Abg analysis

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Arterial Blood Gas (ABG) Analysis

Normal Values

ParameterNormal Range
pH7.35 - 7.45
PaCO235 - 45 mm Hg
PaO270 - 95 mm Hg (age-dependent)
HCO3-22 - 26 mmol/L
Base Excess (BE)-2 to +2 mEq/L
SaO295 - 100%
  • pH < 7.35 = acidemia; pH > 7.45 = alkalemia
  • PaCO2 < 35 = hyperventilation; PaCO2 > 45 = hypoventilation/hypercapnia

Step-by-Step Interpretation

Step 1 - Determine the pH

  • < 7.35 = Acidosis
  • > 7.45 = Alkalosis
  • 7.35-7.45 = Normal (but a disorder may still exist - check other values)

Step 2 - Identify the Primary Disorder

DisorderpHPaCO2HCO3-
Respiratory acidosisNormal/↑
Respiratory alkalosisNormal/↓
Metabolic acidosisNormal/↓
Metabolic alkalosisNormal/↑
Rule: The parameter that matches the pH change is the primary driver.

Step 3 - Assess Compensation

Compensation is never complete - it only partially corrects the pH.
Primary DisorderCompensatory ResponseFormula
Metabolic acidosis↓ PCO2 (hyperventilation)Expected PCO2 = 1.3 × ΔHCO3- below normal; or Winter's formula: PCO2 = (1.5 × HCO3-) + 8 ± 2
Metabolic alkalosis↑ PCO2 (hypoventilation)Expected ΔPCO2 = 0.6 × ΔHCO3-
Respiratory acidosis (acute)↑ HCO3- (buffering)HCO3- ↑ 1 mmol/L per 10 mm Hg ↑ PCO2
Respiratory acidosis (chronic)↑ HCO3- (renal)HCO3- ↑ 4 mmol/L per 10 mm Hg ↑ PCO2
Respiratory alkalosis (acute)↓ HCO3-HCO3- ↓ 2 mmol/L per 10 mm Hg ↓ PCO2
Respiratory alkalosis (chronic)↓ HCO3- (renal)HCO3- ↓ 5 mmol/L per 10 mm Hg ↓ PCO2
Key: If measured compensation does NOT match predicted, a mixed disorder is present.
  • Respiratory compensation for metabolic disorders: rapid (minutes-hours)
  • Metabolic compensation for respiratory disorders: slow (3-5 days for full renal compensation)

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

Anion Gap = Na+ - (Cl- + HCO3-)
  • Normal AG: 8-12 mEq/L (some use 12 as upper limit)
  • Correct for albumin: for every 1 g/dL drop in albumin below 4, add 2.5 mEq/L to measured AG
High AG Metabolic Acidosis (MUDPILES)Normal AG Metabolic Acidosis (HARDUP)
MethanolHyperalimentation / Hospital saline
UremiaAcid infusion / Addison's disease / Carbonic anhydrase inhibitors
DKA (diabetic ketoacidosis)Renal tubular acidosis
Paraldehyde / Propylene glycolDiarrhea
Iron / IsoniazidUreteral diversion
Lactic acidosisPancreatic fistula
Ethylene glycol
Salicylates

Step 5 - Assess Oxygenation

A-a Gradient = FiO2 × (Patm - PH2O) - (PaO2 + PaCO2/0.8)
Simplified estimate of normal A-a gradient: (Age/4) + 4
Mechanism of HypoxemiaA-a Gradient
V/Q mismatch (e.g., pneumonia, PE)Increased
Diffusion impairment (e.g., ILD)Increased
R-to-L shuntIncreased
HypoventilationNormal
Altitude / low FiO2Normal
Hepatopulmonary syndromeIncreased
Normal PaO2 by age (sitting): PaO2 = 104.2 - (0.27 × age in years)

Acid-Base Map

This diagram plots pH vs PCO2 with labeled zones for each primary and mixed disorder:
Acid-Base Map showing zones for metabolic acidosis, metabolic alkalosis, acute/chronic respiratory acidosis and alkalosis, and mixed disorders
Roberts and Hedges' Clinical Procedures in Emergency Medicine
  • Zone 1 (upper right, red): Mixed respiratory + metabolic acidosis
  • Zone 2 (lower left, pink): Mixed respiratory + metabolic alkalosis
  • Zone 3 (lower right, yellow): Metabolic alkalosis + respiratory acidosis
  • Zone 4 (upper left, orange): Metabolic acidosis + respiratory alkalosis
  • N (center): Normal

Worked Examples

Example 1 - Metabolic acidosis with compensation: A 58-year-old with 1 week of diarrhea: Na+ 133, K+ 2.8, pH 7.26, Cl- 118, PCO2 13, HCO3- 5
  1. pH < 7.40 → acidosis
  2. HCO3- is low, PCO2 is not elevated → primary metabolic acidosis
  3. Expected PCO2 = 40 - (1.3 × [25-5]) = 40 - 26 = 14 mm Hg; actual = 13 → appropriate compensation, no mixed disorder
Example 2 - Respiratory alkalosis (sepsis): A 74-year-old with sepsis: pH 7.49, PCO2 25, HCO3- 22
  1. pH > 7.45 → alkalosis
  2. PCO2 low, HCO3- normal → primary respiratory alkalosis
  3. Cause: hyperventilation from sepsis/fever

Quick Reference: Henderson-Hasselbalch Equation

pH = 6.1 + log10([HCO3-] / 0.003 × PaCO2)
This is the backbone of ABG interpretation. Any change in HCO3- (metabolic) or PaCO2 (respiratory) drives a change in pH.

Venous Blood Gas (VBG) vs. ABG

  • Venous pH averages ~0.03 lower than arterial
  • PvCO2 averages 3-8 mm Hg higher than PaCO2
  • VBG is unreliable in hypotensive patients and severe hypercapnia
  • A normal PvCO2 can be used to exclude hypercapnia
Sources: Goldman-Cecil Medicine, Roberts & Hedges' Clinical Procedures in Emergency Medicine, Barash's Clinical Anesthesia, ROSEN's Emergency Medicine

Abg analysis from.basics.to.clinicals

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This is a complete ABG guide covering everything from physiology to clinical application. Here's what's included:
Part 1 - Physiology: Why the body needs tight pH control, Henderson-Hasselbalch equation, the three buffer systems (chemical, respiratory, renal) and their speeds.
Part 2 - Normal Values: All parameters with clinical significance.
Part 3 - The 6-Step Approach:
  1. pH status
  2. Primary disorder identification
  3. Compensation assessment (with all formulas)
  4. Anion gap + albumin correction (MUDPILES / HARDUP)
  5. Urine anion gap for normal-AG acidosis
  6. Delta-delta ratio to unmask hidden mixed disorders
Part 4 - Four Primary Disorders in Depth: Each with pathophysiology, causes, clinical features, and management - including lactic acidosis Type A/B, metabolic alkalosis chloride-responsive vs. resistant, permissive hypercapnia in ARDS, and respiratory alkalosis as an early sepsis sign.
Part 5 - Osmolar Gap: Toxic alcohol ingestion, estimation formulas.
Part 6 - Oxygenation: A-a gradient and all six mechanisms of hypoxemia.
Part 7 - Mixed Disorders: Using the acid-base map and Δ/Δ ratio with classic clinical scenarios.
Part 8 - Four Worked Clinical Cases: DKA with hidden metabolic alkalosis, ethylene glycol ingestion, early sepsis, and acute-on-chronic COPD.
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