Why is it Necessary to Order an ABG Analysis?

The utilization of an ABG analysis becomes necessary in view of the

following advantages:

 Aids in establishing diagnosis.

 Guides treatment plan.
 Aids in ventilator management.
 Improvement in acid/base management; allows for optimal
function of medications.
 Acid/base status may alter electrolyte levels critical to a patient’s
status.

Accurate results for an ABG depend on the proper manner of

collecting, handling, and analyzing the specimen. Clinically important
errors may occur at any of the above steps, but ABG measurements
are particularly vulnerable to preanalytic errors. The most common
problems that are encountered include nonarterial samples, air
bubbles in the sample, inadequate or excessive anticoagulant in the
sample, and delayed analysis of a noncooled sample.

Potential Preanalytical Errors

Preanalytical errors are caused at the following stages:

During preparation prior to sampling

 Missing or wrong patient/sample identification;
 Use of the incorrect type or amount of anticoagulant

- dilution due to use of liquid heparin;

- insufficient amount of heparin;

- binding of electrolytes to heparin;

  Inadequate stabilization of the respiratory condition of the
patient; and
 Inadequate removal of flush solution in arterial lines prior to
blood collection

During sampling/handling
 Mixture of venous and arterial blood during puncturing;
 Air bubbles in the sample. Any air bubble in the sample must be
expelled as soon as possible after withdrawing the sample and
before mixing with heparin or before any cooling of the sample
has been done. An air bubble whose relative volume is up to 1%
of the blood in the syringe is a potential source of significant
error and may seriusly affect the pO2 value.
 Insufficient mixing with heparin.

During storage/transport
 Incorrect storage
 Hemolysis of blood cells
General Storage Recommendation
 Do not cool the sample.
 Analyze within 30 min. For samples with high paO2 e.g., shunt or
with high leukocyte or platelet count also analyze within 5 min.
 When analysis is expected to be delayed for more than 30
minutes, use of glass syringes and ice slurry is recommended.

During preparation prior to sample transfer

 Visually inspect the sample for clots.
 Inadequate mixing of sample before analysis.

Insufficient mixing can cause coagulation of the sample. It is

recommended to mix the blood sample thoroughly by inverting the
syringe 10 times and rolling it between the palms.This prevents
stacking (such as coins or plates) of red blood cells.
During anticoagulation

Modern blood gas syringes and capillary tubes are coated with various
types of heparin to prevent coagulation in the sampler and inside the
blood gas analyzer:

 Liquid nonbalanced heparin

 Dry nonbalanced heparin
 Dry electrolyte-balanced heparin (Na+, K+, Ca2+)
 Dry Ca2+-balanced heparin

Other anticoagulants, e.g., citrate and EDTA are both slightly acidic
which increase the risk of pH being falsely lowered.

Liquid heparin

The use of liquid heparin as the anticoagulant causes a dilution of the

sample, i.e., dilutes the plasma, but not the contents of the blood cells.
As a consequence, parameters such as pCO2 and electrolytes are
affected. Only 0.05 mL of heparin is required to anticoagulate 1 mL of
blood. Dead space volume of a standard 5 mL syringe with 1 inch 22
gauge needle is 0.2 mL; filling the syringe dead space with heparin
provides sufficient volume to anticoagulate a 4-mL blood sample. If
smaller sample volumes are obtained or more liquid heparin is left in
the syringe, then the dilution effect will be even greater. The dilution
effect also depends on the hematocrit value. Plasma electrolytes
decrease linearly with the dilution of the plasma along with pCO2,
cGlucose, and ctHb values. pH and pO2 values are relatively unaffected
by dilution. paO2 is only as little as 2% of the O2 physically dissolved in
the plasma, and so the oximetry parameters given in fractions (or %)
will remain unaffected.

Syringes for blood gas analysis can have a wide range of heparin amounts.
The units are typically given as IU/mL (international units of heparin per
milliliter) blood drawn into the syringe. In order to obtain a sufficient final
concentration of heparin in the sample, blood volume recommended on the
syringe must be drawn. Example: a syringe stated to contain 50 IU/mL
when filled with 1.5 mL of blood means that the syringe contains a total 75
IU of dry heparin. If the user draws 2 mL of blood, then the resulting
heparin concentration will be too low and the sample may coagulate. If the
user draws only 1 mL, then the resulting heparin concentration will be
higher than that aimed for, which may lead to producing falsely low
electrolyte results.

Heparin binds to positive ions such as Ca2+, K+, and Na+. Electrolytes bound
to heparin cannot be measured by ion-selective electrodes, and the final
effect will be measurement of falsely low values. The binding effect and the
resulting inaccuracy of results are especially significant for corrected Ca2+.
The use of electrolyte-balanced heparin significantly reduces the binding
effect and the resulting inaccuracy.

The following steps for rapid interpretation of ABG are recommended:

Check for the consistency of ABG

While making an interpretation of an ABG always check for the consistency of the report
by the modified Henderson equation.

([H+][HCO3])÷PaCO2 = 24

The hydrogen ion is calculated by subtracting the two digits after the decimal point of
pH from 80, e.g., if the pH is 7.23 then

[H+] = 80 - 23 = 57

or

[H+] = 10(9-pH)

Table 1
pH value and corresponding H+ ion concentration
pH H+ pH H+

6.70 200 7.40 40

6.75 178 7.45 35

6.80 158 7.50 32

 pH H+ pH H+

6.85 141 7.55 28

6.90 126 7.60 25

6.95 112 7.65 22

7.00 100 7.70 20

7.05 89 7.75 18

7.10 79 7.80 16

7.15 71 7.85 14

7.20 63 7.90 13

7.25 56 7.95 11

7.30 50 8.00 10

7.35 45

Obtain a relevant clinical history

While making an interpretation of anABG, never comment on the ABG

without obtaining a relevant clinical history of the patient, which gives
a clue to the etiology of the given acid–base disorder. For example, a
patient with a history of hypotension, renal failure, uncontrolled
diabetic status, of treatment with drugs such as metformin is likely to
have metabolic acidosis; a patient, with a history of diuretic use,
bicarbonate administration, high-nasogastric aspirate, and vomiting,
is likely to have metabolic alkalosis. Respiratory acidosis would occur
in COPD, muscular weakness, postoperative cases, and opioid
overdose, and respiratory alkalosis is likely to occur in sepsis, hepatic
coma, and pregnancy.

Look at the oxygenation status of the patient

The oxygenation status of the patient is judged by the paO2;however,

never comment on the oxygenation status without knowing the
corresponding FiO2. Calculate the expected paO2 (generally five times
the FiO2).
Based on the expected paO2 classify as mild, moderate, and severe
hypoxia.

Ventilatory status

Look at paCO2.

Acid–base status

Identify the primary disorder by looking at the pH

pH > 7.40–Alkalemia: – 7.40-Acidemia

Then look at paCO2 which is a respiratory acid, whether it is increased,

i.e., >40 (acidosis) or decreased <40 (alkalosis) and if this explains the
change of pH, then it is respiratory disorder; otherwise, see the trend
of change of HCO3-(whether increased in alkalosis or decreased in
acidosis)–if it explains the change of pH, then it is a metabolic
disorder.

 Remember: an acidosis or alkalosis may be present even if the pH is in the

normal range (7.35 – 7.45)
 You will need to check the PaCO2, HCO3- and anion gap

In a normal ABG
 pH and paCO2 move in opposite directions.
 HCO3 and paCO2 move in same direction.
-

1. When the pH and paCO2 change in the same direction (which

normally should not), the primary problem is metabolic; when
pH and paCO2 move in opposite directions and paCO2 is normal,
then the primary problem is respiratory.
2. Mixed Disorder–if HCO3- and paCO2 change in opposite direction
(which they normally should not), then it is a mixed disorder: pH
may be normal with abnormal paCO2 or abnormal pH and
normal paCO2).

If the trend of change in paCO2 and HCO3- is the same, check the percent difference. The
one, with greater % difference, between the two is the one that is the dominant
disorder.
e.g.: pH = 7.25 HCO3-=16 paCO2=60

Here, the pH is acidotic and both paCO2 and HCO3- explain its acidosis: so look at the %
difference

HCO3-% difference = (24 - 16)/24 = 0.33

paCO2% difference = (60 - 40)/40 = 0.5

Therefore, respiratory acidosis as the dominant disorder.

Respiratory disorders

After the primary disorder is established as respiratory, then the following points will
help us to approach further with regard to the respiratory disorder).

 Ratio of rate of change in H+to change in paCO2

 Alveolar arterial oxygen gradient
 Compensation

Ratio of rate of change in H+to change in paCO2

The above ratio of rate of change in H+to change in paCO2 helps in

guiding us to conclude whether the respiratory disorder is acute,
chronic, or acute on chronic. As we have seen, the hydrogen can be
calculated from Table 1 and the change in H+ is calculated by
subtracting the normal H+ from the calculated H+ ion.

ΔH+ ÷ ΔPaCO2
<0.3–Chronic

>0.8–acute

0.3–0.8–acute on chronic
Alveolar Arterial Oxygen Gradient

It is calculated as follows:

PAO2 = PiO2 −(PaCO2 ÷ R)

PiO2 = FiO2 (PB − PH2O)
PAO2 = FiO2 (PB−PH2O)− (PaCO2 ÷ R)

where PAO2, alveolar partial pressure of oxygen; PiO2, partial pressure of inspired
oxygen; FiO2, fraction of inspired oxygen; PB, barometric pressure (760 mmHg at sea
level); PH2O, water vapor pressure (47 mm Hg), PaCO2, partial pressure of carbon
dioxide in blood; R, respiratory quotient assumed to be 0.8.

= FiO2 (760 − 47) − (PaCO2÷0.8)

Hypoxemic respiratory failure can be associated with normal (10–15 mmHg) or increased
alveolar arterial oxygen gradient. If this gradient is <20, then it indicates an extrapulmonary
cause of respiratory failure.
Differentials of extrapulmonary causes of respiratory failure:

 Central nervous system–Respiratory center depression due to

causes such as drug overdose, primary alveolar hypoventilation,
and myxedema.
 Peripheral nervous system–Spinal cord diseases, Guillain-Barré
syndrome, Amyotrophic lateral sclerosis.
 Respiratory muscles–Hypophosphatemia, muscle fatigue,
myasthenia gravis, and polymyositis.
 Chest wall diseases–Ankylosing spondylitis, flail chest,
thoracoplasty.
 Pleural diseases–Restrictive pleuritis
 Upper air way obstruction–Tracheal Stenosis, vocal cord tumor

Compensation
Rules of compensation
 The compensatory response depends upon the proper
functioning of the organ system involved in the response (lungs
or kidneys) and on the severity of acid–base disturbance. For
example, the likelihood of complete compensation in chronic
respiratory acidosis is <15% when paCO2 exceeds 60 mmHg.
 Acute compensation occurs within 6–24 h and chronic within 1–
4 days. Respiratory compensation occurs faster than metabolic
compensation.
 In clinical practice, it is rare to see complete compensation. The
maximum compensatory response in most cases is associated
with only 50–75% return of pH to normal. However, in chronic
respiratory alkalosis, the pH may actually completely return to
normalcy in some cases.

Respiratory acidosis

Acute: [HCO3-] increase by 1 mEq/L for every 10 mmHg increase in

paCO2 above 40.
Chronic: [HCO3-] increase by 3.5 mEq/L for every 10 mmHg increase in
paCO2 above 40.

Respiratory alkalosis

Acute: [HCO3-] decrease by 2 mEq/L for every 10 mmHg decrease in

paCO2 below 40.

Chronic: [HCO3-] decrease by 5 mEq/L for every 10 mmHg decrease in

paCO2 below 40.

Metabolic disorders

In patients with metabolic acidosis, an excess of acid or loss of base is

present. This causes the HCO3-:H2CO3ratio and pH to fall while no
change occurs in pCO2–uncompensated metabolic acidosis.

As a result of compensatory mechanisms, the lungs in the form of

CO2 excrete H2CO3 and the kidneys retain HCO3-. pCO2 falls and HCO3-:
H2CO3 ratio and pH rise toward normal even though concentrations of
HCO3-and H2CO3 are less than normal. This is called compensated
metabolic acidosis and the expected paCO2 is calculated as paCO2 =
[1.5 × HCO3+ 8] ± 2.

Anion gap

Anion gap is the difference between the charges of plasma anions and cations,
calculated from the difference between the routinely measured concentration of the
serum cations (Na+ and K+) and anions (Cl- and HCO3-). Because electroneutrality must
be maintained, the difference reflects the unmeasured ions. Normally, this difference or
the gap is filled by the weak acids (A-) principally albumin, and to a lesser extent
phosphates, sulfates, and lactates.

When the AG is greater than that produced by the albumin and phosphate, other anions
(e.g., lactates and ketones) must be present in higher than normal concentration.
Calculate the anion gap (if a metabolic acidosis exists): AG= [Na+]-( [Cl-] +
[HCO3-] )-12 ± 2

Anion gap = (Na+ + K+) - [Cl- + HCO3

Because of its low and narrow extracellular concentration, K+ is often omitted from the
calculation The normal value ranges from 12 ± 4 when K+ is considered, and 8 ± 4 when
K+ is omitted. Figure shows the alogrithm for the approach to patients with normal AG
acidosis.

The primary problem with AG is its reliance on the use of the normal
range produced by the albumin and to a lesser extent phosphate, the
level of which may be grossly abnormal in critically ill patients.
Because these anions are not strong anions, their charges will be
altered by changes in pH
Serum protein and phosphate

Normal AG = 2{albumin(gm/L)} + 0.5 {phosphate (mg/dL)}

Acid–base status
In Acidemic state - Anion gap decreases by 1-3

In Alkalemic state - Anion gap increases by 2-5

 A normal anion gap is approximately 12 meq/L.

 In patients with hypoalbuminemia, the normal anion gap is lower than 12
meq/L; the “normal” anion gap in patients with hypoalbuminemia is about 2.5
meq/L lower for each 1 gm/dL decrease in the plasma albumin concentration
(for example, a patient with a plasma albumin of 2.0 gm/dL would be
approximately 7 meq/L.)
 If the anion gap is elevated, consider calculating the osmolal gap in
compatible clinical situations.
o Elevation in AG is not explained by an obvious case (DKA, lactic
acidosis, renal failure
o Toxic ingestion is suspected
 OSM gap = measured OSM – (2[Na+] - glucose/18 – BUN/2.8
o The OSM gap should be < 10
If an increased anion gap is present, assess the relationship between the
increase in the anion gap and the decrease in [HCO 3-].
Assess the ratio of the change in the anion gap (∆AG ) to the change in
[HCO3-] (∆[HCO3-]): ∆AG/∆[HCO3-]
This ratio should be between 1.0 and 2.0 if an uncomplicated anion gap metabolic
acidosis is present.
If this ratio falls outside of this range, then another metabolic disorder is
present:
 If ∆AG/∆[HCO3-] < 1.0, then a concurrent non-anion gap metabolic acidosis is
likely to be present.
 If ∆AG/∆[HCO3-] > 2.0, then a concurrent metabolic alkalosis is likely to be
present.
It is important to remember what the expected “normal” anion gap for
your patient should be, by adjusting for hypoalbuminemia (see Step 5,
above.)
Major clinical uses of the anion gap
 For signaling, the presence of a metabolic acidosis and confirm
other findings.
 Helping to differentiate between causes of metabolic acidosis:
High AG versus normal AG metabolic acidosis. In an inorganic
metabolic acidosis (e.g., due to HCl infusion), the infused
Cl- replaces HCO3-, and the AG remains normal. In an organic
acidosis, the lost bicarbonate is replaced by the acid anion which
is not normally measured. This means that the AG is increased.
 Providing assistance in assessing the biochemical severity of the
acidosis and follow the response to treatment
Disorders associated with low serum anion gap
Cause Comments

Laboratory error Most frequent cause of low anion gap

Hypoalbuminemia Second most common cause of low serum anion gap

Level of anion gap correlates with serum concentration of

Multiple myeloma
paraprotein

Halide intoxication Anion gap depends on serum halide concentration

(bromide, lithium, iodide) (low anion gap with lithium ≥4 mEq/L)

more likely in hypercalcemia associated with 10

Hypercalcemia
hyperparathyroidism

Hypermagnesemia Theoretical cause but not documented in literature

Anion gap depends on serum level; occurs with preparation

Polymyxin B
with chloride

Underestimation of serum
Most frequent with hypernatremia or hypertriglyceridemia
sodium

Overestimation of serum chloride Rare with ion selective electrodes

Overestimation of serum
Spurious in serum HCO3 if cells not separated from sera
bicarbonate

Table 3
Description of the species of unmeasured anions, source of origin, and diagnostic
adjuncts in case of high anion gap metabolic acidosis
High serum anion gap
Cause

Comments

Species Origin Diagnostic adjuncts

Renal
Phosphates, sulphates Protein metabolism BUN/creatinine
failure

Ketocido
Ketoacids Fatty acid metabolism Serum/urine ketones
sis
 High serum anion gap
Cause

Comments

Species Origin Diagnostic adjuncts

β Hydroxybutyrate
Diabetic

Alcoholic

Starvatio Acetoacetate
n

Lactic
Lactate Lactate levels
acidosis

Exogeno
us
Salicylate Salicylate Concomitant
poisonin
g

Respiratory and metabolic

Lactate
alkalosis

Ketoacids

In the patients with metabolic alkalosis, there is an excess of base or a loss of acid which
causes the HCO3-:H2CO3 ratio and pH to rise, but with no change occurring in pCO2,
which is called uncompensated metabolic alkalosis. However, the kidney has a large
capacity to excrete excess bicarbonate and so, for sustaining the metabolic alkalosis, the
elevated HCO3-concentration must be maintained through an abnormal renal retention
of HCO3-.

Compensatory respiratory acidosis may be so marked that pCO2 may rise higher than
55 mmHg. Expected paCO2is calculated as paCO2 = [0.7 × HCO3-+ 21] ± 2 or 40 + [0.7
ΔHCO3]. This is called compensated metabolic alkalosis.
Most of the patients with metabolic alkalosis can be treated with chloride ions in the
form of NaCl (saline responsive) rather than KCl (which is preferable). When NaCl is
given, Cl-ions are supplied, and so the blood volume increases and the secretion of
aldosterone in excess decreases. Thus, excessive urinary loss of K+and excessive
reabsorption of HCO3- stops. When metabolic alkalosis is due to the effects of excessive
aldosterone or other mineralocorticoids, the patient does not respond to NaCl (saline
resistant) and requires KCl.

Based on the urinary chloride, metabolic alkalosis is divided into:

Chloride responsive or extracellular volume depletion (urinary chloride < 20)

 Vomiting
 Diuretic
 Post hypercapnic
 Chronic diarrhea
Chloride resistant (urinary chloride > 20)
 Severe potassium depletion
 Mineralocorticoid excess–Primary hypealdosteronism, Cushing’s
Syndrome, Ectopic ACTH
 Secondary hypereldosteronism–Renovascular disease, malignant
hypertension, CHF, cirrhosis
Aproach to mixed disorder

Mixed metabolic disturbances (e.g., high AG from diabetic ketoacidosis

plus normal AG from diarrhea) can be identified using the relationship
between AG and HCO3-, which is called the gap–gap ratio. It is the ratio
of change in anion gap (ΔAG) to change in HCO3- (ΔHCO3-). When
hydrogen ions accumulate in blood, the decrease in serum HCO3- is
equivalent to the increase in AG and the increase in AG
excess/HCO3- deficit ratio is unity, i.e., pure increase in AG metabolic
acidosis. When a normal AG acidosis is present, the ratio approaches
zero. When a mixed acidosis is present (high AG + normal AG), the
gap–gap ratio indicates the relative contribution of each type to the
acidosis. If it is <1, then it suggests that there is a normal AG metabolic
acidosis associated with it and if >2 it suggests that there is associated
metabolic acidosis.
Rules for rapid clinical interpretation of ABG

When required to make a proper approach towards the evaluation of blood gas and
acid–base disturbances in the body, the following scheme is suggested:

1. Look at pH - < 7.40 - Acidosis; > 7.40 - Alkalosis

2. If pH indicates acidosis, then look at paCO2and HCO3-
3. If paCO2is ↑, then it is primary respiratory acidosis
a. To determine whether it is acute or chronic

ΔH+ / ΔpaCO2 <0.3–chronic

>0.8–acute

0.3-0.8–acute on chronic

b. Calculate compensation by the respective methods

Acute: [HCO3-] ↑ by 1 mEq/L for every 10 mmHg ↑ in paCO2

above 40.

Chronic: [HCO3-] ↑ by 3.5 mEq/L for every 10 mmHg ↑ in

paCO2 above 4

4. If paCO2↓ and HCO3- is also ↓→ primary metabolic acidosis

Calculate expected paCO2as follows:

paCO2 = [1.5 × HCO3+ 8] ± 2 metabolic acidosis only

paCO2 < expected paCO2→ concomitant respiratory alkalosis.

paCO2 > expected paCO2→ concomitant respiratory acidosis

5. If HCO3-is ↓, then AG should be examined.

6. If AG is unchanged → then it is hyperchloremic metabolic
acidosis.
7. If AG is ↑ → then it is wide AG acidosis.
8. Check gap-gap ratio

ΔAG/Δ HCO3- = 1, pure increased AG metabolic acidosis

<1 normal anion gap metabolic acidosis

>2 associated metabolic acidosis.

9. If pH indicates alkalosis, then look at HCO3- and paCO2.

10. If paCO2is ↓ → then it is primary respiratory alkalosis.
a. Whether it is acute or chronic (with the same formula as
above)
b. Calculate compensation by the respective methods:

Acute: [HCO3-]↓ by 2 mEq/L for every 10 mmHg

↓ in paCO2below 40.

Chronic: [HCO3-] ↓ by 5 mEq/L for every

10mmHg ↓ in paCO2 below 40

11. If paCO2 ↑ and HCO3- also ↑ → then it is primary metabolic

alkalosis.

Calculate the expected paCO2

paCO2 = [0.7 × HCO3-+ 21] ± 2 Or 40 + [0.7 ΔHCO3] → metabolic

alkalosis only

paCO2 < expected paCO2 → concomitant respiratory alkalosis.

paCO2 > expected paCO2 → concomitant respiratory acidosis

12. Check urinary chloride

if urinary chloride < 20 → chloride responsive or ECV depletion

 if urinary chloride > 20→ chloride resistant

13. If pH is normal ABG may be normal or mixed disorder

a. ↑paCO2 and ↓HCO3-→ respiratory and metabolic acidosis
b. (b) ↓paCO2 and↑ HCO3-→ respiratory and metabolic
alkalosis.

Calculate % difference (ΔHCO3-/HCO3-and ΔpaCO2/paCO2)

to see which is dominant disorder

Selected etiologies of respiratory acidosis

o Airway obstruction
- Upper
- Lower

o COPD
o asthma
o other obstructive lung disease
o CNS depression
o Sleep disordered breathing (OSA or OHS)
o Neuromuscular impairment
o Ventilatory restriction
o Increased CO2 production: shivering, rigors, seizures, malignant
hyperthermia, hypermetabolism, increased intake of carbohydrates
o Incorrect mechanical ventilation settings
Selected etiologies of respiratory alkalosis
o CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain
trauma, brain tumor, CNS infection
o Hypoxemia or hypoxia: lung disease, profound anemia, low FiO2
o Stimulation of chest receptors: pulmonary edema, pleural effusion,
pneumonia, pneumothorax, pulmonary embolus
o Drugs, hormones: salicylates, catecholamines, medroxyprogesterone,
progestins
o Pregnancy, liver disease, sepsis, hyperthyroidism
o Incorrect mechanical ventilation settings
Selected causes of metabolic alkalosis
o Hypovolemia with Cl- depletion
o GI loss of H+
 Vomiting, gastric suction, villous adenoma, diarrhea with
chloride-rich fluid
o Renal loss H+
 Loop and thiazide diuretics, post-hypercapnia (especially after
institution of mechanical ventilation)
o Hypervolemia, Cl- expansion
o Renal loss of H+: edematous states (heart failure, cirrhosis, nephrotic
syndrome), hyperaldosteronism, hypercortisolism, excess ACTH,
 exogenous steroids, hyperreninemia, severe hypokalemia, renal artery
stenosis, bicarbonate administration
Selected etiologies of metabolic acidosis
o Elevated anion gap:
o Methanol intoxication
o Uremia
o Diabetic ketoacidosisa, alcoholic ketoacidosis, starvation ketoacidosis
o Paraldehyde toxicity
o Isoniazid
o Lactic acidosisa
 Type A: tissue ischemia
 Type B: Altered cellular metabolism
o Ethanolb or ethylene glycolb intoxication
o Salicylate intoxication
a
Most common causes of metabolic acidosis with an elevated anion gap
b
Frequently associated with an osmolal gap
o Normal anion gap: will have increase in [Cl-]
o GI loss of HCO3-
 Diarrhea, ileostomy, proximal colostomy, ureteral diversion
o Renal loss of HCO3-
 proximal RTA
 carbonic anhydrase inhibitor (acetazolamide)
o Renal tubular disease
 ATN
 Chronic renal disease
 Distal RTA
 Aldosterone inhibitors or absence
 NaCl infusion, TPN, NH4+ administration
Selected mixed and complex acid-base disturbances

Disorder Characteristics Selected situations

Respiratory ↓in pH  Cardiac arrest

 Intoxications
acidosis with ↓ in HCO3
 Multi-organ
metabolic ↑ in PaCO 2 failure
acidosis

Respiratory ↑in pH  Cirrhosis with

diuretics
alkalosis ↑ in HCO - 3
 Pregnancy with
with ↓ in PaCO 2 vomiting
metabolic  Over
ventilation of
alkalosis
COPD

Respiratory pH in normal  COPD with

diuretics,
acidosis with range vomiting, NG
metabolic ↑ in PaCO , 2 suction
 alkalosis ↑ in HCO -  Severe
3
hypokalemia

Respiratory pH in normal  Sepsis

 Salicylate
alkalosis range toxicity
with ↓ in PaCO 2  Renal failure
metabolic ↓ in HCO3
with CHF or
pneumonia
acidosis
 Advanced liver
disease

Metabolic pH in normal  Uremia or

ketoacidosis
acidosis with range with vomiting,
metabolic HCO - normal
3 NG suction,
alkalosis diuretics, etc.

Examples on ABG interpretation:

Example 1:

A 17-year-old patient presents to A&E complaining of a tight

feeling in their chest, shortness of breath and some tingling
in their fingers and around their mouth. They have no
significant past medical history and are not on any regular
medication. An ABG is performed on the patient who is not
currently receiving any oxygen therapy.

The ABG result shows the following:

 PaO2: 14 (11-13 kPa) || 105 mmHg (82.5 – 97.5

mmHg)
 pH: 7.49 (7.35 – 7.45)
 PaCO2: 3.6 (4.7-6.0 kPa) || 27 mmHg (35.2 – 45
mmHg)
 HCO3-: 24 (22-26 mEq/L)
Answer:

Oxygenation (PaO2)

A PaO2 of 14 on air is at the upper limit of normal, so the

patient is not hypoxic.
pH

A pH of 7.49 is higher than normal and therefore the patient

is alkalotic. The next step is to figure out whether the
respiratory system is contributing the alkalosis (e.g. ↓ CO2).

PaCO2

The CO2 is low, which would be in keeping with an alkalosis,

so we now know the respiratory system is definitely
contributing to the alkalosis, if not the entire cause of it. The
next step is to look at the HCO3– and see if it is also
contributing to the alkalosis.

HCO3–

HCO3– is normal, ruling out a mixed respiratory and metabolic

alkalosis, leaving us with an isolated respiratory alkalosis.

Compensation

There is no evidence of metabolic compensation of the

respiratory alkalosis (which would involve a lowered HCO 3-)
suggesting that this derangement is relatively acute (as
metabolic compensation takes a few days to develop).

Answer

Respiratory alkalosis with no metabolic compensation. The

underlying cause of respiratory alkalosis, in this case, is a
panic attack, with the hyperventilation, peripheral and peri-
oral tingling being classical presenting features.

Example 2:

A 16-year-old female presents to hospital with drowsiness

and dehydration. They have no previous past medical history
and are on no regular medication. An ABG is performed on
room air.
  PaO2: 14 (11-13 kPa) ||105 mmHg (82.5 – 97.5
mmHg)
 pH: 7.33 (7.35 – 7.45)
 PaCO2: 3.0 (4.7-6.0 kPa) || 22.5 mmHg (35.2 – 45
mmHg)
 HCO3-: 17 (22-26 mEq/L)
Answer:

 Oxygenation (PaO2)
 A PaO2 of 14 on air is at the upper limit of
normal, so the patient is not hypoxic.
 pH
 A pH of 7.33 is lower than normal and
therefore the patient is acidotic. The next
step is to figure out whether the respiratory
system is contributing the acidosis (i.e. ↑
CO2).
 PaCO2
 The CO2 is low, which rules out the
respiratory system as the cause of the
acidosis (as we would expect it to be raised
if this was the case). So we now know the
respiratory system is NOT contributing to
the acidosis and this is, therefore, a
metabolic acidosis. The next step is to look
at the HCO3– to confirm this.
 HCO3–
 HCO3– is low in keeping with a metabolic
acidosis.
 Compensation
 We now know that the patient has a
metabolic acidosis and therefore we can
look back at the CO2 to see if the respiratory
system is attempting to compensate for the
metabolic derangement. In this case, there
is evidence of respiratory compensation as
the CO2 has been lowered in an attempt to
normalise the pH. An important point to
recognise here is that although the
derangement in pH seems relatively minor
this should not lead to the assumption that
 the metabolic acidosis is also minor. The
severity of the metabolic acidosis is masked
by the respiratory system’s attempt at
compensating via reduced CO2 levels.
 Answer
 Metabolic acidosis with respiratory
compensation. The underlying cause of the
metabolic acidosis, in this case, is diabetic
ketoacidosis.