BACKGROUND Improper mechanical ventilation can exacerbate acute lung damage causing a secondary ventilator induced lung injury (VILI). We hypothesize that VILI can be reduced by modifying specific components of the ventilation waveform (mechanical breath) and studied the impact of airway pressure release ventilation (APRV) and controlled mandatory ventilation (CMV) on the lung micro-anatomy (alveoli and conducting airways). The distribution of gas during inspiration and expiration and the strain generated during mechanical ventilation in the micro-anatomy (micro-strain) were calculated. STUDY DESIGN Rats were anesthetized, surgically prepared and randomized into one uninjured Control group (n=2) and four groups with lung injury: 1)APRV 75% (n=2)–time at expiration (TLow) set to terminate appropriately at 75% of Peak Expiratory Flow Rate (PEFR); 2)APRV 10% (n=2)-TLow set to terminate inappropriately at 10% of PEFR; 3)CMV with PEEP 5cmH2O (PEEP 5;n=2) or 4)PEEP 16cmH2O (PEEP 16;n=2). Lung injury was induced in the experimental groups by Tween lavage and ventilated with their respective settings. Lungs were fixed at peak inspiration and end expiration for standard histology. Conducting airway and alveolar air space areas were quantified and conducting airway micro-strain calculated. RESULTS All lung injury groups redistributed inspired gas away from alveoli into the conducting airways. APRV 75% minimized gas redistribution and micro-strain in the conducting airways and provided the alveolar air space occupancy most similar to Control at both inspiration and expiration. CONCLUSIONS In an injured lung, APRV 75% maintained micro-anatomical gas distribution similar to that of the normal lung. The lung protection demonstrated in previous studies using APRV 75% may be due to a more homogeneous distribution of gas at the micro-anatomical level as well as a reduction in conducting airway micro-strain.

Airway pressure release ventilation (APRV) was first described in 1987 and defined as continuous positive airway pressure (CPAP) with a brief release while allowing the patient to spontaneously breathe throughout the respiratory cycle. The current understanding of the optimal strategy to minimize ventilator-induced lung injury is to “open the lung and keep it open”. APRV should be ideal for this strategy with the prolonged CPAP duration recruiting the lung and the minimal release duration preventing lung collapse. However, APRV is inconsistently defined with significant variation in the settings used in experimental studies and in clinical practice. The goal of this review was to analyze the published literature and determine APRV efficacy as a lung-protective strategy. We reviewed all original articles in which the authors stated that APRV was used. The primary analysis was to correlate APRV settings with physiologic and clinical outcomes. Results showed that there was tremendous variation in settings that were all defined as APRV, particularly CPAP and release phase duration and the parameters used to guide these settings. Thus, it was impossible to assess efficacy of a single strategy since almost none of the APRV settings were identical. Therefore, we divided all APRV studies divided into two basic categories: (1) fixed-setting APRV (F-APRV) in which the release phase is set and left constant; and (2) personalized-APRV (P-APRV) in which the release phase is set based on changes in lung mechanics using the slope of the expiratory flow curve. Results showed that in no study was there a statistically significant worse outcome with APRV, regardless of the settings (F-ARPV or P-APRV). Multiple studies demonstrated that P-APRV stabilizes alveoli and reduces the incidence of acute respiratory distress syndrome (ARDS) in clinically relevant animal models and in trauma patients. In conclusion, over the 30 years since the mode’s inception there have been no strict criteria in defining a mechanical breath as being APRV. P-APRV has shown great promise as a highly lung-protective ventilation strategy.

Increasing PEEP during LTVV increased alveolar recruitment and dynamic homogeneity but had a significantly different alveolar size distribution compared with the control group. By comparison, reducing the time at low pressure (EEFR to PEFR ratio of 75%) in the APRV group provided dynamic homogeneity and a closer approximation of the dynamics observed in the control group.

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Increased positive-end expiratory pressure and reduced time at low pressure (decreased T(low)) reduced alveolar microstrain. Reduced microstrain and improved alveolar recruitment using an APRV T-PEFR to PEFR ratio of 75% may be the mechanism of lung protection seen in previous clinical and animal studies.