ARTERIAL BLOOD GAS INTERPRETATION

Lenora C. Fernandez, MD FPCCP

OBJECTIVES
 To review the components of an ABG
examination
 To discuss a systematic way of
interpreting the arterial blood gas
 To recognize existing acid base
disorders
 To become familiar with the concept of
anion gap

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COMPONENTS OF AN ABG

pH
 Measurement of acidity or alkalinity,
based on the hydrogen (H+) ions
present.
 Negative log of the free H+ ion
concentration
 The normal range is 7.35 to 7.45

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COMPONENTS OF AN ABG
PaO2
 The partial pressure of oxygen that is dissolved in
arterial blood.
 The normal range is 80 to 100 mm Hg.
SaO2
 The arterial oxygen saturation.
 The normal range is 95% to 100%.

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COMPONENTS OF AN ABG

PaCO2
 The amount of carbon dioxide dissolved
in arterial blood.
 The normal range is 35 to 45 mm Hg.

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COMPONENTS OF AN ABG
HCO3
 The calculated value of the amount of bicarbonate in
the bloodstream.
 The normal range is 22 to 26 mEq/liter (24 + 2)
B.E.
 The base excess indicates the amount of excess or
insufficient level of bicarbonate in the system.
 The normal range is –2 to +2 mEq/liter (0 + 2).
 (A negative base excess indicates a base deficit in the
blood.)

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Which of these ABG indices is
not directly measured?

A. pH
B. pCO2
C. pO2
D. HCO3
E. None of the above

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Steps in ABG Collection

1. Prepare the materials needed.

2. Prepare the syringe with needle.
3. Select the puncture site.
4. Perform the modified Allen test.
5. Collect the sample.
6. Apply pressure on puncture site.
7. Prepare the specimen for transport.

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Which ABG collection error/s will
falsely elevate the pH?

A. Failure to cool blood

B. Dilution with heparin
C. Venous admixture
D. None of the above

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Which ABG collection error/s will
NOT affect the paO2?

A. Failure to cool blood

B. Dilution with heparin
C. Venous admixture
D. Air contamination

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Effects of ABG collection errors on pH,
paCO2 and paO2

ABG COLLECTION ERROR pH

paCO2 paO2

1. Dilution with heparin INC

DEC NC
2. Air contamination INC
DEC INC
3. Venous admixture DEC
INC DEC
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ANALYSIS OF RESULTS
 The arterial blood gas is used to
evaluate both acid-base balance and
oxygenation, each representing
separate conditions. Acid-base
evaluation requires a focus on three of
the reported components: pH, PaCO2
and HCO3.
pH ~ [HCO3] ~ kidney
PaCO2 lungs
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STEP ONE: Acidosis vs. Alkalosis

 Assess the pH to determine if the blood

is within normal range, alkalotic or
acidotic.
 Normal: 7.35 to 7.45

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STEP ONE: Acidosis vs. Alkalosis

pH Degree of impairment

< 7.20 Severe acidemia

7.20-7.29 Moderate

7.30-7.34 Mild acidemia

7.35-7.45 Normal pH

7.46-7.50 Mild alkalemia

7.51-7.55 Moderate

> 7.55 Severe alkalemia

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STEP TWO: Respiratory vs.
Metabolic

Determine the primary disorder.

pH

< 7.4 >7.4

acidemia alkalemia

HCO3 < 24 pCO2 > 40 HCO3 > 24 pCO2 < 40

metabolic respiratory metabolic respiratory
acidosis alkalosis

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STEP TWO: Respiratory vs.
Metabolic

 To check for the primary disorder

determine the degree of deviation of the
values of pCO2 and HCO3 from the
normal
 Respiratory
Change in PCO2/ 40 > change in HCO3/24
 Metabolic
change in HCO3/24 > Change in PCO2/ 40

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SAMPLE
pH 7.22
PaCO2 55
HCO3 25
Step 1: Acidosis
Step 2:
Change in PCO2 = 37.5%
Change in HCO3 = 4.2%
Therefore, respiratory acidosis

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STEP TWO: Respiratory vs.
Metabolic

HINT:
 If pH and PaCO2 are moving in opposite
directions, then the problem is primarily
respiratory in nature
 If they are moving in the same direction, then
the problem is primarily metabolic in nature.

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Classification of Lab Metabolic Acid-
base Component
Classification [BE] [HCO3]
Meq/L Meq/L
Normal 0+2 24 + 2
metabolic
component
Metabolic < -2 < 22
acidosis
Metabolic > +2 > 26
alkalosis

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STEP THREE: COMPENSATED?

 When a patient develops an acid-base imbalance,

the body attempts to compensate.
 Remember that the lungs and the kidneys are the
primary buffer response systems in the body.
 The body tries to overcome either a respiratory or
metabolic dysfunction in an attempt to return the
pH into the normal range.

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 Compensatory Mechanisms
ex. In acidemia

1. Extracellular buffering primarily by HCO3-

(immediate)
2. Respiratory compensation by an increase in
alveolar ventilation
(minutes to hours)
3. Intracellular buffering primarily by proteins and
phosphates
(2 to 4 hours)
4. Renal compensation by an ↑ in H+ excretion and
↑HCO3- reabsorption
(hours to days)
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 URINE

Cl-

Na+

HCO3- PCT

H+ DT

normal Protein-
anion PO4=,SO4=
gap Organic acids
NH4+
H2PO4-
Regulatory Response to Acidemia
 Once
the primary disorder is identified,
compute the expected value of the
compensating buffering system

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Disorder Primary Compensated Degree of
disorder response change

Metabolic Low Low pCO2 ΔpCO2 = 1.2

acidosis HCO3 ΔHCO3

Metabolic High High pCO2 ΔpCO2 = 0.7

alkalosis HCO3 ΔHCO3

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SAMPLE
 77/F
diagnosed case of ESRD who
missed her dialysis session twice
admitted for decreased responsiveness

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SAMPLE
pH 7.28  Step 1: Acidosis
 Step 2: Metabolic
pCO2 32 Δ pCO2/ 40 = 20%
HCO3 15 Δ HCO3/24 = 38%
 Step 3:
Expected compensation
Δ pCO2 = 1.2 ΔHCO3 =
1.2(9) = 10.8
Expected pCO2 = 29.2
therefore uncompensated
metabolic acidosis

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Respiratory Primary Compensated Degree of
acidosis disorder response change

Acute High High HCO3 ΔHCO3 =

PCO2 1/10 ΔPCO2

Chronic High High HCO3 ΔHCO3 =

PCO2 3/10 ΔPCO2

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Respiratory Primary Compensated Degree of
alkalosis disorder response change

Acute Low Low HCO3 ΔHCO3 =

PCO2 2/10 ΔPCO2

Chronic Low Low HCO3 ΔHCO3 =

PCO2 4/10 ΔPCO2

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 58/F chronic COPD admitted for
elective breast surgery

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SAMPLE
 Step 1: Slight Acidosis
 Step 2: Respiratory
Δ pCO2/ 40 = 20%
Δ HCO3/24 = 17%
 Step 3:
Expected compensation
Δ HCO3 = 3/10 Δ
pCO2 = 3/10 (8) = 2.4
Expected HCO3 = 26.4
therefore compensated
respiratory acidosis

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STEP THREE: COMPENSATED
A patient can then be in a fully
compensated, partially compensated,
uncompensated state.

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HINT

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Uncompensated States

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STEP FOUR: ANION GAP?
If with metabolic acidosis, check for other
existing metabolic derangements; compute
for the anion gap

AG = Na – (Cl + HCO3) = normal 10-12

Represents unmeasured anions in the

plasma

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 Na Cl
136 100
Unmeasured anions
HCO3 Protein-
24 PO4=,SO4=
AG 12 Organic
acids
NORMAL
 Na Cl Na Cl Na Cl
136 100 136 100 136 114

HCO3 HCO3 10
24 HCO3 10
AG 12 AG 26 AG 12

NORMAL HIGH GAP NORMAL GAP

METAB METAB
ACIDOSIS ACIDOSIS

Increased when acidosis due to Gap is normal if metab

Increase in fixed acids (HCO3 acts acidosis due to loss of
as buffer so it is depleted and the base (when HCO3 lost,
unmeasured anions increase to Cl- anions increased to
preserve neutrality) maintain Neutrality)
 CAUSES OF METABOLIC
ACIDOSIS
INCREASED ANION GAP NORMAL ANION GAP

• Ketoacidosis • Associated w/ K loss

Diabetic Diarrhea
Alcoholism RTA
Starvation • Interstitial nephritis
• Lactic Acidosis • Early renal failure
• Uremia • Urinary tract obstrxn
• Toxins • Drug-induced

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 Cl-

M- methanol Na+
U- uremia
D- HCO3-
DKA
P- paraldehyde H+
I- iron, INH
L- lactic
acidosis E- High
ethylene glycol anion
Protein-
S- salicylates gap PO4=,SO4=
Organic acids

States of Systemic Acidosis

 Compute for delta delta value to
determine co-existing metabolic
derangements

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For High Gap: DELTA AnionGap/DELTA HCO3

Na Cl Na Cl Na Cl Na Cl
136 100 136 100 136 106 136 94

HCO3 HCO3
HCO3 14 HCO3 8 20
24
AG 12 AG 22 AG 22 AG 22

NORMAL SIMPLE AG COMBINED AG COMBINED AG

METABOLIC & NAG MET. MET. ACIDOSIS
ACIDOSIS ACIDOSIS & MET. ALKALOSIS

∆ AG 10 ∆ AG = 10 ∆ AG = 10
∆ HCO3= 10 ∆ HCO3 16 ∆ HCO3 4
HAGMA

Δ AG = Δ HCO3  pure HAGMA

Δ AG < Δ HCO3  HAGMA + NAGMA
Δ AG > Δ HCO3  HAGMA + metabolic
alkalosis

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For Normal Gap: DELTA Chloride/DELTA HCO3

Na Cl Na Cl Na Cl Na Cl
136 100 134 110 128 110 140 110

HCO3 HCO3 HCO3

24 14 HCO3 8 20
AG 12 AG 10 AG 10 AG 10

NORMAL SIMPLE NAG COMBINED NAG COMBINED NAG

METABOLIC & AG MET. MET. ACIDOSIS
ACIDOSIS ACIDOSIS & MET. ALKALOSIS

∆ Cl 10 ∆ Cl 10 ∆ Cl 10
= = =
∆ HCO3 10 ∆ HCO3 16 ∆ HCO3 4
NAGMA
Δ Cl = Δ HCO3  pure NAGMA
 Δ Cl < Δ HCO3  NAGMA + HAGMA
 Δ Cl > Δ HCO3  NAGMA + metabolic
alkalosis

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Looking at Base excess to check internal
consistency of blood gas data

 For every change in [BE] of 5 meq/l, pH changes

by 0.1 unit. (assume PaCO2 of 40 mmHg)
pH BE (meq/L)
7.00 -20

7.11 -15
7.22 -10
7.33 -5
7.40 0
7.48 +5
7.55 +10
7.60 +15
7.66 +20
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 Case 2
A 30 year old male with a history of
epilepsy has a grand mal seizure.
Laboratory tests taken immediately after
the seizure has stopped reveal:
Arterial pH = 7.14
pCO2 = 45 mm Hg
Plasma [Na+] = 140 meq/L
[K+] = 4.0 meq/L
[Cl-] = 98 meq/L
[HCO3-] = 17 meq/L
AG = 25
 3. Determine the primary disorder.

pH

< 7.4 >7.4

acidemia alkalemia

HCO3 < 24 pCO2 > 40 HCO3 > 24 pCO2 < 40

metabolic respiratory metabolic respiratory
acidosis alkalosis
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 ∆ HCO3 vs. ∆ pCO2
24 40

24 - 17 vs. 45 - 40
24 40

7 > 5
24 40

∴ The primary disorder is a

metabolic acidosis.
 4. Compute for the compensatory
response.

∆ HCO3 = 24 – 17 = 7
∆ pCO2 = 7 x 1.2 = 8.4
Exp. pCO2 = 40 – 8.4 = 31.6 ± 2

Actual pCO2 of 45 is higher than exp. pCO2

∴ This is a mixed metabolic acidosis
and respiratory acidosis.
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 6. Use the delta-deltas to detect
coexisting metabolic disorders.

∆ AG 25 – 12 13
= =
∆ HCO3 24 – 17 7

∴ This is a combined high anion gap

metabolic acidosis and metabolic
alkalosis.
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STEP FIVE: Assess the PO2
For Adults
Classification PaO2 (mmHg)
Hyperoxemia > 100
Normoxemia 80-100
Mild hypoxemia 60-79
Moderate hypoxemia 45-69
Severe hypoxemia < 45

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 Room air, patient < 60 y.o.
– Mild hypoxemia paO2 < 80 mm Hg
– Moderate hypoxemia paO2 < 60 mm Hg
– Severe hypoxemia paO2 < 40 mm Hg
 For each year > 60 y.o., subtract 1 mm Hg for
limits of mild and moderate hypoxemia
 At any age, a paO2 < 40 mm Hg indicates
severe hypoxemia

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 Quantifying pulmonary dysfunction:
Oxygenation Ratio or PF ratio
(PaO2/FiO2)
Pulmonary status Oxygenation ratio
(PaO2/FiO2)

Normal 400-500

Moderate 200-390
Acute lung injury < 300

Substantial pulmonary < 200

dysfunction

Part of ARDS criterion < 200

(equivalent to shunting > 20%)

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Quantifying pulmonary dysfunction:
Alveolar-arteriolar oxygen tension
gradient
 PAO2 = ideal/alveolar O2 tension
 P(A-a)O2
- quantitates efficiency of oxygen loading
- increased in shunts, V/Q mismatch
- Normal: < 60 yo, 10 mmHg (upper limit 20)
> 60 yo, upper limit 35 mmHg
 When FiO2 < 60%,
PAO2 = PiO2 – 1.2(PaCO2)
PiO2 = (PB-PH2O) x FiO2
at sea level & room air, PiO2 ~ 150 mmHg or
PiO2 = (760-47 mmHg) X 0.21
 Limitations:
– Not helpful when changing FiO2
– Above FiO2 60%, didn’t change anymore
– Not a guide for oxygenation

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REVIEW
 Step 1: Acidosis vs Alkalosis
 Step 2: Respiratory vs. Metabolic
 Step 3: Compensated?
 Step 4: Anion Gap?
 Step 5: Oxygenation

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QUESTIONS ?
THANK YOU!

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BUFFERS IN THE BLOOD
 Extracellular fluid buffers
– Plasma HCO3
– Plasma proteins
– Inorganic phosphates
 Intracellular fluid buffers
– HCO3
– Hb
– Oxyhemoglobin
– Inorganic phosphates
– Organic phosphates
 HCO3 buffering system (open system) responsible
>50% buffering

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