atelectotrauma

(redirected from atelectrauma)

atelectotrauma

, atelectrauma (at″ĕl-ek″tŏ-tro′mă) (-ek″tro′mă) [ atelectasis + trauma]
Injury to the lung caused by shearing forces as alveoli that are next to each other collapse and re-expand during mechanical ventilation. The condition may be prevented by applying enough positive end-expiratory pressure to limit alveolar collapse at end expiration.
References in periodicals archive ?
Results: The pathogenesis of VILI was defined gradually, from traditional pathological mechanisms (barotrauma, volutrauma, and atelectrauma) to biotrauma.
In turn, high PEEP allows for faster alveolar recruitment (73), addressing the causal process leading to diffuse alveolar damage (recruitable ARDS: inflammation, lung water and atelectrauma in addition to atelectasis).
The patient should remain during the treatment (to allow recovery of lung function) with "rest" settings (Fi[O.sub.2] 25-30%, peak inspiratory pressure (PIP) 20-25 cm [H.sub.2]O; positive end expiratory pressure (PEEP) 45 cm [H.sub.2]O; inspiratory time (Ti) 0.5-1.0 seconds; frequency (F) 20-25 breaths per minute) or even in continuous positive airway pressure (CPAP) with a high PEEP (10-12 cm [H.sub.2]O) in order to maintain functional residual capacity (FRC) without causing lung injury (volutrauma, barotrauma, or atelectrauma).
Choosing a ventilator to stockpile for a possible future pandemic leading to a mass critically unwell paediatric population will require a ventilator that can deliver accurate [V.sub.T] to avoid volutrauma, measure the delivered [V.sub.T] accurately to avoid underventilation or overdistension, deliver accurate pressures to avoid barotrauma, and has the ability to optimise PEEP to avoid atelectrauma and maintain the set Fi[O.sub.2] to avoid oxygen toxicity.
VILI is a complex collection of lung deconstuctive elements that manifests itself in a number of forms including but is not limited to the following categories of ventilator induced lung injury; Volutrama, Barotrauma, Biotrauma, RACE and Atelectrauma.
The deleterious effects from loss of positive end expiratory pressure (PEEP) on lung function and mechanics that occurs when patients are disconnected from the ventilator include a reduction in functional residual capacity, possible atelectrauma and a decrease in oxygenation (Amato et al 1998, Barker and Adams 2002, McCann et al 2001, Savian et al 2005).
Major underlying mechanisms have indicated that the injury includes volutrauma due to alveolar overdistension, atelectrauma due to ventilation at low lung volumes, and biotrauma with the release of mediators in the lung.[4] However, there are limited methods to prevent VILI, protect the lung issue, and avoid the damage.
The underlying mechanisms of VILI include alveolar overdistension (volutrauma), alveolar instability leading to alveolar collapse and reopening with each breath (atelectrauma), and the secondary inflammation caused by these mechanical injuries which is known as biotrauma [33].
If intra-airway propagation is a genuine hazard, timing of PEEP application and positioning may be of under-recognized importance for reasons unrelated to atelectrauma. ARDS generally progresses from an edematous to an organizing phase over a few days.
A study of new ventilation strategies guided by transpulmonary pressure in ECMO to determine the optimal PEEP to limit atelectrauma is ongoing in our center (ClinicalTrials.gov Identifier: NCT02439151).[sup][16] Our previous study found that, compared to the traditional “lung rest” strategy, the transpulmonary pressure-guided ventilation strategy can better maintain lung volume to limit atelectasis and provide more effective lung protection.
Ventilator-associated lung injury (VILI) includes barotrauma, volutrauma, atelectrauma, and biotrauma, among which volutrauma, the overexpansion produced by high tidal volume, is the major cause of VILI [1,16,17].