Issues in Ventilator Weaning

system. Examples include volutrauma, cardiac compromise, muscle overload, patient discomfort (and thus continued sedation need), and infection risk. I think it is clear that while good management may not reverse lung disease, bad management can surely worsen it. The focus of clinical attention must include ventilator management during this recovery phase of illness. Second, the authors suggest that in patients failing a liberation trial, subsequent ventilator management could involve any mode or setting “as long as the patient gets adequate rest.”1 Clearly, excessive muscle loading from inadequate ventilatory support can delay recovery and prolong the need for mechanical ventilation. Total muscle rest, however, may not be optimal either. Unlike skeletal muscles, ventilatory muscles (much like cardiac muscles) were never designed to rest. Indeed, there is evidence that only a few days of controlled ventilation can produce muscle dysfunction2 and that near total muscle unloading (as compared to normal loading) may delay fatigue recovery.3 This suggests that perhaps the clinical goal should be focused on near normal muscle loading rather than complete rest. In this regard, partial support modes that can normalize muscle loading by providing variable flows and a continuous pressure bias (eg, pressure support, pressure assist, proportional assist) would seem preferable to fixed flow volume assist-control breaths. Third, as the authors point out, intrinsic positive end-expiratory pressure (PEEP) from airflow limitation can clearly function as a significant inspiratory threshold load and thereby has the potential to delay muscle recovery. Applied circuit PEEP can be helpful in reducing this load, but determining the appropriate amount can be difficult. Manthous and colleagues1 suggest analysis of the flow graphic and use of the expiratory hold maneuver. Unfortunately, in flow-limited patients, expiratory flow may be so slow that incomplete emptying may not be detectable. In addition, the expiratory hold maneuver is often impossible to perform in patients attempting to trigger ventilator breaths. I would therefore suggest that clinicians instead learn to recognize the intrinsic PEEP phenomenon by observing a time delay between ventilatory muscle activity (chest motion or accessory muscle contraction) and either the drop in airway pressure detected by the ventilator or the change in ventilator circuit flow. If clinically indicated, an esophageal pressure tracing can be used to specifically measure this imposed load and guide application of circuit PEEP. It is clear, as Manthous and colleagues point out, that daily assessment for liberation potential is important to do. In the patients who fail to meet liberation criteria, however, it is equally important to manage them properly for the next 24 h until the next liberation assessment can be done. Neil R. MacIntyre, MD, FCCP Duke University Hospital Durham, NC Correspondence to: Neil R. MacIntyre, MD, FCCP, Duke University Medical Center, Respiratory Care Services, Box 3911, Durham, NC, 27710; e-mail: [email protected]

References 1 Manthous CA, Schmidt GA, Hall JB. Liberation from mechanical ventilation: a decade of progress. Chest 1998; 114: 886 –901 2 Anzueto A, Peters JI, Tobin MJ, et al. Effects of prolonged controlled mechanical ventilation on diaphragmatic function in healthy adult baboons. Crit Care Med 1997; 25:1187–1190 3 Uchiyama A, Imanaka H, Nishimura M, et al. Effects of pressure-support ventilation on recovery from acute diaphragmatic fatigue in rabbits. Crit Care Med 1998; 26:1225– 1230 1216

To the Editor: The authors of “Liberation From Mechanical Ventilation: A Decade of Progress”1 would like to thank Dr. MacIntyre for his comments. Regarding his first point, we agree that clinical attention should focus on ventilator management throughout the ventilated course, and we recognize that poor ventilator management can do great harm. Our aim was to emphasize that the solutions to most of the clinician’s questions, (ie, Why is the patient still on a ventilator?) and most of the patient’s problems, ie, shortness of breath, lie within the patient, not the ventilator. We are struck by how frequently doctors think they can free patients from their ventilators by adjusting the machine, while the pathophysiologic processes which cause ventilator dependence remain undefined and untreated. It is our approach to restore the normally compensated balance between respiratory load and neuromuscular competence in the patient, since it is then that the ventilator becomes unnecessary. The role of rest and exercise of the respiratory muscles in mechanically ventilated patients is complex and controversial. We, too, believe that complete rest may lead to dysfunction, although the baboon study cited2 involved continuous muscle relaxation with pancuronium, a drug commonly associated with weakness. The delayed recovery from fatigue in rabbits who were ventilated is interesting and may point to the value of some level of exercise,3 but even the concept of diaphragm fatigue may not pertain to human ventilatory failure. We await additional studies before we can recommend specific strategies for muscle conditioning. Finally, there is no question that intrinsic positive end-expiratory pressure (PEEP) can be very difficult to detect unless flow waveforms are continuously displayed. In a study recently completed by one of us, we were able to quantify the amount of intrinsic PEEP using the end-expiratory occlusion technique in only 30% of all ventilated patients in whom it was present.4 Further, as suggested by Dr. MacIntyre, we confirmed that the clinical examination is very useful in detecting the presence of intrinsic PEEP. In our practice of patients ventilated for exacerbations of COPD, we generally apply 7 to 10 cm H2O extrinsic PEEP when our goal is to reduce the work of triggering, adjusting this value based on shortening of the time delay between obvious patient effort and onset of the ventilator breath, but have not sought to validate this approach. Constantine A. Manthous, MD, FCCP Yale University School of Medicine Bridgeport, CT Gregory A. Schmidt, MD, FCCP Jesse B. Hall, MD, FCCP University of Chicago Chicago, IL Correspondence to: Constantine A. Manthous, MD, FCCP, Bridgeport Hospital, West Tower 6, 267 Grant Street, Bridgeport, CT 06610-2870; e-mail: [email protected]

References 1 Manthous CA, Schmidt GA, Hall JB. Liberation from mechanical ventilation: a decade of progress. Chest 1998; 114: 886 –901 2 Anzueto A, Peters JI, Tobin MJ, et al. Effects of prolonged controlled mechanical ventilation on diaphragmatic function in healthy adult baboons. Crit Care Med 1997; 25:1187–1190 3 Uchiyama A, Imanaka H, Nishimura M, et al. Effects of pressure-support ventilation on recovery from acute diaphragmatic fatigue in rabbits. Crit Care Med 1998; 26:1225– 1230 4 Kress JP, O’connor MF, Schmidt GA. Clinical examination reliably detects intrinsic positive end-expiratory pressure in critically ill, mechanically ventilated patients. Am J Respir Crit Care Med 1999; 159:290 –294 Communications to the Editor