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The value of arterial blood gas analysis is dependent on understanding and correctly interpreting the results in the clinical context.
When abnormalities are detected with arterial blood gas analysis, make sure that the sample was obtained, transported and analysed appropriately.
An arterial blood gas result assists in the assessment of a patient’s gas exchange, ventilatory control and acid–base balance.
Common sampling sites include the radial, femoral, brachial and dorsalis pedis arteries. There is no evidence for the superiority of any site.
The alveolar gas equation establishes the alveolar partial pressure of oxygen (PaO 2 ). The alveolar–arterial difference can then be calculated. An elevated value indicates a ventilation–perfusion defect (high A–a gradient).
Isolated hypoxaemia is referred to as type I respiratory failure; type II respiratory failure is characterized by a partial pressure carbon dioxide (PaCO 2 ) higher than 50 mm Hg (6.7 kPA).
Any of five pathophysiological mechanisms may be responsible for hypoxaemia; they include decreased inspired fractional oxygen, impaired diffusion, shunting, ventilation–perfusion (V/Q) mismatch and hypoventilation.
Type II respiratory failure (hypercapnia) is due to inadequate alveolar ventilation, commonly secondary to poor central respiratory drive, neuromuscular disease or significant mechanical disruption of the lungs or chest wall.
The primary acid–base disturbance is established by assessing the relationship between the direction of change in the pH and the direction of change in the PaCO 2 .
When a metabolic acidosis is diagnosed, calculate the anion gap and delta ratio to narrow the differential diagnosis.
In the presence of a metabolic alkalosis, establish both an initiating and maintaining factor.
Venous pH, bicarbonate and base excess have sufficient agreement to be clinically interchangeable with arterial values in patients who are not shocked.
Arterial blood gas analysis is an essential tool for diagnosing and managing the critically ill emergency department (ED) patient’s respiratory status and acid–base balance ( Box 2.6.1 ). It is, however, imperative to understand and interpret the results correctly to effectively manage patients.
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The technology for arterial blood gas analysis became available more than 50 years ago with the development of electrodes that allowed the measurement of partial pressures of oxygen (PaO 2 ) and carbon dioxide (PaCO 2 ) in arterial blood samples taken directly from the patient.
The Clarke oxygen electrode constitutes a platinum probe suspended in an electrolyte solution and separated from the blood sample by a membrane permeable to oxygen. Oxygen molecules diffuse from blood through the membrane to the electrode, where they are reduced to hydroxyl ions. The partial pressure of oxygen is directly proportional to the current measured from this reduction reaction.
A pH-sensitive glass probe maintained in a bicarbonate solution and protected by a carbon dioxide (CO 2 )–permeable membrane constitutes the Severinghaus CO 2 electrode. In this model, the measured PaCO 2 is proportional to the hydrogen ions produced, as CO 2 reacts with water to form hydrogen and bicarbonate ions.
The pH of arterial blood is measured directly by an electrode that then allows the blood gas analyser’s software to calculate the base excess (BE) and bicarbonate concentration.
The arterial oxygen saturation (SaO 2 ) can be calculated from the PaO 2 ; however, this may still be unreliable even if the shifts in haemoglobin–oxygen affinity secondary to acid–base disturbances are accounted for in this calculation. Most modern blood gas analysers now include a co-oximeter that is capable of measuring concentrations of saturated haemoglobin, reduced haemoglobin, carboxyhaemoglobin and methaemoglobin. Wavelengths of light corresponding to unique absorption spectra for each haemoglobin species allow for these measurements to be determined.
Modern automated blood gas analysers report the pH, PaO 2 and PaCO 2 at either 37°C (the temperature at which the values are measured by the blood gas analyser) or at the patient’s body temperature. Most machines report the values of pH, PCO 2 and PaO 2 at 37°C regardless of the patient’s actual temperature. The corrections are generally minimal and corrected values are no more clinically useful than 37°C values.
Accurate results for arterial blood gases are dependent on appropriate collection and handling. Prepared syringes are pretreated with sodium or lithium heparin to prevent coagulation of the specimen. The presence of air bubbles in the sample syringe that exceed 1% to 2% of the blood volume can spuriously elevate PaO 2 but has little effect on pH and PaCO 2 . Delaying the processing of a specimen beyond 20 minutes may result in a reduction in PaO 2 and pH, with a concomitant elevation in PaCO 2 . These changes reflect ongoing cellular metabolism, which is more pronounced in the presence of a leucocytosis or thrombocytosis. Erythrocytes in the arterial blood sample continue to undergo anaerobic glycolysis, generating lactic acid and thereby lowering the pH of the sample. Placing the specimen on ice immediately after drawing will improve its stability.
The most commonly accessed artery is the radial; other potential sites include the femoral, brachial, dorsalis pedis and axillary arteries. The radial artery is the most frequently accessed as it is convenient and accessible and its puncture is well tolerated. There is no evidence that any single site is superior.
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