THE ASSESSMENT OF PULMONARY FUNCTION. University of Manchester, England

Transcription

1 Brit. J. Anaesth. (1962), 34, 603 THE ASSESSMENT OF PULMONARY FUNCTION The processes of breathing and of perfusion of the body with blood are closely integrated and serve to transfer oxygen from the atmosphere to the tissue cells with minimum loss of tension. By the same processes carbon dioxide is eliminated from the body. There are several stages in these gas transfers, corresponding to the component processes of pulmonary function. These are the ventilation of the lungs, the distribution of blood and gases in the lungs and the diffusion of gases between the alveolar gas and the pulmonary capillaries. This paper will consider the ways in which the normality or otherwise of these processes is determined. In the clinical assessment of pulmonary function three questions have to be answered. (i) Is pulmonary ventilation adequate? (ii) Is the act of ventilation easy or difficult? (iii) Is the arterial blood being oxygenated normally? ADEQUACY OF VENTILATION Breathing is adjusted to keep the carbon dioxide tension (Pco 2 ) of the arterial blood within narrow limits, in normal subjects between 36 and 44 mm Hg. In patients with a reduction of base (metabolic acidosis), e.g. renal failure, diabetic ketosis, the Pco 2 is maintained at lower levels, and in patients with increased base (metabolic alkalosis), the Pco 2 is maintained at higher levels. These adjustments in Pco 2 are such as to minimize the effect on ph of the primary change in base; so it appears that ventilation is altered to maintain a constant hydrogen ion concentration in the tissues. The relationship between Pco 2, hydrogen ion concentration, and base is expressed by the Henderson-Hasselbalch equation [HCO 3 ] Pco 2 x solubility factor BY J. B. L. HOWELL University of Manchester, England Ideally, two of these three variables should be known, for assessment of the ventilatory status of 603 a subject. In practice, measurement of the Pco 2 plus a clinical assessment of the patient enables an intelligent guess to be made, but this is only a guess, and error is possible. A Pco 2 over 44 mm Hg is taken as a criterion of ventilatory failure. While this is usually associated with increased resistance to breathing, such a value could occur in association with an alkalaemia, the ventilatory capacity being normal. The relationship between ventilation and Pco 2 is expressed by the relationship CO, output C -TT r-^ ^ : Alveolar ventilation and alveolar ventilation=total ventilation physiological deadspace x frequency of breathing. Since the adequacy of ventilation is defined in terms of the Pco,, it is pointless to try to estimate it by measuring all of the factors involved in the equations above, especially when one of these (physiological deadspace) requires the measurement of Pco 2, for its determination. Methods of measuring Pco 2 are described elsewhere in this issue (Robinson, 1962; Howell, 1962). THE EFFORT OF BREATHING (a) The mechanical properties of the chest. Ventilation of the lungs is achieved by the force of inspiratory muscle contraction overcoming the resistances of the lungs and thorax to changes in shape and volume. There is therefore a balance of forces represented by the inspiratory muscles on the one hand and the resistances of the chest on the other. These vary in dominance with the phases of breathing and their magnitude determines the ease with which ventilation is achieved. Difficulty in ventilation can occur either due to inspiratory muscle weakness or to excessive resistances to changes in volume. Each of these factors can be measured separately with considerable precision, but this is seldom done in clinical practice,

2 604 BRITISH JOURNAL OF ANAESTHESIA partly because of the technical difficulties involved but mainly because an adequate assessment of the type and magnitude of disturbance can be made from simpler tests. Inspiratory muscle weakness is usually judged on clinical grounds but can be estimated by measuring the maximum negative mouth pressure maintained by a subject at specified lung volumes (Rahn et al., 1946). This procedure requires considerable co-operation from the subject and the range of the normal is wide and ill-defined. Measurement of the resistances of the thorax is difficult and seldom done. The resistances of the lungs are easier to measure and are more important in practice. These are of two main types, (i) elastic resistances and (ii) non-elastic or viscous resistances. The elastic resistances of the lung determine its distensibility. This is expressed as the change in volume per unit change in static transpulmonary pressure (TPP), i.e. the pressure difference between the airways and the pleural surface. This value is sometimes spoken of as the compliance of the lungs, but some caution must be exercised in the use of this term because it implies a linear volume-pressure relationship of the lungs. In fact, the distensibility of the lungs varies at different lung volumes (fig. 1). Starting from the residual volume the distensibility initially is low, but progressively increases until it becomes maximal about the functional residual capacity (FRC) to become less again as total lung capacity is approached. Since the volume-pressure relationship is sigmoid one cannot express it as a single term, i.e. as a compliance. However, over a small range of lung volumes such as the tidal volume this is a reasonable approximation and the term is permissible. Unfortunately, because of the wide range of normal values (Frank, et al., 1956), the measurement is of limited value in comparing different individuals. But this objection does not apply to the estimation of changes occurring in an individual subject. The basic equipment necessary for these measurements is a volume recorder and a manometer capable of recording the differential pressure between mouth and oesophagus (intrathoracic pressure). From these a volume-pressure curve ("V-P loop") can be constructed and the compliance derived (Mead and Whittenberger, 1953). Alternatively, if respiratory airflow or volume is measured with a pneumotachograph with an integrating circuit and recorded on one axis of an oscilloscope and transpulmonary pressure is recorded on the other, it can be arranged electronically that compliance or airway resistance is directly recorded TLC FIG. 1 nu. 1 (a) Volume-pressure relationship of the normal lung. The compartments of total lung capacity are represented on the ordinate. (b) Forced expiratory spirogram to illustrate measurement of F.E.V.

3 THE ASSESSMENT OF PULMONARY FUNCTION 605 during spontaneous breathing. The use of this system requires a more detailed knowledge of pulmonary mechanics than can be described here and the interested reader is referred to the original descriptions (DuBois and Ross, 1951). For routine clinical assessments, valuable information about both the inspiratory muscle power and the elastic properties of the lungs can be obtained from the measurement of the vital capacity (fig. 1). The vital capacity measures the difference in volume between full inspiration and full expiration and its significance depends upon the factors which govern these two positions. Full inspiration is the volume at which the maximal inspiratory muscle power is exactly balanced by the elastic recoil of the thorax and lungs. The elastic recoil of the thorax is not readily measured in the conscious subject and in simple testing must be inferred. The elastic recoil of the lungs is measured as the transpulmonary pressure (TPP) (fig. 1). In the young adult as the total lung capacity (TLC) is reached the TPP rises rapidly, indicating that this volume is limited mainly by the elastic recoil of the lung since further increase in TPP would cause very little increase in volume. However, in the older subject this increase in TPP is not seen, indicating that limitation of effective muscle power governs the TLC (Permutt and Martin, 1960). This partly accounts for the reduction in the vital capacity with increasing age- It was realized only recently that in normal subjects the position of full expiration (the residual volume) is governed by complete airway closure (Slagter and Heemstra, 1955). However, in patients with diffuse airway obstruction the time taken to expire the vital capacity is prolonged and they are often forced to breathe in before they have reached the volume of complete airway closure. When the factors controlling its upper and lower ends are appreciated the vital capacity becomes a valuable measurement in assessing the muscle force and the elastic properties of the lungs. It is possible to interpret the vital capacity only if its place in the total lung capacity is known and this requires estimation or measurement of the residual volume. This can be done clinically, radiologically, or by measurement using either N 2 washout (Darling, Cournand and Richard, 1940), helium dilution (Gilson and Hugh-Jones, 1949),. or body plethysmography (DuBois et al., 1956). The non-elastic (viscous) resistances are present only when air is flowing. They occur both in the tissues (Marshall and DuBois, 1956) and as a resistance to airflow through the bronchial tree. Airflow resistance is measured by relating the rate of airflow to the alveolar-mouth pressure difference which is producing it. Airflow may be measured using a pneumotachograph and the alveolar-tomouth pressure difference using an oesophagealmouth differential manometer, interruptor techniques (Vuilleumier, 1944), or body plethysmography (DuBois, Botelho and Comroe, 1956). These are complex techniques involving expensive equipment which is not generally available. Clements, Sharp and Elam (1959) have recently described a multiple interruptor technique which enables airway resistance to be estimated without requiring flow to be measured. However, for most clinical purposes an adequate estimate of airway resistance can be obtained from measurement of the timed vital capacity. This can be done using conventional recording spirometry or by non-recording spirometry as described by Gaensler (1951) and McKerrow, McDermott and Gilson (1960). Alternative measurements made from the recorded forced vital capacity are the maximum mid-expiratory flow rate (Leuallen and Fowler, 1955) and the mean expiratory flow rate between 50 and 75 per cent of the vital capacity (Franklin, 1958). Because of the lack of portability of equipment for spirometry, the peak flow meter (Wright and McKerrow, 1959) has become popular. The main virtues of this instrument are its simplicity and portability. The results are reproducible but correlate poorly with the FEV,, which is probably the better index of the resistance to airflow through the smaller bronchi. It does not allow a full assessment to be made of the mechanical properties of the thorax and was never intended to do so. Its main use is probably for serial measurements of a value which reflects resistance to airflow. In summary, for most clinical purposes a perfectly adequate assessment of the mechanical status of the chest can be gained from simple spirometric techniques properly interpreted. Precise measurements of the mechanical properties of the thorax require expensive electronic equipment.

4 606 (b) Efficiency of lungs in ventilation. In normal subjects, a part of each breath is wasted in ventilating the nasopharynx, trachea and bronchi, i.e. the anatomical deadspace. In disease states there may be a disturbance of perfusion of many alveoli with blood so that in addition their ventilation is wasted. This may be termed "alveolar deadspace". The combination of alveolar and anatomical deadspace is called the physiological deadspace and may be defined as the volume of «ach breath which does not contribute to gas exchange. In conditions such as asthma, pulmonary fibrosis, chronic bronchitis, and emphysema the physiological deadspace may be increased considerably, as much as threefold, so that each breath has to toe increased a corresponding amount to maintain the level of alveolar ventilation. These subjects already have increased resistances of the chest and this additional factor magnifies their difficulties. The measurement of the physiological deadspace is not often made in routine practice though it is not difficult. It requires the collection of expired air under steady state conditions, over several minutes, noting the number of breaths collected. After measurement or estimation of the alveolar Pco 2, and analysis of the expired air, the physiological deadspace may be calculated from the Bohr equation (Comroe et al., 1955). When the tidal volumes are increased the physiological deadspace is usually increased proportionately. OXYGENATION OF THE ARTERIAL BLOOD The oxygen tension of the arterial blood depends upon three factors, the alveolar Po 2, the degree of venous admixture, and the diffusing capacity of the lungs. These will be considered in turn. (i) Alveolar Po 2 depends upon three factors: inspired Po 2 (Pi O2 ), alveolar Pco 2 (PA C02 ) and the respiratory exchange ratio (R). The relationship between these is expressed by the alveolar air equation PA O2 =PI O 2-PA CO2 [FI O2 1 - Fr 0 o ] R -where Fi o2 is the fractional concentration of oxygen in the inspired mixture (Fenn, Rahn and Otis, 1946). BRITISH JOURNAL OF ANAESTHESIA At a barometric pressure of 760 mm Hg, the warmed moist inspired air contains oxygen at a tension of nearly 150 mm Hg. This is the maximum O 2 tension available to a subject breathing air, and is what the lungs would contain if all of the carbon dioxide were removed. But since the alveolar Pco, is normally maintained at about 40 mm Hg, the Po 2 is reduced proportionately. In fact because oxygen consumption is normally greater than CO, production, the respiratory quotient being approximately 0.8, the oxygen falls by 1 mm Hg for every 0.8 mm Hg rise in Pco 2. This is a slight approximation, and has been used in the presentation of the relationship between alveolar Pco, and Po 2 as shown in figure 2. In the i I JO FIG. 2 Upper. Relationship of PA C02 and PA 02 breathing air at sea level (based on simplification of alveolar air equation PA 02 = Pi O2 PALc z with an assumed R of R 0.8). Lower. Oxygen dissociation of haemoglobin at ph 7 4 Abscissa represents the PA O, corresponding to the PA CO, of the upper diagram. Ordinate is the percentage saturation of pulmonary capillary blood assuming no end-capillary gradient Dotted line represents dissociation curve at ph 7.2. The dotted areas represent the normal range ot alveolar ventilation.

5 THE ASSESSMENT OF PULMONARY FUNCTION 607 lower part of this figure the oxygen saturation of blood in gaseous equilibrium with the alveolar gas at all levels of alveolar Pco, is shown. This diagram shows how severe degrees of hypoventilation may be present without marked arterial unsaturation. Since central cyanosis is usually not apparent until the arterial oxygen saturation falls below 85 per cent, the absence of cyanosis is no indication of the adequacy of alveolar ventilation. For the same reasons, oxygen supplements to the inspired air of only 9 per cent will permit the alveolar Pco 2 to rise to about 130 mm Hg before cyanosis from this cause would occur. Thus underventilation alone will only rarely cause cyanosis. Yet central cyanosis is not infrequently encountered; this is because a second factor influencing arterial oxygenation, venous admixture, is common. (ii) Venous admixture denotes the addition of blood of lower oxygen content to the blood leaving the pulmonary capillaries. This may be purely venous blood passing through shunts (e.g. intracardiac shunts, pulmonary A-V aneurysms, pneumonic consolidation), or blood partly oxygenated which has perfused poorly ventilated regions of the lungs (e.g. asthma, emphysema with diffuse airway obstruction); the latter is by far the more common. The degree of venous admixture through poorly ventilated alveoli can be expressed as an equivalent venous shunt, i.e. the percentage of the venous return which when added to the pulmonary venous blood would produce the observed degree of unsaturation. It is not uncommon, for example, for patients with chronic bronchitis and diffuse airway obstruction to have 25 per cent of the cardiac output effectively "shunted" past the pulmonary alveoli. At normal alveolar Pco, levels this would correspond to an arterial saturation of about 89 to 90 per cent. Inhalation of 30 per cent oxygen will remove most of the unsaturation due to perfusion of poorly ventilated alveoli but will have almost no effect upon that due to true shunts. The measurement of the degree of venous admixture is not often made routinely because of the difficulty of measuring arterial oxygen saturation and tension, but newer techniques should make this easier. (iii) Diffusion. The diffusing surfaces of the lungs consist essentially of two membranes in apposition, the alveolar membrane and the pulmonary capillary membrane. The diffusion behaviour of the lungs is discussed most simply by considering these two membranes as a single flattened-out sheet with alveolar gas on one side and the pulmonary capillary blood on the other. The volumes of gas which will diffuse across these membranes will depend upon their area, their combined thickness, the type of gas, and the difference in gas pressure on either side of the membrane. The diffusion characteristics of a unit area of this membrane are expressed as the diffusion coefficient. This is virtually impossible to measure with any certainty, and the diffusing characteristics of the lung as a whole are usually measured. This is expressed as the Diffusing Capacity and is defined as the volume of gas (in ml) crossing the membrane each minute for each mm Hg pressure difference. This will vary from individual to individual, and may be standardized in terms of body size. The diffusing capacity will also vary according to the gas being measured. For example, a normal subject may have a diffusing capacity for oxygen of 25 ml/min/mm Hg, while for carbon dioxide the diffusing capacity would be of the order of 500 ml/min/mm Hg since carbon dioxide is some twenty times as diffusible. There has been considerable interest in this measurement as it is generally considered to reflect mainly the area of alveolo-capillary membrane, and might serve as an index of the amount of functioning lung tissue. For example, some cases of diffuse airway obstruction have relatively normal diffusing capacity while in others it is greatly decreased. It was hoped that such measurements might allow a recognition of different mechanisms of obstructive airway disease, but this has yet to be established. The subject of diffusing capacity is complicated by the fact that there are several different techniques available for the measurement of diffusing capacity, and since they give different values in the same individual, presumably they are measuring different things. Two measurements are required for the calculation of the diffusing capacity: the volume of gas crossing the membrane in unit time and the average pressure difference across the membrane. In the case of the diffusing capacity for oxygen, the volume of gas crossing the membrane, i.e. the oxygen uptake, is easily measured, but the measurement of the mean oxygen pressure difference

6 608 BRITISH JOURNAL OF ANAESTHESIA is difficult. It has been done (Riley, Coumand and Donald, 1951) but the techniques are too exacting for routine clinical practice. Instead, the diffusing capacity for carbon monoxide (DCO) is usually measured. The capacity of the blood for CO is very great and during short periods of breathing low concentrations of CO the pulmonary capillary blood tension has been assumed to remain at zero. The pressure difference across the membrane is therefore its partial pressure in the alveolar gas. The different methods of measuring the DCO differ in two respects: (i) the methods of measurement of the mean alveolar gas tension of CO and (ii) whether steady state or single breath conditions are employed. The "single breath method" (Ogilvie et al., 1957) is probably the most widely used and gives the most meaningful results. A single breath of a measured volume of a mixture of air, CO, and helium is inspired from the residual volume, the breath is held for a measured time, usually 10 seconds, and the gas is expired. An alveolar sample is delivered and analyzed for He (using a katharometer) and CO (using an infra-red analyzer). The DCO is then calculated from a formula. There are two "steady state" methods, in both of which very low concentrations of CO are inspired over many minutes. The volume of CO absorbed is calculated from the inspired-expired concentration difference, and the minute volume. The methods differ in the way in which mean alveolar CO tension is measured. In one an endtidal sampler collects gas for analysis and this is assumed to represent alveolar gas (Bates and Pearce, 1955). In the other (Filley, Macintosh and Wright, 1954), arterial blood is drawn and the Pco 2 is measured. This value is then used in the alveolar air equation to calculate the mean alveolar Pco. The substitution of a rebreathing method for estimating the arterial Pco 2 has recently been reported. The Bates method is influenced by alterations in the physiological deadspace, while the Filley methods attempts to correct for this. A comprehensive review of diffusing capacity and the problems of its measurement has been made by Forster (1957). The diffusing capacity reflects the area and diffusibility of the alveolo-capillary membrane. Whether a reduction in this will lead to failure to obtain gaseous equilibrium across the membrane causing arterial hypoxia will depend on additional factors including alveolar and mean capillary Po 2 and the level of oxygen consumption. At normal levels of ventilation, breathing air, arterial unsaturation at rest sufficient to cause obvious cyanosis cannot be due solely to an upset of diffusion, for a disturbance of this degree is incompatible with life. In order to invoke a generalized disturbance of diffusion, i.e. a decreased diffusion coefficient, as the cause of arterial unsaturation B y DPhyt. CAPILLARIES VENTILATED BUT NOT PERFUSED ( VD"<") ^ i I \ ALVEOLI PERFUSED BUT NOT VENTILATED (venous admixture) IT i 1 ^ ALVEOLO- CAPILLARY BLOCK V. A. FIG. 3 Diagrammatic illustration of the mechanism of disturbance of pulmonary gas exchange. A: Normal. B: Disturbance of distribution of alveolar ventilation and pulmonary capillary blood flow, e.g. bronchial asthma, chronic bronchitis with emphysema, and diffuse airway obstruction. C: Disturbance of distribution of alveolar ventilation and capillary blood flow plus areas of impaired diffusion, e.g. pulmonary fibrosis.

7 THE ASSESSMENT OF PULMONARY FUNCTION 609 occurring during exercise, it must be shown that this unsaturation is not due to the venous admixture which occurs in those conditions in which an alveolo-capillary block is said to occur. A schematic summary of the mechanisms of disturbed gaseous exchange is presented in figure 3. This review has aimed to outline the main procedures employed in assessing the functional status of the chest. The many techniques available require that careful consideration be given to the selection of those most suitable for each type of study. SUMMARY OF PULMONARY FUNCTIONAL ASSESSMENT (1) Adequacy of ventilation. Measurement or estimation of any two of the following: arterial Pco 2, bicarbonate, or ph. (2) Ease of ventilation. (a) Routine. Full clinical assessment of inspiratory muscle power and degree of inflation of lungs at the end of normal expiration. Measurement of vital capacity inferring whether a reduction is due to a decreased total lung capacity or to an increased residual volume. Estimation of resistance to expiration using a peak flow meter or, preferably, simple spirometry. (b) Additional. Measurement of residual volume. Measurement of physiological deadspace. Measurement of volume-pressure relationships of the thorax and of airway resistance. (3) Efficiency of lungs as an oxygenator. Direct measurement of arterial blood for oxygen tension or saturation, and calculation of degree of venous admixture. Measurement of diffusing capacity. REFERENCES Bates, D. V., and Pearce, J. F. (1955). The pulmonary diffusing capacity: a comparison of methods of measurement and a study of the effect of body posture. J. Physiol.. 132, 232. ents, J. A., Sharp, J. T., and Elam, J. O. (1959). Estimation of pulmonary resistance by repetitive interruption of airflow. /. clin. Invest., 38, Comroe. J. H. jr., Forster. R. E., DuBois. A. B., Briscoe, W. A., and Carlsen, E. (1955). The Lung, p Chicago: Year Book Publishers. Darling. R. C, Cournand, A., and Richard, D. W. (1940). Studies on the intrapulmonary mixture of gases. Ill: An open circuit method for measuring residual air. /. clin. Invest., 19, 609. DuBois, A. B., Botelho, S. Y., Bedell, G. N., Marshall, R., and Comroe, J. H. jr. (1956). A rapid plethysmographic method for measuring thoracic gas volume: a comparison with a nitrogen washout method for measuring functional residual capacity in normal subjects. J. clin. Invest., 35, 322. Comroe, J. H. jr. (1956). A new method for measuring airway resistance in man using a body plethysmograph: values in normal subjects and in patients with respiratory disease. /. clin. Invest., 35, 327. Ross, B. B. (1951). New method for studying mechanics of breathing using cathode ray oscillograph. Proc. Soc. exp. Biol. Med., 78, 546. Fenn, W. O., Rahn, H., and Otis, A. B. (1946). A theoretical study of the composition of the alveolar air at altitude. Amer. J. Physiol., 146, 637. Filley, G. F., Macintosh, D. J., and Wright, G. W. (1954). Carbon monoxide uptake and pulmonary diffusing capacity in normal subjects at rest and during exercise. J. clin. Invest.. 33, 530. Forster, R. W. (1957). Exchange of gases between alveolar air and pulmonary capillary blood: pulmonary diffusing capacity. Physiol. Rev., 37, 391. Frank, N. R., Mead, J., Siebens, A. A., and Storey, C. F. (1956). Measurement of pulmonary compliance in young adults. J. appl. Physiol., 9, 38. Franklin, W. (1958). The effect of smoking on pulmonary function in a working adult population. /. clin. Invest., 37, 895. Gaensler, E. A. (1951). Analysis of the ventilatory defect by timed capacity measurements. Amer. Rev. Tuberc, 64, 256. Gilson, J. C, and Hugh-Jones, P. (1949). The measurement of the total lung volume and breathing capacity. Clin. Sci., 7, 185. Howell, J. B. L. (1962). Rebreathing methods for measurement of blood CO 2 tension. Brit- J. Anaesth., 34, 617. Leuallen, E. C, and Fowler, W. S. (1955). Maximal mid-expiratory flow. Amer. Rev. Tuberc, 72, 783. Marshall, R. and DuBois, A. B. (1956). The measurement of the viscous resistances of the lung tissues in normal man. Clin. Sci., 15, 161. McKerrow, C. B., McDermott, M., and Gilson, J. C. (1960). A spirometer for measuring the forced expiratory volume with a simple calibrating device. Lancet, 1, 149. Mead, J., and Whittenberger, J. L. (1953). Physical properties of human lungs measured during spontaneous respiration. J. appl. Physiol., 5, 779. Ogilvie, C. M., Forster, R. E., Blakemore. W. S., and Morton, J. W. (1957). A standardised breath holding technique for the clinical measurement of the diffusing capacity of the lung for carbon monoxide. /. clin. Invest., 36, 1. Permutt, S., and Martin, H. B. (1960). Static pressurevolume characteristics of lungs of normal males. /. appl. Physiol., 15, 819. Rahn, H., Otis, A. B., Chadwick, L. E., and Fenn, W. O. (1946). The pressure-volume diagram of the thorax and lung. Amer. J. Physiol., 146, 161.

8 610 BRITISH JOURNAL OF ANAESTHESIA Riley, R. L., Cournand, A., and Donald, K. W. (1951). Analysis of factors affecting partial pressures of oxygen and carbon dioxide in gas and blood of lungs: methods. /. appl. Physiol., 4, 102. Robinson, J. B. (1962). ph and Pco 2 measurements in blood. Brit. J. Anaeslh., 34, 611. Slagter, R. B., and Heemstra, H. (1955). Limiting factors of expiration in normal subjects. A eta physiol. pharm. neerl., 4, 419P. Vuilleumier, P. (1944). (Jber eine Methode zur Messung des Intraalveolaren Druckes und der Stromungewilderstandein den Atemwegen des Menschen. Ztschr. f. klin. Med., 143, 698. Wright, B. M., and McKerrow, C. B. (1959). Maximum forced expiratory flow rate as a measure of ventilatory capacity with a description of a new portable instrument for measuring it. Brit. med. J., 2, LIVERPOOL SOCIETY OF ANAESTHETISTS President: Professor CECIL GRAY Vice-Presidents: Dr. R. J. MINNITT, Dr. J. B. HARGREAVES Hon. Treasurer: Dr. J. J. HARGADON, Kingsley, Halewood Road, Gateacre, Nr. Liverpool Tel.: GATeacre 2881 Hon. Secretary : Dr. E. S. N. FENTON, 462 Aigburth Road, Liverpool, 19 Tel.: CREssington Park 1378 Programme for Session FRIDAY, OCTOBER 12, 8 P.M. Ordinary General Meeting at the Liverpool Medical Institution. Speakers: Dr. H. P. L. OZORIO. Special Problems of Anaesthesia in the Far East. Dr. D. JOSEPH. Establishment and Management of a Recovery and Resuscitation Unit. FRIDAY, NOVEMBER 16, 8 P.M. Ordinary General Meeting at the Liverpool Medical Institution. Speaker: Dr. SHEILA KENNY. Anaesthesia and Ophthalmology THURSDAY, JANUARY 10, 8 P.M. Joint Meeting with the Liverpool Medical Institution at the Liverpool Medical Institution. Symposium: Applications of High Pressure Oxygen Therapy. Speakers : Dr. H. H. PINKERTON. Scope of a Pressure Chamber in Surgery and Anaesthesia. I. F. J. CHURCHILL-DAVIDSON. The Use and Effects of High Pressure Oxygen in Radiotherapy FRIDAY, FEBRUARY 15, 8 P.M. Ordinary General Meeting at the Liverpool Medical Institution. Symposium : Circulatory Collapse. Speakers: Dr. GWYN RICHARDS. The Physiological Approach. Dr. JOHN UTTING. The Clinical Approach. FRIDAY, MARCH 22, 8 P.M. Ordinary General Meeting at the Liverpool Medical Institution. Papers to be presented in Competition for the Registrar's Prize. THURSDAY, APRIL 25, 8 P.M. Combined Meeting with the Anaesthetic Section of the Manchester Medical Society at the Liverpool Medical Institution. Speakers: Dr. J. B. MONTGOMERY. Hypothermia in Cardiac Surgery, Dr. I. C. GEDDES. Light Anaesthesia. FRIDAY, MAY 10, 8 P.M. Thirty-First Annual General Meeting at the Liverpool Medical Institution.