Nice

1. ARTERIAL BLOOD GAS
ANALYSIS
Presenter: Dr. M. Krishnaveni
Moderator: Dr. Sri satya

2. • Arterial blood gas analysis is a blood test taken from an artery that measures the
amount of oxygen and carbondioxide that is found in the blood
ABG analysis provides us rapid information on three physiologic processes:
1. Alveolar Ventilation – PaCO₂ is the best index.
2. Oxygenation – PaO₂, SaO₂, PaO₂ /FiO₂.
3. Acid-Base balance.

3. • pH :It is the negative of H+
• The pH = -Log 10[H+ ]
• Because the PH is a negative logarithm of the H+, changes are inversely related to
changes in H+
• An acid: A chemical avid that can acts as a proton donor
• A strong acid. A substance that readily and irreversibly gives up H+ and increases
H+
• A weak acid: A substance that reversibly donates H+ and has less effect on H+
• A base: A chemical substance that can act as a proton acceptor
•

4. • A strong base: A substance that can avidly and almost irrversibly binds H+ and
decreases H+
• A weak base A substace that reversibly binds H+ and has a less effect on H+
• Conjugate base if an acid is the dissociated anionic product of the acid
• Acidosis: It is a process that causes acids to accumulate in arterial blood
• Alkalosis: It is the process that causes bases to accumulate in arterial blood
• Acidemia It is PH <7.36
• Alkalemi it is PH> 7.4
• The PHcompatible with life is 6.8-7.8

5.  Actual bicarbonate: Value collected from the blood gas sample.
 Standard/Corrected bicarbonate: Value of the bicarbonate had the sample been
corrected to 40 mmHg and at room temperature.
Estimate of metabolic component causing acid-base imbalance.
 Base deficit/excess: amount of alkali/ acid that must be added to a solution to restore
its pH to 7.4 after it has been equilibrated to a PaCO₂ of 40 mmHg.
It is the amount of deviation of the standard bicarbonate from the normal.

6. CLINICAL TERMINOLOGY CRITERIA
1. Normal pH
2. Acidemia
3. Alkalemia
4. Normal PaCO₂
5. Resp acidosis
6. Resp alkalosis
7. Normal HCO₃⁻
8. Metabolic acidosis
9. Metabolic alkalosis
7.4 (7.35 – 7.45)
pH < 7.35
pH > 7.45
40(35 – 45 mmHg)
PaCO₂ > 45 mm Hg and low pH.
PaCO₂ < 35 mmHg and high pH.
24(22-26) mEq/L.
HCO₃⁻ < 22 mEq/L and low pH.
HCO₃⁻ > 26 mEq/L and high pH.

7. Methods of acid base regulation
• Propper regulation of acid base balance is important for the proper cellular function
becase H+ ions react highly with cellular proteins resulting in alteration in their
function
• CHEMICAL REGULATION
• 1st line of defence against blood ph changes
• it is the least efficient mechanism
• Acts very rapidly( within seconds)
• Carbonic acid/bicarbonate buffer system: major buffer in ECF, plasma HCO3 acts
immediately, interstitial HCO3 acts within 15-20min
• Phosphate buffer system: major buffer system in ICF and rensl tubular fluid
• Protein buffer system: The most plentiful buffer in body and it is present in ICF,
plasma proteins, Hb, carbonate in the bone

8. • 2. RESPIRATORY REGULATION:
• 2nd line of defense.
• Moderately efficient.
• Acts within 3-15 mins.
• Controls the dissolved CO₂ in the blood.
• Compensatory mechanism against metabolic disorders.
• With increase/decrease in arterial pH changes in CSF 
stimulation/inhibition of chemoreceptors in brain stem  medullary resp
centre Alv.hyperventilation/hypoventilation.

9. • 3. RENAL REGULATION:
• 3 rd line of defense.
• most powerful & efficient mechanism.
• acts within few hrs. & takes 5-6 days for it’s peak effect.
• Controls HCO₃⁻ level in the blood.
• Compensatory mechanism against respiratory disorders.
• Three main mechanisms:
• Excretion of H⁺ ions by tubular secretion.
• Reabsorption of filtered bicarbonate ions.
• Production of new bicarbonate ions.

10. INDICATIONS FOR ABG:
1. Ventilatory status, acid-base balance, oxygenation & oxygen carrying capacity
of blood.
2. Patient’s response to therapeutic intervention like ventilatory management,
circulatory intervention or progression of a disease process.
3. For surgical evaluations(pulmonary resections).

11. • For less than 4 samples/24 hours, collecting sample through arterial puncture
should be performed
• An arterial line should be placed when multiple blood gas studies (more than 4
samples of arterial blood in 24 hours)
• Radial artery on non-dominant hand is the ideal site
Order of site selection for arterial puncture:
1. Radial artery (ideal site).
2. Brachial artery.
3. Femoral artery(risk of infection) &
4. Dorsalis Pedis artery.

12. CONTRAINDICATIONS:
1. Cellulitis/Infection
2. Absence of palpable arterial pulse.
3. Negative Allen’s test( collateral circulation).
4. Coagulopathies/on anti-coagulation therapy.
5. H/o arterial spasms following arterial punctures.
6. Severe peripheral vascular disease.
7. Arterial grafts.

13. • ALLEN’s TEST:
1. Patient elevates hand & makes fist -20 sec.
2. Firm pressure against radial &ulnar ateries.
3. When patient opens hand it should be blanched white.
4. Examiner releases only ulnar compression.
5. Normally, hand color flushes within 5 sec(ulnar collateral
circulation).
6. Abnormal- Delayed/ absent hand flushing (inadequate
collateral circulation).

14. • MODIFIED ALLEN’s TEST: - Dorsalis Pedis/Posterior Tibial artery.
1. Elevate patient’s feet.
2. Occlude Dorsalis Pedis artery.
3. Blanch the great toe by compressing the great toe nail for several
seconds.
4. Release pressure on the nail & observe for flushing(adequate
collateral flow).
• Other means for assessment of collateral circulation:
1. Doppler ultrasound.
2. Finger Plethysmography.

15. PROCEDURE FOR ARTERIAL PUNCTURE
1. Patient should be in comfortable lying down/sitting position.
2. Thoroughly clean & hyperextend the site using rolled towel.
3. Take the 2cc syringe which is already flushed with 0.05-0.1 ml of Heparin (for
anti-coagulation of the sample).
4. Palpate the artery(not too firmly) & pierce it.
5. The sample collected should not contain air bubbles & the sample has to be
analysed within 10-15 mins ( if delayed, can be placed on ice for 1 hr).

16. Venous sample/Arterial sample?
• Dark ,Non-pulsatile blood that requires manual suction to aspirate  Venous
sample (except in severe shock/cardiac arrest).
• When SaO₂ in ABG is lower than that in pulse oximetry  Venous sample.

17. COMPLICATIONS:
1. Pain
2. Bruising &Hematoma
3. Nerve Damage
4. Aneurysms.
5. Spasms
6. AV fistula
7. Infection
8. Vasovagal response.
9. Air/ thromboembolism.
10.Anaphylaxis (Local anaesthetic).

18. BASICS OF ACID BASE DISORDERS
Four primary acid base disorders
Basic disorder pH HCO₃⁻ PaCO₂
Metabolic acidosis Low Low Low
Metabolic alkalosis High High High
Resp acidosis Low High High
Resp alkalosis High Low Low

19. Primary acid – base disorders
RESPIRATORY METABOLIC
(If primary disturbance
involves PaCO₂)
(If primary disturbance
involves HCO₃⁻)
ACIDOSIS ALKALOSIS ACIDOSIS ALKALOSIS

20. PHYSIOLOGICAL EFFECTS OF ACID BASE DISORDERS
ACIDOSIS ALKALOSIS
1. Right shift of O₂-Hb dissociation
curve.(severe acidosis tissue hypoxia).
1. Left shift of O₂ –Hb dissociation
curvetissue hypoxia.
2. Hyperkalemia, increased ionised plasma Ca₂⁺. 2. Hypokalemia & decreased ionised plasma
Ca₂⁺  tetany.
3. Vasodilatation- Systemic and cerebral vessels.
Vasoconstriction- pulmonary vessels.
3. Vasoconstriction- systemic
vessels,cerebral,coronary vessels.
Vasodilatation – pulmonary vessels.
4. Direct myocardial depression, decreased
threshold for ventricular fibrillation.
4. Anaerobic glycolysis lactic acidosis,
ketoacidosis.
5. Insulin resistance & inhibition of anaerobic
glycolysis.
5. Hypoventilation Hypoxia &hypercarbia.
- Bronchospasm.
5. Metabolic acidosis – Kussmaul’s respiration
and dyspnea.
Respiratory acidosis- Hypercapnia.

21. ACIDOSIS
RESPIRATORY ACIDOSIS METABOLIC ACIDOSIS
DEF: primary defect is primary increase in
PaCO₂  decreased [HCO₃⁻]/0.03 PaCO₂ ratio
 decreases pH.
DEF: primary defect is primary decrease in
[HCO₃⁻] decreased [HCO₃⁻]/0.03 PaCO₂ ratio.
CAUSES:
A) Alveolar Hypoventilation:
1. CNS depression.
2. Neuromuscular disorders.
3. Chest wall disorders.
4. Pleural disorders.
5. Airway obstruction.
6. Parenchymal diseases.
B) Increased CO2 production:
1. Large carbohydrate load.
2. Malignant hyperthermia.
3. Intensive shivering.
4. Increased seizures.
5. Thyroid storm.
6. Burns.
7. Permissive hypercarbia(ARDS).
CAUSES:
A) Anion Gap Metabolic Acidosis:
1. Increased endogenous non-volatile acids:
a) ARF,CRF.
b) Diabetic, Alchoholic,starvation
ketoacidosis.
c) Lactic acidosis.
2. Toxin ingestion.
3. Rhabdomyolysis.
B) Non-anion Gap Metabolic
Acidosis/Hyperchloremic metabolic acidosis:
1. Increased Renal HCO₃⁻ loss.
2. Increased gastrointestinal HCO₃⁻ loss.
3. Dilution of extracellular buffer by
bicarbonate free solutions.
4. Increased intake of Cl⁻ contaning acids.

22. RESPIRTORY ACIDOSIS METABOLIC ACIDOSIS
TREATMENT:
A. Rx of the cause.
B. Improve alveolar ventilation:
1. Mild cases:
Bronchodilators,Diuretics.
2. Moderate cases(pH< 7.2):
CO₂ narcosis,resp muscle fatigue
 Mech ventilation.
3. Severe cases(pH< 7.1):
IV NaHCO₃, Increased FiO₂.
TREATMENT:
A. Rx the cause.
B. Alkali therapy: NaHCO₃
- (When pH<7.1 or HCO₃⁻ <10
mmol/L.
- Dose: fixed dose -1 mmol/Kg or
acc. to the base deficit.
- Half correction:
- NaHCO₃ = BW x base deficit x 0.4 x
½.
- Serial blood gas measurements
done – to avoid overcorrection.
C. Other alkali therapy: Carbicarb, THAM.

23. ACIDOSIS- ANAESTHETIC CONSIDERATIONS.
1. Elective surgeries postponed.
2. Emergency surgeries- Invasive BP monitoring, repeated ABGs are
required.
3. Acidemia causes
a. Increase in depressant effects of sedatives & anaesthetic agents
on CNS &CVS.
b. Increase in non-ionised form of opioids (weak bases) 
penetration into brain.
c. Depression of airway reflexes Pulmonary aspiration.
d. Halothane  Arrhythmogenic effects.
e. Avoid Scoline (due to raised serum K⁺).
4. Respiratory acidosis  increase in non-depolarising blockade.

24. ALKALOSIS
RESPIRATORY ALKALOSIS METABOLIC ALKALOSIS
DEF: primary defect is primary decrease
in PaCO₂  increase in [HCO₃⁻]/ 0.03
PaCO₂ ratio  increases pH.
DEF: primary defect is primary increase in
HCO₃⁻  increased [HCO₃⁻]/ 0.03 PaCO₂
ratio  increases pH.
CAUSES:
A. Central stimulation: Pain,Anxiety,
Trauma, Infection, tumor, fever.
B. Peripheral stimulation: Hypoxemia,
high altitude, asthma, pulm emboli,
severe anemia.
C. Unknown mech: shock,metabolic
cirrhosis encephalopathy,
pregnancy.
D. iatrogenic: Ventilator-induced.
CAUSES:
A. Chloride-sensitive ( Volume or saline
responsive):
- Hypovolemia.
- Urine Cl⁻ < 10 mmol/L.
B. Chloride resistant:
- Volume overload
- Urine Cl⁻ >20 mmol/L.

25. RESPIRATORY ALKALOSIS METABOLIC ALKALOSIS
TREATMENT:
1. Rx the cause.
2. For severe alkalemia (pH>7.55):
- IV HCl 0.1 mmol/L.
- IV NH4Cl 0.1 mmol/L.
TREATMENT:
1. Rx the cause.
2. Chloride sensitive metabolic
alkalosis:
- NaCl, KCl.
- In severe alkalemia- IV diluted
HCl.
- Hemodialysis.
- On controlled ventilation.
3. Chloride resistant metabolic
alkalosis:
- Spironolactone ( for increased
mineralocorticoid activity).
- Stop exogenous
mineralocorticoids.

26. ANAESTHESTIC CONSIDERATIONS- ALKALOSIS
1. Elective surgeries –postponed.
2. Emergency surgeries- Invasive BP & repeated ABGs.
3. Alkalemia 
a. Increase in opioid induced respiratory depression.
b. Decrease in serum K⁺ 
Severe atrial & ventricular arrhythmias.
Potentiation of non-depolarizing blockade.
4. Respiratory alkalosis
a. Decrease in cerebral blood flow  cerebral ischemia.
b. Decrease in coronary blood flow  coronary ischemia.

27. METHODS OF ANALYSING ACID – BASE DISORDERS
1. Classic/traditional approach –
- Respiratory disorders are due to change in PaCO₂ &
- Metabolic disorders are due to change in HCO₃⁻.
2. STEWART approach –
- It’s variables are PaCO₂, Strong Ion Difference (SID) and Atot (total weak
acids).
3.THE SEMI-QUANTITATIVE (BASE DEFICIT/ EXCESS
[COPENHAGEN]) APPROACH
4. BOSTON APPROACH

28. STEPS FOR ABG ANALYSIS
1. What is pH? - Acidemia/Akalemia?
2. What is the primary disorder present?
3. Is there appropriate compensation?
4. Is the compensation acute/chronic?
5. Is there an anion gap?
6. If there is a anion gap, check for delta gap.

29. 1. Is there acidemia / alkalemia?
pH < 7.35 acidemia.
pH> 7.45  alkalemia.
Acidosis/ Alkalosis may also be present even if pH is in normal range.
Then, we need to check for PaCO₂, HCO₃⁻ and anion gap.

30. 2. What is the primary disorder?
Is the disturbance Respiratory / Metabolic?
- Direction of change in pH and change in PaCO₂.
- If pH and PaCO₂change in same direction METABOLIC disorder.
If pH and PaCO₂change in opposite direction  RESPIRATORY disorder.
Acidosis Respiratory pH ↓ PaCO₂ ↑
Acidosis Metabolic pH ↓ PaCO₂ ↓
Alkalosis Respiratory pH ↑ PaCO₂ ↓
Alkalosis Metabolic pH ↑ PaCO₂ ↑

31. 3. Is there appropriate compensation for primary disturbance?
4. Is the compensation acute / chronic?
The body’s response to neutralise the effect of the initial insult on pH homeostasis is
called compensation.
Compensatory changes are in same direction as the primary changes.
Rules of compensation:
1. Compensatory response depends on proper functioning of the organ system
involved(lungs & kidneys) and on severity of acid-base disturbance.
2. Kidneys- acute compensation- 6-24 hrs
- chronic compensation – 1-4 days

32. • Respiratory compensation occurs faster than metabolic compensation
3. .Maximum compensatory response- with only 50-75% return of pH to
normal.
4. Overcompensation never occurs.

33. Is there appropriate compensation for primary disturbance?
4. Is the compensation acute / chronic?
I. METABOLIC ACIDOSIS
↓ HCO₃⁻ 1 mEq/L below 24 mEq/L  ↓ PaCO₂ 1.2 mmHg.
∆PaCO₂ = 1.2 x ∆ HCO₃⁻
Expected PaCO₂ = 40 – [1.2 x (24 – HCO₃⁻)].
II. METABOLIC ALKALOSIS
↑HCO₃⁻ 1 mEq/L above 24 mEq/L  ↑ PaCO₂ 0.7 mm Hg.
∆ PaCO₂ = 0.7 x ∆ HCO₃⁻.
Expected PaCO₂ = 40 + [0.7 x (HCO₃⁻ – 24)].

34. III. RESPIRATORY ACIDOSIS
A. ACUTE RESP ACIDOSIS
↑ PaCO₂ 10 mm Hg above 40 mmHg  ↑ HCO₃⁻ 1 mEq/L.
∆ HCO₃⁻ = 0.1 x ∆ PaCO₂.
Expected HCO₃⁻ = 24 + [ 0.1 x (PaCO₂ -40)].
B. CHRONIC RESP ACIDOSIS
↑ PaCO₂ 10 mmHg above 40 mmHg  ↑ HCO₃⁻ 4 mEq/L.
∆ HCO₃⁻ = 0.4 x ∆ PaCO₂.
Expected HCO₃⁻ = 24 + [ 0.4 x (PaCO₂ – 40)].

35. IMPORTANCE OF CALCULATING AND CHECKING COMPENSATION:
1. Useful in differentiating simple from mixed disorder.
2. Expected change = actual change  simple disorder.
3. Expected change >/< actual change  mixed disorder.
4. If changes in compensation are in opposite direction  mixed
disorder.

36. MIXED DISORDER:
• If the directions of change in HCO₃⁻ and PaCO₂ are opposite to each
other (with pH either normal/abnormal).
• If the observed compensation is not the expected compensation, it is
likely that more than one acid-base disorder is present.

37. 5. Calculate anion gap (if metabolic acidosis exists).
Total serum cations = Total serum anions.
Normal Anion Gap = [Na⁺] – [ (Cl⁻) + (HCO₃⁻)]
=12 ± 2 mEq/L.
Anion Gap (modern) = 14-18 mEq/L (included lactates)
In patients with hypoalbuminemia, the normal anion gap is lower than 12 mEq/L;
(for 1 gm/dl decrease in albumin – 2.5 mEq/L decrease in normal anion gap)
Corr. Anion gap = Cal. Anion gap + 0.25 ( Normal Alb –Observed Alb.)

39. High anion gap
• Ketoacidosis
• Lactic acidosis
• Uremia
• Toxins
Methanol ,Ethylene glycol
Propylene glycol ,Salicylates
Paraldehyd
Decreased anion gap acidosis
Hypoalbuminemia
Paraproteinemia (multiple myeloma)
Spurious hypercholeremia
Bromide intoxication
Spurious hyponatremia
Hypermagnesemia

40. • Normal anion gap acidosis
• 1. Hypokalemic
a) GI losses of HCO3
Ureteral diversion
Diarrhea
Ileostomy
b) Renal loss of HCO3
proximal RTA
Carbonic anhydrase inhibitors
2. Normokalemic or hyperkalemic
a)Renal tubular disease
Acute tubula necrosis
chronic tubulo interstitial necrosis
Distal RTA
Hypoaldosteronisn
b)Pharmacological
Ammonium chloride
Hyperalimentation
dilutional acidosis

41. With elevated anion gap, calculate osmolar gap
OSM GAP = measured OSM – (2 [Na⁺]- Glucose/18 – BUN/2.8)
Normal OSM gap < 10.
If calculated osmolality differ from the measured osmolality by 15 mosm/Kg
H2O, this is called osmolar gap.

42. 6. If increased anion gap is present, assess the relationship between the increase in
the anion gap and the decrease in [HCO3].
DELTA RATIO:
Assess the ratio of the change in the anion gap to the change in HCO3 =
∆ AG / ∆ HCO 3= [AG -12]/[24 – HCO3]
(or) DELTA GAP: ∆ AG - ∆ HCO₃⁻
1.0 -2.0  uncomplicated anion gap metabolic acidosis.
If <1.0  concurrent non-anion gap metabolic acidosis.
If > 2.0  concurrent metabolic alkalosis.

43. • URINE SAMPLE ANALYSIS:
1. Urine Anion Gap = [Na⁺] + [K⁺] –[Cl⁻].
for hyperchloremic (non-anion gap) metabolic
acidosis.
If it is positive  Renal cause;
If it negative  Non-Renal cause.
2. Urinary Cl⁻ conc.: for metabolic alkalosis
Urinary Cl⁻ <10 mmol/L  Chloride sensitive;
Ur.Cl⁻ > 20mmol/L  chloride resistant.

44. pH
↑pH
(Alkalosis)
↓pH
(Acidosis)
Normal (or)
Abnormal HCO₃⁻ &
PaCO₂.
Metab (↑/ ↑) Resp (↑ / ↓)
Urine Cl⁻ level
<10 mmol/L
(Cl⁻ –sensitive)
>20 mmol/L
(Cl⁻ – resistant)
MIXED disorder
Metab (↓/ ↓) Resp (↑/ ↓)
Anion gap
High Normal
Urine anion
gap
Bicarbonate gap
> +6
(Met.alkalosis)
< -6
(Hyperchloremic
met acidosis)

46. References
• Clinical anesthesia- Barash 8th edition
• Millers anesthesia- 9th edition
• Objective anesthesia - 5th edition