Department of Anaesthesiology, University Hospital Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany
LMA® is the property of Intervent Limited.
Accepted for publication: April 12, 2000
![]() |
Abstract |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Br J Anaesth 2000; 85: 41016
Keywords: equipment, mask; equipment, tubes tracheal; airway, resistance
![]() |
Introduction |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
The LMA provides an adjunct which can be joined to the airway end-to-end, to avoid the reduction in diameter that happens when one tube (the ETT) is inserted into the lumen of another (the trachea).1 Indeed, the tube part of a standard LMA is shorter and wider than a corresponding ETT. Bhatt and co-workers2 found the resistance of an LMA was between one-sixth and half of that of a comparable ETT, depending on size and flow. They suggested that a patient breathing spontaneously would have to expend less work breathing on an LMA. This ignores the fact that the ETT ends in the trachea, i.e. beyond the glottis, while the LMA ends before the laryngeal entrance. The inspiratory resistance of the larynx should be added to that of the LMA for a true comparison.
We compared the inspiratory resistance of a standard ETT with that of a corresponding LMA plus the larynx. We hypothesized that any difference in resistance of the devices alone would be offset by the additional resistance of the larynx. Another aim of the study was to investigate how LMA position affected airflow resistance. Previous studies39 have shown that deviations from a central position are common and that the epiglottis can project into a considerable proportion of the air passage in many patients. It has been suggested8 10 that these variations in position are associated with increased airflow resistance, but no data have been presented to support or reject this assumption.
![]() |
Materials and methods |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
The patients received oral midazolam (5.07.5 mg). For the study they were placed supine with the head resting on a 5 cm thick foam cushion. Anaesthesia was induced and maintained with propofol (23 mg kg1 and infusion 612 mg kg1 h1) and ketamine (1.01.5 mg kg1 initially with repeated doses) after atropine 0.51.0 mg for reduction of secretions. Ketamine was used for analgesia in order to avoid the effects of opioids on chest wall mechanics.
Positioning of LMA and ETT
For the first part of the study, a size 4 LMA (Intavent (Cyprus) Ltd, Nicosia, Cyprus) was inserted by a standard technique, and its cuff was inflated with the recommended amount of air (30 ml). Absence of leaks was verified by ventilation with positive pressure. If leaks were detected by auscultation, the LMA was repositioned up to three times. The study was continued only if an apparently leak-free position was obtained. The position of the LMA relative to the structures of the larynx was inspected with a fibre-bronchoscope (type BF P30, Olympus Optical Co. (Europe), Hamburg, Germany). Special attention was given to lateral deviation and to the proportion of the field of vision occupied by the epiglottis when looking from inside the distal opening. In all patients, the same experienced anaesthetist inserted the LMA and did the laryngoscopy.
A standard cuffed ETT (Mallinckrodt lopro, Mallinckrodt Medical, Hennef, Germany, internal diameter (i.d.) 7.5 mm for female patients, 8.5 mm for males) was used in the second part of the study, inserted through the mouth by conventional direct laryngoscopy. The position in the trachea was checked fibreoptically. Because of the limited length of the pressure-measuring catheter (see below), the ETTs had to be shortened to 24 cm at the proximal end. Since the length of an airway has only minor impact on its resistance,11 this shortening should not have influenced our results.
The devices were attached to the patient circuit of a standard anaesthesia machine (Cicero, Drägerwerk AG, Lübeck, Germany) via a 90° swivel bronchoscopy connector, a bacterium filter (type BB22-15M; Pall, Newquay, UK), and a combination of pneumotachygraph and proximal airway opening pressure (Pao) tap (side stream spirometer; Datex Instrumentarium Corp., Helsinki, Finland).
Measuring equipment
A pressure-measuring catheter of 2.5 mm outer diameter, with closed tip and side holes (K-31; Baxter Healthcare Corporation, Deerfield, IL, USA) was placed through the LMA or ETT with the tip guided into the trachea under direct vision using a bronchoscope (distal catheter). An identical catheter was placed with its tip in the proximal end of the devices close to the swivel connector (connector catheter) and both were attached to individual transducers (Medex, Klein Winternheim, Germany) measuring pressure relative to atmosphere. The catheters were flushed with air frequently throughout the study; this reliably prevented plugging by mucus or condensation. Signals from these pressure transducers and from the sidestream spirometer (flow and Pao) were displayed on a monitor (ASIII; Datex) and stored on a personal computer after digitizing at 100 Hz. The monitor was calibrated according to the manufacturers specifications; standard pressures and a standard volume were recorded on the computer before each study for correction of the digitized signals. Earlier tests had shown that the ASIII monitor delays signal output by 50 ms (pressures) or 250 ms (signals from the sidestream spirometer). The tracks of the digital recordings were shifted appropriately, so the remaining phase shift between signals was <10 ms. Linearity and symmetry were verified for pressure measurements by appropriate reference pressures and for the flow measurement by applying the calibration volume (1 litre) in both directions with a wide range of flows.
Arterial pressure (cuff), heart rate (ECG), oxyhaemoglobin saturation (pulse oximeter) and endtidal PCO2 were monitored throughout the study (Marquette Electronics Inc., Milwaukee, WI, USA; Draegerwerk AG).
Experimental procedure
The patients were ventilated with 50% oxygen in nitrogen in intermittent positive pressure ventilation mode with 12 breaths min1, a tidal volume of 10 ml kg1 and an inspiratory:expiratory time (I:E) ratio of 1:1.5. To obtain measurements at different inspiratory flow rates while keeping tidal volume and I:E ratio constant, the relation between the inspiratory flow phase and end inspiratory pause was varied: Each measurement block consisted of three sets of 1030 breaths each with an end inspiratory pause of 0%, 30% and 60% of inspiratory time, respectively, resulting in flows of 5.5, 7.5 and 12.5 ml kg1 s1, respectively. With each device, one block of measurements was made with the distal catheter located in the trachea and one after retraction of this catheter to the connector position. By comparing the data from the two blocks, the effect of the catheter on the devices resistance could be estimated. In eight patients, another block of measurements was made with the tip of the distal catheter located in the distal opening of the LMA, so in these patients the resistance of the LMA could be distinguished from that of the larynx.
To avoid unnecessary manipulation in the patients upper airway, the LMA was studied first in all patients. The ETT was then placed and left there for the rest of the anaesthesia. Since the variables measured were bound to be independent of time, we did not expect the order to have any effect. As endotracheal intubation was facilitated routinely by neuromuscular blockade, both devices were studied after administration of vecuronium (0.1 mg kg1 initially, repeat doses of 0.05 mg kg1 after 30 min) to allow comparability. In five patients additional measurements were made with the LMA before giving the relaxant, to provide data on the effects of neuromuscular blockade.
Data analysis
The recorded signals were supplemented with a trace for the drop in resistive pressure along the devices and the larynx. This was obtained by digitally subtracting the pressure measured with the distal catheter from that at the connector catheter. The flow signal was digitally integrated for calculation of tidal volume. Flow during the last 500 ms of inspiration was used as the denominator in resistance calculations. All respiratory mechanics results were means from the last six breaths of each setting.
Resistance values were calculated primarily by dividing the drop in resistive pressure between the connector and the trachea (and between the connector and tip of the LMA in eight patients) by the simultaneously measured flow values. However, this resistance was, inevitably, increased artificially by the distal catheter passing through the devices and the larynx. The data were corrected for this artefact by a second method for resistance calculation: When inspiratory flow stops, pressures throughout the respiratory system decrease suddenly, because the resistive loads distal to any point of measurement no longer have to be addressed by a driving pressure component. If an end inspiratory pause follows the cessation of flow, as in our study in the setting with medium and high flows, the difference between the peak pressure immediately preceding the cessation and the value directly after it (P1) can be divided by the flow before cessation, yielding resistance of all structures distal to the point of measurements 12. In this study the
P1 method was applied to Pao; comparison of the values with the distal catheter in the trachea or at the tip of the LMA, respectively, to those after retraction to the connector position allowed quantification of the increased resistance caused by the catheter passing through the structures of interest when in the distal position. The catheter-derived resistances were corrected for this artefact. Since the artefact could only be quantified at medium and high flows (see above), corrected resistance values are available only for those settings. Since the
P1 method is prone to noise, the artefact correction introduced a certain amount of scatter, but this did not influence the main findings of the study.
Theoretically, simple differences between the resistances of the devices could have been measured entirely based on the P1 method, obviating the need for catheter measurements. This simplification, however, would have generated several problems: (i) no absolute values of resistance would have been available, making comparison with published data difficult; (ii) intubation-related changes in resistance of structures distal to the trachea, i.e. bronchi, lung parenchyma and chest wall, could not have been distinguished from changes of the values under study, thus introducing a substantial source of error; (iii) separate consideration of LMA and larynx would not have been possible.
Data are reported as means (SD) unless stated otherwise. Since comparison of devices always included ETTs, only the data for the male patients were tested by Wilcoxons ranked sign test; differences were considered significant if P was <0.05 (SYSTAT version 5.1 under MacOS). There were too few female patients for statistical testing to be valid for data from these patients.
![]() |
Results |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
|
|
|
|
P = (K1 x flow) + (K2 x flow2)
In this study, K1 and K2 for the LMA were 0.08 and 1.54 respectively (so P was 1.62 mbar at a flow rate of 1 litre s1), while those for the ETT were 0.32 and 3.21, respectively (so
P was 3.53 mbar at a flow rate of 1 litre s1). This underscores the similarity between the resistance found in the present study and those reported previously.2 11
Confidence intervals for resistance values are not reported, because the variability caused by individual differences in flow rate would have to be eliminated first by deriving a resistance value at a normalized flow. For the devices alone this can be done by fitting the data as described in the paragraph above. However, the absence of such a clear relationship for the most interesting data, namely those from the LMA plus larynx, precludes such procedure in this context.
Table 2 summarizes endoscopic findings and other observations. Resistance data for the LMA plus larynx are included as reference. Two patients made a whooping noise during inspiration when ventilated through the LMA, and one showed a marked lateral deviation of the LMA; these were the three patients with especially high resistance of LMA plus larynx. In eight patients the epiglottis covered between one-tenth and two-thirds of the distal opening of the LMA, but this was not associated with increased resistance. In the two patients with a whoop and high resistance, the epiglottis could not be seen; the entire glottis could be seen from the distal opening of the LMA.
|
![]() |
Discussion |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
The resistance of artificial airways is of interest because a spontaneously breathing patient has to work to overcome it. Previous in vitro studies2 13 found that the resistance and the additional work of breathing caused by standard LMAs are approximately one-sixth to half of those elicited by comparable ETTs (the range reflects the fact that there is a range of ETT sizes corresponding to a single LMA size). This difference is not surprising considering the larger diameter of the LMA tube: the work of breathing is inversely related to the third to fourth power of the tube diameter,14 depending on breathing pattern, while length only makes a minor difference.11 The recently introduced reinforced LMAs have narrower tubes, so their resistance is greater than that of standard LMAs and similar to that of ETTs.13 However, an ETT bridges the larynx and thus eliminates its resistance. Thus, work while breathing through an ETT has been found to be equivalent to that during breathing through a standard LMA, and even less than that during breathing through a reinforced LMA with its narrower tube.13 We found that the anatomical structures between the LMA and trachea had a sizeable and highly variable resistance of their own. On average, this resistance (the difference between the resistance determined for the LMA alone and that of the LMA plus larynx) amounted to 2.3 mbars litre1 at high flow and reduced the differences between LMA and ETT resistance to insignificant and clinically irrelevant amounts. These results support those of Ferguson and colleagues,15 who studied spontaneously breathing awake volunteers. They found that the resistance of the airways including an LMA was similar to that found for airways including an ETT by Gal and Suratt.16 Normal upper airway resistance is between 0.5 and 1.0 mbars litre1 during quiet breathing,17 i.e. at flows comparable to the medium or low flows in our study. In contrast, Boisson-Bertrand and co-workers18 found that the upper airways did not contribute to the overall resistance of the respiratory system resistance during mechanical ventilation via an LMA. The discrepancy might be result from the fact that upper airway resistance was not measured directly in that study.
Because of the small number of patients, the present study might not show a true difference between the resistance of the ETT and that of an LMA plus larynx. However, because of the high variability of laryngeal resistance, many patients would have to be studied to find a difference, which cannot be expected to be of a clinically relevant magnitude.
The relevance of the additional work of breathing imposed by airways can also be questioned in general. This work component is of the same order of magnitude as that naturally imposed by the respiratory system, and healthy adults should be able to easily overcome it with the force reserve of their respiratory muscles.
However, the resistance of the structures between a LMA and the trachea is clinically relevant from a different point of view: major complications known to be associated with the use of the LMA,19 i.e. laryngospasm and bronchospasm, likewise increase resistance, often immediately after LMA insertion. The anaesthetist has to distinguish these complications from an increase in resistance for mechanical reasons. The latter requires a different therapy, if any (namely repositioning of the device), which is not indicated in the case of laryngospasm or bronchospasm.19 20 It might be reasonable to increase the depth of anaesthesia at first, perform auscultation for differential diagnosis, and then attempt to reposition the device.
The study also aimed to discover the degree to which highly variable resistance of the larynx and the surrounding structures might be related to individual differences in the interactions of the LMA with the upper airway. The position of the epiglottis relative to the LMA has been of concern for several authors. Studies using magnetic resonance imaging, conventional radiography and/or fibreoptic endoscopy showed that, in 3565% of patients, the epiglottis comes to lie within the cuff of the LMA and in most of these is folded down.3 59 The epiglottis might occupy up to 100% of the field of view when looking down on the distal opening of the LMA with a fibrescope. This has been postulated to be a potential reason for obstruction,8 10 but a correlation has not been found. As Brain points out,20 the endoscopic view is two-dimensional, so the fact that the epiglottis can be seeneven in large parts of the field of viewdoes not preclude air from passing around it. Our study supports the notion that visibility of the epiglottis is not associated with a marked increase in resistance. Indeed, in the two patients in whom resistance was greatest, the view of the glottis was completely unobstructed. As the visibility of the epiglottis was not associated with increased resistance, no attempts were made to quantify the area of visual obstruction more precisely or to correct for the geometry of the fibrescope.
Nandi and co-workers7 point to an important potential mechanism for obstruction. They found that the typical anterior displacement of the cricoid cartilage by the blocked LMA might render the vocal cords short, slack and partially adducted. In our study, both patients with high resistance were ventilated with relatively high tidal volumes (and, thus, inspiratory flows) because of their high body weight. The whooping sound associated with inspiration in these, and only these, patients gave rise to the suspicion that the inspiratory flow itself caused a narrowing of the glottis by a Bernoulli-like effect of flow limitation in an elastic tube. We also noted that, in one patient, the overall resistance diminished when the measuring catheter was retracted from the glottis. This resembled findings by Pedersen and Ingram,21 who showed that a foreign body introduced into an elastic tube can promote collapse and aggravate flow limitation.
Righini and colleagues22 found that the inspiratory resistance shown by a size 3 LMA while in situ in five patients was almost twice that measured in vitro. These authors speculated that this was caused by a narrowing of the distal LMA opening brought about by blocking the LMA cuff within the hypopharynx. However, the distal pressure was measured with a catheter extending 15 mm beyond the distal opening. Our endoscopic findings suggest that, in this position, Righini and co-workers were already measuring a considerable part of the resistance posed by the anatomical structures, so that conformational changes of the LMA outlet might not have had the impact ascribed to it by these authors.
In conclusion, we found no statistically significant or clinically relevant difference between the resistance of a size 4 LMA plus that of the larynx and that of an 8.5 mm i.d. ETT. The resistance of the anatomical structures between the LMA and the trachea is sizeable and highly variable. These findings extend and complement previous in vitro studies. In addition, they suggest that an LMA might change upper airway geometry in a way that promotes elevation of resistance.
![]() |
Acknowledgements |
---|
![]() |
Footnotes |
---|
![]() |
References |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
2 Bhatt SB, Kendall AP, Lin ES, Oh TE. Resistance and additional inspiratory work imposed by the laryngeal mask airway. Anaesthesia 1992; 47: 3437[ISI][Medline]
3 Brimacombe J. Analysis of 1500 laryngeal mask uses by one anaesthetist in adults undergoing routine anaesthesia. Anaesthesia 1996; 51: 7680[ISI][Medline]
4 Brimacombe J, Berry A. Insertion of the laryngeal mask airwaya prospective study of four techniques. Anaesth Intens Care 1993; 21: 8992[ISI][Medline]
5 Pothmann W, Füllekrug B, Schulte am Esch J. Fiberoptische Befunde zum Sitz der Kehlkopfmaske. Anaesthesist 1992; 41: 77984[ISI][Medline]
6 Füllekrug B, Pothmann W, Werner C, Schulte am Esch J. The laryngeal mask airway: anesthetic gas leakage fiberoptic control of positioning. J Clin Anesth 1993; 5: 35763[ISI][Medline]
7 Nandi PR, Nunn JF, Charlesworth CH, Taylor SJ. Radiologic study of the laryngeal mask. Eur J Anaesthesiol 1991; Suppl 4: 339
8 Payne J. The use of fibreoptic laryngoscope to confirm the position of the laryngeal mask. Anaesthesia 1989; 44: 865
9 Shorten GD, Opie NJ, Graziotti P, Morris I, Khangure M. Assessment of upper airway anatomy in awake, sedated and anaesthetized patients using magnetic resonance imaging. Anaesth Intens Care 1994; 22: 1659[ISI][Medline]
10 Brodrick PM, Webster NR, Nunn JF. The laryngeal mask airwaya study of 100 patients during spontaneous breathing. Anaesthesia 1989; 44: 23841[ISI][Medline]
11 Guttmann J, Eberhard L, Fabry B, Bertschmann W, Wolff G. Continuous calculation of intratracheal pressure in tracheally intubated patients. Anesthesiology 1993; 79: 50313[ISI][Medline]
12 von Neergard K, Wirz R. Die Messung der Strömungswiderstände in den Atemwegen des Menschen, insbesondere bei Asthma und Emphysem. Z Klin Med 1927; 105: 5182
13 Al-Hasani A. Resistance to constant air flow imposed by the standard laryngeal mask, the reinforced laryngeal mask and RAE tracheal tubes. Br J Anaesth 1993; 71: 5946[Abstract]
14 Bolder PM, Healy TEJ, Bolder AR, Beatty PCW. Kay B. The extra work of breathing through adult endotracheal tubes. Anesth Analg 1986; 65: 8539[Abstract]
15 Ferguson C, Herdman M, Evans K, Hayes M, Cole PV. Flow resistance of the laryngeal mask in awake subjects. Br J Anaesth 1991; 66: 400P
16 Gal TJ, Suratt PM. Resistance to breathing in healthy subjects following endotracheal intubation under topical anesthesia. Anesth Analg 1980; 59: 27074[ISI][Medline]
17 Ferris BG Jr, Mead J, Opie LH. Partitioning of respiratory flow resistance in man. J Appl Physiol 1964; 19: 6538[ISI]
18 Boisson-Bertrand D, Hannhart B, Rousselot JM, Duvivier C, Quilici N, Peslin R. Comparative effects of laryngeal mask and tracheal tube on total respiratory resistance in anaesthetized patients. Anaesthesia 1994; 49: 8469[ISI][Medline]
19 Leach AB, Alexander CA. The laryngeal maskan overview. Eur J Anaesthesiol 1991; Suppl 4: 1931
20 Brain AIJ. Studies on the laryngeal maskfirst, learn the art. Anaesthesia 1991; 46: 4178[ISI][Medline]
21 Pedersen OF, Ingram RH Jr. Configuration of maximum expiratory flowvolume curve: model experiments with physiological implications. J Appl Physiol 1985; 58: 130513
22 Righini ER, Marangoni E, Volta CA, Alvisi R, Bortolazzi S, Gritti G. Additional inspiratory resistance imposed by the laryngeal mask airway: in vitro versus in vivo comparison. Anaesthesia 1997; 52: 8728[ISI][Medline]