ABGs Flashcards
What are the normal blood gas values?
What is an acid and a base?
What is pH homeostasis?
- Respiratory
• Δ resp. rate can change PaCO₂ rapidly
• Lung pathology can change PaCO₂ - Metabolic
• Kidneys regulate HCO₃⁻ levels more slowly
• Many pathologies can change [HCO₃⁻] and other acids/bases
Low CO2 -> high pH…
Respiratory alkalosis
Eg. Altitude→hyperventilation
High CO2 -> low pH…
Respiratory acidosis
Eg. Trauma→hypoventilation
Low HCO3 -> low pH…
Metabolic acidosis
Eg. Diabetic ketoacidosis→gain in fixed acid
High HCO3 -> high pH…
Metabolic alkalosis
Eg. Chronic vomiting→loss of fixed acid
What are the steps to interpreting an ABG?
- Step 0: oxygenation
- Step A: acidosis/alkalosis
- Step B: buffers/bases (CO₂ & HCO₃⁻)
- Step C: compensation/chronic
- Step D: differential diagnoses
What happens in step 0- oxygenation?
- Normal = 10 – 13 kPa
- PaO₂ <8 kPa = respiratory failure (RF)
- Type I RF = normal or low PaCO₂ (hypoxaemic)
• Impaired gas exchange at alveolar-capillary interface; V/Q mismatch
• O₂ gas exchange more vulnerable than CO₂
• Solubility: CO₂»_space; O₂ → 20× more rapid diffusion
• Proportion: In lungs, < 10% CO₂ lost; > 25% O₂ gained
• See Fick’s Law: O₂ exchange is often compromised before CO₂ - Type II RF = high PaCO₂ (hypercapnic)
• Global underventilation - Type I & II can occur together
What happens in step A- acidosis or alkalosis?
- Check the pH
- Normal pH = 7.35 – 7.45
- If pH < 7.35 → acidosis
- If pH > 7.45 → alkalosis
What happens in step B- buffers (CO2)
- FIRST: check PaCO₂ (N = 4.7 – 6.0 kPa)
- Q. Is PaCO₂ contributing to or compensating for pH?
- If pH < 7.35 (acidotic) then…
• PaCO₂ > 6.0 → contributing → RESPIRATORY ACIDOSIS
• PaCO₂ < 4.7 → compensating → METABOLIC ACIDOSIS - If pH > 7.45 (alkalotic)
• PaCO₂ > 6.0 → compensating → METABOLIC ALKALOSIS
• PaCO₂ < 4.7 → contributing → RESPIRATORY ALKALOSIS - SECOND: Check bases (HCO₃⁻ & base excess)
- HCO₃⁻ has two possible values:
• Actual – derived from pH and PaCO₂ using HH Equation
• Estimate of [HCO₃⁻] actually in plasma
• Used to assess both metabolic and respiratory causes of acid- base disturbances
• (if there is only 1 reported value, it is likely to be this one)
• Standard – derived plasma [HCO₃⁻] in blood equilibrated with normal PaCO₂ (5.3 kPa), PaO₂ & temperature (37°C)
• When PaCO₂ (et al) is normal, aHCO₃⁻ = sHCO₃⁻
• sHCO₃⁻ is a measure solely of the metabolic component of imbalance - Base excess (BE) measures ALL bases not just HCO₃⁻
• HCO₃⁻ accounts for 75% of total buffering
• In metabolic acid-base disturbances BE provides similar information to sHCO₃⁻ - Amount of acid/base causing a deviation from pH 7.40, at normal PaCO₂ & temperature
- Normal range is easy to interpret (-2 to +2 mEq/L)
• BE > +2 mEq/L = high HCO₃⁻ = metabolic alkalosis
• BE < -2 mEq/L = low HCO₃⁻ = metabolic acidosis - mEq/L: an ‘equivalent’ is amount required to react with one mole of H⁺
What happens in step C- compensation/chronic?
- If pH and PaCO₂ point to a primarily metabolic cause,
BE (and sHCO₃⁻) will confirm, i.e.,
• high in alkalosis and low in acidosis - If pH and PaCO₂ point to a 1° respiratory cause, then BE (and sHCO₃⁻) can give insight into duration…
- In a respiratory acidosis…
• Normal BE = no compensation yet = acute
• High BE = compensation = chronic
• Low BE indicates mixed respiratory and metabolic! - In a respiratory alkalosis
• Normal BE = no compensation yet = acute
• Low BE = compensation = chronic
• High BE indicates mixed respiratory and metabolic!
What happens in step D- differential diagnoses?
- How can things go wrong?
- How can things be compensated?
- Lungs
• V/Q mismatch (V = ventilation / Q = perfusion)
• ↑ or ↓ respiratory rate - Metabolic & kidney
• Gain/loss of acid/base
• ↑ or ↓ HCO₃⁻ elimination
What is ventilation-perfusion mismatch vs compensation?
What is the response to respiratory acidosis by the kidney?