Clinical Trial: Work of Breathing and Mechanical Ventilation in Acute Lung Injury
Study Status: Withdrawn
Recruit Status: Withdrawn
Study Type: Interventional
Official Title: Prospective Study on the Effects of Artificial Breathing Patterns on Work of Breathing in Patients With Acute Lung Injury.
Brief Summary:
The primary goal of this study is to measure changes in biological markers of inflammation in critically-ill patients with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) while they are treated with different styles of lung-protective, artificial breathing assistance.
Secondary goals are to measure the breathing effort of patients using different artificial breathing patterns from the breathing machine.
The primary hypothesis is that volume-targeted artificial patterns will produce less inflammation. The secondary hypothesis is that volume-targeted artificial patterns will increase breathing effort compared to pressure-targeted artificial patterns.
Detailed Summary:
Ventilator-induced lung injury contributes to the progression of ALI/ARDS,1 and is thought to occur partly from the unequal distribution of a super-normal tidal volume to normal areas of the lung.2 Alveolar overdistension causes alveolar-capillary membrane damage,3 increased-permeability pulmonary edema4 and hyaline membrane formation.5 Therefore, it is recommended that tidal volume should be reduced to 6-7 mL/kg, and that the peak alveolar pressure, or the end-inspiratory plateau pressure (PPLAT), should be limited to < 30 cm H2O.6 The National Heart Lung and Blood Institute's ARDS Network demonstrated a 22% reduction in mortality using a "lung-protective" (low tidal volume) ventilation strategy in patients with ALI/ARDS.7 High tidal volume ventilation causes a rapid and substantial increase plasma levels of proinflammatory mediators which decrease in response to lung protective ventilation.8,9 A consequence of lung-protective ventilation is dyspnea and increased work of breathing.10 Our recent study11 on work of breathing during lung-protective ventilation found that inspiratory pleural pressure changes were extraordinarily high, averaging 15-17 cm H2O. Whereas tidal volume was well controlled during volume ventilation, in contrast, it exceeded target levels in 40% of patients during pressure control ventilation.
High tidal volume-high negative pressure ventilation causes acute lung injury in animal models.12,13 Thus ventilator-induced lung injury results from excessive stress across lung tissue created by high transpulmonary (airway-pleural).pressure.14 This suggests the possibility that despite pressure control ventilation being set with a low positive airway pressure, "occult" high tidal volume-high transpulmonary pressure ventilation still may occur.11 However, during spontaneous breathing diaphragmatic contractions cause ventilation to be dis
Sponsor: University of California, San Francisco
Current Primary Outcome: proinflammatory cytokine expression in plasma [ Time Frame: 2 hours ]
Original Primary Outcome: Same as current
Current Secondary Outcome: work of breathing [ Time Frame: 2 hours ]
Original Secondary Outcome: Same as current
Information By: University of California, San Francisco
Dates:
Date Received: August 16, 2009
Date Started: September 2009
Date Completion: September 2013
Last Updated: March 3, 2015
Last Verified: March 2015
