BJA Advance Access originally published online on February 24, 2006
British Journal of Anaesthesia 2006 96(4):522-532; doi:10.1093/bja/ael033
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The effect of bi-level positive airway pressure mechanical ventilation on gas exchange during general anaesthesia
1Department of Anaesthetics, University of Sydney and Royal Prince Alfred Hospital Sydney, NSW, Australia
2Department of Respiratory Medicine, University of Sydney and Royal Prince Alfred Hospital Sydney, NSW, Australia
*Corresponding author: Department of Anaesthetics, University of Sydney and Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW, Australia 2050. E-mail: bbaker{at}usyd.edu.au
Accepted for publication January 6, 2006.
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Abstract |
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Background. Atelectasis may occur and ventilation–perfusion mismatch may increase during general anaesthesia with neuromuscular paralysis and mechanical ventilation, though preservation of some intermittent muscle contraction might mitigate this process. There is still no ideal manoeuvre to minimize such mismatch or atelectasis. Bi-level positive airway pressure (BiPAP) ventilation adjusts to extra breaths and improves gas exchange during recovery of diaphragm function after neuromuscular paralysis. We hypothesize that BiPAP ventilation may limit the development of pulmonary shunt and may improve ventilation–perfusion mismatch when compared with standard IPPV, with or without PEEP when neuromuscular paralysis has been used during surgery.
Methods. Twenty ventilated patients either on BiPAP or IPPV with or without PEEP were studied randomly using the multiple inert gas elimination technique (MIGET) at 60 and 120 min after rocuronium at induction and after 60 min. Non-invasive cardiac output (NICO®) monitoring and plasma concentrations of rocuronium were measured. We compared the data of MIGET, gas exchange, haemodynamic variables and pulmonary mechanics measurements between the different ventilatory modes.
Results. Intrapulmonary shunt (blood flow to 
) did not increase at 60 min of anaesthesia in any of the different ventilation modes compared with the shunt value before anaesthesia. Log standard deviation of perfusion increased in IPPV, with and without PEEP groups, compared with the baseline (P<0.05) but did not increase in the BiPAP group. BiPAP ventilation generated a higher level of PaO2 than IPPV with or without PEEP (P<0.05).
Conclusion. BiPAP ventilation was beneficial in decreasing ventilation–perfusion mismatch and improving oxygenation when compared with conventional IPPV (with or without PEEP).
Keywords: airway, bi-level positive airway pressure (BiPAP); lung, gas exchange; technique, multiple inert gas elimination technique (MIGET); ventilation, mechanical; ventilation, ventilation–perfusion match
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Introduction |
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Impairment of gas exchange during general anaesthesia with mechanical ventilation is common.1–3 A major cause for this is atelectasis forming in the dependent regions of the lungs4 which increases intrapulmonary shunt and ventilation–perfusion mismatch.5 This impairment of gas exchange often extends into the early postoperative period for cardiopulmonary and abdominal surgery,6 7 though studies have not been done to show that the cause is similar. Conventional IPPV is unable to prevent this atelectasis completely after induction even when using different ventilation settings and other manoeuvres.8–10
Bi-level positive airway pressure (BiPAP) ventilation has recently been introduced into clinical anaesthesia. The continuous airflow from a BiPAP ventilator develops two independent levels of inspiratory and expiratory positive airway pressure (IPAP and EPAP). BiPAP may deliver adaptive pressures to prevent the dynamic airway collapse which tends to occur with standard IPPV in chronic obstructive pulmonary disease.11 12 The flow triggering during BiPAP allows unrestricted spontaneous breathing throughout the mechanical ventilatory cycle which enables unrestricted movement of the diaphragm.13 This sensitive flow triggering function of BiPAP may be a key factor in allowing diaphragmatic movement which may reduce atelectasis in the dependent parts of the lungs when compared with conventional IPPV using non-synchronized ventilation.9 13 14 BiPAP has been shown to improve mismatch and gas exchange in postoperative patients and experimental animals with bronchoconstriction.13 15
We therefore hypothesize that BiPAP may be beneficial in preventing the development of impaired gas exchange in general anaesthesia. In order to test this hypothesis we evaluated ventilation–perfusion relationships using the multiple inert gas elimination technique (MIGET), arterial blood gases (ABGs) and a number of measurements of pulmonary mechanics during BiPAP and IPPV modes of ventilation.
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Materials and methods |
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Patients, anaesthesia and ventilation
This study was approved by the Ethics Committee of The Royal Prince Alfred Hospital, University of Sydney, Australia (# X01-0184) and informed consent was obtained from each participating patient. Twenty patients, of ASA physical status II–IV, undergoing surgery for elective femoral to popliteal (or further distal) artery bypass grafting were enrolled in the study (Table 1). They were not specifically screened for respiratory disease. The patients were divided randomly into two groups for mechanical ventilation. In the first group, each patient received a period with BiPAP and a period with IPPV, and in the second BiPAP was compared with IPPV with PEEP (4 cm H2O). In both groups the order of application of BiPAP and IPPV was randomized. The PEEP level of 4 cm H2O for IPPV was chosen to match the BiPAP level, not to attempt to counter any atelectatic tendency which requires higher PEEP levels.16 17
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The patients received no pre-medication and were supine for the operative procedure. Anaesthesia was induced and maintained by a target controlled infusion technique with propofol (10 mg ml–1 at 3–4 µg ml–1 target level) and remifentanil (50 µg ml–1 at 2–3 µg kg–1 h–1). Tracheal intubation was performed after administering rocuronium 0.6 mg kg–1, and 100% oxygen until tracheal intubation. Each patient's lungs were ventilated mechanically for 60 min with one of the ventilation modes. MIGET and other data collections were performed for 10 min, then an additional bolus dose of rocuronium 0.4 mg kg–1 was injected i.v. and the lungs were expanded by manual hyperventilation to 35–40 cm H2O to match the same initial hyperventilation conditions immediately after tracheal intubation. The other ventilation mode was then used for a further 60 min and the tests repeated. Neuromuscular activity, particularly diaphragmatic activity, was allowed to return gradually over the hour for each part of the study. Clinical monitoring of neuromuscular block showed return of train-of-four impulses at 60 min for each study for all patients. Metaraminol 0.5 mg ml–1 was continuously infused at a varying rate of 0–0.05 mg min–1 to maintain a mean arterial blood pressure (BP) of 80–85 mm Hg.
Two ventilatory models of IPPV were applied by a Dräger Cato anaesthetic machine (Dräger Inc., Germany) and BiPAP was applied by a BiPAP Vision ventilator (Respironics Inc., USA) with air and oxygen without any volatile or gaseous anaesthetic agents. The expiratory minute volumes (VE) were controlled to maintain the same VE in all ventilation modes using a volume meter (Dräger Inc., Germany) connected at the outlet of the expired gas mixing box (Fig. 1). The ventilation settings were initiated with a tidal volume (Vt) of 9–10 ml kg–1, respiratory frequency (Rf) of 10 bpm, inspiratory:expiratory time ratio (I:E) of 1:2, fractional inspired oxygen (FIO2) of 0.35 and timed inspiration equal to 2.0 s in both IPPV and BiPAP ventilation modes. The inspired oxygen for IPPV and IPPV+PEEP was measured at 0.35 but when using the BiPAP machine on a setting of 0.35 the measured FIO2 was 0.40. The time of IPAP increase was 0.2 s in the BiPAP Vision mode only. During this study, 4 cm H2O of EPAP was kept unchanged in the BiPAP Vision mode.
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Measurements
Routine clinical monitoring including ECG, BP and
was executed by a Dräger monitor system (Dräger Inc., Germany). A radial artery catheter was inserted for clinical monitoring and used for sampling, and two i.v. lines were established for administration of the MIGET solution of inert gases, and other drugs and fluids.
Non-invasive cardiac output measurement
Non-invasive cardiac output (NICO) measurement was obtained using a NICO monitor system (Novametrix Medical Systems Inc., USA). The technique uses measurements of end-tidal CO2 and CO2 elimination both during normal ventilation and during 35 s of partial rebreathing based on a differential form of the CO2 Fick Equation.18 19 The NICO sensor, including rebreathing valve, NICO loop and CO2 flow and pressure sensor, were connected between the tracheal tube and the one-way valve system (Fig. 1). NICO automatically cycles through brief periods of partial rebreathing, providing a rapidly repeating display of cardiac output.
One-way valve system
A one-way valve system was designed for collecting expiratory gases while maintaining the ventilation regimen (Fig. 1). It consisted of an Ambu one-way valve together with an Ambu PEEP valve (model: 22/15, Ambu international A/S, Denmark) both contained in a special housing to enable connection to the ventilators and the mixing box. Diaphragm 1 in the one-way valve was opened when the ventilators delivered gas flow into the system and diaphragm 2 was closed (Fig. 2A). The expiratory flow from the patient generated the pressure to close diaphragm 1 and to impede EPAP flow from the BiPAP ventilator, meanwhile the expiratory flow forced diaphragm 2 to open for gas flow into the mixing box (Fig. 2B). The PEEP valve was able to maintain enough pressure to close diaphragm 1 at the end of expiration during BiPAP ventilation. During BiPAP ventilation, the one-way valve and PEEP system was set at 5 cm H2O pressure to prevent gas mixing during expiration (Fig. 2).
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MIGET
MIGET was used to assess pulmonary gas exchange during general anaesthesia.3 20 Six inert gases [sulfur hexafluoride (SF6), ethane, cyclopropane, enflurane, diethylether and acetone] were dissolved in normal saline and infused continuously (4 ml min–1) into a peripheral vein for at least 40 min to ensure equilibration of the inert gases in body tissues and stable mixed venous concentrations. Arterial blood and mixed expired gas samples were collected simultaneously and analysed by an HP 68900 gas chromatography system (Hewlett Packard Inc., Avondale, USA) to yield retention and excretion plots of six inert gases.21 22 Subsequent computer processing of the retention and excretion data allowed description of a 50 compartment model of
distribution which can be defined by a number of parameters. Intrapulmonary shunt (), low regions (0.005<<0.1), high regions (10<<100) and dead space (>100) were calculated according to the Wagner model.22 The mean of the ventilation and perfusion distributions (
of and 
of ) and log standard deviations of ventilation (logSDV) and perfusion (logSDQ) were also calculated. The remaining sums-of-squares for the data fit were used to monitor experimental error and a value of 6 or less was regarded as satisfactory.
Rocuronium assay
Because of the return of monitored neuromuscular function to normal, and because of the relationship between blood levels and monitoring,23 the rocuronium serum concentrations were measured as additional confirmation of return of neuromuscular function.
Arterial blood samples (5 ml each) were drawn into tubes containing sodium heparin. Plasma was decanted and acidified by the addition of 0.2 ml NaH2PO4 1 M to 1 ml plasma, and then stored at –20°C until analysis.
Plasma concentrations of rocuronium were determined using a gas chromatographic-mass spectrometry technique with 3-desacetylvecuronium as the internal standard. Selective ion monitoring using the most abundant (base) peak was performed in quantifying rocuronium (m/z 413) and the internal standard (m/z 425). The extraction procedure of rocuronium from plasma was carried out by liquid–liquid extraction with dichloromethane using potassium iodide as the ion-pairing agent. The precision (reproducibility) of the method was within 6% over the range 50–5000 ng ml–1 for rocuronium.24
Physiological gas analysis
Arterial blood samples were analysed immediately for pH, PaO2, PaCO2, Hb, Hct, 
and acid–base status with blood gas electrodes (model: 582, Instrumentation Laboratories, USA).
Experimental procedure and protocol
After 40 min of infusion of the inert gas solution at 4 ml min–1, arterial and expiratory gas samples for MIGET analysis were obtained for the pre-anaesthetic baseline. Cardiac output was also measured by the NICO monitor system at this time. Duplicate measurements were made in each physiological state.
Anaesthesia was then induced as described above. Mechanical ventilation was carried out using BiPAP or IPPV (either with or without PEEP) for 60 min. Arterial blood samples for rocuronium assay were drawn at 5, 20 and 60 min after injection of rocuronium. ABG samples were obtained at 20 and 60 min after rocuronium administration. Arterial blood samples and mixed expiration gas samples for 
were obtained at 60 min after the rocuronium administration. Mechanical ventilation was switched to the other mode of ventilation for a further 60 min after which all samplings described above were repeated. Data on cardiac output (CO), cardiac index (CI), stroke volume (SV), VE, peak inspiratory pressure (PIP), PEEP and airway resistance (Raw) from NICO monitor system were recorded during the ventilation modes.
Statistical analysis
Statistical results were expressed as mean (SD). Statistical analysis was performed using SPSS (Statistical Package for the Social Science; SPSS Software Co., USA). Data before anaesthesia (baseline) and during BiPAP and IPPV (with or without PEEP) were compared using one-way ANOVA. Homogeneity of variance was carried out by the Levene test. Non-parametric tests for several related samples were performed by Friedman and Kendall's W-tests for data with skewed distribution. A P-value <0.05 was considered to be statistically significant.
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Results |
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Results of the MIGET analyses are summarized in Table 2. Data for baseline measurement for MIGET were unobtainable in two patients who were unable to finish the full procedure of baseline measurements because of their clinical disability and old age. The percentage shunt was not significantly different after 60 min of ventilation when compared with baseline measurements. Dead space ventilation did not show significant change between baseline and 60 min of mechanical ventilation with the different ventilation modes. The logSDQ distribution increased in both IPPV groups (P<0.05) when compared with the baseline values. The logSDQ showed no significant change for the BiPAP group. Total blood flow was decreased during anaesthesia and mechanical ventilation in both groups (P<0.01). The PaO2 in the BiPAP group was increased (P<0.01) at 60 min when compared with the IPPV groups. The PaCO2 did not change significantly between the ventilatory modes. Haemoglobin concentrations were recorded because the patients were undergoing lower limb vascular operations during which variable amounts of blood are lost, but there were no statistical differences between the BiPAP group and either of the IPPV groups. Comparisons of inert gas exchange, ABG, cardiac output and ventilation data between the present study and previous studies are shown in Table 3.
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: n=8 in Pre-An2 for MIGET analysis. logSDQ, log standard deviation of perfusion distribution; logSDV, log standard deviation of ventilation; total flow, total pulmonary blood flow; total ventilation, total minute ventilation (litre min–1); PaO2, arterial carbon dioxide tension; PaCO2, arterial cartan dioxide tension; Hb, haemoglobin; Pre-An, before anaesthesia; BiPAP1-60', BiPAP2-60', IPPV-60' and IPPV+PEEP-60', the time for sampling in different groups
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Ventilation–perfusion distributions are shown for typical Patients 11 and 12 of this study in Figure 3. Blood flow in all patients decreased because of propofol and remifentanil anaesthesia. There were small changes in the distribution with IPPV compared with BiPAP in Patient 11, but there was no major change in the distribution between BiPAP and IPPV with PEEP in Patient 12.
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Haemodynamic variables were decreased during anaesthesia (Table 4). The changes in plasma rocuronium concentration conformed to the pharmacokinetic characteristics of rocuronium in these elderly patients.25 26 There was no significant difference in rocuronium plasma concentration measured at 5, 20 and 60 min after injection in the different ventilatory groups (Tables 5 and 6). Total dosages of propofol, remifentanil and metaraminol were not statistically different between the various groups.
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Discussion |
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Two broad findings from this study are of particular interest: (i) the lack of shunt development between pre-induction and 60 min of post-induction for all three ventilating regimens, and (ii) the maintenance of an unchanged log standard deviation of perfusion distribution (logSDQ) with the BiPAP intervention, but increased logSDQ values for IPPV and IPPV with PEEP.
Anaesthesia and mechanical ventilation: effects on gas exchange
Atelectasis and increased intrapulmonary shunt have been found in patients who undergo general anaesthesia.4 5 Shunt showed a significant increase after induction of anaesthesia in all the previous studies (Table 3) except Gunnarsson's study in chronic obstructive pulmonary disease patients.27 LogSDQ was also increased during anaesthesia compared with baseline (awake). In our study there were no significantly increased shunt or dead space measurements at 60 min for either BiPAP or IPPV when compared with baseline. The sampling times for MIGET were performed at 15–30 min after induction of anaesthesia in almost all of the published studies which might indicate that these changes have resolved at our longer time period. Atelectasis has been demonstrated by CT scan, coinciding with the increased shunt at 20–30 min after induction of anaesthesia in most studies.27–29 All the previous studies shown in Table 3 were undertaken with full neuromuscular paralysis, and the duration and degree of neuromuscular block affects the shape and motion of the diaphragm and chest wall resulting in a cephalic shift of the diaphragm consequently decreasing the functional residual capacity (FRC), which may have led to the increased atelectasis and shunt. Soluble gas (N2O) was also administered as part of the anaesthesia in all the other studies shown in Table 3.
Hedenstierna and colleagues9 demonstrated that diaphragm contraction could decrease the area of atelectasis and Tokics and colleagues30 found no atelectasis formed during ketamine anaesthesia with spontaneous breathing. Maintaining muscular tone and an active diaphragm action with spontaneous breathing appear to be an important factor in attenuating atelectasis and pulmonary shunt during anaesthesia. Muscle relaxation is a major factor affecting muscular tone during general anaesthesia, and the time to 90% electromyographic recovery after rocuronium administration has been shown to be 30–35 min.31 32 The plasma concentration of rocuronium in our study decreased by 60–70% at 60 min when compared with values at 5 min after injection (Tables 5 and 6). A curve with negative exponential decay for rocuronium plasma concentration and time was shown after a single dose of rocuronium in our study. The change in FRC may reverse gradually after rehabilitation of diaphragmatic function because of improving muscle tone. Atelectasis and shunt may be improved with recovery of diaphragmatic function resulting in increasing PaO2.9 Allowing minimal spontaneous breathing, towards the end of anaesthesia, might improve overall matching. This may explain why shunt did not increase at 60 min of anaesthesia in our study. However, BiPAP ventilatory support techniques which allow unrestricted breathing throughout mechanical ventilation may promote recovery of diaphragm function which may contribute to improving mismatch and oxygenation. This may explain why logSDQ was unchanged for BiPAP at 60 min of anaesthesia from pre-induction in our study.
Propofol causes a decrease in cardiac output during i.v. anaesthesia33 34 and a decrease in cardiac output would be expected to decrease shunt, particularly in dependent parts of the lung. This is thought to be the major mechanism improving PaO2 during PEEP rather than alveolar recruitment.35 36 The effect of propofol on the cardiovascular system decreases blood flow to shunt regions as a consequence of a general reduction in cardiac output without necessarily changing overall match. Hemmer and Suter37 and Matamis and colleagues38 used dopamine to prevent the decrease in cardiac output during PEEP, yet found an improvement in relationships with a redistribution of blood flow from regions of shunt units towards normal units suggesting that when cardiac output was maintained, improvement in PaCO2 was because of a true improvement in pulmonary gas exchange.
BiPAP vs IPPV with or without PEEP: effects on gas exchange
In mechanically ventilated and anaesthetized patients in the supine position, the distribution of inspired gas is altered from the awake state, although the distribution of regional perfusion does not change significantly. During spontaneous breathing, inspired gas is predominately distributed to the dependent alveoli. Active contraction of the diaphragm causes greater displacement in the dependent portions of the lung and provides better ventilation to these regions39 though subsequent studies by Warner and colleagues40 dispute the magnitude of this and none measure the distribution of ventilation specifically. During mechanical ventilation, inspiratory gas is preferentially distributed to the non-dependent lung (posterior area in the supine patient). During positive pressure ventilation, an equal airway pressure is applied throughout the lung and is opposed by the hydrostatic pressure gradient of the abdomen in the supine position. Consequently, during anaesthesia and mechanical ventilation, the distribution of ventilation to perfusion is altered, with lung regions having both increased low and high ventilation to perfusion ratios.
In this study the inspiratory waveforms differed with the different ventilators. BiPAP was pressure-controlled with a rectangular pressure waveform, and the IPPV mode was volume-controlled with an approximately ascending ramp pressure waveform. The feature of a constant inspiratory pressure in BiPAP may result in improvement of alveolar ventilation in dependent regions of the lung. For similar ventilatory volumes, pressure-controlled ventilation generated by BiPAP might provide a more ideal pressure to maintain alveoli open, or to reopen collapsed alveoli, than IPPV does. Whether for this reason or not, BiPAP was able to maintain better ventilation in low areas in our study. PaO2 was also better in BiPAP ventilation.
IPPV with PEEP (4 cm H2O) was applied in one of our groups to compare with BiPAP ventilation because EPAP with 4 cm H2O pressure was set for the BiPAP Vision ventilator in the present study. PaO2 was increased in the IPPV mode with PEEP when compared with the IPPV mode. BiPAP displayed a statistically significant greater oxygenation than occurred in IPPV with PEEP. The slightly higher FIO2 during BiPAP ventilation in this study would be expected to worsen logSDQ if it had any effect. This did not occur and if anything the beneficial effect observed may have been masked to some extent by the small increased FIO2. There were no significant changes for shunt after 60 min of ventilation with any of the different modes of ventilation. LogSDQ values were worse for IPPV plus PEEP than for BiPAP. This suggests that BiPAP may be better for low regions in the dependent lung. The physiological dead space (VD/VT) usually increases from 0.3 in awake subjects to approximately 0.4 in anaesthetized mechanically ventilated subjects. Because anatomic dead space is reduced by tracheal intubation, this change is considered to indicate an increase in alveolar dead space attributable to increased distribution of ventilation to areas of lung having high ratios. Alveolar dead space did not increase with low level of PEEP (4 cm H2O) in our study. High PEEP does not seem to be ideal because arterial oxygenation is not improved on average and the lung rapidly collapses after discontinuation of PEEP,9 and the high level of PEEP may cause lung damage.
In pressure-controlled ventilation, a low PEEP seems necessary to prevent tidal end-expiratory airway closure or collapse of alveoli.41 During general anaesthesia, failure to provide an adequate level of end-expiratory alveolar pressure often manifests as reduced respiratory compliance with distinct points of inflection on the static pressure–volume curve. These features are attenuated or obliterated entirely by sufficient end-expiratory alveolar pressure.41 The total end-expiratory alveolar pressure can be raised either by applying PEEP or by encouraging dynamic hyperinflation with auto-PEEP.42 It is possible that sustaining end-inspiratory volume in BiPAP ventilation may aid the recruitment process independently of auto-PEEP so that BiPAP shows a beneficial effect on gas exchange and oxygenation because BiPAP can generate consistent and continuous airflow in both inspiratory and expiratory phases.
In conclusion, this study has found that pulmonary shunt did not increase in 60 min of anaesthesia with a single dose of rocuronium in the three ventilatory modes studied. This may have been because of recovery of muscular tone resulting in FRC recovery and pulmonary blood redistribution. LogSDQ was better with BiPAP ventilation which may improve ventilation–perfusion mismatch and gas exchange because of its sensitive airflow trigger function and ideal bi-level pressure recruitment manoeuvres. These results indicate a clinically small but statistically significant improvement in ventilation–perfusion mismatch when BiPAP ventilation was used in these elderly patients.
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Acknowledgments |
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We thank Mayo Healthcare P/L, Australia and Respironics Inc., USA for the loan of a BiPAP Vision ventilator. We acknowledge salaries provided by the University of Sydney and Royal Prince Alfred Hospital and research funds for MIGET gases from the Royal Prince Alfred Hospital.
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Footnotes |
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3Present address: Department of Anaesthesia, Guangzhou Medical College, Guangzhou, China
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References |
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