HUMIDIFICATION IN ANAESTHESIA

Transcription

1 Brit. J. Anaesth. (1972), 44,879 HUMIDIFICATION IN ANAESTHESIA A review of the present situation J. E. BOYS AND T. HILARY HOWELLS It is well established that humidification of the inspired gas is an essential part of the long term care of patients following endotracheal intubation or tracheostomy to prevent the drying of secretions, crusting and inflammatory changes in the trachea. For similar reasons, intubated patients, under nonrebreatbing anaesthesia, might be expected to run the same risks, especially as the inspired gases are completely dry. However, the time of exposure is short, and perhaps for this reason the problem has not received widespread attention. A recent editorial (1970) suggested there was need of a full appraisal of humidified anaesthesia and in this paper we reviewed the situation from a theoretical point of view in the hope of finding the most useful avenues of research. The questions we examined are: how feasible is the provision of humidification during anaesthesia and what system appears to be most useful; what benefit may be expected from its adoption; and what dangers or problems, if any, are involved? HUMIDITY The amount of water present in a gas may be described by the expression of: relative humidity, absolute humidity, water vapour partial pressure. Absolute humidity is the weight of water per unit volume of a gas. Relative humidity is the absolute humidity expressed as a percentage of the maximum quantity of water vapour which can exist in the gas at the same temperature. Temp. ( Q TABLE I Saturated water vapour partial pressure (mmhg) Absolute humidity (mg/1-) Partial pressure of water vapour is an index of its molar concentration. The table gives examples of saturated vapour pressure and equivalent absolute humidities at different temperatures. To avoid any drying of the respiratory tract whatsoever, the inspired gas must be completely saturated at body temperature and carry 43.4 mg/1. of water vapour. Normal air at 20 C in England is about 70 per cent saturated, containing approximately 12 mg/l water vapour, and even if saturated at this temperature can only hold 17.1 mg/1. To enable the air to carry 43.4 mg/1. of water, it must be heated to 37 C and saturated with water vapour, or the extra water must be suspended as droplets. NORMAL MECHANISM OF RESPIRATORY HUMIDIFICATION Dery and associates (1967), have demonstrated that the upper respiratory tract (i.e., upper anatomical deadspace) functions as a heat and moisture eychanger. They showed that the temperature and humidity, at any given point, rise and fall with expiration and inspiration respectively. Fluctuations become less marked and the mean temperature and humidity rise as the respiratory tract is descended. Saturated body temperature conditions are reached quite high in the respiratory tract; cf figure I where it will be seen that the curve steepens in the bronchi where the epithelial surface area increases because of branching. Their study was made on intubated patients using a circle absorber system with an inspired humidity of 80 per cent at 20 C. Although these conditions are artificial, the basic mechanism of heat and moisture exchange was clearly demonstrated. In addition to the respiratory tract deadspace the apparatus deadspace was shown also to have an appreciable heat and moisture exchange function. These deadspace components are shown thus to J. E. BOYS, B.SC., M.B., B.S., F.F.A.R.C.S.; T. HILARY HOWELLS. M.B., CH.B., F.F.A.R.C.S.; The Royal Free Hospital, London.

2 880 BRITISH JOURNAL OF ANAESTHESIA have an important function and are not to be regarded purely as a hindrance to ventilation. The upper respiratory tract can augment any deficiency in this mechanism by supplying water by transpiration through the mucosa. Lowering the inspired humidity moves the curve (fig. 1) to the right and increases the slope. This results in cooler, drier mean conditions in the proximal upper respiratory tract. The lower respiratory tract is always subjected to body temperature saturated gas as the branching bronchial tree rapidly (almost exponentially) increases in surface area with a parallel increase in humidification efficiency. The humidity of the gases reaching the alveoli is thus shown to be derived from the following compenents: (1) the conservation process of heat and moisture exchange; (2) the inspired humidity; (3) mucosal transpiration of water. The expired air is always saturated with water vapour but its temperature and hence the absolute humidity is determined by the heat and moisture exchange efficiency of the upper respiratory tract. The normal expiratory water loss amounts to 28 mg/1. (Han and Lowe, 1968). HUMIDIFIERS We find it convenient to divide humidifiers into suppliers and conservers of water and to subdivide the former. A. Suppliers: (1) Ambient temperature vapour suppliers. (2) Heated vapour suppliers. (3) Ambient temperature aerosol suppliers. (4) Heated aerosol suppliers. (5) Instillers. B. Conservers: (1) Heat and moisture exchangers (HME) or condenser humidifiers. A. Suppliers: 1. Ambient temperature vapour suppliers. These have a maximum output of saturated water vapour at the ambient temperature. Their ability to approach this ceiling is determined by the area of gas to water surface and the gas flow. They function by bubbling gas through water or passing it through wet tubing. By passing the gas through a sieve it is broken up into very fine bubbles providing large gas to liquid surface area. The absolute humi- 20 TO 0 TO 2O O D'»tanc«Irom th» Incuor te«th (Cm.) FIG. 1. Withdrawal temperature curve from the lower airway through to the inspiratory limb of the circle, during anaesthesia with the semi-closed system. The upper peaks on the curve represent temperature in expiration. (Figure and caption reproduced from Canad. Anaesth. Soc. J., 14, 287 (1967), with kind permission of the Authors and Editor.) dity output falls with time because of cooling from loss of latent heat and resultant fall in saturated vapour pressure. Their maximum theoretical output, which is seldom attained, is 17.1 mg/1. at 20 C which is 30 per cent of body temperature saturated gas humidity. They are only suitable for supplementary humidification. 2. Heated vapour suppliers. These are in the form of a heated water bath over, or through, which the gas passes. The output is determined by both temperature and gas flow. In practice they are highly efficient, producing body temperature saturated gas even at high flow rates, but the water tends to condense in the inspiratory tubing with loss of temperature and resultant loss of absolute humidity. This can be reduced by shortening, insulating or heating the tubing. 3. Ambient temperature aerosol suppliers. These form the majority of humidifiers and there are several mechanisms for producing aerosols. Their ability to suspend water droplets depends on the aerosol density and size of the droplets produced. Only the smaller droplets remain in suspension long enough to reach the patient, the larger ones condensing on the way. Droplets are stabilized by the presence of a solute. Water is broken up into droplets by such mechanisms as allowing it to impinge on a rotating disc or ultrasonic vibrator or by being drawn through a jet at right angles to a gas jet.

3 HUMIDIFICATION IN ANAESTHESIA 881 Output varies widely from the equivalent of ambient temperature saturated vapour up to 2-3 times the equivalent of body temperature saturated vapour. The upper respiratory tract must supply considerable latent heat to vaporize the droplets. 4. Heated aerosol suppliers. Heating the aerosol increases the vapour phase of the water and reduces the latent heat required from the upper respiratory tract to vaporize die droplets. 5. Instillation. Direct drip feed into an endotracheal tube produces some humidification. Availablility of body heat makes it more efficient than an ambient temperature vapour humidifier despite small gas/water interface. Examples and performances: A. Suppliers: 1. Ambient temperature Vapour suppliers a. Woulffe bottle (Freedman, 1967) Absolute humidity (mg/1.) 6-12 b. Wet tube (Chase, Kilmore and Trotta, 1962) (pouring water into inspiratory tube and shaking out excess) 2. Heated Vapour Suppliers a. Water bath, e.g., East b. Bubble heater, e.g., Loosco infant Ambient Temperature Aerosol a. Bernoulli, e.g., Air Shields ") Hydrojet! b. Bernoulli and anvil, e.g. f Bird J c. Ultrasound, e.g., D;Vilbiss 801 d. Spinning disc, e.g., Air 20 Shields Hydrojet II 4. Heated Aerosol a. Cascade, e.g., Bennett Cascade b. Heated Bernoulli, e.g., Ohio heated nebulizer 5. Instillation (Absolute Humidity values in sections 2-5 arc taken from Hayes and Robinson (1970). B. Conservers: 1. Heat and moisture exchanger (Condenser humidifiers, "Swedish nose"). This is a different mechanism relying on the condensation and the release of latent heat in added deadspace, on expiration and its subsequent evaporation and cooling on inspiration. This is similar to the normal upper respiratory tract humidification and will be discussed later. Performance of a heat and moisture exchanger depends on the humidity and temperature of die inspired gas, efficiency being high widi cool or moist gas. Anaesdietic gases are cool on exit from their cylinders due to latent heat loss and/or expansion, but after passing through die anaesthetic machine and tubing they are close to room temperature and completely dry. Normal upper respiratory tract humidities in a non-rebreathing anaesdietic system can only be achieved by a heat and moisture exchanger provided tliat these gases are humidified to 60 per cent at 20 C (Mapleson, Morgan and Hfflard, 1963). Damage resulting from the use of inadequately humidified anaesthetic gases. The following changes have been suggested to result from die use of dry anaesthetic gases (Burton, 1962; Dalhamn, 1956; Rashad et al., 1967): a. local tracheal inflammation; fc. alveolar dessication; c. ciliary paralysis; d. decreased pulmonary compliance; e. micro-atelectasis and right to left shunt. a. Local tracheal inflammation below the endotracheal tube has been observed following extended use of unhumidified anaesdietic systems. The changes range from local drying and inspissation of mucus to frank crusting, inflammation and ulceration (Burton, 1962). These local changes were shown to be prevented by humidification of die anaesdietic gases. b. Alveolar dessication is extremely unlikely as die normal mechanism of respiratory humidification ensures diat only body temperature gas saturated with water vapour can exist in die lower respiratory tract (see above). Only die trachea and larger bronchi are affected direcdy by dry gas. c. Ciliary paralysis has been demonstrated at humidities less than 70 per cent, and using dry gas, mucus flow is slowed to 15 per cent of die rate observed using gas saturated at 35'C. (Dalhamn, 1936). Atropine slows mucus flow to 80 per cent, die effects being completely reversed in 3 to 5 hours (Burton, 1962). An inflated endotracheal tube cuff produces local obstruction to mucus flow and adds to die problem. d. Decreased pulmonary compliance has been

4 882 BRITISH JOURNAL OF ANAESTHESIA demonstrated by Rashad and associates (1967) in dogs during unhumidified anaesthesia. The fall in compliance using 18 per cent saturated gas at 20 C was progressive over l± hours, whereas dogs breathing saturated gas at 35 C showed an insignificant 5 per cent fall with no evidence of further progression. Pulmonary surfactant activity was within normal limits for both groups. Under the controlled conditions of the experiment the reduction of pulmonary compliance results either from an increase in surface tension or a reduction in the number of ventilated alveoli. Increased surface tension involves a reduction in surfactant activity which was shown to be normal. Therefore atelectasis is the most likely basis for the falling compliance during low humidity anaesthesia. e. Micro-atelectasis and right to left shunt. An increased alveolar/arterial oxygen tension gradient has been widely demonstrated during non-rebreathing anaesthesia (Morgan, Lumley and Sykes, 1970; Frumin et al., 1959; Marshall et al., 1969; (Sykes, Young and Robinson, 1965; Nunn, 1964; Nunn, Bergman and Coleman, 1965). Nunn and Pouliot (1962) using varying inspired oxygen tensions, have demonstrated that right-toleft shunt constitutes the whole or major part of this gradient change. There seems to be little doubt among these workers that atelectasis is the basis for this right to left shunt. Alveolar mechanics render them liable to collapse when exposed to certain conditions. We propose the following combination of factors, operating during unhumidified non-rebreathing anaesthesia, to predispose to atelectasis: (1) Secretion retentien; (2) Reduced expiratory reserve volume; (3) The occupation of the alveoli by gases having a high alveolar/ mixed venous tension gradient. In order to demonstrate the relevance of inadequate humidification it is pertinent to consider the above factors in some detail. It is first necessary to review the alveolar mechanics. Alveolar mechanics. The alveoli are essentially a population of intercommunicating elastic spheres. Their resistance to inflation is composed mainly of surface tension arising from the fluid lining and, to a much lesser degree, to tissue elasticity of the alveolar walls (Selkurt, 1966). The surface tension of a liquid is constant and as a consequence of Laplace's Law the pressure inside a liquid sphere is inversely proportional to the radius. It would therefore be expected that the alveolar size would be very unstable and that the majority of small alveoli would empty into the few distended alveoli. Two mechanisms serve to maintain inflation of the alveolus: (a) pulmonary surfactant, (b) terminal airway closure at residual volume. (a) Pulmonary surfactant is a lipoprotein found in small concentration in the fluid lining the alveoli (Schoedel and Rufer, 1969). It has an extremely high affinity for the surface layer where it lowers the surface tension from 44 dyne/cm to around 24 dyne/cm. When the surface area of the alveolus is reduced the surface tension falls to between 0 and 5 dyne/cm (Tierney and Johnson, 1965), thus opposing the tendency to a rise in pressure as a consequence of Laplace's Law. A further property of surfactant is its requirement for repeated stretching of the surface film. As the surface is stretched, new surface is created from molecules in the bulk of the liquid. Since water molecules are in great excess some will enter the surface film despite the higher affinity of the few surfactant molecules and the surface tension will rise, thus opposing the tendency to a pressure drop and overdistension. During expiration the surface film is reduced in area, water molecules will preferentially leave the surface and surface surfactant concentration will rise reducing the surface tension (Tierney and Johnson, 1965). Hence to maintain efficient surfactant function the surface requires not only repeated but also extensive stretching. (fc) Expiration is limited by closure of the terminal airways (Slagter and Heemstra, 1955) which prevents extreme alveolar emptying, otherwise even small surface tensions would result in high alveolar pressures due to the small alveolar radius. The volume of gas in the alveoli when all are isolated by terminal airway closure together with the anatomical deadspace constitutes the residual volume. The transpulmonary pressure at which terminal airways close is less than that required to reopen them (Laver et al., 1964). This is partly because as the surface is held at a relatively constant area the surface tension will rise (Tierney and Johnson, 1965). It is also because isolated alveolar gas volume tends to slowly decrease (see below) reducing the radius and therefore increasing the pressure (Coryllos and Birnbaum, 1932 a, b). The volume decrease is too slow for surfactant to exert its surface tension reducing action to any degree. Alveoli are of variable dimensions throughout the

5 HUMIDIFICATION IN ANAESTHESIA 883 lung so that they will become isolated sequentially as lung volume decreases, the smaller ones with narrow, terminal, supplying airways of low elastic recoil being isolated first. The dependent lung contains most of the readily isolated alveoli (Clarke, Jones and Glaister, 1,969). So at one extreme there is a small group of alveoli which are isolated permanently during quiet breathing and are only ventilated during deep inspiration (Clements, Brown and Johnson, 1958). Others are subjected to isolation and reopening during quiet breathing. But the majority remain in permanent continuity with the bronchial tree. Any reduction in the expiratory reserve volume (see next section) will cause a larger number of alveoli to be subjected to permanent or intermittent isolation. As a consequence of this, not only the number of alveoli subjected to isolation increases with reduction of the expiratory reserve volume, but also the duration of their isolation during each respiratory cycle. Furthermore, increase in alveolar opening pressure, above that at which isolation occurs, is related to the duration of isolation (see below). Factors tending to produce atelectasis during unhumidified non-rebreathing anaesthesia (1) Secretion retention. The well-documented ciliary paralysis resulting from exposure t» dry gases (Dalhamn, 1956) would be expected to impair the clearance of mucus from the normally humidified and mucus secreting lower respiratory tract. This results in secretion retention which would favour the narrowing or obstruction of the smaller airways, and increase the probability of terminal airway closure which is a prerequisite for atelectasis. It would be extremely difficult to demonstrate secretion retention in the smaller airways but the resultant atelectasis may be detected by a raised alveolar/arterial oxygen tension gradient and reduced compliance. A progressive fall in compliance during low humidity anaesthesia has been demonstrated compared with an insignificant non-progressive fall in humidified cases (Rashad et al., 1967). The alveolar/arterial oxygen tension gradient was not measured in this study and only an insignificantly lower arterial oxygen tension was demonstrated in the lower humidity group. Estimations of pulmonary surfactant showed no difference between the groups, thus eliminating effeas on surfactant as a basis for the compliance reduction. Stevens and Kennedy (1968) have shown that per-anaesthetic humidification is associated with a lower incidence of gross radiological collapse. However, while such massive collapse is unusual, diffuse atelectasis is a widespread problem. Some support for the concept of secretion retention induced atelectasis comes from the study of chronic bronchitis, where the retention results from excessive mucus production. This condition is also associated with diffuse atelectasis and a raised alveolar/arterial oxygen tension gradient (2) Reduced expiratory reserve volume. Ventilation of the lungs, whether spontaneous or artificial, with a reduced expiratory reserve volume increases the liability of alveoli to isolation, which increases the probability of their collapse. This has been well demonstrated in normal subjects breathing with a reduced expiratory reserve volume by conscious effort (Ferris and Pollard, 1960; Caro, Butler and Dubois, I960). This manoeuvre resulted in collapse within a few minutes as evidenced by reduced compliance, total lung capacity and arterial oxygen tension. Nunn and associates (1965) in a similar study demonstrated the production of basal radiological opacities in erect subjects associated with reduced arterial oxygen tension. The expiratory reserve volume is reduced by increasing age (Clarke and Jones, 1969) by supine posture (Hanson, Tabakin and Caldwell, 1962) and in the most dependent parts of the lung (Clarke, Jones and Glaister, 1969). The dependent effect is increased by high positive gravitation such as occurs in fighter pilots (Glaister, 1967), when they develop radiologically visible basal atelectasis while breathing pure oxygen. (3) Occupation of the alveoli by gases having a high alveolar/mixed venous tension gradient. It is apparent from the above that even a normal (unanaesthetized) patient will subject a small number of his alveoli to isolation during expiration. If the duration of isolation is very brief and the rate of rise in opening pressure during isolation very gradual the closed terminal airways will be reopened at the next breath. Otherwise the alveoli will remain isolated until an extra large transpulmonary pressure is applied to overcome the increasing opening pressure. This eventuality is overcome in the conscious subject by periodically taking a deep breath. These events have been demonstrated by inducing volunteers to breathe air at a consciously maintained minimal expiratory reserve volume which resulted in

6 884 BRITISH JOURNAL OF ANAESTHESIA radiologically visible basal collapse in the erect posture and an associated fall in arterial oxygen tension (Caro, Butler and Dubois, 1960). Both these changes were readily reversed by the subjects taking a few very large breaths. It may be expected that the atelectasis developing during anaesthesia could be similary controlled and early work was encouraging (Hedley-Whyte et al., 1964; Bendixen et al., 1964). But it has now been shown that the reversal of per-anaesthetic atelectasis requires exceedingly high transpulmonary pressures, to the extent of dangerous reduction in venous return (Nunn, Bergman and Coleman, 1965). Apparently, alveoli isolated during anaesthesia develop greatly increased opening pressures. This could be related to an alteration in the dynamic behaviour of surfactant which would be difficult to demonstrate, but it is more likely to be related to an increased rate of alveolar volume reduction following isolation. This more rapid volume reduction is explained by the high alveolar/mixed venous gas tension gradient of oxygen, and gaseous anaesthetic agents totally occupying the alveoli, which undergo rapid absorption. In contrast air breathing alveoli contain at least 80 per cent nitrogen which has a very small alveolar/ mixed venous tension gradient resulting in much slower alveolar volume reduction in isolation. This difference has been well demonstrated by the persistance of atelectasis, induced during the breathing of pure oxygen at minimal expiratory reserve volume, for up to 48 hours (Caro, Butler and Dubois, 1960). The development of atelectasis in fighter pilots breathing pure oxygen while exposed to increased positive acceleration is of similar aetiology. This has been successfully prevented by adding as little as 5 per cent nitrogen to the inspired gas mixture (Dubois et al., 1966). Similarly the incidence of radiological atelectasis in the dependent lung during thoracotomy has been reduced by adding 30 per cent nitrogen to the inhaled gas (Browne et al, 1970). Dangers of artificial humidification (1) Infection. All supplier humidifiers are subject to the risk of bacterial contamination of their water reservoir. (2) Water intoxication. Highly efficient humidifiers (notably ultrasound aerosol suppliers) can produce considerable positive water balance and infants during prolonged exposure could theoretically suffer from water intoxication (Harris and Riley, 1967). However most anaesthetics are of sufficiently short duration to prevent an appreciable degree of this. Nevertheless, careful regulation of the efficient humidifiers is essential to eliminate this risk. (3) Mucosal cooling. Ambient temperature aerosols of high concentration will produce considerable cooling of the upper respiratory tract as latent heat is absorbed to vaporize the droplets. However, rich respiratory mucosal blood supply and condensation during expiration would reduce this effect. (4) Mucosal heating and pyrexia. Heated vapour suppliers can release considerable heat on reaching the upper respiratory tract unless the temperature is carefully regulated. While this may be a hazard to infants (Graff and Benson, 1969) the short exposure time of anaesthesia reduces this risk. (5) Inactivation of surfactant. Pulmonary lavage has been shown to reduce surfactant activity thus predisposing to atelectasis (Strunin, Abrams, and Simpson, 1968). Instillation humidification and excessive aerosol or heated vapour supply would be expected to have similar effects (Harris and Riley, 1967). Increased alveolar/arterial oxygen tension gradient (Modell et al., 1968) and an increased post-anaesthetic incidence of severe bronchopneumonia (Modell, Giammona and Davis, 1967) have been demonstrated in different series using ultrasonic nebulizers. On the other hand Shakoor and associates (1968) failed to demonstrate any significant change in blood gases or compliance using an ultrasonic nebulizer. The conflict of results may be due to differing outputs (which were not measured) and differing routes of administration. In any event it seems unlikely that either lavage or aqueous droplets could reach the alveoli to result in a "wash out" of surfactant. It is more likely that any loss of surfactant activity is by inhibition, possibly by cellular debris released by mucosal damage from hypotonic solutions (Tierney and Johnson, 1965) higher in the respiratory tract. It is, however, most likely that excess fluid acts purely as a mechanical blockage to small terminal airways, and secondary loss of surfactant would then follow the resultant collapse (Sutnick and Soloff, 1963).

7 HUMIDIFICATION IN ANAESTHESIA 885 (6) Deadspace and resistance. Heat and moisture exchangers have certain potential drawbacks not shared with the suppliers. They add both apparatus deadspace and airway resistance. The added deadspace is only 17 ml which is less than 10 per cent of the physiological deadspace using 600 ml tidal volumes and can easily be compensated for. Added airway resistance is 0.1 cm HjO/l./sec at 0.3 l./sec which is only a 5 per cent addition. The gauzes do tend to clog up following repeated use and sterilization but can easily be replaced (Mapleson, Morgan and Hillard, 1963). CHOICE OF HUMIDIFIER Normal in vivo respiratory humidification is a combination of ambient supply and conservation. During intubated non-rebreathing anaesthesia both are impaired. It is commonly accepted that it is desirable to aim to supply body temperature saturated gas to a patient when humidification is considered necessary. This is far from reproducing the normal condition. Because of its conservation potential a condenser humidifier with an initial inefficient ambient temperature vapour supply of not less dian 60 per cent relative humidity at room temperature (within the capabilities of a Woulffe Bottle) (Freedman, 1,967) provides humidification of well within the in vivo range (Dalhamn, 1956). It also most closely reproduces the normal fluctuating temperature and humidity in the respiratory tract, which may or may not be advantageous. Compared with other humidifiers, this equipment is small, light, convenient to use, silent in operation, relatively cheap and prevents water contamination of the rest of the apparatus. It also has many less potential hazards than other humidifiers. As ambient air in all but very dry climates contains a relative humidity of more than 60 per cent, it is dear that an HME used with air breathing requires no accessory water. We suggest, therefore, the HME humidifying system is the best choice for all patients with endotracheal tubes or tracheostomies. If short term therapeutic respiratory overhydration is required a high output humidifier, such as an ultrasound aerosol supplier, would be necessary. CONCLUSION Normal respiratory humidification is carried out mainly by heat and moisture exchange in the anatomical deadspace and, to a lesser extent, by transpiration through the respiratory mucosa. During anaesthesia, apparatus deadspace functions as a heat and moisture exchanger but of lower efficiency. To compensate for the humidity deficit water can be supplied either as aerosol or vapour, or conserved by additional heat and moisture exchange. The artificial supply of humidity introduces the risk of infection, water overload and heat overload. A suggestion has also been made that aerosol humidifiers may increase airway resistance (Editorial, 1970). Heat and moisture exchangers introduce a small additional respiratory resistance and deadspace but without the above risks. From the consideration of the damage that might result from inadequate humidification during anaesthesia, we conclude that micro-atelectasis is the most important. This is caused by three factors secretion retention due to impaired ciliary function, reduced expiratory reserve volume and the occupation of the alveoli by gases having high alveolar/mixed venous tension gradients. We recognize that the use of nitrogen containing mixtures and manoeuvres increasing the expiratory reserve volume will help to prevent atelectasis. However, we wish to stress that secretion retention is a neglected factor and tends to occur in every patient receiving anaesthesia in which attention to respiratory humidification has been ignored. Although a few potential risks obtain, we conclude that humidification is worthwhile for all patients undergoing anaesthesia, particularly when endotracheal and non-rebreathing arrangements are used. We recommend the use of an HME supplied with water vapour by gases diverted through water in a standard Boyle bottle. It remains to say, however, that a critical assessment of the benefits deriving from humidified anaesthesia is yet to be established. REFERENCES Bendixen, H. H., Bullwinkel, B., Hedley-Whyte, J., and Laver, M. B. (1964). Atelectasis and shunting during spontaneous ventilation in anaesthetized patients. Anesthesiology, 25, 297. Browne, D. R. G., Rochford, J., O'Connell, V., and Jones, G. J. (1970). The incidence of postoperative atelectasis in die dependent lung following Thoracotomy: the value of added nitrogen. Brit. J. Anaesth., 42, 340. Burton, J. D. K. (1962). Effects of dry anaesthetic gases on the respiratory mucus membrane. Lancet, 1, 235. Caro, C. G., Butler, J., and Dubois, A. B. (1960). Some effects of restriction of chest cage expansion on pulmonary function in man: an experimental study. J. din. Invest., 39, 573. Chase, H. F., Trotta, R., and Kilmore, M. A. (1962). Simple methods for humidifying non-rebreathing anesthesia gas systems. Anesth. Atwlg. Curr. Res., 41, 249.

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