Acid-Base Disorders PDF

C H APT E R
Fluid, Electrolyte, and Acid-Base 21

Disorders
ROBERT B. SCHONBERGER
ABNORMALITIES OF WATER, OSMOLALITY,

AND ELECTROLYTES
Abnormalities of Water, Osmolality, and Electrolytes
Water and Osmolal Homeostasis
Water and Osmolal Homeostasis
Disorders of Sodium
Hyponatremia In the nonobese adult, total body water comprises approximately
Transurethral Resection of the Prostate (TURP) Syndrome 60% of body weight (obesity decreases this proportion). Body
Hypernatremia water is divided into intracellular fluid (ICF) and extracellular
Disorders of Potassium fluid (ECF) compartments according to the location of the water
Hypokalemia relative to cell membranes (Fig. 21.1). ECF consists primarily of
Hyperkalemia an interstitial compartment (three-fourths of ECF) and an intra-
Disorders of Calcium vascular plasma compartment (one-fourth of ECF). Water shifts
Hypocalcemia between compartments according to the balance of hydrostatic
Hypercalcemia and oncotic pressure across membranes, and thus water homeo-
Disorders of Magnesium stasis relies on the maintenance of osmolality within a narrow
Hypomagnesemia physiologic range. The integrity of living cells depends on pres-
Hypermagnesemia ervation of water homeostasis, as well as on the energy-intensive
Acid-Base Disorders maintenance of intracellular and extracellular concentrations of
Respiratory Acidosis ions termed electrolytes. These electrolytes, in addition to being
Respiratory Alkalosis a major determinant of both osmolality and acid-base balance,
Metabolic Acidosis are responsible for electrical potentials across cell membranes.
Metabolic Alkalosis Changes in electrolyte homeostasis especially impact excitable
Key Points cells in the CNS and musculature that rely on action potentials
for rapid and organized transfer of information.
Water and osmolal homeostasis are predominantly medi-
ated by osmolality-sensing neurons located in the anterior
hypothalamus. In response to osmolal elevations, these neu-
Alterations of water, osmolal, and electrolyte content and dis- rons stimulate thirst and cause pituitary release of vasopres-
tribution as well as acid-base disturbances are common in the sin (antidiuretic hormone). Vasopressin is stored as granules
perioperative period and rarely happen in isolation, because in the posterior pituitary and acts through G protein–coupled
they are inherently interrelated. They both affect and are receptors in the collecting ducts of the kidney to cause water
affected by the function and stability of several organ systems. retention, which in turn decreases serum osmolality. Vaso-
Central nervous system (CNS) impairment, cardiac dysfunc- pressin receptors are also present in other tissues and, most
tion, and neuromuscular changes are especially common in noticeably for the anesthesiologist, are present in high density
the presence of water, osmolal, electrolyte, and acid-base dis- on vascular smooth muscle cells, where they induce vasocon-
turbances. Several perioperative events can exacerbate such striction. As a major site of vasopressin effects, the kidney is
alterations (Table 21.1). Management of patients with these responsible for maintaining water homeostasis by excreting
disturbances is based on an assessment of the cause and sever- urine with large variations in total osmolality. Under normal
ity of the condition, an understanding of the interrelationships circumstances, serum osmolality is tightly regulated by thirst
among these disturbances, and an awareness of the patient’s and renal control of water excretion. The normal range of
comorbid conditions. serum osmolality is 280–290 mOsm/kg.
407
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408 STOELTING’S ANESTHESIA AND CO-EXISTING DISEASE
may be encountered as a result of free water depletion (e.g.,

TABLE 21.1 Common Causes of Water, Osmolal,
Electrolyte, and Acid-Base Disturbances
dehydration or diabetes insipidus) or the presence of addi-
During the Perioperative Period tional solutes (most commonly from ingestion of ethanol or
other toxins, hyperglycemia, or iatrogenic administration
Disease states of osmolal loads such as mannitol or glycine). Perioperative
Endocrinopathies attempts to induce fluid shifts by deliberate administration
Nephropathies
Gastroenteropathies
of osmolal loads should take into consideration the patient’s
Drug therapy preexisting serum osmolality to avoid extreme increases in
Diuretics serum osmolality (>320 mOsm/kg). Mannitol should not be
Corticosteroids administered to an intoxicated patient with elevated intracra-
Nasogastric suction nial pressure, for example, without prior consideration of the
Surgery
preexisting effects of ethanol molecules and water diuresis on
Transurethral resection of the prostate
Translocation of body water due to tissue trauma the osmolal state of the patient.
Resection of portions of the gastrointestinal tract Although vasopressin is predominantly secreted in
Management of anesthesia response to increased osmolality, its release is also stimulated
Intravenous fluid administration by large isoosmolar decreases in effective circulating volume.
Alveolar ventilation
In addition, the pain and stress of the perioperative period are
Hypothermia
upregulators of vasopressin release, and the stress response to
critical illness can include water retention, oliguria, and dilu-
TOTAL BODY WATER 0.6 BODY WEIGHT tional hyponatremia (Table 21.2).
100 In contrast to osmolal homeostasis, the homeostatic
response to isotonic changes in total body water relies on
juxtaglomerular sensation of changes in effective circulating
volume and consequent changes in kidney renin excretion.
Renin converts angiotensinogen into angiotensin I, which is
Intracellular fluid
converted to angiotensin II in the lung. Angiotensin II induces
adrenal release of aldosterone, which promotes sodium reab-
sorption and potassium loss in the distal tubules and also leads
Total body water %
to increases in water resorption. Elevations in circulating vol-

50
ume also cause increased release of natriuretic peptides that
Cell promote a return to water homeostasis.
membrane Fluid resuscitation in patients with hypovolemia necessi-
tates consideration of the cause and severity of the hypovolemia
Extracellular fluid
Interstitial fluid (3/4 of ECF)

and patient comorbid conditions. Crystalloid administration
should take into consideration a patient’s electrolyte and acid-
base balance as well as concerns regarding the acute cardiovas-
Capillary cular effects of additional volume and the neurologic effects of
membrane
Plasma (1/4 of ECF) changes in volume, osmolality, and glucose levels.
0
Infusion of colloids, including blood products, should
be done in the context of appropriate goals for hemoglobin
FIG. 21.1 Total body water (≈60% of total body weight) is desig-
nated as intracellular fluid (ICF) or extracellular fluid (ECF) depending
concentration, platelet numbers, and coagulation factors and
on the location of the water relative to cell membranes. ECF is fur- must take into consideration the course of any ongoing blood
ther divided into interstitial and plasma compartments depending on loss and the health status of the patient. Synthetic volume
its location relative to vascular walls. Two-thirds of total body water expanders have been advocated to achieve volume expansion
is ICF. Of ECF, 75% is interstitial, 25% is intravascular. with reduced tissue edema compared to crystalloids. However,
there is no good evidence that they provide advantages in out-
The osmolality of serum represents the total number of comes in comparison to appropriately balanced crystalloid
osmotically active particles (i.e., solutes) per kilogram of solutions. Indeed, some have been associated with increased
solvent. When osmolality is assessed, a shorthand indirect bleeding and a higher incidence of renal dysfunction in addi-
measurement of expected serum osmolality can easily be tion to their increased cost in comparison with crystalloids.
calculated as 2[Na] + [Glucose]/18 + [Blood urea nitrogen
(BUN)]/2.8, and this calculated value should always be com-
DISORDERS OF SODIUM
pared with direct laboratory-measured actual osmolality. A
significant difference in these values (known as an osmolal As the ion with the highest concentration in the ECF, sodium
gap) should alert the clinician to the presence of unmeasured contributes most of the effective osmoles to serum. This under-
osmotically active particles. Increases in serum osmolality lying connection between serum sodium concentration and
Chapter 21 Fluid, Electrolyte, and Acid-Base Disorders 409
TABLE 21.2 Factors and Drugs Affecting Vasopressin Secretion

Drugs That Stimulate Vasopressin Release and/or
Stimulation of Vasopressin Release Inhibition of Vasopressin Release Potentiate Renal Action of Vasopressin
Contracted ECF volume Expanded ECF volume Amitriptyline

Hypernatremia Hyponatremia Barbiturates
Hypotension Hypertension Carbamazepine
Nausea and vomiting Chlorpropamide
Congestive heart failure Clofibrate
Cirrhosis Morphine
Hypothyroidism Nicotine
Angiotensin II Phenothiazines
Catecholamines Selective serotonin reuptake inhibitors
Histamine
Bradykinin
ECF, Extracellular fluid.
osmolality is critical for understanding disorders of sodium TABLE 21.3 Symptoms and Signs of Hyponatremia
homeostasis. Under normal circumstances, serum sodium
concentration is maintained between 136 and 145 mmol/L, Symptoms Signs
primarily by the action of vasopressin on water and osmolal
Anorexia Abnormal sensorium
homeostasis. Nausea Disorientation, agitation
Variations in measured sodium concentration frequently Lethargy Cheyne-Stokes breathing
occur along with derangements in total body water. Assess- Apathy Hypothermia
ment and treatment of changes in sodium concentration must Muscle cramps Pathologic reflexes
Pseudobulbar palsy
therefore consider osmolality as well as the total body water
Seizures
of the patient. Total body water can be increased, normal, or Coma
decreased in the context of derangements in sodium concen- Death
tration, and the cause and treatment of serum sodium disor-
ders depend on the osmolality and volume status of the patient.
movement of potassium and organic solutes out of brain cells.
This reduces water movement into the intracellular space.
Hyponatremia
However, when adaptive mechanisms fail or hyponatremia
Hyponatremia commonly exists in concert with hypoosmolal- progresses, CNS dysfunction can manifest as a change in sen-
ity when water retention or water intake exceeds renal excre- sorium, seizures, brain herniation, or death.
tion of dilute urine. Hyponatremia exists in approximately
15% of hospitalized patients, most commonly as a dilutional Diagnosis
effect in the setting of increased vasopressin release. In the Although hyponatremia usually co-exists with hypoosmolality,
outpatient setting, hyponatremia is more likely to be a result of osmolality should be measured in all cases of hyponatremia,
chronic disease, and in heart failure has been shown to be an particularly to avoid overlooking a pathologic hyperosmolar
independent predictor of 30-day and 1-year mortality. state caused by dangerous concentrations of glucose or exog-
enous toxins, or iatrogenic infusions of osmolal loads.
Signs and Symptoms In such hyperosmolal situations, plasma volume expands
The signs and symptoms of hyponatremia depend on the as interstitial and intracellular water migrates into the intra-
rate at which the hyponatremia has developed and are less vascular space, causing a relative dilution of the serum sodium
pronounced in chronic cases. In addition, younger patients concentration without a reduction in the amount of total
appear to tolerate a decrease in serum sodium better than body sodium. Total body water may be increased, unchanged,
elderly patients. or decreased depending on the competing effects of water
Anorexia, nausea, and general malaise may occur early, but administered with the osmolal load and the likely presence of
CNS signs and symptoms predominate later in the course and an osmotic diuresis.
in acutely deteriorating cases of hyponatremia (Table 21.3). As In patients with normal osmolality, a pseudohyponatremia
mentioned earlier, hyponatremia usually occurs along with can be seen as a laboratory artifact in cases of severe hyperlip-
extracellular hypotonicity. The associated osmolal gradient idemia or hyperproteinemia when plasma volume is increased
allows water to move into brain cells, which results in cerebral in the presence of normal serum sodium concentrations. Mea-
edema and increased intracranial pressure. Brain cells may suring sodium concentrations in serum rather than in plasma
compensate over time by lowering intracellular osmolality by avoids this misinterpretation of laboratory data.
Hypotonic hyponatremia
Hypovolemia Euvolemia Hypervolemia
Decreased skin turgor Peripheral edema

Flat neck veins Rales
Dry mucous membranes Ascites
Orthostatic hypotension
Tachycardia
Oliguria
UNa 20 UNa 20 UNa 20 UNa 20 UNa 20 UNa 20
Renal Extrarenal Salt- Renal Avid sodium

losses losses restricted diet losses reabsorption
Diuretic excess Vomiting Glucocorticoid deficiency Acute renal failure Nephrotic syndrome
Mineralocorticoid deficiency Diarrhea Hypothyroidism Chronic renal failure Cardiac failure
Salt-losing nephritis 3rd space losses High sympathetic drive Cirrhosis
Renal tubular acidosis Burns Drugs
Metabolic alkalosis Pancreatitis SIADH
Ketonuria Muscle trauma
Osmotic diuresis
FIG. 21.2 Diagnostic algorithm for hypotonic hyponatremia. SIADH, Syndrome of inappropriate
antidiuretic hormone secretion; UNa, urinary sodium concentration (mEq/L) in a spot urine sample.
(Adapted from Schrier RW. Manual of Nephrology. 6th ed. Philadelphia: Lippincott Williams &
Wilkins; 2006.)
Once the two situations of hyperosmolality and normal context does not lead to a diagnosis, urinary sodium concentra-
osmolality have been excluded, the approach to the diagno- tion measured from a spot urine sample can help further differ-
sis of hypoosmolal hyponatremia includes evaluation of the entiate among the various causes of hyponatremia (Fig. 21.2).
severity of the electrolyte derangement and the underlying
volume status of the patient. Hypervolemic hyponatremia sug- Treatment
gests the possibility of renal failure, congestive heart failure, Treatment of hypotonic hyponatremia will depend on the
or a hypoalbuminemic state such as cirrhosis or nephrotic volume status of the patient. In hypovolemic hyponatremia,
syndrome. Euvolemic hyponatremia is commonly seen in the appropriate volume resuscitation should be pursued, usu-
syndrome of inappropriate antidiuretic hormone secretion ally with normal saline. If renal sodium losses are suspected,
(SIADH) or in situations of habitual ingestion of hypotonic mineralocorticoid deficiency and the possibility of adrenal
solutions (e.g., water), as seen in psychogenic polydipsia. insufficiency should not be overlooked. Cases of massive
Hypovolemic hyponatremia should prompt an investigation third spacing, such as often accompany pancreatitis or burns,
into the source of free water loss. This free water loss may be require tailored resuscitation based on the totality of electro-
from renal losses (e.g., from diuretics, mineralocorticoid defi- lyte and hematologic derangements.
ciency, or other salt-wasting nephropathy) or extrarenal losses In euvolemic or hypervolemic patients, treatment involves
(e.g., gastrointestinal [GI] losses or third spacing). withholding free water and encouraging free water excretion
Often the clinical context of hyponatremia offers the prin- with a loop diuretic. Administration of saline is necessary only
cipal clue to its cause. For example, massive absorption of if significant symptoms are present. In these as in all cases of
irrigating solutions that do not contain sodium, such as dur- hyponatremia, the rate of correction depends on whether the
ing transurethral resection of the prostate, is a relatively com- development of hyponatremia was acute (i.e., occurred in <48
mon cause of intraoperative hyponatremia. When the clinical hours) or was chronic.
TABLE 21.4 Signs and Symptoms of TURP Syndrome

System Signs and Symptoms Cause
Cardiovascular Hypertension, reflex bradycardia, pulmonary edema, Rapid fluid absorption (reflex bradycardia may be
cardiovascular collapse secondary to hypertension or increased ICP)
Hypotension Third spacing secondary to hyponatremia and
hypoosmolality; cardiovascular collapse
ECG changes (wide QRS, elevated ST segments, Hyponatremia
ventricular dysrhythmias)
Respiratory Tachypnea, oxygen desaturation, Cheyne-Stokes breathing Pulmonary edema
Neurologic Nausea, restlessness, visual disturbances, confusion, Hyponatremia and hypoosmolality causing cerebral edema
somnolence, seizures, coma, death and increased ICP, hyperglycinemia, hyperammonemia
Hematologic Disseminated intravascular hemolysis Hyponatremia and hypoosmolality
Renal Renal failure Hypotension, hyperoxaluria (oxalate is a metabolite of
glycine)
Metabolic Acidosis Deamination of glycine to glyoxylic acid and ammonia
ECG, Electrocardiogram; ICP, intracranial pressure, TURP, transurethral resection of the prostate.
Acute symptomatic hyponatremia must be treated promptly. necessary to avoid overly rapid correction of hyponatre-
Solute-free fluids are withheld and hypertonic saline (3% mia with resultant osmotic demyelination or overcorrection
NaCl) and furosemide are administered to enhance renal resulting in hypernatremia. If the treatment of hyponatremia
excretion of free water. Serum electrolyte levels should be includes hypertonic sodium infusion during surgery, it should
checked frequently and this treatment continued until symp- be infused via a pump while losses caused by the surgery
toms disappear, which will likely occur before the serum are replaced with standard crystalloid or colloid solutions as
sodium concentration returns to normal. required. Treatment of the underlying cause of the hyponatre-
Chronic symptomatic hyponatremia should be corrected mia should also continue throughout the perioperative period.
slowly to avoid the risk of osmotic demyelination. During the Induction and maintenance of anesthesia in patients with
development of chronic hyponatremia, brain cells retain their hypovolemic hyponatremia are fraught with the risk of hypo-
normal intracellular volume as the serum sodium decreases by tension. In addition to fluid therapy, vasopressors and/or ino-
exporting “effective osmoles.” Approximately half of these effec- tropes may be required to treat the hypotension, and these
tive osmoles are potassium ions and anions, and the remainder should be available before the start of induction. Hypervolemic
are small organic compounds. While hyponatremia is being cor- hyponatremic patients, particularly those with heart failure,
rected, brain cells must reaccumulate these effective osmoles or may benefit from invasive hemodynamic monitoring to assess
water will move out of the cells into the now relatively hypertonic cardiac function and guide fluid therapy.
ECF, causing cell shrinkage. Such shrinkage can trigger central
pontine myelinolysis, which can result in quadriplegia, seizures,
Transurethral Resection of the Prostate (TURP)
coma, and death. The risk of osmotic demyelination is higher in
Syndrome
patients who are malnourished or potassium depleted. Guide-
lines for correction of chronic symptomatic hyponatremia call for Benign prostatic hyperplasia is often treated surgically by
an initial correction in serum sodium concentration of approxi- transurethral resection of the prostate (TURP). This procedure
mately 10 mEq/L. Thereafter, correction should not exceed 1 to involves resection via a cystoscope, with continuous irriga-
1.5 mEq/L/hr or a daily maximum increase of 12 mEq/L. tion of the bladder to aid visualization of the surgical field and
Treatment of chronic asymptomatic hyponatremia should removal of blood and resected material. The irrigating fluid is
consider the underlying cause of the electrolyte disturbance. usually a nearly isotonic nonelectrolyte fluid containing glycine
Appropriate sodium intake and volume restriction are often or a mixture of sorbitol and mannitol. This irrigating fluid can
the cornerstones of treatment. Patients with hypervolemic be absorbed rapidly via open venous sinuses in the prostate
hyponatremia due to congestive heart failure respond very gland and can cause volume overload and hyponatremia. The
well to the combination of an angiotensin-converting enzyme constellation of findings associated with absorption of bladder
inhibitor and a loop diuretic. irrigation solution is known as TURP syndrome. This syndrome
is more likely to occur when resection is prolonged (>1 hour),
Management of Anesthesia when the irrigating fluid is suspended more than 40 cm above
If at all possible, significant hyponatremia, especially if symp- the operative field, when hypotonic irrigation fluid is used, and
tomatic, should be corrected before surgery. If the surgery when the pressure in the bladder is allowed to increase above
is urgent, appropriate corrective treatment should continue 15 cm H2O. TURP syndrome (Table 21.4) manifests principally
throughout the surgery and into the postoperative period. with cardiovascular signs of fluid overload and neurologic signs
Frequent measurement of serum sodium concentration is and symptoms of hyponatremia. Use of hypotonic irrigating
solutions can also induce hemolysis because red blood cells

TABLE 21.5 Symptoms and Signs of Hypernatremia
encounter a significant influx of free water from hypotonic ECF.
Hypertension and pulmonary edema are common. If a glycine Symptoms Signs
irrigant is used, transient blindness can occur that is thought
Polyuria Muscle twitching
to result from the inhibitory neurotransmitter effects of glycine
Polydipsia Hyperreflexia
on several populations of retinal ganglion cells. Glycine breaks Orthostasis Tremor
down into glyoxylic acid and ammonia, and excessive ammonia Restlessness Ataxia
levels are themselves known to cause encephalopathy. Irritability Muscle spasticity
Monitoring for the development of TURP syndrome Lethargy Focal and generalized seizures
Death
includes direct neurologic assessment in patients under
regional anesthesia and measurement of hemodynamics,
serum sodium concentration, and osmolality in patients under
general anesthesia. Treatment consists of terminating the sur- been reported. As the brain cells shrink, cerebral blood vessels
gical procedure so no more fluid is absorbed, administration may stretch and tear, which results in intracranial hemorrhage.
of loop diuretics if needed for relief of cardiovascular symp- Usually the signs and symptoms are more severe when
toms, and administration of hypertonic saline if severe neu- hypernatremia is acute rather than chronic and when exces-
rologic symptoms or signs are present or the serum sodium sive elevations in serum sodium levels are present. Mortality
concentration is less than 120 mEq/L. rates of up to 75% have been reported in adults with severe
acute hypernatremia (serum sodium concentration > 160
mEq/L), and survivors of severe acute hypernatremia often
Hypernatremia
have permanent neurologic deficits. During the development
Hypernatremia is defined as a serum sodium concentration of chronic hypernatremia, brain cells generate “idiogenic
above 145 mEq/L. It is much less common than hyponatremia osmoles” that restore intracellular water in spite of the ongoing
because the vasopressin-driven thirst mechanism is very effec- hypernatremia and protect against brain cell dehydration. If
tive in responding to the hypertonic state of hypernatremia. chronic hypernatremia is corrected too rapidly, these idiogenic
Even in patients with renal disorders of sodium retention or osmoles predispose to the development of cerebral edema.
severe water loss, patients will regulate their serum sodium
concentration close to or within the normal range if they have Diagnosis
access to water. Therefore hypernatremia is much more likely The diagnosis and treatment of hypernatremia should focus
to be seen in the very young, the elderly, and those people who on the severity of the derangement and the volume status
are debilitated, have altered mental status, or are unconscious. of the patient. The presence of hypervolemia, euvolemia, or
In the perioperative setting, hypernatremia is most likely a hypovolemia dictates the appropriate diagnostic and treat-
result of iatrogenic overcorrection of hyponatremia or treatment modalities (Fig. 21.3).
ment of acidemia with sodium bicarbonate. Free water losses In hypovolemic hypernatremia the patient has lost more
from diabetes insipidus and extrarenal GI losses may also lead water than sodium via renal or extrarenal routes. This may
to hypernatremia. Because sodium is the major contributor occur as a result of excessive diuresis, GI losses, or insensible
to ECF osmolality, hypernatremia induces the movement of fluid losses from burns or sweating.
water across cell membranes into the ECF. Hypernatremia Patients with hypervolemic hypernatremia will show signs
and the associated hyperosmolality will always lead to cellular of ECF volume expansion, such as jugular venous distention,
dehydration and shrinkage. peripheral edema, and pulmonary congestion. The differential
diagnosis includes a history of hypertonic fluid administra-
Signs and Symptoms tion, oral intake of salt tablets, and endocrine abnormalities
Signs and symptoms of hypernatremia can vary from mild to marked by excessive aldosterone secretion.
life threatening (Table 21.5). The earliest signs and symptoms Euvolemic and hypovolemic hypernatremia occur second-
include restlessness, irritability, and lethargy. As hypernatre- ary to water loss without salt loss and may be seen with either
mia progresses, muscular twitching, hyperreflexia, tremors, extrarenal pathologic conditions (e.g., GI tract losses or insen-
and ataxia may develop. The signs and symptoms progress as sible losses from burns or sweating) or from renal losses (e.g.,
the osmolality increases above 325 mOsm/kg. Muscle spastic- diabetes insipidus, loop diuretics, or osmotic diuresis).
ity, seizures, and death may ensue. The very young, the very As with hyponatremia, testing of a spot urine sample for
old, and those with preexisting CNS disease exhibit more sodium concentration and osmolality can help distinguish
severe symptoms at any given serum sodium concentration or among the causes of hypernatremia (see Fig. 21.3).
degree of hyperosmolality.
The most prominent abnormalities in hypernatremia are Treatment
neurologic. Dehydration of brain cells occurs as water shifts Treatment is determined by how severe the hypernatremia
out of the cells into the hypertonic interstitium. Capillary and is, how rapidly it developed, and whether the ECF volume is
venous congestion as well as venous sinus thrombosis have all increased or decreased.
Hypernatremia
Hypovolemia Euvolemia Hypervolemia
Decreased skin turgor Peripheral edema

Flat neck veins Rales
Dry mucous membranes Ascites
Orthostatic hypotension
Tachycardia
Oliguria
UNa 20 UNa 20 UNa variable UNa 20
Renal salt Extrarenal salt Renal Extrarenal Sodium gains

and water loss and water loss water loss water loss
Osmotic diuretic Diarrhea Diabetes insipidus Insensible losses

Hyperaldosteronism
Loop diuretic GI fistulas • Central • Respiratory tract
Cushing’s syndrome
Postrenal obstruction Burns • Nephrogenic • Skin
Hypertonic dialysis
Intrinsic renal disease Sweating • Gestational
Intravenous sodium bicarbonate
Profound glycosuria
Sodium chloride tablets
Hyperalimentation
Hypertonic saline enemas
Salt water drowning
FIG. 21.3 Diagnostic algorithm for hypernatremia. GI, Gastrointestinal; UNa, urinary sodium con-
centration (mEq/L) in a spot urine sample. (Adapted from Schrier RW. Manual of Nephrology. 6th
ed. Philadelphia: Lippincott Williams & Wilkins; 2006.)
In hypovolemic hypernatremia the water deficit is replen- abated. Frequent serum sodium measurement and urine out-
ished with normal saline or a balanced electrolyte solution put monitoring will be required perioperatively, and invasive
until the patient is euvolemic, and then the plasma osmolality hemodynamic monitoring may be useful to assess volume sta-
is corrected with hypotonic saline or 5% dextrose solution. tus. Hypovolemia will be exacerbated by induction and main-
In patients with hypervolemic hypernatremia the primary tenance of anesthesia, and prompt correction of hypotension
treatment is diuresis with a loop diuretic unless the cause is with fluids, vasopressors, and/or inotropes may be required.
renal failure, in which case hemofiltration or hemodialysis The volume of distribution of hydrophilic drugs will be altered
may be needed. in hypovolemia and hypervolemia. However, the accentuated
Patients with euvolemic hypernatremia require water hemodynamic responses to anesthetic drug administration
replacement either orally or with 5% dextrose intravenously. are most likely a consequence of the vasodilation and negative
Treatment of diabetes insipidus depends on whether there is a inotropic effects of anesthetic drugs rather than the result of
central deficit of vasopressin release or a renal insensitivity to changes in their volume of distribution.
vasopressin’s actions.
Acute hypernatremia should be corrected over several
DISORDERS OF POTASSIUM
hours. However, to avoid cerebral edema, chronic hypernatre-
mia should be corrected more slowly over 2–3 days. Ongoing Potassium is the major intracellular cation. The normal total
sodium and water losses should also be calculated and replaced. body potassium content depends on muscle mass; it is maxi-
mal in young adults and decreases progressively with age. Less
Management of Anesthesia than 1.5% of total body potassium is found in the extracellu-
If at all possible, surgery should be delayed until the hyperna- lar space. Therefore serum potassium concentration is more
tremia has been corrected and its associated symptoms have a reflection of factors that regulate transcellular potassium
distribution than of total body potassium. Total body potas-

TABLE 21.6 Causes of Hypokalemia
sium is regulated over long periods of time, principally by the
distal nephron in the kidneys; the distal nephron secretes potas- HYPOKALEMIA DUE TO INCREASED RENAL POTASSIUM
sium in response to aldosterone, which leads to an increase in LOSS
urine volume and nonresorbable anions and metabolic alkalo- Thiazide diuretics
Loop diuretics
sis. More than 90% of potassium taken in by diet is excreted in
Mineralocorticoids
the urine, and most of the remainder is eliminated in the feces. High-dose glucocorticoids
As the glomerular filtration rate decreases in renal failure, the Antibiotics (penicillin, nafcillin, ampicillin)
amount of potassium excreted by the GI route increases. Drugs associated with magnesium depletion (aminoglycosides)
Surgical trauma
Hyperglycemia
Hypokalemia Hyperaldosteronism
Signs and Symptoms HYPOKALEMIA DUE TO EXCESSIVE GASTROINTESTINAL

Signs and symptoms of hypokalemia are generally restricted to LOSS OF POTASSIUM
the cardiac and neuromuscular systems and include dysrhyth- Vomiting and diarrhea
mias, muscle weakness, cramps, paralysis, and ileus. Zollinger-Ellison syndrome
Jejunoileal bypass
Malabsorption
Diagnosis Chemotherapy
Hypokalemia is diagnosed by the presence of a serum potas- Nasogastric suction
sium concentration below 3.5 mmol/L and results from
decreased net potassium intake, intracellular shifts, or HYPOKALEMIA DUE TO TRANSCELLULAR POTASSIUM
SHIFT
increased potassium losses. The differential diagnosis requires β-Adrenergic agonists
determining whether the hypokalemia is acute and secondary Tocolytic drugs (ritodrine)
to intracellular potassium shifts, such as might be seen with Insulin
hyperventilation or alkalosis, or whether the hypokalemia is Respiratory or metabolic alkalosis
chronic and associated with depletion of total body potassium Familial periodic paralysis
Hypercalcemia
stores (Table 21.6). If the hypokalemia is the result of potassium
Hypomagnesemia
losses, a spot urinary potassium reading will guide the diag-
nosis to either renal or extrarenal causes. Appropriately low Adapted from Gennari JF. Hypokalemia. N Engl J Med. 1998;339:451-458.
urine potassium concentrations in the setting of hypokalemia
point to a normally functioning kidney in the setting of inad- dysrhythmia appears during potassium repletion, the rate of
equate potassium intake or GI losses. Renal potassium losses potassium administration may be the cause. Therefore electro-
are indicated by a spot urinary potassium value of more than cardiographic (ECG) monitoring is required whenever rapid
15–20 mEq/L despite the presence of hypokalemia. In cases potassium repletion is undertaken. In the setting of urgent
of renal potassium loss, assessment of the transtubular potas- potassium repletion, potassium solutions without dextrose are
sium concentration gradient, hemodynamics, and acid-base preferred. Otherwise the insulin secretion stimulated by the
status will further help to elucidate the diagnosis. Hyperten- glucose will induce intracellular potassium transfer.
sion with hypokalemia is usually the result of a hyperaldoste- The enteral route of potassium repletion is preferred in
rone state. Renal losses in the setting of acidemia point to a cases of nonemergent potassium repletion to avoid the risks
diagnosis of renal tubular acidosis or diabetic ketoacidosis. of high-dose intravenous (IV) potassium administration. If
Renal losses in the setting of alkalemia can indicate a response IV repletion is chosen in a nonemergency situation, it should
to diuretics or can be seen in genetic disorders such as Liddle proceed at a rate of less than 20 mEq/h. Peripheral infusion
syndrome (associated with hypertension) or Bartter syndrome of a concentrated potassium solution will result in pain and/
(which has tubular effects similar to those of loop diuretics). or inflammation at the IV site, so administration via a central
Hypomagnesemia can also exacerbate renal potassium losses. venous catheter is preferred.
Hypokalemia without a change in total body potassium stores
can be caused by familial hypokalemic periodic paralysis. Management of Anesthesia
Whether or not to treat hypokalemia before surgery is an
Treatment ongoing subject of debate and depends on the chronicity and
Treatment of hypokalemia depends on the degree of potas- severity of the deficit. Because of the limitations on the rate of
sium depletion and the underlying cause. If the hypokale- potassium repletion and the large total body potassium deficits
mia is profound or is associated with life-threatening signs, that accompany chronic hypokalemia, safe repletion of total
potassium must be administered intravenously. In the pres- body potassium stores often requires days. Although total body
ence of paralysis or malignant dysrhythmias, the rate of potas- depletion is variable in its relationship to serum potassium con-
sium repletion can be as high as 20 mEq over 30 minutes (via centrations, chronic hypokalemia with serum concentrations
an infusion pump) and repeated as needed. If a malignant of less than 3.0 mEq/L may require delivery of 600 mEq or
V1 V2 V3 V4 V5 V6
TABLE 21.7 Causes of Hyperkalemia

INCREASED TOTAL BODY POTASSIUM CONTENT
Day 1
Acute oliguric renal failure

Chronic renal disease
Hypoaldosteronism
Drugs that impair potassium excretion
Triamterene
Spironolactone
Day 2
Nonsteroidal antiinflammatory drugs

Drugs that inhibit the renin-angiotensin-aldosterone system
A ALTERED TRANSCELLULAR POTASSIUM SHIFT

Succinylcholine
Respiratory or metabolic acidosis
Day 1
Lysis of cells resulting from chemotherapy

Iatrogenic bolus
PSEUDOHYPERKALEMIA
Hemolysis of blood specimen
Thrombocytosis/leukocytosis
Day 4
administration of insulin, glucose, β-adrenergic agonists,

B
bicarbonate, and diuretics, as well as by avoiding hyperventi-
FIG. 21.4 Electrocardiographic changes in hyperkalemia (A) and
lation and respiratory alkalosis.
hypokalemia (B). A, On day 1, at a K+ level of 8.6 mEq/L, the P
wave is no longer recognizable and the QRS complex is diffusely
Because of the effect of hypokalemia on skeletal muscle,
prolonged. Initial and terminal QRS delays are characteristic of there is the theoretical possibility of prolonged action of
K+-induced intraventricular conduction slowing and are best illus- muscle relaxants. Doses of neuromuscular blockers should, as
trated in leads V2 and V6. On day 2, at a K+ level of 5.8 mEq/L, the P always, be guided by nerve stimulator testing.
wave is recognizable, with a PR interval of 0.24 seconds; the dura- Potassium levels should be measured frequently if repletion
tion of the QRS complex is approximately 0.10 seconds, and the T is ongoing or changes resulting from drug administration, sur-
waves are characteristically “tented.” B, On day 1, at a K+ level of 1.5 gical progress, or ventilation are expected.
mEq/L, the T and U waves are merged. The U wave is prominent and
the QU interval is prolonged. On day 4, at a K+ level of 3.7 mEq/L,
the tracing is normal. (From Bonow R, Mann D, Zipes D, et al., eds. Hyperkalemia
Braunwald’s Heart Disease: A Textbook of Cardiovascular Medi-
Hyperkalemia is defined as a serum potassium concentration
cine. 9th ed. Philadelphia: Saunders; 2011. Courtesy Dr. C. Fisch.)
of more than 5.5 mEq/L. As with hypokalemia, hyperkalemia
can result from transcellular movement of potassium out of
more of potassium to achieve a normal total body potassium. cells or from alterations in potassium intake or excretion. In
It is therefore unlikely that administration of small aliquots of hospitalized patients, hyperkalemia is frequently the result of
potassium immediately before surgery will make any significant iatrogenic potassium loads (Table 21.7).
difference in potassium balance. Moreover, such interventions
carry the risk of inadvertent hyperkalemia that may exacerbate Signs and Symptoms
the risk of dysrhythmias in the perioperative period. However, Signs and symptoms of hyperkalemia depend on the acuity
it has been suggested that even small improvements in potas- of the increase. Chronic hyperkalemia is often asymptomatic,
sium balance may help normalize transmembrane potentials and dialysis-dependent patients can withstand considerable
and reduce the incidence of perioperative dysrhythmias. Rec- variations in serum potassium concentration between dialy-
ommendations on this controversial issue are based more on sis sessions (usually 2–3 days) with remarkably few symptoms.
expert opinion, clinical judgment, and local practice patterns Chronic hyperkalemia may be associated with nonspecific
than on evidence from peer-reviewed studies. symptoms such as general malaise and mild GI disturbances.
It may be prudent to correct significant hypokalemia in More acute or significant increases in serum potassium mani-
patients with other risk factors for dysrhythmias, such as fest as complications of a change in membrane depolarization,
those with congestive heart failure, those taking digoxin, and and neuromuscular and cardiac changes including weakness,
those with ECG evidence of hypokalemia. ECG abnormalities paralysis, nausea, vomiting, bradycardia, or asystole may result.
associated with potassium derangement are illustrated in (Fig.
21.4). Classically, U waves are seen. Anesthetic management Diagnosis
of patients with significant hypokalemia should prevent fur- The first step in the diagnosis of hyperkalemia is to rule out
ther decreases in serum potassium concentration by avoiding a spuriously high potassium level due to hemolysis of the
specimen. A spuriously high potassium level may also occur if there is muscle weakness from the hyperkalemia. Both respi-
with thrombocytosis and leukocytosis, because potassium ratory and metabolic acidosis must be avoided, since either
may leak from these cells in vitro. True hyperkalemia can be will exacerbate the hyperkalemia and its effects. Potassium-
identified on ECG first as a peaked T wave, followed in more containing IV fluids such as lactated Ringer solution (which
severe cases by disappearance of the P wave and prolongation contains 4 mEq/L of potassium) and Normosol (which con-
of the QRS complex, which progresses to sine waves and then tains 5 mEq/L of potassium) should be avoided. Dialysis
eventually to asystole (see Fig. 21.4). patients who are scheduled for surgery in which intraopera-
Common causes of hyperkalemia in the perioperative tive potassium loads are anticipated can be managed preop-
period include acidosis, rhabdomyolysis, and succinylcho- eratively by decreasing the potassium content of the dialysate
line administration. If the increase in serum potassium level to reduce serum potassium levels in anticipation of surgery.
is thought to be associated with increased total body potas-
sium, decreased renal excretion or increased potassium intake
DISORDERS OF CALCIUM
is likely. Measurement of the urinary potassium excretion rate
can aid in the differential diagnosis between cellular potas- Only 1% of total body calcium is present in the ECF. The
sium shifts and problems with potassium excretion. remainder is stored in bone. In the ECF, 60% of calcium is free
or coupled with anions and is thus filterable, and the remain-
Treatment ing 40% is bound to proteins, mainly albumin. Only the ion-
Immediate treatment of hyperkalemia is required if life-threat- ized calcium in the extracellular space is physiologically active.
ening dysrhythmias or ECG signs of severe hyperkalemia are Ionized calcium concentrations are affected by both albumin
present. This treatment is aimed at antagonizing the effects of concentration and the pH of plasma. Net calcium balance
a high potassium level on the transmembrane potential and occurs when absorption from the diet equals losses of calcium
redistributing the potassium intracellularly. Calcium chloride in feces and urine. Several hormones regulate calcium metab-
or calcium gluconate is administered intravenously to stabilize olism: parathyroid hormone, which increases bone resorp-
cellular membranes. The onset of action is immediate. Potas- tion and renal tubular reabsorption of calcium; calcitonin,
sium can be driven intracellularly by the action of insulin with which inhibits bone resorption; and vitamin D, which aug-
or without glucose. This measure will be effective within 10–20 ments intestinal absorption of calcium. The activity of these
minutes. Other adjuvant therapies include sodium bicarbon- hormones is altered in response to changes in plasma ionized
ate administration and hyperventilation to promote alkalosis calcium concentration. Other hormones, including thyroid
and movement of potassium intracellularly. Potassium driven hormone, growth hormone, and adrenal and gonadal steroids,
intracellularly may eventually move out of the cells again, so also affect calcium homeostasis, but their secretion is deter-
therapy may need to continue beyond acute correction of the mined by factors other than plasma calcium concentration.
derangement.
When hyperkalemia is due to increased total body stores
Hypocalcemia
of potassium, potassium must be eliminated from the body.
This can be achieved by administration of a loop diuretic such Hypocalcemia is defined as a reduction in serum ionized cal-
as furosemide, infusion of saline to encourage diuresis, or use cium concentration. It is important to note that many blood
of an ion exchange resin. The primary potassium exchange chemistry analysis systems measure total calcium rather than
resin in use is sodium polystyrene sulfonate (Kayexalate) given ionized calcium. Several formulas exist to convert total cal-
either orally or by enema. Dialysis may be required to remove cium to ionized calcium, but none of these is totally reliable.
potassium in cases of emergent hyperkalemia or in patients Binding of calcium to albumin is pH dependent, and acid-
with poor renal function. base disturbances can change the bound fraction and therefore
the concentration of ionized calcium without changing total
Management of Anesthesia body calcium. Alkalosis reduces the ionized calcium concen-
It is recommended that the serum potassium concentration be tration, so ionized calcium may be significantly reduced after
less than 5.5 mEq/L for elective surgery. Correction of hyper- bicarbonate administration or in the setting of hyperventila-
kalemia before surgery is preferable, but if this is not feasible, tion. Many hospitalized patients are also hypoalbuminemic,
steps should be taken to lower the potassium level immedi- and the reduction in bound calcium will reduce the measured
ately before induction of anesthesia by one or more of the serum calcium level. When serum calcium concentration is
methods indicated previously. Potassium levels may influence interpreted in the setting of a low albumin level, corrected
selection of drugs for induction and maintenance of anesthe- calcium concentration can be calculated as follows: measured
sia, because preoperative medications that induce some degree calcium (mg/dL) + 0.8 [4 − albumin (mg/dL)].
of hypoventilation and respiratory acidosis may cause further
transcellular potassium shifts. Also, succinylcholine (which Signs and Symptoms
only increases serum potassium concentration by ≈0.5 mEq/L The signs and symptoms of hypocalcemia depend on the
in healthy patients) is best avoided in the absence of an urgent rapidity and degree of reduction in ionized calcium. Most of
need for it. The effects of muscle relaxants may be exaggerated these signs and symptoms are evident in the cardiovascular
and neuromuscular systems and include paresthesias, irri- Management of Anesthesia

tability, seizures, hypotension, and myocardial depression. Symptomatic hypocalcemia must be treated before surgery,
ECG changes associated with hypocalcemia are marked by and every effort must be made to minimize any further
prolongation of the QT interval (Fig. 21.5). In the post- decrease in serum calcium level intraoperatively, as might
operative period following thyroid or parathyroid resec- occur with hyperventilation or administration of bicarbonate.
tion, hypocalcemia-induced laryngospasm can be life A decrease in ionized calcium levels should always be consid-
threatening. ered during massive transfusion of blood containing citrate.
Hypothermia, liver disease, and renal failure impair citrate
Diagnosis clearance and further increase the likelihood of significant
Hypocalcemia is often caused by decreased parathyroid hor- hypocalcemia in transfusion recipients.
mone secretion, end-organ resistance to parathyroid hormone, Sudden decreases in ionized calcium levels may be seen in
or disorders of vitamin D metabolism. These are usually seen the early postoperative period after thyroidectomy or parathy-
clinically as complications of thyroid or parathyroid surgery, roidectomy and may precipitate laryngospasm.
magnesium deficiency, and renal failure. In the operating
room, acute hypocalcemia is often encountered as a result of
Hypercalcemia
calcium binding to the citrate preservative in blood products
during massive transfusion. Hypercalcemia results from increased calcium absorption from
the GI tract (milk-alkali syndrome, vitamin D intoxication,
Treatment granulomatous diseases such as sarcoidosis), decreased renal
Acute symptomatic hypocalcemia with seizures, tetany, and/ calcium excretion in renal insufficiency, and increased bone
or cardiovascular depression must be treated immediately with resorption of calcium (primary or secondary hyperparathy-
IV calcium. The duration of treatment will depend on serial roidism, malignancy, hyperthyroidism, and immobilization).
calcium measurements. Treatment of hypocalcemia in the
presence of hypomagnesemia is ineffective unless magnesium Signs and Symptoms
is also replenished. Metabolic or respiratory alkalosis should be Hypercalcemia is associated with neurologic and GI signs
corrected. If metabolic or respiratory acidosis is present with and symptoms such as confusion, hypotonia, depressed deep
hypocalcemia, the calcium level should be corrected before tendon reflexes, lethargy, abdominal pain, and nausea and
the acidosis is treated; correcting an acidosis with bicarbon- vomiting, especially if the increase in serum calcium level is
ate or hyperventilation will only exacerbate the hypocalcemia. relatively acute. A shortened ST segment and QT interval are
Less acute and asymptomatic hypocalcemia may be treated seen on ECG (see Fig. 21.5). Chronic hypercalcemia is often
with oral calcium and vitamin D supplementation. associated with polyuria, hypercalciuria, and nephrolithiasis.
Hypocalcemia Normal Hypercalcemia
I I I
II II II
III III III
QT 0.48 sec QT 0.36 sec QT 0.26 sec

QTC 0.52 QTC 0.41 QTC 0.36
FIG. 21.5 Electrocardiographic changes in calcium disorders. Prolongation of the QT interval (ST-
segment portion) is typical of hypocalcemia. Hypercalcemia may cause abbreviation of the ST seg-
ment and shortening of the QT interval. QTC, Corrected QT interval. (Data from Goldberger AL.
Clinical Electrocardiography: A Simplified Approach. 6th ed. St Louis, MO: Mosby; 1999.)
Diagnosis Magnesium is absorbed from and secreted into the GI tract

Almost all patients with hypercalcemia have either hyperpara- and filtered, reabsorbed, and excreted by the kidneys. Renal
thyroidism or cancer. Primary hyperparathyroidism is typi- reabsorption and excretion are passive, following sodium and
cally associated with a serum calcium concentration below 11 water.
mEq/L and no symptoms, whereas malignancy often presents
with acute symptoms and a serum calcium level higher than
Hypomagnesemia
13 mEq/L.
Some degree of hypomagnesemia occurs in up to 10% of
Treatment hospitalized patients. An even higher percentage of patients
Treatment of hypercalcemia is directed toward increasing uri- in intensive care units (ICUs), especially those receiving
nary calcium excretion and inhibiting bone resorption and parenteral nutrition or dialysis, have hypomagnesemia.
further GI absorption of calcium. Coronary care unit patients with hypomagnesemia have a
Since hypercalcemia is frequently associated with hypovo- higher mortality rate than those with normal serum levels
lemia secondary to polyuria, volume expansion with saline of magnesium.
not only corrects the fluid deficit but also increases urinary
excretion of calcium along with the administered sodium. Signs and Symptoms
Loop diuretics also enhance urinary excretion of both sodium Signs and symptoms of hypomagnesemia are similar to those
and calcium but should be used only after appropriate volume of hypocalcemia and involve mostly the cardiac and neuro-
resuscitation. muscular systems. Dysrhythmias, weakness, muscle twitching,
Calcitonin, bisphosphonates, or mithramycin may be tetany, apathy, and seizures can be seen. Hypokalemia and/or
required in disorders associated with osteoclastic bone resorp- hypocalcemia that had been refractory to supplementation
tion. Hydrocortisone may reduce GI absorption of calcium in will respond after correction of hypomagnesemia.
granulomatous disease, vitamin D intoxication, lymphoma,
and myeloma. Oral phosphate may also be given to reduce GI Diagnosis
uptake of calcium if renal function is normal. Dialysis may be Hypomagnesemia is most commonly due to reduced GI
required for life-threatening hypercalcemia. Surgical removal uptake (reduced dietary intake or reduced absorption from
of the parathyroid glands may be required to treat primary or the GI tract) or to renal wasting of magnesium. These entities
secondary hyperparathyroidism. can be differentiated by measuring the urinary magnesium
excretion rate. Much less frequently, hypomagnesemia is due
Management of Anesthesia to intracellular shifts of magnesium with no overall change in
Management of anesthesia for emergency surgery in a patient total body magnesium, to hungry bone syndrome after para-
with hypercalcemia is aimed at restoring intravascular vol- thyroidectomy, or to exudative cutaneous losses after burn
ume before induction and increasing urinary excretion of cal- injury.
cium with loop diuretics (thiazide diuretics should be avoided
because they increase renal tubular reabsorption of calcium). Treatment
Ideally, surgery should be postponed until calcium levels have Treatment of hypomagnesemia depends on the severity of
normalized. the deficiency and the signs and symptoms that are present.
Central venous pressure or pulmonary artery pressure If cardiac dysrhythmias or seizures are present, magnesium
monitoring may be advisable in some patients requiring is administered intravenously as a bolus (2 g of magnesium
fluid resuscitation and diuresis as part of the perioperative sulfate = 8 mEq of magnesium), and the dose is repeated until
treatment of hypercalcemia. Dosing of muscle relaxants symptoms abate. After life-threatening signs have resolved, a
must be guided by neuromuscular monitoring if muscle slower infusion of magnesium sulfate can be continued for
weakness, hypotonia, or loss of deep tendon reflexes is several days to allow for equilibration of intracellular and total
present. body magnesium stores. If renal wasting is present, supple-
mentation must be increased to account for the magnesium
lost in urine.
DISORDERS OF MAGNESIUM
Hypermagnesemia is a potential side effect of the treatment
Magnesium is predominantly found intracellularly and in of hypomagnesemia, so the patient should be monitored for
mineralized bone. Between 60% and 70% of serum magne- signs of hypotension, facial flushing, and loss of deep tendon
sium is ionized, with 10% complexed to citrate, bicarbonate, or reflexes.
phosphate and approximately 30% bound to protein, mostly
albumin. There is little difference between extracellular and Management of Anesthesia
intracellular ionized magnesium concentrations, so there is Management of anesthesia in patients with hypomagne-
only a small transmembrane gradient for ionized magnesium. semia includes attention to the signs of magnesium defi-
It is the ionized fraction of magnesium that is associated with ciency, magnesium supplementation, and treatment of
clinical effects. refractory hypokalemia or hypocalcemia if needed. If the
hypomagnesemia is secondary to malnutrition or alcohol- Management of Anesthesia

ism, the anesthetic implications of these diseases must also Invasive cardiovascular monitoring may be necessary peri-
be considered. Intraoperative magnesium supplementation operatively to measure and treat the hypotension and vaso-
to reduce postoperative dysrhythmias has been suggested dilation associated with hypermagnesemia and to guide fluid
but was recently found to make no difference in rates of resuscitation and ongoing replacement of fluids during forced
postoperative atrial fibrillation in a randomized trial of car- diuresis. Acidosis exacerbates hypermagnesemia, so careful
diac surgery patients. attention must be paid to ventilation and arterial pH. Initial
Ventricular dysrhythmias (typically polymorphic ventricu- and subsequent doses of muscle relaxants should be reduced
lar tachycardia) should be anticipated and treated as necessary. in the presence of muscle weakness and guided by results of
Muscle relaxation should be guided by the results of periph- peripheral nerve stimulation. Hypermagnesemia and skeletal
eral nerve stimulation, since hypomagnesemia can be associ- muscle weakness are not uncommon causes of failure to wean
ated with both muscle weakness and muscle excitation. Fluid from mechanical ventilation in the ICU setting, especially in
loading (particularly with sodium-containing solutions) and patients with renal failure.
diuretic use should be avoided because renal excretion of mag-
nesium passively follows sodium excretion.
ACID-BASE DISORDERS
Arterial acid-base balance is normally tightly regulated within
Hypermagnesemia
the pH range of 7.35–7.45 to ensure optimal conditions for
Hypermagnesemia (i.e., serum magnesium concentration cellular enzyme function. Values of arterial blood pH less
> 2.5 mEq/L) is much less common than hypomagnesemia, than 7.35 are termed acidemia, and values higher than 7.45
because a magnesium load can be briskly excreted if renal are termed alkalemia. The related terms acidosis and alkalo-
function is normal. Even patients with renal failure rarely sis refer to acid-base derangements that produce either excess
have symptomatic hypermagnesemia unless there is a signifi- H+ or excess OH−, respectively, that may be present regardless
cant increase in dietary or IV intake. However, milder eleva- of arterial pH. Intracellular pH is lower than extracellular pH
tions in serum magnesium levels are frequently found in ICU and is maintained at a closely regulated level of 7.0–7.3. Acid-
and dialysis patient populations. Hypermagnesemia may be base regulation in the setting of normal metabolism requires
a complication of magnesium sulfate administration to treat handling of the continuous production of acidic metabolites,
preeclampsia/eclampsia or to provide perinatal neurologic totaling approximately 1 mEq/kg body weight per day.
protection in premature delivery. Magnesium infusion during Stability of pH is accomplished by a system of intracellu-
pheochromocytoma surgery is popular in some centers but lar and extracellular buffers, most importantly the HCO3/CO2
may also result in hypermagnesemia. buffer pair. Carbon dioxide can enter or leave the body via
the lungs, and bicarbonate can enter or leave the body via the
Signs and Symptoms kidneys. Maintenance of a normal bicarbonate concentration
Signs and symptoms of hypermagnesemia begin to occur at relative to carbon dioxide tension results in an optimal ratio
serum levels of 4–5 mEq/L and include lethargy, nausea and of approximately 20:1. Maintenance of this ratio of 20:1 allows
vomiting, and facial flushing. At levels above 6 mEq/L, a loss of for a relatively normal pH despite deviations from normal of
deep tendon reflexes and hypotension occur. Paralysis, apnea, either bicarbonate concentration or carbon dioxide tension.
heart block, and/or cardiac arrest are likely if the magnesium Other buffers include proteins, bone apatite, and phosphate
level exceeds 10 mEq/L. ions.
The relationship of the CO2/HCO3 buffer system to pH is
Diagnosis expressed by the Henderson-Hasselbalch equation: pH = 6.1 +
Evaluation of hypermagnesemia involves assessing renal func- log (serum bicarbonate concentration/0.03 × Paco2).
tion (creatinine clearance) and detecting any source of excess Changes in respiration regulate carbon dioxide tension,
magnesium intake, such as parenteral infusion, oral ingestion whereas renal regulation adjusts bicarbonate concentration.
of antacids, and administration of magnesium-based enemas These changes may be the cause of a primary acid-base dis-
or cathartics. Once these have been excluded, less common order or can occur as a compensatory mechanism in response
causes of hypermagnesemia, including hypothyroidism, to another underlying disorder. In non–mechanically venti-
hyperparathyroidism, Addison’s disease, and lithium therapy, lated, nonsedated patients, compensatory respiratory or renal
can be considered. responses can normalize an altered pH but will not overcom-
pensate and alter the pH to the point of reversing the pri-
Treatment mary disorder. This is not always true in the operating room,
Life-threatening signs of hypermagnesemia may be temporar- where mechanical ventilation and sedation/unconsciousness
ily ameliorated with IV calcium administration, but hemodi- allow for potential overcompensation or undercompensation
alysis may be required. Lesser degrees of hypermagnesemia of acid-base disorders. Familiarity with the clinical history is
can be treated with forced diuresis with saline and loop diuret- then a key part of understanding the patient’s primary acid-
ics to increase renal excretion of magnesium. base abnormality.
Arterial blood [H+] (nmol/L)

100 90 80 70 60 50 40 30 20
60
120 110 100 90 80 70 60 50 40
56
52
35
48
Arterial plasma [HCO3– ] (mmol/L)

METABOLIC
44 CHRONIC ALKALOSIS
30
RESPIRATORY
40 ACIDOSIS
36 25
32
ACUTE
28 RESPIRATORY
20
ACIDOSIS
24 NORMAL
ACUTE 15
20 RESPIRATORY
ALKALOSIS
16 CHRONIC
10
RESPIRATORY
12 ALKALOSIS
METABOLIC
8 ACIDOSIS
PCO (mm Hg)
2
4
0
7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8
Arterial blood pH
FIG. 21.6 Acid-base nomogram (map). Shaded areas represent the 95% confidence limits of the
normal respiratory and metabolic compensations for primary acid-base disturbances. Data falling
outside the shaded areas denote a mixed disorder if a laboratory error is not present. (Data from
Brenner B, Clarkson M, Oparil S, et al., eds. Brenner and Rector’s The Kidney. 8th ed. Philadel-
phia: Saunders; 2007.)
Renal compensation for acid-base derangements may secondary disorder that brings the ratio of bicarbonate to
include increases in resorption or secretion of filtered bicar- carbon dioxide tension back toward 20:1.
bonate in the proximal tubule. In addition, protons (i.e., 4. If bicarbonate and Paco2 change in opposite directions,
hydrogen ions) can be reabsorbed in the distal tubule and col- there is a mixed acid-base disorder.
lecting duct or excreted into the urine. Hydrogen ion excretion 5. Determine the primary acid-base disorder by comparing
in the urine regenerates the bicarbonate originally consumed the fractional change of the measured bicarbonate or car-
by buffering a hydrogen ion in the ECF. The excreted hydrogen bon dioxide tension to the normal value.
ions are themselves buffered by titratable renal buffers (mainly 6. There are equations and nomograms that calculate the
ammonia) and lost in the urine. expected change in one of the three parameters involved
Evaluation of acid-base disturbances begins with a deter- in acid-base determination (pH, bicarbonate, or carbon
mination of the primary pH derangement by measurement dioxide tension) for a given change in one of the other two
of arterial pH, Paco2, and HCO3. A high or low pH will dem- parameters (Fig. 21.6). If the actual change is markedly dif-
onstrate the primary acid-base disorder and allow evaluation ferent from the expected change, there is a mixed acid-base
of whether there is appropriate compensation. In cases of disorder.
normal pH, there may still be chronic compensated acidosis 7. Finally, calculate the anion gap to determine whether there
or alkalosis that can offer insight into a patient’s comorbid is an anion gap metabolic acidosis. Elevation in the anion
condition. gap requires subsequent identification of the unmeasured
Identification of acid-base disturbance follows a series of anion.
steps:
1. Identify whether the pH is increased or decreased. An Signs and Symptoms
increase defines alkalemia, and a decrease defines acidemia. Major adverse consequences of severe systemic acidosis (pH
2. Identify the change in Paco2 and bicarbonate from their < 7.2) can occur independently of whether the acidosis is of
normal levels of 40 mm Hg and 24 mEq/L, respectively. respiratory, metabolic, or mixed origin (Table 21.8). The effects
3. If both Paco2 and bicarbonate change in the same direc- of acidosis are particularly detrimental to the cardiovascular
tion (i.e., both are increased or both are decreased), there system. Acidosis decreases myocardial contractility, although
is a primary acid-base disorder with a compensatory clinical effects are minimal until the pH decreases to less than
TABLE 21.8 Adverse Consequences of Severe Acidosis TABLE 21.9 Adverse Consequences of Alkalosis

NERVOUS SYSTEM NERVOUS SYSTEM
Obtundation Decreased cerebral blood flow
Coma Seizures
Lethargy
CARDIOVASCULAR SYSTEM Delirium
Impaired myocardial contractility Tetany
Decreased cardiac output
Decreased arterial blood pressure CARDIOVASCULAR SYSTEM
Sensitization to reentrant cardiac dysrhythmias Arteriolar vasoconstriction
Decreased threshold for ventricular fibrillation Decreased coronary blood flow
Decreased responsiveness to catecholamines Decreased threshold for angina pectoris
Predisposition to refractory dysrhythmias
VENTILATION
Hyperventilation VENTILATION
Dyspnea Hypoventilation
Fatigue of respiratory muscles Hypercarbia
Arterial hypoxemia
METABOLISM
Hyperkalemia METABOLISM
Insulin resistance Hypokalemia
Inhibition of anaerobic glycolysis Hypocalcemia
Hypomagnesemia
Adapted from Adrogué HJ, Madias NE. Management of life-threatening acid-base Hypophosphatemia
disorders. N Engl J Med. 1998;338:26-34.
Stimulation of anaerobic glycolysis
7.2, which perhaps reflects the effects of catecholamine release Adapted from Adrogué JH, Madias NE. Management of life-threatening acid-base
disorders. N Engl J Med. 1998;338:107-111.
in response to the acidosis. When the pH is less than 7.1, car-
diac responsiveness to catecholamines decreases and compen-
satory inotropic effects are diminished. The detrimental effects TABLE 21.10 Causes of Respiratory Acidosis

of acidosis may be accentuated in those with underlying left
ventricular dysfunction or myocardial ischemia and in those Drug-induced ventilatory depression
Permissive hypercapnia
in whom sympathetic nervous system activity is impaired, Upper airway obstruction
such as by β-adrenergic blockade or general anesthesia. Status asthmaticus
Major adverse consequences of severe systemic alka- Restriction of ventilation (rib fractures/flail chest)
losis (pH > 7.60) reflect impairment of cerebral and coro- Disorders of neuromuscular function
nary blood flow caused by arteriolar vasoconstriction (Table Malignant hyperthermia
Hyperalimentation
21.9). Associated decreases in serum ionized calcium con-
centration probably contribute to the neurologic abnormali-
ties associated with systemic alkalosis. Alkalosis predisposes period is drug-induced depression of ventilation by opioids,
patients, especially those with co-existing heart disease, to general anesthetics, or neuromuscular blockers. Respiratory
significant and even refractory ventricular dysrhythmias. acidosis may be complicated by metabolic acidosis when renal
Alkalosis depresses ventilation and can frustrate efforts to perfusion is decreased to the extent that reabsorption mecha-
wean patients from mechanical ventilation. Hypokalemia nisms in the renal tubules are impaired. For example, cardiac
accompanies both metabolic and respiratory alkalosis but is output and renal blood flow may be so decreased in patients
more prominent in the presence of metabolic alkalosis. Alka- with chronic obstructive pulmonary disease and cor pulmo-
losis stimulates anaerobic glycolysis and increases the pro- nale as to lead to metabolic acidosis.
duction of lactic acid and ketoacids. Although alkalosis can Respiratory acidosis is treated by correcting the disorder
decrease the release of oxygen to the tissues by tightening the responsible for hypoventilation. Mechanical ventilation is
binding of oxygen to hemoglobin, chronic alkalosis negates necessary when the increase in Paco2 is marked and carbon
this effect by increasing the concentration of 2,3-diphospho- dioxide narcosis is present. It must be remembered that rapid
glycerate in erythrocytes. lowering of chronically increased Paco2 levels by mechani-
cal ventilation decreases body stores of carbon dioxide much
more rapidly than the kidneys can produce a corresponding
Respiratory Acidosis
decrease in serum bicarbonate concentration. The resulting
Respiratory acidemia is present when a decrease in alveolar metabolic alkalosis can cause neuromuscular irritability and
ventilation results in an increase in the Paco2 sufficient to excitation of the CNS, including seizures. It is best to decrease
decrease arterial pH to less than 7.35 (Table 21.10). The most the Paco2 slowly to permit sufficient time for renal tubular
likely cause of respiratory acidosis during the perioperative elimination of bicarbonate.
TABLE 21.11 Causes of Respiratory Alkalosis TABLE 21.12 Causes of Metabolic Acidosis

Iatrogenic (mechanical hyperventilation) Lactic acidosis
High altitude Diabetic ketoacidosis
Central nervous system injury Renal failure
Hepatic disease Hepatic failure
Pregnancy Methanol and ethylene glycol intoxication
Salicylate overdose Aspirin intoxication
Increased skeletal muscle activity
Cyanide poisoning
Metabolic alkalosis may accompany respiratory acidosis Carbon monoxide poisoning
when the body stores of chloride and potassium are decreased.
For example, decreased serum chloride concentrations facili-
tate renal tubular reabsorption of bicarbonate, which leads electrical neutrality. Therefore a normal anion gap acidosis
to metabolic alkalosis. Hypokalemia stimulates renal tubules is often called a hyperchloremic metabolic acidosis. The most
to excrete hydrogen, which may produce metabolic alkalosis common causes of a normal–anion gap acidosis are IV infu-
or aggravate a co-existing alkalosis caused by chloride defi- sion of sodium chloride and GI and renal losses of bicarbonate
ciency. Treatment of metabolic alkalosis associated with these (diarrhea, renal tubular acidosis, early renal failure).
electrolyte disturbances requires administration of potassium
chloride. Signs and Symptoms
Since acidosis is secondary to an underlying disorder, the pre-
sentation of acidosis is complicated by the signs and symp-
Respiratory Alkalosis
toms of the causative disorder. Derangements of pH have
Respiratory alkalosis is present when an increase in alveolar wide-ranging effects on tissue, organ, and enzyme function,
ventilation results in a decrease in Paco2 sufficient to increase and the signs and symptoms attributable to an acidosis relate
the pH to greater than 7.45 (Table 21.11). The most likely to these effects. The clinical features of metabolic acidosis
cause of acute respiratory alkalosis during the perioperative depend also on the rate of development of acidosis and are
period is iatrogenic hyperventilation. Respiratory alkalosis likely to be more dramatic in rapidly developing acidosis in
occurs normally during pregnancy and is an important adap- which compensatory respiratory or renal changes are not able
tive response to high altitude. to limit the fall in pH.
Treatment of respiratory alkalosis is directed at cor-
recting the underlying disorder responsible for alveolar Diagnosis
hyperventilation. During anesthesia, this is most often Diagnosis depends on a high index of suspicion and labora-
accomplished by adjusting the ventilator to decrease alveo- tory testing. Most commonly, arterial blood is analyzed for
lar ventilation. The hypokalemia and hypochloremia that pH, carbon dioxide tension, bicarbonate concentration, and
may co-exist with respiratory alkalosis may also require anion gap. Common causes of metabolic acidosis are listed in
treatment. Table 21.12.
Metabolic acidosis can be of renal or extrarenal origin.
Metabolic acidosis of renal origin involves a primary disor-
Metabolic Acidosis
der of renal acidification. This occurs when the kidneys are
Metabolic acidosis lowers blood pH, which stimulates the unable to regenerate sufficient bicarbonate to replace that lost
respiratory center to hyperventilate and lower carbon dioxide by the buffering of normal endogenous acid production (distal
tension. Respiratory compensation does not in general fully renal tubular acidosis) or when an abnormally high fraction of
counterbalance the increased acid production, but the pH will filtered bicarbonate is not reabsorbed in the proximal tubule
return toward normal. and is subsequently lost in the urine (proximal renal tubular
Acidoses of metabolic origin are typically divided into those acidosis or acetazolamide use). Combined defects occur in
with a normal anion gap and those with a high anion gap. renal failure. The most common causes of extrarenal sources
A high anion gap occurs when a fixed acid is added to the of metabolic acidosis are GI bicarbonate losses, ketoacidosis,
extracellular space. The acid dissociates, the hydrogen ion and lactic acidosis.
combines with bicarbonate forming carbonic acid, and the
decreased bicarbonate concentration produces an increased Treatment
anion gap. Lactic acidosis, ketoacidosis, renal failure, and the Treatment of metabolic acidosis includes treatment of the
acidoses associated with many poisonings are examples of cause of the acidosis—for example, insulin and fluids for
high–anion gap metabolic acidoses. diabetic ketoacidosis and improvement in tissue perfusion
Non–anion gap metabolic acidosis is the result of a net for lactic acidosis. Administration of sodium bicarbonate
increase in chloride concentration. Bicarbonate loss is for acute treatment of metabolic acidosis is very controver-
counterbalanced by a net gain of chloride ions to maintain sial. Many recommend that bicarbonate be given only if the
increased renal bicarbonate reabsorption in an attempt to

TABLE 21.13 Causes of Metabolic Alkalosis
maintain electroneutrality. Therefore metabolic alkaloses can
Hypovolemia be characterized as chloride responsive or chloride resistant.
Vomiting Another classification of metabolic alkalosis is volume-deple-
Nasogastric suction tion alkalosis (resulting from vomiting, diarrhea, or chloride
Diuretic therapy losses) and volume-overload alkalosis (resulting from primary
Bicarbonate administration
Hyperaldosteronism
or secondary mineralocorticoid excess).
Chloride-wasting diarrhea Metabolic alkalosis can also occur secondary to renal com-
pensation for chronic respiratory disease with hypercarbia. In
these patients, bicarbonate levels may be quite high and associ-
pH is less than 7.1 or the bicarbonate concentration is less than ated with urinary losses of chloride along with obligatory losses
10 mEq/L. There is concern that the bicarbonate reacts with of sodium and potassium. If the respiratory disorder is treated
hydrogen ions, generating carbon dioxide, which diffuses into with mechanical ventilation and the carbon dioxide tension is
cells and lowers intracellular pH even more than before the reduced rapidly, a profound metabolic alkalosis may result.
bicarbonate treatment. It is also postulated that administration
of bicarbonate to patients with chronic metabolic acidosis may Signs and Symptoms
result in transient tissue hypoxia because acute changes in pH Progressively more binding of calcium to albumin occurs as
toward normal (or alkalosis) may negate the rightward shift an alkalosis develops, so the signs and symptoms of alkalosis,
of the oxyhemoglobin dissociation curve caused by acidemia especially those related to the neuromuscular and central ner-
(Bohr effect) and result in increased hemoglobin affinity for vous systems, may be very similar to those of hypocalcemia.
oxygen, which reduces oxygen delivery at the tissue level. Metabolic alkalosis may be accompanied by volume contrac-
The 2015 American Heart Association Guidelines Update tion, hypochloremia and hypokalemia, or volume overload
for Cardiopulmonary Resuscitation and Emergency Car- and sodium retention, depending on the cause.
diovascular Care do not recommend administering sodium
bicarbonate routinely during cardiac arrest and cardiopul- Diagnosis
monary resuscitation. However, sodium bicarbonate may be As with metabolic acidosis, the diagnosis of metabolic alkalosis
considered for life-threatening hyperkalemia or cardiac arrest is dependent on a high index of suspicion and laboratory test-
associated with hyperkalemia, or for cardiac arrest associated ing. Metabolic alkaloses secondary to chloride losses are associ-
with a significant prearrest metabolic acidosis. ated with low urinary chloride levels (typically <10 mEq/L) and
volume contraction. In contrast, metabolic alkaloses associated
Management of Anesthesia with mineralocorticoid excess are typically associated with vol-
Elective surgery should be postponed until an acidosis has ume overload and spot urine chloride values above 20 mEq/L.
been treated. For urgent surgery in a patient with metabolic
acidosis, invasive hemodynamic monitoring should be con- Treatment
sidered to guide fluid resuscitation and monitor cardiac func- Volume-depletion metabolic alkalosis is treated by chloride
tion in marked acidosis. Laboratory measurement of acid-base replacement along with fluid resuscitation using saline, which
parameters should be performed frequently throughout the is itself weakly acidic. If the alkalosis has been caused by gas-
perioperative period because pH can change rapidly and sig- tric losses of hydrochloric acid, proton pump inhibitors can
nificantly in response to changes in ventilation, volume status, be given to stop perpetuation of the alkalosis. Metabolic alka-
circulation, and drug administration. losis associated with loop diuretics can be improved by add-
Acidosis affects the proportion of drug in the ionized and ing or substituting potassium-sparing diuretics. In the case
un-ionized states. Volume of distribution may also be affected of volume-overload metabolic alkalosis due to excess miner-
in patients who have uncorrected hypovolemia. alocorticoid concentrations, administration of spironolactone
plus potassium chloride may be useful if the source of miner-
alocorticoid secretion cannot be eliminated.
Metabolic Alkalosis
Metabolic alkalosis is marked by an increase in plasma bicar- Management of Anesthesia
bonate concentration and is usually compensated for by an Management of anesthesia includes judicious volume replace-
increase in carbon dioxide tension. Common causes of meta- ment and adequate supplementation with chloride, potas-
bolic alkalosis are listed in Table 21.13. sium, and magnesium as needed. Invasive monitoring may be
Metabolic alkalosis can be of renal or extrarenal origin and helpful in some patients. Care must be taken not to eliminate
can be caused by either a net loss of hydrogen ions (e.g., loss a compensatory metabolic alkalosis in patients with chronic
of hydrochloric acid with vomiting) or a net gain of bicarbon- lung disease and significant carbon dioxide retention, because
ate (e.g., caused by tubular defects of bicarbonate reabsorp- successful weaning from mechanical ventilation will likely
tion). Abnormal losses of chloride with or without hydrogen necessitate a return to the chronic respiratory acidosis and
ion (e.g., in cystic fibrosis or villous adenoma) also induce metabolic alkalosis the patient had at presentation.
• Binding of calcium to albumin is pH dependent, and acid-

KEY POINTS
base disturbances can change the fraction and therefore the
• Total body water content is categorized as ICF and ECF, concentration of ionized calcium without changing total
according to the location of the water relative to cell mem- body calcium. Alkalosis reduces the ionized calcium con-
branes. The distribution and concentration of electrolytes centration, so ionized calcium may be significantly reduced
can differ greatly between fluid compartments. The electro- after bicarbonate administration or with hyperventilation.
physiology of excitable cells is dependent on the intracellu- • Signs and symptoms of hypermagnesemia begin to occur
lar and extracellular concentrations of sodium, potassium, at serum levels of 4–5 mEq/L and include lethargy, nausea
and calcium. and vomiting, and facial flushing. At levels above 6 mEq/L,
• Water balance is predominantly mediated by osmolality a loss of deep tendon reflexes and hypotension occur. Paral-
sensors, neurons located in the anterior hypothalamus that ysis, apnea, and/or cardiac arrest are likely if the magne-
stimulate thirst and cause pituitary release of vasopressin sium level exceeds 10 mEq/L.
(antidiuretic hormone). Vasopressin is stored as granules • Major adverse consequences of severe systemic acidosis
in the posterior pituitary and acts through G protein–cou- (pH < 7.2) can occur whether the acidosis is of respiratory,
pled receptors in the collecting ducts of the kidney, causing metabolic, or mixed origin. Acidosis decreases myocardial
water retention that in turn corrects serum osmolality. contractility, although clinical effects are minimal until the
• As hyponatremia develops, it is usually associated with pH decreases below 7.2, which perhaps reflects the effects
extracellular hypotonicity, which results in water move- of catecholamine release in response to the acidosis. When
ment into cells and can manifest as cerebral edema and the pH is less than 7.1, cardiac responsiveness to catechol-
increased intracranial pressure. Initial compensation amines decreases and compensatory inotropic effects are
is afforded by the movement of brain extracellular fluid diminished. The detrimental effects of acidosis may be
into the cerebrospinal fluid. Later compensation includes accentuated in those with underlying left ventricular dys-
the lowering of intracellular osmolality by the movement function or myocardial ischemia and in those in whom
of potassium and organic solutes out of brain cells. This sympathetic nervous system activity is impaired, such as by
reduces water movement into the intracellular space. β-adrenergic blockade or general anesthesia.
However, when these adaptive mechanisms fail or hypo- • Major adverse consequences of severe systemic alkalosis (pH
natremia progresses, CNS manifestations of hyponatre- > 7.60) reflect impairment of cerebral and coronary blood
mia occur. flow due to arteriolar vasoconstriction. Associated decreases
• The volume overload, hyponatremia, and hypoosmolal- in serum ionized calcium concentration contribute to the
ity that may accompany transurethral resection of the neurologic abnormalities associated with systemic alkalosis.
prostate is known as TURP syndrome. This syndrome Alkalosis predisposes patients—especially those with co-
is more likely to occur when resection is prolonged (>1 existing heart disease—to severe, often refractory, ventricu-
hour), when the irrigating fluid is suspended more than lar dysrhythmias. Alkalosis also depresses ventilation.
40 cm above the operative field, and when the pressure
in the bladder is allowed to increase above 15 cm H2O. RESOURCES
TURP syndrome manifests principally with cardiovas- Adrogué HJ, Madias NE. Management of life-threatening acid-base disorders.
cular signs of volume overload and neurologic signs of N Engl J Med. 1998;338:26-34: 107-111.
hyponatremia. Berend K, de Vries A, Gans R. Disorders of fluids and electrolytes: physio-
• Hypokalemia is diagnosed by testing the serum potassium logical approach to assessment of acid-base disturbances. N Engl J Med.
concentration. The differential diagnosis requires deter- 2014;371:1434-1445.
Bonow R, Mann D, Zipes D, et al, eds. Braunwald’s Heart Disease: a Textbook
mining whether the hypokalemia is acute and secondary of Cardiovascular Medicine. Philadelphia: Saunders; 2011.
to intracellular potassium shifts, such as might be seen with Brenner B, Clarkson M, Oparil S, et al, eds. Brenner and Rector’s The Kidney.
hyperventilation or alkalosis, or is chronic and associated Philadelphia: Saunders; 2007.
with depletion of total body potassium stores. Fauci AS, Braunwald E, Hauser SL, et al, eds. Harrison’s Principles of Internal
• Immediate treatment of hyperkalemia is required if life- Medicine. New York: McGraw Hill; 2007.
Gennari FJ. Hypokalemia. N Engl J Med. 1998;339:451-458.
threatening dysrhythmias or ECG signs of severe hyperka- Link MS, Berkow LC, Kudenchuk PJ, et al. 2015 American Heart Associa-
lemia are present. This treatment is aimed at antagonizing tion guidelines update for cardiopulmonary resuscitation and emergency
the effects of a high potassium on the transmembrane cardiovascular care. Part 7: adult advanced cardiovascular life support.
potential and redistributing potassium intracellularly. Circulation. 2015;132:S444-S464.
Calcium chloride or calcium gluconate is administered to Sterns RH. Disorders of plasma sodium—causes, consequences, and correc-
tion. N Engl J Med. 2015;372:55-65.
stabilize cellular membranes. Hyperventilation, sodium Wahr JA, Parks R, Boisvert D, et al. Preoperative serum potassium levels and
bicarbonate administration, and insulin administration perioperative outcomes in cardiac surgical patients. JAMA. 1999;281:
promote movement of potassium intracellularly. 2203-2210.

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C H APT E R

Fluid, Electrolyte, and Acid-Base 21

ABNORMALITIES OF WATER, OSMOLALITY,

may be encountered as a result of free water depletion (e.g.,

to increases in water resorption. Elevations in circulating vol-

Interstitial fluid (3/4 of ECF)

TABLE 21.2 Factors and Drugs Affecting Vasopressin Secretion

Contracted ECF volume Expanded ECF volume Amitriptyline

ECF, Extracellular fluid.

Hypovolemia Euvolemia Hypervolemia

Decreased skin turgor Peripheral edema

UNa  20 UNa  20 UNa  20 UNa  20 UNa  20 UNa  20

Renal Extrarenal Salt- Renal Avid sodium

TABLE 21.4 Signs and Symptoms of TURP Syndrome

solutions can also induce hemolysis because red blood cells

Hypovolemia Euvolemia Hypervolemia

Decreased skin turgor Peripheral edema

UNa  20 UNa  20 UNa variable UNa  20

Renal salt Extrarenal salt Renal Extrarenal Sodium gains

Osmotic diuretic Diarrhea Diabetes insipidus Insensible losses

distribution than of total body potassium. Total body potas-

Signs and Symptoms HYPOKALEMIA DUE TO EXCESSIVE GASTROINTESTINAL

Acute oliguric renal failure

Nonsteroidal antiinflammatory drugs

A ALTERED TRANSCELLULAR POTASSIUM SHIFT

Lysis of cells resulting from chemotherapy

administration of insulin, glucose, β-adrenergic agonists,

and neuromuscular systems and include paresthesias, irri- Management of Anesthesia

Hypocalcemia Normal Hypercalcemia

III III III

QT 0.48 sec QT 0.36 sec QT 0.26 sec

Diagnosis Magnesium is absorbed from and secreted into the GI tract

hypomagnesemia is secondary to malnutrition or alcohol- Management of Anesthesia

Arterial blood [H+] (nmol/L)

Arterial plasma [HCO3– ] (mmol/L)

increased renal bicarbonate reabsorption in an attempt to

• Binding of calcium to albumin is pH dependent, and acid-

S-ar putea să vă placă și

TABLE 21.2 Factors and Drugs Affecting Vasopressin Secretion

UNa 20 UNa 20 UNa 20 UNa 20 UNa 20 UNa 20

TABLE 21.4 Signs and Symptoms of TURP Syndrome

UNa 20 UNa 20 UNa variable UNa 20

• Binding of calcium to albumin is pH dependent, and acid-