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
• 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.
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 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
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.