Arterial Blood Gas (ABG) Analysis

Table of Contents

Image: “Cobas b 121 (Roche Diagnostics) – measurement chamber (detail). From the left: Reference electrode Sample’s conductivity electrode Na+ electrode Cl- electrode pH (glass) electrode Sample’s conductivity electrode Ca2+ electrode K+ electrode pO2 (Clark) electrode pCO2) (Sveringhaus) electrode Hemoglobin/Hematocrit chamber. Emergency Laboratory, Hospital de Niños, Córdoba, Arg.” by J3D3 – Own work. License: CC BY-SA 3.0

Overview of ABG Analysis

Analysis of arterial blood gases (ABG) is an essential investigation in the management of critically ill patients as it provides important information about alveolar ventilation, oxygenation, and acid-base balance.

Measurement of ABG includes measurement of three parameters, i.e., pH, PaCO₂, and PaO₂; however, measurement of bicarbonate (HCO_3^–) and electrolytes is almost always done simultaneously to complete the whole picture of acid-base & electrolyte balance/imbalance.

Important values

Normal blood pH: 7.36–7.44
Acidemia: pH < 7.35
Alkalemia: pH > 7.45

PaCO₂& PaC0₂

Normal PaO₂: 80–100 mm Hg
Normal PaCO₂: 36–44 mm Hg
Respiratory acidosis: Acidemia with PaCO₂ > 44 mm Hg
Respiratory alkalosis: Alkalemia with PaCO₂ < 36 mm Hg

HCO_3^–

Normal HCO₃-: 20–28 mEq/L
Metabolic acidosis: Acidemia with HCO_3^– < 20 mEq/L
Metabolic alkalosis: Alkalemia with HCO_3^– > 28 mEq/L
Normal base excess/deficit: 0 ± 2 mEq/L

Anion Gap

Normal Anion Gap (AG): 12 mEq/L
Anion Gap Metabolic Acidosis (AGMA): Metabolic acidosis with AG > 12
Non-Anion Gap Metabolic Acidosis (NAGMA): Metabolic acidosis with normal AG

“Acidosis and Alkalosis” by Kapil Pal

Basic Physiological Concepts

PaCO₂ is the best parameter that reflects alveolar ventilation; high (> 44 mm Hg) and low (< 36 mm Hg) PaCO₂ levels suggest alveolar hypoventilation and alveolar hyperventilation respectively.

The status of oxygenation is affected mainly by PaO₂, FiO₂, and hemoglobin content along with its affinity and saturation with oxygen. The presence of hypoxemia (PaO₂ < 80 mm Hg at sea level while breathing room air) does not necessarily mean the presence of hypoxia.

Blood pH is maintained in the narrow range (7.36–7.44) by lungs, kidneys and blood buffers. In general, the blood buffer system (H₂CO₃/HCO_{3^–) acts within a fraction of seconds, the respiratory system takes about 1–15 minutes, and kidneys may take many minutes to many days to adjust H⁺ ions concentration.}

PaCO₂ is mainly controlled by lungs and is a marker of respiratory acid-base disturbance. HCO_3- is mainly controlled by kidneys and blood buffers, but it does not always purely indicate metabolic acid-base disturbance as it is affected by hydrolysis effect.

Plasma bicarbonate can be calculated using the Henderson-Hasselbalch equation; while standard bicarbonate is plasma bicarbonate obtained after blood has been equilibrated at 37°C with a PaCO₂ of 40 mm Hg.

Henderson-Hasselbalch equation: pH = 6.1 + log10 ([HCO3-]/0.03 x PaCO2)

The difference between the measured bicarbonate and the calculated bicarbonate is known as base excess (if positive value) or base deficit (if negative value).

In acidemia, an excess of H⁺ ions enter intracellular space, hence, K⁺ ions move out from intracellular space into the plasma to maintain electroneutrality. Thus, acidemia is associated with hyperkalemia.

In distal renal tubular cells, K⁺ or H⁺ ions are exchanged for Na⁺ ions. In alkalemia, as H⁺ ions are retained, K⁺ ions are exchanged for Na⁺ ions, leading to hypokalemia.

Compensation: In response to primary acid-base disturbance, the respiratory system or kidneys attempt to maintain normal pH by the compensatory response. Compensation “moves the pH towards normal”, but compensation can never “overshoot” the normal pH.

Respiratory compensation for a primary metabolic derangement is immediate and usually improves over the course of hours, while renal compensation for a primary respiratory derangement is gradual and improves over days as it takes time for the kidneys to generate/eliminate HCO₃.

“Davenport (Acid/Base) Diagram” by Kapil Pal

Anion Gap (AG)

Calculation of anion gap is very important for metabolic acidosis. In electroneutrality:

Unmeasured anions + Cl^– + HCO₃– = Unmeasured cations + Na⁺

Unmeasured anions are usually proteins, SO₄, PO₄, organic anions, etc. and unmeasured cations are K⁺, Ca⁺⁺, Mg⁺⁺, etc. Therefore:

Anion Gap (AG) = Na⁺ – (Cl^– + HCO₃–) = Unmeasured anions – Unmeasured cations

An elevated anion gap refers to an increase in unmeasured anions. Normal AG: 12 mEq/L

Respiratory Acidosis

Key features: pH < 7.35 with PaCO₂ > 44 mm Hg

Causes: Basically, causes of respiratory acidosis are those that cause CO₂ retention or hypoventilation.

Upper airway disorders such as obstruction, laryngospasm, obstructive sleep apnea
Lower airway disorders such as COPD, asthma
Thoracic cage abnormalities restricting respiratory movements such as flail chest, kyphoscoliosis
Neuromuscular disorders affecting ventilation such as AIDP
CNS depression due to CNS disorders, opioids, sedatives, etc.
Respiratory muscle fatigue following any prolonged/severe respiratory disease

Respiratory Alkalosis

Key features: pH > 7.45 with PaCO₂ < 36 mm Hg

Causes: Basically, causes of respiratory alkalosis are those that cause CO₂ washout or hyperventilation.

Hyperventilation due to pain, anxiety, hysteria, CNS tumor/disorder, pulmonary embolism, etc.
Hypoxemia due to high altitude or any other cause
Early salicylate poisoning

Metabolic Acidosis

Key features: pH < 7.35 with HCO₃– < 20 mEq/L

Metabolic acidosis is further sub-classified on the basis of anion gap.

Anion Gap (AG) = Na⁺ – (Cl^– + HCO₃-)/p>

Causes of high Anion Gap Metabolic Acidosis (AGMA) (AG > 12 mEq/L):

Methanol (formic acid) poisoning
Uremia
Diabetic ketoacidosis, Drugs
Propylene glycol poisoning
Iron poisoning, Isoniazid
Lactic acidosis
Ethylene glycol (→ oxalic acid) poisoning, Ethanol poisoning (Alcoholic ketoacidosis)
Salicylate poisoning

⇒ Mnemonic: MUDPILES

Lactic acidosis
Uremia
Salicylate poisoning
Iron poisoning, Isoniazid
Diabetic ketoacidosis, Drugs
Alcohol poisoning (methanol, ethanol, ethylene glycol, propylene glycol)

⇒ Mnemonic: LUSID Alcohol

Causes of Normal Anion Gap Metabolic Acidosis (NAGMA):

Hyperalimentation (TPN)
Aldosterone related (Addison disease, spironolactone, RTA type IV)
Acetazolamide
Renal tubular acidosis
D iarrhea, ureteral Diversion (ileal loop), after DKA treatment
Fluids (after volume resuscitation with low HCO₃– fluids such as normal saline)

⇒ Mnemonic: HAARD Fluids

Metabolic Alkalosis

Key features: pH > 7.45 with HCO₃– > 28 mEq/L

Metabolic alkalosis is further sub-classified into saline-responsive (generally low urine Cl^–) and saline-resistant (generally high urine Cl^–) metabolic alkalosis. Causes of saline-responsive metabolic alkalosis:

Gastrointestinal losses (emesis, nasogastric tube aspiration, villous adenoma, etc)
Diuretics
Post-hypercapnia

⇒ Mnemonic: GDP

Causes of saline-resistant metabolic alkalosis:

Licorice ingestion
Mineralocorticoid excess (hyperaldosteronism, Cushing’s syndrome, exogenous administration)
Bartter’s syndrome
Exogenous Alkali load
Gitelman’s syndrome

⇒ Mnemonic: LiMi BAG

Stepwise Approach to Interpret ABG Analysis

Step 1: Is there acidemia or alkalemia?

If pH < 7.35 → Acidemia
If pH > 7.45 → Alkalemia

“Step 1” by Kapil Pal

Step 2: Use PCO₂ to determine the primary derangement

In acidemia:

If PCO₂ > 40 mm Hg → Respiratory acidosis
If PCO₂ < 40 mm Hg → Metabolic acidosis

In alkalemia:

If PCO₂ > 40 mm Hg → Metabolic alkalosis
If PCO₂ < 40 mm Hg → Respiratory alkalosis

“Step 2” by Kapil Pal

Step 3: Determine if compensation is adequate

For primary metabolic derangement, respiratory compensation is usually immediate and improves over the course of hours. For primary respiratory derangement, renal compensation is usually gradual and improves over days. It also depends on whether the condition is acute or chronic.

“Arterial Blood Gases” by Kapil Pal

In respiratory acidosis, for every 10 mm Hg increase in PaCO₂:

In acute condition: pH decreases by 0.08 and HCO₃– increases by 1
In chronic condition: pH decreases by 0.03 and HCO₃– increases by 4

In respiratory alkalosis, for every 10 mm Hg decrease in PaCO₂:

In acute condition: pH increases by 0.08 and HCO₃– decreases by 2
In chronic condition: pH increases by 0.03 and HCO₃– decreases by 4

“Step 3” by Kapil Pal

Step 3a: If the expected value for the level of compensation does not correlate with the measured value (pH or HCO₃-), then there is likely a mixed disorder present

In metabolic derangements:

If PCO2 is higher than expected → Concomitant respiratory acidosis
If PCO2 is lower than expected → Concomitant respiratory alkalosis

In respiratory derangements:

If pH is higher than expected → Concomitant metabolic alkalosis
If pH is lower than expected → Concomitant metabolic acidosis

“Step 3a” by Kapil Pal

Step 4: For all metabolic acidosis, calculate the Anion Gap

Anion gap = Na⁺ – (Cl- + HCO₃-) (Normal: 12 mEq/L)

AG should be corrected for hypoalbuminemia: For every 1 mg/dL below 4 → subtract 3 to the “normal” anion gap.

“Step 4” by Kapil Pal

For elevated anion gap metabolic acidosis (AGMA):

Important work up for AGMA includes urine ketones, renal function tests, serum lactate, toxin screen and osmolar(OG). (See the causes.)

OG = Measured osmolality – Calculated osmolality
Calculated osmolality = 2(Na⁺) + Glucose/18 + BUN/2.8
If OG > 10 → suggests the possibility of ingestion as a cause of AGMA

Another important consideration is to calculate ΔAG (change in AG) and ΔHCO₃– (change in bicarbonate).

ΔAG = Patient’s AG – Normal AG

If ΔAG = ΔHCO₃– → pure AGMA
If Δ AG > Δ HCO₃– → concomitant metabolic alkalosis
If Δ AG < Δ HCO₃– → concomitant non-anion gap metabolic acidosis or chronic respiratory acidosis

Example 1: HCO₃– = 16, AG = 20

Unmeasured anions Δ AG = 20 – 12 = 8 (normal AG = 12)

Δ HCO₃– = 24 – 16 = 8 (normal HCO₃– = 24)

Thus, ΔHCO₃– = Δ AG = 8 → pure AGMA

Example 2: HCO₃– = 10, AG = 20

Unmeasured anions Δ AG = 20 – 12 = 8

ΔHCO₃– = 24 – 10 = 14

Thus, Δ HCO< _{3- ≠ Δ AG}

8 mEq of change in HCO₃– is accounted for by AG acidosis; additional (14 – 8=) 6 mEq of change in HCO₃– must have been caused by non-AG acidosis → combined AG and non-AG acidosis.

For normal anion gap metabolic acidosis (NAGMA):

Check Urine Anion Gap: UNa⁺ + UK⁺ – UCl^–

If urine AG is positive, it implies HCO₃– loss by the kidneys as in renal tubular acidosis.
If urine AG is negative, it implies HCO₃– loss from an external source as in gastrointestinal losses.

Step 5: Review differential diagnosis

Refer to causes of acid-base disorders described above and correlate them with the conclusion before making a final diagnosis.

Review Questions

The correct answers can be found below the references.

1. Which of the following is not associated with high anion gap metabolic acidosis?

Salicylate poisoning
Iron poisoning
Acetazolamide poisoning
Ethanol poisoning
Isoniazid poisoning

2. Which of the following conditions is associated with saline-responsive metabolic alkalosis?

Post-hypercapnia
Licorice ingestion
Cushing’s syndrome
Exogenous alkali administration
Gitelman’s syndrome

3. In a patient with metabolic acidosis, anion gap is 22 mEq/L and serum HCO3- is 16 mEq/L. What is the acid-based imbalance?

Pure anion gap metabolic acidosis
Anion gap metabolic acidosis with concomitant non-anion gap metabolic acidosis
Anion gap metabolic acidosis with concomitant respiratory acidosis
Anion gap metabolic acidosis with concomitant metabolic alkalosis
Anion gap metabolic acidosis with concomitant non-anion gap metabolic acidosis and respiratory acidosis

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