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METABOLIC ALKALOSIS
Keep Me in the Loop . . . . . . . . . . . . . . . . . . . . . . . . . . . . Level I
Jennifer Confer, PharmD, BCPS, BCCCP
Generalized weakness and fatigue cause a 60-year-old woman to
seek treatment in the emergency department (ED). She complains
of weakness, fatigue, myalgias, and polyuria that have occurred over
the past 2 days. She has also felt bloated and has taken extra doses of
her “water pill.” She has thrown up three times since last night’s dinner and attributes this to eating bad food. Her past medical history
is significant for HTN, heart failure (HF), type 2 diabetes mellitus,
and dyslipidemia. Physical exam reveals signs of volume depletion (dry mucous membranes, hypotension, tachycardia, and dry/
wrinkled extremities). Laboratory values indicate the presence of
metabolic alkalosis. Appropriate treatment measures include fluid
administration with isotonic (0.9%) sodium chloride, intravenous
potassium chloride supplementation, and temporary discontinuation of the loop diuretic. Identification of the patient’s baseline fluid
status when not dehydrated will guide further modifications of the
current drug regimen. The student must determine what parameters
should be monitored after fluid administration to assess the effectiveness of treatment. Further, after the response to initial IV fluids
is known, the student must determine whether alternative treatments are required based on physical exam and laboratory values.
QUESTIONS
Problem Identification
1.a. Identify the type of acid–base disturbance present in this
patient. Interpret the patient’s arterial blood gas results and
identify potential causes to support your response.
• To assess arterial blood gas results, five steps should be taken:
1. What is the pH—normal, acidotic, or alkalotic?
✓The patient’s arterial blood pH of 7.54 signifies an alkalemia (pH 7.45 or greater).
2. What is the PaCO2—high, normal, or low?
✓ The patient’s PaCO2 of 46 is high (normal range 35–45 mm
Hg.
3. What is the serum HCO3—high, normal, or low?
✓The patient’s serum HCO3 of 39 is high (normal range
22–30 mEq/L).
4. Is the primary problem respiratory or metabolic?
✓The patient has an elevated serum bicarbonate concentration, but the PaCO2 is not considerably increased. This
information is evidence that the acid–base disturbance
this patient is experiencing is metabolic. The fact that
the PaCO2 is not considerably increased indicates that this
disturbance does not yet contain a respiratory component.
5. Is the problem acute, partially compensated, or compensated?
✓For a compensation to occur, the arterial PaCO2 is estimated to increase 0.5–0.7 mm Hg for every 1 mEq/L
✓ Since this patient’s PaCO2 is 46 mm Hg, a partial compensatory response is beginning.
• Evaluating the above results, it is determined that this patient’s
disturbance is a partially compensated metabolic alkalosis.
• When metabolic alkalosis occurs, the body attempts to compensate leading to alveolar hypoventilation, which causes a rise
in the PaCO2, reducing the elevation in pH that is occurring.1
• The use of diuretics (typically thiazide or loop diuretics) causes
an inhibition of ion reabsorption (sodium, chloride, potassium, and hydrogen) through either the loop of Henle or the
distal tubules. This leads to increased excretion of sodium,
chloride, potassium, hydrogen, and water.
• Vomiting of gastric contents, which are abundant in hydrochloric acid (HCl), will cause an increase in serum bicarbonate.
Although compensation can occur through the renal excretion
of bicarbonate, the rapid loss of chloride anions with hydrogen
causes an abrupt increase in serum bicarbonate producing a
metabolic alkalosis.2
1.b. Create a list of this patient’s drug therapy problems.
• Hypotension secondary to volume depletion.
• Metabolic alkalosis secondary to excessive loop diuretic use
and vomiting.
• Constitutional symptoms (ie, generalized weakness, fatigue,
and myalgias) likely the result of volume depletion.
• Electrolyte abnormalities, including hyponatremia, hypokalemia, hypochloremia, hypocalcemia, hypomagnesemia, and
elevated serum bicarbonate.
• HF with poor medication adherence exhibited by excessive
diuretic use.
• Type 2 diabetes mellitus—diet controlled.
• Dyslipidemia—obtain fasting lipid panel to assess the adequacy of current treatment.
1.c. Describe the physical exam and laboratory findings that are
consistent with metabolic alkalosis and those that are inconsistent with this acid–base disorder.
Consistent findings (physical):
• Many of the signs of metabolic alkalosis are not specific and
depend on the severity of the alkalosis. Findings that can be
seen such as weakness, fatigue, and myalgias are due primarily
to the volume depletion and electrolyte abnormalities that are
associated with alkalosis; but not directly due to the alkalosis.3
Consistent findings (laboratory):
• Elevated arterial blood pH
• Elevated arterial bicarbonate
• Elevated serum bicarbonate
• Decreased serum chloride
• Decreased serum sodium
• Decreased serum potassium
• Decreased serum calcium
• Decreased serum magnesium
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Metabolic Alkalosis
CASE SUMMARY
✓This patient’s serum bicarbonate concentration of
39 mEq/L is 13 mEq/L above the normal expected serum
value; therefore, a compensatory PaCO2 response would
be a PaCO2 of approximately 48 mm Hg (13 × 0.6, or
7.8 mm Hg above the expected value of 40 mm Hg).
CHAPTER 62
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increase in serum bicarbonate above a normal expected
value.1
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• Decreased urine chloride
SECTION 5
• Elevated urine potassium
• Elevated urine pH
Inconsistent findings:
Renal Disorders
• An elevated white blood cell (WBC) count is generally not a
sign of metabolic alkalosis. This finding in the case may be
caused by physical stress the patient is experiencing because
of hypotension and tachycardia secondary to volume depletion. Because of volume depletion, this elevated WBC count
may also simply reflect hemoconcentration. While obtaining a WBC differential may assist in differentiating stress
from infection, both can cause abnormalities (increases and
decreases) in the percentage of each type of WBC. At this time,
it is not necessary to obtain a WBC differential in this patient.
If the WBC count did not decrease after fluid administration,
then ordering a differential to rule out infection could be
considered.
• Constitutional symptoms (ie, generalized weakness, fatigue,
and myalgias) do not result directly from metabolic alkalosis.
This patient’s physical constitutional symptoms are suggestive
of volume depletion. Secondary to the volume depletion are
electrolyte disturbances (hypokalemia, hyponatremia, and
hypocalcemia) that can be manifested as weakness, myalgia, or
polyuria due to hypokalemia and/or muscle spasms or twitching due to hypocalcemia.
• Polyuria alone is not a characteristic sign of metabolic alkalosis. In this patient, polyuria may be multifactorial caused by
excessive diuretic use resulting in electrolyte abnormalities.
Hypokalemia can cause polyuria, which would increase fluid
excretion worsening the volume depletion. As fluids and/or
potassium supplements (see question 4.a) are administered
and the metabolic alkalosis is corrected, the potassium should
normalize and the patient should not experience polyuria at
that point. In addition, with a past medical history of diabetes
mellitus that is currently diet controlled, the patient may benefit from a urinalysis and labs (ie, hemoglobin A1C) to assure
that the diabetes mellitus is not progressing.
• Extracellular fluid volume contraction can also intensify the
increase in serum bicarbonate by limiting the volume in which
bicarbonate can distribute.
• Many of the causes of metabolic alkalosis are associated with
hypokalemia, which in turn prolongs alkalosis. Hypokalemia will stimulate the shift of hydrogen ions intracellularly,
enhancing bicarbonate reabsorption in the collecting duct,
producing extracellular alkalosis. When potassium depletion
occurs in conjunction with chloride depletion, metabolic alkalosis is four times as likely to occur.3
• Gastric secretions contain high concentrations of hydrochloric
acid. Normally, gastric acid secretions stimulate the pancreas
to secrete bicarbonate once the hydrochloric acid reaches the
duodenum. These substances are then neutralized and there is
equilibrium between hydrogen and bicarbonate. When gastric secretions are lost through vomiting, the pancreas is not
stimulated to release bicarbonate and a net gain of bicarbonate
in the serum occurs, leading to metabolic alkalosis.2 Volume
depletion is also observed when gastric secretions are lost and
metabolic alkalosis then occurs as described above.
1.e. What medications, dietary supplements, and medical procedures could contribute to metabolic alkalosis? Include those
that may not apply to this patient.
• Medications that can contribute to metabolic alkalosis
include:1,4
✓Thiazide diuretics
✓Loop diuretics
✓Nonabsorbable antacids (ie, magnesium, calcium, or aluminum with a hydroxide or carbonate base)
✓Excessive use of laxatives causing sufficient losses through
diarrhea
✓
Mineralocorticoids
glucocorticoids)
(ie,
fludrocortisone,
some
✓ Excessive administration or retention (in renal insufficiency)
of sodium bicarbonate
✓Intravenous penicillins (eg, ampicillin, penicillin)
1.d. What is the pathophysiology underlying this patient’s metabolic alkalosis?
• This patient is taking the loop diuretic furosemide in an unprescribed manner
• As described above (see question 1.a.), this patient’s metabolic
alkalosis is due to excessive loop diuretic use, combined with
three episodes of recent vomiting.
• Glycyrrhizinic acid-containing compounds (eg, licorice, chewing tobacco)
• Loop and thiazide diuretics cause metabolic alkalosis (also
referred to as “contraction alkalosis” or “chloride depletion
alkalosis”) through the enhanced excretion of sodium, chloride, potassium, and water in the ascending limb of the Loop of
Henle and distal convoluted tubule, respectively. Evaluation of
urine electrolytes demonstrates increased urine concentrations
secondary to the enhanced excretion. This results in increased
osmolality in the renal tubules and a subsequent reduction of
extracellular fluid volume.3
• Hemodialysis utilizing citrate-containing dialysate solutions
• Extracellular fluid volume contraction promotes the secretion of renin and aldosterone that leads to an increase in the
reabsorption of sodium in the distal tubule and accelerated
secretion of potassium and hydrogen ions, leading to alkalosis and hypokalemia. The increased secretion of hydrogen
ions leads to increased luminal bicarbonate. The kidneys are
normally able to secrete excess bicarbonate through an apical
chloride–bicarbonate exchanger. With an excessive renal loss
of chloride, the kidneys are unable to appropriately secrete
bicarbonate, thus elevating the concentration in the serum.1
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• Hemodialysis utilizing bicarbonate-rich dialysate solutions
• Blood transfusions that contain citrate as a preservative agent
Desired Outcome
2.What are the desired therapeutic outcomes for this patient?
Hypotension:
• Normalize blood pressure (goal <140/90 mm Hg).
• Maintain mean arterial pressure (MAP) ≥65 mm Hg.5
• Achieve urine output 0.5 mL/kg/hour or more.5
• Maintain adequate organ perfusion [based on MAP ≥65 and
either superior vena cava oxygenation saturation (Scvo2)
or mixed venous oxygen saturation (Svo2) of ≥70% or 65%,
respectively].5
Metabolic alkalosis/electrolyte abnormalities:
• Cessation of vomiting
• Correction of pH to 7.35–7.45
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• Correction of serum bicarbonate to 22–30 mEq/L
• Correction of serum potassium to 3.5–5.0 mEq/L
• Correction of serum sodium to 135–145 mEq/L
• Correction of serum calcium (corrected) to 8.5–10.5 mg/dL
• Correction of serum magnesium to 1.6–2.4 mEq/L
• Correction of urine pH to <6.0
• Correction of volume depletion
Constitutional symptoms:
• Cessation of vomiting
• Correction of volume depletion
• Normalization of body temperature
• Resolution of weakness, fatigue, and myalgias
Congestive HF:
• Improve patient’s quality of life.
• Minimize fluid overload.
• Avoid exacerbations of HF requiring hospitalization.
• Maintain vital signs within normal limits.
• Maintain adequate urine output.
Therapeutic Alternatives
3.What pharmacologic and nonpharmacologic alternatives
should be considered for the treatment of metabolic alkalosis
in this patient?
• The first step in determining a pharmacologic plan is to determine the cause of the metabolic alkalosis and to predict if the
alkalosis is chloride responsive or chloride resistant. The most
likely cause(s) of the alkalosis in this patient are excessive use
of furosemide and recent vomiting, which are considered chloride-responsive states (see answer to questions 1.d and 1.e).
• IV fluid resuscitation with isotonic sodium chloride is firstline therapy in chloride-responsive cases (urine chloride
<10 mEq/L). Isotonic sodium chloride will restore extracellular
fluid volume and in patients with normal renal function, bicarbonate excretion will be enhanced as sodium, potassium, and
chloride stores are repleted. Fluid therapy should be administered to patients who can tolerate the volume load. Fluid therapy
should be cautiously administered or not given in patients who
are volume overloaded or who may have difficulty with excess
volume (ie, patients with HF or renal insufficiency).1,4 Although
this patient has a history of HF, it is obvious based on presentation that she is severely volume depleted; therefore, cautious
administration of isotonic sodium chloride should be initiated.
• Ringer’s lactate IV solution contains less chloride than sodium
and should not be used to treat metabolic alkalosis. In addition, the lactate in the solution is a precursor to bicarbonate,
which could further exacerbate the existing alkalosis.
• Potassium supplementation (either orally or intravenously
depending on severity) is usually needed because metabolic
alkalosis resulting from diuretic therapy and/or vomiting
causes potassium depletion. Given that this patient is experiencing chloride-responsive alkalosis with volume depletion,
potassium supplementation should be initiated with appropriate electrolyte monitoring. Caution should be given when
potassium supplementation is initiated in patients with renal
insufficiency, as hyperkalemia could develop.
• Acidifying agents (ie, ammonium chloride, arginine monohydrochloride, and hydrochloric acid) may be considered in
patients with severe (pH >7.55) symptomatic metabolic alkalosis, as well as patients who are not responsive to sodium chloride hydration therapy and those who are not able to endure
excessive volume replacements due to edematous states.1,3
✓Ammonium chloride, metabolized by the liver to urea and
hydrochloric acid, is an alternative treatment for metabolic
alkalosis. Caution must be used for patients with hepatic
and/or kidney impairment. Patients with hepatic dysfunction are unable to properly convert ammonia to urea, leading to increased serum ammonia levels, which can cause or
worsen encephalopathy. In patients with renal insufficiency,
the generation of increased urea may worsen uremic symptoms. If prescribed, ammonium chloride can be administered through a peripheral vein.
✓Arginine hydrochloride, similar to ammonium chloride,
undergoes metabolism by the liver that results in the production of hydrogen ions. Additionally, because arginine
binds to circulating ammonia that leads to the production
of urea, it may be used safely in patients with hepatic insufficiency. Patients with renal insufficiency should not be given
arginine hydrochloride. Arginine may cause intracellular to
extracellular shifts in potassium, which in renal insufficiency
may lead to severe hyperkalemia.
✓Hydrochloric acid is indicated when sodium or potassium
chloride cannot be administered because of volume overload or advanced renal failure, or in states where prompt
correction is needed and other acidifying agents are contraindicated (eg, cardiac arrhythmias, hepatic encephalopathy).
Due to the potential for severe adverse effects such as metabolic acidosis, hemolysis, and extravasation, hydrochloric
acid should be administered slowly through a central vein
and the infusion rate should not exceed 0.2 mEq/kg/hour.7
• Hemodialysis may be considered in patients with advanced
renal failure, who are volume overloaded and resistant to
acetazolamide.3 With hemodialysis, the use of either a lowbicarbonate or acetate-free solution is recommended in patients
with metabolic alkalosis. Based on the laboratory data (ie, SCr
and BUN), it does not appear that this patient is in advanced
renal failure; therefore, hemodialysis is not recommended.
Optimal Plan
4.a. What drug, dosage form, dose, schedule, and duration of
therapy are best for this patient?
• IV hydration with 0.9% sodium chloride solution is the firstline therapy for this patient.
• Based on the patient’s vital signs and laboratory values, this
patient is volume depleted. Intravenous boluses of 1000 mL
of 0.9% sodium chloride can be given repeatedly, each one
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
Metabolic Alkalosis
• Prevent/minimize complications
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• Correction of serum chloride to 95–105 mEq/L
• Acetazolamide is an alternative for patients who are unable
to tolerate increased fluid volume. The drug inhibits carbonic
anhydrase, thereby reducing the reabsorption of sodium
and bicarbonate in the proximal tubule and leading to their
enhanced excretion. In addition, acetazolamide stimulates the
excretion of potassium and phosphate. It is not recommended
if the patient is experiencing hypokalemia, but if it used in
the setting of hypokalemia then potassium supplementation
should be initiated. A single 500-mg IV dose has been shown
to correct metabolic alkalosis and return serum bicarbonate
levels to normal.6 This patient should be reassessed after an
initial fluid challenge before administering acetazolamide.
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SECTION 5
infused over 1 hour, keeping the following goals of fluid resuscitation in mind: MAP ≥65 mm Hg, urine output ≥0.5 mL/
kg/hour and Scvo2 ≥70% or a Svo2 ≥65%.5 Typically, goals are
achieved after 3–4 L of fluid.
• Because this patient’s metabolic alkalosis is chloride responsive, the estimated volume of isotonic fluid needed can be
calculated based on the chloride (Cl) deficit using the following
equation:1,4
Renal Disorders
Cl deficit (mEq) = 0.2 × wt (kg) × (normal Cl – actual Cl)
The factor 0.2 signifies the extracellular volume as a fraction of body weight. Once the chloride deficit is calculated, the
volume can be determined as a ratio of Cl deficit/154, where
154 represents the amount of chloride in mEq in 1 L of isotonic
sodium chloride. For this patient, who weights 80 kg and has
a serum chloride level of 85 mEq/L, the chloride deficit can be
calculated as follows:
Step 1: Calculate the Cl deficit (mEq)
= 0.2 × 80 × (100 – 85) = 240 mEq
Step 2: Determine the minimum volume
(L) of NaCl to infuse = 240 mEq/154 mEq/L = 1.6 L
• Fluid resuscitation should be completed gradually and cautiously to avoid fluid overload in this patient with a history of
HF. The patient should be reassessed for signs and symptoms
of fluid overload after each liter of isotonic saline infused.
• Furosemide therapy should be discontinued until the metabolic alkalosis has been resolved and the hypotension/volume
depletion has been corrected.
• Potassium chloride supplementation should be initiated at a
dose of 20–40 mEq per day, with the understanding that the
patient’s requirements may need to be modified as volume
depletion resolves and furosemide is reinitiated. Potassium
supplementation may be given either orally in divided doses or
added to the sodium chloride solution (ie, 20–40 mEq/L) and
given as a continuous infusion. Further monitoring of serum
potassium should continue to ensure that overcorrection has
not occurred.
4.b. What other modifications in the patient’s current drug regimen are warranted? Include your rationale.
• The patient should first be asked, or medical records reviewed,
for any changes that the patient may have experienced or may
be experiencing that are different from baseline due to HF (eg,
difficulty breathing, noticeable weight gain or loss, increase
edema, etc.). Currently, it is not appropriate to change therapy
based on the presentation of the patient because she is volume
depleted.
• If the patient is not fluid overloaded at baseline, it would be
suitable to decrease the dose of the furosemide to 20 mg daily
after the metabolic alkalosis resolves and the hypotension/
volume depletion have been corrected. Dietary restriction
of sodium should be reiterated to the patient to avoid fluid
overload.
• If the patient is fluid overloaded at baseline, adding a
potassium-sparing diuretic, such as spironolactone 25 mg
PO once daily, would assure proper diuresis and may prevent
hypokalemia.
• Currently, the doses of carvedilol, lisinopril, and atorvastatin
are within appropriate dosing recommendations for the disease states of the patient. The lisinopril dose may need to be
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
adjusted or discontinued if the patient is receiving potassium
as a treatment option for metabolic alkalosis in the acute treatment phase. Once the metabolic alkalosis is corrected and the
underlying cause treated, dose adjustments for the lisinopril
may need to be modified back to the original dose. In addition, routine monitoring of potassium levels should occur to
avoid hyperkalemia while the patient is receiving potassium.
The patient does not appear to be having adverse effects from
atorvastatin, but it would be beneficial to obtain a baseline fasting lipid panel to assess the efficacy of therapy and adherence.
In addition, the patient presented with complaints of myalgias
(likely secondary to electrolyte abnormalities), but it would be
beneficial to obtain a myoglobin and creatine kinase level to
assure the statin does not need to be discontinued.
• Patient education on adherence to the prescribed regimen (as
described in question 6) is necessary to avoid potential adverse
effects.
Outcome Evaluation
5.a. What clinical and laboratory parameters are necessary to
evaluate the therapy for achievement of the desired outcome
and to detect or prevent adverse effects?
Efficacy:
• Obtain repeat arterial blood gas in 24 hours and reassess treatment response.
• Obtain serum electrolytes (ie, sodium, potassium, chloride,
and bicarbonate), calcium, BUN, and serum creatinine every
12 hours for the first 24 hours and then reassess.
• Obtain vital signs every 4 hours.
• Obtain repeat set of urine electrolytes (ie, sodium, potassium,
and chloride).
✓Urine sodium when a patient is euvolemic is generally
>40 mEq/L.
✓Urine potassium concentration should be between 20 and
30 mEq/L.
✓Urine chloride concentration should be between 25 and
40 mEq/L.
• Measure fluid intake and urine output every 2 hours for
24 hours, then once every shift.
Toxicity:
• Assess the patient for signs and symptoms of fluid overload
(shortness of breath, crackles on chest auscultation, and
peripheral edema).
5.b. What is your assessment of the patient’s response to the IV
fluids? What modifications in therapy are warranted, if any?
• The infusion of 0.9% sodium chloride, along with potassium
chloride supplementation, appears to have facilitated the normalization of sodium, potassium, and chloride.
• There has also been improvement of the volume depletion as
noted by a normalization of serum creatinine and BUN.
• While there has been an improvement in several parameters
of the arterial blood gas (ie, pH, PaCO2, HCO3) and serum
bicarbonate, the values are still slightly elevated.
• Although the patient is experiencing 1+ pitting edema in the
lower extremities, evaluation of the full appearance of the
patient is necessary to assess fluid status before continuing
treatment. This includes (but is not limited to) lung auscultation, repeat chest X-ray, and assessment for the presence of
JVD.
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✓ A single dose of acetazolamide 500 mg IV (if utilized) should
result in correction of the metabolic alkalosis.6
Patient Education
6.What information should be provided to the patient to help
enhance adherence, ensure successful outcomes, and prevent
future complications?
• The extra doses of the diuretic furosemide that you were taking for treatment of congestive HF have caused you to lose
too much fluid and essential electrolytes such as potassium,
sodium, and chloride. This caused you to become dehydrated
and feel weak and tired. To avoid this in the future, do not take
your furosemide more than as prescribed. If you consistently
feel bloated or if you develop difficulty breathing, dizziness,
weakness, fatigue, or muscle aches, let your doctor know as
soon as possible.
• It is beneficial to weigh yourself on a daily basis to assess if
you are experiencing any fluid retention due to your congestive HF. In addition, if you find your weight is decreasing, this
can be due to a depletion of fluid that can result in electrolyte
imbalances and possible injury to your kidneys. Some of the
medications that you are taking (eg, furosemide and lisinopril)
may also worsen electrolyte imbalances and kidney injury. For
• It is highly recommended to limit the amount of salt you use
when you eat. Extra salt will cause your body to hang on to
fluid, which will cause your heart to work harder. This can
also cause symptoms such as shortness of breath and swelling
of your feet.
• Furosemide removes fluid from your body, but it also causes
loss of potassium in the urine. Potassium is very important for
normal heart function. For this reason, please keep all followup appointments with your doctor so your lab work can be
monitored.
• Store these and all other medications in the original container
in a cool, dry place out of the reach of children.
REFERENCES
1. Shah N, Shaw C, Forni LG. Metabolic alkalosis in the intensive care
unit. Neth J Crit Care 2008;12(3):113–119.
2. Gennari FJ, Weise WJ. Acid–base disturbances in gastrointestinal disease. Clin J Am Soc Nephrol 2008;3:1861–1868.
3. Soifer JT, Kim HT. Approach to metabolic alkalosis. Emerg Med Clin
N Am 2014;32:453–463.
4. Seifter JL. Integration of acid–base and electrolyte disorders. N Engl
J Med 2014;371(19):1821–1831.
5. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign:
international guidelines for management of severe sepsis and septic
shock: 2012. Crit Care Med 2013;41:580–637.
6. Moviat M, Pickkers P, van der Hoeven PHJ, et al. Acetazolamidemediated decrease in strong ion difference accounts for the correction
of metabolic alkalosis in critically ill patients. Crit Care 2006;10:R14.
doi: 10.1186/cc3970.
7. Oh YK. Acid–base disorders in ICU patients. Electrolyte Blood Press
2010;8:66–71.
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
Metabolic Alkalosis
• If it appears that the patient cannot tolerate any further treatment with IV fluids due to fluid overload, acetazolamide
should be considered as an option to assist with further excretion of bicarbonate.1,3 As described above (see question 3),
acetazolamide will also cause potassium excretion, and therefore it is important to follow electrolytes carefully while
administering this medication. Supplementation of potassium
may be considered to avoid hypokalemia.
this reason, it is important that you let your doctor know if you
are unable to maintain your normal fluid intake or if you are
not going to the bathroom as often as you normally do.
CHAPTER 62
• Continued treatment with 0.9% sodium chloride is warranted
if no further symptoms of fluid overload are apparent. Full
normalization of the serum bicarbonate and pH should occur
within 24 hours.