Arterial Blood Gas Analysis

FK UPH
May26th, 2022
Why Order an ABG?

• Aids in establishing a diagnosis

• Helps to guide treatment
• Aids in ventilator management
• Improvement in acid-base management allows for optimal function
of medications
• Acid-base status may alter electrolyte levels critical to patient status
Puncture sites

• The options
• Radial
• Femoral
• Brachial
• Dorsalis Pedis
• Axillary
Radial artery

• Superficial, easily accessible, easily stabilized.

• Easily compressible with better control of bleeding
• No nerve near by to worry about.
• Collateral arch with ulnar artery minimizes the risk of occlusion.
Allen Test
Contraindication

• Wound or infection over the site.

• Negative Allen test.
• Severe coagulopathies.
• Arterial spasms.
• Severe peripheral vascular disease.
• Arterial grafts.
• AV Shunt.
Taking sample

• Aseptic technique
• Heparinized syringe
• Avoid bubbles
• Analyze immediately
ERRORS

Pre-analytical
•bubbles
•contamination of line with flush solution
•extreme leukocytosis -> pseudohypoxaemia (from excessive in vitro O2
consumption)
•ice storage in polypropylene syringes (rather than glass) -> artefactual PaCO2
elevation

Analytical
•inter-analyser variability
•inadequate heparinization
•non-linearity of Clark electrode when PaO2 > 150mmHg
•lack of appropriate electrolyte temperature
•interference of NO and halothane
•poor quality control
•ABG tensions fluctuate constantly even in stable patients
ABG Interpretation
The Components
• pH 7.35 - 7.45
• PaCO2 35-45 mmHg directly measured
• PaO2 80-100 mmHg
• HCO3- 22-26
• SaO2 95-98% derived
• Base Excess +/-2 mEq/L

• HCO3- derived from the Henderson–Hasselbalch equation

• Base excess (BE) = amount of titratable acid in mmol/L needed to titrate one litre
of blood to a pH of 7.4, with Hb of 150g/L, PCO2 of 40mmHg, @ 37C

• Standard Base Excess (SBE) = same as above but corrected for haemoglobin as Hb
is a buffer of acid (more accurately reflects the BE in the ECF)

• SaO2 = ratio of oxyHb to total Hb

paO2

• Partial pressure (tension) of oxygen

in arterial blood
• N : 80-100 mmHg
HbO2 Dissociation Curve

Age corrected pO2 : 100 – (1/3 X age)

SpO2 90% equivalent to paO2 of 60

mmHg  ICU point
P/F ratio

• Normal pO2 = roughly 5x FiO2

• Ventilated patient PaO2 / FiO2 (with PEEP>=5)
• <300  Mild ARDS
• <200  Moderate
• <100  Severe

• eg: FiO2=100% PO2=90 mmHg

P/F ratio= 90/1 = 90
pO2 100mmHg in room air?
Alveolar gas equation

pAO2 = (FIO2 x (Barometric Pressure – Water Vapour)) – PaCO2 / R

R = respiratory quotient (RQ)

= CO2 Production / O2 Consumption
~ 0.8 (0.7 – 1.0)

Barometric Pressure = 760 mmHg at sea level

Water Vapour in 37 degree C = 47 mmHg
pAO2

Partial pressure O2 in alveoli

For a person breathing room air (FiO2 0.21)

pAO2= piO2 – (paCO2/RQ)
pAO2= [0.21 x (760-47)]-(40/0.8) = 100

Calculated: breathing 100% O2 = 663 mmHg

(Reality: roughly 500 x FiO2)
A-a gradient (A-a DO2)

The difference of pO2 in Alveoli and in arterial blood (pAO2 – paO2)

•Reflects efficiency of gas exchange between alveolus and artery

•N: 10 – 20 mmHg
•Age related: 1/3 x age
•Increases 5 to 7 mmHg for every 10% increase FIO2
• Room Air: A-a gradient = 10 to 20 mmHg
• 100% oxygen: A-a gradient 60 to 70 mmHg
Oxygen Cascade
pH

•7.35 – 7.45 mmHg (7.4 + 0.05)

•Acidaemic or alkalaemic
7.35 7.45
7.25 7.55

6.8 N 7.8

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paCO2

• Partial pressure of CO2 in arterial blood

• 35-45 mmHg ( 40 + 5)
• Volatile acid
• CO2 + H2O H2CO3 HCO3- + H+
HCO3-

• Main buffer to maintain a constant pH

• N: 22-26 mEq/L = mmol/L (24 ± 2)
• Actual bicarbonate: the calculated concentration of HCO3- derived from
pH and pCO2.
• Standard bicarbonate: the calculated concentration of HCO3- if the
sample were at 'standard conditions', that is at a temperature of 37°C,
and a pCO2 of 40mmHg
Base Excess

• Assessment of the metabolic component of acid-base disorders.

• Assuming 'standard conditions', this is the amount of strong acid
required to bring the pH to 7.40
• A negative base excess (acid excess) indicates that the patient has
metabolic acidosis.
• A positive base excess indicates that the patient has metabolic alkalosis.
Buffer

• A buffer keeps something where it should be.

• Prevents swings
• Shields
• Cushions
• Protects
pH buffering agents

• Substance that can reversibly bind hydrogen ions

• Minimize changes in pH
• Extracellular eg: bicarbonate system, haemoglobin, plasma proteins.
(CSF has low buffering capacity)
• Intracellular: proteins, phosphates
INTERPRETATION Step 1

Acidaemia or Alkalaemia?  pH
• < 7.35 – acidaemia
• > 7.45 – alkalaemia

INTERPRETATION Step 2

Is the primary disturbance respiratory or metabolic?

 see pCO2 and HCO3-
 Respiratory  alter pCO2

 Metabolic  alter HCO3 –

 Classification pH pCO2 HCO3 Classification pH pCO2 HCO3

(Acute respiratoric ↓ ↑ N Acute metab acidosis ↓ N ↓

Acidosis)

Chronic metab acidosis ↓/N ↓ ↓

(Chronic respiratoric ↓/N ↑ ↑

Acidosis)
Acute metab alkalosis ↑ N ↑

Chronic metab alkalosis ↑/N ↑ ↑

(Acute respiratoric ↑ ↓ N
alkalosis)

Mixed metab + resp ↓↓ ↑ ↓

acidosis

(Chronic respiratoric ↑/N ↓ ↓

alkalosis)
Mixed metab + resp ↑↑ ↓ ↑
alkalosis
INTERPRETATION Step 3

For a respiratory disturbance, determine whether it is acute or chronic?

• Acute: For every 10 mmHg changes in pCO2

 changes in pH 0.08 unit

• Chronic: For every 10 mmHg changes in pCO2

 changes in pH 0.03
pH 7.31
pCO2 50 Respiratoric acidosis…… Acute!
HCO3 24

pCO2 N: 40 changes: 50 - 40 = 10 mmHg

Estimated pH Acute: 7.4 – 0.08 = 7.32

Chronic: 7.4 – 0.03 = 7.37
Anion Gap

• Difference between calculated serum anions and cations

• Metabolic acidosis with a high AG is associated with the addition of

endogenously or exogenously generated acids.

• Metabolic acidosis with a normal AG is associated with the loss of HCO3

from the kidney or GI tract, or the failure of the kidney to excrete H+.
Unmeasured anions Unmeasured cations

Proteins, mostly albumin Calcium

15 mEq/L 5 mEq/L
Organic acids Potassium
5 mEq/L 4.5 mEq/L
Phosphates Magnesium
2 mEq/L 1.5 mEq/L
Sulfates
1 mEq/L
Totals: 23 mEq/L 11 mEq/L
 INTERPRETATION Step 4

For metabolic acidosis, determine whether an anion gap is increased

Anion Gap = Na+ – (Cl- + HCO3-) Normal: 12 ± 4 mmol/L

A gap > 30 indicates a significant concentration of unmeasured anions

 Organic acids retention: MUDPILES

MUDPILES

Methanol
Uremia
DKA
Propylene glycol
INH
Lactic acidosis
Ethylene glycol
Salicylates
INTERPRETATION Step 5

Determine whether other metabolic disturbaces co-exist with AG

metabolic acidosis

∆ HCO3– = ∆ AG
Corrected HCO3 – measured HCO3 = AG - 12

Corrected HCO3 < 24  co-exist with another metab acidosis

Corrected HCO3 > 24  co-exist with another metab alkalosis
Example:
1. DKA pt, measured HCO3 10, AG 26 

corrected HCO3 – 10 = 26-12

corrected HCO3 = 24 (N)
no secondary metabolic disturbances co-exist

2. DKA pt, vomiting  gastric acid losses (metab alkalosis)

HCO3 18, AG 24

corrected HCO3 – 18 = 24-12

corrected HCO3 = 30 (>N)
 metab acidosis co-exist with metab alkalosis
INTERPRETATION Step 6

Assess the normal compensation by the respiratory system for a metabolic

disturbance.

For a simple metab acidosis, pCO2 will fall within the range predicted by
Winter’s Formula:

expected pCO2 = (1.5 x HCO3-) + (8 ± 2)

(rule of thumb: pCO2 = 2 last digit of pH)

! Compensation to metab alkalosis cannot be predicted because

hypovetilation response to retain CO2 rarely > 50-55 mmHg
Example:

pH: 7.25
HCO3 : 10
Expected pCO2 = (1.5 x 10) + 8 ± 2 = 23 ± 2

21 - 25 : adequate respiratory alkalosis response

>25 : poor compensation (lung or ventilation problem)
ACIDOSIS CORRECTION

NaHCO3 (mmol) = 0.3 X BW X Base Excess

Example: pH 7.1
BE – 15
BW 60 kg

NaHCO3 dose = 0.3 x 60 x 15 = 270 mmol

Half amount = 135 mmol given as slow bolus or drip

Routine administration is not recommended now, because of its possible

unfavorable effects, including paradoxical intracellular acidosis
CASE

• 23 yo male, confusion state. DM since 12 yo. Abdominal pain, vomiting.

High blood glucose, urine keton +++.

ABG
• pH 7.25
• pCO2 25 mmHg
• PO2 68 mmHg
• HCO3 10 mmol/L
• Na 130 mmol/ L
• Cl 80 mmol/L
 pH 7,25
pCO2 25 mmHg

A. Oxygenation and ventilation status PO2 68 mmHg

HCO3 10 mEg/L
Na 130 meq/ L
Cl 80 mEq

• 22 yo  pO2 should be 100-(1/3X22)=93

 hypoxaemia

• A-a DO2= [150-1.25(pCO2)] – pO2

= [ 150 – 1,25 (25) ] – 68
= 51
High A-a gradient  evidence of increase in shunt
 lung problem (Aspiration?)
 pH 7,25
pCO2 25 mmHg

B. Acid – base status PO2 68 mmHg

HCO3 10 mEg/L
Na 130 meq/ L
Cl 80 mEq

1. Asidosis or Alkalosis?
2. Respiratory or metabolic?
3. If respiratory: acute or chronic?
4. If metab acidosis: is there increased anion gap?
5. If anion gap metab acidosis, is there any co-exist metab disturbance?
6. Is there adequate respiratory compensation?
Answer Step 1 – 6 pH 7,25
pCO2 25 mmHg
PO2 68 mmHg
HCO3 10 mEg/L
1. pH 7.25 (<7.35)  Acidosis Na 130 meq/ L
Cl 80 mEq

2. pCO2 low (<35)  not respiratory acidosis

HCO3 low (<22)  metabolic acidosis

3. Skip (not respiratory cause)

4. AG=130 - (80+10) = 40 (>12)  AG increased

5. Corrected HCO3- = 10 + (40-12) = 38 (>24)  metab alkalosis co-exist

6. Expected pCO2 = (1.5 X 10) + (8 + 2) = 23 + 2

(measured pCO2 = 25)  adequate resp compensation
 pH 7,25
pCO2 25 mmHg
PO2 68 mmHg
HCO3 10 mEg/L
Na 130 meq/ L
Cl 80 mEq

Conclusion:

1. Hypoxaemia d/t lung problem (aspiration?)

2. Metab acidosis
- With high anion gap
- With co-exist metab alkalosis
- With adequate respiratory compensation
Respiratory Acidosis

• CNS depression
• Lung and/or pleural disease
• Musculoskeletal disorders
Respiratory Alkalosis

• Catastrophic CNS event (CNS haemorrhage)

• Drugs (salycilates, progesterone)
• Pregnancy 3rd trimester
• Liver cirrhosis
• Anxiety
Anion Gap Acidosis

• Uraemia
• Ketoacidosis
• Alcohol or drugs intoxication (methanol, ethylene glycol, salicylates)
• Lactic acidosis
Non Anion Gap Acidosis

• GI loss of HCO3- (diarrhoea, fistula)

• Renal loss of HCO3-
• Compensation for resp alkalosis
• Carbonic anhydrase inhibitor
• Renal tubular acidosis
• Ureteral diversion
• Other causes: acid infusion, hyperalimentation
Metabolic Alkalosis

• Volume contraction (vomiting, overdiuresis, ascites)

• Hypokalaemia
• Alkali ingestion
• Excess gluco- or mineralocorticoids
Temperature and Gas Partial Pressure
Alpha-stat vs pH-stat

• https://derangedphysiology.com/main/cicm-primary-exam/required-
reading/acid-base-physiology/Chapter%20115/alpha-stat-and-ph-sta
t-models-blood-gas-interpretation

• https://www.anaesthesiamcq.com/AcidBaseBook/ab1_6.php