This document provides information on arterial blood gas analysis, including contraindications for arterial puncture, reasons to order an ABG, normal values, equations, and approaches to interpreting ABG results. It discusses how to determine if a patient has acidosis or alkalosis, whether it is respiratory or metabolic, and if the compensation is adequate. It provides steps to classify the acid-base disorder, consider anion and osmolal gaps, and evaluate for mixed disorders. Causes and treatments of different acid-base imbalances are outlined.

2. CONTRAINDICATION FOR ARTERIAL PUNCTURE :
 INFECTION AT SITE.
 ALLEN’S TEST NEGATIVE.
 ON ANTICOAGULANT THERAPY.
 SEVERE PERIPHERAL VASCULAR DISEASE.
 DISTAL TO SURGICAL SHUNT.

3. WHY TO ORDER AN ABG
 Aids in establishing a diagnosis
 Helps guide treatment plan
 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/care
 Follow up

5. NORMAL VALUES
 Ph- 7.35-7.45
 Po2- 95mmhg- 100mmhg
 PCO2- 36mmhg -44mmhg
 HCO3- 22 – 26mEq/L
 AG – 8-12
 OG- -10 - +10

6. EQUATIONS
Henderson Hasselbalch equation: pH = 6.1 + log [HCO3-]
0.03( Pco2)
Kassirer-Bleich equation: [H+] = 24 × PCO2 / [HCO3-]

7. DERIVATION OF HH EQUATION
 (H+) ∞(acid) / (base)
 (H+) =Ka(HA)/ (A-)
 pH=pKa + log (A-)/ (HA)
 pH= pKa + log (HCO3) / 0.03 ( CO2)

8. HYDROGEN ION CONC AT dif PH
pH [H+]
7.7 20
7.5 31
7.4 40
7.3 50
7.1 80
7.0 100
6.8 160

9. APPROACH TO ABG
 Acidosis or alkalosis.
 Respiratory or metabolic.
 If respiratory – Acute or chronic.
 If metabolic acidosis – High AG or normal AG
 Is the compensation adequate
 Rule out mixed disorders

10. STEP 1
PH < 7.35 - ACIDOSIS
PH > 7.45 - ALKALOSIS

11. STEP 2
ACID BASE CHANGES
Acid-Base Disorder Primary Change Compensatory
Change
Respiratory acidosis PCO2 up HCO3 up
Respiratory alkalosis PCO2 down HCO3 down
Metabolic acidosis HCO3 down PCO2 down
Metabolic alkalosis HCO3 up PCO2 up

12. Compensation
Primary Disorder Compensatory Mechanism
Metabolic acidosis Increased ventilation
Metabolic alkalosis Decreased ventilation
Respiratory acidosis Increased renal reabsorption of HCO3-
in the proximal tubule
Increased renal excretion of H in the
distal tubule
Respiratory alkalosis Decreased renal reabsorption of HCO3-
in the proximal tubule
Decreased renal excretion of H+ in the
distal tubule

13. The Boston formulae*
State Rule Formula Range
Metabolic acidosisfor acid-base derangementPCOsimply guesstimated using the Boston formulae: + 8
1.Compensation
1.5+8 can be 2
(mmHg) = 1.5*bicarbonate 2
Metabolic alkalosis 0.7+20 PCO 2 (mmHg) = 0.7*bicarbonate +20 5
Acute respiratory bicarbonate (mmol/l) drops 2 mmol/l
2 for 10 ?
alkalosis for every 10 mmHg PCO 2 drop
Chronic respiratory
4 for 10 likewise, but 5 mmol/l ?
alkalosis
bicarbonate (mmol/l) increases 1
Acute respiratory
1 for 10 mmol/l ?
acidosis
for every 10 mmHg
Chronic respiratory
4 for 10 likewise, but 4 mmol/l ?
acidosis

14. HARRISON
METABOLIC ACIDOSIS-
HCO3 – 1.25 PCO2
METABOLIC ALKALOSIS:
HCO3- 0.75 PCO2

15. STEP 4 ANION GAP
 The principle of electroneutrality
 (Na+ + K+) – (Cl- + HCO3- )
 Usually 12-16 mEq/l
 Difference is due to the unmeasured –
ve charge on the proteins, and SO4- and
PO4-
 Low albumin will reduce the ‘normal’
gap

16. HIGH AG NORMAL AG
•LACTIC ACIDOSIS •DIARRHOEA
•UREMIC ACIDOSIS •FITUL A
•KETO ACIDOSIS •RTA
•SALISYLSTE •ACETOZOLAMIDE
•ETHELENE GLYCOL •MASSIVE NS INFUSION
•ETHANOL •HYPERALIMENTATION

17. HAGMA
 SAG increased. (Na – Cl + HCo3)
 The added Acid is buffered by
Hco3, Hco3 Falls and Anion Gap is increased.
Key Point : Increased Anion Gap means an acid has been
added to the blood. HAGMA.

18. NAGMA
 SAG normal.( Na – Cl + HCo3)
 When Hco3 is lost, to maintain electro neutrality
Cl is conserved by the kidney’s and so Anion Gap is
normal.
 Key Point : Normal Gap acidosis denotes loss of
Hco3. Also called hypercholeremic acidosis.
 NAGMA.

19. HIGH AG NORMAL AG
•LACTIC ACIDOSIS •DIARRHOEA
•UREMIC ACIDOSIS •FITUL A
•KETO ACIDOSIS •RTA
•SALISYLSTE •ACETOZOLAMIDE
•ETHELENE GLYCOL •MASSIVE NS INFUSION
•ETHANOL •HYPERALIMENTATION

20. OSMOLAL GAP
 osmolal gap = MO - CO
 MO = Measured Osmolality
 CO = Calculated Osmolality.
 2 x Na + GLU/18 + UN/2.8
 Normal OG = -10 to +10
 An OG value greater than + 14 has traditionally been
considered a critical value or cutoff.

21. Urine Anion Gap
 UAG = (UNa +UK) – UCl.
 Normal UAG = -10 to +10.
 If UAG is negative,more than -20
it is due GI loss.
If the UAG is positive, more than +10 then it is due
to renal loss of Hco3.
UAG is an indirect measure of NH3 secretion in
the Distal Tubule.

22. STEP 6
 If the decrease in bicarbonate is more than the rise
in the AG, concurrent with the AG metabolic
acidosis there is also a second type of metabolic
acidosis present, a non-AG metabolic acidosis.
AG/ HCO3 < 1
 If the decrease in bicarbonate is less than the rise
in AG, a metabolic alkalosis is concurrently
present with the AG metabolic acidosis.
AG/ HCO3 > 1

23. RESPIRATORY ACIDOSIS
 Upper airway obstruction
 Lower airway obstruction
 Cardiogenic or non-cardiogenic pulmonary edema
 Pneumonia
 Pulmonary emboli
 Fat emboli
 Central nervous system depression
 Neuromascular impairment
 Ventilatory restriction

24. RESPIRATORY ALKALOSIS
 Central nervous system stimulation: Fever, pain, fear,
cerebrovascular accident, CNS infection, trauma,
tumor.
 Hypoxia: High altitude, profound anemia, pulmonary
disease.
 Stimulation of chest receptors: Pulmonary edema,
pulmonary emboli, pneumonia, pneumothorax,
pleural effusion.
 Drugs or hormones : Salicylates,
medroxyprogesterone, catecholamines.
 Miscellaneous: Sepsis, pregnancy, liver disease,
hyperthyroidism.

25. METABOLIC ALKALOSIS
CHLORIDE RESPONSIVE CHLORIDE RESISTANT
URINE CL < 25 URINE CL> 25
•DIURETICS •HYPERALDOOSTERONE STATE
•CORTICOSTEROIDS •CUSHING
•GI LOSS- DIARRHOEA, VILLOUS •BARTTERS
ADENOMA
•POTTASIUM DEPLETION
•VOMITING
•MASSIVE BLOOD TRANSFUSION
•SUCTION
•Rx – K+ REPLACEMENT
•Rx – 0.9% NS , K+ REPLENIHMENT

26. TIPS
 Do not interpret any blood gas data for acid-base
diagnosis without closely examining the serum
electrolytes: Na+, K+, Cl-,
 Single acid-base disorders do not lead to normal
blood pH. Although pH can end up in the normal
range (7.35 - 7.45) with a single mild acid-base
disorder, a truly normal pH with distinctly
abnormal HCO3- and PaCO2 invariably suggests
two or more primary disorders. and CO2.

27. TIPS
 Simplified rules predict the pH and HCO3- for a
given change in PaCO2. If the pH or HCO3- is
higher or lower than expected for the change in
PaCO2, the patient probably has a metabolic acid-
base disorder as well.
 In maximally-compensated metabolic acidosis, the
numerical value of PaCO2 should be the same (or
close to) as the last two digits of arterial pH. This
observation reflects the formula for expected
respiratory compensation in metabolic acidosis:
Expected PaCO2 = [1.5 x serum hco3] + (8 ± 2)

28. correction
 Ph< 7.1
 HCO3 < 10
 BICARB DEFICIT
 VOD=Body wt( 0.4 + 2.4 / 5 )
 Correction = Vod ( bicarb defict)
400 mEq increases Hco3 by 12 mEq

29.  JAYARAMAN
 AKI

30.  LATHA
 MYASTHENIA GRAVIS

31.  LATHA
 IN VENTILLATOR

32.  SAMUNDESHWARI

33.  DIABETIC KETO ACIDOSIS

34. THANK YOU