2. 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
3. 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%.
4. COMPONENTS OF AN ABG
PaCO2
The amount of carbon dioxide dissolved
in arterial blood.
Normal range is 35 to 45 mm Hg (40 + 5)
5. 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.)
6. Effects of ABG collection errors on
pH, paCO2 and paO2
ABG COLLECTION
ERROR
pH paCO2 paO2
Dilution with heparin
Air contamination
Venous admixture
Failure to cool
blood
7. STEPWISE APPROACH
Obtain clues from the clinical setting
Determine primary disorder
Check the compensatory response
Calculate the anion gap
Calculate the delta/deltas
Identify specific etiologies for the acid-base
disorder
Prescribe treatment
9. CLUES FROM CLINICAL SETTING
HIGH ANION GAP METABOLIC ACIDOSIS
HIGH AG, normal Cl
Lactic acidosis
Ketoacidosis
Ingestions; alcohol, INH, methanol, ethylene glycol
Renal failure
Massive rhabdomyolysis
10. CLUES FROM CLINICAL SETTING
NORMAL ANION GAP METABOLIC ACIDOSIS
Normal AG, HIGH Cl
Diarrhea- GI loss of HCO3
RTA- renal loss of HCO3
Ingestion of ammonium chloride or
hyperalimentation fluids
Acetazolamide therapy
11. CLUES FROM CLINICAL SETTING
METABOLIC ALKALOSIS
(urine Cl < 10 mEq/d)
Vomiting
Remote diuretic use
Post hypercapnea
Chronic diarrhea
Cystic fibrosis
12. CLUES FROM CLINICAL SETTING
METABOLIC ALKALOSIS
(urine Cl > 10 mEq/d)
Bartter’s syndrome
Severe potassium depletion
Current diuretic use
Hypercalcemia
Hyperaldosteronism
Cushing’s syndrome
22. Characteristics of primary
acid base disturbances
Disorder pH Primary
Disturbance
Compensatory
Response
Metabolic
Acidosis
Decreased Dec HCO3 Dec pCO2
Metabolic
Alkalosis
Increased Inc HCO3 Inc pCO2
Respiratory
Acidosis
Decreased Inc pCO2 Inc HCO3
Respiratory
Alkalosis
Increased Dec pCO2 Dec HCO3
23. Disorder Primary
abnormality
Secondary
response
Metabolic acidosis Loss of HCO3 or
gain H+
Hyperventilation
Metabolic alkalosis Gain of HCO3 or
lose H+
hypoventilation
Resp acidosis hypoventilation HCO3 generation-
kidneys
Resp alkalosis hyperventilation HCO3
consumption
24. 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
25. DETERMINE PRIMARY DISORDER
Check the trend of the pH, HCO3, pCO2
The change that produces the pH is the primary
disorder
pH = 7.25 HCO3 = 12 pCO2 = 30
ACIDOSIS ACIDOSIS ALKALOSIS
METABOLIC ACIDOSIS
26. DETERMINE PRIMARY DISORDER
Check the trend of the pH, HCO3, pCO2
The change that produces the pH is the primary
disorder
pH = 7.25 HCO3 = 28 pCO2 = 60
ACIDOSIS ALKALOSIS ACIDOSIS
RESPIRATORY ACIDOSIS
27. DETERMINE PRIMARY DISORDER
Check the trend of the pH, HCO3, pCO2
The change that produces the pH is the primary
disorder
pH = 7.55 HCO3 = 19 pCO2 = 20
ALKALOSIS ACIDOSIS ALKALOSIS
RESPIRATORY ALKALOSIS
28. DETERMINE PRIMARY DISORDER
If the trend is the same, check the percent
difference
The bigger %difference is the 10 disorder
pH = 7.25 HCO3 = 16 pCO2 = 60
ACIDOSIS ACIDOSIS ACIDOSIS
RESPIRATORY ACIDOSIS
(16-24)/24 = 0.33 (60-40)/40 = 0.5
29. DETERMINE PRIMARY DISORDER
If the trend is the same, check the percent
difference
The bigger %difference is the 10 disorder
pH = 7.55 HCO3 = 38 pCO2 = 30
ALKALOSIS ALKALOSIS ALKALOSIS
METABOLIC ALKALOSIS
(38-24)/24 = 0.58 (30-40)/40 = 0.25
31. COMPENSATED?
When a patient develops an acid-
base imbalance, the body attempts
to compensate.
Primary buffer response systems in the
body: lungs and the kidneys
The body tries to overcome either a
respiratory or metabolic dysfunction
in an attempt to return the pH into the
normal range.
32. Compensatory Responses
DISORDER RESPONSE
Metabolic acidosis Dec HCO3 1.2 mmHg dec in
PCO2 foe every 1
meq/L fall in HCO3
Metabolic alkalosis Inc HCO3 0.7 mmHg inc in CO2
for every 1 meq/L rise
in HCO3
Respiratory acidosis Inc PCO2 1 meq/L inc in HCO3
for every 10 mmHg
rise in PCO2
Respiratory alkalosis Dec PCO2 2 meq/L dec in HCO3
for every 10 mmHg fall
in PCO2
33. 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)
34. Na+
Regulatory Response to Acidemia
Cl-
H+
Protein-
PO4
=,SO4
=
Organic acids
normal
anion
gap
URINE
HCO3
-
NH4
+
H2PO4
-
PCT
DT
35. Compensation
If compensation is < or > predicted then there may
be ≥2 disorders:
pCO2 too low: concomitant primary respiratory
alkalosis
pCO2 too high: concomitant primary respiratory
acidosis
HCO3 too low: concomitant primary metabolic
acidosis
HCO3 too high: concomitant primary metabolic
alkalosis
36. Compensation
Normal pH but increased pCO2 + increased
HCO3: respiratory acidosis + metabolic alkalosis
Normal pH but decreased pCO2 + decreased
HCO3: respiratory alkalosis + metabolic acidosis
(e.g., salicylates, DKA)
Normal pH & normal pCO2 & HCO3 but
increased AG: HAGMA + metabolic alkalosis
(e.g., Alcoholic ketoacidosis w/ vomiting) +
respiratory alkalosis (due to hyperventilation of
hepatic dysfunction or alcohol withdrawal)
37. Compensation
Normal pH & normal pCO2 & HCO3 & AG: no
disturbance or NAGMA + metabolic alkalosis
Metabolic acidosis + respiratory acidosis: DKA<
sedatives.
Cannot have respiratory acidosis & respiratory
alkalosis simultaneously (one either hypo- or
hyperventilates)
38.
39. Example 1
If patient presents with pH=7.2 and HCO3=16,
what is the normal compensated value for
pCO2?
24-16= 8 meq/L 8 x 1.2 = 9.6 mmHg fall in PCO2
40 mmHg-9.6 mmHg = 30.4 mmHg
Normal compensation PCO2 = 30.4 mmHg
40. Example 2
If patient presents with pH= 7.23. HCO3= 22
meq/L, and pCO2= 9, what is your
interpretation?
Note the pH and tell whether it is acidosis or
alkalosis?
Note the HCO3 and pCO2 values to determine
which causes the primary disturbance?
Determine the compensatory response
What is our diagnosis?
52. Calculate 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
54. ANION GAP
Na – (HCO3 + Cl) = 12 + 4
Na = 135 HCO3 = 15
Cl = 97 RBS = 100 mg%
AG = 135 – 112 = 23
55. ANION GAP
Na – (HCO3 + Cl) = 12 + 4
Na = 135 HCO3 = 15
Cl = 97 RBS = 500 mg%
Corrected Na = Na + RBS mg% -100 x 1.6
100
AG = 135 + 6.4 – 112 = 29.4
56. ANION GAP IN MAJOR CAUSES OF
METABOLIC ACIDOSIS
High Anion Gap
A. Lactic acidosis: Lactate
B. Ketoacidosis: B-hydroxybutyric acid
C. Renal failure: Sulfate, phosphate, urate
D. Ingestions
1. Salicylate: ketones, lactate, salicylate
2. Methanol or formaldehyde
3. Ethylene glycol: glycolate, oxalate
Normal Anion Gap
A. Gastrointestinal loss of HCO3-
1. Diarrhea
B. Renal HCO3- loss
1. Type I and Type II Renal Tubular Acidosis
C. Ingestion:
1. Ammonium Chloride
57. Na+
States of Systemic Acidosis
Cl-
High
anion
gap
H+
Protein-
PO4
=,SO4
=
Organic acids
HCO3
-
M- methanol
U- uremia
D- DKA
P- paraldehyde
I- iron, INH
L- lactic acidosis
E- ethylene glycol
S- salicylates
59. Na
136
Cl
100
AG 12
HCO3
24
NORMAL
Na
136
Cl
100
AG 26
HCO3 10
HIGH GAP
METAB
ACIDOSIS
Increased when acidosis due to
Increase in fixed acids (HCO3 acts
as buffer so it is depleted and the
unmeasured anions increase to
preserve neutrality)
Na
136
Cl
114
AG 12
HCO3 10
NORMAL GAP
METAB
ACIDOSIS
Gap is normal if metab
acidosis due to loss of
base (when HCO3 lost,
Cl- anions increased to
maintain Neutrality)
60. Na
136
Cl
100
AG 12
HCO3
24
NORMAL
Na
136
Cl
94
AG 22
HCO3
20
COMBINED HAG
MET. ACIDOSIS
& MET. ALKALOSIS
AG
HCO3
=
10
4
Na
136
Cl
106
AG 22
HCO3 8
COMBINED HAG
& NAG MET.
ACIDOSIS
AG
HCO3
=
10
16
Na
136
Cl
100
AG 22
HCO3
14
SIMPLE HAG
METABOLIC
ACIDOSIS
AG
HCO3
=
10
10
HAGMA: DELTA AG/DELTA HCO3
61. HAGMA
Δ AG = Δ HCO3 pure HAGMA
Δ AG < Δ HCO3 HAGMA + NAGMA
Δ AG > Δ HCO3 HAGMA + metabolic alkalosis
62. Na
136
Cl
100
AG 12
HCO3
24
NORMAL
Na
134
Cl
110
AG 10
HCO3
14
SIMPLE NAG
METABOLIC
ACIDOSIS
Cl
HCO3
=
10
10
Na
128
Cl
110
AG 10
HCO3 8
COMBINED NAG
& HAG MET.
ACIDOSIS
Cl
HCO3
=
10
16
Na
140
Cl
110
AG 10
HCO3
20
COMBINED NAG
MET. ACIDOSIS
& MET. ALKALOSIS
Cl
HCO3
=
10
4
For Normal Gap: DELTA Chloride/DELTA HCO3
66. Room air, patient < 60 y.o.
Mild hypoxemia paO2 < 80 mm Hg
Moderate paO2 < 60 mm Hg
Severe 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
