4.

Fluid, Electrolyte & Acid-Base Disorders

QRS, and QT intervals.
c. Treatment. Cessation of exogenous Mg2+ is necessary. Calcium gluconate
10% (10 to 20 mL over 5 to 10 minutes intravenously) is indicated in the
presence of life-threatening symptoms (e.g., hyporeflexia, respiratory depression,
or cardiac conduction disturbances) to antagonize the effects of Mg2+. A 0.9%
NaCl (250 to 500 mL/hour) infusion with loop diuretic (furosemide, 20 mg
intravenously every 4 to 6 hours) in the patient with intact renal function promotes
renal elimination. Dialysis is the definitive therapy in the presence of intractable
symptomatic hypermagnesemia.
IV. Parenteral Fluid Therapy. The composition of commonly used parenteral fluids is
presented in Table 4-3.
A. Crystalloids, in general, are solutions that contain sodium as the major osmotically
active particle. Crystalloids are relatively inexpensive and are useful for volume
expansion, maintenance infusion, and correction of electrolyte disturbances.
1. Isotonic crystalloids (e.g., lactated Ringer's solution and 0.9% NaCl) distribute
uniformly throughout the extracellular fluid compartment so that after 1 hour, only
25% of the total volume infused remains in the intravascular space. Lactated
Ringer's solution is designed to mimic extracellular fluid and is considered a
balanced salt solution. This solution provides a HCO3- precursor and is useful for
replacing GI losses
P.112
P.113
P.114
and extracellular fluid volume deficits. In general, lactated Ringer's solution and
0.9% NaCl can be used interchangeably. However, 0.9% NaCl is preferred in the
presence of hyperkalemia, hypercalcemia, hyponatremia, hypochloremia, or
metabolic alkalosis.

Table 4-3 Composition of Common Parenteral Fluidsa

Solution

Volumeb

Na+

K+

Ca2+ Mg2+

Cl-

HCO3(as Dextrose
lactate)
(g/L)
mOsm/L

Extracellular
fluid

142

103

27

280
310

Lactated
Ringer's

130

109

28

273

0.9% NaCl

154

154

308

0.45% NaCl

77

77

154

D5 W

50

252

D5/0.45%
NaCl

77

77

50

406

D5LR

130

109

28

50

525

3% NaCl

513

513

1,026

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4. Fluid, Electrolyte & Acid-Base Disorders

7.5% NaCl

1,283

1,283

2,567

6%
hetastarch

500

154

154

310

10%
dextran-40

500

0/154c

0/154c

300

6% dextran70

500

0/154c

0/154c

300

5% albumin

250,500

130
160

<2.5

130
160

330

25%
albumin

20,50,100

130
160

<2.5

130
160

330

Plasma
protein
fraction

250,500

145

145

300

a Electrolyte concentrations in mmol/L.

b Available volumes (mL) of colloid solutions.
c Dextran solutions available in 5% dextrose (0 Na+, 0 Cl) or 0.9% NaCl (154 mmol Na+, 154 mmol Cl).
D5LR, 5% dextrose in lactated Ringer's solution; D5/0.45% NaCl, 5% dextrose per 0.45% NaCl; D5 W, 5%
dextrose in water.

2. Hypertonic saline solutions alone and in combination with colloids, such as

dextran, have generated interest as a resuscitation fluid for patients with shock or
burns. These fluids are appealing because, relative to isotonic crystalloids, smaller
quantities are required initially for resuscitation. A randomized, double-blinded study
of a 250-mL dose of hypertonic saline (7.5% NaCl, 6% dextran-70) compared to
placebo (0.9% NaCl) given to patients in hemorrhagic shock after sustaining blunt
trauma showed that the patients receiving the hypertonic saline bolus had
significant blunting of neutrophil activation and alteration of the pattern of monocyte
activation and cytokine secretion with a only a transient increase in serum sodium
that normalized within 24 hours. This immunomodulatory effect of hypertonic saline
plus dextran may help to prevent widespread tissue damage and multiorgan
dysfunction seen after traumatic injury (Ann Surg. 2006;243:47). However, another
recent randomized controlled trial of patients with blunt trauma in hypovolemic
shock that compared resuscitation with either lactated Ringer solution or 7.5%
hypertonic saline and 6% dextran 70 demonstrated no significant difference in
ARDS-free survival (Arch Surg. 2008;143(2):139). The possible side effects of
hypertonic solutions include hypernatremia, hyperosmolality, hyperchloremia,
hypokalemia, and central pontine demyelination with rapid infusion and should be
administered with caution until more research becomes available.
B. Hypotonic solutions (D5 W, 0.45% NaCl) distribute throughout the total body water
compartment, expanding the intravascular compartment by as little as 10% of the
volume infused. For this reason, hypotonic solutions should not be used for volume
expansion. They are used to replace free water deficits.
C. Colloid solutions contain high-molecular-weight substances that remain in the
intravascular space. Early use of colloids in the resuscitation regimen may result in
more prompt restoration of tissue perfusion and may lessen the total volume of fluid
required for resuscitation. However, there are no situations in which colloids have
unequivocally been shown to be superior to crystalloids for volume expansion. In fact,

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the SAFE (Saline versus Albumin Fluid Evaluation) study, which randomized 6,997
patients in the ICU to receive either 4% albumin or normal saline for fluid
resuscitation, found no significant difference in outcomes, including mortality and
organ failure, between the two groups (N Engl J Med. 2004;350:2247). Because
colloid solutions are substantially more expensive than crystalloids, their routine use in
hypovolemic shock is controversial. In addition, a post hoc study of ICU patients with
traumatic brain injury revealed that patients who underwent fluid resuscitation with
albumin compared to saline had significantly higher mortality rates (N Engl J Med.
2007;357:874). The use of colloids is indicated when crystalloids fail to sustain
plasma volume
P.115
because of low colloid osmotic pressure (e.g., increased protein loss from the vascular
space, as in burns and peritonitis).
1. Albumin preparations ultimately distribute throughout the extracellular space,
although the initial location of distribution is the vascular compartment. Preparations
of 25% albumin (100 mL) and 5% albumin (500 mL) expand the intravascular
volume by an equivalent amount (450 to 500 mL). Albumin 25% is indicated in the
edematous patient to mobilize interstitial fluid into the intravascular space. The cost
per liter of albumin is more than that of other colloid solutions and 30 times the cost
of the intravascular volume-equivalent amount of crystalloid solutions; thus, albumin
preparations should be used judiciously. They are not indicated in the patient with
adequate colloid oncotic pressure (serum albumin >2.5 mg/dL, total protein >5
mg/dL), for augmenting serum albumin in chronic illness (cirrhosis or nephrotic
syndrome), or as a nutritional source.
2. Dextran is a synthetic glucose polymer that undergoes predominantly renal
elimination. In addition to its indications for volume expansion, dextran also is used
for thromboembolism prophylaxis and promotion of peripheral perfusion. Dextran
solutions expand the intravascular volume by an amount equal to the volume
infused. Side effects include renal failure, osmotic diuresis, coagulopathy, and
laboratory abnormalities (i.e., elevations in blood glucose and protein and
interference with blood cross-matching). Preparations of 40- and 70-kD dextran are
available (dextran-40 and dextran-70, respectively).
3. Hydroxyethyl starch (hetastarch) is a synthetic molecule resembling glycogen
that is available as a 6% solution in 0.9% NaCl. Hetastarch, like 5% albumin,
increases the intravascular volume by an amount equal to or greater than the
volume infused. Hetastarch is less expensive than albumin and has a more
favorable side effect profile than dextran formulations, making it an appealing colloid
preparation. Hextend is a colloid that contains 6% hetastarch, balanced
electrolytes, a lactate buffer, and physiologic levels of glucose. Relative to
hetastarch in saline, Hextend seems to have a more beneficial coagulation profile,
less antigenicity, and antioxidant properties.
a. Indications include use as a plasma volume-expanding agent in shock from
hemorrhage, trauma, sepsis, and burns. Urine output typically increases acutely
secondary to osmotic diuresis and must not be misinterpreted as a sign of
adequate peripheral perfusion in this setting.
b. Elimination is hepatic and renal. Patients with renal impairment are particularly
subject to initial volume overload and tissue accumulation of hetastarch with
repeated administration. In these patients, initial volume resuscitation
accomplished with hetastarch should be maintained with another plasma volume
expander, such as albumin or crystalloid.
c. Laboratory abnormalities include elevations in serum amylase to approximately
twice normal without alteration in pancreatic function.
P.116
d. Dosing of hetastarch 6% solution is 30 to 60 g (500 to 1,000 mL), with the total
daily dose not exceeding 1.2 g/kg (20 mL/kg) or 90 g (1,500 mL). In hemorrhagic

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4. Fluid, Electrolyte & Acid-Base Disorders

shock, hetastarch solution can be administered at a rate of 1.2 g/kg/hour (20
mL/kg/hour). Slower rates of administration generally are used in patients with
burns or septic shock. In individuals with severe renal impairment (creatinine
clearance <10 mL/minute), the usual dose of hetastarch can be administered
initially, but subsequent doses should be reduced by 50% to 75%.
D. Principles of fluid management. A normal individual consumes an average of 2,000
to 2,500 mL of water daily. Daily water losses include approximately 1,000 to 1,500
mL in urine and 250 mL in stool. The minimum amount of urinary output that is
required to excrete the catabolic end products of metabolism is approximately 800 mL.
An additional 750 mL of insensible water loss occurs daily via the skin and respiratory
tract. Insensible losses increase with hypermetabolism, fever, and hyperventilation.
1. Maintenance. Maintenance fluids should be administered at a rate that is sufficient
to maintain a urine output of 0.5 to 1 mL/kg/hour. Maintenance fluid requirements
can be approximated on the basis of body weight as follows: 100 mL/kg/day for the
first 10 kg, 50 mL/kg/day for the second 10 kg, and 20 mL/kg/day for each
subsequent 10 kg. Maintenance fluids in general should contain Na+ (1 to 2
mmol/kg/day) and K+ [0.5 to 1 mmol/kg/day (e.g., D5/0.45% NaCl + 20 to 30 mmol
K+/L)].
2. Preoperative management. Pre-existing volume and electrolyte abnormalities
should be corrected before operation whenever possible. Consideration of duration
and route of loss provides important information regarding the extent of fluid and
electrolyte abnormalities.
3. Intraoperative fluid management requires replacement of preoperative deficit as
well as ongoing losses (Table 4-4). Intraoperative losses include maintenance fluids
for the duration of the case, hemorrhage, and third-space losses. The
maintenance fluid requirement is calculated as detailed previously (see Section
IV.D.1). Acute blood loss can be replaced with a volume of crystalloid that is three
to four times the blood loss or with an equal volume of colloid or blood.
Intraoperative insensible and third-space fluid losses depend on the size of the
incision and the extent of tissue trauma and dissection and can be replaced with an
appropriate volume of lactated Ringer's solution. Small incisions with minor tissue
trauma (e.g., inguinal hernia repair) result in third-space losses of approximately 1
to 3 mL/kg/hour. Medium-sized incisions with moderate tissue trauma (e.g.,
uncomplicated sigmoidectomy) result in third-space losses of approximately 3 to 7
mL/kg/hour. Larger incisions and operations with extensive tissue trauma and
dissection (e.g., pancreaticoduodenectomy) can result in third-space losses of
approximately 9 to 11 mL/kg/hour or greater.
4. Postoperative fluid management requires careful evaluation of the patient.
Sequestration of extracellular fluid into the sites of injury or operative trauma can
continue for 12 or more hours after operation. Urine output should be monitored
closely and intravascular volume repleted to maintain a urine output of 0.5 to 1
mL/kg/hour. GI losses that exceed 250 mL/day from nasogastric or gastrostomy
tube suction
P.117
should be replaced with an equal volume of crystalloid. Mobilization of perioperative
third-space fluid losses typically begins 2 to 3 days after operation. Anticipation of
postoperative fluid shifts should prompt careful evaluation of the patient's volume
status and, if needed, consideration of diuresis before the development of
symptomatic hypervolemia.

Table 4-4 Estimation of Intraoperative Fluid Loss and Guide for

Replacement
Preoperative deficit

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4. Fluid, Electrolyte & Acid-Base Disorders

Maintenance IVF hr NPO, plus preexisting deficit related to disease state
Maintenance fluids
Maintenance IVF duration of case
Third-space and insensible losses
13 mL/kg/hr for minor procedure (small incision)
37 mL/kg/hr for moderate procedure (medium incision)
911 mL/kg/hr for extensive procedure (large incision)
Blood loss
1 mL blood or colloid per 1 mL blood loss, or 3 mL crystalloid per 1 mL
blood loss
IVF, intravenous fluids; NPO, nothing by mouth.

V. ACIDBASE DISORDERS
A. Diagnostic approach
1. General concepts
a. Acidbase homeostasis represents equilibrium among the concentration of
H+, partial pressure of CO 2 (Pco2), and HCO3-. Clinically, H+ concentration is
expressed as pH.
b. Normal pH is 7.35 to 7.45. Acidemia refers to pH of less than 7.35, and
alkalemia refers to pH of greater than 7.45.
c. Acidosis and alkalosis describe processes that cause the accumulation of acid
or alkali, respectively. The terms acidosis and acidemia and the terms alkalosis
and alkalemia are often used interchangeably, but such usage is inaccurate. A
patient, for example, may be acidemic while alkalosis is occurring.
d. Laboratory studies that are necessary for the initial evaluation of acidbase
disturbances include arterial pH, arterial Pco2 (Paco2) (normal is 35 to 45 mm
Hg), and serum electrolytes [HCO3P.118
(normal is 22 to 31 mmol/L)]. Although base-excess or base-deficit calculations
can be made, this information does not add substantially to the evaluation.

Table 4-5 Expected Compensation for Simple AcidBase Disorders

Primary
Disorder

Initial
Change

Compensatory
Response

Expected
Compensation

Metabolic
acidosis

HCO3decrease

Pco2
decrease

Pco2 decrease = 1.2

HCO3-

Metabolic
alkalosis

HCO3increase

Pco2 increase

Pco2 increase = 0.7

HCO3-

Respiratory
acidosis

Pco2
increase

HCO3increase

Acute: HCO3- increase

= 0.1 Pco2
Chronic: HCO3increase = 0.35
Pco2

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4. Fluid, Electrolyte & Acid-Base Disorders

Respiratory
alkalosis

Pco2
decrease

HCO3decrease

Acute: HCO3- decrease

= 0.2 Pco2
Chronic: HCO3decrease = 0.5 Pco2

2. Compensatory response to primary disorders. Disorders that initially alter

Paco2 are termed respiratory acidosis or alkalosis. Alternatively, disorders that
initially affect plasma HCO3- concentration are termed metabolic acidosis or
alkalosis. Primary metabolic disorders stimulate respiratory responses that act to
return the ratio of Pco2 to HCO3- (and therefore the pH) toward normal. Similarly,
primary respiratory disturbances elicit countervailing metabolic responses that also
act to normalize pH. As a general rule, these compensatory responses do not
normalize pH because to do so would remove the stimulus for compensation. By
convention, these compensating changes are termed secondary, respiratory , or
metabolic compensation for the primary disturbance. The amount of compensation
to be expected from either a primary respiratory or metabolic disorder is presented
in Table 4-5. Significant deviations from these expected values suggest the
presence of a mixed acidbase disturbance.
B. Primary metabolic disorders
1. Metabolic acidosis results from the accumulation of nonvolatile acids, reduction in
renal acid excretion, or loss of alkali. The most common causes of metabolic
acidosis are listed in Table 4-6. Metabolic acidosis
P.119
has few specific signs. The appropriate diagnosis depends on the clinical setting
and laboratory tests.

Table 4-6 Causes of Metabolic Acidosis

Increased anion gap
Increased acid production
Ketoacidosis
Diabetic
Alcoholic
Starvation
Lactic acidosis
Toxic ingestion (salicylates,
ethylene glycol, methanol)
Renal failure
Normal anion gap
(hyperchloremic)

Renal tubular dysfunction

Renal tubular acidosis
Hypoaldosteronism
Potassium-sparing diuretics
Loss of alkali
Diarrhea
Ureterosigmoidostomy
Carbonic anhydrase inhibitors
Administration of HCl (ammonium
chloride, cationic amino acids)

a. The anion gap (AG; normal = 12 2 mmol/L) represents the anions, other than
Cl- and HCO3-, which are necessary to counterbalance Na+ electrically (all
values are in mmol/L):
It is useful diagnostically to classify metabolic acidosis into increased or normal
AG metabolic acidosis.
1. Increased AG metabolic acidosis (Table 4-6).
2. Normal AG (hyperchloremic) metabolic acidosis (Table 4-6).

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b. Treatment of metabolic acidosis must be directed primarily at the underlying
cause of the acidbase disturbance. Bicarbonate therapy should be considered
in patients with moderate-to-severe metabolic acidosis only after the primary
cause has been addressed. The HCO3- deficit (mmol/L) can be estimated using
the following equation:

P.120
This equation serves to provide only a rough estimate of the deficit because the
volume of HCO3- distribution and the rate of ongoing H + production are
variable.
1. Rate of HCO 3- replacement. In nonurgent situations, the estimated HCO3deficit can be repaired by administering a continuous intravenous infusion over
4 to 8 hours [a 50-mL ampule of 8.4% NaHCO3 solution (provides 50 mmol
HCO3-) can be added to 1 L of D5 W or 0.45% of NaCl]. In urgent situations,
the entire deficit can be repaired by administering a bolus over several
minutes. The goal of HCO3- therapy should be to raise the arterial blood pH
to 7.20 or the HCO3- concentration to 10 mmol/L. One should not attempt to
normalize pH with bicarbonate administration because the risks of bicarbonate
therapy (e.g., hypernatremia, hypercapnia, cerebrospinal fluid acidosis, or
overshoot alkalosis) are likely to be increased. Serial arterial blood gases and
serum electrolytes should be obtained to assess the response to HCO3therapy.
2. Lactic acidosis. Correction of the underlying disorder is the primary therapy
for lactic acidosis. Reversal of circulatory failure, hypoxemia, or sepsis reduces
the rate of lactate production and enhances its removal. Because the use of
NaHCO3 in lactic acidosis is controversial, no definite recommendations can
be made.
2. Metabolic alkalosis (Table 4-7)
a. Causes
1. Chloride-responsive metabolic alkalosis in the surgical patient is typically
associated with extracellular fluid volume deficits. The most common causes of
metabolic alkalosis in the surgical patient include inadequate fluid resuscitation
or diuretic therapy (e.g., contraction alkalosis), acid loss through GI secretions
(e.g. nasogastric suctioning and vomiting), and the exogenous administration
of HCO3- or HCO3- precursors (e.g. citrate in blood). Posthypercapnic
metabolic alkalosis occurs after the rapid correction of chronic respiratory
acidosis. Under normal circumstances, the excess in bicarbonate that is
generated by any of these processes is excreted rapidly in the urine.
Consequently, maintenance of metabolic alkalosis requires impairment of renal
HCO3- excretion, most commonly due to volume and chloride depletion.
Because replenishment of Cl- corrects the metabolic alkalosis in these
conditions, each is classified as Cl--responsive metabolic alkalosis.
2. Chloride-unresponsive metabolic alkalosis is encountered less frequently
in surgical patients and usually results from mineralocorticoid excess.
Hyperaldosteronism, marked hypokalemia, renal failure, renal tubular Clwasting (Bartter syndrome), and chronic edematous states are associated with
chloride-unresponsive metabolic alkalosis.
b. Diagnosis. Although the cause of metabolic alkalosis is usually apparent in the
surgical patient, measurement of the urinary

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4. Fluid, Electrolyte & Acid-Base Disorders

P.121
chloride concentration may be useful for differentiating these disorders. A urine
Cl- concentration of less than 15 mmol/L suggests inadequate fluid resuscitation,
ongoing GI loss from emesis or nasogastric suctioning, diuretic administration, or
post-hypercapnia as the cause of the metabolic alkalosis. A urine Clconcentration of greater than 20 mmol/L suggests mineralocorticoid excess, alkali
loading, concurrent diuretic administration, or the presence of severe
hypokalemia.

Table 4-7 Causes of Metabolic Alkalosis

Associated with extracellular fluid volume (chloride) depletion
Vomiting or gastric drainage
Diuretic therapy
Posthypercapnic alkalosis
Associated with mineralocorticoid excess
Cushing syndrome
Primary aldosteronism
Bartter syndrome
Severe K+ depletion
Excessive alkali intake

c. Treatment principles in metabolic alkalosis include identifying and removing

underlying causes, discontinuing exogenous alkali, and repairing Cl-, K+, and
volume deficits. Because metabolic alkalosis generally is well tolerated, rapid
correction of this disorder usually is not necessary.
1. Initial therapy should include the correction of volume deficits (with 0.9%
NaCl) and hypokalemia. Patients with vomiting or nasogastric suctioning also
may benefit from H2-receptor antagonists or other acidsuppressing
medications.
2. Edematous patients. Chloride administration does not enhance HCO3excretion because it does not correct the reduced effective arterial blood
volume. Acetazolamide (5 mg/kg/day intravenously or orally) facilitates fluid
mobilization while decreasing renal HCO3- reabsorption. However,
tachyphylaxis may develop after 2 to 3 days.
P.122
3. Severe alkalemia (HCO3- >40 mmol/L), especially in the presence of
symptoms, may require more aggressive correction. The infusion of acidic
solutions is occasionally indicated in the patient with severe refractory
metabolic alkalosis and chloride loss, typically due to massive nasogastric
drainage or complete prepyloric obstruction. Ammonium chloride (NH4Cl) is
hepatically converted to urea and HCl. The amount of NH4Cl that is required
can be estimated using the following equation:
NH4Cl is prepared by adding 100 or 200 mmol (20 to 40 mL of the 26.75%
NH4Cl concentrate) to 500 to 1,000 mL of 0.9% NaCl. This solution should be
administered at a rate that does not exceed 5 mL/minute. Approximately one
half of the calculated volume of NH4Cl should be administered, at which time
the acidbase status and Cl- concentration should be repeated to determine
the necessity for further therapy. NH4Cl is contraindicated in hepatic failure.
4. HCl [0.1 N (normal), administered intravenously] corrects metabolic alkalosis

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4. Fluid, Electrolyte & Acid-Base Disorders

more rapidly. The amount of H+ to administer can be estimated using the
following equation:
To prepare 0.1 N HCl, mix 100 mmol of HCl in 1 L of sterile water. The
calculated amount of 0.1 N HCl must be administered via a central venous
catheter over 24 hours. The HCO3- concentration can be safely reduced by 8
to 12 mmol/L over 12 to 24 hours.
5. Dialysis can be considered in the volume-overloaded patient with renal failure
and intractable metabolic alkalosis.
C. Primary respiratory disorders
1. Respiratory acidosis occurs when alveolar ventilation is insufficient to excrete
metabolically produced CO2. Common causes in the surgical patient include
respiratory center depression (e.g., drugs and organic disease), neuromuscular
disorders, and cardiopulmonary arrest. Chronic respiratory acidosis may occur in
pulmonary diseases, such as chronic emphysema and bronchitis. Chronic
hypercapnia may also result from primary alveolar hypoventilation or alveolar
hypoventilation related to extreme obesity (e.g., Pickwickian syndrome) or from
thoracic skeletal abnormalities. The diagnosis of acute respiratory acidosis usually
is evident from the clinical situation, especially if respiration is obviously depressed.
Appropriate therapy is correction of the underlying disorder. In cases of acute
respiratory acidosis, there is no indication for NaHCO3 administration.
2. Respiratory alkalosis is the result of acute or chronic hyperventilation. The
causes of respiratory alkalosis include acute hypoxia (e.g.,
P.123
P.124
pneumonia, pneumothorax, pulmonary edema, and bronchospasm), chronic hypoxia
(e.g., cyanotic heart disease and anemia), and respiratory center stimulation (e.g.,
anxiety, fever, Gram-negative sepsis, salicylate intoxication, central nervous system
disease, cirrhosis, and pregnancy). Excessive ventilation may also cause
respiratory alkalosis in the mechanically ventilated patient. Depending on its
severity and acuteness, hyperventilation may or may not be clinically apparent.
Clinical findings are nonspecific. As in respiratory acidosis, the only effective
treatment is correction of the underlying disorder.

Table 4-8 Common Causes of Mixed AcidBase Disorders

Metabolic acidosis and respiratory acidosis
Cardiopulmonary arrest
Severe pulmonary edema
Salicylate and sedative overdose
Pulmonary disease with superimposed renal failure or sepsis
Metabolic acidosis and respiratory alkalosis
Salicylate overdose
Sepsis
Combined hepatic and renal insufficiency
Metabolic alkalosis and respiratory acidosis
Chronic pulmonary disease, with superimposed:
Diuretic therapy
Steroid therapy
Vomiting
Reduction in hypercapnia by mechanical ventilation
Metabolic alkalosis and respiratory alkalosis
Pregnancy with vomiting

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Chronic liver disease treated with diuretic therapy
Cardiopulmonary arrest treated with bicarbonate therapy and mechanical
ventilation
Metabolic acidosis and alkalosis
Vomiting superimposed on
Renal failure
Diabetic ketoacidosis
Alcoholic ketoacidosis

D. Mixed acidbase disorders. When two or three primary acidbase disturbances occur
simultaneously, a patient is said to have a mixed acidbase disorder. As summarized in
Table 4-5, the respiratory or metabolic compensation for a simple primary disorder
follows a predictable pattern. Significant deviation from these patterns suggests the
presence of a mixed disorder. Table 4-8 lists some common causes of mixed acid
base disturbances. The diagnosis of mixed acidbase disorders depends principally
on evaluation of the clinical setting and on interpretation of acidbase patterns.
However, even normal acidbase patterns may conceal mixed disorders.

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