Pressure support ventilation in tetraplegia

Abstract

Editor'I read with interest the case reports describing an apparent failure of flow triggering when using pressure support ventilation (PSV) for two patients with high cervical cord lesions.1Kannan S Sherwood N Armfield A Flow-by induced hypoventilation in high spinal cord lesions'report of two cases.Br J Anaesth. 2002; 89: 512-514Abstract Full Text PDF PubMed Google Scholar Case 1 involved a 66-yr-old man with an odontoid fracture, managed with halo stabilization. Using the Puritan Bennett 7200 with inspiratory pressure support of 16 cm H2O and 7.6 cm H2O PEEP, the initial inspiratory pressure support trigger was pressure dependent, set at 0.5 cm H2O. It had been noted the patient was unable to trigger at a sensitivity of 1.0 cm H2O. A trial of flow triggering (using ‘flow-by’) at basal flow 5 and trigger 3 litre min−1 resulted in a fall in respiratory rate from 25 bpm to 14 bpm. We are not told the corresponding tidal volume but that the vital signs were unchanged, the patient appeared comfortable and oxygenated, and no evidence of accessory muscle activity was apparent. ‘An error in the flow-by settings was suspected’, but it is not clear why? I would be surprised if this machine was not in working order when it was checked after this critical incident. This patient had advanced and profound weakness with complete tetraparesis'the requirement of a 0.5 cm H2O pressure trigger is evidence of this. Flow-by and flow triggering generally were originally devised to meet the initial inspiratory ‘gas demand’ of a dyspnoeic patient, and reduce the possible time delay to effective inspiratory pressure support delivery.2Sykes K Young JD Modern ventilator technology.in: Hahn CEW Adams AP Respiratory Support in Intensive Care. BMJ, London1999: 263-266Google Scholar Whether it achieves this or not remains controversial, with a number of conflicting studies, as referenced in this report. However, having noted a failure to trigger at 1.0 cm H2O, the authors then tried a flow trigger of 3 litre min−1: this is probably closer to an equivalent 1.0 cm H2O pressure trigger rather than the 0.5 cm H2O hoped for, especially as no triggering was observed.3Goulet R Hess D Kacmarek RM Pressure vs flow triggering during pressure support ventilation.Chest. 1997; 111: 1649-1653Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar 4Hill LL Pearl RG Flow triggering, pressure triggering, and autotriggering during mechanical ventilation.Crit Care Med. 2000; 28: 579-581Crossref PubMed Scopus (55) Google Scholar The patient was effectively moved to a higher trigger setting on flow-by and so it should be no surprise if triggering ‘failed’, but this is a direct consequence of patient weakness, not ventilator failure. The authors then increased the base flows up to 20 litre min−1, with no change. This is not surprising'the base flow is largely irrelevant if the patient is too weak to even reach the trigger flow. This is not a patient with a high initial inspiratory flow requirement, potentially left ‘gasping’ by using a pressure trigger. The authors note that their second patient with an epidural abscess at C2–C4, could trigger at 1 litre min−1 and conclude ‘…it is likely the first patient could have responded in the same way’. Why was 1 litre min−1 not tried? A poorly set up ventilator is the fault of the clinician, and the title ‘Flow-By Induced Hypoventilation…’, implying ventilator failure, is misleading. I suspect that if like was compared with like, i.e. pressure trigger of 0.5 cm H2O vs flow trigger 1–2 litre min−1, little difference would have been found. I am left wondering what the desired effect of flow-by was in this patient and why the pressure trigger was ever changed; we are told this was an ‘assessment’ of the patient's ability to trigger the ventilator. A patient with neuromuscular weakness is unlikely to require high initial flows and the initial trigger, set at 0.5 cm H2O, appeared appropriate to the authors. I am also concerned about using the PSV mode for this patient. We are told that the patient suffered an odontoid fracture (C1/C2) with clinical involvement at least from below the C3 dermatome. The intercostal muscles will not therefore function and both phrenic nerves/hemidiaphragms are likely to be impaired. There is likely to be no respiratory innervation and therefore no facility for triggering inspiratory pressure support. This patient needs a more complete assessment. It is imperative to demonstrate diaphragmatic function/innervation with this C1–C3 lesion if PSV is to be used, otherwise triggering is impossible. In Case 2, we are told that ultrasonography revealed reduced diaphragmatic movements. The deficiencies of this particular imaging technique for this purpose are alluded to in the accompanying editorial,5Watt JWH Pressure support ventilation and the critically ill patient with muscle weakness.Br J Anaesth. 2002; 89: 373-375Abstract Full Text PDF PubMed Google Scholar but the patient was also observed making weak respiratory efforts on an (excessively) high set flow trigger. This is at least compatible with the potential to trigger. In contrast, Case 1 may well have a ‘disconnected’ diaphragm and chest wall. Electromyography, diaphragmatic fluoroscopy or even a Wright's respirometer should have been employed to determine the possibility of triggering, particularly when no respiratory efforts were noted. No diaphragm innervation makes pressure support ventilation meaningless'and one is left speculating as to what was triggering the ventilator on either trigger setting. Was false triggering (e.g. transmitted pulsations) on a low pressure trigger at 25 bpm erroneous, and the rate of 14 bpm on a higher flow trigger nearer the endogenous neural rhythm, particularly if the patient appears comfortable and oxygenated on these settings? Finally, I am concerned by one small detail that makes a huge difference'the PEEP setting. We have established that this patient's weakness prevented triggering above 0.5 cm H2O. Expiration at rest is a passive phenomenon, but during exercise (and possibly a trial of inappropriate trigger settings) this can become active, because of abdominal musculature contraction'not an option in tetraparesis. Patients cannot be expected to exhale against +7.6 cm H2O PEEP if they cannot generate –0.5 cm H2O inspiratory trigger pressure. What was the indication for this excessive level of PEEP? Was it poor oxygenation; which is unlikely if the FIO2 was only 0.35. A more appropriate measure would be to increase the FIO2 slightly, accepting a mechanical benefit for reduced oxygenation. Or was it recruitment of atelectatic lung? This is again inappropriate as tetraparesis reduces FRC to a significant degree. Including occasional mandatory breaths (or specifically using the ‘automatic sigh’ facility on the Puritan Bennett 7200) would achieve recruitment, as would physiotherapy. PEEP is a therapy titrated to end points of oxygenation and lung recruitment, and has the potential to cause harm. I would argue that PEEP much above physiological levels (>2.5 cm H2O) for patients with severe weakness is probably counterproductive and incompatible with PSV. Case 2 was also managed with 5 cm H2O PEEP while unable to tolerate an inspiratory trigger above 0.5 cm H2O. These levels of PEEP, for patients with no active expiration, will produce air trapping, closing the total thoracic pressure/volume ratio (compliance) to a less favourable level, requiring elevated inspiratory pressure support, and producing chronic lung hyperexpansion with associated baro/volutrauma, cardiovascular and neuroendocrine responses. The role of abdominal supports/splinting in aiding expiration for tetraplegia is often overlooked. The excellent accompanying editorial mentions the problems that may affect inspiratory/expiratory cycling with PSV and the consequences thereof.5Watt JWH Pressure support ventilation and the critically ill patient with muscle weakness.Br J Anaesth. 2002; 89: 373-375Abstract Full Text PDF PubMed Google Scholar While high intrinsic PEEP is mentioned, extrinsic PEEP (which may produce the former) is not. When we set up ventilators we would do well to consider each setting and its consequences. The recent ARDS Network trial6ARDS Network Investigators Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.N Engl J Med. 2000; 342: 1301-1308Crossref PubMed Scopus (10080) Google Scholar is a good example of the morbidity and mortality that an inappropriately set up ventilator will cause. Curiously, in neither article is mention made of volume support as an alternative to inspiratory pressure support for patients with inadequate inspiratory efforts. I think pressure and flow triggering were probably both applicable for these two patients had they been set ‘equally’. I presume no faults were subsequently found on either ventilator. The odontoid fracture patient required evaluation of their diaphragm function. In both patients, inappropriately high levels of PEEP were used, for no clear reason. Editor'Thank you for the opportunity to reply to Dr Morris. The purpose of these case reports was to demonstrate that small changes in trigger sensitivity settings could be significant in patients with severe muscle weakness. Studies assessing the various trigger modes and settings have shown that the time differences between them are in the range of milliseconds. In one study, the difference in the mean triggering time between a trigger sensitivity setting of 0.5 cm H2O and 3 litre min−1 was 17 ms (0.017 s).3Goulet R Hess D Kacmarek RM Pressure vs flow triggering during pressure support ventilation.Chest. 1997; 111: 1649-1653Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar The difference between a trigger sensitivity of 1 cm H2O and 3 litre min−1 was 12 ms (0.012 s). We are not sure how many intensivists are aware of these tiny differences. In practice, for most patients, it does not matter whether the flow sensitivity is 2 litre min−1 or 3 litre min−1. We wanted to emphasize the point that even the ‘default’ trigger setting of 3 litre min−1 in ventilators such as the Puritan Bennett 7200 can prove to be ‘too much’ for patients with severe muscle weakness. We suspect that the purpose of having such default setting in these ventilators was to avoid the possibility of ‘autotriggering’. We did not intend to blame the ventilator for the hypoventilation in these patients. If the patient fails to trigger the ventilator, there can be several other reasons apart from failure of the machine, which is unusual if it has undergone the preoperational checks. As to his query regarding the first patient not being put on a flow sensitivity of 1 litre min−1, it was not done so because, at that time, it was not suspected that the flow sensitivity was the reason for failure to trigger. These two patients presented about two months apart. When the second patient also failed to trigger the ventilator at the default flow sensitivity, a more sensitive trigger setting was tried. The decision to change over to flow sensitivity was taken since a pressure sensitivity setting of 0.5 cm H2O carried the perceived risk of autotriggering,7Willatts SM Drummond G Brain stem death and ventilator trigger settings.Anaesthesia. 2000; 55: 676-677Crossref PubMed Scopus (42) Google Scholar and the fact that the patient was unable to trigger the ventilator at a trigger sensitivity of 1 cm H2O. Dr Morris questions the suitability of using pressure support ventilation in the first patient. This patient was quadriparetic when he was first admitted to the hospital, but lost all motor power in his limbs subsequently. The patient was able to trigger the ventilator when pressure support ventilation was first attempted with no evidence of autotriggering. The switch from pressure sensitivity to flow sensitivity settings used at that time led to the ‘hypoventilation’ because of failure to trigger. The time duration of flow sensitivity settings was not continued beyond a couple of minutes for obvious reasons. This was possibly not long enough for the patient to exhibit discomfort or desaturation, especially when there was some ventilation of the lungs occurring. As regards the positive end expiratory pressure (PEEP) settings, the intention was to prevent atelectasis rather than alveolar recruitment. Alveolar recruitment generally needs a PEEP of 10 cm H2O or more.8Shapiro BA Cane RD Harrison RA Positive end expiratory pressure therapy on adults with special reference to acute lung injury: a review of the literature and suggested clinical correlations.Crit Care Med. 1984; 12: 127-141Crossref PubMed Scopus (92) Google Scholar The first patient had required a high inspired oxygen concentration during the preceding three weeks and the PEEP was being gradually brought down. Dr Morris has expressed concern about the possible complications of PEEP in these patients. If these patients did not have adequate expiration, auto-PEEP would have been inevitable. There was no evidence of this in either of these patients as seen on the ventilator graphic waveforms. Volume support was the back up mode for these patients in the event of pressure support failure. The inadequate inspiratory efforts were noted only during the trial of flow sensitivity settings and not otherwise. Hence, pressure support ventilation was continued in both patients. We do not think that the ventilatory management in these two patients was inappropriate at any stage. Weaning quadriplegic patients from ventilatory support is a challenging task, probably best done in specialist centres, which may be more familiar with the triggering issues we have highlighted. However, because of service constraints, many patients similar to the two cases we have reported will continue to be cared for in non-specialist critical care units throughout the country. S. Kannan N. Sherwood Birmingham, UK