Airway Pressure Release Ventilation Reduces Conducting Airway Micro-Strain in Lung Injury

Abstract

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.

RETRACTED: Mechanical Ventilation as a Therapeutic Tool to Reduce ARDS Incidence

“…Th ese studies thus confi rm, perhaps somewhat counterintuitively, that increasing PTI is actually protective, at least in the context of APRV, and reduces both alveolar and alveolar duct m -strain ( Figs 3, 4 ). 30,44 Th e result is reduced development of ARDS as measured by the Pa o 2 /F io 2 ratio ( Fig 5A ) and gross pathology ( Fig 6 ). 31 APRV has also been shown to be eff ective at reducing ARDS incidence in patients in the ICU.…”

“…In secondary ARDS, trauma, hemorrhagic shock, or sepsis can incite SIRS and cause an increase in capillary permeability that ultimately results in surfactant deactivation that, together with alveolar fl ooding, alters alveolar mechanics and, in particular, can lead to RACE. Lung tissue injury caused by RACE can be exacerbated by the development of 44 ) stress concentrations between air-fi lled alveoli and alveoli that are either collapsed 36 or edema fi lled. 37 Th us, heterogeneous ventilation, which creates stress concentrators, can also cause excessive strain on alveolar walls and combined with RACE drive progressive lung injury.…”

“…Given that APRV is superior to CMV for the most severely injured lungs (ie, rescue mode) and that the MBP of APRV is theoretically ideal for minimizing ventilator injury cost function, we chose to study the effi cacy of this mechanical breath at reducing ARDS incidence. We hypothesized that the mechanism by which APRV protected the lung 24,[30][31][32][33][34]44,45 was reduced alveolar microstrain ( m -strain). We found that appropriately set APRV with an extended duration at plateau pressure (duration at high pressure [THigh]) and a very brief duration at pressure release (duration at low pressure [TLow]) is essential to minimizing m -strain in the alveoli and the alveolar ducts ( Figs 3 , 4 ).…”

“…We found that appropriately set APRV with an extended duration at plateau pressure (duration at high pressure [THigh]) and a very brief duration at pressure release (duration at low pressure [TLow]) is essential to minimizing m -strain in the alveoli and the alveolar ducts ( Figs 3 , 4 ). 30,44 m -Strain is defi ned as the change in size and shape of the alveoli and alveolar ducts in response to a given stress. In this case the stress applied is airway pressure.…”

“…Th ere are three possible mechanisms by which the extended PTI produced by APRV reduces ARDS incidence: (1) preserving the integrity of the blood-gas barrier and thereby reducing pulmonary edema formation ( Fig 2 , increased permeability), 47 thus blocking the sequence of events leading to surfactant deactivation, alveolar collapse, and subsequent alveolar instability ( Fig 2 , RACE); (2) minimizing alveolar collapse ( Fig 3 , RACE) with the very brief expiration that occurs during TLow, which limits the time for alveolar derecruitment to occur before the lung is reinfl ated ( Figs 3, 4 ) 30,44 ; and (3) maximally recruiting the lung with the extended inspiratory duration THigh, which maintains distal airspace patency and creates a homogeneously ventilated lung so as to minimize stress concentrations in the parenchyma ( Fig 4 ). 30 Th ese factors have all been linked to lung protection.…”