INTERPRETATION OF ARTERIAL BLOOD GASES (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 Stewarts 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.
Readers are welcome to discuss their observations and share their comments on the ATS
Critical Care Forums.

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 PaCO2? In primary

respiratory disorders, the pH and PaCO2 change inopposite directions; in metabolic

disorders the pH and PaCO2 change in the same direction.

Acidosis

Respiratory

pH

PaCO2

Acidosis

Metabolic
&

pH

PaCO2

Alkalosi
s

Respiratory

pH

PaCO2

Alkalosi
s

Metabolic

pH

PaCO2

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 compensation

Correction
factor

Metabolic acidosis

PaCO2 = (1.5 x [HCO3-]) +8

Acute respiratory acidosis

Increase in [HCO3-]=
PaCO2/10

Chronic respiratory
acidosis (3-5 days)

Increase in [HCO3-]= 3.5(

PaCO2/10)

Metabolic alkalosis

Increase in PaCO2 = 40 +
0.6(HCO3-)

Acute respiratory
alkalosis

Decrease in [HCO3-]= 2(
PaCO2/10)

Chronic respiratory
alkalosis

Decrease in [HCO3-] = 5(
PaCO2/10) to 7( PaCO2/10)

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-] +
[HCO3-] )-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 problem

Compensation

Metabolic acidosis

in HCO3-

in PaCO2

Metabolic alkalosis

in HCO3-

in PaCO2

Respiratory acidosis

in PaCO2

in [HCO3-]

Respiratory alkalosis

in PaCO2

in [HCO3-]

Table 2: Selected etiologies of respiratory acidosis

Airway obstruction
- Upper
- Lower

COPD

asthma

other obstructive lung disease

CNS depression

Sleep disordered breathing (OSA or OHS)

Neuromuscular impairment

Ventilatory restriction

Increased CO2 production: shivering, rigors, seizures, malignant hyperthermia,

hypermetabolism, increased intake of carbohydrates

Incorrect mechanical ventilation settings

Table 3: Selected etiologies of respiratory alkalosis

CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain trauma,
brain tumor, CNS infection

Hypoxemia or hypoxia: lung disease, profound anemia, low FiO2

Stimulation of chest receptors: pulmonary edema, pleural effusion, pneumonia,

pneumothorax, pulmonary embolus

Drugs, hormones: salicylates, catecholamines, medroxyprogesterone, progestins

Pregnancy, liver disease, sepsis, hyperthyroidism

Incorrect mechanical ventilation settings

Table 4: Selected causes of metabolic alkalosis

Hypovolemia with Cl- depletion

GI loss of H+

Vomiting, gastric suction, villous adenoma, diarrhea with

chloride-rich fluid

Renal loss H+

Loop and thiazide diuretics, post-hypercapnia (especially after

institution of mechanical ventilation)

Hypervolemia, Cl- expansion

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

Elevated anion gap:

Methanol intoxication
Uremia
Diabetic ketoacidosisa, alcoholic ketoacidosis, starvation ketoacidosis
Paraldehyde toxicity
Isoniazid
Lactic acidosisa

Type A: tissue ischemia

Type B: Altered cellular metabolism

Ethanolb or ethylene glycolb intoxication

Salicylate intoxication

a
b

Most common causes of metabolic acidosis with an elevated anion gap

Frequently associated with an osmolal gap

Normal anion gap: will have increase in [Cl-]

GI loss of HCO3
Diarrhea, ileostomy, proximal colostomy, ureteral diversion

Renal loss of HCO3

proximal RTA

carbonic anhydrase inhibitor (acetazolamide)

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

in pH
in HCO3
in PaCO2

Cardiac arrest
Intoxications
Multi-organ failure

in pH
in HCO3 in PaCO2

Cirrhosis with diuretics

Pregnancy with vomiting
Over ventilation of COPD

Respiratory acidosis
with metabolic
alkalosis

pH in normal
range
in PaCO2,
in HCO3-

Respiratory alkalosis
with metabolic
acidosis

pH in normal
range
in PaCO2
in HCO3

Respiratory acidosis
with metabolic
acidosis
Respiratory alkalosis
with metabolic
alkalosis

Metabolic acidosis
with metabolic
alkalosis

pH in normal
range
HCO3- normal

COPD with diuretics,

vomiting, NG suction
Severe hypokalemia

Sepsis
Salicylate toxicity
Renal failure with CHF or
pneumonia
Advanced liver disease
Uremia or ketoacidosis with
vomiting, NG suction,
diuretics, etc.

Interpreting Arterial Blood Gases

Understanding Basic Physiology Eases Arterial Blood Gas Analysis

Quiz Yourself
Case 1
A 60 year old man with a history of chronic obstructive pulmonary disease presents to the
emergency department with increasing shortness of breath, pyrexia, and a cough productive
of yellow-green sputum. He is unable to speak in full sentences. His wife says he has been
unwell for two days. On examination, a wheeze can be heard with crackles in the lower
lobes; he has a tachycardia and a bounding pulse. Measurement of arterial blood gas shows
pH 7.2, PaCO2 9.3 kPa (70 mm Hg), HCO3 - 27 mmol/L, and PaO2 7.9 kPa (59 mm Hg). How
would you interpret this?
Answer
This patient has respiratory acidosis (raised carbon dioxide) resulting from an acute
exacerbation of chronic obstructive pulmonary disease, with no apparent compensation. He
is in type II respiratory failure as he is both hypoxaemic and hypercapnic. He should be
treated with bronchodilators, oral steroids, antibiotics, and controlled oxygen.[5] Most patients
can be treated safely with oxygen, but a few with chronic obstructive pulmonary disease rely
on their hypoxic drive to breathe. Take care when giving them oxygen, and remember to
recheck their arterial blood gas levels. If the patient does not improve, he or she may require
assisted ventilation either non-invasively with a mask or invasively after sedation and
endotracheal intubation.
Any condition leading to inadequate ventilation and consequent retention of carbon dioxide
will lead to respiratory acidosis. Causes include:

Airways disorderslife threatening asthma, acute exacerbation of chronic obstructive

pulmonary disease

Drugsopioids, sedatives, muscle relaxants

Central nervous system disordersbrainstem stroke, status epilepticus

Neuromuscular disordersmyasthenia gravis.

Case 2
A six year old boy is taken to the emergency department with vomiting and a decreased level
of consciousness. His breathing is slow and deep (Kussmaul breathing), and he is lethargic
and irritable in response to stimulation. He appears to be dehydratedhis eyes are sunken
and mucous membranes are dryand he has a two week history of polydipsia, polyuria, and
weight loss. Measurement of arterial blood gas shows pH 7.2, PaO2 13.3 kPa (100 mm Hg),
PaCO2 3.3 kPa (25 mm Hg), and HCO3 -10 mmol/L; other results are Na+ 126 mmol/L, K+ 5
mmol/L, and Cl- 95 mmol/L. What is your assessment?
Answer
The boy has diabetes mellitus. These results show that he has metabolic acidosis (low
HCO3 -) with respiratory compensation (low CO2). He has an increased anion gap (26 mm
Hg). Sometimes the anion gap in patients with diabetic ketoacidosis is less than expected as
a result of urinary excretion of ketoacids and metabolic alkalosis associated with the
vomiting.[1]
This patient should be treated in the paediatric intensive care unit. He should be given
intravenous fluids, insulin by infusion, and potassium replacement, and he may need cardiac
monitoring.[6]
Metabolic acidosis has many causes, and the anion gap can be used to help differentiate
between the causes. An increase in anion gap occurs when there is increased production of
organic acids, such as ketones and lactic acid, or reduced excretion of them. Causes include:

Lactic acidosisshock, infection, tissue ischaemia

Ketoacidosisdiabetes mellitus, alcohol abuse

Uraterenal failure

Poisoningsalicylates, biguanides, ethylene glycol, methanol.[7]

There is no increase in anion gap when there is a loss of bicarbonate. It is usually associated
with a concomitant rise in plasma chloride.[1] Causes include:

Renal tubular acidosis

Severe diarrhoea (intestinal secretions below the stomach contain a large amount of
bicarbonate).

Case 3
A 12 year old girl attends the emergency department after falling and hurting her arm. In
triage she is noted to be tachycardic and tachypnoeic. She is given some pain killers. While
waiting to be seen by the doctor, she becomes increasingly hysterical, complaining that she
is still in pain and now experiencing muscle cramps, tingling, and paraesthesia.
Measurement of arterial blood gas shows pH 7.5, PaO2 15.3 kPa (115 mm Hg), PaCO2 3.9
kPa (29 mm Hg), and HCO3 - 24 mmol/L. What does this mean?
Answer
The primary disorder is acute respiratory alkalosis (low CO2) due to the pain and anxiety
causing her to hyperventilate. There has not been time for metabolic compensation. She
should be treated with a stronger analgesic and given reassurance to slow down her
breathing. Some people breathe in and out of a paper bag so that CO2 is reinhaled and
PaCO2 is brought back to normal.
Note that muscle cramps, tingling, and paraesthesia are caused by low serum calcium, which
results from the low H+ ion concentration (increased pH) promoting an increased binding of
calcium to proteins and a reduction in ionised serum calcium.[1]
Respiratory alkalosis results from hyperventilation. There are many causes, such as:

Lung disorderspneumonia, pulmonary embolism, pulmonary oedema

Hypoxiaanaemia, high altitude, right to left cardiac shunt

Central nervous system disordersmeningitis

Psychogenesispain and anxiety

Drugscatecholamines, theophylline, and early stage of salicylates overdose.

Case 4
An 80 year old woman presents with a two day history of persistent vomiting. She is lethargic
and weak and has myalgia. Her mucous membranes are dry and her capillary refill takes >4
seconds. She is diagnosed as having gastroenteritis and dehydration. Measurement of
arterial blood gas shows pH 7.5, PaO2 11.3 kPa (85 mm Hg), PaCO2 6.0 kPa (45 mm Hg),
and HCO3 - 37 mmol/L. What acid-base disorder is shown?
Answer
The primary disorder is metabolic alkalosis (high HCO3 -). As CO2 is the strongest driver of
respiration, it generally will not allow hypoventilation as compensation for metabolic alkalosis.
The patient should be treated with normal saline and an appropriate amount of KCl, which
should be delivered slowly, to expand the extracellular fluid volume.[1] As the body rehydrates,
the kidneys will excrete the excess HCO3 - and correct the alkalosis.
Metabolic alkalosis is most commonly associated with:

Loss of gastric acid from vomiting

Diuretichypokalaemia

Burnsdue to volume depletion

Antacid overdose

Primary hyperaldosteronism.

Adult values for PaO2 and oxygen saturation[4]

PaO2 (kPa)

SaO2 (%)

Normal (range)

13(10.7)

97 (95-100)

Hypoxaemia

<10.7

<95

Mild hypoxaemia

8-10.5

90-94

Moderate hypoxaemia

5.3-7.9

75-89

Severe hypoxaemia

<5.3

<75