ARTERIAL BLOOD GAS

ANALYSIS
Presenter: Dr. M. Krishnaveni
Moderator: Dr. Sri satya
• 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.
• 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
•
• 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
 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.
CLINICAL TERMINOLOGY CRITERIA

1. Normal pH 7.4 (7.35 – 7.45)

2. Acidemia pH < 7.35
3. Alkalemia pH > 7.45
4. Normal PaCO₂ 40 (35 – 45 mmHg)
5. Resp acidosis PaCO₂ > 45 mm Hg and low pH.
6. Resp alkalosis PaCO₂ < 35 mmHg and high pH.
7. Normal HCO₃⁻ 41 (22-26) mEq/L.
8. Metabolic acidosis HCO₃⁻ < 22 mEq/L and low pH.
9. Metabolic alkalosis HCO₃⁻ > 26 mEq/L and high pH.
 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
• 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.
• 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.
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).
• 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.
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.
• 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).
• 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.
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).
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.
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).
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

 Primary acid – base disorders

RESPIRATORY METABOLIC

(If primary disturbance (If primary disturbance

involves PaCO₂) involves HCO₃⁻)

ACIDOSIS ALKALOSIS ACIDOSIS ALKALOSIS

PHYSIOLOGICAL EFFECTS OF ACID BASE DISORDERS
ACIDOSIS ALKALOSIS
1. Right shift of O₂-Hb dissociation curve. 1. Left shift of O₂ –Hb dissociation
(severe acidosis tissue hypoxia). curvetissue hypoxia.

2. Hyperkalemia, increased ionised plasma 2. Hypokalemia & decreased ionised plasma

Ca₂⁺. Ca₂⁺  tetany.

3. Vasodilatation- Systemic and cerebral 3. Vasoconstriction- systemic

vessels. vessels,cerebral,coronary vessels.
Vasoconstriction- pulmonary vessels. Vasodilatation – pulmonary vessels.

4. Direct myocardial depression, decreased 4. Anaerobic glycolysis lactic acidosis,

threshold for ventricular fibrillation. ketoacidosis.
5. Insulin resistance & inhibition of anaerobic 5. Hypoventilation Hypoxia &hypercarbia.
glycolysis. - Bronchospasm.

5. Metabolic acidosis – Kussmaul’s respiration

and dyspnea.
Respiratory acidosis- Hypercapnia.
 ACIDOSIS
RESPIRATORY ACIDOSIS METABOLIC ACIDOSIS

DEF: primary defect is primary increase in DEF: primary defect is primary decrease in
PaCO₂  decreased [HCO₃⁻]/0.03 PaCO₂ ratio [HCO₃⁻] decreased [HCO₃⁻]/0.03 PaCO₂ ratio.
 decreases pH.

CAUSES: CAUSES:
A) Alveolar Hypoventilation: A) Anion Gap Metabolic Acidosis:
1. CNS depression. 1. Increased endogenous non-volatile
2. Neuromuscular disorders. acids:
3. Chest wall disorders. a) ARF,CRF.
4. Pleural disorders. b) Diabetic, Alchoholic,starvation
5. Airway obstruction. ketoacidosis.
6. Parenchymal diseases. c) Lactic acidosis.
B) Increased CO2 production: 2. Toxin ingestion.
7. Large carbohydrate load. 3. Rhabdomyolysis.
8. Malignant hyperthermia. B) Non-anion Gap Metabolic
9. Intensive shivering. Acidosis/Hyperchloremic metabolic acidosis:
10. Increased seizures. 1. Increased Renal HCO₃⁻ loss.
11. Thyroid storm. 2. Increased gastrointestinal HCO₃⁻ loss.
12. Burns. 3. Dilution of extracellular buffer by
13. Permissive hypercarbia(ARDS). bicarbonate free solutions.
4. Increased intake of Cl⁻ contaning acids.
RESPIRTORY ACIDOSIS METABOLIC ACIDOSIS
TREATMENT: TREATMENT:
A. Rx of the cause. A. Rx the cause.
B. Improve alveolar ventilation: B. Alkali therapy: NaHCO₃
1. Mild cases: - (When pH<7.1 or HCO₃⁻ <10
Bronchodilators,Diuretics. mmol/L.
2. Moderate cases(pH< 7.2): - Dose: fixed dose -1 mmol/Kg or
CO₂ narcosis,resp muscle fatigue acc. to the base deficit.
 Mech ventilation. - Half correction:
3. Severe cases(pH< 7.1): - NaHCO₃ = BW x base deficit x 0.4 x
IV NaHCO₃, Increased FiO₂. ½.
- Serial blood gas measurements
done – to avoid overcorrection.
C. Other alkali therapy: Carbicarb, THAM.
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.
 ALKALOSIS
RESPIRATORY ALKALOSIS METABOLIC ALKALOSIS
DEF: primary defect is primary decrease DEF: primary defect is primary increase in
in PaCO₂  increase in [HCO₃⁻]/ 0.03 HCO₃⁻  increased [HCO₃⁻]/ 0.03 PaCO₂
PaCO₂ ratio  increases pH. ratio  increases pH.

CAUSES: CAUSES:
A. Central stimulation: Pain,Anxiety, A. Chloride-sensitive ( Volume or saline
Trauma, Infection, tumor, fever. responsive):
B. Peripheral stimulation: Hypoxemia, - Hypovolemia.
high altitude, asthma, pulm emboli, - Urine Cl⁻ < 10 mmol/L.
severe anemia. B. Chloride resistant:
C. Unknown mech: shock,metabolic - Volume overload
cirrhosis encephalopathy, - Urine Cl⁻ >20 mmol/L.
pregnancy.
D. iatrogenic: Ventilator-induced.
RESPIRATORY ALKALOSIS METABOLIC ALKALOSIS
TREATMENT: TREATMENT:
1. Rx the cause. 1. Rx the cause.
2. For severe alkalemia (pH>7.55): 2. Chloride sensitive metabolic
- IV HCl 0.1 mmol/L. alkalosis:
- IV NH4Cl 0.1 mmol/L. - 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.
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.
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
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.

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.
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 ↑
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
• Respiratory compensation occurs faster than metabolic compensation
3. .Maximum compensatory response- with only 50-75% return of pH to
normal.
4. Overcompensation never occurs.
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)].
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)].
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.
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.
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.)
High anion gap Decreased anion gap acidosis
• Ketoacidosis Hypoalbuminemia
• Lactic acidosis Paraproteinemia (multiple myeloma)
• Uremia Spurious hypercholeremia
• Toxins Bromide intoxication
Methanol ,Ethylene glycol Spurious hyponatremia
Propylene glycol ,Salicylates Hypermagnesemia
Paraldehyd
• Normal anion gap acidosis
• 1. Hypokalemic 2. Normokalemic or hyperkalemic
a) GI losses of HCO3 a)Renal tubular disease
Acute tubula necrosis
Ureteral diversion
chronic tubulo interstitial necrosis
Diarrhea Distal RTA
Ileostomy Hypoaldosteronisn
b) Renal loss of HCO3 b)Pharmacological
Ammonium chloride
proximal RTA
Hyperalimentation
Carbonic anhydrase inhibitors dilutional acidosis
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.
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.
• 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.
 pH

↑pH Normal (or) ↓pH

(Alkalosis) Abnormal HCO₃⁻ & (Acidosis)
PaCO₂.

Metab (↓/ ↓) Resp (↑/ ↓)

Metab (↑/ ↑) Resp (↑ / ↓) MIXED disorder

Anion gap
Urine Cl⁻ level

High Normal
<10 mmol/L >20 mmol/L
(Cl⁻ –sensitive) (Cl⁻ – resistant) Bicarbonate gap
Urine anion
gap
> +6 < -6
(Met.alkalosis) (Hyperchloremic met
acidosis)
 References
• Clinical anesthesia- Barash 8th edition
• Millers anesthesia- 9th edition
• Objective anesthesia - 5th edition