Arterial blood gas analysis in clinical practice

1. ABG IN CLINICAL
PRACTICE
Chairperson : Dr Ardaman Singh
Speaker : Dr Ashok Kumar
1

2. What is an ABG
•Arterial Blood Gas
•Drawn from artery- radial, brachial, femoral
•It is an invasive procedure.
•Caution must be taken with patient on
anticoagulants.
•Arterial blood gas analysis is an essential
part of diagnosing and managing the patient’s
oxygenation status, ventilation failure and
acid base balance in medical emergency. 2

3. What is an ABG?
• The Components
– pH / PaCO2 / PaO2 / HCO3 / O2sat / BE
• Desire Ranges
– pH - 7.35 - 7.45
– PaCO2 - 32-45 mmHg
– PaO2 - 72-104 mmHg
– HCO3 - 22-30mEq/L
– O2sat - 95-100%
– Base Excess - +/-2 mEq/L
3

4. COMPONENTS OF THE ABG
pH: Measurement of acidity or alkalinity, based on the hydrogen
(H+)
7.35 – 7.45
Pao2 The partial pressure oxygen that is dissolved in
arterial blood.
72-104 mm Hg.
PCO2: The amount of carbon dioxide dissolved in arterial blood.
32– 45 mmHg
HCO3
: The calculated value of the amount of bicarbonate in the blood
22 – 30mEq/L
B.E:
The base excess indicates the amount of excess or insufficient
level of bicarbonate. -2 to +2mEq/L
SaO2:The arterial oxygen saturation.
>95% 4

5. Why Order an ABG?
• Aids in establishing a diagnosis
• Helps guide treatment plan
• Aids in ventilator management
• Improvement in acid/base management allows
for optimal function of medications
• Acid/base status may alter electrolyte levels
which are critical to patient status.
5

6. Logistics
• When to order an Arterial line --
– Need for continuous BP monitoring
– Need for multiple ABGs
• Where to place --
– Radial
– Femoral
– Brachial
– Dorsalis Pedis
– Axillary
6

7. The Terms
• ACIDS
– Acidemia
– Acidosis
• Respiratory
↑CO2
• Metabolic
↓HCO3
• BASES
– Alkalemia
– Alkalosis
• Respiratory
↓CO2
• Metabolic
↑HCO3
7

8. STEPWISE APPROACH TO
ABG
• Step 1: Acidemic or Alkalemic?
• Step 2: Is the primary disturbance respiratory
or metabolic?
• Step 3. Asses to Pa O2. A value below 80mm Hg
indicates Hypoxemia. For a respiratory
disturbance, determine whether it is acute or
chronic.
• Step 4. For a metabolic acidosis, determine
whether an anion gap is present.
• Step 5. Assess the normal compensation by the
respiratory system for a metabolic disturbance
8

9. STEPS TO AN ABG
INTERPRETATION
• STEP:1
• Assess the pH –
acidotic/alkalotic
• If above 7.45 – alkalotic
• If below 7.35 – acidotic
9

10. • STEP: 2
• Assess the paCO2 level.
• pH decreases below 7.35, the paCO2
should rise.
• If pH rises above 7.45 paCO2 should fall.
• If pH and paCO2 moves in opposite
direction – PRIMARY respiratory
problem.
10

11. • STEP:2
• Assess HCO3 value
• If pH increases the HCO3 should also
increase
• If pH decreases HCO3 should also decrease
• They are moving in the same direction
• PRIMARY problem is metabolic
11

12. Respiratory
acidosis
pH PaCo2 HC03
normal
Respiratory
Alkalosis
normal
Metabolic
Acidosis
normal
Metabolic
Alkalosis
normal
12

13. • STEP: 3
Assess pao2 < 80 mm Hg - Hypoxemia
For a resp. disturbance : acute or chronic
If the change in paco2 is associated with
the change in pH, the disorder is acute.
In chronic process the compensatory
process brings the pH to within the
clinically acceptable range ( 7.30 – 7.50)
13

14. Anion GAP
STEP:4
• It represent maeasured anions in plasma
AG = (Na+ ╋ K+) – (cl- ╋ Hco3-)
(Normally 10-12mmol/L)
• * A change in the pH of 0.08 for each 10
mm Hg pCo2 indicates an ACUTE
condition.
* A change in the pH of 0.03 for each 10
mm Hg pCo2 indicates a CHRONIC
condition.
14

15. BASE EXCESS
• Is a calculated value which estimates the
metabolic component of an acid- base
abnormality.
• It is an estimate of the amount of strong
acid or base needed to correct the met.
component of an acid- base disorder
15

16. Formula
BE=( Patient’s Anion Gap -10 )
In a 50kg person with metabolic
acidosis Hco3 needed for correction is:
Hco3 = 0.3 X body weight X BE
= 0.3 X 50 X10 = 150 mmol/L
16

17. EXPECTED CHANGES IN ACID-BASE DISORDERS
Primary Disorder Expected Changes
Metabolic acidosis PCO2 = 1.5 × HCO3 + (8 ± 2)
Metabolic alkalosis PCO2 = 0.7 × HCO3 + (21 ± 2)
Acute respiratory acidosis delta pH = 0.008 × (PCO2 - 40)
Chronic respiratory acidosis delta pH = 0.003 × (PCO2 - 40)
Acute respiratory alkalosis delta pH = 0.008 × (40 - PCO2)
Chronic respiratory alkalosis delta pH = 0.003 × (40 - PCO2)
17

18. STEP: 5
Determine if there is a compensatory
mechanism working to try to correct the
pH.
ie: if have primary respiratory acidosis
will have increased PaCO2 and decreased
pH. Compensation occurs when the
kidneys retain HCO3.
18

19. Assess the PaCO2
• In an uncompensated state – when the pH
and paCO2 moves in the same direction: the
primary problem is metabolic.
• The decreasing paco2 indicates that the
lungs acting as a buffer response (blowing
of the excess CO2)
• If evidence of compensation is present but
the pH has not been corrected to within the
normal range, this would be described as
metabolic disorder with the partial
respiratory compensation.
19

20. Assess the HCO3
• The pH and the HCO3 moving in the
opposite directions, we would
conclude that the primary disorder is
respiratory and the kidneys acting as
a buffer response: are compensating
by retaining HCO3 to return the pH to
normal range.
20

21. COMPENSATION
• Step 5
• A patient can be uncompensated or
partially compensated or fully
compensated
• pH remains outside the normal range
• pH has returned within normal range-
fully compensated though other
values may be still abnormal
• Be aware that neither the system has
the ability to overcompensate
21

22. COMPENSATED
pH paco2 Hco3
Resp.Acidosis Normal
but<7.40
Resp.Alkalosis Normal
but>7.40
Met. Acidosis Normal
but<7.40
Met. Alkalosis Normal
but>7.40
22

23. ~ PaCO2 – pH Relationship
80 7.20
60 7.30
40 7.40
30 7.50
20 7.60
23

24. 24

25. 25

26. 26

27. PRECAUTIONS
 Excessive Heparin Decreases bicarbonate and
PaCO2
 Large Air bubbles not expelled from sample
PaO2 rises, PaCO2 may fall slightly.
 Fever or Hypothermia, Hyperventilation or
breath holding (Due to anxiety) may lead to
erroneous lab results
 Care must be taken to prevent bleeding
27

28. ACID/BASE BALANCE
 The pH is a measurement of the acidity or alkalinity
of the blood.
 It is inversely proportional to the no. of (H+) in the
blood.
 The normal pH range is 7.35-7.45.
Changes in body system functions that occur in an
acidic state decreases the force of cardiac contractions,
decreases the vascular response to catecholamines,
and a diminished response to the effects and actions of
certain medications.
An alkalotic state interferes with tissue oxygenation
and normal neurological and muscular functioning.
Significant changes in the blood pH above 7.8 or
below 6.8 will interfere with cellular functioning, and if
uncorrected, may lead to death.
28

29. H2O + CO2  H2CO3  HCO3
+ H+
Acid/Base Relationship
29

30. There are two buffers that work in
pairs
H2CO3 NaHCO3
Carbonic acid base bicarbonate
These buffers are linked to the
respiratory and renal compensatory
system
BUFFERS
30

31. THE RESPIRATORY BUFFER
RESPONSE
• The blood pH will change acc.to the
level of H2CO3 present.
• This triggers the lungs to either
increase or decrease the rate and
depth of ventilation
• Activation of the lungs to
compensate for an imbalance starts
to occur within 1-3 minutes
31

32. THE RENAL BUFFER RESPONSE
• The kidneys excrete or retain
bicarbonate(HCO3-).
• If blood pH decreases, the kidneys will
compensate by retaining HCO3
• Renal system may take from hours to
days to correct the imbalance.
32

33. RESPIRATORY ACIDOSIS
• Defined as a pH less than 7.35 with a pco2
greater than 45 mmHg.
• Acidosis –accumulation of co2, combines
with water in the body to produce carbonic
acid, thus lowering the pH of the blood.
• Any condition that results in
hypoventilation can cause respiratory
acidosis.
33

34. RESPIRATORY ACIDOSIS
∀↓PH, ↑CO2, ↓Ventilation
• Causes
– CNS depression(drug,stroke,inf.)
– Parenchymal disease(Emphysema,ARDS)
– Airway disease(obstruction,asthma)
– Musculoskeletal disorders(polio,MG)
– Compensation for metabolic alkalosis
34

35. RESPIRATORY ACIDOSIS
• Acute vs Chronic
– Acute - little kidney involvement. Buffering via
cellular buffering for example
• HCO3↑ 1mmol/Lfor 10mmHg ↑ in CO2
– Chronic –(>24hr) Renal compensation via
synthesis and retention of HCO3 (↓Cl to
balance charges hypochloremia)
• HCO3 ↑4mmol/L for 10mmHg ↑in CO2
35

36. SIGNS & SYMPTOMS OF
RESPIRATORY ACIDOSIS
• Respiratory : Dyspnoea, respiratory distress
and/or shallow respiration.
• CNS : Headache, restlessness and
confusion. If co2 level extremely high
drowsiness and unresponsiveness may be
noted.
• CVS: Tacycardia and dysrhythmias
36

37. MANAGEMENT
• Restoration of alveolar ventilation.
• Causes should be treated rapidly
include pneumothorax, pain and CNS
depression r/t medication.
• Mechanical ventilation.
• Rapid correction of hypercapnia
should be avoided.
37

38. RESPIRATORY ALKALOSIS
∀ ↑pH, ↓CO2, ↑Ventilation
∀ ↓ CO2 , ↓ HCO3 (↑Cl to balance charges
hyperchloremia)
• Causes
– CNS Stimulation(Pain,fever,anxiety,tumour)
– Hypoxia(high altitude,pneumonia,anemia)
– Drugs and harmones(salicylate,pregnancy)
– Chest receptors stimulation(Hemothorex,CCF)
– Sepsis,Hepatic failure
38

39. RESPIRATORY ALKALOSIS
• Acute vs. Chronic
– Acute - ↓HCO3 by 2 mEq/L for every 10mmHg
↓ in PCO2
– Chronic - Ratio increases to 4 mEq/L of HCO3
for every 10mmHg ↓ in PCO2
– Decreased bicarb reabsorption and
decreased ammonium excretion to normalize
pH
39

40. SIGNS & SYMPTOMS
• CNS: Light Headedness, numbness,
tingling, confusion, inability to
concentrate and blurred vision.
• Dysrhythmias and palpitations
• Dry mouth, diaphoresis and tetanic
spasms of the arms and legs.
40

41. MANAGEMENT
• Resolve the underlying problem
• Monitor for respiratory muscle
fatigue
• Hyperventilation syndrome
benefit by rebreath into paper bag
• Antidepressents and sedative
avoided
41

42. METABOLIC ACIDOSIS
∀ ↓Ph(<7.35), ↓HCO3 (<22mEq/L)
• 12-24 hours for complete activation of
respiratory compensation
∀ ↓PCO2 by 1.2mmHg for every 1 mEq/L
↓HCO3
• The degree of compensation is assessed via
the Winter’s Formula
PCO2 = 1.5(HCO3) +8 ± 2
42

43. METABOLIC ACIDOSIS CAUSES
• High anion Gap
metabolic Acidosis
– Lactic Acidosis
– Ketoacidosis
– Toxins(Ethylene
glycol,Methanol,Salicyl
ate)
– Renal failure(Acute
and chr.)
• Non Gap Metabolic
Acidosis
– GI bicarbonate loss
– Renal acidosis(k↑,K↓)
– Drug induced
hyperkalamia
43

44. • K etoacidosis
• U remia
• S epsis
• S alicylate & other drugs
• M ethanol
• A lcohol (Ethanol)
• L actic acidosis
• E thylene glycol
REMEMBER
KUSSMALE
44

45. SIGN & SYMPTOMS
• CNS: Headache, confusion and
restlessness progressing to lethargy,
then stupor or coma.
• CVS: Dysrhythmias
• Kussmaul’s respirations
• Warm, flushed skin as well as nausea
and vomiting
45

46. MANAGEMENT
• Treat the cause
• Hypoxia of any tissue bed will produce
metabolic acids as a result of anaerobic
metabolism even if the pao2 is normal
• Restore tissue perfusion to the hypoxic
tissues
• The use of bicarbonate is indicated for non
metabolizable anion with renal failure or if
pH<7.10
• 50-100meq of NaHCO3 over 30-45 min
• Goal increase HC03 to 10meq/L ,pH to 7.2046

47. METABOLIC ALKALOSIS
• Bicarbonate more than 30m Eq /L with a
pH more than 7.45
• Excess of base /loss of acid can cause
• Ingestion of excess antacids, excess use of
bicarbonate, or use of lactate in dialysis.
• Protracted vomiting, gastric suction,villous
adenoma ,hypokalemia,excess use of
diuretics, high levels of aldosterone.
• ↑PCO2 by 0.75 for every 1mEq/L ↑ in HCO3
47

48. SIGNS/SYMPTOMS
• CNS: Dizziness, lethargy
disorientation, siezures & coma.
• M/S: weakness, muscle twitching,
muscle cramps and tetany.
• Nausea, vomiting and respiratory
depression.
• Cause should treated.
• It is difficult to treat.
48

49. MIXED ACID-BASE
DISORDERS
• Patients may have two or more acid-base disorders
at one time
• Metabolic acidosis and alkalosis both present pH
may normal
• Discrepancy in △AG(prevailing-normal) and △HCO3
(Normal- prevailing) indicate this condition
• DKA with renal failure ,alcoholic ketoacidosis due
to vomiting develop metabolic alkalosis.
49

50. • EXAMPLE :1
• A 45 years old female admitted with the severe attack
of asthma. She has been experiencing increasing
shortness of breath since admission three hours ago.
Her arterial blood gas result is as follows:
• pH : 7.22
• paCO2 : 55
• HCO3 : 25
• Follow the steps
• pH is low – acidosis
• paCO2 is high – in the opposite direction of the pH.
• Hco3 is Normal.
• Respiratory Acidosis
• Need to improve ventilation by oxygen therapy,
mechanical ventilation, pulmonary toilet or by
administering bronchodilators.
50

51. • EXAMPLE 2:
• Mr. D is a 55 years old admitted with
recurring bowel obstruction has been
experiencing intractable vomiting for
the last several hours. his ABG is:
• pH : 7.5
• paCO2 :42
• HCO3 : 33
• Metabolic alkalosis
• Management: IV fluids, measures to
reduce the excess base
51

52. EXAMPLE :3
• Mrs. H is admitted, he is kidney
dialysis patient who has missed his
last 2 appointments at the dialysis
centre his ABG results:
• pH : 7.32
• paCo2 : 32
• HCO3 : 18
• Pao2 : 88
• Partially compensated metabolic
Acidosis 52

53. EXAMPLE: 4
• Mr. K with COPD.his ABG is:
• pH : 7.35
• PaCO2 : 48
• HCO3 : 28
• PaO2 : 90
• Fully compensated Respiratory
Acidosis
53

54. EXAMPLE: 5
• Mr. S is a 53 year old man presented
to ED with the following ABG.
• pH : 7.51
• PaCO2 : 50
• HCO3 : 40
• Pao2 : 40 (21%O2)
• He has metabolic alkalosis
• compensatory respiratory acidosis.
54

55. TAKE HOME MESSAGE:
Valuable information can be gained from an
ABG as to the patients physiologic condition
Remember that ABG analysis only part of the
patient assessment.
Be systematic with your analysis, start with ABC’s
as always and look for hypoxia (which you can
usually treat quickly), then follow the four steps.
A quick assessment of patient oxygenation can be
achieved with a pulse oximeter which measures
SaO2.
55

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