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Acid-base disorders Last updated: November 2, 2023

Summary

Acid-base disorders are characterized by changes in the concentration of hydrogen ions (H+) in the body.
Increased H+ concentration (acidosis) can lead to an abnormally low blood pH (acidemia) and decreased H+
concentration (alkalosis) can lead to an abnormally high blood pH (alkalemia); however, if compensation occurs,
acidosis and/or alkalosis may be present without acidemia or alkalemia. Acidosis and alkalosis may be respiratory
or metabolic in origin depending on the cause of the imbalance; they can also coexist as mixed acid-base disorders
. Diagnosis is made based on arterial blood gas (ABG) results. In metabolic acidosis, calculation of the anion gap
can also help determine the cause and reach a precise diagnosis. In metabolic alkalosis, urine chloride (Cl-)
concentration can help identify the cause. Treatment is based on the underlying cause.

De�nition

• Acid-base processes [1]

◦ Acidosis: the processes by which H+ concentration is increased

◦ Alkalosis: the processes by which H+ concentration is decreased

• pH scale

◦ A logarithmic scale that expresses the acidity or alkalinity of a solution based on the concentration of H+ (pH
= -log[H+])

◦ Neutral pH is 7; lower values are acidic and higher values are alkaline.

• Blood pH abnormalities

◦ Acidemia; : abnormally low blood pH (pH < 7.35)

◦ Alkalemia; : abnormally high blood pH (pH > 7.45)

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Pathophysiology

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• The Henderson-Hasselbalch equation allows for the calculation of pH from HCO3- and PCO2: pH = 6.1 + log([
HCO3-]/[0.03 × pCO2])
◦ 6.1 = pKa of carbonic acid

◦ 0.03 = solubility constant of PCO2

Pathophysiology of acid-base disorders [2]

Respiratory acidosis Respiratory alkalosis Metabolic acidosis Metabolic alkalosis

pH • ↓ • ↑ • ↓ • ↑

PCO2 • ↑ • ↓ • Expected • Expected

compensatory compensatory
response: ↓ response: ↑

HCO3- • Expected • Expected • ↓ • ↑

compensatory compensatory
response: ↑ response: ↓

Mechanism • Alveolar • ↑ Respiratory rate • ↑ Production • Loss of H+ or ↑

hypoventilation → and/or tidal volume and/or ingestion production/ingestion
CO2 retention → alveolar of H+ or loss of of HCO3-
hyperventilation → HCO3-
CO2 washout

Compensation • Acute • Acute • ↓ Arterial and CSF • ↑ Arterial and CSF pH

mechanisms in compensation: compensation: pH (with ↓ HCO3- (with ↑ HCO3-) → ↓
buffers in blood buffers in blood ) → ↑ stimulation stimulation of the
acid-base
of the medullary medullary
• Chronic • Chronic
disorders chemoreceptors chemoreceptors → ↓
compensation compensation:
→↑ respiratory rate
◦ ↓ Arterial pH ◦ ↑ Arterial pH
respiratory rate and/or tidal volume (
(with ↑ PCO2) → (with ↓ PCO2) →
and/or hypoventilation) → ↑
↑ HCO3- via: ↓ HCO3- via:
tidal volume ( CO2 retention → ↑
▪ ↑ ▪ ↓
hyperventilation) PCO2
Reabsorption Reabsorption
→ ↑ CO2 washout
of HCO3- by of HCO3- by • The compensatory
the the → ↓ PCO2
process in
proximal proximal metabolic alkalosis is
convoluted convoluted not as ef�cient as the
tubule tubule process in
▪ ↑ Excretion of ▪ ↓ Renal metabolic acidosis
excretion of because
H+ as H2PO4-
hypoventilation
H+
and NH4+ -induced hypoxia
from the blunts the decrease in
distal ventilatory drive.
convoluted
tubule
and
collecting
duct

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Diagnostics

Approach to acid-base disorders [1][3]

• Perform an initial clinical evaluation: to help identify the most likely underlying cause

• Order initial laboratory studies: ABG, BMP [4][5]

• Determine the primary acid-base disorder: i.e., using pH, PCO2, and HCO3-

• Calculate the expected compensatory (or secondary) response.

◦ Mixed acid-base disorder: The expected compensatory response differs from the laboratory �ndings.

◦ No mixed acid-base disorder: The expected compensatory response aligns with the laboratory �ndings.

• Perform further diagnostic workup (to determine the mechanism and the cause), e.g.:

◦ In metabolic acidosis: anion gap and delta gap

◦ In metabolic alkalosis: urinary chloride and potassium levels

Careful clinical evaluation is an important �rst step in the assessment of acid-base disorders, as it
can provide important diagnostic clues that can help determine the underlying cause.

Initial blood gas analysis

There are different methods for the assessment of acid-base status; the following method is just one example.

Suggested approach

1. Evaluate blood pH (reference range: 7.35–7.45).

2. Evaluate HCO3- (reference range: 22–28 mEq/L).

3. Evaluate PCO2 (reference range: 33–45 mm Hg).

Interpretation

• pH < 7.35 (acidemia): Primary disorder is an acidosis.

◦ ↓ pH and ↓ HCO3-: metabolic acidosis

◦ ↓ pH and ↑ PCO2: respiratory acidosis

• pH > 7.45 (alkalemia): Primary disorder is an alkalosis.

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◦ ↑ pH and ↑ HCO3-: metabolic alkalosis

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◦ ↑ pH and ↓ PCO2: respiratory alkalosis

Further considerations

• Evaluate PO2.

◦ High: hyperoxemia

◦ Low: hypoxemia

• See also “Respiratory failure.”

SMORE: change in PCO2 in the Same direction as pH → Metabolic disorder; change in PCO2 in the
Opposite direction to pH → REspiratory disorder

Corrections to central venous blood gas values [6][7]

Reference values for venous blood gas (VBG) are different from those for ABG; central VBG results can be
corrected to approximate ABG.

• Arterial pH = venous pH + 0.03–0.05 units

• Arterial PCO2 = venous PCO2 – 5 mm Hg

Compensation (acid-base) [1][8]

• De�nition: physiological changes that occur in acid-base disorders in an attempt to maintain normal body pH

• Compensatory changes

◦ In metabolic disorders: rapid compensation within minutes through changes in minute ventilation
(respiratory compensation)

◦ In respiratory disorders: typically slow compensation over several hours to days through changes in urine pH
(metabolic compensation)
◦ See also “Compensation mechanisms in acid-base disorders.”

• Assessment and interpretation: Calculate the expected compensation; see “Calculation of compensatory
response.”

◦ Primary respiratory disorders

▪ Measured HCO3- > expected HCO3-: metabolic alkalosis in addition to respiratory disturbance

▪ Measured HCO3- < expected HCO3-: metabolic acidosis in addition to respiratory disturbance

◦ Primary metabolic disorders

▪ Measured PCO2 > expected PCO2: respiratory acidosis in addition to metabolic disturbance

▪ Measured PCO2 < expected PCO2: respiratory alkalosis addition to metabolic disturbance

Calculation of compensatory response

Primary acid-base disturbance Expected compensation [1][9]

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Calculation of compensatory response

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Primary acid-base disturbance Expected compensation [1][9]

Metabolic acidosis • Winter formula: expected PCO2 (mm Hg) = (1.5 × HCO3-) + 8 ± 2

• OR (rule of thumb) expected PCO2 (mm Hg) = last two digits of the pH value

Metabolic alkalosis • Expected PCO2 (mm Hg) = [0.7 × (HCO3- - 24)] + 40 ± 2

• OR expected PCO2 (mm Hg) = HCO3- + 15

Respiratory acidosis Acute • Expected HCO3- (mEq/L) = 24 + [0.1 × (PCO2 - 40)]

• OR expected HCO3- (mEq/L): HCO3- increases by 1 mEq/L for every 10 mm Hg

increase in PCO2 above 40 mm Hg.

Chronic • Expected HCO3- (mEq/L) = 24 + [0.35 × (PCO2 - 40)]

• OR expected HCO3- (mEq/L): HCO3- increases by 4–5 mEq/L for every 10 mm Hg

increase in PCO2 above 40 mm Hg.

Respiratory Acute • Expected HCO3- (mEq/L) = 24 - [0.2 × (40 - PCO2)]

alkalosis • OR expected HCO3- (mEq/L): HCO3- decreases by 2 mEq/L for every 10 mm Hg
decrease in PCO2 below 40 mm Hg.

Chronic • Expected HCO3- (mEq/L) = 24 - [0.4 × (40 - PCO2)]

• OR expected HCO3- (mEq/L): HCO3- decreases by 4–5 mEq/L for every 10 mm Hg

decrease in PCO2 below 40 mm Hg.

Discordance between the measured compensatory response and the expected compensatory
response suggests a secondary acid-base disturbance.

In primary metabolic disorders, respiratory compensation develops quickly (within hours),

whereas metabolic compensation may take 2–5 days to develop in primary respiratory disorders.

Metabolic acidosis

General principles

• Calculation of the anion gap is the �rst step in the evaluation of metabolic acidosis.

◦ Maintenance of electrical neutrality requires that the total concentration of cations approximate that of
anions.

◦ Anion gap: the difference between the concentration of measured cations and measured anions

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◦ High anion gap: increased concentration of organic acids such as lactate, ketones (e.g., beta-hydroxybutyrate,
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acetoacetate), oxalic acid, formic acid, or glycolic acid, with no compensatory increase in Cl-.

◦ Normal anion gap: primary loss of HCO3- compensated with ↑ Cl-

• The measured serum sodium (Na+), not the corrected serum Na+, should be used in the formulas, even if
glucose levels are high.

• Depending on the results, further evaluation and calculations may be needed (see speci�c subsections below).

Metabolic acidosis formulas [1][10][11]

Anion gap Serum anion gap • [Na+] - ([Cl-] + [HCO3-])

• Reference range: 6–12 mEq/L

• Correction for hypoalbuminemia: Increase the anion gap by 2.5 mEq/L for every 1 g/dL
reduction in serum albumin.

• If potassium levels are taken into consideration: ([Na+] + [K+]) - ([Cl-] + [HCO3-]) (
reference range: 10–16 mmol/L)

Urine anion gap • [Urine Na+] + [urine K+] - [urine Cl-]

Osmolal Serum • Measured serum osmolality - calculated serum osmolality

gap osmolal gap • Calculated serum osmolality = (2 × [Na+]) + ([glucose in mg/dL]/18) + ([BUN in
mg/dL]/2.8)

Urine osmolal • Measured urine osmolality - calculated urine osmolality

gap • Calculated urine osmolality = (2 × [urine Na+ + urine K+]) + ([urine urea in mg/dL]/2.8)
+ ([urine glucose in mg/dL]/18)

Delta gap • ∆ Anion gap/∆ bicarbonate

• ∆ Anion gap = measured anion gap - 12

• ∆ Bicarbonate = 24 - measured HCO3-

• Anion gap: the difference between the concentration of measured cations and measured anions

• Osmolal gap: the difference between the measured osmolality and the calculated osmolality

• Delta gap: a ratio of the change in anion gap to the change in bicarbonate

High anion gap metabolic acidosis [1][11]

Review clinical features and initial studies and follow a stepwise approach to identify the underlying cause of high
anion gap metabolic acidosis.

1. Exclude accumulation of endogenous organic acids.

◦ Exclude ketoacidosis : Consider measuring ketone levels in urine or serum (e.g., beta-hydroxybutyrate).

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◦ Exclude lactic acidosis: Measure or review lactate levels.

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◦ Exclude uremia: Measure or review BUN and creatinine levels.

2. Consider accumulation of exogenous organic acids (ingestion) as the cause: e.g., if the cause remains unclear,
or initially if the patient is comatose

◦ Consider obtaining serum or urine toxicology screen.

◦ Calculate serum osmolal gap: If elevated (≥ 10 mOsm/kg), consider propylene glycol, ethylene glycol,
diethylene glycol, methanol, and isopropanol as potential causes.

3. Calculate the delta gap: to exclude concomitant acid-base disturbances

Etiology of high anion gap metabolic acidosis

Mechanism Causes

Accumulation of • Ketoacidosis (e.g., diabetic ketoacidosis, starvation ketoacidosis, alcoholic ketoacidosis)

endogenous organic acids • Lactic acidosis
◦ Type A lactic acidosis (related to hypoxia): e.g., caused by septic shock, hypovolemic shock,
hypoxemia, carbon monoxide poisoning

◦ Type B lactic acidosis (not related to hypoxia): e.g., caused by liver failure , seizures,
intoxication with methanol or toxic alcohols, toluene, medications such as isoniazid and
metformin

◦ D-lactic acidosis: e.g., caused by short bowel syndrome (can also occur in other forms of
malabsorption)

• Renal insuf�ciency, uremia

• Massive rhabdomyolysis

Accumulation of • Ingestion of methanol → ↑ formic acid

exogenous organic acids • Ingestion of ethylene glycol (a component of antifreeze products) → ↑ oxalic acid

• Ingestion of propylene glycol → ↑ lactic acid

• Toluene [12]

• Long-term acetaminophen use → ↑ 5-oxoproline (pyroglutamic acid)

• Salicylate toxicity

• Iron overdose

• Isoniazid (INH) overdose

• Djenkol bean poisoning

• Use of penicillin-derived antibiotics

Causes of high anion gap acidosis (MUDPILES): Methanol toxicity, Uremia, Diabetic ketoacidosis,
Paraldehyde, Isoniazid or Iron overdose, Inborn error of metabolism, Lactic acidosis, Ethylene
glycol toxicity, Salicylate toxicity

Concomitant acid-base disturbances [10][11]

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Calculation of the delta gap can help determine if another acid-base disturbance is present in addition to a
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high anion gap metabolic acidosis. Cut-off values may vary depending on the source.

• Delta gap < 1 : Hyperchloremic or normal anion gap metabolic acidosis is present in addition to
high anion gap metabolic acidosis. [10]

• Delta gap 1–2 : Only high anion gap metabolic acidosis is present.

• Delta gap > 2 : A metabolic alkalosis is present in addition to high anion gap metabolic acidosis. [11]

Normal anion gap metabolic acidosis

Review clinical features and initial studies and consider further diagnostic workup to determine the underlying
cause of normal anion gap metabolic acidosis.

• Calculate the urine anion gap

◦ Negative urine anion gap: Acidosis is likely due to loss of bicarbonate.

◦ Positive urine anion gap: Acidosis is likely due to decreased renal acid excretion.

• Consider calculating the urine osmolal gap

◦ Preferred over urine anion gap if the urine pH is > 6.5 or urine Na+ is < 20 mEq/L

◦ ↓ Urine osmolal gap (< 80–100 mOsm/kg) suggests impairment in the excretion of urinary ammonium. [13]

[14]

Etiology of normal anion gap metabolic acidosis

Mechanism Causes

Loss of bicarbonate (negative urine anion gap) • Diarrhea

• GI �stulas (e.g., biliary or pancreatic �stula)

• Toluene ingestion

• Medications (e.g., carbonic anhydrase inhibitors such as acetazolamide,

spironolactone)

• Type 2 renal tubular acidosis

Decreased renal acid excretion (positive • Hyperchloremia (e.g., due to excess saline infusion, ammonium chloride)
urine anion gap) • Renal failure (early uremic acidosis)

• Addison disease

• Renal tubular acidoses: type 1 renal tubular acidosis,

type 4 renal tubular acidosis

Causes of normal anion gap acidosis (FUSEDCARS): Fistula (biliary, pancreatic), Ureterogastric
conduit, Saline administration, Endocrine (Addison disease, hyperparathyroidism), Diarrhea,
Carbonic anhydrase inhibitors, Ammonium chloride, Renal tubular acidosis, Spironolactone

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A neGUTive urine anion gap may be due to GI loss of bicarbonate.

Abnormal anion gap without metabolic acidosis [15]

• Etiology of low anion gap

◦ Hypoalbuminemia → ↓ unmeasured anions → ↓ anion gap

◦ Paraproteinemia (e.g., in multiple myeloma), severe hypercalcemia, severe hypermagnesemia, and/or

lithium toxicity → ↑ unmeasured cations → ↓ anion gap

• Etiology of high anion gap

◦ Severe hyperphosphatemia → ↑ unmeasured anions → ↑ anion gap [16]

◦ Severe hypocalcemia and/or hypomagnesemia → ↓ unmeasured cations → ↑ anion gap

Metabolic alkalosis

Approach [1]

• Assess the patient's blood pressure and volume status.

• Evaluate for exogenous ingestion (e.g., laxatives, calcium, alkali load, diuretics).

• Obtain BMP and serum calcium, urinary chloride, and urinary potassium levels.

◦ Low urine chloride (< 25 mEq/L): chloride-responsive metabolic alkalosis

◦ High urine chloride (> 40 mEq/L): chloride-resistant metabolic alkalosis ; check urine potassium.

▪ High urine potassium (> 30 mEq/L): Review blood pressure.

▪ Elevated blood pressure: Consider mineralocorticoid excess as a potential cause.

▪ Low or normal blood pressure: Consider Gitelman syndrome or Bartter syndrome as a potential cause.

▪ Low urine potassium (< 20 mEq/L): Consider laxative abuse as a potential cause.

Elevated calcium with renal failure suggests milk-alkali syndrome.

Etiology

Etiology of metabolic alkalosis [1][17]

Mechanism Causes

Chloride-responsive metabolic alkalosis (urine chloride • Hypovolemia (e.g., contraction alkalosis )

< 25 mEq/L) ◦ Gastrointestinal losses: due to vomiting, nasogastric suction,
or diarrhea

◦ Other: hemorrhage

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Etiology of metabolic alkalosis [1][17] Collapse all sections START FREE TRIAL LOG IN

Mechanism Causes

• Renal losses: due to loop or thiazide diuretics

• Cystic �brosis

• Dietary chloride de�ciency with a high alkali dietary load

Chloride-resistant metabolic alkalosis (urine chloride > • Severe magnesium de�ciency

40 mEq/L) • Extreme hypercalcemia, hypokalemia

• High alkali load (e.g., due to antacid use, alkalization therapy)

• Loop or thiazide diuretics

• Other (less common causes)

◦ Associated with low or normal blood pressure
▪ Bartter syndrome

▪ Gitelman syndrome

◦ Associated with high blood pressure

▪ Hyperaldosteronism

▪ Cushing syndrome

▪ Liddle syndrome

▪ Licorice ingestion [18]

◦ Ingestions or drugs [17]

▪ Laxative abuse

▪ Clay ingestion

▪ Carbenicillin, ampicillin, penicillin

◦ Recovery from starvation

◦ Hypoalbuminemia

Respiratory disorders

Respiratory acidosis

• Seen in alveolar hypoventilation; see also “Respiratory insuf�ciency.”

• Establish the expected chronicity based on clinical presentation using the following rule:

◦ HCO3- increases by 1 mEq/L for every 10 mm Hg increase in PCO2 above 40 mm Hg: suggests
acute respiratory acidosis

◦ HCO3- increases by 4–5 mEq/L for every 10 mm Hg increase in PCO2 above 40 mm Hg: suggests chronic
respiratory acidosis
• Expected and measured HCO3- values may differ if additional metabolic disturbances are present; see
“Compensation (acid-base).”

Etiology of respiratory acidosis [1]

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Mechanism Causes
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Acute respiratory acidosis • Acute lung disease (e.g., pneumonia , pulmonary edema)

• Acute exacerbation of chronic obstructive airway disease (e.g., COPD, asthma)

• CNS depression due to:

◦ Head trauma

◦ Postictal state

◦ Drug toxicity (e.g., from opiates, barbiturates, benzodiazepines)

◦ Central sleep apnea

Chronic respiratory acidosis • Airway obstruction (e.g., COPD, asthma)

• Respiratory muscle weakness, e.g., due to:

◦ Myasthenia gravis

◦ ALS

◦ Guillain-Barré syndrome

◦ Poliomyelitis

◦ Multiple sclerosis

◦ Severe hypokalemia

Respiratory alkalosis

• Seen in hyperventilation; see also “Respiratory insuf�ciency.”

• Establish the expected chronicity based on clinical presentation using the following rule:

◦ HCO3- decreases by 2 mEq/L for every 10 mm Hg decrease in PCO2 below 40 mm Hg: suggests
acute respiratory alkalosis

◦ HCO3- decreases by 4–5 mEq/L for every 10 mm Hg decrease in PCO2 below 40 mm Hg: suggests chronic
respiratory alkalosis

• Expected and measured values may differ if additional metabolic disturbances are present; see “Compensation
(acid-base).”

Etiology of respiratory alkalosis [19]

Mechanism Causes

Acute respiratory • Pulmonary disease (e.g., pneumonia, pulmonary embolism, pulmonary edema,
alkalosis aspiration pneumonitis), interstitial �brosis

• Pain, anxiety, panic attacks

• Fever

• Drug toxicity (e.g., from salicylate , theophylline, progesterone)

• CNS infections (e.g., meningitis, encephalitis)

• Stroke

• Severe anemia

• Congestive heart failure

• Sepsis

• Hypoxemia (e.g., upon arrival at high altitude)

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Etiology of respiratory alkalosis [19] Collapse all sections START FREE TRIAL LOG IN

Mechanism Causes

• Hyperventilation while on mechanical ventilation

Chronic • Pulmonary embolism during pregnancy

respiratory alkalosis • Liver failure

• Hyperthyroidism

• Brainstem tumor (may cause central neurogenic hyperventilation)

Gastrointestinal disorders

Acid-base disturbances associated with GI disorders [20][21]

GI disturbance Acid-base disturbance Cl- K+ Na+

Severe diarrhea or laxative use Metabolic acidosis ↑ ↓ ↑

Prolonged vomiting or nasogastric suctioning Metabolic alkalosis ↓ ↓ ↑

The loss of bicarbonate-rich �uid in severe diarrhea may cause non-anion gap metabolic acidosis.

Treatment

General considerations [2]

• Treatment of acid-base disorders should target the underlying cause.

• Medications (e.g., sodium bicarbonate, acetazolamide) used to correct acid-base abnormalities should be
initiated in consultation with a specialist (e.g., nephrologist).

• Mechanical ventilation may be indicated in severe respiratory disorders and severe metabolic acidosis.

• Optimize ventilation in mechanically ventilated patients as needed.

• Electrolyte imbalances should be corrected: See “Disorders of potassium balance” and “Electrolyte repletion.”

Respiratory acidosis

• Severe acute respiratory acidosis: Consider noninvasive or invasive mechanical ventilation.

• See also “COPD,” “Opioid intoxication,” and “Benzodiazepine overdose.”

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Respiratory alkalosis
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• Acute respiratory alkalosis accompanied by increased work of breathing: Consider mechanical ventilation.

• See also “Treatment of congestive heart failure,” “Treatment of pulmonary embolism,” and “Salicylate toxicity.”

Metabolic acidosis

• Acute severe metabolic acidosis

◦ Consider intravenous sodium bicarbonate and mechanical ventilation (see “High-risk indications for
mechanical ventilation”)

◦ See also “Diabetic ketoacidosis” and “Salicylate toxicity.” [4][22]

• Chronic metabolic acidosis

◦ Consider oral sodium bicarbonate

◦ See also “Chronic kidney disease,” and “Diarrhea.”

Metabolic alkalosis

• Chloride-responsive metabolic alkalosis

◦ Start isotonic saline to increase urinary bicarbonate excretion and correct extracellular volume loss

◦ See “Intravenous �uid therapy” and “Treatment” in “Dehydration and hypovolemia.”

• Chloride-resistant metabolic alkalosis

◦ Consider bicarbonate excess as a potential cause and administer acetazolamide.

◦ See also “Cushing Syndrome” and “Primary hyperaldosteronism.”

References

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2. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal
Medicine. McGraw-Hill Education ; 2015
3. Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nature Reviews
Nephrology. 2010; 6 (5): [Link]: 10.1038/nrneph.2010.33 . | Open in Read by QxMD

4. Jaber S, Paugam C, Futier E, et al. Sodium bicarbonate therapy for patients with severe metabolic
acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled,
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5. Kasper DL, Hauser SL, Loscalzo J, Longo DL, Jameson JL, Fauci AS. Harrison's Principles of Internal
Medicine Vol 1 20e. McGraw-Hill Education / Medical ; 2018
6. Dufour DR. Laboratory Recognition and Testing in Acid-Base Disorders. Lab Med. 1999; 30 (12):
[Link]: 10.1093/labmed/30.12.776 . | Open in Read by QxMD

7. Walkey AJ, Farber HW, O’Donnell C, Cabral H, Eagan JS, Philippides GJ. The Accuracy of the Central
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8. Chong WH, Saha BK, Medarov BI. Comparing Central Venous Blood Gas to Arterial Blood Gas and
Determining Its Utility in Critically Ill Patients: Narrative Review. Anesth Analg. 2021; 133 (2):
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9. Marano M. Evaluation of the expected ventilatory response to metabolic acidosis in chronic

hemodialysis patients. Hemodial Int. 2017; 22 (2): [Link]: 10.1111/hdi.12602 . | Open in Read
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10. Adrogué HJ, Madias NE. Secondary Responses to Altered Acid-Base Status: The Rules of Engagement. J
Am Soc Nephrol. 2010; 21 (6): [Link]: 10.1681/asn.2009121211 . | Open in Read by QxMD

11. Rastegar A. Use of the DeltaAG/DeltaHCO3- ratio in the diagnosis of mixed acid-base disorders.. J Am
Soc Nephrol. 2007; 18 (9): [Link]: 10.1681/ASN.2006121408 . | Open in Read by QxMD
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High-Anion-Gap Metabolic Acidosis. Am J Kidney Dis. 2011; 58 (3): [Link]:
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13. Tuchscherer J, Rehman H. Metabolic acidosis in toluene snif�ng. CJEM. 2013; 15 (04): [Link]:
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14. Kim G-H, Han JS, Kim YS, Joo KW, Kim S, Lee JS. Evaluation of urine acidi�cation by urine anion gap and
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10.1016/s0272-6386(96)90029-3 . | Open in Read by QxMD

15. Halperin ML, Margolis BL, Robinson LA, Halperin RM, West ML, Bear RA. The urine osmolal gap: a clue
to estimate urine ammonium in "hybrid" types of metabolic acidosis.. Clin Invest Med. 1988; 11 (3):
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16. Lee S, Kang KP, Kang SK. Clinical usefulness of the serum anion gap.. Electrolyte & blood pressure : E &
BP. 2006; 4 (1): [Link]: 10.5049/EBP.2006.4.1.44 . | Open in Read by QxMD

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