Approach to arterial blood gas (ABG) analysis

1. ABG
Dr. Rohit Saini

2. Definition
• It is a diagnostic procedure in which a blood is
obtained from an artery by direct puncture or
through indwelling arterial catheter.

3. Information
• Basic physiologic processes:
1. Alveolar ventilation (PaCO2)
2. Oxygenation (PaO2, SaO2)
3. Acid base balance

4. Indications
1. To assess ventilatory status, oxygenation, acid base
balance
2. Oxygen carrying capacity of blood
3. Aids in diagnoses / etiology
4. To assess patients response (MV, circulatory
intervention)
5. Electrolyte level

5. Contraindications
1. Local site infection
2. Absence of arterial pulse
3. Negative Allen’s or modified Allen’s test
4. Coagulopathies
5. Anticoagulants/thrombolytics
6. Peripheral vascular disease
7. Arterial grafts

6. Sites
• Radial artery (non dominant hand) – most preferred
Other sites:
• Brachial
• Femoral
• Dorsalis pedis
• Posterior tibial artery (pediatric)

7. Complications
• Bruise / hematoma
• Spasms
• Aneurysm
• Nerve damage
• Infection
• Pain
• Distal ischemia
• Anaphylaxis to LA

8. Sources of error
• Preanalytic errors (MC) – collection, storage and
transportation
• Nonarterial sample
• Air bubbles
• Inadequate or excessive anticoagulant
• Delayed analysis of uncooled sample

10. Normal values
• pH : 7.35 – 7.45
• PaO2 : 80 – 100 mmHg
• PCO2 : 35 – 45 mmHg
• HCO3 : 22 – 28 mEq/L
• SaO2 : 94 – 100 %
• Base excess : +/- 2

11. Components of ABG
1. pH – measures hydrogen concentration in blood,
shows acidity or alkalinity
2. pCO2 – partial pressure of CO2 dissolved in blood,
shows respiratory parameter
3. pO2 – partial pressure of O2 dissolved in blood
4. HCO3 – reflects kidney’s ability to retain or excrete
bicarbonate, shows metabolic parameter

12. Components of ABG
5. SaO2 - measures the percentage of Hb combined
with O2
6. Base excess - amount of acid or base (in mmol)
required to titrate 1 L of blood to pH 7.4, at 37◦C and
pCO2 of 40mmHg.

13. Abnormal values

14. Methods to analyse
• Two methods:
1. Classic / traditional approach – bicarbonate based
2. Stewart approach – non bicarbonate based

15. Classic approach
• Henderson Hasselbalch equation:
• pKa – dissociation constant (6.1)
• Conjugate base – bicarbonate
• Acid – pCO2

16. Classic approach
• Based on this approach – 6 primary disorders:
1. Metabolic acidosis (high or normal AG)
2. Metabolic alkalosis
3. Acute and chronic respiratory acidosis
4. Acute and chronic respiratory alkalosis

17. Stewart approach
• Non bicarbonate based
• Variables :
1. Respiratory – pCO2
2. Metabolic – strong ion difference (SID) and total
weak acids (ATOT)
 SID : [cations]-[anions]
 ATOT : represent all non bicarbonate buffer

20. Step 2

21. Compensation
• Maintainance of acid base balance
• Goal : to return pH back to normal
• Accomplished by buffer system (by changing H+)
• Respiratory compensation faster than metabolic
• No complete compensation (only 50 – 75%)

25. Expected compensation
• Metabolic acidosis : 1-1.3 pCO2↓ (1 HCO3 ↓)
• Metabolic alkalosis : 0.5-0.7 pCO2↑ (1 HCO3 ↑)
• Respiratory acidosis :
o Acute – 1 HCO3↑ (10 pCO2 ↑)
o Chronic – 3.5 HCO3 ↑ (10 pCO2 ↑)
• Respiratory alkalosis :
o Acute – 2 HCO3 ↓ (10 pCO2 ↓)
o Chronic – 5 HCO3 ↓ (10 pCO2 ↓)

26. Anion gap
• Difference between measured cations and measured
anions :
[Na + K] – [Cl + HCO3]
Normal value : 14-16
Or
[Na] – [Cl + HCO3]
Normal value : 8 -12
• Unmeasured anions : significant proportion e.g –
proteins, phosphates, sulfates, lactates, ketones etc.

27. High anion gap acidosis
Mnemonic – KULT
• Ketoacidosis : Diabetic, starvation, alcoholic
• Uremia : renal failure
• Lactic acidosis
• Toxins : ethylene glycol, salicylates

28. Normal anion gap acidosis
Hypokalemic :-
• GI loss HCO3 : diarrhea, ileostomy
• Renal loss HCO3 : RTA (type II)
Normokalemic / Hyperkalemic :-
• RTA (type I and IV)
• Hypoaldosteronism
• Acute tubular necrosis

29. Approach to normal AG acidosis

30. Low anion gap acidosis
• Hypoalbuminemia (MC)
• Paraproteinemia (multiple myeloma)
• Spurious hyponatremia
• Hypermagnesemia
• Hypercalcemia
Corrected anion gap :
observed AG + 2.5X(normal alb. – observed alb.)

31. Metabolic alkalosis
• Loss of H+ ions (vomiting, diuretics)
• Increased reabsorption of bicarbonate (low
intravascular volume)
• Alkali administration in renal failure (Ringer’s lactate)
• Hyperaldosteronism

32. Respiratory acidosis
Any condition causes hypoventilation:
• Airway / lung disease
• CNS depression – trauma, sedatives, narcotics
• Neuromuscular disease – spinal cord injury, NMD
residual effect, GBS etc
• Ventilation restriction – pain, obesity, chest wall
injury/deformity

33. Respiratory alkalosis
Any condition causes hyperventilation:
• CNS stimulation – fever, pain, CVA
• Hypoxemia – pulmonary edema, pneumonia
• Drugs – catecholamines, salicylates
• Misc. – sepsis, pregnancy
• Psychologic – anxiety, fear

34. Delta gap
Delta gap : to rule out co existence of 2 acid base disorders

35. Correlate with patient’s clinical
status is more important
Treat patient, not ABG.