Arterial blood gas

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Here is a thorough reference guide on Arterial Blood Gas (ABG) analysis, synthesized from multiple authoritative textbooks.

Arterial Blood Gas (ABG) Analysis

What Is an ABG?

An ABG directly measures pH, PaCO2, and PaO2 from an arterial blood sample and is the gold standard for assessing oxygenation, ventilation, and acid-base status. HCO3- is calculated using the Henderson-Hasselbalch equation. Blood gas analyzers may also report lactate, total hemoglobin, and serum electrolytes. - Tintinalli's Emergency Medicine, p. 121

Normal Values

Parameter	Normal Range
pH	7.35 - 7.45
PaCO2	35 - 45 mmHg (4.5 - 6 kPa)
PaO2	80 - 100 mmHg (11 - 14 kPa)
HCO3-	22 - 28 mEq/L
Anion Gap	10 - 16 mEq/L
SaO2	95 - 100%

Bailey and Love's Short Practice of Surgery, 28th Edition, p. 5115

Step-by-Step Interpretation

Step 1: Determine pH Status

Acidosis = pH < 7.35
Alkalosis = pH > 7.45
Normal = pH 7.35-7.45 (but a disorder + compensation may still exist)

Step 2: Identify the Primary Disorder

pH	PaCO2	HCO3-	Primary Disorder
Low (< 7.35)	High (> 45)	Normal/High	Respiratory Acidosis
High (> 7.45)	Low (< 35)	Normal/Low	Respiratory Alkalosis
Low (< 7.35)	Normal/Low	Low (< 22)	Metabolic Acidosis
High (> 7.45)	Normal/High	High (> 26)	Metabolic Alkalosis

Step 3: Assess for Expected Compensation

Compensation is never complete - it only moves pH toward normal, not to normal.

Primary Disorder	Compensation	Expected Change
Metabolic acidosis	Hyperventilation (↓ PCO2)	ΔPCo2 = 1.3 × ΔHCO3- (Winter's formula: PCO2 = 1.5×HCO3- + 8 ± 2)
Metabolic alkalosis	Hypoventilation (↑ PCO2)	ΔPCO2 = 0.6 × ΔHCO3-
Acute respiratory acidosis	Renal HCO3- retention	HCO3- ↑ by 1 mEq/L per 10 mmHg ↑ PCO2
Chronic respiratory acidosis	Full renal compensation	HCO3- ↑ by 3.5-5 mEq/L per 10 mmHg ↑ PCO2
Acute respiratory alkalosis	Renal HCO3- excretion	HCO3- ↓ by 2 mEq/L per 10 mmHg ↓ PCO2
Chronic respiratory alkalosis	Full renal compensation	HCO3- ↓ by 5 mEq/L per 10 mmHg ↓ PCO2

Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 4814

If compensation is outside the expected range, a mixed disorder is present.

Step 4: Calculate the Anion Gap (if metabolic acidosis)

Anion Gap (AG) = Na+ - (Cl- + HCO3-)

Normal = 8-12 mEq/L (or up to 16 if albumin-uncorrected)

Acid-Base Map

The diagram below plots pH vs. PCO2 and maps each acid-base zone, including mixed disorders:

Roberts and Hedges' Clinical Procedures in Emergency Medicine, Figure A.1

The Four Primary Disorders

1. Respiratory Acidosis

Cause: hypoventilation, COPD exacerbation, neuromuscular failure, opioid overdose
ABG: pH ↓, PaCO2 ↑, HCO3- normal (acute) or ↑ (chronic)
Acute: pH falls 0.08 per 10 mmHg rise in PCO2
Chronic: kidneys compensate over 3-5 days by retaining HCO3-

2. Respiratory Alkalosis

Cause: anxiety/hyperventilation, sepsis, PE, pregnancy, high altitude, pain
ABG: pH ↑, PaCO2 ↓, HCO3- normal (acute) or ↓ (chronic)
Example: The sepsis case above showed acute respiratory alkalosis with appropriate compensation (HCO3- drop of 3 from expected 3) - Roberts and Hedges', p. 4871

3. Metabolic Acidosis

ABG: pH ↓, HCO3- ↓, PCO2 ↓ (compensation)
Classified by anion gap:

Wide Anion Gap (MUDPILES):

M - Methanol
U - Uremia
D - Diabetic/alcoholic ketoacidosis
P - Paraldehyde/Polyethylene glycol/Paracetamol
I - Iron
L - Lactic acidosis (most common, ~50% of high-AG metabolic acidosis)
E - Ethylene glycol
S - Salicylates

Normal Anion Gap / Hyperchloremic (HARDUP):

H - Hyperalimentation / Hospital saline administration
A - Acid infusion / Addison's / Carbonic anhydrase inhibitors
R - Renal tubular acidosis
D - Diarrhea (GI bicarbonate loss)
U - Ureteral diversion
P - Pancreatic fistula

ROSEN's Emergency Medicine, p. 1647-1651

4. Metabolic Alkalosis

Cause: vomiting, NG suctioning, diuretics, hyperaldosteronism
ABG: pH ↑, HCO3- ↑, PCO2 ↑ (compensation)
Divided into chloride-responsive (urine Cl- < 20) and chloride-unresponsive (urine Cl- > 20)

Winter's Formula (Quick Check for Metabolic Acidosis Compensation)

Expected PCO2 = (1.5 × HCO3-) + 8 ± 2

If measured PCO2 > expected → additional respiratory acidosis (possible impending respiratory failure)
If measured PCO2 < expected → additional respiratory alkalosis (e.g., salicylate toxicity)
Useful mnemonic: expected pH last two digits ≈ PCO2 (e.g., PCO2 23 → pH ~7.23)

Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 4876-4891

ABG vs. Pulse Oximetry

Feature	ABG	Pulse Oximetry
pH	Yes	No
PaCO2	Yes	No
PaO2	Yes	Indirect (via saturation curve)
SaO2	Yes (directly)	Yes (SpO2)
Detects hypercarbia	Yes	No (especially on O2 therapy)
Detects CO/MetHb	Yes	No (falsely elevated SpO2)

A critical point: pulse oximetry cannot detect hypoventilation in patients on supplemental oxygen, because the added O2 keeps SpO2 on the flat portion of the oxyhemoglobin dissociation curve even as PCO2 rises significantly. Capnography or ABG is required for these patients. - Murray & Nadel's Textbook of Respiratory Medicine, p. 956-957

Alveolar-Arterial (A-a) Gradient

A-a PO2 = PAO2 - PaO2

Where: PAO2 = FiO2 × (PB - 47) - (PaCO2 / 0.8)

Normal A-a gradient on room air: ~10 mmHg (increases with age)
A-a > 20 mmHg with hypercapnia → underlying lung disease contributing (e.g., COPD, PE, pneumonia)
Normal A-a with hypercapnia → pure hypoventilation (e.g., CNS depression, neuromuscular disease)

Murray & Nadel's Textbook of Respiratory Medicine, p. 974

Worked Examples

Example 1 - Metabolic Acidosis with Compensation: 58-year-old with diarrhea: Na 133, K 2.8, Cl 118, pH 7.26, PCO2 13, HCO3- 5

Acidosis present (pH 7.26)
Primary: metabolic (HCO3- 5, low)
Check compensation: ΔPCO2 = 1.3 × (25-5) = 26 → predicted PCO2 = 40-26 = 14 (actual = 13) → appropriate compensation only, no mixed disorder

Example 2 - Respiratory Alkalosis (Sepsis): 74-year-old, septic: pH 7.49, PCO2 25, HCO3- 22

Alkalosis (pH 7.49)
Primary: respiratory (PCO2 25, low)
Expected ΔHCO3- for 15 mmHg drop in PCO2 = 3 mmol/L → predicted HCO3- = 25-3 = 22 (actual = 22) → pure acute respiratory alkalosis

Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 4824-4871

Difference between spo2 vs sao2

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Here is a detailed comparison drawn from multiple authoritative textbooks.

SpO2 vs SaO2

Quick Definitions

	SpO2	SaO2
Full name	Peripheral oxygen saturation	Arterial oxygen saturation
Method	Pulse oximetry (non-invasive)	Co-oximetry on ABG (invasive)
What it measures	Functional saturation	Fractional saturation
Continuous?	Yes	No (point-in-time)
Requires blood draw?	No	Yes (arterial sample)

The Key Mathematical Difference

This is the most important distinction - they use different formulas:

SpO2 (functional saturation) - what pulse oximetry measures:

SpO2 = HbO2 / (HbO2 + Hb) × 100%

It only considers oxyhemoglobin vs. deoxyhemoglobin - it ignores dyshemoglobins entirely.

SaO2 (fractional saturation) - what ABG co-oximetry measures:

SaO2 = HbO2 / (HbO2 + Hb + COHb + MetHb) × 100%

It accounts for ALL hemoglobin species, including dysfunctional forms. - Barash Clinical Anesthesia, 9e, p. 2100

How Pulse Oximetry Works (and Why It Can Be Wrong)

Pulse oximetry uses two wavelengths of light:

660 nm (red) - absorbed more by deoxyhemoglobin
940 nm (near-infrared) - absorbed more by oxyhemoglobin

It performs a plethysmographic analysis to isolate the pulsatile (arterial) signal from venous blood and tissue background. The ratio of absorbance at these two wavelengths determines SpO2. - Barash Clinical Anesthesia, 9e, p. 2099-2100

The problem: this 2-wavelength system cannot distinguish other hemoglobin species that absorb light at the same wavelengths.

The Oxyhemoglobin Dissociation Curve - Why Both Matter

Oxyhemoglobin dissociation curve showing normal, left-shifted, and right-shifted curves relating saturation to pO2

Barash Clinical Anesthesia, 9e - Oxyhemoglobin dissociation curve

SpO2 and SaO2 relate to PaO2 via this sigmoid curve. At PaO2 > 75 mmHg, both measurements plateau on the flat upper portion - meaning large drops in PaO2 can occur with minimal change in either saturation. This is why a normal SpO2 does not rule out significant hypoxemia. - Barash Clinical Anesthesia, 9e, p. 2099

When SpO2 and SaO2 Diverge

1. Dyshemoglobins (most clinically important)

Condition	SpO2 reads	Actual SaO2	Reason
Carbon monoxide poisoning (COHb)	Falsely HIGH (SpO2 ~90%+ even at 70% COHb)	Low	COHb absorbs at 660 nm like O2Hb - pulse ox mistakes it for oxyHb
Methemoglobinemia (MetHb)	Approaches 85% regardless of true SaO2	Variable	MetHb absorbs 660/940 nm equally (R-ratio = 1 = 85%)
Sulfhemoglobin	SpO2 ~85%	Variable	Hb absorbs red light heavily

Miller's Anesthesia, 10e, p. 5464 and Barash, 9e, p. 2100

2. Accuracy at Low Saturations

When SaO2 > 90%: average SpO2 vs SaO2 difference is < 2% - clinically acceptable. When SaO2 drops below 90%: the discrepancy increases, making SpO2 unreliable in severe hypoxemia. - Fishman's Pulmonary Diseases, p. 2596

3. Racial Disparity

SpO2 overestimates SaO2 in Black patients. In one study, occult hypoxemia (true SaO2 <88%) was three times more frequent in Black patients with an SpO2 reading of 92-96% compared with white patients. Skin pigmentation alters light absorption at the probe site. - Fishman's Pulmonary Diseases, p. 2596

4. Technical / Physiologic Errors in SpO2

Source of Error	Effect on SpO2 vs SaO2
Hypotension / poor perfusion	SpO2 ↓ (falsely low)
Motion artifact	SpO2 ↓
Dark nail polish	SpO2 ↓
Methemoglobin	SpO2 → 85% (either ↑ or ↓)
Carboxyhemoglobin	SpO2 falsely ↑
Anemia	SpO2 ↓
Polycythemia	No significant effect
Venous pulsations (e.g., TR, Trendelenburg)	SpO2 ↓ (venous O2 detected)
Excessive ambient light	Variable

Miller's Anesthesia, 10e - Table 37.1, p. 5465

When to Use ABG (SaO2) Instead of Pulse Oximetry (SpO2)

Use ABG/co-oximetry for SaO2 when:

Suspected CO poisoning (SpO2 will be falsely normal)
Suspected methemoglobinemia (SpO2 locks near 85%)
Critically ill patients where ±2% error is not acceptable
Patient on supplemental oxygen with suspected hypoventilation (SpO2 cannot detect rising PaCO2)
Suspected dyshemoglobinemia (e.g., sulfhemoglobin from dapsone/nitrates)
Any situation where SpO2 and clinical picture do not match

Fishman's Pulmonary Diseases, p. 2597

Summary in One Line

SpO2 is a convenient continuous estimate; SaO2 from co-oximetry is the ground truth - they agree well in normal physiology, but diverge critically when dyshemoglobins are present, in severe hypoxemia, or in low-perfusion states. In CO poisoning especially, SpO2 can be dangerously misleading.

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