Patient-Ventilator Trigger Asynchrony in Prolonged Mechanical Ventilation*

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1 Patient-Ventilator Trigger Asynchrony in Prolonged Mechanical Ventilation* David C. Chao, MD, FCCP; David]. Scheinhorn, MD, FCCP; and Meg Stearn-Hassenpflug, MS, RD Study objective: To investigate patient-ventilator trigger asynchrony (TA), its prevalence, physiologic basis, and clinical implications in patients requiring prolonged mechanical ventilation (PMV). Study design: Descriptive and prospective cohort study. SeUing: Barlow Respiratory Hospital (BRH), a regional weaning center. Patients: Two hundred consecutive ventilator-dependent patients, transferred to BRH over an 18-month period for attempted weaning from PMV. Methods and interventions: Patients were assessed clinically for TA within the first week of hospital admission, or once they were in hemodynamically stable condition, by observation of uncoupling of accessory respiratory muscle efforts and onset of machine breaths. Patients were excluded if they had weaned by the time of assessment or if they never achieved hemodynamic stability. Ventilator mode was patient triggered, flow control, volume cycled, with a tidal volume of 7 to 10 mllkg. Esophageal pressure (Peso), airway-opening pressure, and airflow were measured in patients with TA wbo consented to esophageal catheter insertion. Attempts to decrease TA in each patient included application of positive end-eapiratory pressure (PEEP) stepwise to 10 em H 2 0, flow triggering, and reduction of ventilator support in pressure support (PS) mode. Patients were followed up until hospital discharge, when outcomes were scored as weaned (defined as >7 days of ventilator independence), failed to wean, or died. Results: Of the 200 patients screened, 26 were excluded and 19 were found to have TA. Patients with TA were older, carried the diagnosis of COPD more frequently, and had more severe hypercapnia than their counterparts without TA. Only 3 of 19 patients (16%), all with intermittent TA, weaned from mechanical ventilation, after 70, 72, and 108 days, respectively. This is in contrast to a weaning success rate of 57%, with a median (range) time to wean of 33 (3 to 182) days in patients without TA. Observation of uncoupling of accessory respiratory muscle movement and onset of machine breaths was accurate in identifying patients with TA, which was confirmed in all seven patients consenting to Peso monitoring. TA appeared to result from high auto-peep and severe pump failure. Adjusting trigger sensitivity and application of flow triggering were unsuccessful in eliminating TA; external PEEP improved but rarely led to elimination of TA that was transient in duration. Reduction of ventilator support in PS mode, with resultant increased respiratory pump output and lower tidal volumes, uniformly succeeded in eliminating TA. However, this approach imposed a fatiguing load on the respiratory muscles and was poorly tolerated. Conclusion: TA can be easily identified clinically, and when it occurs in the patient in stable condition with PMV, is associated with poor outcome. (CHEST 1997; 112: ) Key words: auto-peep; patient-ventilator trigger asynchrony; prolonged mechanical ventilation; regional weaning center; ventilator-dependent; ventilator weaning Abbreviations: AI=asynchrony index; BRH=Barlow Respiratmy Hospital; EMG=electromyogram; MIP=maximum inspiratory pressure; Pao=pressure at airway-opening; Peso=esophageal pressure; Pmus = inspiratory muscle pressure; Ppl=pleura pressure; PEEP= positive end-expiratory pressure; PIP= peak inspiratory pressure; PMV=prolonged mechanical ventilation; PS=pressure suppmt; RWC=regional weaning center; TA=trigger asynchrony *From the Barlow Respiratmy Hospital and Barlow Respiratmy Research Center, Los Angeles. Presented in part at \Veaning '96: Weaning from Prolonged Mechanical Ventilation, Palm Springs, April 1996; and at the 62nd Annual Scientific Assembly of the Ame1ican College of Chest Physicians, San Francisco, October 27-31, Manuscript received September 26, 1996; revision accepted May 23, Reprint requests: David C. Chao, MD, FCCP, Barlow Respiratory Research Center, 2000 Stadium Way, Los Angeles, CA patient-ventilator trigger asynchrony (TA) refers to the phenomenon of a mechanically ventilated patient failing to trigger the ventilator in an assist mode, resulting in a machine rate that is less than the rate of the patient's inspiratory efforts. TA is a common observation in mechanically ventilated infants and neonates. TA has only recently been reported in adults in the ICU setting, related to 1592 Clinical Investigations in Critical Care

2 either ventilator factors, eg, inappropriate bias flow, 1 high levels of pressure support (PS ), 2 or patient factors, eg, patients not sedated or paralyzed. 3 To our knowledge, T A has not been studied in the setting of prolonged mechanical ventilation (PMV). Patients who experience difficulty weaning from PMV would be expected to be prone to T A because of factors such as decreased inspiratory muscle pressure (Pmus). Barlow Respiratory Hospital (BRH) functions as a regional weaning center (RWC), accepting ventilator-dependent patients from the ICU s of surrounding hospitals for attempted weaning. 4 We investigated the prevalence and physiologic basis of T A, and outcome of weaning attempts in these patients. MATERIALS AND METHODS \'\Te screened 200 consecutive ventilator-dependent patients transferred to BRH for attempted weaning over an 18-month period. Initial assessments for TA were performed within 1 week of hospital admission. Patients were excluded if they had weaned by the time of assessment, or if they were in hemodynamically unstable condition, in which case they were reassessed once their conditions stabilized. The assessment was performed as follows: all patients were ventilated via tracheostomy tubes using ventilators (PB7200ae; Nellcor Puritan-Bennett; Carlsbad, Calif) in patient-triggered, flow-control, volume-cycled (AC) mode. Tidal volume was set between 7 and 10 mukg, inspiratory flow rate was set no lower than 70 Umin, and trigger sensitivity was set to 0.5 ern H 2 0 and titrated up only if auto-cycling could not be corrected. Maximum inspiratory pressure (MIP) was determined using the ventilator pressure transducer and automated airway occlusion maneuver (7200ae ventilator option 31). The trigger sensitivity was first decreased to 5 em H 2 0 and the airway occlusion maneuvers were activated in rapid succession over a 20-s period to prevent intetim inspiration, while coaching the patients in maximizing their efforts. Measurements were abandoned if rapid occlusion maneuvers could not prevent interim inspiration, or if patients could not cooperate or tolerate the maneuvers. TA was identified by observing uncoupling of the patient's accessory respiratory muscle efforts and onset of ventilator breaths. The patient was observed for a minimum of 2 min for consistently failed efforts. In selected patients who consented to esophageal pressure (Peso) monitoring, TAwas confirmed using a monitor (BICORE CP-100 Pulmonaty Monitor; Allied Healthcare Products; Riverside, Calif) that digitizes signals from three transducers: a pressure transducer (50 Hz sampling rate) in the esophagus, and pressure (50 Hz)lflow (100 Hz) transducers attached b etween the tracheostomy tube and the circuit "Y." Correct positioning of the Peso transducer was confirmed by agreement between Peso change and airway pressure (Pao) change during a Mueller maneuver. 5 The three digitized signals were directly downloaded into a laptop computer and saved into one file for each ventilator setting. These files (ASCII) were imported into a spreadsheet program (Microsoft Excel for \Vindows version 4; Redmond, Wash), then displayed graphically, and plotted against time. In addition to directly downloading the digitized data for analysis, intrinsic positive end-expiratory pressure (auto-peep) measurements performed by the monitor (BICORE CP-100) in real-time over 1 min duration were also downloaded into a computer spreadsheet. The monitor (BICORE) calculates the dynamic auto-peep using a method described by Marini, 6 measming the difference between the Peso plateau near endexpiration and the Peso at the onset of flow. This value minus the corresponding Pao swing (the trigger sensitivity) approximates the intrathoracic pressure change required to overcome auto PEEP. At the time of identification, attempts were made to eliminate TA as follows: applying PEEP of 5, 8, and 10 em H 2 0 stepwise, switching to flow triggering, and reducing ventilator support in PS mode. Flow trigger setting was 6 to 8 Umin for base flow, 1 to 2 Umin for sensitivity. PS was reduced by first titrating pressure to match machine breath volume and then r educing stepwise 4 em H 2 0 each time until TA resolved. If respiratory distress developed, patients were returned to original level of ventilator support. After the assessment, patients were treated b y their attending pulmonologists. Patients were followed up until they were discharged from the hospital, at which time outcomes were scored as weaned (defin ed as > 7 days of ventilator independence), fail ed to wean, or died. The study was approved by the Institutional Review Board of BRH, and informed consent was obtained from subjects agreeing to Peso monitoting. Data are expressed as mean:±:sd; median (range) of values is reported when the distribution of data was not normal. Statistical tests used to compare patients \vith and without T A w ere as follows: x 2 test for gender, the prevalence of smoking and COPD, elevated PaC0 2, and weaning outcome; Student's t test for continuous variables including age, MIP, amount of tobacco smoked, serum albumin, and PaC0 2 ; Mann-Whitney test for time to wean. RESULTS Of the 200 patients screened, 26 were excluded. The remaining 174 patients had a median duration of mechanical ventilation prior to transfer of 29 (3 to 371 ) days. Nineteen of the 174 patients (10.9%) were found to have T A on initial assessment. In these 19 patients, the set tidal volume was 576±75 ml, inspiratory flow was decelerating with peak flow of 81.9±7.2 Umin, effective respiratory rate was 14.7±3.0 with all breaths patient triggered, and ineffective efforts constituted 45.2± 13.8% of all efforts. Comparison of demographics and selected measurements of patients with and without T A are shown in Table l. Significant differences are noted in age, diagnosis of COPD, PaC0 2, and MIP. Seven of the 19 patients with TA consented to Peso monitoring. Representative pressure and flow tracings in these patients are shown in Figure 1 (PEEP=O) and Figure 2 (PEEP=10). In each case in which Peso was monitored, the clinical observation of inspiratory muscle effort corresponded to a negative deflection on the Peso tracing. The expiratory airflow vs time waveform was also characteristic, showing either transient spikes in expiratory flow rate just as the futile inspiratory efforts ended (see asterisk in Fig 1) or transient drop in expiratory flow rate during the futile efforts (see double asterisk in Fig 2). CHEST I 112 I 6 I DECEMBER,

3 Table!-Comparison of Demographics and Selected Measurements in PMV Patients With and Without Trigger Asynchrony Patients With Patients Without TA (n=19) TA (n= l55) Age, yr 75:!:6 69:!:13* Gender, % female Prior ventilated days 27 (4-120) 29 (3-371 ) Smoking history (pack-yr) 8.3% (57:!:16) 65% (48:!:36) Diagnosis of COPD 84% 40%* Albumin, gldl 2.4:!: :!:0.6 2 ~ 46 P a C Hg 68% 58% Average PaC0 2, mm Hg 52:!:10 45:!:12* ph 7.40:!: :!:0.06 MIP :!: :!:10.8* *p< Data obtained in 12 of 19 TA patients and 80 of 155 non-ta patients. The graphic pressure and flow monitoring data were analyzed to determine the potential causes of T A. The inspiratory efforts were identified by the negative Peso deflections, which appeared to retard the expiratory flow to variable degrees, depending on the magnitude of Peso, phase of expiration, and severity of flow limitation. The corresponding Pao, however, was minimally affected by the intrathoracic pressure swing. T1igger failures were found to result from low Pmus that was inadequate to overcome the high inspiratory trigger threshold associated with auto-peep. Adjusting tiigger sensitivity and application of flow triggering were unsuccessful in eliminating T A; external PEEP improved coupling in general but only led to transient elimination of T A in three patients. Figure 2 shows that while TAwas persistent, the rate of successful triggering was improved after PEEP of 10 was applied, even as the apparent Pmus has decreased. Reduction of ventilator support in PS mode uniformly succeeded in eliminating T A, at a PS level of 11.2±3.3 em H 2 0. Figure 3 shows complete elimination of T A when the patient was switched to low-level PS, due to increased Pmus and lower tidal volume. This maneuver, though successful in eliminating T A in every patient, also led to development of a rapid and shallow breathing pattern, and subsequent respiratory distress. The outcome of weaning attempts in the 19 patients with T A is summarized in Table 2. Three of 19 patients (16%), all with intermittent TA, weaned compared to a 57% weaning success rate in the 155 patients without TA during the same period (p < 0.01 ). The median time to wean for patients with T A was more than twice as long as those without T A, 72 (70 to 108) days vs 33 (3 to 182) days. This difference is statistically significant (p=0.013) despite having only three patients in the TA group. DISCUSSION T A has also been called patient-ventilator "dyssynchrony,"7 "desynchronization," 2 "mismatching," 8 and trigger failurey We prefer the term TA because it has been used in the pediatric literature, and because we consider T A to be one of several conditions in which there is lack of synchrony in the interaction between patient and ventilator (Table 3). We found a prevalence of 10.9% TA in patients in stable condition with PMV on transfer to our RWC. These patients were older, weaker, and had a higher prevalence of COPD and severity of hypercapnia, compared to peers in the cohort. It is perhaps surprising that TA is less prevalent at the RWC than in reports from the ICU population. This is probably accounted for by differences in both ventilator mode and patient treatment factors. Fabry et al 2 observed a small number of patients in the ICU at PS settings of 20 em H 2 0, with TA attributed to expiratmy phase delay due to persistent inspiratory flow well past patients' termination of inspiration. In contrast, all of our patients were ventilated in the volume-cycled mode with tidal volume set between 7 and 10 mukg and flovv rate of 70 Umin or higher. Varon et al, 3 in an abstract reporting 97% prevalence ofta in the ICU, found no association between TA and etiology of ventilator dependency, ventilator mode, inspiratmy flow rate, or tidal volume. However, their patients were acutely intubated and lightly sedated, unlike patients in the PMV population, who were comfmtably tracheostomized and rarely required sedation. These authors also relied only on the printed airway pressure and flow waveform downloaded from the ventilators, as opposed to direct patient observation or Peso tracing, to identify TA. Identifying T A There are little data in the literature on how to identify or quantify T A. Ideally, inspiratory efforts should be identified by respiratmy center output, phrenic nerve activity, or diaphragm activation. Attempts to monitor diaphragm activation in the clinical s etting using electromyography (EMG) have suffered from lack of standardization and frequent signal contamination, whether surface or esophageal electrodes were used. The EMG pattern of asynchronous breaths has not been well characterized. We validated visual observation of TA vvith Peso monitoring. Although cardiac and other artifacts can be present, and pressure may be low from respiratory muscle weakness, we found that in all seven patients vvith clinically identified TA who underwent Peso monitoring, each observed effmt corresponded to a negative Peso deflection. Thus, clinical observa Clinical Investigations in Critical Care

4 80! 60 Peso \ ~ time(s) FIGURE l. Peso, Pao, and flow at the tracheostomy in a patient with T A on flow-controlled, volume-cycled (assist/control) mode. The units are em H 2 0 for the pressure tracing and Umin for flow. The patient's inspiratory efforts are identified by the negative Peso swings. The PEEP is set at 0. Pao appropriately drops to 0 during expiration, demonstrating little circuit or valve resistance. TA is evident, with one triggered breath every three to four efforts. Prolonged expiratory flow is due to airflow limitation. Peso swings have little effect in retarding the expiratory flow and even less effect on Pao, depending on the phase of expiration. tion is probably highly specific in identifying TA. We believe that clinical observation is probably sensitive as well, since observation of thoracoabdominal movement has been the standard method of counting respiratory rate, and patients with T A often have heightened and prominent accessory muscle activity associated with inspiratory efforts. The use of airway pressure and flow waveforms to detect T A deserves comment, as these are now commonly displayed on mechanical ventilator monitoring systems. Since airway pressure and flow measured at the ventilator can be affected by various artifacts (eg, hiccup, cough, sudden displacement or compression of the ventilator tubing), this may not be a reliable way to identify TA. Even when measured with a transducer directly attached to the tracheostomy tube, we found that the morphology of the expiratory flow disturbance due to futile efforts varies and can be subtle. When severe airflow limitation is present, as in Figure 1, only small transients in expiratory flow were observed. Quantifying T A QuantifYing TA is also problematic. Varone et ap defined asynchrony index (AI) as the percentage of monitored breaths that fail to trigger. However, we found that AI varied with applied PEEP, confirming 80 time(s) FIGURE 2. PEEP is now increased to 10 so the Pao during expiration is now 10. There is persistent flow at end-expiration, thus auto-peep is still present. TA has improved \vith one breath triggered every two to three inspiratory efforts. There is less limitation of expiratory flow, and the Peso swings are more effective in retarding the persistent expiratory flow. PIP and the Peso have increased slightly compared to Figure 1, most likely indicating a higher end-expiratory lung volume and total PEEP level. CHEST/112/6/DECEMBER,

5 i time(s) FIGURE 3. Ventilator mode is now set to pressure support of 10 em H 2 0. The patient's Peso S \ \ is ~ n g approximately 18 em H 2 0 and TA is completely eliminated. The rapid respiratory rate of 44 developed immediately, with a shallow average tidal volume of240 ml. The patient showed increasing respiratoty distress and decreased minute volume. Full ventilator support was resumed. the findings of Nava et ap 0 We also found that AI varied with level of PS, consistent with the findings of Patessio et al 8 that AI could vary from 0 to 75% in the same patient, depending on the PS level. In our patients, PS reduction was not the only maneuver capable of eliminating TA; a similar effect was observed in AC mode by reducing tidal volume. We also noted that if a spontaneous breathing trial was poorly tolerated by a patient with T A, upon resumption of full ventilatory suppmt, T A would frequently be abolished temporarily until the patient's heightened respiratory drive lessened. We found the arousal state of the patient affects AI. The asleep patient exhibiting TA may show reduced AI with arousal, as would a relaxed patient who became agitated. Therefore the respiratory drive, controlling the respiratory pump output, had profound effect on AI. Without defining all the factors influencing AI, we found its great variability lessened its usefulness as an index. Further studies are needed on the effects of respiratory mechanics and respiratmy drive on TA. Causes ofta T A occurs when inspiratory pressure is less than the trigger threshold. While the ventilator trigger Table 2-0utcome of Weaning Attempts in 19 Patients With T A on Admission to the RWC Outcome Group Weaned Failed to Wean Died 1596 n Remark Time ventilated at BRH=83:'::2l d BRH length of stay= 127::'::48 d BRH length of stay=77:<::60 d sensitivity may be very high, this "trigger" is usually a pressure transducer, located within the ventilator on either the inhalation or exhalation side of the circuit. The actual trigger threshold for the patient is the pleural pressure drop (LlPpl) generated in order to effect the pressure change at this pressure transducer. Several potential barriers exist between activation of respiratory muscles and pressure change at the transducer, which equals LlPpl only under the ideal conditions where auto-peep is 0, the exhalation valve is closed, bias flow is 0, and energy dissipation along the circuit due to system leak, compliance, and friction is negligible. Thus, either patient or ventilator factors can affect the balance behveen inspiratmy pressure and trigger threshold (Table 4). Auto-PEEP has been shown to be an important trigger threshold load in flow-limited patients, ll and consistent with this, we found auto PEEP and low Pmus to be the predominant causes ofta. Auto-PEEP and Trigger Threshold Close examination of Figures l and 2 reveals how a patient reached the effective trigger threshold every three to four efforts with 0 PEEP, and every two to three efforts with 10 cn,1 H 2 0 PEEP. The patient, subsequent to each failed effort, increased Pmus stepvvise. At the same time, continued expiration allowed end-expiratory lung volume to decrease, lowering the auto-peep. It is clear that the endexpiratory occlusion method to measure auto-peep cannot be used in these patients, since inspiratory efforts are persistent and multiple. However, we found dynamic auto-peep measurement using Peso Clinical Investigations in Critical Care

6 Table 3-A Classification of Patient-Ventilator Asynchrony Asynchrony Phase asynchrony TA Trigger and posttrigger delay Autocycling Double triggering Expiratory asynchrony (inappropriate cycling-off algorithm for PS mode, volume setting for volume-cycled mode, or!-time setting for time-cycled mode) Flow asynchrony Inadequate ("flow starvation") or excessive inspiratory flow rate Inadequate or excessive flow acceleration ("attack rate," "rise time") Inappropriate inspiratory flow profile to be problematic as well. The measurement cannot be obtained for asynchronous breaths since the Peso drop did not overcome the auto-peep and result in breath delivery. For the successfully triggered breaths, we found large variation in auto-peep between breaths. Patel and Yang 12 found that even for patients without TA, the degree of variability in dynamically measured auto-peep is high due to variability in breathing pattern. Furthermore, active expiratory muscle use is found to be prevalent in COPD patients and can substantially increase the measured auto-peep In measuring auto-peep, it is assumed that the measurement reflects the elastic recoil pressure. This assumption is violated when expiratory muscles are active, increasing either the occlusion pressure (end-expiratory occlusion technique) or the endexpiratory plateau pressure (dynamic Peso technique). There is no easy way to accurately measure the contribution of expiratory Pmus to the measured auto-peep. Appendini et al 16 suggested that the portion of Ppl change associated with gastric pressure change is due to expiratory muscle relaxation. However, this accounts only for abdominal muscles and assumes all the gastric pressure drop is due to relaxation. For the above reasons, we could not report specific and accurate auto-peep levels, but it is more important to note that auto-peep overestimation due to expiratory muscle activity does not contribute to trigger failure. As long as relaxation of expiratory muscles occurs at the onset of inspiration, as documented with needle EMG by Lessard et al,l5 it may even facilitate triggering. This is because if endexpiratory lung volume were pushed below the relaxation volume by the expiratory muscles, the thorax would expand upon relaxation of these muscles. Application of PEEP Application of external PEEP has been shown to reduce the effective triggering threshold in patients with high auto-peep,l7 and improve triggering in TA. 10 An example is found in Figure 2, showing the following: (1) 10 em H 2 0 increase in airway pressure (the applied PEEP) far exceeded the corresponding increase in Peso, which was about 3 em H 2 0; (2) smaller deflection of Peso compared to Figure 1 for the successfully triggered breaths, resulting in more triggered breaths. Thus, applying PEEP resulted in a reduction in TA secondary to reduction in auto PEEP. It is important to note that the concept of PEEP reducing auto-peep is oversimplified and is correct only if PEEP in the amount equal to the auto-peep were applied instantaneously just before the onset of every breath-an impossible scenario. In reality, PEEP is applied continuously, so it may have an effect on expiratory airflow that in turn affects the auto-peep and/or total PEEP levelj7 In a non-flow-limited patient, the expiratory flow is driven by the gradient between alveolar pressure and PEEP. Application of PEEP leads to decreased driving pressure and expiratory flow for the first breath, and higher alveolar pressure and total PEEP for all subsequent breaths. If flow limitation were present, then applying PEEP below a critical level would not decrease overall expiratory flow, nor would it increase alveolar pressure, peak inspiratory pressure (PIP), or total PEEP level. Auto-PEEP would be reduced proportionate to the increase in applied PEEP.l 8 Figure 1 shows that expiratory flow limitation was indeed present, and appears to improve \vith improved triggering after PEEP was applied (Fig 2). Table 4-Ventilator and Patient Determinants ofta Factors Ventilator factors Affecting trigger threshold Low trigger sensitivity Pressure trigger \vith a high bias flow High circuit resistance/compliance/leak Affecting auto-peep High tidal volume (either set or resulting from high PS setting) Low inspiratory flow Patient factors Affecting inspiratmy pressure Severe respiratory muscle weakness Marked hyperinflation Flail chest Affecting auto-peep High time constant High minute ventilation demand CHEST I 112 I 6 I DECEMBER,

7 However, examination of Figure 2 also shows the following: (1) auto-peep was still persistent; and (2) hyperinflation was more pronounced, evidenced by the increase in Peso and significantly higher PIP compared to Figure l. We conclude that in our flow-limited patients, although auto-peep can be reduced, it cannot be eliminated completely by applying PEEP, even at a level that leads to increased total PEEP. This finding is best explained by two hypotheses: that flow-limited and non-flowlimited pathways coexist as suggested by Marini, 19 and that auto-peep level varies between different lung regions due to time-constant inhomogeneity, which is undoubtedly true. Although applying PEEP has been shown to reduce the work of breathing by reducing threshold load, 20 we found two reasons why this maneuver was unsuccessful in resolving T A in our patients. First, as noted in the preceding paragraph, applied PEEP did not eliminate auto-peep. Equally important, we found that patients' Pmus decreased after application of PEEP. This is likely due to decreased respiratory center output, as reported by Smith and Marini, 17 who found that respiratory drive, reflected by inspiratory occlusion pressure at 0.1 s, was reduced with the application of PEEP in patients with auto-peep but without TA. However, differences in lung volume have not been specifically accounted for, raising the possibility that the decrease in Pmus might partially result from a more mechanically disadvantaged diaphragm due to higher total PEEP. Other Approaches to Decrease T A It is also not surprising that flow triggering did not eliminate T A. Diverting bias flow from the circuit is required for flow triggering. Flow cannot be diverted until alveolar pressure drops below airway pressure, ie, until auto-peep is overcome by the patient's inspiratory pressure. By similar reasoning, more sensitive transducers will not help so long as they are located within the ventilator circuit. Even tracheal pressure triggering, clearly effective in reducing the work of breathing, 21 is unlikely to be helpful in decreasing TA. Peso triggering holds the greatest promise, since changes in Peso are not directly affected by auto-peep. However, false triggering due to low signal to noise ratio is a problem with esophageal triggering. One potential solution to resolving T A is to utilize measurement of the end-expiratory flow due to the auto-peep. As noted in Figure 2, the patient's failed inspiratory efforts, while inadequate to overcome auto-peep, often retarded the expiratory flow significantly. Both first- and second-order time differ- entia! of this expiratory flow signal may be incorporated into a trigger algorithm. We found that the most effective of the methods attempted to eliminate TAwas reduction of patients' ventilatory support. We accomplished this by using PS ventilation at a relatively low support level that varied between patients. This maneuver essentially forced the patients to increase their Pmus. Patessio et al, 8 studying eight flow-limited patients with TA, found that synchronization improved from 1: 4 on PS of 25 em H 2 0 to 1: 1 on PS of 15 em H 2 0. They also noted the improvement to be a result of increased Pmus. We found that this maneuver, although successful in eliminating T A, was poorly tolerated, with development of respiratory distress in these patients. Clinical Implications Patients with TA took substantially longer to wean, and overall, had a very poor prognosis. Although we did not specifically control for age, gender, or oxygenation parameters in our analysis, we speculate that T A, as an index of the severity of obstruction and pump failure, would likely be somewhat independent of these variables in its association with poor outcome. Indexes reflecting pump and airway functions, however, may covariate with T A. Prognostically, TA may simply mark the far end of the spectrum of severity of respiratory pump failure and airflow obstruction. It is of interest to note that the three patients who weaned showed only intermittent TA (ie, they must be on the borderline of the balance between auto-peep and sustainable Pmus). Clinicians should exercise caution in applying this prognostic finding early in the ICU course, when bronchodilator and anti-infection/anti-inflammatory treatments may not have achieved maximal therapeutic effect, and many causes of acute respiratory muscle weakness would still have great potential for resolution. Yet to be investigated, as well, is whether eliminating T A itself will be of significant benefit in terms of outcome of these patients if, despite TA, they are adequately oxygenated and ventilated. CONCLUSION In patients with PMV, the observation of uncoupling of accessory respiratory muscle movement and onset of machine breaths is highly specific and probably sensitive in identifying T A. T A is associated with low respiratory pump output and high auto PEEP. Ventilator factors contribute to reduced pump output vvith high levels of ventilator support, and increased auto-peep vvith high tidal volume; patient factors include severe pump failure and expiratory airflow limitation. T A can be eliminated 1598 Clinical Investigations in Critical Care

8 by decreasing ventilator support, causing patients to increase respiratory pump output and decrease tidal volume, but this approach imposes a fatiguing load on the respiratory muscles and is poorly tolerated. TA, when it occurs in the patient in stable condition with PMV, is associated with poor outcome. ACKNOWLEDGMENT: The authors thank Catherine S. H. Sassoon, MD, for her expert and thoughtful criticism and advice in manuscript preparation. REFERENCES 1 Gurevitch M, Gelmont D. Importance of trigger sensitivity to ventilator response delay in advanced chronic obstructive pulmonary disease with respiratory failure. Crit Care Med 1989; 17: Fabry B, Guttmann J, Eberhard L, et al. An analysis of desynchronization between the spontaneously breathing patient and ventilator during inspiratory pressure support. Chest 1995; 107: Varon J, Fromm R, Rodarte J, et a!. Prevalence of patient ventilator asynchrony in critically ill patients [abstract]. Chest 1994; 106:141S 4 Scheinhorn DJ, Artinian BM, Catlin JL. Weaning from prolonged mechanical ventilation: the experience at a regional weaning center. Chest 1994; 105: Baydur A, Behraks K, Zin WA, et a!. A simple method for assessing the validity of esophageal balloon technique. Am Rev Respir Dis 1982; 126: Marini JJ. Monitoring during mechanical ventilation. Clin Chest Med 1988; 9: Hubmayr RD. Setting the ventilator. In: Tobin MJ, ed. Principles and practice of mechanical ventilation. New York: McGraw-Hill, 1994; Patessio A, Purro A, Appendini L, e t al. Patient-ventilator mismatching dming pressure support ventilation in patients with intrinsic PEEP. Am Rev Respir Dis 1994; 149:A65 9 Younes M. Patient -ventilator interaction with pressureassisted modalities of ventilatory support. Semin Respir Med 1993; 14: lo Nava S, Bruschi C, Rubini F. Respiratory response and inspirat01y effort during pressure support ventilation in COPD patients. Intensive Care Med 1995; 21: Younes M. Proportional assist ventilation and pressure support ventilation: similarities and differences. In: Marini JJ, Roussos C, eds. Ventilat01y failure (update in intensive care and emergency medicine, 15). Berlin: Springer, 1992; Patel H, Yang KL. Variability of intrinsic positive endexpiratory pressure in patients receiving mechanical ventilation. Crit Care Med 1995; 23: Ninane V, Yernault JC, de Troyer A. Intrinsic PEEP in patients with chronic obstructive pulmonal)' disease: role of expiratmy muscles. Am J Respir Crit Care Med 1993; 148: Ninane V, Rypens F, Yernault JC, et al. Abdominal muscle use during breathing in patients with chronic airflow obstruction. Am J Respir Crit Care Med 1992; 146: Lessard MR, Lofaso F, Brochard L. Expiratory muscle activity increases inhinsic positive end-expiratory pressure independently of dynamic hypetinflation in mechanically ventilated patients. Am J Respir Crit Care Med 1995; 151: Appendini L, Patessio A, Zanaboni S, et al. Physiologic effects of positive end-expiratory pressure and mask pressure support during exacerbation of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1994; 149: Smith TC, Marini JJ. Impact of PEEP on lung mechanics and work of breathing in severe airflow obstruction. J Appl Physiol 1988; 65: Gay PC, Rodarte JR, Hubmayr RD. The effect of positive expiratory pressure on isovolume flow and dynamic hyperinflation in patients receiving mechanical ventilation. Am Rev Respir Dis 1989; 139: Marini JJ. Should PEEP be used in airflow obstruction? [editorial]. Am Rev Respir Dis 1989; 140: Petrof BJ, Legare!vl, Goldberg P, et al. Continuous positive airway pressure reduces work of breathing and dyspnea during weaning from mechanical ventilation in severe chronic obstructive pulmonary disease. Am Rev Respir Dis 1990; 141: Messinger G, Banner MJ, Blanch PB, et a!. Using tracheal pressure to trigger the ventilator and control airway pressure during continuous positive aitway pressure decreases work of breathing. Chest 1995; 108: CHEST /1 12 /6 I DECEMBER,

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