Blood Gases Section

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

Note (scribble down) if the patient has an acidaemia or an alkalaemia?
What is the primary acidosis or alkalosis?
If it is a Metabolic Acidosis (MA):
1. Is the anion gap wide (R[raised] AGMA) or (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]?
If it is a metabolic alkalosis
1. Is the respiratory compensation as expected? [see below]
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
If it is a respiratory alkalosis:
1. Is the metabolic compensation as expected?
If the pH is normal check the anion gap, the base excess, and the PaCO₂ as there may be hidden disturbances
Check the PaO₂ and the A-a oxygen difference. Is it what is expected given the FiO₂?
Check the Hb, the glucose, and the electrolytes
Does the gas fit the patient?

Acidosis

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

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^-
Take normal AG as 12 and normal HCO₃^- as 24
ΔAG-ΔHCO₃- = (AG-12)-(24-HCO₃^-) = Na⁺ - Cl^- - 36

Na⁺ - Cl^- - 36

<-6 = Mixed high and normal anion gap acidosis
-6 to 6 = Only a high anion gap acidosis exists
>+6 = Mixed high AG acidosis and metabolic alkalosis

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

Resp. compensation in Metab acidosis:

Expected PaCO₂ = (1.5*bicarbonate) + 8

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

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)

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

Blood gases

Introduction

VBG vs ABG

Normal ranges

Approach

Acidosis

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

Delta gap

Na+ - Cl- - 36

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

Causes of a wide anion gap

Causes of a low anion gap

Resp. compensation in Metab acidosis:

Causes of respiratory acidosis

Disorders of gas exchange

Respiratory muscle abnormalities

Respiratory centre abnormalities

Metabolic compensation for respiratory acidosis

Alkalosis

Causes of respiratory alkalosis:

Metabolic compensation for resp. alkalosis

Causes of metabolic alkalosis

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

Saline unresponsive - normovolaemia

Unclassified

Respiratory compensation for metabolic alkalosis

Other compensations

Corrected K+

Corrected Na+

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

Formula (kPa)

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

↑ A-a gradient = V/Q mismatch:

A-a gradient (assume at sea level)

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

Approx. FiO2 on O2 flow rate nasal cannulae

PaO2 and age

Causes of a low PaO2

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

Na⁺ - Cl^- - 36

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

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

Corrected K⁺

Corrected Na⁺

A-a oxygen gradient [P(A-a)O₂]

A-a = FiO₂ - (1.25 x PaCO₂) - PaO₂

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

Approx. FiO₂ on O₂ flow rate nasal cannulae

PaO₂ and age

Causes of a low PaO₂