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Interpretation of ABGs

Interpretation of Arterial Blood Gases (ABGs)

David A. Kaufman, MD
Chief, Section of Pulmonary, Critical Care & Sleep Medicine
                Bridgeport Hospital-Yale New Haven Health
Assistant Clinical Professor, Yale University School of Medicine
(Section of Pulmonary & Critical Care Medicine)

Introduction:

Interpreting an arterial blood gas (ABG) is a crucial skill for physicians, nurses, respiratory therapists,
and other health care personnel. ABG interpretation is especially important in critically ill patients.

The following six-step process helps ensure a complete interpretation of every ABG. In addition, you
will find tables that list commonly encountered acid-base disorders.

Many methods exist to guide the interpretation of the ABG. This discussion does not include some
methods, such as analysis of base excess or Stewart’s strong ion difference. A summary of these
techniques can be found in some of the suggested articles. It is unclear whether these alternate
methods offer clinically important advantages over the presented approach, which is based on the
“anion gap.”

6-step approach:
Step 1:  Assess the internal consistency of the values using the Henderseon-Hasselbach equation:

[H+] = 24(PaCO2)
           [HCO3-]

If the pH and the [H+] are inconsistent, the ABG is probably not valid.

pH Approximate [H+]
(mmol/L)

7.00 100

7.05 89

7.10 79

7.15 71

7.20 63

7.25 56

7.30 50

7.35 45

7.40 40

7.45 35

7.50 32

7.55 28

7.60 25

7.65 22

Step 2:  Is there alkalemia or acidemia present?

 pH < 7.35  acidemia
pH > 7.45  alkalemia

 This is usually the primary 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

Step 3:  Is the disturbance respiratory or metabolic?  What is the relationship between the direction
of change in the pH and the direction of change in the PaCO 2? In primary respiratory disorders, the
pH and PaCO2 change in opposite directions; in metabolic disorders the pH and PaCO2 change in
the same direction.

Acidosis Respiratory pH ↓  PaCO   ↑

2

Acidosis Metabolic& pH ↓ PaCO   ↓

2

Alkalosis Respiratory pH ↑ PaCO   ↓

2

Alkalosis Metabolic pH ↑ PaCO    ↑

2

Step 4:  Is there appropriate compensation for the primary disturbance?  Usually, compensation
does not return the pH to normal (7.35 – 7.45).

Disorder Expected Correction

compensation factor

Metabolic PaCO  = (1.5 x

2 ±2
acidosis [HCO -]) +8
3

Acute Increase  in  ±3

respiratory [HCO -]= ∆
3

acidosis PaCO /10

2

Chronic Increase  in   

respiratory [HCO -]= 3.5(∆
3

acidosis PaCO /10)

2

(3-5 days)
 Metabolic Increase in PaCO  = 2  
alkalosis 40 + 0.6(∆HCO -) 3

Acute Decrease in   

respiratory [HCO -]= 2(∆
3

alkalosis PaCO /10)

2

Chronic Decrease in   

respiratory [HCO -] = 5(∆
3

alkalosis PaCO /10) to 7(∆

2

PaCO /10)
2

If the observed compensation is not the expected compensation, it is likely that more than one acid-
base disorder is present.

Step 5:  Calculate the anion gap (if a metabolic acidosis exists): AG= [Na+]-( [Cl-] + [HCO 3-] )-12 ± 2

 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

Step 6:  If an increased anion gap is present, assess the relationship between the increase in the
anion gap and the decrease in [HCO3-].

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.)

Table 1:  Characteristics of acid-base disturbances

Disorder pH Primary Compensation

problem

Metabolic ↓ ↓ in ↓ in PaCO 2

acidosis HCO - 3

Metabolic ↑ ↑ in ↑ in PaCO 2

alkalosis HCO - 3

Respiratory ↓ ↑ in ↑ in [HCO -]
3

acidosis PaCO 2

Respiratory ↑ ↓ in ↓ in [HCO -]
3

alkalosis PaCO 2

Table 2:  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

Table 3:  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

Table 4:  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

Table 5:  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

Table 6:  Selected mixed and complex acid-base disturbances

Disorder Characteristics Selected situations

 Cardiac
Respiratory ↓in pH
arrest
acidosis ↓ in HCO 3
 Intoxications
with ↑ in PaCO 2  Multi-organ
metabolic failure
 
acidosis

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

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

 Sepsis
Respiratory pH in normal
 Salicylate
alkalosis range toxicity
with ↓ in PaCO 2  Renal failure
metabolic ↓ in with CHF or
pneumonia
acidosis HCO           
3
  Advanced
 
liver disease

 Uremia or
Metabolic pH in normal
ketoacidosis
acidosis range with
with HCO - normal  
3 vomiting, NG
metabolic suction,
 
diuretics,
alkalosis
etc.

Suggested additional reading:

 Rose, B.D. and T.W. Post. Clinical physiology of acid-base and electrolyte disorders, 5th ed.
New York: McGraw Hill Medical Publishing Division, c2001.
 Fidkowski, C And J. Helstrom. Diagnosing metabolic acidosis in the critically ill: bridging the
anion gap, Stewart and base excess methods. Can J Anesth 2009;56:247-256.
 Adrogué, H.J. and N.E. Madias. Management of life-threatening acid-base disorders—first of
two parts. N Engl J Med 1998;338:26-34.
 Adrogué, H.J. and N.E. Madias. Management of life-threatening acid-base disorders—
second of two parts. N Engl J Med 1998;338:107-111.  

 
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