As the name suggests, MB was thought to protect against
overdistention of the RV.[7] The mechanical stretch and misarranged cardiomyocyte renders the insertion sites more vulnerable to arrhythmia generation.
Although the use of NIMV strategies has not gained universal approval in this setting because of the increased transpulmonary pressure and the uncontrolled
overdistention of the alveoli, the commonly advocated advantages include the preservation of airway defence mechanisms, the decreased need for sedation and improvements in gas exchange.
The uterine
overdistention, cervical diseases, breakdown of maternal-fetal tolerance, decidual senescence, vascular disorders, infections, and stress are the major mechanisms of the disease implicated in spontaneous preterm labor, but probably there are still unknown factors included in this pathology [1].
Uterine
overdistention in multiple gestations (and in polyhydramnios) has been implicated in preterm birth (3,6).
It was thought to be a structure protecting against
overdistention of the RV, hence the name "moderator" [3].
Additionally, in ARDS, the presence of RVD (hemodynamic status) and not Pa[O.sub.2]/Fi[O.sub.2] ratio could be an indication for proning to unload the RV by recruiting collapsed alveoli without causing
overdistention and reducing airway pressure and hypercapnia ("RV-protective" ventilation strategy) [77-79].
(17) It is thought that the antecedent to preterm delivery in multiples is uterine
overdistention. (18,19) Currently, there are no established therapies to reduce the risk of preterm delivery in higher order multiples.
While normally the pericardium exerts a mild containing force that somewhat prevents
overdistention of the cardiac chambers, in CP this extrinsic pressure is increased and most commonly transmitted uniformly to all cardiac chambers equalizing chamber pressures.
Pneumonia accompanied with pneumopericardium caused by anaerobic bacteria Staphylococci and Klebsiella have been described before.3 Moreover mechanical ventilation predisposed alveoli to both barotrauma and volutrauma which aggravated
overdistention of the friable alveoli.
This mode of ventilation provides small tidal volumes and high mean airway pressures that prevent both collapse and
overdistention of the alveoli, a key goal in ARDS treatment (Chan, Stewart, & Mehta, 2007).
Additionally, because all PFC15 lungs presented rupture of alveolar septae due to
overdistention, we decided to exclude the 15 mL/kg dose experiments.
The only complications were bradycardia, which responded to atropine, and
overdistention of the lung if the tube was too large.