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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
pH = Alkalemia (Alkalosis)
pH = Acidemia (Acidosis)
Maintained within narrow limits
pH 7.36 to 7.44
BLOOD pH
NORMAL
RESPIRATORY COMPONENT METABOLIC COMPONENT
ACID(CO2)
BASE (HCO3)
7.4
ACIDOSIS ALKALOSIS
7.87.0
BLOOD pH
The challenge
Volatile ACID (CO2) &
Fixed acids
7.4
ACIDOSIS
7.87.0
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 acidCO2 + 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.
CO2 15000 mmol/day
CO2 + H2O H2CO3 H+ + HCO3-
Noncarbonic acids 70 mmol/day
HYDROGEN ION SOURCES
Acute (minutes to hours)
Ventilation
Buffering
DEFENCE AGAINST pH CHANGE
Acute (minutes to hours)
Long term
Renal excretion
Hepatic metabolism
DEFENCE AGAINST pH CHANGE
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
1. Intracellular Buffers1. Proteins
2. Haemoglobin
3. Phosphate
2. Extracellular Buffers1. Proteins
2. Bicarbonate
BUFFERS
Buffer systems
Intracellular
Phosphate buffers
Protein buffers
Haemoglobin
Amino acidAll proteins
Plasma proteins
Exracellular
Carbonic acid 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
20
BICARBONATE BUFFER SYSTEM H2CO3 H+ + HCO3
-
• Hydrogen ions generated by metabolism or by ingestion react with bicarbonate base to form more carbonic acid
HCO3-H2CO3
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
H+ HCO3-
H2CO3
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
Hemoglobin6.5
Relative Buffering power:
Most important buffer is protein. 75% of all buffering 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
ACID(CO2)
BASE (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
7.8
7.4
7.0
RESPIRATORY ACIDOSIS
H2O + CO2 H2CO3 H+ + HCO3
-
Cause - hypoventilation
Retention of CO2
Drives equation rightward
Increases both [H+] and [HCO3-]
RESPIRATORY ALKALOSIS
ACID(CO2)
BASE (HCO3)
7.0
7.4
7.8
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
ACID(CO2)
BASE (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
7.8
7.4
7.0
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
ACID(CO2)
BASE (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
7.0
7.4
7.8
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
ACID(CO2)
BASE (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
7.4
7.87.0
PARTIALLY COMPENSATED RESPIRATORY ALKALOSIS
METABOLIC COMPONENT
ACID(CO2)
BASE (HCO3)
RESPIRATORY COMPONENT
7.4
7.0 7.8
ACID(CO2)
BASE (HCO3
)RESPIRATORY COMPONENT METABOLIC COMPONENT
7.4
7.87.0
PARTIALLY COMPENSATED METABOLIC ACIDOSIS
PARTIALLY COMPENSATED METABOLIC ALKALOSIS
ACID(CO2)
BASE (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
7.4
7.0 7.8
MIXED ACIDOSIS
ACID(CO2)
BASE (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
7.8
7.4
7.0
COMPENSATED STATE
ACID(CO2)
BASE (HCO3)
RESPIRATORY COMPONENT METABOLIC COMPONENT
7.4ACIDOSIS ALKALOSIS
7.87.0
pH PaCO2 HCO3-
Acute ventilatory failure (acute respiratory acidosis)
N
Chronic ventilatory failure(compensated respiratory acidosis)
pH PaCO2 HCO3-
Normal
pH PaCO2 HCO3-
N
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
Renal tubular acidosis
Dirrhoea
Carbonic anhydrase inhibition
Ureteral diversion
Early renal failure
Hydronephrosis
HCL administration
Saline administration
Elevated anion gap
Uremia
Ketoacidosis
Lactic acidosis
Methanol toxicity
Ethylene glycol toxicity
Salicylate
Paraldehyde
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
2. ? If this Pt has pH = 7.2
3. ? If this Pt has pH = 7.33
60 - 40 = 20 X ½ =10 = 0.10
pH = 7.40 – 0.10 = 7.30
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
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
Determining the Metabolic component
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 7.15pCO2 22 mm HgPO2 90 mmHgHCO3 9 mmol/L
•Partially compensated Metabolic acidosis
Diagnosis
Clinical case
pH 7.29pCO2 33 mm HgPO2 90 mmHgHCO3 19 mmol/L
•Partially compensated Metabolic acidosis
Diagnosis
Clinical case
pH 7.50pCO2 29 mm HgPO2 92 mmHgHCO3 24 mmol/L
• Acute respiratory Alklosis
Diagnosis
Clinical case
pH 7.30pCO2 55 mm HgPO2 74 mmHgHCO3 30 mmol/L
•Partially compensated Respiratory acidosis
Diagnosis
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
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