慢性阻塞性肺疾病急性发作期患者对比例辅助通气的生理反应

目的　探讨比例辅助通气 (PAV)不同辅助水平对慢性阻塞性肺疾病 (COPD)急性发作期患者生理反应的影响。方法　 9例COPD急性发作期患者接受三个不同比例辅助水平的PAV通气 ,观察患者吸气肌肉用力情况和呼吸方式的变化。结果　 (1)与自主呼吸 (SB)相比 ,PAV各辅助水平时的潮气量 (VT)、分钟通气量 (V·E)和呼吸频率 (RR)均稍增高 (P >0 0 5 )。各比例辅助水平之间的VT、V·E 和RR比较差异无显著性 (P >0 0 5 )。 (2 )与SB相比 ,各比例辅助水平时的跨膈压 (Pdi)、压力时间乘积 (PTP)和患者呼吸做功均明显减少 (P >0 0 1) ,Pdi、PTP和患者呼吸做功分别平均减少 8 36cmH2 O、11 4 9cmH2 O·s-1·L-1和 0 5 3J/L。随比例辅助水平的升高 ,Pdi、PTP和患者呼吸功无明显变化(P >0 0 5 )。 (3)PAV可减轻患者呼吸困难 (P <0 0 5 )。结论　本试验证实了无创PAV在COPD急性发作期患者中应用的可行性。患者感觉最舒适的PAV辅助比例水平是 (5 7± 11) %。根据患者感觉舒适情况而设定比例辅助水平的无创PAV可减轻患者的呼吸肌肉负担 ,最舒适水平时呼吸功减少5 7% ,Pdi减少 72 % ,PTP减少 6 5 % ;并改善患者的呼吸方式和呼吸困难     

Pulmonary rehabilitation and non-invasive ventilation in COPD

A multidisciplinary pulmonary rehabilitation program has become an important part of the treatment of chronic obstructive pulmonary disease. It can improve both exercise tolerance and health related quality of life in these patients. Exercise training has to be included for the program to be successful. The intensity of the training is of great importance: there is more physiological benefit in high-intensity training, compared to moderate-intensity training. High-intensity training results in reduced levels of blood lactate and pulmonary ventilation at a given heavy work rate. High-intensity training is limited in COPD patients because of exercise-induced dyspnoea. Flow limitation, as a consequence of increased ventilatory demands of exercise, causes a breathing pattern with greater demands on their inspiratory muscles: this results in a pattern of low tidal volume and high-frequency breathing. Increased inspiratory muscle work causes dyspnoea and limitation in exercise intensity. Artificial ventilatory assistance could improve exercise tolerance and hence help severe COPD patients to achieve a higher level of training. It could help to unload and assist the overburdened ventilatory muscles and give a possibility for higher levels of exercise intensity. In this review article we will discuss the effectiveness and feasibility of training with ventilatory aids.     

Inspiratory muscle unloading by neurally adjusted ventilatory assist during maximal inspiratory efforts in healthy subjects

BACKGROUND: Neurally adjusted ventilatory assist (NAVA) is a mode of mechanical ventilation in which the ventilator is controlled by the electrical activity of the diaphragm (EAdi). During maximal inspirations, the pressure delivered can theoretically reach extreme levels that may cause harm to the lungs. The aims of this study were to evaluate whether NAVA could efficiently unload the respiratory muscles during maximal inspiratory efforts, and if a high level of NAVA would suppress EAdi without increasing lung-distending pressures. METHOD: In awake healthy subjects (n = 9), NAVA was applied at increasing levels in a stepwise fashion during quiet breathing and maximal inspirations. EAdi and airway pressure (Paw), esophageal pressure (Pes), and gastric pressure, flow, and volume were measured. RESULTS: During maximal inspirations with a high NAVA level, peak Paw was 37.1 +/- 11.0 cm H(2)O (mean +/- SD). This reduced Pes deflections from - 14.2 +/- 2.7 to 2.3 +/- 2.3 cm H(2)O (p < 0.001) and EAdi to 43 +/- 7% (p < 0.001), compared to maximal inspirations with no assist. At high NAVA levels, inspiratory capacity showed a modest increase of 11 +/- 11% (p = 0.024). CONCLUSION: In healthy subjects, NAVA can safely and efficiently unload the respiratory muscles during maximal inspiratory maneuvers, without failing to cycle-off ventilatory assist and without causing excessive lung distention. Despite maximal unloading of the diaphragm at high levels of NAVA, EAdi is still present and able to control the ventilator.     

Physiologic effects of noninvasive ventilation during acute lung injury

A prospective, crossover, physiologic study was performed in 10 patients with acute lung injury to assess the respective short-term effects of noninvasive pressure-support ventilation and continuous positive airway pressure. We measured breathing pattern, neuromuscular drive, inspiratory muscle effort, arterial blood gases, and dyspnea while breathing with minimal support and the equipment for measurements, with two combinations of pressure-support ventilation above positive end-expiratory pressure (10-10 and 15-5 cm H2O), and with continuous positive airway pressure (10 cm H2O). Tidal volume was increased with pressure support, and not with continuous positive airway pressure. Neuromuscular drive and inspiratory muscle effort were lower with the two pressure-support ventilation levels than with other situations (p < 0.05). Dyspnea relief was significantly better with high-level pressure-support ventilation (15-5 cm H2O; p < 0.001). Oxygenation improved when 10 cm H2O positive end-expiratory pressure was applied, alone or in combination. We conclude that, in patients with acute lung injury (1) noninvasive pressure-support ventilation combined with positive end-expiratory pressure is needed to reduce inspiratory muscle effort; (2) continuous positive airway pressure, in this setting, improves oxygenation but fails to unload the respiratory muscles; and (3) pressure-support levels of 10 and 15 cm H2O provide similar unloading but differ in their effects on dyspnea.     

Ventilatory muscle support in respiratory failure with nasal positive pressure ventilation

Long-term intermittent mechanical ventilation results in improvements in ventilatory performance and clinical status between ventilation sessions in patients with chronic respiratory failure. The application of intermittent positive pressure ventilation through a nasal mask (NPPV) is a simple, noninvasive method for the provision of chronic intermittent ventilatory support. We investigated the effects of NPPV on inspiratory muscle activity in three normal subjects and nine patients with acute or chronic ventilatory failure due to restrictive (four subjects) or obstructive (five subjects) respiratory disorders. NPPV resulted in reductions of phasic diaphragm electromyogram amplitude to 6.7 +/- 0.7 percent (mean +/- SEM) of values obtained during spontaneous breathing in the normal subjects, 6.4 +/- 3.2 percent in the restrictive group, and 8.3 +/- 5.1 percent in the obstructive group. Simultaneous decreases in activity of accessory respiratory muscles were observed. The reductions in inspiratory muscle activity were confirmed by the finding of positive intrathoracic pressure swings on inspiration in all subjects. With NPPV, oxygen saturation and PCO2 remained stable or improved as compared with values obtained during spontaneous breathing. These results indicate that NPPV can noninvasively provide ventilatory support while reducing inspiratory muscle energy expenditure in acute and chronic respiratory failure of diverse etiology. Long-term assisted ventilation with NPPV may be useful in improving ventilatory performance by resting the inspiratory muscles.     

无创正压通气不同呼气末正压水平对慢性阻塞性肺疾病急性加重患者呼吸做功的影响

目的 探讨无创正压通气(NPPV)不同呼气末正压水平对慢性阻塞性肺疾病急性加重(AECOPD)患者的呼吸做功影响.方法 12例AECOPD患者接受相同压力支持和不同呼气末正压水平的NPPV,观察患者吸气肌肉用力和呼吸方式的变化.结果 ①与自主呼吸(SB)相比,4 cm H2O(L-PEEP)、6 cm H2O(PEEP...     

神经调节辅助通气研究进展

近年,引人了通过横膈电活动控制的神经调节辅助通气(neurally adjusted ventilatory assist,NAVA)这一机械通气模式,它能同时在时间和通气水平上与患者自身作功相协调一致.NAVA使呼吸机的通气支持能够与呼吸中枢所要求的通气量相匹配,从而提高了人机之间的协调性.在吸气过程中,NAVA能安全有效地使呼吸肌得以放松,且不会出现辅助通气的脱节和产生过度肺膨胀.此外,NAVA也不受漏气的影响,能够松弛呼吸肌并能与患者通气需求相协调.总之,NAVA开创了机械通气的新时代.     

神经调节辅助通气研究进展

近年,引人了通过横膈电活动控制的神经调节辅助通气(neurally adjusted ventilatory assist,NAVA)这一机械通气模式,它能同时在时间和通气水平上与患者自身作功相协调一致.NAVA使呼吸机的通气支持能够与呼吸中枢所要求的通气量相匹配,从而提高了人机之间的协调性.在吸气过程中,NAVA能安全有效地使呼吸肌得以放松,且不会出现辅助通气的脱节和产生过度肺膨胀.此外,NAVA也不受漏气的影响,能够松弛呼吸肌并能与患者通气需求相协调.总之,NAVA开创了机械通气的新时代.     

Inspiratory pressure support prevents diaphragmatic fatigue during weaning from mechanical ventilation

Persistent inability to tolerate discontinuation from mechanical ventilation is frequently encountered in patients recovering from acute respiratory failure. We studied the ability of inspiratory pressure support, a new mode of ventilatory assistance, to promote a nonfatiguing respiratory muscle activity in eight patients unsuccessful at weaning from mechanical ventilation. During spontaneous breathing, seven of the eight patients demonstrated electromyographic signs of incipient diaphragmatic fatigue. During ventilation with pressure support at increasing levels, the work of breathing gradually decreased (p less than 0.02) as well as the oxygen consumption of the respiratory muscles (p less than 0.01), and electrical signs suggestive of diaphragmatic fatigue were no longer present. In addition, intrinsic positive end-expiratory pressure was progressively reduced. For each patient an optimal level of pressure support was found (as much as 20 cm H2O), identified as the lowest level maintaining diaphragmatic activity without fatigue. Above this level, diaphragmatic activity was further reduced and untoward effects such as hyperinflation and apnea occurred. When electrical diaphragmatic fatigue occurred, the activity of the sternocleidomastoid muscle was markedly increased, whereas it was minimal when the optimal level was reached. We conclude that in patients demonstrating difficulties in weaning from the ventilator: (1) pressure support ventilation can assist spontaneous breathing and avoid diaphragmatic fatigue (pressure support allows adjustment of the work of each breath to provide an optimal muscle load); (2) clinical monitoring of sternocleidomastoid muscle activity allows the required level of pressure support to be determined to prevent fatigue.     

Inspiratory muscle activity during pulmonary edema in anesthetized dogs.

Pulmonary edema is known to induce a rapid and shallow breathing pattern. However, its effects on the level and pattern of distribution of motor activity to the respiratory muscles is unclear. In the present study we evaluated the effect of oleic acid induced pulmonary edema on the electrical activity of the inspiratory muscles (costal and crural diaphragm and parasternal and external intercostal muscles) in the dog, and related it to the transdiaphragmatic pressure and ventilatory parameters over the course of CO2 rebreathing. Pulmonary edema, reflected by a 7.1 +/- 0.6 wet to dry ratio, decreased lung compliance by 57%, increased pulmonary shunt to 35%, and was associated with a rapid and shallow breathing pattern. When compared at equal levels of PCO2 during CO2 rebreathing before and during edema, ventilation and mean inspiratory flow were increased only at lower levels of hypercapnia and their responses to increasing levels of PCO2 were significantly diminished during edema. Transdiaphragmatic pressures were elevated during edema as compared to control values. The rate of rise of the electrical activity of all inspiratory muscles increased significantly during edema at all levels of PCO2. Peak activity, however, remained unchanged, due to shortening of the inspiratory duration. The EMG responses to progressive hypercapnia were not affected by edema. Pulmonary edema did not change the pattern of breathing and neural output to the inspiratory muscles in vagotomized dogs. We conclude that stimulation of pulmonary proprioreceptors during edema increases neural output to all inspiratory muscles. The neural response to hypercapnia is not altered by edema, and is additive to the vagal input. The ventilatory response to CO2 is blunted during severe edema, due to alterations in lung mechanics.     

Mechanical load on the inspiratory muscles during exercise hyperpnea in patients with Type 1 (insulin-dependent) diabetes mellitus

Summary The aim of this study was to evaluate the difference between Type 1 (insulin-dependent) diabetic patients and healthy control subjects regarding inspiratory muscle load during exercise hyperpnea. For this purpose an incremental progressive exercise test on a cycle ergometer was performed by 36 Type 1 diabetic patients and 40 healthy subjects. In order to determine the mechanical load on the inspiratory muscles breath by breath, we selected the following two parameters, which represent the pressure generated by the inspiratory muscles as well as the duration and velocity of their contraction: (1) the oesophageal tension time index, which is the product of the duty cycle (ratio of inspiratory time to total breath cycle duration) and the mean oesophageal pressure expressed as a percentage of the maximal oesophageal pressure and (2) the mean oesophageal pressure change per time unit during the inspiratory phase of each breathing manoeuver, which is expressed as a fraction of the subject's maximal oesophageal pressure. Comparison of the two groups revealed that at similar levels of ventilation the mechanical load on the inspiratory muscles was significantly higher in the Type 1 diabetic patients than in the control subjects. When the loading was stopped the maximal ventilation was lower in the patients. Nevertheless, they reported a degree of respiratory effort sensation comparable to the control group, which seems to have been caused by an increase of the mechanical load on the ventilatory muscles.     

Proportional assist ventilation, a new approach to ventilatory support. Theory.

The relation between inspiratory effort and ventilatory return (flow and volume) is usually abnormal in patients who require ventilatory support because of respiratory distress. Although all available support methods provide the patient with greater ventilation than would obtain with the same effort while unsupported, the relation between instantaneous effort and ventilatory consequences is not normalized. We describe an approach with which the ventilator simply amplifies patient instantaneous effort throughout inspiration while leaving the patient with complete control over all aspects of breathing pattern (tidal volume, inspiratory and expiratory durations, and flow patterns). This approach is implemented by monitoring the instantaneous rate (V) and volume (V) of gas flow from ventilator to patient and causing applied pressure (P) to change according to the equation of motion [P = f1(V) + f2(V)], where f1 and f2 are appropriately selected functions for the relation between pressure and volume (elastic assist) and pressure and flow (resistive assist). There are several potential advantages to this approach: (1) greater comfort; (2) reduction of peak airway pressure required to sustain ventilation and, hence, the potential for avoiding intubation; (3) less likelihood of overventilation; (4) preservation and enhancement of patient's own reflex, behavioral, and homeostatic control mechanisms since the ventilator essentially becomes an extension of the patient's own muscles; and (5) improved efficiency of negative pressure ventilation.     

Mechanical load on the ventilatory muscles during an incremental cycle ergometer test

An incremental cycle ergometer test performed with a total of 40 healthy subjects (25 male, 15 female) was used to study the mechanical load on the ventilatory muscles. The parameters for the mechanical load on the ventilatory muscles are the time integral of the oesophageal pressure and the mean oesophageal pressure change per time unit (dPoe/dTI) of each breathing manoeuvre. The pressure-time integral is the area delimited by the oesophageal pressure trace and the inspiratory time axis. It is expressed as a fraction of the product of the subject's maximum oesophageal pressure (Poe(max)) and total breath cycle duration (TTOT). This parameter is called oesophageal tension time index (TTIoe). The relationship between minute ventilation and these two parameters during ergometer test showed gender-specific variations because of the differences between men and women as to anthropometric data, lung function parameters and maximum ventilatory muscle strength. Moreover, the dPoe/dTI values significantly depend on the breathing frequency. The present study has provided evidence that, in general, the TTIoe and dPoe/dTI values in terms of a specific minute ventilation (VE) are higher in women than in men. Parameters for the mechanical load on the ventilatory muscles regarding the level of pressure to be generated as well as the duration and velocity of muscle contraction should therefore also allow for the gender of the patients.     

Response of ventilator-dependent patients to different levels of pressure support and proportional assist.

The ventilator's response to the patient's effort is quite different in proportional assist ventilation (PAV) and pressure support ventilation (PSV). We wished to determine whether this results in different ventilatory and breathing pattern responses to alterations in level of support and, if so, whether there are any gas exchange consequences. Fourteen patients were studied. Average elastance (E) was 22.8 (range, 14 -36) cm H2O/L and average resistance (R) was 15. 7 (range, 9-21) cm H2O/L/s. The highest PSV support (PSVmax) was that associated with a tidal volume (VT) of 10 ml/kg (20.4 +/- 3.2 cm H2O), and the highest level of PAV assist (PAVmax) was 78 +/- 7% of E and 76 +/- 7% of R. Level of assist was decreased in steps to the lowest tolerable level (PSVmin, PAVmin). Minute ventilation, VT, ventilator rate (RRvent), and arterial gas tensions were measured at each level. We also determined the patient's respiratory rate (RRpat) by adding the number of ineffective efforts (DeltaRR) to RRvent. There was no difference between PSVmin and PAVmin in any of the variables. At PSVmax, VT was significantly higher (0.90 +/- 0.30 versus 0.51 +/- 0.16 L) and RRvent was significantly lower (13.2 +/- 3.9 versus 27.6 +/- 10.5 min-1) than at PAVmax. The difference in RRvent was largely related to a progressive increase in ineffective efforts on PSV as level increased (DeltaRR 12.1 +/- 10.1 vs 1.4 +/- 2.1 with PAVmax); there was no significant difference in RRpat. The differences in breathing pattern had no consequence on arterial blood gas tensions. We conclude that substantial differences in breathing pattern may occur between PSV and PAV and that these are largely artifactual and related to different patient-ventilator interactions.     

Measurement of inspiratory muscle performance with incremental threshold loading

We found that breathing strategies affect measurement of sustainable inspiratory pressure (SIP). After allowing time for learning, the maximum sustainable inspiratory pressure (SIPmax) was 46% greater than SIP. We therefore developed a test of ventilatory muscle performance that used progressive 2-minute increments in threshold inspiratory resistance. Subjects started with a low load and continued to breathe until they could no longer inspire. With increasing load there was a fall in minute ventilation and time of inspiration, and an increase in oxygen consumption and PETCO2. Power was greatest when loads were 55 to 75% of maximum static inspiratory pressure (MIP). The inspiratory mouth pressure corresponding to the greatest load achieved (PmPeak) was the same in trained and naive subjects. PmPeak/MIP was reproducible and was not influenced by fixing subjects' breathing frequency. We concluded that tests of ventilatory muscle performance should allow subjects to develop breathing strategies to handle high inspiratory loads. Two-minute incremental loading is a simple assessment of ventilatory muscle performance and the test may have clinical application where reproducibility is necessary.     

Pressure support. Changes in ventilatory pattern and components of the work of breathing

To evaluate the interaction between patient and ventilator during widely varying levels of pressure support (PS) ventilation, we studied 33 patients who had undergone aortocoronary bypass. All patients were without preoperative evidence of lung disease and had left ventricular ejection fractions greater than 45 percent. We assessed both changes in ventilatory pattern and the use of an extension of the Campbell technique to determine the components of the mechanical work of breathing (WOB). Patients were placed on 0, 10, 20, and 30 cm H2O of PS. We found that increasing the pressure support level (PSL) did not change minute ventilation, PCO2, or pH despite large changes in both rate and depth of breathing. The inspiratory time fraction was consistently and progressively reduced as PS increased. Although mean inspiratory flow (MIF) increased by 75 +/- 9 (SE) percent as the PSL increased to 30 cm H2O, mean airway pressure rose only 3.5 +/- 0.1 cm H2O. Observed changes in the resistive and elastic components of WOB at PSL greater than 0 were consistent with values predicted from baseline observations and changes in VT and MIF demonstrating that the Campbell technique of separating resistive and elastic components of the patient's WOB during unassisted ventilation can be extended to the analysis of WOB during mechanical ventilation. We were surprised to observe that although inspiratory WOB fell 67 +/- 13 percent as the PSL increased to 30 cm H2O, postinspiratory work by the inspiratory muscles (WOBPIIM) did not show significant change. The persistence and substantial values of WOBPIIM in some patients suggested the presence of significant patient-ventilator dyssynchrony, especially at higher levels of PS. Total inspiratory WOB per minute, including both patient WOB and WOB by the ventilator, increased by 186 +/- 29 percent, demonstrating that PS results in a respiratory pattern requiring substantially greater total mechanical work.     

Physiologic effects of negative pressure ventilation in acute exacerbation of chronic obstructive pulmonary disease

To assess the physiologic effects of continuous negative extrathoracic pressure (CNEP), negative pressure ventilation (NPV), and negative extrathoracic end-expiratory pressure (NEEP) added to NPV in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD), we measured in seven patients ventilatory pattern, arterial blood gases, respiratory mechanics, and pressure- time product of the diaphragm (PTPdi) under four conditions: (1) spontaneous breathing (SB); (2) CNEP (-5 cm H(2)O); (3) NPV; (4) NPV plus NEEP. CNEP and NPV were provided by a microprocessor-based iron lung capable of thermistor-triggering. Compared with SB, CNEP improved slightly but significantly Pa(CO(2 ))and pH, and decreased PTPdi (388 +/- 59 versus 302 +/- 43 cm H(2)O. s, respectively, p < 0.05) and dynamic intrinsic positive end-expiratory pressure (PEEPi) (4.6 +/- 0.5 versus 2.1 +/- 0.3 cm H(2)O, respectively, p < 0.001). NPV increased minute ventilation (V E), improved arterial blood gases, and decreased PTPdi to 34% of value during SB (p < 0.001). NEEP added to NPV further slightly decreased PTPdi and improved patient-ventilator interaction by reducing dynamic PEEPi and nontriggering inspiratory efforts. We conclude that CNEP and NPV, provided by microprocessor-based iron lung, are able to improve ventilatory pattern and arterial blood gases, and to unload inspiratory muscles in patients with acute exacerbation of COPD.     

Similarities between behavior of respiratory muscles in breath-holding and in elastic loading

Breath-holding subjects often exhibit involuntary contractions of respiratory muscles which are much stronger and faster than the efforts they would make during unrestricted breathing at the same level of CO2 and O2. To gain a better understanding of the genesis of these contractions, we compared them with the respiratory response to external elastic loading. Normal men rebreathed a mixture of 8% CO2 in oxygen against no load, elastic loads of 25 and 75 cm H2O/L, and held their breath, equivalent to an elastic load of 226 cm H2O/L. At iso-CO2, increasing loads led to progressively smaller tidal volumes, inspiratory flow rates and ventilation. However, respiratory muscles were progressively activated by the loads, as indicated by increasing occlusion pressure, so that inspiratory flow rate and ventilation were defended much better than could be expected if no neural compensation occurred. The pattern of respiratory muscle activity in breath-holding was qualitatively similar to that in elastic loading, and seemed quantitatively to be an extreme form of reaction to a large load. The reduction in inspiratory time and therefore of peak inspiratory pressure and ratio of inspiratory to total time with very large loads could be viewed as an adaptive response to limit respiratory muscle fatigue.     

Proportional assist ventilation

Partial ventilatory support techniques are intended for patients who are unable to maintain a normal alveolar ventilation, despite normal central control for respiration. Proportional assist ventilation (PAV) is a novel mode of partial ventilatory support in which the ventilator generates an instantaneous inspiratory pressure in proportion to the instantaneous effort of the patient. In theory, PAV should normalize the neuro-ventilatory coupling by making the ventilator an extension of patient's respiratory muscles, while leaving to the patient the entire control of all aspects of breathing. PAV, however, shares a common problem with the conventional partial ventilatory support modes. In mechanically ventilated patients, the respiratory system impedance may change over time. These changes may impair the good matching between ventilator output and patient's ventilatory demand and lead to patient-ventilator asynchrony. To take full advantage of PAV, the authors believe that PAV should continuously and automatically adapt to the respiratory system passive mechanics, assessed by continuous noninvasive measurement of total elastance and resistance.     

Ventilatory control in patients with hypoxemia due to obstructive lung disease.

In 20 patients with chronic hypoxemia due to chronic obstructive pulmonary disease, we measured responses to CO2 and hypoxia in terms of ventilation and P0.1, the pressure generated by the respiratory muscles during the first 0.1 s of inspiratory effort against a closed airway at functional residual capacity. These responses were compared to those of a control group of 17 patients with similar ventilatory abnormality but without hypoxemia. Hypoxemic patients demonstrated significantly less response to hypoxia than did control subjects in terms of both ventilation and P0.1 The decreased hypoxic response might be analogous to that reported in high altitude dwellers and patients with cyanotic congenital heart disease. Ventilatory responses to CO2 were depressed in hypoxemic patients, but P0.1 responses were not significantly decreased. While breathing at rest with arterial O2 saturation of 95 per cent, hypoxemic patients demonstrated the same minute ventilation as control subjects, but tidal volume was smaller, inspiratory duration was shorter, and breathing frequency was slightly higher. This breathing pattern appeared to be independent of whether or not these patients retained CO2.