EMed

Blood gases

Introduction

Look at the patient and see and predict what should be going on based on clinical suspicion.

Then look at the blood gas.

"Gases" get confusing if you don't note (scribble down) each finding as you work through the printout.

VBG vs ABG

VBGs used in EDs in preference to ABGs.

Correlation good, apart from pO2.

pCO2 correlates well at normal ranges. Correlation worsens with sepsis/shock/rising pCO2.

Normal ranges

pH = 7.4 (7.35-7.45)

PaCO2 = 4.7 - 6.0 kPa.

HCO3- = 24 mmol/l (22-26)

BE = 0 (±2)

Approach

  1. Note (scribble down) if the patient has an acidaemia or an alkalaemia?
  2. What is the primary acidosis or alkalosis?
  3. If it is a Metabolic Acidosis (MA):
    1. Is the anion gap wide (R[raised] AGMA) or not (N[normal] AGMA)?
    2. If RAGMA check delta gap [see below] (to see if another problem)?
    3. Is the respiratory compensation as expected [see below]?
  4. If it is a metabolic alkalosis
    1. Is the respiratory compensation as expected? [See below]
  5. If it is a respiratory acidosis:
    1. Is the metabolic compensation as expected?[see below]
    2. If the anion gap is wide there is probably a concurrent RAGMA
  6. If it is a respiratory alkalosis:
    1. Is the metabolic compensation as expected?
  7. If the pH is normal check the anion gap, the base excess, and the PaCO2 as there may be hidden disturbances
  8. Check the PaO2 and the A-a oxygen difference. Is it what is expected given the FiO2?
  9. Check the Hb, the glucose, and the electrolytes
  10. Does the gas fit the patient?

Acidosis

Anion gap : K+ + Na+ - Cl- - HCO3 = 8 - 16 mmol/l

Metabolic Acidosis & Anion Gap
Metabolic acidosis
with a high anion gap		 Metabolic acidosis
with a normal AG
C CO (or Cyanide)
A Alcohol
T Toluene P Potassium sparing diuretics
  A Acetazolamide
M Methanol R Rhabdomyolysis /RTA
U Urea A Alimentation feeding
D DKA (and AKA) M Mineral Acids
P Paraldehyde / Phenformin E Enterostomy
I Iron / isoniazid D Diarrhoea
L Lactic acidosis I Intestinal fistula
E Ethanol/Ethylene glycol C Cholestyramine
S

Salicylate/Solvents/Starvation

Delta gap

  • If a wide-anion-gap metabolic acidosis is the only disturbance, then the change in value of the anion gap should equal the change in bicarbonate (ie) ↑ AG = ↓ HCO3-
  • The delta gap = increase AG - decrease HCO3-
  • For purposes of calculation take normal AG as 12 and normal HCO3- as 24
  • Shortcut calculation: Δ AG - Δ HCO3- = (AG -12) - (24 - HCO3-) = Na+ - Cl- - 36
  • If the delta gap is < -6 there is also a non-anion gap metabolic acidosis
  • Other causes of a delta gap < -6 are a respiratory alkalosis (with compensating non-anion gap acidosis), or a low anion gap state
  • If the delta gap > +6 there is a concurrent metabolic alkalosis
  • Other causes of a delta gap > +6 are respiratory acidosis (with compensating metabolic alkalosis), or a non-acidotic high anion gap state

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

Upper limit normal is about 15 using (Na+) - (HCO3- + Cl-)

More than 20 definitely abnormal

Causes of a wide anion gap

  • Ketoacidosis
  • Lactic acidosis
  • Rhabdomyolysis
  • Non-ketotic hyperosmolar coma
  • Uraemia (or other Organic acidosis)
  • Haemoconcentration
  • Hypomagnesaemia
  • Hypocalcaemia
  • Hypokalaemia
  • IgA myeloma
  • Lactate or Citrate
  • Acetate

Causes of a low anion gap

  • Haemodilution
  • Hypoalbuminaemia
    • Adjusted anion gap = observed anion gap + 0.25 (normal albumin - observed albumin): Where albumin concentrations are in g/l
  • IgG myeloma
  • Hypercalcaemia
  • Hypermagnesaemia
  • Hyperkalaemia
  • Lithium XS
  • Analytical error: ↑Na+, hyperlipidaemia

In lone metabolic acidosis:

Expected PaCO2 = (1.5*bicarbonate) + 8

or

In mmHg .... 7.xx rule (mmHg) : PaCO2 = decimal digits of pH ± 5 mmHg

Respiratory compensation for metabolic acidosis

Causes of respiratory acidosis

Disorders of gas exchange

Acute:

  • Asthma
  • Bronchiolitis
  • Pneumonia
  • Pulmonary oedema
  • Laryngospasm
  • Foreign body aspiration
  • Mechanical ventilation

Chronic:

  • COPD
  • Prolonged pneumonia

Respiratory muscle abnormalities

Acute:

  • Chest wall trauma
  • Tension pneumothorax
  • Aminoglycosides
  • Familial periodic paralysis

Chronic:

  • Muscle weakness
  • Myasthenia gravis
  • Poliomyelitis
  • Amyotrophic lateral sclerosis
  • Kyphoscoliosis
  • Pickwickian syndrome

Respiratory centre abnormalities

Acute:

  • Opiates
  • Sedatives
  • General anaesthesia
  • Cardiac arrest

Chronic:

  • CNS abnormalities

Metabolic compensation for respiratory acidosis

  • Acute Resp. acidosis - Δ HCO3- = 1 mmol/l for each 1 kPa change in pCO2
  • Chronic Resp. acidosis - Δ HCO3- = 4 mmol/l for each 1 kPa change in pCO2

Alkalosis

Causes of respiratory alkalosis:

  • CNS diseases
  • Anxiety / hysteria
  • Hypermetabolic states
  • Hepatic insufficiency
  • Assisted ventilation
  • Pregnancy/Altitude/Exercise
  • Hypoxia
  • Toxins

Metabolic compensation for resp. alkalosis

Respiratory acidosis and alkalosis are characterized by a primary change in pCO2. Secondary physiological compensation is seen in blood gas results as a change (Δ) in bicarbonate concentration (↑ in the case of acidosis and ↓ in alkalosis). So expect:

  • Acute Resp. alkalosis - Δ HCO3- = 2 mmol/l for each 1 kPa change in pCO2
  • Chronic Resp. alkalosis - Δ HCO3- = 3 mmol/l for each 1 kPa change in pCO2

Causes of metabolic alkalosis

Saline responsive
(urine chloride < 10 mmol/l ) - hypovolaemia

  • Diuretics
  • Vomiting, NG suctioning
  • Following respiratory acidosis
  • Exogenous alkalis
  • Contraction alkalosis

Saline unresponsive - normovolaemia

  • Hyperaldosteronism ( primary, secondary, exogenous )
  • Cushing's syndrome
  • Severe hypokalaemia

Unclassified

  • Milk alkali syndrome
  • Metabolism of organic anions
  • Massive blood transfusion
  • Nonparathyroid hypercalcaemia

Respiratory compensation for metabolic alkalosis

Other compensations

Corrected K+

= Each pH ↓, K+ should ↑ by from 5mmol/L by 0.5 mmol/L

E.g. Expect K+ for pH 7.2 = 5.0 + 2 = 6.0 mmol/L

Corrected Na+

= Na+ + (Glucose -5)/3

A-a oxygen gradient [P(A-a)O2]

Formula (kPa)

A-a = FiO2 - (1.25 x PaCO2) - PaO2

Normal A-a : young <3, >60 years <4

↑ A-a gradient = V/Q mismatch:

  • LVF/Pulm. oedema
  • PE
  • ARDS
  • LRTI
  • Other resp.membrane disease

A-a gradient (assume at sea level)

Result:

Approx. FiO2 on O2 flow rate in a rigid mask:

Flow rate l/min 4 6 8 10 12 15
FiO2 0.35 0.5 0.55 0.6 0.65 0.7

Approx. FiO2 on O2 flow rate nasal cannulae

Flow rate l/min 1 2 3 4 5 6
FiO2 25 29 33 37 41 45

PaO2 and age

The normal value for the partial pressure of arterial oxygen (PaO2) irrespective of age is >10.6 kPa.

The normal PaO2 for a given age can be predicted from:

  • Seated PaO2 = 13.8 kPa - 0.27 x age
  • Supine PaO2 = 13.8 kPa - 0.42 x age

If PaO2 is < 10.7 kPa, the patient has arterial hypoxemia.

Causes of a low PaO2

  • Shunt (pulmonary, cardiovascular)
  • Ventilation perfusion imbalance
  • Diffusion block
  • Hypoventilation
  • ↓ PiO2
  • Low mixed venous oxygen content

Last review Dr Simon Walsh, Dr ÍOS 20/07/22.