The respiratory system presents a uniquely vulnerable aspect of our bodies to the outside world. It is, for example, the only place where capillaries continuously come into direct contact with the outside air. Admittedly, that air is well conditioned before being presented to the respiratory surface, but attacks on the respiratory system and its function are extremely common. It is to be hoped that our readers will never suffer from coronary heart disease or renal failure, but which of us will go through life without a disease of the respiratory system, if only the common cold?

Most malfunctions of the respiratory system are reliably diagnosed by clinicians after taking a history of the patient’s complaint and making a clinical examination. Radiological examination at appropriate levels of sophistication, microbiological and cytological investigations, blood tests, lavage, bronchoscopy, and a pantheon of other ingenious tests are available to confirm or refute the original diagnosis.

Such a diagnosis is, however, usually qualitative. It does not quantitatively measure the effect the disease is having on the functioning of the respiratory system, and hence on the quality of life. This is the province of the lung function test.

These tests range from the relatively simple to those that are the province of the specialized lung function laboratory. We have placed the tests roughly in increasing order of exoticism.

A simple spirometer (Fig. 5.2, p. 63) will provide much useful information about a patient’s lungs. Large people have larger lungs than small people and age exerts its malign effect. Extensive study of these relationships has provided us with tables which, for example, relate vital capacity to height (see Appendix).

Measurements made on a spirometer may be classified as:

Although such measurements as inspiratory reserve volume (IRV) and expiratory reserve volume (ERV) can be informative, the most usual and useful static spirometric test is the forced vital capacity (FVC). This is ‘forced’ because the subject is enthusiastically urged to breathe in as far as he can and out as far as he can (Fig. 11.1). This test, which can be classed as static because it does not involve an element of time, is often combined with a dynamic test, the FEV₁:

FEV₁ is commonly expressed as a percentage of FVC. This takes into account the problem that a very small person (with very small, perfectly healthy lungs) would never be able to breathe out the same amount in 1 second as a very large person, whose lungs may not be so healthy. You can expect a healthy person to force out at least 70% of his vital capacity in 1 second. Using this percentage alone can create problems in restrictive lung diseases, which restrict the expansion of the lungs: both VC and FEV₁ are reduced, therefore in those cases that percentage may be normal. For this reason both absolute values and percentage are measured. Many years ago a ratio of 70% VC was considered acceptable, but that was when smoking was considered normal. A higher percentage is required today.

Characteristic traces in normals and patients with chronic obstructive (emphyzematous/bronchitic) or restrictive (fibrotic) lung disease are shown in Figure 11.1.

Although emphysema is the ‘classic’ obstructive lung disease it can only be diagnosed with certainty at post mortem (pathologists are the only people who invariably make the perfect diagnosis, but by then it’s too late). We therefore describe obstructive patterns of lung disease as asthma (reversible) or chronic obstructive pulmonary disease (COPD, irreversible).

In the helium dilution method the principle is simple. The patient breathes out to FRC or RV, whichever is being measured, and is connected to a spirometer of known volume containing helium (He) at known concentration. The patient breathes normally for an appropriate length of time and the dilution of the He by the RV or FRC in his lungs is measured. The level of the trace of his breathing is carefully watched and oxygen added at the same rate as it is used up to keep the overall volume in lungs + spirometer constant (Fig. 11.2).

An interesting disparity is often seen between RV measured by plethysmography and by dilution. This arises because air trapped in the lungs, which is not in contact with the mouth, is measured by the plethysmographic method but does not take part in the dilution of He.

Restrictive lung diseases decrease TLC, FRC, RV and VC. Frequently RV is first to be affected. Care should be taken in interpreting results from obese patients, where the outward recoil of the chest wall is reduced, resulting in lower FRC.

Obstructive lung diseases show an increasing RV as gas is trapped behind the collapsed airways (see above). Increased FRC and TLC in these patients is the result of reduced lung recoil and breathing at increased lung volumes in an instinctive attempt to keep the airways open.

Peak expiratory flow is the maximum expiratory flow (L.s²¹) that a subject can produce. Of course this is dependent on the subject’s motivation even with healthy lungs. The advantage of this measurement is that it can be made with simple apparatus – where the subject blows against a paddle or propeller which records flow. Although not precise this has been found to be a useful domiciliary measurement in asthma with the patient keeping a diary of his progress.

Flow-volume loops. With the subject breathing through a pneumotachograph (Fig. 4.6, p. 45) which measures flow, and by integrating that flow to provide volume, loops of inspiratory and expiratory flowvolume relationships can be recorded. (Fig. 11.3). These loops are constructed by having the patient breathe from total lung capacity down to residual volume several times. They are particularly useful in assessing chronic obstructive pulmonary disease (COPD) where the inspiratory part of the loop has a normal shape, although being of reduced volume, while the expiratory part of the loop has a characteristic ‘scooped out’ shape as flow is restricted by airway collapse.

This instrument is described in Chapter 4 and consists of an airtight box in which the subject sits. To understand the principles on which this instrument works, consider the subject’s chest as a syringe with the diaphragm represented by the plunger.

The subject first pants against a closed shutter – the neck of the syringe is blocked.

In terms of gas law the situation is as in Figure 11.4A, where a large enclosed volume of gas (the contents of the box) surrounds a small enclosed volume of gas (the air in the lungs) which increases and decreases in volume as it is compressed or decompressed. This change in volume of the syringe compresses and decompresses the air in the box, and so the pressure in the box changes proportionately and in the opposite sense to the pressure in the lungs.

Measuring the pressure changes in the box while the subject pants against a closed shutter enables us to calculate pressure within the lungs (Fig. 11.4) and therefore from the gas laws calculate lung volume, and is usually used to measure functional residual capacity (FRC) and residual volume (RV).

Plethysmography is also used to measure lung volumes (TLC) in patients with severe airflow obstruction in preference to the usual helium (He) dilution technique. This is because in these patients air trapping is so bad that the He cannot get to closed off volumes in the lungs, which are therefore not registered. In plethysmography, however, these closed off volumes are still subject to the gas laws (see the Appendix) on which this technique is based.

The principle of the relationship between box pressure and lung airway pressure does not depend on the ‘syringe’, which represents the lungs, being closed. In Figure 11.4B the narrow tube represents the resistance of the airways, and although air is being forced in to or out of the syringe the relationship between this driving pressure and box pressure still holds. In this case, measuring the driving alveolar pressure (by measuring box pressure) and flow (using a pneumotachograph), we can measure airways resistance.

Plethysmography offers an almost ideal way of measuring a number of pulmonary variables. One of its major limitations is that many subjects object to being locked inside an airtight box. This may reflect the incidence of claustrophobia in the population, or the mistrust in which respiratory physiologists are held.

The theory behind the method of measuring transfer factor was outlined in Chapter 6 (p. 82). Methods of indirectly measuring transfer factor for O₂ which are based on a number of questionable assumptions have been developed, but are really only of theoretical interest.

Transfer factor is now measured using carbon monoxide under steady-state or single-breath methods, both of which require us to know the partial pressure driving CO from the inhaled air into the blood, and the rate of uptake of CO.

It is the business of the respiratory system to ‘condition’ arterial blood for the benefit of the tissues it perfuses. Measuring the properties of arterial blood with the subject at rest and, if necessary, during the increased demands of exercise, tells us whether the respiratory system is up to the job.

Where arterial blood samples are available Po₂, Pco₂ and pH are measured by bringing the blood into contact with electrodes whose resistance to current or whose accumulation of H⁺ is determined by the Po₂, Pco₂ and pH of the blood being tested. By bringing the blood into contact with standard gas mixtures and carrying out a variety of calculations, modern blood gas analysers calculate other variables, such as standard bicarbonate and base excess/deficit. These instruments have displaced all other methods of measuring blood gases and pH, but they still depend on the operator presenting a sample which has been correctly collected. The causes of error in collection are mainly due to contamination of the sample by air; delayed analysis, which Xresults in oxygen being consumed within the stored blood; and secondarily, the effect of temperature, a drop in which can result in the measured Po₂ being less than the Po₂ of the blood when it was in the subject (most modern instruments get round this problem by automatically ensuring that the blood is kept at body temperature during analysis).

Obtaining a sample of arterial blood is not a trivial or unskilled procedure, and capillary blood from a pinprick can be used with techniques that do not need more than 0.1 mL to measure CO₂ tension, haemoglobin saturation and lactic acid. A number of non-invasive alternatives have also been developed.

Oxygen saturation used to be measured photometrically by monitoring light of the appropriate wavelength for oxygenated or deoxygenated haemoglobin transmitted through the finger or earlobe. The problem with this technique was that the blood being monitored was mainly venous or capillary, rather than arterial. This technique has now been almost completely replaced by pulse oximetry. In this technique, light of appropriate wavelengths is monitored as it passes through the earlobe or finger and related to the pulse pressure wave in the vessels under the sensor. The difference between the extra light signal at the peak of the pulse and that between pulses is due to the inflow of blood and reflects arterial saturation.

Another approach is to apply miniature O₂ and CO₂ electrodes to heated skin. The plan being to measure the gas tensions in the blood in the dilated vessels below the electrodes. These transcutaneous (Tc) measurements are more successful in neonates, who have thin well-vascularized skin (as soft as a baby’s bottom), than in adults where TcPo₂ is approximately 80% Pao₂ and TcPo₂ is greater than Paco₂.

The uniformity of distribution of inspired air throughout the lungs is important to their efficient function (assuming that blood is also uniformly distributed). The uniformity of ventilation can be investigated by measuring the appearance of an inhaled inert gas at the lips in a single- or multiple-breath test.

Exercise tests are generally safe because they do not, as might be assumed, involve striving to maximum effort but are aimed to provide information at loads which the patient can perform reasonably comfortably. Nevertheless, this form of testing should have a physician in attendance as cardiac dysrhythmias are not infrequent. An electrocardiogram should be continuously taken from patients suspected of cardiac disease and all subjects over 40. Walking with the patient or asking him to climb stairs are traditional and useful guides to incapacity and assessment of fitness for surgery.

Because the respiratory system has such enormous reserves many of the tests outlined above are carried out when the increased demands of exercise are being placed on it. More sophisticated exercise tests involve exercising the patient on a treadmill or stationary bicycle. In particular, minute ventilation, pattern of breathing, composition of the expired air and O₂ consumption, together with cardiovascular measurements of blood pressure, heart rate and ECG at different levels of exercise, can help to assess a patient’s disability. Assessment of exercise capacity is measured as maximum O₂ uptake per minute . This is obtained directly by increasing the exercise level until the patient can no longer continue. Because the relationship between heart rate, cardiac output and oxygen consumption is linear this information can be projected from submaximal responses in vulnerable patients.

The most usual reason for performing an exercise test is to determine whether the symptoms of breathlessness that the patient complains of are of cardiac or respiratory origin. To do this it is useful to compare the ventilation and heart rate obtained with predicted values from age and size matched normals.

Patients with impaired heart valves, for example, reach normal maximum heart rates at lower than normal workloads.

Patients with airflow obstruction have higher than expected minute ventilation for the level of exercise, which reflects wasted ventilation. Patients with restrictive diseases respond in the same way, except that their increased minute ventilation is made up of a pattern of high frequency and low V_T.

For good diagnosis we wish to see the patient’s complaint under the best (or, from his point of view, worst) condition. This is very clearly seen in asthmatic patients who are remarkably normal when not in status asthmaticus. Frequently the exercise tests described above will provoke an asthmatic attack in these patients but there are a variety of other challenges to which they can be put. These include tests of bronchial responsiveness which have been developed to exploit the fact that asthmatics show abnormally large bronchoconstrictor responses to inhalation of specific allergens and non-specific chemical and physical stimuli. Thus, even the exercise test described above or the inhalation of cold air may trigger an attack. Of the chemical agents, histamine and methacholine are the most popular, administered as an aerosol. Histamine is rapidly metabolized and so repeated doses are not cumulative. Methacholine seems to be more discriminatory between normal subjects and asthmatics. An aerosol of saline is first administered as saline is the vehicle in which the histamine or methacholine is administered and we wish to see if the saline itself produces an effect. The histamine or methacholine in saline is then administered in increasing doses (usually starting with about 0.003 mg mL⁻¹ histamine acid phosphate and doubling with each administration). After 2 minutes of breathing the aerosol and 3 minutes for the drug to take effect the subject’s FEV₁ or specific airways conductance is measured. The procedure is repeated at 10-minute intervals doubling the concentration each time until FEV₁ falls by more than 20%. The concentration which produces a 20% fall is then interpolated and this provocation concentration is reported as PC 20.