By Richard Kallet, MS, RRT, FAARC, FCCM
Director of Quality Assurance, Respiratory Care Services, San Francisco General Hospital
Mr. Kallet reports no financial relationships relevant to this field of study.
SYNOPSIS: Although pressure-controlled ventilation (PCV) and volume-controlled ventilation (VCV) approach mechanical breath delivery differently in terms of inspiratory flow and airway pressure characteristics, this comprehensive review found no significant differences in terms of their impact on breathing mechanics or gas exchange in patients with various forms of acute respiratory failure.
SOURCE: Rittayamai N, et al. Pressure-controlled vs volume-controlled ventilation in acute respiratory failure: A physiology-based narrative and systematic review. Chest 2015 Apr 30 [Epub ahead of print].
The study was divided into two parts: 1) a concise description of the working principles of pressure-controlled ventilation (PCV) and volume-controlled ventilation (VCV) modes, and 2) a comprehensive review of the literature. In the first section, the authors reviewed how each breath delivery style functions during both continuous mechanical ventilation (CMV) and partial support modes, such as synchronized intermittent mandatory ventilation (SIMV). In the systematic review, the authors de-limited the search to studies that directly compared modes in critically ill patients with various causes of acute respiratory failure and reported data on respiratory system compliance (Crs), patient work of breathing (WOB), gas exchange, hemodynamics, and patient outcomes. Thirty-four studies met inclusion criteria and included 880 patients using random effects models. Approximately half of these patients had acute respiratory distress syndrome (ARDS). In general, the studies were small, varied widely in terms of quality, and were at high risk for bias.
No statistically significant differences were found between modes in their effects on Crs, oxygenation, ventilation efficiency, hemodynamics, mortality, or ICU length of stay. The only difference distinguishing these modes was a reduction in patient WOB during PCV, and this result was limited to situations when the peak inspiratory flow rate was lower during VCV. The authors concluded that the choice of ventilator mode should be based on the clinical context and focused almost exclusively on whether the impact of patient-ventilator asynchrony on patient WOB was problematic. There was no compelling evidence that the inspiratory flow pattern itself impacts gas exchange in any clinically meaningful way.
This study is a welcome contribution to the medical literature, as it provides an elegant and masterful description of mechanical ventilation as well as a comprehensive review of the impact of ventilator modes. My own research on the effects of PCV and VCV was piqued by my experiences in the early years of the AIDS epidemic. By the fall of 1981, our medical ICU consisted almost entirely of young men suffering from pneumocystis pneumonia managed with the only modes available at the time: VC-CMV or VC-SIMV. I vividly recall these young men writing detailed notes about their breathing sensations.
Despite tailoring their settings according to their feedback, the improvement in synchrony was at best ephemeral. In April 1982, we purchased our first ventilator with PCV and PSV. Despite a complete lack of evidence, we were desperate to try anything. The positive impact of these modes was immediately noticeable.
The important lessons learned over the past 30 years can be distilled down to the following: First, patient demand for flow and tidal volume reflects the velocity and shortening of the inspiratory muscles. Any mismatch between demand and ventilator performance imposes additional tension on the inspiratory muscles that induces or magnifies dyspnea. Second, the natural response to dyspnea and increased WOB is increase respiratory drive and includes abdominal muscle recruitment to enhance inspiratory muscle performance. Third, the resulting large negative and positive cyclical changes in pleural pressure exaggerate gas exchange dysfunction by enhancing alveolar edema formation on inspiration and derecruitment during expiration. Fourth, the humane impulse to let patients dictate their breathing pattern or use generous amounts of sedation to control breathing are both problematic, as they paradoxically worsen patient outcomes.
The most helpful guide is to place asynchronous patients on a brief trial of continuous positive airway pressure to assess their ventilator demand. This provides immediate feedback about whether satisfying a patient’s ventilatory demand significantly increases the risk of ventilator-induced lung injury. It also allows for assessing whether increasing sedation or using paralytics presents even greater risks. Oversedation is often due to an inadequate evaluation of analgesic needs. It is important to emphasize that breathing patterns also express emotional states and bodily sensations.
Moreover, moderately increased WOB and mild asynchrony generally are well tolerated, and therefore, do not necessarily require optimization in those with stable gas exchange or in those not at risk for muscle fatigue. Optimal synchronization and guaranteeing passive ventilation is likely to impact outcomes only during the acute phase among the most critically ill, unstable patients.
Balancing lung protection and sedation are crucial. Modes are of secondary importance in dealing with patient-ventilator asynchrony. It behooves ICU clinicians to possess both an in-depth understanding of the physiology, mechanics, and proprioceptive aspects of the problem and the wisdom to know what context requires meticulous attention to optimizing patient-ventilator asynchrony.