# Blood Gas Interpretation

The blood gas is used to rapidly assess ventilatory function and identify acid-base disorders – and will also generally provide point-of-care testing of a number of values such as electrolytes, blood glucose and haemoglobin.

Interpretation occurs in a systematic manner to identify the primary disorder, secondary disorders and therefore the differential diagnoses that could be contributing to the patient’s clinical state.

**Use the following steps and flowchart to approach blood gas interpretation in a comprehensive and structured manner:**

**Interpreting the blood gas in a step-wise manner:**

- Step 1. pH
- Step 2. Assess the pCO
_{2}and HCO_{3}to identify the primary disorder - Step 3. Consider the cause of the primary disorder
- Step 4. Assess for secondary processes
- Step 5. Apply corrections to certain measured values

##### Step 1. pH

A normal pH is between 7.35 and 7.45 (use 7.4 as the ‘normal’ value for all calculations)

- If pH < 7.35 there is acidaemia
- If pH > 7.45 there is alkalaemia

*If pH is normal – there could be no acid-base disorders occurring, or there could be multiple processes occurring concurrently*

Remember – acidaemia/alkalaemia describe the pH status of the blood, not the process(es) driving the abnormality

##### Step 2. Assess the pCO_{2} and HCO_{3} to identify the primary disorder

- A normal pCO
_{2}is between 35 – 45mmHg (use 40mmHg as the ‘normal’ value for all calculations) - A normal HCO
_{3}is between 22 – 26mmol/L (use 24mmol/L as the ‘normal’ value for all calculations)

If there is ** acidaemia**:

- An elevated pCO
_{2}indicates a respiratory acidosis - A reduced HCO
_{3}indicates a metabolic acidosis

If there is *alkalaemia*

- A reduced pCO
_{2}indicates a respiratory alkalosis - An elevated HCO
_{3}indicates a metabolic alkalosis

##### Step 3. Consider the cause of the primary disorder

**Respiratory acidosis (elevated pCO2)**

**Respiratory acidosis (elevated pCO _{2})**

Consider causes of *hypoventilation*

- CNS depression (head injury, stroke, drugs)
- Respiratory depression (myopathy, spinal cord injury, drugs)
- Hypoventilation (pain, chest wall injury/deformity, raised intra-abdominal pressures)
- Respiratory failure (pneumonia, pneumothorax, oedema, bronchial obstruction)
- Airway obstruction
- Chronic respiratory acidosis – COPD, restrictive lung disease

**Metabolic acidosis (reduced HCO3)**

**Metabolic acidosis (reduced HCO _{3})**

The first step involves calculating the *anion gap*, where there are different categories of differentials for either a *normal anion gap metabolic acidosis* (NAGMA) or a *high anion gap metabolic acidosis *(HAGMA)

Anion Gap = [Na^{+}] – ([Cl^{–}] + [HCO_{3}^{–}])

**Normal anion gap metabolic acidosis (NAGMA**)

A normal anion gap is 12 ± 4. Differentials for a normal anion gap metabolic acidosis can be remembered with “**USED CRAP**”

**USED CRAP**

**U**reterostomy**S**mall bowel fistula**E**xtra chloride (hyperchloraemic metabolic acidosis)**D**iarrhoea**C**arbonic anhydrase inhibitor**R**enal tubular acidosis**A**ddison disease**P**ancreatic duodenal fistula

*The anion gap can also be low (<3) or negative, with the differentials for a low or negative anion gap metabolic acidosis including: *

- Analytical error (severe hypernatraemia, pseudohyponatraemia, hyperviscosity, hyperlipidaemia)
- Reduced unmeasured anions (dilution, hypoalbuminaemia)
- Increased unmeasured cations (lithium, calcium, magnesium, potassium)
- Pseudohyperchloraemia (bromide, iodide, salicylates, thiocyanate)

**High anion gap metabolic acidosis (HAGMA**)

The differentials for a high anion gap (>16) metabolic acidosis can be remembered with “**CAT MUD PILES**” or more simply *“Left Total Knee Replacement *(**L TKR**)”

**CAT MUD PILES**

**C**arbon monoxide, cyanide**A**lcoholic ketoacidosis**T**oluene**M**ethanol, metformin (phenformin)**U**raemia**D**iabetic ketoacidosis, D-lactic acidosis**P**aracetamol, pyroglutamic acid, paraldehyde, propylene glycol**I**soniazid, iron**L**actate**E**thanol, ethylene glycol**S**alicylates

**L TKR**

- Lactate
- Toxins
- Ketones
- Renal

**Respiratory alkalosis (reduced pCO2)**

**Respiratory alkalosis (reduced pCO _{2})**

Related to processes that cause *hyperventilation *– differentials can be remembered with “**CHAMPS**“

**C**NS disease (stroke, haemorrhage, psychogenic)**H**ypoxia (pneumonia, PE, asthma, altitude)**A**nxiety, pain**M**echanical or excessive ventilation**P**rogesterone, pregnancy**S**alicylates and sepsis

**Metabolic alkalosis (elevated HCO3)**

**Metabolic alkalosis (elevated HCO _{3})**

Differentials can be remembered with “* CLEVER PD*“

**C**ontraction (volume contraction)**L**iquorice, laxative abuse**E**ndocrine (Conn syndrome, Cushing syndrome)**V**omiting, GI losses Excess alkali (antacids)**R**enal (Bartter syndrome)**P**ost-hypercapnia Diuretics

##### Step 4. Assess for secondary processes

If there is a primary metabolic disorder, there is an expected respiratory compensation that can be calculated, and vice versa for a primary respiratory disorder. Respiratory compensation occurs quickly (within 30 minutes and complete within 12-24 hours), whereas metabolic compensation begins within 5-10 minutes (with whole body buffering) but requires 3-5 days to complete with further renal processes.

If the degree of compensation is not appropriate (e.g. the expected pCO_{2} or HCO_{3} is above or below the measured value) this is indicative of concurrent additional acid base disorders occurring.

**A respiratory acidosis is compensated for by increasing HCO _{3}**

- Calculate the expected HCO
_{3}using**1-2-3-4-5 rule**

- This rule states that for
the expected HCO*acute respiratory acidosis*_{3}will increase by 1mmol/L (from the normal value of 24) for every 10mmHg that the pCO_{2}rises above normal (40mmHg)- For
the expected HCO**chronic respiratory acidosis**_{3}will increase by 4mmol/L for every 10mmHg rise in pCO_{2}above normal

- For

**A metabolic acidosis is compensated for by reducing pCO _{2}**

- Calculate the expected pCO
_{2}using**Winter’s formula**:

pCO_{2 expected} = (1.5 x [HCO_{3}^{–}]) + 8 ±2

- The expected pCO
_{2 }can also be approximated using the two digits to the right of the decimal point (e.g. expected pCO_{2 }= 25 if the pH = 7.25)- If the measured pCO
_{2 }is more than the expected pCO_{2}– there is**also**a*respiratory acidosis*

- If the measured pCO

###### Delta ratio

In the context of a metabolic acidosis, a further calculation can be performed to assess whether the metabolic acidosis is due to single process or a mixed acid-base disorder. This is called the delta ratio, and reflects whether the change in the anion gap from normal (delta AG) is proportional to the expected change in the HCO_{3} from normal (delta HCO_{3}).

Delta ratio = (AG – 12) / (24 – HCO_{3}^{–})

If the denominator is larger (i.e. the HCO_{3} has changed more than the change in anion gap) this could reflect that a NAGMA is present (either by itself or concurrently with a HAGMA). If the numerator is larger (i.e. the anion gap has changed more than the change in HCO_{3}) this could reflect that there is predominantly a HAGMA occurring – or if the ratio is very high (>2) this could reflect that there is an additional process present (such as a concurrent metabolic alkalosis or a chronic respiratory acidosis which is raising the HCO_{3} and reducing the delta HCO_{3})

**Delta ratio interpretation:**

<0.4 | Pure NAGMA |

0.4 – 0.8 | Mixed NAGMA and HAGMA |

0.8 – 2.0 | Pure NAGMA |

>2.0 | HAGMA and either metabolic alkalosis or chronic respiratory acidosis |

**A respiratory alkalosis is compensated for by reducing HCO _{3}**

- Calculate the expected HCO
_{3}using**1-2-3-4-5 rule** - This rule states that for
the expected HCO*acute respiratory alkalosis*_{3}will reduce by 2mmol/L (from the normal value of 24) for every 10mmHg that the pCO_{2}drops below normal (40mmHg)- For
the expected HCO*chronic respiratory alkalosis*_{3}will reduce by 5mmol/L for every 10mmHg reduction in pCO_{2}below normal

- For
- If the measured HCO
_{3}is**less than**the expected HCO_{3}– there is also a**metabolic acidosis**occurring. - If the measured HCO
_{3}is**greater**than expected – there is also a**metabolic alkalosis**.

**A metabolic alkalosis is compensated for by increasing pCO _{2}**

- Calculate the expected pCO
_{2}using:

pCO_{2 expected} = (0.7 x [HCO_{3}^{–}]) + 20 ± 5

- If the measured pCO
_{2}is more than the expected pCO_{2}– there is also a respiratory acidosis occurring - If the measured pCO
_{2}is less than expected – there is a concurrent respiratory alkalosis.

##### Step 5. Apply corrections to certain measured values

In certain acid base disturbances, particular measured values may be falsely normal/abnormal and correction factors can be applied to assess for further abnormalities.

**Albumin correction of anion gap**

Albumin is an anion, therefore hypoalbuminaemia may under-estimate the anion gap. To correct the anion gap for hypoalbuminaemia – for every 10g/L that the albumin is below normal (40g/L) add 2.5 to the calculated anion gap

Anion gap_{Albumin corrected} = Anion gap + 0.25 (40 – Albumin)

**Osmolar gap **

The osmolar gap technically compares two different values – the osmolality (measured in the laboratory with freezing point depression, mOsm/kg), and the osmolarity (calculated, mOsm/L). Normally the gap between these two values is less than 10, and if the osmolar gap is elevated it can reflect the presence of an abnormal solute (e.g. toxic alcohol)

Osmolarity = (2x [Na^{+}]) + urea + glucose + (1.25 x EtOH)

** Note**: Ethanol must be converted to SI units (mmol/L)

EtOH (mmol/L) = EtOH (%) x 217 = EtOH (mg/dL) ÷ 4.6

*Exogenous agents* associated with an elevated osmolar gap

- Acetone
- Ethanol
- Ethylene glycol
- Glycerol
- Glycine
- Isopropyl alcohol
- Maltose
- Mannitol
- Methanol
- Propylene glycol

*Other conditions *(non-toxicological) associated with an elevated osmolar gap

- Alcoholic ketoacidosis
- Chronic renal failure
- Diabetic ketoacidosis
- Hyperlipidaemia
- Hyperproteinaemia
- Severe lactic acidosis
- Shock
- Trauma and burns

**Sodium correction in hyperglycaemia**

In patients with marked hyperglycaemia, the elevated serum glucose raises the serum tonicity (as the glucose cannot enter cells) which pulls water out of cells and expands the extracellular water compartment – thereby lowering the concentration of sodium.

The corrected serum sodium can be calculated, which represents what the serum sodium concentration would be if the glucose level was reduced back to normal. If the corrected sodium is in a normal range – the patient does not have a concurrent hypotonic hyponatraemia.

[Na]_{ corrected} = [Na] + 1.5x([Glucose – 5.5]/5.5)

*Roughly approximate to* [Na]_{ corrected} = [Na] + (Glucose – 5)/3

**Potassium correction with pH abnormalities**

Acid-base disturbances will affect the serum concentration of potassium – where *acidaemia *will **increase** the measured serum potassium by causing extracellular shift, and *alkalaemia *will **reduce **the measured serum potassium by causing intravascular shift.

The described relationship is that for every 0.1 unit change in pH, there will be a 0.6mEq/L change in serum potassium

K^{+}_{corrected} = [K^{+}] _{measured} – 0.6 ([7.4 – pH] / 0.1 )

## Critical Care

Compendium

Physician in training. German translator and lover of medical history.

Thank you… very helpful

The aniongap is usually calculated without potassium en that value is used to calculate the delta ratio. What if the potassium is high? Is that a reason to include it, which will give a change in the delta-ratio compared to not using the potassium?

This question was raised when interpreting the following ABG:

pH 6.98; pCO2 14 mmHg (1.9 kPa); HCO3 3 mmol/l; Na 138 mmol/l; K 7.0 mmol/l; Cl 114 mmol/l

With kind regards,

René