Mechanical Breath Profile of Airway Pressure Release Ventilation

Abstract

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.

The role of high airway pressure and dynamic strain on ventilator-induced lung injury in a heterogeneous acute lung injury model

“…2) vs a set PEEP in clinically relevant animal models of ARDS resulted in superior gas exchange, compliance, surfactant preservation, less microstrain, and reduced lung inflammatory and histopathology injury. In particular, the histology showed significantly less atelectasis in the time-controlled PEEP vs set PEEP as well as less edema and intra-alveolar debris and alveolar septal thickening [13, 14, 38–41]. …”

“…A difference of only 0.67 s expiratory time raised the end-expiratory pressure (EEP) from 3.0 ± 1.2 (25%) to 12.9 ± 2.7 (75%) cmH 2 O (Table 2, EEP, T6). We postulate that this time-controlled PEEP, combined with an expiratory duration less than the collapse time constant of the alveolus [35], works additively or synergistically to stabilize the lung and prevent alveolar collapse and reopening [13, 14, 38]. Better lung inflation was suggested in the group with the PEF/EEF ratio set at 75% as an increase in the P/F ratio and PO 2 at a lower FiO 2 , fall in lung elastance over time (Table 2), and improved gross lung (Fig.…”

“…ARDS causes a more rapid lung collapse due to decreased lung compliance. Our preliminary studies have shown that if the ratio of the peak expiratory flow (PEF, 60 L/min) to the end-expiratory flow (EEF, 45 L/min) (EEF/PEF) is equal to 75%, this expiratory duration (0.5 s) is sufficiently brief to stabilize alveoli [14, 38]. The lung with ARDS collapses more rapidly such that the EEF/PEF of 75% identifies a shorter expiratory duration of 0.45s is necessary to stabilize alveoli.…”

“…However, this can be arduous, when in the heterogeneous lung there is both normal tissue (N T ) and acutely injured lung tissue (ALI T ), which must be ventilated with a single mechanical breath. In the heterogeneous lung, airway pressure must be sufficient to open alveoli with altered surfactant or edema, without causing over-distension of normal alveoli [14]. …”

Physiology in Medicine: Understanding dynamic alveolar physiology to minimize ventilator-induced lung injury

“…The failure of HFOV to reduce mortality may be due to a misdistribution of ventilation in the heterogeneously injured lung (29). A very specific strategy of personalized APRV (30) has been shown to be effective at stabilizing alveoli (35,36) and protecting from the development of ARDS in a clinically applicable porcine model (34,51,52). In a meta-analysis this personalized APRV strategy significantly reduced ARDS incidence and mortality in a surgical intensive care unit (8), but it has not been tested in a prospective clinical trial.…”