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
Normal Blood Gases
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+].
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)
22 to 26 mEq/liter
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.
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
–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
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 =
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
-------------------------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
-4 to -6
-6 to -9
-9 to -13
to < -13
Metabolic alkalosis: > +2 mmol/L
9 to 13
6 to 9
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
1] Calculate the anion gap:
Anion gap = Na+ - [CL- + HCO3-]
Difference between calculated serum anions and
Based on the principle of electrical neutrality, the
serum concentration of cations (positive ions) should
equal the serum concentration of anions (negative
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-.
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
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
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
Diabetic ketoacidosis: incomplete oxidation of fatty acids causes a build up of betahydroxybutyric and acetoactic acids (ketoacids).
Ischemia: causes lactic acidosis.
Lactic acidosis: Lactic acid is the end product of glucose breakdown if pyruvic acid,
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.
Causes of common acid-base disturbances:
Metabolic acidosis (non-respiratory)
High anion gap.
Ketoacidosis (diabetes, chronic
alcoholism, malnutrition, fasting).
Toxins metabolized to acids:
Methanol (formic acid)
Ethylene glycol (oxalate)
Paraldehyde (acetate, chloracetate)
Toxins causing lactic acidosis
Toluene (initially high gap,
subsequent excretion of metabolites
Renal HCO3- loss:
Tubulointerstitial renal disease.
Renal tubular acidosis, types 1, 2, 4.
Ingestions (acetazolamide, CaCl2, MgSO4)
Parenteral infusion of arginine, lysine,
Rapid NaCl infusion. Toluene (late).
pCO2 decreases 1.2 for each mEq/L change
in HCO3 or
pCO2 = last two digits of pH
Ventilation of the lungs increases through
stimulation of central chemoreceptors (H+
ion receptors) in the medulla and peripheral
chemoreceptors in the carotid and aortic
Loss of base bodies. Consequently PCO2 falls below
Normal anion gap (hyperchloremic normal, and H+ ion concentration falls.
Respiratory compensation increases the
GI HCO3- loss (diarrhea, ileostomy, acidic pH towards normal. The respiratory
colostomy, enteric fistulas, use of ion- system responds to metabolic acidosis
quickly and predictably by hyperventilation,
so much so that pure metabolic acidosis is
Ureterosigmoidostomy, ureteroileal seldom seen.
CNS disorders or lesions, hypoxia
pulmonary receptor stimulation
(asthma, pneumonia, pulmonary
edema, PE), Pulmonary vascular
disease, anxiety, fear, pain, drugs
(ASA, theophylline), liver failure,
- Acute: HCO3 decreases 0.22 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.
- Chronic: HCO3 decreases 0.5 for
every mmHg change in pCO2
Increase in base
Administration/ingestion of HCO3Hypochloremia (HCO3 retained).
Contraction of blood volume.
Loss of fixed acid.
Severe vomiting (loss of H+).
Hypokalemia - Potassium deficiency.
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
- Acute: HCO3 increases 0.1 for every
mmHg change in pCO2
pCO2 increases 0.6 for each mmol/L
change in HCO3
- Chronic: HCO3 increases 0.35 for every
mmHg change in pCO2
The respiratory response to metabolic Compensation: In the presence of
alkalosis is hypoventilation. PCO2
respiratory acidosis the kidneys compensate
rises above normal. Respiratory
for the fall in pH by excreting H+ ions and
compensation to metabolic alkalosis retaining HCO3 - ions. As a result, pH rises
is variable and unpredictable. It is
towards normal and HCO3 - concentration
unlikely that a conscious patient
rises above normal. Renal compensation
breathing spontaneously will
(also called metabolic compensation) to
hypoventilate to a PCO2 > 7.3 kPa
respiratory acidosis is a slow process.
(55 mmHg) to compensate for
Compensation is not obvious for several
hours and takes 4 days to complete.
Sample Problems - Arterial Blood Gases
Chronic ventilation failure
acute ventilation failure
Respiratory alkalosis (chronic
Chronic alveolar hyperventilation HCO3:
Chronic ventilation failure
Respiratory alkalosis (acute
Acute Respiratory Acidosis
Dx - heroin overdose.
Breathing - shallow, slow.
PaCO2: 55 mm/Hg
HCO3-: 27 mEq/L
Chronic Respiratory Acidosis
Hx/Dx: 73yo, emphysema, labored
breathing at rest.
PaCO2: 64 mmHg
HCO3-: 35 mEq/L
Acute Respiratory Alkalosis
Hx/Dx: 77yo, anxiety,
psychosomatic origin. Rapid
breathing and slurred speech.
PaCO2: 23 mmHg
HCO3-: 21 mEq/L
Persistent bacterial pneumonia.
Mild cyanosis and labored
PaCO2: 26 mmHg
HCO3-: 17 mEq/L
PaO2: 53 mmHg
80 yo with heart disease. RX:
PaCO2: 48 mmHg
HCO3-: 44 mEq/L
BE: + 19 mEq/L
Serum CL- 95 mEq/L