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Background Ventilator-associated pneumonia (VAP) is the most common nosocomial infection in intensive care units. Distal airway mucus clearance has been shown to reduce VAP incidence. Studies suggest that mucus clearance is enhanced when the rate of expiratory flow is greater than inspiratory flow. The time-controlled adaptive ventilation (TCAV) protocol using the airway pressure release ventilation (APRV) mode has a significantly increased expiratory relative to inspiratory flow rate, as compared with the Acute Respiratory Distress Syndrome Network (ARDSnet) protocol using the conventional ventilation mode of volume assist control (VAC). We hypothesized the TCAV protocol would be superior to the ARDSnet protocol at clearing mucus by a mechanism of net flow in the expiratory direction. Methods Preserved pig lungs fitted with an endotracheal tube (ETT) were used as a model to study the effect of multiple combinations of peak inspiratory (IPF) and peak expiratory flow rate (EPF) on simulated mucus movement within the ETT. Mechanical ventilation was randomized into 6 groups (n = 10 runs/group): group 1—TCAV protocol settings with an end-expiratory pressure (PLow) of 0 cmH2O and PHigh 25 cmH2O, group 2—modified TCAV protocol with increased PLow 5 cmH2O and PHigh 25 cmH2O, group 3—modified TCAV with PLow 10 cmH2O and PHigh 25 cmH2O, group 4—ARDSnet protocol using low tidal volume (LTV) and PEEP 0 cmH2O, group 5—ARDSnet protocol using LTV and PEEP 10 cmH2O, and group 6—ARDSnet protocol using LTV and PEEP 20 cmH2O. PEEP of ARDSnet is analogous to PLow of TCAV. Proximal (towards the ventilator) mucus movement distance was recorded after 1 min of ventilation in each group. Results The TCAV protocol groups 1, 2, and 3 generated significantly greater peak expiratory flow (EPF 51.3 L/min, 46.8 L/min, 36.8 L/min, respectively) as compared to the ARDSnet protocol groups 4, 5, and 6 (32.9 L/min, 23.5 L/min, and 23.2 L/min, respectively) (p

Background Acute respiratory distress syndrome causes a heterogeneous lung injury with normal and acutely injured lung tissue in the same lung. Improperly adjusted mechanical ventilation can exacerbate ARDS causing a secondary ventilator-induced lung injury (VILI). We hypothesized that a peak airway pressure of 40 cmH2O (static strain) alone would not cause additional injury in either the normal or acutely injured lung tissue unless combined with high tidal volume (dynamic strain). Methods Pigs were anesthetized, and heterogeneous acute lung injury (ALI) was created by Tween instillation via a bronchoscope to both diaphragmatic lung lobes. Tissue in all other lobes was normal. Airway pressure release ventilation was used to precisely regulate time and pressure at both inspiration and expiration. Animals were separated into two groups: (1) over-distension + high dynamic strain (OD + HDS, n = 6) and (2) over-distension + low dynamic strain (OD + LDS, n = 6). OD was caused by setting the inspiratory pressure at 40 cmH2O and dynamic strain was modified by changing the expiratory duration, which varied the tidal volume. Animals were ventilated for 6 h recording hemodynamics, lung function, and inflammatory mediators followed by an extensive necropsy. Results In normal tissue (NT), OD + LDS caused minimal histologic damage and a significant reduction in BALF total protein (p

It has been shown that mechanical ventilation in patients with, or at high-risk for, the development of acute respiratory distress syndrome (ARDS) can be a double-edged sword. If the mechanical breath is improperly set, it can amplify the lung injury associated with ARDS, causing a secondary ventilator-induced lung injury (VILI). Conversely, the mechanical breath can be adjusted to minimize VILI, which can reduce ARDS mortality. The current standard of care ventilation strategy to minimize VILI attempts to reduce alveolar over-distension and recruitment-derecruitment (R/D) by lowering tidal volume (Vt) to 6 cc/kg combined with adjusting positive-end expiratory pressure (PEEP) based on a sliding scale directed by changes in oxygenation. Thus, Vt is often but not always set as a “one-size-fits-all” approach and although PEEP is often set arbitrarily at 5 cmH2O, it may be personalized according to changes in a physiologic parameter, most often to oxygenation. However, there is evidence that oxygenation as a method to optimize PEEP is not congruent with the PEEP levels necessary to maintain an open and stable lung. Thus, optimal PEEP might not be personalized to the lung pathology of an individual patient using oxygenation as the physiologic feedback system. Multiple methods of personalizing PEEP have been tested and include dead space, lung compliance, lung stress and strain, ventilation patterns using computed tomography (CT) or electrical impedance tomography (EIT), inflection points on the pressure/volume curve (P/V), and the slope of the expiratory flow curve using airway pressure release ventilation (APRV). Although many studies have shown that personalizing PEEP is possible, there is no consensus as to the optimal technique. This review will assess various methods used to personalize PEEP, directed by physiologic parameters, necessary to adaptively adjust ventilator settings with progressive changes in lung pathophysiology.

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.

It was recently shown that acute respiratory distress syndrome (ARDS) mortality has not been reduced in over 15 years and remains ~40 %, even with protective low tidal volume (LVt) ventilation. Thus, there is a critical need to develop novel ventilation strategies that will protect the lung and reduce ARDS mortality. Protti et al. have begun to analyze the impact of mechanical ventilation on lung tissue using engineering methods in normal pigs ventilated for 54 h. They used these methods to assess the impact of a mechanical breath on dynamic and static global lung strain and energy load. Strain is the change in lung volume in response to an applied stress (i.e., Tidal Volume-Vt). This study has yielded a number of exciting new concepts including the following: (1) Individual mechanical breath parameters (e.g., Vt or Plateau Pressure) are not directly correlated with VILI but rather any combination of parameters that subject the lung to excessive dynamic strain and energy/power load will cause VILI; (2) all strain is not equal; dynamic strain resulting in a dynamic energy load (i.e., kinetic energy) is more damaging to lung tissue than static strain and energy load (i.e., potential energy); and (3) a critical consideration is not just the size of the Vt but the size of the lung that is being ventilated by this Vt. This key concept merits attention since our current protective ventilation strategies are fixated on the priority of keeping the Vt low. If the lung is fully inflated, a large Vt is not necessarily injurious. In conclusion, using engineering concepts to analyze the impact of the mechanical breath on the lung is a novel new approach to investigate VILI mechanisms and to help design the optimally protective breath. Data generated using these methods have challenged some of the current dogma surrounding the mechanisms of VILI and of the components in the mechanical breath necessary for lung protection.

Background Lung injury is often studied without consideration for pathologic changes in the chest wall. In order to reduce the incidence of lung injury using preemptive mechanical ventilation, it is important to recognize the influence of altered chest wall mechanics on disease pathogenesis. In this study, we hypothesize that airway pressure release ventilation (APRV) may be able to reduce the chest wall elastance associated with an extrapulmonary lung injury model as compared with low tidal volume (LVt) ventilation. Methods Female Yorkshire pigs were anesthetized and instrumented. Fecal peritonitis was established, and the superior mesenteric artery was clamped for 30 min to induce an ischemia/reperfusion injury. Immediately following injury, pigs were randomized into (1) LVt (n = 3), positive end-expiratory pressure (PEEP) 5 cmH2O, Vt 6 cc kg−1, FiO2 21 %, and guided by the ARDSnet protocol or (2) APRV (n = 3), PHigh 16–22 cmH2O, PLow 0 cmH2O, THigh 4.5 s, TLow set to terminate the peak expiratory flow at 75 %, and FiO2 21 %. Pigs were monitored continuously for 48 h. Lung samples and bronchoalveolar lavage fluid were collected at necropsy. Results LVt resulted in mild acute respiratory distress syndrome (ARDS) (PaO2/FiO2 = 226.2 ± 17.1 mmHg) whereas APRV prevented ARDS (PaO2/FiO2 = 465.7 ± 66.5 mmHg; p 0.05). This was because the pleural pressure was significantly lower in LVt (7.6 ± 0.5 cmH2O) as compared with APRV (17.4 ± 3.5 cmH2O; p