Proportional Assist Ventilation and Lung Protection in Acute Respiratory Distress Syndrome: A Way Forward
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: A post-hoc analysis found that once patients were allowed to control their breathing pattern on high-level proportional assist ventilation, they continued to maintain an estimated driving pressure remarkably close to that measured during lung protective ventilation.
SOURCE: Georgopoulos D, Xirouchaki N, Tzanakis N, Younes M. Driving pressure during assisted mechanical ventilation. Is it controlled by patient brain? Respir Physiol Neurobiol 2016;228:69-75.
A post-hoc analysis of a 2008 study that compared proportional assist ventilation (PAV+) to pressure support ventilation in patients with acute respiratory failure examined 108 patients in the PAV+ arm (59% of whom had acute respiratory distress syndrome or ARDS).1 Preclinical studies have shown that animals with acute lung injury (who possess an inherently strong Hering-Breuer inspiratory-inhibitory reflex) instinctively adopt a lung-protective breathing pattern. Because the Hering-Breuer reflex is weaker in humans, the study inquired whether animal model findings are generalizable to patients with ARDS. Baseline chest mechanics were measured during both controlled mechanical ventilation (CMV) and during PAV+. The focus was plateau pressure (PPLAT) and the elastic driving pressure (∆P = PPLAT – positive-end expiratory pressure or PEEP), which was recently shown to be a robust mortality predictor.2 Although patients increased their tidal volume (VT) on PAV+, they maintained almost identical PPLAT and ∆P as during CMV. When chest compliance measured on PAV+ was lower than on CMV, patients modestly increased their VT (~ 0.6-0.8 mL/kg). Moreover, a higher ∆P during CMV was associated with subsequent decreased PAV+ support (and vice versa), signifying decreased breathing effort at higher loads and suggesting neuromuscular load adaptation.
Beyond these intriguing results is their application to the practical problem regarding the management of patients recovering from ARDS. That is, how best to manage competing, often contradictory, issues that negatively affect patient outcomes. These include maintaining lung protection, preventing respiratory muscle fatigue, and ameliorating dyspnea and asynchrony, while minimizing sedation to expedite weaning. This study suggests that PAV+, a closed-loop, within-breath form of pressure support ventilation, may provide the best approach to solve this conundrum.
PAV+ provides a clinician-set level of the total work of breathing performed by the patient, based on instantaneous measurements of flow and volume change integrated with real-time estimations of total elastic and resistive ventilatory work. It can be thought of as “pressure support with power steering,” such that increases or decreases in muscle pressure is met with a proportional increase or decrease in pressure support. Therefore, this mode is contraindicated both in those with respiratory muscle weakness and in those in the acute phase of severe respiratory failure. The patients in this study were clearly in the recovery phase (i.e., median PEEP, fraction of inspired oxygen [FiO2], and minute ventilation of 6 cm H2O, 0.40, and 9.9 L/minute, respectively). In addition, the median chest compliance on CMV, PPLAT, and PaO2/FiO2 ratio were 44 mL/cm H2O, 18 cm H2O, and 215 mmHg, respectively.
Nonetheless, PAV+ with relatively higher PEEP remains a plausible strategy in stable patients with ARDS who remain ventilator dependent, particularly those with abnormal chest wall compliance. Often, these patients have stable gas exchange on reasonable settings (e.g., PEEP/FiO2 ~ 10 cmH2O/< 0.60), yet they cannot tolerate pressure support ventilation low enough to limit stretch-related injury and avoid acute muscle fatigue, nor can they tolerate CMV with a protective VT without requiring generous sedation to control asynchrony and dyspnea.
Finally, it’s unclear whether apparent autoregulation of ∆P actually signifies neural control of stretch in this setting. During brief periods of unassisted breathing, ventilator-dependent ARDS patients generate muscle pressures approximating the cutoff point for increased mortality risk (16.5 vs. 15 cm H2O, respectively) while limiting VT to 4-5 mL/kg.2,3 However, this merely may reflect an adaptive strategy to avoid respiratory muscle injury when chest elastance is high as originally proposed by Otis’ theory of minimal work. Both inspiratory muscle fatigue and dyspnea occur when inspiratory muscle pressure exceeds approximately 50% of maximal force generating capacity. Thus, this level of muscle pressure or ∆PAV+ may only reflect adaptation in the face of incipient muscle fatigue. Regardless, PAV+, if not misapplied, may become an important tool in the armamentarium in managing ARDS and should be studied in prospective clinical trials.
- Xirouchaki N, Kondili E, Vaporidi K, et al. Proportional assist ventilation with load-adjustable gain factors in critically ill patients: Comparison with pressure support. Intensive Care Med 2008;34:2026-2034.
- Amato MB, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med 2015;372:747-755.
- Kallet RH, Hemphill JC, Dicker RA, et al. Spontaneous breathing pattern and work of breathing of patients with acute respiratory distress syndrome and acute lung injury. Respir Care 2007;52:989-995.
A post-hoc analysis found that once patients were allowed to control their breathing pattern on high-level proportional assist ventilation, they continued to maintain an estimated driving pressure remarkably close to that measured during lung protective ventilation.
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