Blood Gas analysis

DR. MANSOOR AQIL

ASSOCIATE PROFESSOR,
KING SAUD UNIVERSITY HOSPITALS
RIYADH.
 Clinical case

pH 7.62
pCO2 30mmHg
PO2 80 mmHg
HCO3 30 mmol/L

Diagnosis

Respiratory Alklosis
• With Metabolic Alklosis
 BLOOD pH

 Maintained within narrow limits

pH 7.36 to 7.44

pH = Alkalemia (Alkalosis)

pH = Acidemia (Acidosis)
 NORMAL
7.4
ACIDOSIS ALKALOSIS

7.0 7.8

ACID BASE
(CO2) (HCO3)

RESPIRATORY COMPONENT METABOLIC COMPONENT

BLOOD pH
 The challenge
7.4
ACIDOSIS

7.0 7.8
Volatile ACID (CO2)
&
Fixed acids

Defense of normal alkalinity

 Types of Acids

 Volatile acids

• Easily move from liquid to gas state within

the body
– Lung can remove

– H2CO3 + renal enzyme  H2O + CO2 (both of which are

exhaled)

– Carbon dioxide is therefore considered an acid

 Types of Acids

 Nonvolatile acids (Fixed acids)

• Cannot be changed to gas state within the

body
– Examples
– Keto acids

– Lactic acids
 The challenge
 Sources of acids:
Volatile acid
CO2 + H2O  H2CO3  H+ + HCO3

Fixed acids
• Organic and inorganic source
– Lactic acid, ketones, Sulfuric and phosphoric acid

• Kidney plays an important role handling fixed

acids.
 HYDROGEN ION SOURCES
 CO2 15000 mmol/day
CO2 + H2O H2CO3 H+ + HCO3-

 Noncarbonic acids 70 mmol/day

DEFENCE AGAINST pH CHANGE

Acute (minutes to hours)

Ventilation
Buffering
DEFENCE AGAINST pH CHANGE

Acute (minutes to hours)

Long term
Renal excretion
Hepatic metabolism
Chemical Buffers
• The body uses pH buffers in the blood to guard
against sudden changes in acidity
• A pH buffer works chemically to minimize
changes in the pH of a solution

Buffer
 BUFFERS
1. Intracellular Buffers
1. Proteins

2. Haemoglobin

3. Phosphate

1. Extracellular Buffers
1. Proteins

2. Bicarbonate
 Phosphate
Intracellular buffers Haemoglobin

Amino acid
Protein buffers All proteins

Buffer
systems

Plasma
proteins
Carbonic acid
Exracellular
bicarb buffers
 Biological systems and Buffering:

 The power of a buffer depends on:

1.Concentration of the buffer.

2.Whether the pK is close to the pH of the system.

 Bicarbonate buffer systems:

CO2 + H2O  H2CO3  H+ + HCO3-

Maintains a ratio of 20 parts bicarbonate to 1 part

carbonic acid
 Bicarbonate Buffer System

 If strong acid is added:

HCl + NaHCO3 = H2CO3 + NaCl

Hydrogen ions released combine with the bicarbonate ions and form carbonic acid (a weak acid)

The pH of the solution decreases only slightly

 BICARBONATE BUFFER SYSTEM
 H2CO3 H+ + HCO3-
• Hydrogen ions generated by metabolism or by
ingestion react with bicarbonate base to form more
carbonic acid

H2CO3 HCO -
3

20
 BICARBONATE BUFFER SYSTEM
 Equilibrium shifts toward the formation of acid

• Hydrogen ions that are lost (vomiting) causes

carbonic acid to dissociate yielding replacement
H+ and bicarbonate
H2CO3
H+ HCO3-
 Bicarbonate Buffer System
If strong base is added:

NaOH + H2CO3 = NaHCO3 + H2O

 It reacts with the carbonic acid to form sodium

bicarbonate (a weak base)

 The pH of the solution rises only slightly

 This system is the only important ECF buffer

 Bicarbonate buffer systems:

CO2 + H2O  H2CO3  H+ + HCO3-

 pK = 6.1 [HCO3-] = 24 mmol/L

 Bicarbonate buffer systems:

Can eliminate CO2 & H+ by VA

pK is not very close to blood pH of

7.4
 Phosphate buffer systems

 Phosphate buffer H2PO4- / HPO4

 pK = 6.8 and has a low concentration.

 Role as intracellular and urinary buffer.

 Phosphate buffer systems

H2PO4- / HPO4-2
 Protein buffers:

A. Amino acid residues of proteins take up H+

(pK=7.0) are most important

NH2  NH3-

B. Hemoglobin is important due to high concentration

and its increased buffering capacity when deoxygenated.
Relative Buffering power:

Phosphate 0.3

HCO3- 1

Plasma proteins 1.4

Hemoglobin 6.5
 Relative Buffering power:

Most important
75% of all buffering
buffer is protein.
power of the body is
within cells as
protein
 Compensation

A. Compensatory response involves

the system opposite to the one that
caused the primary disturbance.

B. Compensation moves pH towards

the original normal value but not
completely.
 Renal buffering mechanisms

Renal - kidney excretes H+ and

replenishes [HCO3-] .

But, this is a slow process taking hours

to days.
Renal buffering mechanisms
Renal buffering mechanisms
METABOLIC DISORDERS
RESPIRATORY ACIDOSIS
7.4

7.0 7.8

ACID BASE
(CO2) (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
RESPIRATORY ACIDOSIS

H2O + CO2  H2CO3  H+ + HCO3-

Cause - hypoventilation

Retention of CO2

Drives equation rightward

Increases both [H+] and [HCO3-]

RESPIRATORY ALKALOSIS
7.4

7.0 7.8

ACID BASE
(CO2) (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
 RESPIRATORY ALKALOSIS

H2O + CO2  H2CO3  H+ + HCO3-

2. Respiratory Alkalosis
cause - hyperventilation

Blows off CO2

Drives equation leftward decreasing both [H+] and [HCO3-]

METABOLIC ACIDOSIS
7.4

7.0 7.8

ACID BASE
(CO2) (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
 Metabolic Acidosis
Deficit in HCO3- and decreased pH

Causes:

1. Increased production of nonvolatile acids.

2. Decreased H+ secretion in the kidney

3. Increased HCO3- loss in kidney

4. Increased Cl- reabsorption by the kidney.

 Metabolic Acidosis

Body response is increased

ventilation to blow off excess
CO2
METABOLIC ALKALOSIS
7.4

7.0 7.8

ACID BASE
(CO2) (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
 Metabolic Alkalosis

Primarily due to Increased HCO3- , increased pH

Causes
• Administration of excess HCO3-
• Increased secretion of H+ by kidney and gut
• Sudden volume contraction which leads to increased Na+ retention.This
leads to water and HCO3- to follow the Na+
PARTIALLY COMPENSATED RESPIRATORY
ACIDOSIS
7.4

7.0 7.8

ACID BASE
(CO2) (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
PARTIALLY COMPENSATED RESPIRATORY
ALKALOSIS
7.4

7.0 7.8

ACID BASE
(CO2) (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
PARTIALLY COMPENSATED METABOLIC
ACIDOSIS
7.4

7.0 7.8

ACID BASE
(CO2) (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
PARTIALLY COMPENSATED METABOLIC
ALKALOSIS

7.4

7.0 7.8

ACID BASE
(CO2) (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
MIXED ACIDOSIS
7.4

7.0 7.8

ACID BASE
(CO2) (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
COMPENSATED STATE

7.4
ACIDOSIS ALKALOSIS

7.0 7.8

ACID BASE
(CO2) (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
Acute ventilatory failure (acute respiratory acidosis)

pH PaCO2 HCO3-

N
Chronic ventilatory failure
(compensated respiratory acidosis)

pH PaCO2 HCO3-

pH PaCO2 HCO3-

Normal
Acute alveolar hyperventilation
(acute respiratory alkalosis)

pH PaCO2 HCO3-

Normal
Chronic alveolar hyperventilation
(compensated respiratory alkalosis)
pH PaCO2 HCO3-

Normal

pH PaCO2 HCO3-

Normal
Acute metabolic acidosis

pH PaCO2 HCO3-

Normal
Chronic metabolic acidosis

pH PaCO2 HCO3-

Normal

pH PaCO2 HCO3-

Normal
Acute Metabolic Alkalosis

pH PaCO2 HCO3-

Normal
Chronic metabolic alkalosis

pH PaCO2 HCO3-

Normal

pH PaCO2 HCO3-

Normal
 Anion Gap

AG = [Na + ] - [Cl ‾ + HCO3‾ ]

• AG represents unaccounted for anions (R ‾ )

• Normal anion gap = 10

 Anion Gap

 Cations are Na + & K +

 Major Anions are Cl ‾ & HCO3 ‾

 Anion gap

Unmeasured Anions vs Unmeasured Cations

Proteins, mostly albumin 15 mEq/L Calcium 5 mEq/L

Organic acids 5 mEq/L Potassium 4.5 mEq/L

Phosphates 2 mEq/L Magnesium 1.5 mEq/L

Sulfates 1 mEq/L
Totals: 23 mEq/L 11 mEq/L
 Rules For Analyzing The ABG’s

• Look at the anion gap.

If elevated and metabolic acidosis is present,

it’s anion gap metabolic acidosis.

If not elevated, it’s non-anion gap metabolic

acidosis.

If more than 20, there is definitely anion gap

acidosis even if the PH and the HCO3 are
normal.
 Differential diagnosis of
metabolic acidosis
Normal anion gap Elevated anion gap

 Renal tubular acidosis  Uremia

 Dirrhoea  Ketoacidosis

 Carbonic anhydrase inhibition  Lactic acidosis

 Ureteral diversion  Methanol toxicity

 Ethylene glycol toxicity

 Early renal failure
 Salicylate
 Hydronephrosis
 Paraldehyde
 HCL administration

 Saline administration
DIAGNOSIS OF ACID BASE
DISTURBANCE
 Determining the predicted
“Respiratory pH”

 Acute 10 mmHg increase in PCO2 results in pH

decrease of approximately 0.05 units

 Acute 10 mmHg decrease in PCO2 results in pH

increase of approximately 0.10 units

 Determining the predicted
“Respiratory pH”

First determine the difference between the measured

PaCO2 and 40 mmHg and move the decimal point two
places left.

60 - 40 = 20 X 1/2 0.10

40 – 30 = 10 0.10
 Determining the predicted
“Respiratory pH”

1. If the PaCO2 is greater than 40 subtract half of the

difference from 7.40

60 - 40 = 20 X ½ =10 = 0.10

pH = 7.40 – 0.10 = 7.30

2. ? If this Pt has pH = 7.2
3. ? If this Pt has pH = 7.33
 Determining the predicted
“Respiratory pH”

If the PaCO2 is less than 40 add the difference to 7.40

40 - 30 = 10 0.10

pH = 7.40 + 0.10 = 7.50

Determining the predicted
“Respiratory pH”
pH 7.04
PCO2 76

76 - 40 = 36 X ½ = 18 0.18

7.40 - 0.18 = 7.22

Determining the predicted
“Respiratory pH”
pH 7.21
PCO2 90

90 - 40 = 50 X ½ = 25 0.25

7.40 – 0.25 = 7.15

Determining the predicted
“Respiratory pH”
pH 7.47
PCO2 18

40 – 18 = 22 0.22

7.40 + 0.22 = 7.62

 Determining the
Metabolic component

RULE

10 mmol/L variance from the normal buffer

base represents a pH change of
approximately 0.15 units.
 pH 7.21
PCO2 90

90 - 40 = 50 X ½ = 0.25

7.40 – 0.25 = 7.15

Determining the Metabolic component

7.21 -7.15 = 0.06 X 2/3 = 0.04 = 4 mmol/L base excess
 pH 7.04
PCO2 76

76 - 40 = 36 X ½ = 0.18

7.40 - 0.18 =7.22

Determining the Metabolic component
7.22 -7.04 = 0.18 X 2/3 =12 mmol/L base deficit
 Determining the Metabolic component
pH 7.47
PCO2 18

40 – 18 = 22 = 0.22

7.40 + 0.22 = 7.62

Determining the Metabolic component
7.62-7.47 = 0.15 X 2/3 =10 mmol/L base deficit
 Diagnosis of acid base disturbance
1. Examine arterial pH: Is acidemia or alkalemia present?

2. Examine PaCO2: Is the change in PaCO2 consistent with a

respiratory component?

3. If the change in PaCO2 does not explain the change in

arterial pH, does the change in [HCO3–] indicate a
metabolic component?

4. Make a tentative diagnosis (see Table).

 Diagnosis of acid base disturbance

5. Compare the change in [HCO3–] with the change in PaCO2. Does a

compensatory response exist (Table)?

6. If the compensatory response is more or less than expected, by definition

a mixed acid–base disorder exists.

7. Calculate the plasma anion gap in the case of metabolic acidosis.

8. Measure urinary chloride concentration in the case of metabolic

alkalosis.
Table . Normal Compensatory Responses in Acid–Base Disturbances.

Disturbance Response Expected Change

Respiratory acidosis

Acute [HCO3–] 1 mEq/L/10 mm Hg increase in PaCO2

Chronic [HCO3–] 4 mEq/L/10 mm Hg increase in PaCO2

Respiratory alkalosis

Acute [HCO3–] 2 mEq/L/10 mm Hg decrease in PaCO2–

Chronic [HCO3–] 4 mEq/L/10 mm Hg decrease in PaCO2

Metabolic acidosis PaCO2 1.2 x the decrease in [HCO3–]

Metabolic alkalosis PaCO2 0.7 x the increase in [HCO3–]

 Clinical case

pH 7.62
pCO2 30mmHg
PO2 80 mmHg
HCO3 30 mmol/L

Diagnosis

Respiratory Alklosis
• With Metabolic Alklosis
 Clinical case

pH 7.15
pCO2 22 mm Hg
PO2 90 mmHg
HCO3 9 mmol/L

Diagnosis

•Partially compensated Metabolic acidosis

 Clinical case

pH 7.29
pCO2 33 mm Hg
PO2 90 mmHg
HCO3 19 mmol/L

Diagnosis

•Partially compensated Metabolic acidosis

 Clinical case

pH 7.50
pCO2 29 mm Hg
PO2 92 mmHg
HCO3 24 mmol/L

Diagnosis

• Acute respiratory Alklosis

 Clinical case

pH 7.30
pCO2 55 mm Hg
PO2 74 mmHg
HCO3 30 mmol/L

Diagnosis

•Partially compensated Respiratory acidosis

Thank U
 Base Excess/ Deficit

 The degree of deviation from normal total body buffer base

can be calculated independent of compensatory PCO2
changes

 The amount of acid of base that must be added to return the

blood pH to 7.4 and PCO2 to 40 at full O2 saturation and 370
C