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In hypoventilating patients, less air will be moved in and out of the lungs, causing CO2 to be
retained. As the PaCO2 rises, the respiratory acid load is increased leading to respiratory
acidosis. This can be caused by:
- Airway obstruction, as in inhalation of a foreign body;
- Impaired alveolar filling, as in bronchopneumonia;
- Depression of respiratory centre, as in a drug overdose or with semiconscious patients.
Respiratory alkalosis
In respiratory alkalosis, the blood pH is greater than 7.45 and the PaCO2 is less than 4.5kPa.
Hyperventilating patients move large amounts of air in and out of the lungs. This lowers the CO2
and therefore the PaCO2. The respiratory acid load is therefore reduced. The effect of this on the
acid-base balance is to cause an excess of alkali (base) which leads to respiratory alkalosis. This
can be caused by:
- A fall in oxygen levels, as in severe anaemia, pulmonary disease or high altitude;
- Stimulation of the central nervous system, as in aspirin overdose or raised intracranial pressure.
Assessing the patients acid-base balance
The normal pH of arterial blood (7.35-7.45) is maintained by a delicate balance between the
alkalis and acids in the body. This balance is needed for the functioning of the enzyme systems.
An acidotic pH of less than 7.35 decreases the force of cardiac contractions, while an alkalotic
pH of greater than 7.45 interferes with tissue oxygenation: pH is inversely related to acidity,
meaning that the more hydrogen ions (H+) or acids there are, the lower the pH value will be.
The bicarbonate-carbonic acid system is the main buffer system in the body. The carbonic acid
element has already been explored when assessing patient ventilation. Bicarbonate (HCO3-)
reflects the metabolic component of acid-base regulation. The normal level of bicarbonate in the
blood is 24-27mmol/L. An HCO3- of greater than 27 reflects a metabolic alkalosis (excess of
base), and a HCO3- of less than 24 reflects a metabolic acidosis (deficit of base).
The base excess (BE) measures the amount of excessive base or acid in the blood. It gives
information on the metabolic aspect of acid-base balance.
The normal value ranges from -5 to +5. The value indicates the amount of strong acid (or base)
to be added to the sample of blood to produce a pH of 7.4.
For example, a base deficit of -3 indicates that 3mmol of base added to a litre would produce a
pH of 7.4.
A base deficit is a negative figure and shows a deficit of base or excess of acid: this represents a
metabolic acidosis. A base excess is a plus figure and shows an excess of base or deficit of acid:
this represents a metabolic alkalosis.
Metabolic acidosis
In metabolic acidosis, the blood pH is less than 7.35, the HCO3- is less than 24mmol/L and the
BE is less than -5.
An increase in the metabolic acid load depletes the bicarbonate available for buffering and, as a
result, the HCO3- and base excess levels fall.
Conditions that increase the acid load causing a metabolic acidosis include:
- Increased production of H+ ions (acids), as in cardiac arrest or diabetic ketoacidosis;
- Ingestion of H+ ions or substances that metabolise to H+ ions, as in alcohol, methanol
(methylated spirits) or ethylene glycol (antifreeze);
- Increased HCO3- losses, as in losses from diarrhoea, kidney failure through renal tubular
disease or drugs such as acetazolamide.
Metabolic alkalosis
In metabolic alkalosis, the blood pH is greater than 7.45, the HCO3- is greater than 27mmol/L
and the BE is greater than +5.
A decrease in the metabolic acid load increases the bicarbonate available for buffering, and
therefore HCO3- and base excess levels rise. Conditions that decrease the acid load and lead to a
metabolic alkalosis include:
- Gastric losses, as in vomiting or excessive gastric aspiration;
- Depletion of H+ ions, as in prolonged diuretic therapy;
- Excessive ingestion of base, as in chronic milk alkali ingestion.
the elimination of hydrogen ions (acids) and absorbing more bicarbonate (alkali). This metabolic
compensation usually takes between two and five days.
Patients with chronic obstructive airways disease or emphysema will therefore often have
elevated PaCO2 and HCO3- levels, but with a normal pH. They are said to have compensated
respiratory acidosis.
In metabolic abnormalities, the body attempts to restore a pH to normal by altering the buffer
system. Respiratory compensation takes place through changes in the respiratory pattern and
depth of breathing. This will influence the CO2 excretion and so restore pH balance. Respiratory
compensation is rapid and starts within minutes. It is complete within 12 to 24 hours.
The radial artery is the usual puncture site, although the brachial and femoral arteries are suitable
for patients who are in shock or shutdown.
All ABG samples must be anticoagulated with heparin and taken aseptically and anaerobically.
To prevent haemorrhage or a haematoma, especially in patients with coagulopathies, manual
pressure must be applied for a minimum of five minutes after the needle is withdrawn.
This blood sample should be treated in the same manner as all blood samples taken from a
patient, that is, correctly labelled with particular attention to the date and time of sample and
level of oxygen therapy the patient is receiving.
Managing an ABG sample
ABGs reflect the patients physiological condition at the moment of sampling.
If the patient has been recently postured or given nebulisers or an oxygen change, this will affect
the results. Unless it is an emergency, 20 to 30 minutes should elapse before taking a sample
from spontaneously breathing patients, with 10 minutes for ventilated patients.
All arterial samples taken without immediate access to blood gas analysers should be placed in
ice to reduce metabolic activity and gas exchanges and must be analysed within an hour. Noniced samples must be analysed within 10 to 15 minutes.
Ensuring safe practice
To minimise distress, arterial sampling must be undertaken only by competent clinicians.
Multiple attempts must not be tolerated as this can cause problems for future access. Before
obtaining a radial arterial sample, a modified Allens test should be performed on the patient.
This ensures that there is adequate collateral blood flow through the ulnar artery.
Arterial sampling should not be performed in limbs with evidence of: Raynauds or Bergers
disease; skeletal trauma; a surgical shunt, for example in a dialysis patient; infection; or
peripheral vascular disease. Alternative sites must be chosen.
His PaCO2 is within normal limits. This indicates that respiration is not the primary problem.
The HCO3- is depleted at 19mmol/L and this is reflected by a base deficit of -9. The cause must
be metabolic.
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