VOL: 97, ISSUE: 27, PAGE NO: 36
Maureen Coombs, PhD, RN, is consultant nurse, critical care, Southampton General Hospital
Arterial blood gas (ABG) analysis may appear a complex and daunting task, but a little guidance can make it much simpler.
It is important to understand the physiological principles underpinning blood gas analysis, so these will be outlined briefly before exploring some practice issues for patients undergoing arterial blood gas sampling.
The key to making sense of arterial blood gases is to use a structured approach. Some patient case studies show this in action.
Why analyse arterial blood gases?
As we care for more acutely ill patients with respiratory, cardiac, renal and metabolic disorders, so more of them will have arterial blood gas samples taken. Understanding these results is an essential part of patient care, making patient assessment more informed and patient management more specific. Essentially, arterial blood gases are taken to evaluate the patient’s:
- Acid base balance.
Arterial blood gas analysis requires a clear understanding of the terms used. The key measurements are shown in Table 1.
Assessing the patient’s oxygenation
The oxygen partial pressure (PaO2), the measurement of oxygen dissolved in the blood, is an important indicator of potential tissue oxygenation.
The normal value is between eight and 12 kilopascals (kPa).
Hypoxaemia, or a low PaO2, deprives cells of oxygen and leads to irreversible cell damage. It can result from hypoventilation, airway obstruction and atelectasis. Older patients and those with chronic respiratory disease tend to have lower oxygen levels. It is therefore important to establish the acceptable PaO2 for each patient to administer appropriate oxygen therapy.
The oxygen saturation, SaO2, is the percentage of saturated haemoglobin carrying oxygen compared with the total amount of oxygen it could carry.
An SaO2 of more than 95% is normal for a healthy adult and can be determined by ABG analysis or by pulse oximetry.
Assessing the patient’s ventilation
The lungs eliminate the respiratory acid (carbonic acid) as carbon dioxide (CO2). When the patient is breathing effectively and moving adequate volumes of air in and out of the lungs, the PaCO2 will stay within the normal limits of 4.5-6kPa.
However, changes in the patient’s ventilation (breathing) will affect CO2 levels. The PaCO2 may reveal the conditions of respiratory acidosis or respiratory alkalosis.
In respiratory acidosis, the blood pH is less than 7.35 and the PaCO2 greater than 6kPa.
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.
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 patient’s 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.
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.
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.
Metabolic and respiratory compensation
The body is very sensitive to pH changes. It attempts to restore a normal pH by altering the buffer system. In respiratory conditions, therefore, the kidneys will compensate. In chronic respiratory acidosis, the kidneys will attempt to balance the respiratory acid load by increasing 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.
How are ABGs sampled?
ABG samples are usually obtained from a single percutaneous needle puncture into a peripheral artery. Patients who need frequent arterial blood gas analysis, for example those in intensive care, may have an indwelling catheter which is then kept patent using a heparinised, pressurised system.
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 patient’s 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. Non-iced 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 Allen’s 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: Raynaud’s or Berger’s disease; skeletal trauma; a surgical shunt, for example in a dialysis patient; infection; or peripheral vascular disease. Alternative sites must be chosen.
A systematic approach to analysing ABGs
An approach that applies four simple steps to analysing arterial blood gases demystifies the process. The steps are:
- Analyse the patient’s oxygenation - look at the PaO2, SaO2;
- Establish the patient’s pH - look at the pH;
- Check if there is respiratory or metabolic disturbance - look at the PaCO2, -HCO3, BE;
- If the pH is normal, establish whether there is any compensation - look at the pH, PaCO2, -HCO3.
The following case studies show how this works.
Ted Wilcox is admitted to your ward with an extensive anterior-wall myocardial infarction. He is hypotensive and in cardiogenic shock. His ABGs are: pH 7.26, PaCO2 4.9kPa, HCO3- 19mmol/L, BE -9, PaO2 8.5kPa and SaO2 92% on 40% O2. Apply the four analytical steps.
Mr Wilcox is hypoxaemic with a low PaO2 and SaO2 on 40% O2.
His pH is less than 7.35 and he is therefore acidotic.
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.
His pH is not normal. There is no compensation.
Analysis: This patient has an uncompensated metabolic acidosis. This is most likely because of a low cardiac output arising from the cardiac insult. Low blood pressure leads to poor tissue perfusion and therefore poor oxygenation. Lactic acid would build up as a result of aerobic metabolism and cause an excess metabolic acid load.
Paul Bannerman is 48 hours post-laparotomy for a perforated duodenal ulcer. Since surgery he has continued to have large gastric losses via his nasogastric tube. There is a query of postoperative ileus. His ABGs are: pH 7.52, PaCO2 5.5kPa, HCO3- 34mmol/L, BE +7, PaO2 10.1kPa and SaO2 96% on air.
Apply the four analytical steps.
Mr Bannerman has an adequate PaO2 and SaO2 on air. He is not hypoxaemic.
His pH is greater than 7.35 and he is therefore alkalotic.
The PaCO2 is within normal limits. This indicates that respiration is not the primary problem. The HCO3- is raised and this is reflected by base excess (acid deficit). The cause must be metabolic.
The pH is not normal. There is therefore no compensation.
Analysis: This patient has an uncompensated metabolic alkalosis. This is a result of continued acid loss from high-volume gastric aspirates.
This acid loss would lead to a high base load causing metabolic alkalosis.
Freda Thomas is admitted from outpatients with increasing dyspnoea and a productive cough. She has a pyrexia of 37.9°C. She has a long-standing diagnosis of chronic obstructive airways disease. Her ABGs are: pH 7.38, PaCO2 8.6kPa, HCO3- 33 mmol/L, BE +10, PaO2 7kPa and SaO2 88% on air.
Apply the four analytic steps.
Ms Thomas is hypoxaemic with a low PaO2 and SaO2 on air. However, with her history of chronic respiratory disease it is important to establish what is a normal PaO2 for her. This will then direct the oxygen therapy given.
Her pH is within normal limits.
Both the PaCO2, HCO3- and BE are outside normal limits. All are elevated.
There is both a respiratory acidosis and metabolic alkalosis.
The pH is normal, therefore the patient’s problem must be chronic leading to compensation. To establish whether the respiratory or metabolic component came first, the patient’s history must be examined more closely.
Analysis: This patient has compensated respiratory acidosis. Impaired respiratory function has led to a chronic elevation of the PaCO2 and respiratory acidosis. The kidneys have compensated for this by raising the HCO3-.
Although you will care for patients with complex ABG results showing mixed and combined acid-base imbalances, the systematic approach outlined here will enable you to interpret most uncomplicated results.
Remember that ABG analysis is only part of the patient assessment. However, from these results you can gain valuable information on patient oxygenation, ventilation and acid-base balance. Systematic interpretation of the results must therefore be performed in conjunction with the patient’s history and physical examination.