Blood Gas Analysis
Arterial blood gases
Arterial blood gas analysis provides
information about oxygenation (O2) and ventilation (CO2),
and metabolic disturbance. Some machines also provide electrolytes, lactate and
carbon monoxide levels.
Indications for blood gas
measurement
•
Diagnostic.
•
Severe
shortness of breath.
•
Possible
pulmonary embolus.
•
Assessment of
severity of illness.
•
Shock, severe
sepsis.
•
Diabetic ketoacidosis.
•
Severe
vomiting and diarrhoea.
•
Specific situations.
•
Overdose of
tricyclic antidepressants or aspirin.
Arterial puncture is painful and
should only be performed if theresultis goingtochangemanagement. Thisis
particularlyimportant in young adults with chronic conditions. If just the pH
is required, e.g. for a patient with diabetes, this may be obtained from
venousblood.
The blood gas machine has three main
sensors: pH, PaO2 and PaCO2. Other values
such as bicarbonate and base excess are calculated from these values, not
measured directly. Therefore you can deduce the problem using just these three
values.
Oxygenation
Hypoxia occurs in two situations:
•
Not enough
oxygen reaches the blood.
•
High
altitude: not enough oxygen in the air.
•
Hypoventilation:
neuromuscular disease, extreme fatigue
•
Obstruction: asthma.
•
Not enough
blood reaches the oxygen.
•
Ventilation/perfusion
(V/Q) mismatch: the lung tissue is intact but there is no blood passing through
it, e.g. pulmonary embolus. If the arterial oxygen level fails to correct with 100%
oxygen, this implies ‘shunting’, i.e. blood is bypassing the lung altogether.
•
Alveolar dysfunction:
the apparatus for gas exchange is not working, e.g. interstitial lung disease, pulmonary
oedema.
The A-a gradient
If we know the fraction (%) of oxygen
the patient is breathing in (=FiO2) we can calculate the A-a gradient.
The A-a gradient compares the expected amount of oxygen in the blood (=
the amount of oxygen in the Alveolus), PAO2, with the actual
amount of arterial oxygen, PaO2. Common causes of
a large A-a gradient are:
•
The blood not
reaching the oxygen, e.g. pulmonary embolus.
•
A barrier to effective
gas exchange, e.g. pulmonary oedema. Calculating the partial pressure of alveolar
oxygen is shown oppo- site (R is the respiratory quotient and is related to diet).
Pulse oximetery
Pulse oximetry is very useful for
monitoring patients, as it is non- invasive. The oxygen saturation is
calculated by shining two beams of light through soft tissue, e.g. finger or
earlobe, to estimate the fraction of haemoglobin carrying oxygen.
Unfortunately pulse oximetry has a
significant flaw that can trip up
the unwary. The
blood value we
want to measure
is the PaO2 =
the amount of oxygen carried in arterial blood. Oxygen saturation is only a
surrogate measure of the PaO2: the graph (opposite) shows the
relationship between the two.
Under normal circumstances, with an
oxygen saturation of 100%, the PaO2
Acid–base disturbance
Acidosis and alkalosis have a chicken/egg
relationship with ventilation, (measured by PaCO2) and
respiratory effort: sometimes it is not always clear which came first. To
analyse these problems, start with the acid–base disturbance, and then look at
the PaCO2.
Acidosis (pH < 7.35)
CO2 low = metabolic
acidosis
If the patient is acidotic and the PaCO2
is low, it is likely the patient is breathing deeply to expel CO2,
to compensate for the metabolic acidosis by hyperventilation. This is often
seen in diabetic ketoacidosis and is called Kussmaul breathing.
CO2 high = respiratory acidosis
If the CO2 is high, it is
likely that this is at least partially responsible for the acidosis, although
usually the acidosis is mixed (partly metabolic and partly respiratory).
The normal stimulus to breathe is
increased blood CO2 levels, so a high CO2 level implies
failure of adequate ventilation.
Some patients with lung disease (e.g.
COPD) lose their sensitivity to increased blood CO2 levels and
therefore rely on low O2 levels to drive their breathing. Giving
these patients high concentrations of oxygen dangerously reduces their
respiratory drive, resulting in a build-up of CO2. The increase in
CO2 makes the patient sleepy, further reducing respiratory effort.
If faced with a patient who is on home
oxygen or is known to have advanced COPD, the safest action is to give enough
oxygen to ensure an oxygen saturation of about 91%. Any more than this may
abolish the patient’s drive to breathe.
Patients with chronically elevated CO2
levels compensate for this by excreting acid (H) renally to rebalance the
equation:
CO2 +
H2O ó HCO3- + H +
Therefore these patients will have a
chronically raised HCO (bicarbonate) level.
Alkalosis (pH > 7.45)
CO2 low = respiratory
alkalosis
Respiratory alkalosis is usually due
to anxiety-related hyperventilation although marked hypoxia, e.g. from
pulmonary embolus, may also cause this.
CO2 high = metabolic alkalosis
Metabolic alkalosis is usually caused
by loss of acid and/or dehye.g. diarrhoea and vomiting.
