of COPD who is stimulated to increase ventilation by a pulmonary embolism.
Arterial oxygenation
In addition to the acid/base balance, arterial blood gas analysis provides valuable information on arterial oxygen tension (PaO2).
Respiratory failure
‘Respiratory failure’ is a clinical term used to describe a failure to maintain oxygenation (usually taken as an arbitrary cut‐off point of PO2 8.0 kPa [60 mmHg]).
Type I respiratory failure is hypoxaemia in the absence of hypercapnia. Overall alveolar ventilation is therefore normal. This pattern of abnormality usually indicates a disturbance of the V/Q matching system within the lung. Such a disturbance can be caused by any intrinsic lung disease affecting the airways, parenchyma or vasculature (e.g. acute asthma, lung fibrosis or pulmonary embolism).
Type II respiratory failure is hypoxaemia with hypercapnia and indicates alveolar hypoventilation. Note this is not merely a severe form of type I respiratory failure; it is brought about by an entirely different mechanism. This may occur from reduced ventilatory drive (e.g. sedative overdose), reduced neuromuscular power (e.g. myopathy) or resetting of the chemoreceptors that drive ventilation in chronic lung disease (e.g. COPD).
Of course, type I and type II respiratory failure can coexist (and commonly do). These matters are dealt with in more detail in Chapter 1.
Oxygen saturation can be measured non‐invasively and continuously using a pulse oximeter. Oxygenated blood appears red, whereas reduced blood appears blue (clinical sign of cyanosis). An oximeter measures the ratio of oxygenated to total haemoglobin in arterial blood using a probe placed on a finger or earlobe, which comprises two light‐emitting diodes – one red and one infrared – and a detector. The light absorbed varies with each pulse, and measurement of light absorption at two points on the pulse wave allows the oxygen saturation of arterial blood to be determined. The accuracy of measurement is reduced if there is reduced arterial pulsation (e.g. low‐output cardiac states) or increased venous pulsation (e.g. tricuspid regurgitation, venous congestion). Skin pigmentation or the use of nail varnish may interfere with light transmission. Oximetry is also inaccurate in the presence of carboxyhaemoglobin (e.g. in carbon monoxide poisoning), which the oximeter detects as oxyhaemoglobin.
The relationship of PO2 to oxygen saturation is described by the oxyhaemoglobin dissociation curve (see Fig . 1.9). This curve is sigma‐shaped, so that oxygen saturation is closely related to PO2 only over a short range of about 3–7 kPa. Above this level, the dissociation curve begins to plateau and there is only a small increase in oxygen saturation as the PO2 rises. Oximetry can reduce the need for arterial puncture, but arterial blood gas analysis is necessary to determine accurately the PO2 on the plateau part of the oxyhaemoglobin dissociation curve, to measure CO2 level and to assess acid/base status.
A simple algorithm for reviewing blood gas results
Most blood results in medicine are relative easy to make sense of; there’s one value, and it’s either high or low. When faced with the results of an arterial blood gas measurement, the clinician has to handle six different values, which must be drawn together and interpreted as one. The inexperienced often find their attention skipping from one number to the next, declaring each as either high or low, before becoming utterly confused and giving up. A simple stepwise system for interpreting blood results would help. The following algorithm is easy to follow and will make sense of most of the results you’ll come across in clinical practice.
1 Look at the pH. Decide whether this is an acidosis or alkalosis. Once that fact is determined, don’t be diverted from it after reviewing the other values. It won’t change. If the pH is in the normal range, note whether it is erring towards one end of the range or the other. If there is a compensated abnormality, the position of the pH within the range may indicate the nature of the primary disturbance. Remember that physiological compensatory mechanisms don’t overcompensate.
2 Look at the PCO 2 . Ask whether the PCO2 is contributing to or attempting to compensate for the abnormality identified in the pH. That will allow you to know whether the primary disturbance is respiratory (contributing) or metabolic (attempting to compensate).
3 Look at the bicarbonate. I would suggest either the sHCO3 – or base excess. In the case of a primary metabolic problem, the bicarbonate may hold no surprises. In a metabolic acidosis, it will be low; in a metabolic alkalosis, high. In the case of a primary respiratory problem, the bicarbonate may be normal (suggesting the problem is acute, having not had time to change), attempting to correct the respiratory effect on the pH (suggesting the problem is chronic) or compounding the problem (suggesting a mixed disturbance).
4 Look at the PO 2 .Knowing the inspired partial pressure of oxygen, ask whether the PO2 is what you’d expect given the level of ventilation (i.e. given the PCO2) or lower than expected. This may be difficult to gauge, in which case the alveolar gas equation should be applied (see Chapter 1). You can then determine whether type I respiratory failure, type II respiratory failure or both are present.
A reduced FEVI:VC ratio indicates airways obstruction (e.g. asthma, COPD).
A reduced KCO indicates disease of the lung parenchyma or its blood supply (e.g. emphysema, lung fibrosis, pulmonary embolism).
Type I respiratory failure is hypoxia without hypercapnia and may occur in any disease intrinsic to the lung (e.g. asthma, pulmonary oedema, pulmonary embolism, lung fibrosis).
Type II respiratory failure is hypoxia with hypercapnia and indicates hypoventilation (e.g. sedative overdose, neuromuscular disease or moderate to severe COPD where it occurs in conjunction with a type I respiratory failure).
An elevated alveolar–arterial gradient implies a problem intrinsic to the lung.
1 Burns GP. Arterial blood gases made easy. Clin Med 2014; 14: 66–8.
2 Maynard RL, Pearce SJ, Nemery B, Wagner PD, Cooper BG. Cotes’ Lung Function. Oxford: Wiley Blackwell, 2020.
3 Flenley DC. Interpretation of blood‐gas and acid–base data. Br J Hosp Med 1978; 20: 384–94.
4 Gibson GJ. Clinical Tests of Respiratory Function. Oxford: Oxford University Press, 2009.
5 Gibson GJ. Measurement of respiratory muscle strength. Respir Med 1995; 89: 529–35.
6 Hanning CD, Alexander‐Williams JM. Pulse oximetry: a practical review. BMJ 1995; 311: 367–70.
Multiple choice questions
1 3.1 The volume of gas in the lungs after a full expiration is: residual volumetotal lung capacity minus residual volumefunctional residual capacitytidal volume plus functional residual capacityvital capacity minus residual volume
2 3.2 Lung function test results of: FEV 1 reduced, FEV 1 :VC normal, KCO reduced would be most in keeping with: kyphoscoliosisidiopathic pulmonary fibrosispulmonary hypertensionasthmaCOPD
3 3.3