ABG INTERPRETATION

Emma Nyakuri.
RN, BNS, MNSc CCN, PGDME
 Objectives
1. Explain Acid-Base Relationship.
2. Explain the clinical causes of Abnormal
ABG’s.
3. Explain the general approach to ABG
Interpretation.

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 Why acid base balance?
If the pH changes whether up or down:

 Protein and enzymes becomes stop functioning.

 Loss of muscles and nerves function.

 Metabolic activities becomes impaired.

 Blood pH below 6.9 or above 7.9 would be life

threatening.

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 Buffering system.
There are two major buffers in the acid-base
balance, these work in pairs

H2CO3 NaHCO3
Carbonic acid base bicarbonate

To alter any acid base imbalance thus maintain

a constant plasma pH.
These buffers are linked to the respiratory and
renal compensatory system.

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By balancing back and forward, a normal
pH is achieved

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 Respiratory mechanism.
 Function of the lungs

 Carbonic acid H2CO3

 Approximately 98% normal metabolites are in the

form
of CO2
CO2 + H2O  H2CO3
Exhalation of excess CO2 . Or retention of CO2.

Adjust body pH by changing rate and depth of

breathing.
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 Renal Mechanism.
 Process of kidneys excreting H+ into the urine and reabsorbing
HCO3- into the blood from the renal tubules;

1) active exchange Na+ for H+ between the tubular

cells and glomerular filtrate.

2) carbonic anhydrase is an enzyme that accelerates

hydration/dehydration CO2 in renal epithelial cells.

 Most effective regulator of pH but slow.

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Normal Acid-base ranges.

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 Related terms.
pH [H+]

PCO2 Partial pressure CO2

PO2 Partial pressure O2

HCO3 Bicarbonate

BE Base excess

SaO2 Oxygen Saturation

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 Acidosis and alkalosis:
There are two abnormalities of acid-base
balance:
1. Acidosis: Too much acid or too little base,
resulting in a decrease in blood pH<7.35
2. Alkalosis: Too much base or too little acid,
resulting in an increase in blood pH>7.45

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Acidosis Alkalosis

pH < 7.35 pH > 7.45

PCO2 > 45 PCO2 < 35

HCO3 < 22 HCO3 > 26

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 Acid-base imbalance.
Acidosis and alkalosis are categorized as metabolic or
respiratory.

Depends on their primary cause.

1. Metabolic acidosis and metabolic alkalosis are
caused by an imbalance acids or bases production
or excretion by the kidneys.
2. Respiratory acidosis and respiratory alkalosis are
caused by amount of carbon dioxide exhalation
due to lung or breathing disorders.

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 Respiratory Acidosis

 Think of CO2 as an acid

 Failure of the lungs to exhale adequate CO2

 pH < 7.35
 PCO2 > 45

 CO2 + H2CO3   pH

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 Cause of Respiratory Acidosis.
1. Lung diseases e.g. COPD, asthma or pneumonia,
Pulmonary edema,ARDS.
2. Airway obstruction e.g. swelling, sputum retention,
foreign bodies.
3. Drugs (anesthetics, sedatives, and narcotics)induce
respiratory depression.
4. Neuromuscular diseases(GBS, MG) impair
breathing effort.
5. Head injury.
6. Chest wall dysfunction or deformities.

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 Respiratory Alkalosis

 Too much CO2 exhaled (hyperventilation)

  PCO2, H2CO3 insufficiency =  pH

 pH > 7.45
 PCO2 < 35 mmHg.

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Cause of Respiratory Alkalosis.
• Hyperventilation (rapid, deep breathing).
• Mechanical overventilation.
• Anxiety.
• Fever.
• Sepsis.

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 Metabolic Acidosis
 Failure of kidney function

  blood HCO3 which results in  availability of renal

tubular HCO3 for H+ excretion.

 pH < 7.35
 HCO3 < 22

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 Cause of Metabolic Acidosis.
• Diabetic Ketoacidosis.
• Starvation.
• Lactic acidosis (anaerobic metabolism during heavy
exercise, hypoxia or CPR).
• Renal failure(acute and chronic).
• Severe diarrhea (excreted large amounts of
bicarbonate).
• Drugs: Methanol or excessive salicylate drug
(aspirin).
• Pancreatic fistula.

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 Metabolic Alkalosis

  plasma bicarbonate

 pH > 7.45
 HCO3 > 26

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 Cause of Metabolic Alkalosis.
• Loss of gastric acid (vomiting, gastric suctioning).
• Long-term diuretics therapy(thiazide, Furosemide).
• Excessive NaHCO3 administration.
• Massive blood transfusion (metabolism of
citrate>>>HCO3).
• Hypercalcemia.
• Acute anemia.

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 Compensation.
• Our body regulates pH by using the opposing
system to balance pH.
• It involves 2 opposing system :
1. Respiratory system.
2. Renal system.

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 Compensation.
• If pH is out of balance because of primary
respiratory disorder.
 Renal system will make the corrections of pH.
• If the renal system is the primary cause of pH
disorder.
 Respiratory system will make the corrections of
pH.
This is called compensation.
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Summary

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 Arterial Blood Gas(ABG) sampling.
• Drawn from artery; Radial(common site), Brachial,
Femoral.
• It is an invasive procedure.
• Caution must be taken with patient on
anticoagulants.

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Steps of ABG sampling.

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 Indication of ABG.
1. Assess respiratory function: PaO2, PaCO2.
2. Assess metabolic status (Acid-Base).
3. Assess any electrolyte imbalance.

Significant deviations from normal pH ranges are

poorly tolerated and may be life threatening.

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Introduce yourself to the patient

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Equipment required for measuring arterial
blood gases

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ABG kit contents

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Locate the radial artery with your index
and middle fingers.

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Remove the cap from the needle

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Prepare to insert the needle

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Remove the needle.

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Place the needle into the bung.

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Remove the needle from the syringe.

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Safely discard the needle into the sharps bin

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Cap the syringe

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Factors affecting ABG results.
 Temperature.
 The presence of air bubbles in ABG
sample.
 Excessive heparin sodium in the sample.
 Clotted sample.
 Time between taken and analysis.
 Site of sampling (venous, arterial)

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Normal ABG ranges.

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 How to Analyze an ABG.
1. PO2 NR = 80 – 100 mmHg

2. pH NR = 7.35 – 7.45
Acidotic <7.35
Alkalotic >7.45

3. PCO2 NR = 35 – 45 mmHg
Acidotic >45
Alkalotic <35

4. HCO3 NR = 22 – 26 mmol/L
Acidotic < 22
Alkalotic > 26
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 Four-step ABG Interpretation
Step 1:

 Examine PaO2
 Determine oxygen status(SPO2).

 Low PaO2 (<80 mmHg) means hypoxia

 Normal range or elevated oxygen means

adequate oxygenation

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Four-step ABG Interpretation
Step 2:

 pH acidosis <7.35

alkalosis >7.45

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 Four-step ABG Interpretation.
Step 3:

 Study PaCO2 & HCO 3

 Respiratory irregularity if PaCO2 abnormal & HCO3 normal

 Metabolic irregularity if HCO3 abnormal & PaCO2 Normal

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 Four-step ABG Interpretation
Step 4:

Determine if there is a compensatory mechanism working

to try to correct the pH.

Look here!
 If have primary respiratory acidosis will have
increasedPaCO2 and decreased pH.
 Compensation occurs when the kidneys retain
HCO3.

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 What are the compensations?
Respiratory acidosis  metabolic alkalosis

Respiratory alkalosis  metabolic acidosis

In respiratory conditions, therefore, the kidneys will

attempt to compensate and visa versa.

In chronic respiratory acidosis (COPD) the kidneys increase

the elimination of H+ and absorb more HCO3. The ABG will
Show NL pH, CO2 and HCO3.
Buffers kick in within minutes. Respiratory compensation
is rapid and starts within minutes and complete within 24
hours. Kidney compensation takes hours and up to 5 days.
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Examples
Get a pen & paper.
Lets do it!

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 Ex.1

pH. 7.30
Respiratory Acidosis
PaCO2 60

HCO3 26

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 Ex.2.
pH 7.50
Respiratory Alkalosis
PaCO2 30

HCO3 22

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 Ex. 3.

pH 7.30
Metabolic Acidosis
PaCO2 40

HCO3 15

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 Ex. 4.

pH 7.50
Metabolic Alkalosis

PCO2 40

HCO3 30

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 Take Home Message.
1. Valuable information can be gained from an ABG as to the
patients physiologic condition
2. Remember that ABG analysis if only part of the patient
assessment.
3. Be systematic with your analysis, start with ABC’s as
always and look for hypoxia, then follow the four steps.
4. A quick assessment of patient oxygenation can be achieved
with a pulse oximeter which measures SPO2.

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It’s not magic understanding
ABG’s, it just takes a little practice!

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Any Questions?

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 References
1. 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.
2. https://www.thoracic.org/professionals/clinical-
resources/critical-care/clinical-education/abgs.php.
3. Irvine, David;ABG Interpretation, A Rough and Dirty
Production.
4. 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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