = electrocardiograph.

  1. Calcium
  2. 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).

Table 14-28 Signs and Symptoms of Hypocalcemia

Cardiac dysrhythmias
ECG changes (prolongation of the Q-T interval, T-wave inversion)
Congestive heart failure
Skeletal muscle spasm
Skeletal muscle weakness

ECG = electrocardiograph.

  1. P.173

Table 14-29 Treatment of Hypocalcemia

Administer calcium.
10 mL of 10% calcium gluconate IV over 10 min followed by a continuous infusion of 500 to 1000 mg of calcium orally every 6 hr.
Administer vitamin D.
Monitor ECG.

ECG = electrocardiograph; IV = intravenous; PO = per os.

  1. The hallmark of hypocalcemia is increased neuronal membrane irritability and tetany (Table 14-28).
  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 trauma, after cardiopulmonary bypass, massive transfusion [citrate]).
  3. Treatment of hypocalcemia (Table 14-29).
  4. 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.

Table 14-30 Signs and Symptoms of Hypercalcemia

Heart block
Digitalis sensitivity
Skeletal muscle weakness
Sedation to coma
Polyuria (renal tubular concentration defect)
Peptic ulcer disease

  1. P.174

Table 14-31 Signs and Symptoms of Hypomagnesemia

Coronary vasospasm
Cardiac dysrhythmias (especially after myocardial infarction or after cardiopulmonary bypass)
Refractory ventricular fibrillation
Congestive heart failure
Neuronal irritability (tetany)
Skeletal muscle weakness
Hypokalemia (magnesium-induced potassium wasting)
Hypocalcemia (magnesium-induced suppression of parathyroid hormone secretion)

  1. Signs and symptoms (Table 14-30).
  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).
  3. Magnesiumis principally intracellular and is necessary for enzymatic reactions.
  4. 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.
  5. Signs and symptoms (Table 14-31).
  6. Treatment of hypomagnesemia (Table 14-32). 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.

Table 14-32 Treatment of Hypomagnesemia

Administer magnesium.*
Administer IV magnesium 8 to 16 mEq over 1 hr followed by 2 to 4 mEq/hr.
Administer IM magnesium 10 mEq every 4 to 6 hr.

*MgSO4 1 g = 8 mEq; MgCl2 1 g = 10 mEq.
IM = intramuscular; IV = intravenous.

Table 14-33 Signs and Symptoms of Hypermagnesemia

Plasma Magnesium Concentration (mg/dL)



Therapeutic range (pre-eclampsia)




Deep tendon hyporeflexia




Deep tendon areflexia




Heart block


Cardiac arrest


  1. Hypermagnesemia(>2.5 mg/dL) is usually iatrogenic (e.g., treatment of pregnancy-induced hypertension or premature labor).
  2. Signs and symptoms (Table 14-33).
  3. Hypermagnesemia antagonizes the release and effect of acetylcholine at the neuromuscular junction, manifesting as potentiation of the action of nondepolarizing muscle relaxants.
  4. 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.

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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