A brief presentation on ABG analysis, mainly sourced from The ICU Book by Paul Marino

1. ARTERIAL
BLOOD
GAS
ANALYSIS
Chairperson: Dr. Vandana Gogate
Presenters: Dr. Priyanka Gadvi
Dr. Ashwin Haridas
JNMC, Belagavi

2. • Life is a struggle, not against sin, not against money,
power... but against hydrogen ions.
- H.L. Mencken

3. Outline
• What is an ABG?
• Why order one?
• How to take a sample?
• Basics of acid-base balance
• Compensation
• Steps to analyse an ABG report
• Individual disorders

4. What does an ABG
report tell you?
• pH, PaCO2 and HCO3
-
• PaO2 and SaO2
• BE
• Electrolytes like Na+,
K+, Ca2+, Cl-
• RBS

5. Why Order An ABG?
• Aids in establishing a diagnosis
• Helps to guide a treatment plan
• Aids in ventilator management
• Improvement in acid/base manage allows for optimal
function of drugs

6. How to take an ABG sample?
• Consent & patient identification
• Equipment
• Heparinized syringe* with 23G hypodermic needle
• Cotton swabs
• Spirit
• Allen’s test

8. Not what you want to see

9. How to take an ABG sample?
• Radial artery is preferred
• Easily accessible
• Easily compressible
• Good collaterals
• Brachial, femoral and dorsalis pedis may be used
• May be harder to locate and have poor collaterals
• Higher risk of hematoma
• Supinate and extend the wrist, you can use an NS bottle

10. How to take an ABG sample?
• Palpate the radial artery and disinfect the puncture site
• Steady the patient’s hand
• Hold the heparinised syringe like a pen and go at a 45
degree angle
• Syringe should fill by itself
• 1-2 ml should suffice

11. How to take an ABG sample?
• Remove the needle and put pressure on the puncture site for
five minutes or till the bleeding stops
• Remove air bubbles
• Cap and the send the syringe ASAP
• If there is a delay in sending the sample you may keep it in a
cold box with ice packs
• Mention FiO2 while sending the sample
• Dress the puncture site

12. BASICS

13. pH
• pH is the negative common logarithm of the hydrogen ion concentration
• ‘Power of hydrogen’
pH = -log[H+]

14. Logarithm

15. Why is the pH important?
• Enzymes
• Proteins get denatured
• Cardiac conduction
• Neuronal conduction
• Drugs might not act

16. The Balance
•

17. How is the balance maintained?
• Pulmonary regulation
• Changes in the tidal volume and minute ventilation
• pH sensed through arterial chemoreceptors
• Takes place in minutes to hours
• Renal regulation
• Adjusting the amount of HCO3- that is excreted and reabsorbed
• HCO3- reabsorption is equivalent to excreting an H+ ion
• Mainly in the proximal collecting tubule
• Can also synthesise ammonia

18. Renal Regulation

19. How is the balance maintained? contd.
• Buffers
• React immediately
• Carbonate buffer
• Phosphate buffer
• Haemoglobin buffer
• Protein buffers

20. NORMAL VALUES

21. • pH = 7.35 – 7.45
• PaO2 = 80 – 100 mmHg on room air
• HCO3 = 22 – 26 mEq/L
• PaCO2 = 35 – 45 mmHg
• BE = -2 to +2 mEq/L

22. DISORDERS

24. Compensation or the Secondary
Responses

25. Responses to Metabolic Disorders
• Metabolic Acidosis
• PaCO2 = 1.2 * HCO3
• Expected PaCO2 = 40 – (1.2 * (24 – current HCO3)
• Metabolic Alkalosis
• PaCO2 = 0.7 * HCO3
• Expected PaCO2 = 40 + (0.7 * (current HCO3 – 24)

26. Responses to Respiratory Disorders
• Acute respiratory acidosis
• HCO3 = 0.1 * PaCO2
• Acute respiratory alkalosis
• HCO3 = 0.2 * PaCO2
• Neither of the above changes are significant
• For chronic respiratory disorders
• HCO3 = 0.4 * PaCO2
• Expected HCO3 = 24 + [0.4 * (current PaCO2 – 40)] for acidosis
• Expected HCO3 = 24 - [0.4 * (40 – current PaC02)] for alkalosis

27. Rule of same direction
• In simple acid base disorder HCO3 and PaCO2 compensatory changes
are in the same direction
• HCO3 leads to PaCO2
• HCO3 leads to PaCO2
• This will bring pH towards normal although not to normal
• Change in opposite direction or not equal to expected suggestive of
mixed disorder

28. A Stepwise Approach to Acid-Base
Interpretation
• The first stages will allow to identify major acid-base
abnormalities using only three variables: pH, PaCO2, and
HCO3
• The last stage allows to further investigate cases of
metabolic acidosis using commonly measured serum
electrolytes.

29. Stage I: Identify the Primary Acid-
Base Disorder
• In the first stage the PaCO2 and pH are used to determine if
an acid-base disturbance is present and, if so, to identify the
primary acid-base disorder.

30. Stage I
• Rule 1: An acid-base abnormality is present if either the
PaCO2 or the pH is outside the normal range.

31. Stage I
• Rule 2: If the pH and PaCO2 are both abnormal, compare
the directional change.
• If both change in the same direction the primary disorder is
metabolic.
• If both change in opposite directions, the primary acid-base
disorder is respiratory.

32. Stage I
• Rule 3: If either the pH or PaCO2 is normal, there is a mixed
metabolic and respiratory acid-base disorder.
• If the pH is normal, the direction of change in PaCO2
identifies the respiratory disorder
• If the PaCO2 is normal, the direction of change in the pH
identifies the metabolic disorder.

33. Stage II: Evaluate Compensatory
Responses
• The second stage of the approach is for cases where a
primary acid-base disorder has been identified in Stage I.
• If a mixed acid-base disorder was identified in Stage I, go
directly to Stage III
• The goal in Stage II is to determine if the compensatory
responses are adequate and if there are additional acid-base
derangements.

34. Stage II
• Rule 4: If there is a primary metabolic acidosis or alkalosis,
use the measured HCO3 to identify the expected PaCO2.
• If the measured and expected PaCO2 are equivalent, the
condition is fully compensated.
• If the measured PaCO2 is higher than the expected PaCO2,
there is a superimposed respiratory acidosis.
• If the measured PCO2 is less than the expected PCO2, there
is a superimposed respiratory alkalosis.

35. Stage II
• Rule 5: For a primary respiratory disorder, a normal or near-
normal HCO3 indicates that the disorder is acute.
• Rule 6: For a primary respiratory disorder where the HCO3
is abnormal, determine the expected HCO3 for a chronic
respiratory disorder.

36. Stage II: Rule 6
• For a chronic respiratory acidosis, if the HCO3 is lower than
expected, there is an incomplete renal response, and if the
HCO3 is higher than expected, there is a secondary metabolic
alkalosis.
• For a chronic respiratory alkalosis, if the HCO3 is higher than
expected, there is an incomplete renal response, and if the
HCO3 is lower than expected, there is a secondary metabolic
acidosis.

37. Stage III: Use The Anion Gap to
Evaluate Metabolic Acidosis
• The final stage of this approach is for patients with a
metabolic acidosis, and it involves determination of the
anion gap
• It is an estimate of unmeasured anions that helps to identify
the cause of a metabolic acidosis.

38. • A 20 year old primipara with severe protracted vomiting
presents to you in a confused and irritable state. ABG
revealed pH – 7.6, PCO2 -

39. Metabolic Alkalosis
• Characterized by hyperbicarbonatemia (>27 mEq/L) and by an alkalemic
pH (>7.45)
• Factors that generate metabolic alkalosis include vomiting and diuretic
use

40. Metabolic Alkalosis
• Associated with
• Hypokalemia
• Ventricular arrhythmias
• Hypercarbia, although compensation rarely results in PaCO2 >55 mmHg.

41. Metabolic Alkalosis
•Causes
•Saline responsive (urine chloride <15mEq/L)
•Vomiting/Gastric suction
•Diuretics (K+)
•Multiple transfusion
•Saline resistant (urine chloride>20mEq/L)
•Hyperaldosteronism
•Cushing syndrome

42. Metabolic Alkalosis
• Clinical features
• CNS: Neuromuscular excitability, paresthesia, light headache
• CVS : Hypotension,cardiac arrhythmias
• RS: Compensatory hypo-ventilation

43. Metabolic Alkalosis
•Treatment
•Treat the underlying cause
•Saline responsive alkalosis
•Adequate correction of volume, IV isotonic saline
•H1 inhibitor or PPI to decrease gastric secrection
•Avoid exogenous sources of alkali such as NaHCO3 infusion,

44. Metabolic Alkalosis
• If alkalosis is due to diuretics, dose reduction may be
required, KCL supplementation, spironolactone or carbonic
anhydrase inhibitor.
• Saline resistant metabolic acidosis
• Needs specific treatment of underlying causes (surgical treatment of
pitutary tumor or adrenal adenoma in cushing syndrome)
• Supportive treatment such as spiranolactone

45. • Type 1 DM patient who missed his last three doses of
insulin presents with vomiting, abdominal pain and deep
sighing breathing. ABG revealed pH- 7.1, PaO2- 88mmHg,
HCO3- 8 mEq/L, and PaCO2 – 20 mmHg. Na – 140 mEq/L,
Cl – 106 mEq/L and urine ketone bodies were positive.

46. Metabolic Acidosis
• Metabolic acidosis, characterized by hypobicarbonatemia (<21 mEq/L)
and by an acidemic pH (<7.35).
• Metabolic acidosis occurs as a consequence of buffering by bicarbonate
of endogenous or exogenous acid loads or as a consequence of abnormal
external loss

47. Pathophysiology of Metabolic
Acidosis
1. Loss of base HCO3 via GI tract
2. Over production of metabolic acids in the body
3. Ingestion or infusion of acid or potential acids
4. Failure of H+ excretion by kidney

48. Metabolic Acidosis
• Causes of high anion gap metabolic acidosis
• DKA
• Alcoholic ketoacidosis
• Lactic acidosis
• Methanol poisoning
• Salicylate poisoning
• Ethlylene glycol poisoning

49. Metabolic Acidosis
• Causes of normal anion gap acidosis
• Diarrhoea
• RTA
• Acetazolamide
• Pancreatic fistula

50. Metabolic Acidosis
• Clinical features
• RS : Kussumal breathing
• CVS: Arrhythmias, decrease in response to inotropes, secondary
hypotension
• CNS: Headache, confusion, lethargy

51. Metabolic Acidosis - Treatment
• Treat the underling cause
• Alkali therapy
• Correct volume status and electrolyte imbalance

52. Metabolic Acidosis - Treatment
• Alkali therapy
• Amount of HCO3 required = (desired HCO3-actual
HCO3)×0.5× body weight in kg
Carbicarb- generates bicarbonate rather than CO2

53. • Patient with a history of overdosing on her sleeping pills
presents in a drowsy state with sluggish respiration. ABG
revealed pH – 7.1, HCO3 – 28 mEq/L, PaCO2 – 72 mmHg
and PaO2 of 78 mmHg.

54. Respiratory Acidosis
• Characterized by hypercarbia (PaCO2 ≥ 45 mm Hg) and
low pH (<7.35), occurs because of a decrease in minute
alveolar ventilation
• Respiratory acidosis may be either acute, without
compensation by renal or chronic, with compensation
• A reduction in minute ventilation may be due to an overall
decrease an increase in production of carbon dioxide (VCO2)

55. Respiratory Acidosis
• Decreases in minute ventilation may occur
• Central ventilatory depression by drugs
• Central nervous system injury
• Increased work of breathing
• Airway obstruction
• Neuromuscular dysfunction.

56. Respiratory Acidosis
• Increases in dead space volume occur with
• COPD
• Pulmonary embolism
• Consolidations
• Mucus plugs or foreign body

57. Respiratory Acidosis
• Clinical features
• Hypercapnia causes neurological features - anxiety,
headache, confusion, psychosis, hallucination & coma
• Mild to moderate chronic Hypercapnia may cause sleep
disturbance, loss of memory, daytime somnolence,
personality changes, impairment of coordination, tremors
and myoclonic jerks

58. Treatment of Respiratory Acidosis
• Identify and treat the underlying cause
• Establish patent airway to restore OXYGENATION
• Oxygen therapy
• Mechanical ventilation - hyperventilate

59. • A 26 year old male with septic shock is on volume control
ventilation since the last 4 hours. ABG reveals pH – 7.8,
HCO3 – 14 mEq/L, PaCO2 – 22 mmHg, PaO2 – 250mmHg.

60. Respiratory Alkalosis
• Respiratory alkalosis, characterized by hypocarbia (PaCO2 ≤
35 mmHg) and an alkalaemic pH (>7.45)
• Results from an increase in minute ventilation that is
greater than that required to excrete metabolic CO2
production.

61. Respiratory Alkalosis
• Respiratory alkalosis may be a sign of pain, anxiety,
hypoxemia, central nervous system disease or systemic
sepsis
• Development of spontaneous respiratory alkalosis in a
previously normo-carbic patient requires prompt evaluation.

62. Respiratory Alkalosis
• Most frequently encountered acid base disorder, since it
occurs in normal pregnancy and high altitude
• Anxiety or pain induced hyperventilation
• Excessive mechanical ventilation

63. Respiratory Alkalosis
• Clinical features
• Light headache, tingling of the extremities, circumoral
anaesthesia, headache, shortness of breath and chest wall
tightness

64. Respiratory Alkalosis
• Treatment of respiratory alkalosis per se is often not
required.
• The most important steps are recognition and treatment of
the underlying cause.

65. Summary
• ABG analysis requires a thorough understanding of acid-
base physiology
• There are no shortcuts
• Always correlate with the clinical scenario
• Just trying to correct any derangement from the normal
values is not enough
• Correct the underlying cause

66. References
• Marino L. The ICU Book, Fourth Edition, Wolters Kluwer, New Delhi,
2016
• Miller RD, Eriksson LI, Fleisher LA, Wiener-Kronish JP, Young WL,
editors. Miller’s Anesthesia: 8th edition. Philadelphia: Elsevier
Saunders; 2015
• Barash P, Cullen B, Stoelting R, Cahalan M, Stock M, editors. Clinical
Anesthesia: 7th edition. Lippincott Williams and Wilkins, 2013.
• Thomas EJ Healy, Paul RK, Editors. Wylie and Churchill- Davidson’s
A practice of Anaesthesia: 7thEdn, London: Arnold;2003

67. Thank you for listening