Laboratory VALUES Home Page

Arterial Blood Gases

Arterial blood gas analysis provides information on the following:
1] Oxygenation of blood through gas exchange in the lungs.  2] Carbon dioxide (CO2) elimination through respiration.  3] Acid-base balance or imbalance in extra-cellular fluid (ECF).

Normal Blood Gases

Arterial Venous
pH 7.35 – 7.45 7.32 – 7.42
Not a gas, but a measurement of acidity or alkalinity, based on the hydrogen (H+) ions present. The pH of a solution is equal to the negative log of the hydrogen ion concentration in that solution: pH = – log [H+].
PaO2 80 to 100 mm Hg. 28 – 48 mm Hg
The partial pressure of oxygen that is dissolved in arterial blood.
New Born – Acceptable range 40-70 mm Hg.  Elderly: Subtract 1 mm Hg from the minimal 80 mm Hg level for every year over 60 years of age:  80 – (age- 60)  (Note: up to age 90)
HCO3  22 to 26 mEq/liter
(21–28 mEq/L)
19 to 25 mEq/liter
The calculated value of the amount of bicarbonate in the bloodstream. Not a blood gas but the anion of carbonic acid.
PaCO2 35-45 mm Hg 38-52 mm Hg
The amount of carbon dioxide dissolved in arterial blood.  Measured.  Partial pressure of arterial CO2.  (Note: Large A= alveolor CO2).  CO2 is called a “volatile acid” because it can combine reversibly with H2O to yield a strongly acidic H+ ion and a weak basic bicarbonate ion (HCO3 -) according to the following equation: CO2 + H2O <— –> H+  +  HCO3
B.E. –2 to +2 mEq/liter

Other sources:  normal reference range is between -5 to +3.

The base excess indicates the amount of excess or insufficient level of bicarbonate in the system.  (A negative base excess indicates a base deficit in the blood.) A negative base excess is equivalent to an acid excess. A value outside of the normal range (-2 to +2 mEq) suggests a metabolic cause for the abnormality.  Calculated value.  The base excess is defined as the amount of H+ ions that would be required to return the pH of the blood to 7.35 if the pCO2 were adjusted to normal.

It can be estimated by the equation:
Base excess = 0.93 (HCO3 – 24.4 + 14.8(pH – 7.4))
Alternatively: Base excess = 0.93×HCO3 + 13.77×pH – 124.58

A base excess > +3 = metabolic alkalosis a base excess < -3 = metabolic acidosis

SaO2 95% to 100% 50 – 70%
The arterial oxygen saturation.

Step by Step ABG Analysis

Step One –   Assessing pH

Look at pH and determine if it is acidotic (<7.35), normal (7.35 – 7.45), or alkalotic (> 7.45).

pH is the best overall indicator in determining the acid-base status of the patient.

Step Two –  Determine respiratory involvement

Review the PaCO2 to assess respiratory involvement [The lungs control the level of carbon dioxide in the arterial blood]. The PaCO2 must be evaluated in light of the arterial pH. That is, if the pH is abnormal, we then ask ourselves: would this observed PaCO2, by itself, cause this pH abnormality? For example, suppose that the pH is below 7.35 (denoting acidosis) and the PaCO2 is above 45 mmHg. According to the Henderson-Hasselbalch equation, a high PaCO2 would indeed cause a low pH (i.e., acidosis). Therefore we know that the respiratory system is at least in part, if not entirely, responsible for the acidosis. On the other hand, if the pH is less than 7.35 and the PaCO2 is in the normal range, then we know that the acidosis must be of non-respiratory (metabolic) origin.

Normal: 35 – 45 mmHg (4.6 – 6 kPa)
Respiratory acidosis: > 45 mmHg (> 6 kPa)
Respiratory alkalosis: <35 mmHg (< 4.6 kPa)

Step Three – Determine metabolic involvement

Review the plasma [HCO3-] or B.E. (Base excess) to determine metabolic involvement (both controlled by non-respiratory factors.)   Each of these components must be evaluated based on the current pH.  If the pH is abnormal, we ask: would this observed [HCO3-] by itself, cause this pH abnormality?  For example, suppose that the pH is less that 7.35 (denoting acidosis) and the [HCO3-] is below 22 mEq/L. Indeed, according to the Henderson-Hasselbalch equation, the low [HCO3-] is consistent with acidosis. Thus, we know that non-respiratory factors are in part, if not entirely, responsible for the acidosis. If [HCO3-] were in the normal range in the presence of this acidosis, then we would know that the acidosis must be of respiratory origin.

Normal: 22 – 26 mEq/L
Metabolic acidosis: <22 mEq/L
Metabolic alkalosis: > 26 mEq/L[Standard Bicarbonate: Calculated value. Similar to the base excess. It is defined as the calculated bicarbonate concentration of the sample corrected to a PCO2 of 5.3kPa (40mmHg).
BE (Base Excess):
Normal: -2 to +2 mmol/L
Metabolic acidosis: < -2 mmol/L

Mild -4 to -6
Moderate -6 to -9
Marked -9 to -13
Severe to < -13

Metabolic alkalosis: > +2 mmol/L

Severe > +13
Marked 9 to 13
Moderate 6 to 9
Mild 4 to 6

[Base excess (BE) is the mmol/L of base that needs to be removed to bring the pH back to normal when PCO2 is corrected to 5.3 kPa or 40 mmHg. During the calculation any change in pH due to the PCO2 of the sample is eliminated, therefore, the base excess reflects only the metabolic component of any disturbance of acid base balance.]

Step Four – Assess for compensation

Look at the pH, PaCO2, and B.E. / HCO3–  to decide whether compensatory mechanisms are at work.

Once the acid-base disorder is identified as respiratory or metabolic, we must look for the degree of compensation that may or may not be occurring. we know that the system not primarily responsible for the acid-base abnormality must assume the responsibility for returning the pH to the normal range. This compensation may be complete (pH is brought into the normal range) or partial (pH is still out of the normal range but is in the process of moving toward the normal range.) In pure respiratory acidosis (high PaCO2, normal [HCO3-], and low pH) we would expect an eventual compensatory increase in plasma [HCO3-] that would work to restore the pH to normal. Similarly, we expect respiratory alkalosis to elicit an eventual compensatory decrease in plasma [HCO3-]. A pure metabolic acidosis (low [HCO3-], normal PaCO2, and a low pH) should elicit a compensatory decrease in PaCO2, and a pure metabolic alkalosis (high [HCO3-], normal PaCO2, and high pH) should cause a compensatory increase in PaCO2. All compensatory responses work to restore the pH to the normal range (7.35 – 7.45)

[ See sample problems near the bottom of the page]

Step Five – Further analysis in cases of METABOLIC ACIDOSIS

Metabolic acidosis:

1] Calculate the anion gap:

Anion gap = Na+ – [CL- + HCO3-]

Difference between calculated serum anions and cations.
Based on the principle of electrical neutrality, the serum concentration of cations (positive ions) should equal the serum concentration of anions (negative ions).
However, serum Na+ ion concentration is higher than the sum of serum Cl- and HCO3- concentration.
Na+ = CL- + HCO3- + unmeasured anions (gap).

Normal anion gap: 12 mmol/L (10 – 14 mmol/L)

2] Based on the anion gap and patient history – review potential causes:

Normal anion gap (hyperchloremic) metabolic acidosis:
Normal anion gap acidosis: The most common causes of normal anion gap acidosis are GI or renal bicarbonate loss and impaired renal acid excretion. Normal anion gap metabolic acidosis is also called hyperchloremic acidosis, because instead of reabsorbing HCO3- with Na, the kidney reabsorbs Cl-.    Many GI secretions are rich in bicarbonate (eg, biliary, pancreatic, and intestinal fluids); loss from diarrhea, tube drainage, or fistulas can cause acidosis. In ureterosigmoidostomy (insertion of ureters into the sigmoid colon after obstruction or cystectomy), the colon secretes and loses bicarbonate in exchange for urinary Cl- and absorbs urinary ammonium, which dissociates into NH3+ and H+.

Loss of HCO3 ions is accompanied by an increase in the serum Cl- concentration. The anion gap remains normal. Disease processes that can lead to normal anion gap (hyperchloremic) acidosis. Useful mnemonic (DURHAM):
a) Diarrhea (HCO3- and water is lost).
b) Ureteral diversion: Urine from the ureter may be diverted to the sigmoid colon due to disease (uretero-colonic fistula) or after bladder surgery. In such an event urinary Cl- is absorbed by the colonic mucosa in exchange for HCO3-, thus increases the gastrointestinal loss of HCO3-.
c) Renal tubular acidosis: dysfunctional renal tubular cells causes an inappropriate wastage of HCO3- and retention of Cl-.
d) Hyperalimentation
e) Acetazolamide
f) Miscellaneous conditions: They include pancreatic fistula, cholestyramine, and calcium chloride (CaCl) ingestion, all of which can increase the gastrointestinal wastage of HCO3-.

Increased anion gap metabolic acidosis
High anion gap acidosis
: The most common causes of a high anion gap metabolic acidosis are ketoacidosis, lactic acidosis, renal failure, and toxic ingestions. Renal failure causes anion gap acidosis by decreased acid excretion and decreased bicarbonate reabsorption. Accumulation of sulfates, phosphates, urate, and hippurate accounts for the high anion gap.   Toxins may have acidic metabolites or trigger lactic acidosis.

In increased anion gap metabolic acidosis, the nonvolatile acids are organic or other inorganic acids (e.g., lactic acid, acetoacetic acid, formic acid, sulphuric acid). The anions of these acids are not Cl- ions. The presence of these acid anions, which are not measured, will cause an increase in the anion gap. Useful mnemonic (MUD PILES):

Methanol poisoning: Methanol is metabolized by alcohol dehydrogenase in the liver to formic acid.
Uremia: In end-stage renal failure in which glomerular filtration rate falls below 10—20 ml/min, acids from protein metabolism are not excreted and accumulate in blood.

Diabetic ketoacidosis: incomplete oxidation of fatty acids causes a build up of beta-hydroxybutyric and acetoactic acids (ketoacids).

Paraldehyde poisoning.

Ischemia: causes lactic acidosis.

Lactic acidosis: Lactic acid is the end product of glucose breakdown if pyruvic acid, the end
product of anaerobic glycolysis, is not oxidized to CO2 and H2O via the Tricarboxylic Acid Cycle.  (Causes: hypoxia, ischemia, hypotension, sepsis).

Ethylene glycol poisoning:  Ethylene is metabolized by alcohol dehydrogenase to oxalic acid in the liver. Usually there is also a coexisting lactic acidosis.

Salicylate poisoning

Causes of common acid-base disturbances:

Metabolic acidosis (non-respiratory)

High anion gap.
Ketoacidosis (diabetes, chronic alcoholism, malnutrition, fasting).
Lactic acidosis.
Renal failure.Toxins metabolized to acids:
Methanol (formic acid)
Ethylene glycol (oxalate)
Paraldehyde (acetate, chloracetate)
SalicylatesToxins causing lactic acidosis
Toluene (initially high gap, subsequent excretion of metabolites normalizes gap)Rhabdomyolysis (rare)

Loss of base –
Normal anion gap (hyperchloremic acidosis)
GI HCO3- loss (diarrhea, ileostomy, colostomy, enteric fistulas, use of ion-exchange resins)

Ureterosigmoidostomy, ureteroileal conduit

Renal HCO3- loss:
Tubulointerstitial renal disease.
Renal tubular acidosis, types 1, 2, 4.
Hyperparathyroidism.Ingestions (acetazolamide, CaCl2, MgSO4) OthersHypoaldosteronism,  Hyperkalemia
Parenteral infusion of arginine, lysine, NH4Cl.
Rapid NaCl infusion.  Toluene (late).Formulas (Compensation):
pCO2 decreases 1.2 for each mEq/L change in HCO3 or  
= last two digits of pHCompensation
Ventilation of the lungs increases through stimulation of central chemoreceptors (H+ ion receptors) in the medulla and peripheral chemoreceptors in the carotid and aortic bodies. Consequently PCO2 falls below normal, and H+ ion concentration falls.  Respiratory compensation increases the acidic pH towards normal. The respiratory system responds to metabolic acidosis quickly and predictably by hyperventilation, so much so that pure metabolic acidosis is seldom seen.

Respiratory Alkalosis:

CNS disorders or lesions, hypoxia [Hypoxia-causing conditions], pulmonary receptor stimulation (asthma, pneumonia, pulmonary edema, PE), Pulmonary vascular disease,  anxiety, fear, pain,  drugs (ASA, theophylline), liver failure, sepsis.

Formulas (Compensation):
Acute: HCO3 decreases 0.22 for every mmHg change in pCO2

Chronic: HCO3 decreases 0.5 for every mmHg change in pCO2

In the presence of respiratory alkalosis the kidneys compensate for the increase in pH by retaining H+ ions and excreting HCO3 – ions. As a result, pH falls towards normal and HCO3 – concentration falls below normal. Renal compensation to respiratory alkalosis is a slow process and the pH does not completely return to normal.

Metabolic (non-resp) alkalosis:

Respiratory Acidosis:

Increase in base
Administration/ingestion of HCO3-
Hypochloremia (HCO3 retained).
Diuretic therapy
Contraction of blood volume.
Loss of fixed acid.
Severe vomiting (loss of H+).
Nasogastric suction.
Hypokalemia – Potassium deficiency.
Corticosteroid administration.Formulas (Compensation):
pCO2 increases 0.6 for each mmol/L change in HCO3 Compensation:
The respiratory response to metabolic alkalosis is hypoventilation. PCO2 rises above normal. Respiratory compensation to metabolic alkalosis is variable and unpredictable. It is unlikely that a conscious patient breathing spontaneously will hypoventilate to a PCO2 > 7.3 kPa (55 mmHg) to compensate for metabolic alkalosis.
Central nervous depression: sedatives etc.
Neuromuscular disease (Guillain-Barr, myasthenia gravis). Trauma.
Severe restrictive disorders: scoliosis.
COPD. Acute airway obstruction: choking etc.  CVA, pneumothorax, chest wall disorder, tumor. Acute and chronic lung disease.Formulas (Compensation):
Acute: HCO3 increases 0.1 for every mmHg change in pCO2- Chronic: HCO3 increases 0.35 for every mmHg change in pCO2 Compensation: In the presence of respiratory acidosis the kidneys compensate for the fall in pH by excreting H+ ions and retaining HCO3 – ions. As a result, pH rises towards normal and HCO3 – concentration rises above normal. Renal compensation (also called metabolic compensation) to respiratory acidosis is a slow process. Compensation is not obvious for several hours and takes 4 days to complete.

Sample Problems – Arterial Blood Gases

Respiratory alkalosis
(chronic alveolar hyperventilation)
 Respiratory acidosis.
Chronic ventilation failure
Uncompensated metabolic alkalosis pH:
(Respiratory acidosis.
acute ventilation failure
uncompensated metabolic alkalosis pH:
Respiratory alkalosis (chronic alveolar hyperventilation) pH:
 Respiratory acidosis.

Chronic ventilation failure

 Respiratory alkalosis.
Chronic alveolar hyperventilation
Uncompensated metabolic acidosis pH:
Respiratory alkalosis (acute alveolar hyperventilation) pH:
Acute Respiratory Acidosis Dx – heroin overdose.
Breathing – shallow, slow.
pH: 7.30
PaCO2: 55 mm/Hg
HCO3-: 27 mEq/L
Chronic Respiratory Acidosis Hx/Dx: 73yo, emphysema, labored breathing at rest.
pH: 7.36
PaCO2: 64 mmHg
HCO3-: 35 mEq/L
Acute Respiratory Alkalosis  Hx/Dx: 77yo, anxiety, psychosomatic origin. Rapid breathing  and slurred speech.
pH: 7.57
PaCO2: 23 mmHg
HCO3-: 21 mEq/L
Compensated Respiratory Alkalosis  Persistent bacterial pneumonia.   Mild cyanosis  and labored breathing.
pH: 7.44
PaCO2: 26 mmHg
HCO3-: 17 mEq/L
PaO2: 53 mmHg
Metabolic Alkalosis 80 yo with heart disease.  RX:   diuretic
pH: 7.58
PaCO2: 48 mmHg
HCO3-: 44 mEq/L
BE: + 19 mEq/L
Serum CL- 95 mEq/L