Measurement of respiratory function: ventilation

RESPIRATORY PHYSIOLOGY

Measurement of respiratory function: ventilation Iain Campbell James Waterhouse

As outlined on page 349, the mechanics of getting oxygen into the bloodstream and removing carbon dioxide from it is brought about by a combination of the movement of air in and out of the lung (ventilation) and the ability to transfer oxygen and carbon dioxide in and out of the bloodstream via the alveoli (perfusion). A typical value for alveolar ventilation with the individual at rest is about 4–5 litres/min and pulmonary blood flow (cardiac output) is about 5 litres/min, thus the ratio of ventilation (V) to perfusion (Q) is about 0.8–1. Minute ventilation, calculated from tidal volume (500 ml) and respiratory frequency (15 breaths/min) is about 7.5 litres, anatomical dead space is 150 ml and alveolar gas volume (functional residual capacity: FRC) is 3 litres. The volume of blood in the pulmonary capillaries is only about 70 ml. Gas transfer may be limited by the time the blood spends in the capillary. When blood is diverted from other parts of the lung (e.g. following a large pulmonary embolus) the time taken for the blood to traverse the capillaries that are still open is reduced and gas transfer may be incomplete. With exercise at altitude, the lower atmospheric partial pressure of oxygen results in a decrease in the driving pressure of oxygen across the capillary membrane, and equilibration may be incomplete, worsening the hypoxaemia. Equilibration between the alveolus and the blood is normally limited by perfusion. However, it may be limited if the resistance to gas transfer is increased by diffusion, for example in chronic chest diseases with thickening of the alveolar capillary membrane or if fluid is present. In health, diffusion reserves are huge and, with a normal alveolar–capillary membrane, disturbances in gas transfer are mainly caused by alterations in the matching of perfusion to ventilation.

Iain Campbell is Consultant Anaesthetist at the University Hospitals of South Manchester NHS Trust and Visiting Professor of Human Physiology at Liverpool John Moores University. He qualified from Guy’s Hospital Medical School, London, and trained in anaesthesia in Zimbabwe, Southend, Montreal and Leeds. James Waterhouse is Professor of Biological Rhythms at the Research Institute for Sport and Exercise Sciences at Liverpool John Moores University. He qualified as an animal physiologist from Oxford University and gained his DPhil there. His research interests are circadian rhythms, with particular reference to jet lag and assessing the clock-driven components of measured circadian rhythms.

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Lung volumes Air flow in and out of the lung is dependent on the generation of pressure differences between the alveoli and the atmosphere. Air flow is a mixture of laminar and turbulent flow, the latter occurring particularly at airway junctions. At high rates of flow, the amount of turbulence increases and resistance rises disproportionately. Quiet expiration to FRC is a passive process driven by elastic forces in the lung, while the inspiratory muscles gradually relax. At FRC, intrapleural pressures are negative, but in the upright individual there is a difference between the top (atmospheric pressure (A) – 8 cm H2O) and the base (A – 2 cm H2O) of the lung, as a result of which, alveoli at the base of the lung (in the upright position) are relatively compressed and smaller (less full with gases) than those at the top. During expiration to residual volume the intrapleural (intrathoracic) pressure becomes positive and compresses alveoli and airways. Alveolar pressure is thus made up of the intrapleural (intrathoracic) pressure plus the elastic recoil pressure of the lung (Figure 1). Pressure at the mouth is atmospheric, therefore there is a point along the airway from alveoli to the mouth where the intraluminal pressure equals the surrounding intrathoracic pressure – the so-called ‘equal pressure point’.

Towards the mouth from this equal pressure point mainly comprises the large, relatively rigid, airways and towards the alveoli, the smaller airways, which are less well supported and less rigid. Any increase in muscular effort tends to compress these small airways at or on the alveolar side of the equal pressure point. The alveolar pressure is thus a combination of elastic recoil of the lung plus the raised intrathoracic pressure, but this raised intrathoracic pressure is also compressing the airways at the equal pressure point, therefore the expiratory flow rate is determined by the elastic recoil of the lung only and is independent of muscular effort (Figure 1). When the rise in intrathoracic pressure completely blocks off the airways, the alveoli cease to empty and gas trapping occurs. In a healthy young adult, breathing quietly down to residual volume in the upright position, this is seen at about 10% of vital capacity. Other factors that predispose to premature small airway closure and air trapping are those that cause a reduction in calibre of the smaller airways (e.g. smooth muscle contraction, mucosal swelling, secretions), a loss of supporting tissues and elasticity (emphysema, age), increased intrathoracic pressure (obesity), or decreased elastic recoil of the lung. This occurs first at the lung bases because of the higher intrapleural (intrathoracic) pressure. With a forced expiratory manoeuvre and high intrathoracic pressure, airway closure occurs at a higher lung volume.

Respiratory pressures during a forced expiration

Tests of ventilation Ventilation is normally assessed from measurement of static lung volumes and various indices of expiration, namely forced expiratory volume (FEV), forced expiratory volume in 1 second (FEV1), peak expiratory flow rate (PEFR) and flow–volume curves.

Equal pressure Mouth 0 cm H2O

Static lung volumes Static lung volumes are traditionally measured using a conventional bell-type spirometer or a dry rolling seal-type spirometer, which is essentially a piston in a cylinder with a pliant seal between the two which is free to move as the piston moves in and out. The volumes obtained are compared with published tables of normal values for age, height, weight and gender. All measurements can be read directly from the spirometer trace (see Figure 1 on page 350) except for FRC (and residual volume) which is measured with helium dilution, or using a whole-body plethysmograph or calculated from nitrogen washout.

Alveolar 27 cm H2O Elastic (lung) 12 cm H2O

15 cm H2O

Muscular 18 cm H2O Elastic (chest wall) 3 cm H2O

FRC is the oxygen reservoir from which gas exchange takes place and which is replenished by tidal ventilation. It is affected by a number of conditions (e.g. obesity, pregnancy, abdominal surgery) and such changes affect oxygenation mechanisms, particularly via the relationship between FRC and small airway closure. FRC cannot be read off the spirometer trace and is most commonly measured using helium dilution because helium is easily analysed and virtually insoluble in the tissues. The spirometer is filled with a mixture of a known concentration of helium (C1) and oxygen-enriched air. The volume (V1) of the spirometer is known. The individual, wearing a nose clip, breathes into the spirometer via a mouthpiece. The mouthpiece is initially open to room air. At the end of a normal quiet expiration (i.e. at FRC:V2) the individual is switched into the spirometer circuit and continues to breath quietly via the circuit. Carbon dioxide is

Muscular effort (18 cm H2O) produces a positive intrathoracic (intrapleural) pressure equal to the effort (18 cm H2O) minus the elastic recoil of the chest wall (3 cm H2O) of 15 cm H2O. The pressure gradient down the airway ranges from the intra-alveolar pressure (27 cm H2O) to zero at the mouth. Intra-alveolar pressure (27 cm H2O) is made up of the elastic recoil of the lung (12 cm H2O) plus the positive intrathoracic pressure (15 cm H2O) therefore a point must exist along the airway where airway pressure equals intrathoracic pressure. Any further increase in pressure compresses the airways at and below the equal pressure point and does not increase the rate of airflow which is thus determined only by the elastic recoil of the lung (12 cm H2O) and so is independent of muscular effort 1

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absorbed and oxygen added as necessary to maintain the end-tidal position. The helium equilibrates between the spirometer and the lung and its concentration in the circuitry is observed to fall to a final concentration C2. Thus:

Figure 2. The individual takes a maximal inspiration then breathes out as far and as forcibly as possible. FVC and FEV1 are derived from the tracing. The ratio FEV1:FVC (× 100) gives a measure of airways obstruction; its normal value is 75–80%. FVC is slightly less than VC (measured with a slow quiet expiration) because of airway trapping. It is affected by diseases of the thoracic cage (e.g. kyphosis, acute injury), of the respiratory muscles (e.g. poliomyelitis), of the pleural cavity (e.g. pneumothorax) or by decreased compliance (e.g. chronic bronchitis, fibrosis, obesity). It is also affected by obstructive conditions (e.g. asthma). The ratio FEV1: FVC gives more information about obstruction than either of the two measurements alone. The point of greatest resistance in the normal respiratory tract is in the medium-size bronchi, about the fourth or fifth generation, just beyond the origin of the bronchopulmonary segments. With a forced expiratory manoeuvre, the intrathoracic pressure rises and compresses the alveoli, causing the small airways to be compressed as well. In the latter part of such a manoeuvre, the point of greatest resistance is the small airways. Other measurements of flow that can be derived from the FVC curve are PEFR (by taking a tangent to the steepest part, normally the start of the curve) and mid-expiratory flow rate (FEV25–75: by measuring the slope of a line drawn between the two points on the curve at 25% and 75% of FVC).

C1 V1 = C2(V1 + V2) from which V2(FRC) = V1 × C1 – C2 C2 The individual normally takes a couple of quiet vital capacity breaths to facilitate mixing. The whole process takes 5–10 min depending on the type and degree of lung pathology (poorly ventilated alveoli take longer to equilibrate). Other techniques for measuring FRC include the whole-body plethysmograph and nitrogen washout. A body plethysmograph (unlike helium dilution) measures gas volumes trapped behind closed airways. The plethysmograph is a closed airtight box. Changes in closed volumes within the box produce changes in box pressures from which the volume changes can be inferred. It is not in common use in anaesthetic practice. Readers interested in body plethysmography and nitrogen washout should refer to the Further Reading for details. Dynamic lung volumes Forced expiratory lung volumes: the most common measurement of ventilation is forced vital capacity (FVC). This can be measured using a wedge spirometer (or Vitalograph) which is easily transported to the bedside. A typical FVC trace is shown in

Flow volume loops: the above measurements are more an index of large or medium airway function. Small airways are studied specifically using the flow volume loop, an example of which is shown in Figure 3. The individual carries out an FVC manoeuvre;

Forced expiratory lung volume measured by wedge spirometry

Flow volume loops

PEFR

Normal

Volume

Mild obstructive lung disease FVC

Severe obstructive lung disease

Flow rate

FEV1

1

2

3

4

5

Time (s)

TLC Lung volume

The graph shows the derivation of forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1) and the line from which peak expiratory flow rate (PEFR) can be determined

Note the scooped out appearance of the obstructive curves and the limitation of peak flow with severe obstructive lung disease RV, residual volume; TLC, total lung capacity

2

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RV

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flow rate is measured and plotted against lung volume. The peak of the curve denotes peak flow; beyond that point, airway compression occurs and increased muscular effort does not increase the expiratory flow rate. With worsening disease of the small airways the flow rate declines earlier in expiration to give a typical scooped out appearance (Figure 3). With obstructive disease, vital capacity may be decreased and residual volume increased (i.e. the patient breathes at a higher lung volume because of the obstruction to expiration).

Single breath nitrogen test

Nitrogen concentration

Phase 1

Modern spirometers are often electronic, integrating flow signals from various types of flowmeter to derive volumes such as FVC, FEV1, FEV25–75. All of the parameters discussed above can be derived electronically from a single forced expiration. Lightweight portable instruments are available, but have to be calibrated and, though more convenient than the traditional ones, are not as robust nor as accurate. It is conventional to present respiratory volumes at body temperature and pressure saturated (BTPS). All of the measurements are made under ambient conditions, therefore volumes are corrected for temperature, including the difference in saturated vapour pressures at ambient and body temperatures.

Phase 2 Phase 3

A1

CC

CV

RV

A2 0

VD

Lung volume

The graph shows nitrogen concentration in exhaled breath following inhalation of 100% oxygen. While oxygen is washed out of the upper airway (phase 1) nitrogen concentration rises (phase 2) to alveolar plateau (phase 3). Closing volume (CV) is the transition from phase 3 to phase 4. Steepness of phase 3 denotes unevenness of ventilation. RV, residual volume; CC, closing capacity; VD anatomical dead space

Assessment of uneven ventilation Two tests give a ready assessment of uneven ventilation. The single breath nitrogen test is a research tool, but is much loved by examiners and has other applications in terms of measuring the volume at which small airways start to close. The single breath carbon dioxide washout curve is used in everyday anaesthetic practice.

4

The single breath nitrogen test: the individual takes in a single vital capacity inspiration of pure oxygen then exhales to residual volume and the concentration of nitrogen at the mouth is monitored. A typical tracing is shown in Figure 4. Four phases are recognized. • Phase 1: pure oxygen is exhaled from the upper airways and the nitrogen concentration is zero. • Phase 2: there is a rapid rise in nitrogen concentration as the anatomical dead space is washed out with alveolar gas. • Phase 3 is known as the alveolar plateau. With uneven ventilation the nitrogen concentration rises steadily. The slope is a measure of the unevenness of ventilation. • Phase 4: towards the end of phase 3 there is a sharp rise in nitrogen concentration. This signals the onset of small airway closure at the base of the lung. The inflection from phase 3 to phase 4 occurs because, at residual volume, alveoli at the base of the lung are smaller and expand more than those at the top. Towards residual volume, the (small) airways to some of them are closed, because the intrathoracic (pleural) pressure exceeds the airway pressure. With a vital capacity inspiration the alveoli at the base of the lung, which are closed at residual volume, expand far more than those at the top, so when breathing in 100% oxygen, the nitrogen in the alveoli at the base is more diluted by oxygen than in those at the apex. During expiration, upper and lower zones tend to empty together, producing the alveolar plateau, but as soon as the airways at the base start to close, the higher nitrogen concentrations in alveoli in the upper zones, which are still emptying, produce the abrupt rise in nitrogen concentration.

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Phase 4

Carbon dioxide washout curve

Residual volume

End-tidal

Normal

PCO2

Arterial

COAD

Volume expired Expired partial pressure of carbon dioxide (PCO2) breathing quietly from normal inspiration to residual volume. End-tidal PCO2 approximates to the partial pressure of carbon dioxide in arterial blood (PaCO2). The steepness of the alveolar plateau gives an index of unevenness of ventilation. PCO2 at residual volume is higher than PaCO2. The lower trace shows that in chronic obstructive airways disease (COAD) end-tidal PCO2 does not approximate to PaCO2 5

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Carbon dioxide washout curve: expired carbon dioxide concentrations are monitored routinely during anaesthesia. Figure 5 shows a typical carbon dioxide concentration curve during a slow quiet expiration to residual volume in a normal individual and in a patient with airway obstruction and uneven ventilation. Also indicated are the normal end-tidal points, the expired partial pressure of carbon dioxide (PCO2) at residual volume and the partial pressure of carbon dioxide in arterial blood (PaCO2). The slope of the curve is analogous to the slope of the nitrogen washout curve following a vital capacity inspiration of 100% oxygen. End-tidal PCO2 at the end of a normal quiet tidal expiration approximates closely to PaCO2 and in clinical practice can be used as an indicator of PaCO2. If the individual breathes slowly and steadily to residual volume, PaCO2 rises further and tends to venous PCO2. The slope of the tracing is an indication of abnormalities in ventilation (and perfusion), the steeper the slope the more uneven the ventilation in relation to alveolar perfusion. The lower curve in Figure 5 shows the type of curve seen in individuals with obstructive airways disease. It is also similar to that seen during a forced expiratory manoeuvre; airway trapping occurs at relatively high lung volumes, the alveolar slope is steeper and there is a significant difference between end-tidal (end expiratory) PCO2 and PaCO2. 

FURTHER READING Ganong W F. Review of medical physiology. 19th ed. Stamford, CT: Appleton and Lange, 1997. Hedenstierna G. Respiratory measurement. London: BMJ Books, 1998. Lumb A B. Nunn’s applied respiratory physiology. Oxford: ButterworthHeinemann, 2000. West J B. Respiratory physiology – The essentials. 5th ed. Baltimore: Williams and Wilkins, 1999.

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