top of page

Arterial Blood Gas Interpretation

ABG Interpretation

  1. Oxygenation

  2. Ventilation

  3. Acid-Base Status

  4. Acid-Base Compensation

  5. Other

Oxygenation
Oxygenation

Key Variables:

  • SaO2

    • % of Hb molecules bound to O2​

    • This is the equivalent to saturations measured via a sats probe (though less prone to error)

  • PaO2

    • Partial pressure​ of oxygen molecules dissolved in blood (ie. not bound to haemoglobin)

  • FiO2

    • Fraction of inspired oxygen​

      • Room air = 21%​

    • FiO2 varies with oxygen delivery device, flow rate and oxygen concentration delivered by device, inspiratory flow rate of patient

  • Hb concentration​​

​

Key Questions:​​​

  1. Does the patient have adequate oxygen content?

  2. How well is the patient oxygenating their blood?

​

Oxygen Content

  • Oxygen content = (Hb concentration X SaO2 X 1.34) + (0.03 X PaO2)

    • Normal content ~ 200 ml O2 / Litre of blood​

    • Normal O2 consumption = 250 ml O2 / minute

  • Oxygen saturation is main determinant of oxygen content of arterial blood​

  • Relationship between PaO2 and SaO2

    • At a PaO2 above 60 mmHg, there are only small changes in SaO2 for a given change in PaO2

    • Below 60 mmHg, SaO2 will rapidly fall as PaO2 falls​​​​

Shunt

Oxygenation

  • Key Terms

    • Hypoxia​

      • Refers to​ inadequate levels of tissue oxygenation for cellular respiration

      • If oxygen uptake or utilisation is impaired, a patient may be hypoxic without the presence of hypoxaemia

    • Hypoxaemia

      • Abnormally low arterial oxygen partial pressure (< 60 mmHg)​

      • Hypoxaemia may not result in hypoxia if compensatory mechanisms increase oxygen delivery or reduce oxygen utilisation

  • Causes of hypoxaemia

    • Inadequate inspired oxygen concentration​

      • Eg. High altitude

    • Hypoventilation​

      •  ​Alveolar gas is not refreshed with oxygen as quick as it is taken up by haemoglobin and consumed by peripheral tissues

    • Ventilation-perfusion mismatch​

    • Diffusion abnormalities

    • Dead space ventilation

      • Results in hypoxaemia via:​

        • Decreased minute ventilation​ (ie. hypoventilation)

        • Altered blood flow, resulting in concurrent shunting

  • Shunt or V/Q mismatch refer to processes by which blood moves from the venous circulation to the arterial circulation without adequate oxygenation

    • It is the most common cause of hypoxaemia in the critically ill​

    • Bedside measures:

      • P:F Ratio​

        • The ratio of PaO2 relative to the FiO2 delivered​​​

        • Values:

          • Normal = 500

            • ie. 100 mmHg / 0.21

          • < 100 = severely impaired arterial oxygenation​​

          • < 300 = mildly impaired arterial oxygenation

      • A-a Gradient
        • The difference between Alveolar oxygen partial pressure and arterial oxygen partial pressure​
        • Calculation:
          • PAO2 (alveolar) = (FiO2 x 713)​ - (PaCO2 / 0.8)
          • PaO2 is measured via arterial blood gas
        • Values​

          • As V/Q mismatch increases, A-a gradient will increase

          • Normal = 5 - 10 mmHg​​

            • Increases with age; Normal = (age/4) + 4​

Ventilation
Ventilation

Key Questions:​​​

  1. Do I need to worry about the PaCO2 in this patient?

  2. How does the respiratory rate relate to the PaCO2?

​

PaCO2 is:​​

  • Inversely proportional to alveolar ventilation

    • As minute ventilation increases, PaCO2 decreases​

      • Minute ventilation = tidal volume X respiratory rate​

  • Directly proportional to CO2 production (ie. metabolic rate)

​

Normal PaCO2 = 35 - 45 mmHg

​

Do I need to worry?​

  • If the patient has an acidaemia, is obtunded, is tachypnoeic/bradypnoeic or has any other concerning signs or symptoms, then this must be immediately escalated!!!

  • Chronic hypercapnoea may be adequately compensated and of no particular concern

    • ie. the COPD patient who is mentating well, with a normal pH​ due to a compensatory metabolic alkalosis

  • Mild - moderate hypercapnoea may be tolerated in certain circumstances (permissive hypercapnoea)

    • This should be discussed with a more senior clinician​

​

How does the respiratory rate relate to the PaCO2?

  • Hypercapnoea with tachypnoea (The patient who CAN'T breathe)

    • The hypercapnoea is likely driving the minute ventilation​

    • Consider respiratory or metabolic causes of hypercapnoea

​

  • Hypercapnoea with reduced respiratory rate (The patient who WON'T breathe)

    • The hypopnoea is likely the cause of hypercapnoea​

    • Consider neurological or metabolic causes

    • Beware the tiring or obtunded patient who was initially tachypnoeic!

​

  • Hypocapnoea with tachypnoea

    • The tachypnoea is likely the cause of the hy​pocapnoea

    • Consider respiratory, neurological or metabolic causes

Acid - Base Status
Acid Base Status

Key Questions:​​​

  1. What is the overall Acid-Base State?

  2. What are the underlying Acid-Base Disorders?

​

​

Step 1:

  • Assess the pH

    • Acidaemia (pH < 7.35) vs alkalaemia (pH > 7.45)​

​

Step 2:

  • Assess the process:

    • Acidosis​

      • Elevated PaCO2 (respiratory) or reduced HCO3 (metabolic)​

    • Alkalosis

      • Reduced PaCO2 (respiratory) or elevated HCO3 (metabolic)

​

Step 3:

  • Assess the cause:

    • For respiratory derangements, see above​.

    • Metabolic Acidosis

      • Check Anion Gap​

        • AG = Na - (Cl + HCO3)​

        • Normal = 12 (+/- 4)

      • High anion gap metabolic acidosis (HAGMA)

        • Lactate​

        • Toxins

        • Ketones

        • Renal failure

      • Normal anion gap metabolic acidosis (NAGMA)​​

        • GIT loss of bicarbonate (eg. diarrhoea)​

        • Renal tubular acidosis

        • Hyperchloraemia

          • Eg. Excessive 0.9% NaCl administration​

    • Metabolic Alkalosis

      • Excess HCO3​

        • Renal retention​

          • eg. diuretics, Cushings/excessive steroid administration

        • Exogenous administration

          • eg. Sodium bicarbonate solution​

      • Loss of H+

        • GIT loss​

          • Eg. Excessive vomiting​

      • Hypochloraemia/Hypernatraemia

        • Eg. Dehydration​/hypovolaemic states

​

​

Step 4:

  • Assess compensation

    • Compensation for respiratory acidosis​

      • Acute acidosis​

        • For every 10 mmHg increase above PCO2 = 40, HCO3 should increase 1 mmol/L above 24​

      • Chronic acidosis

        • For every 10 mmHg increase above PCO2 = 40, HCO3 should increase 4 mmol/L above 24​

    • Compensation for respiratory alkalosis

      • Acute alkalosis​

        • For every 10 mmHg decrease below PCO2 = 40, HCO3 should decrease 2 mmol/L below 24​

      • Chronic alkalosis

        • For every 10 mmHg decrease below PCO2 = 40, HCO3 should decrease 5 mmol/L below 24​

    • Compensation for metabolic acidosis

      • For every 1 mmol/L decrease of HCO3 below 24, CO2 decreases 1.25 mmHg​

    • Compensation for metabolic alkalosis

      • For every 1 mmol/L increase of HCO3 above 24, CO2 increases 0.75 mmHg​

​

  • If PCO2 or HCO3 is not compensated as expected, consider a secondary acid-base process occurring simultaneously

    • Respiratory compensation has limits; unusual to rise above 60 mmHg or decrease below 10 mmHg​

Compensation
Other
Other

Other information obtained from a blood gas sample:

  • Electrolytes

    • Sodium​

    • Potassium

    • Chloride

    • Ionised Calcium

  • Glucose

  • Lactate

  • Methaemoglobin levels

    • Normal < 1.5% ​

  • Carboxyhaemoglobin (Carbon monoxide levels)

    • Normal < 0.5%​

    • Signs/symptoms generally begin when levels increase above 10%

       Author: Matt Guest, Peer Reviewer: Irma Bilgrami, Date: 20/05/20

bottom of page