Lung protective ventilation (ARDSNet) versus airway pressure release ventilation

Abstract

Background Concomitant lung/brain traumatic injury, results in significant morbidity and mortality. Lung protective ventilation (ARDSNet) has become the standard for managing acute respiratory distress syndrome (ARDS); however, the resulting permissive hypercapnea may compound traumatic brain injury (TBI). Airway pressure release ventilation (APRV) offers an alternative strategy for management of this patient population. APRV was hypothesized to retard the progression of acute lung/brain injury to a greater degree than ARDSNet in a swine model. Methods Yorkshire swine were randomized to ARDSNet, APRV, or sham. Ventilatory settings and pulmonary parameters, vitals, blood gases, quantitative histopathology, and cerebral microdialysis were compared between groups using chi-square, Fisher’s exact, Student’s t-test, Wilcoxon rank-sum, and mixed effects repeated measures modeling. Results 22 swine (17 male, 5 female), weighing 25±6.0kg, were randomized to APRV (n=9), ARDSNet (n=12), or sham (n=1). PaO2/FiO2 (P/F) ratio dropped significantly while intracranial pressure increased significantly for all three groups immediately following lung and brain injury. Over time, peak inspiratory pressure, mean airway pressure, and P/F ratio significantly increased, while total respiratory rate significantly decreased within the APRV group compared to the ARDSNet group. Histopathology did not show significant differences between groups in overall brain or lung tissue injury; however, cerebral microdialysis trends suggested increased ischemia within the APRV group compared to ARDSNet over time. Conclusion Previous studies have not evaluated the effects of APRV in this population. While our macroscopic parameters and histopathology did not observe a significant difference between groups, microdialysis data suggest a trend toward increased cerebral ischemia associated with APRV over time. Additional and future studies should focus on extending the time interval for observation to further delineate differences between groups. Level of Evidence II Study Type Therapeutic

The 30-year evolution of airway pressure release ventilation (APRV)

“…Similar to the F-APRV studies, P-APRV either resulted in improved outcomes or no change as compared with CPPV and in none of the studies was APRV shown to be harmful. Unlike the F-APRV studies that were mainly crossover studies, all of the P-APRV animal studies were randomized prospective cohort trials that compare non-protective CPPV or low tidal volume (LTV) with APRV [ 5 , 49 , 52 , 54 , 55 , 57 , 61 , 62 ]. P-APRV was shown to reduce heterogeneity and both alveolar and alveolar duct micro-strain (i.e., change in alveolar size with applied stress) [ 54 – 56 ] suggesting a mechanism for the improvement in the efficacy experiments (Table 3 ) [ 5 , 49 , 57 , 61 , 62 ].…”

“…In prospective outcome animal experiments, P-APRV resulted in an increase in oxygenation along with a decrease in histopathologic injury as compared with CPPV and LTV ventilation strategies [ 5 , 52 , 57 , 61 , 62 ]. Several studies showed that P-APRV resulted in an increase in surfactant protein concentration [ 5 , 57 , 62 ], while two showed a reduction of inflammatory markers (Table 2 ) [ 49 , 57 ].…”

“…Davies et al [ 52 ] showed increased oxygenation with P-APRV as compared with LTV, with no significant differences in cerebral ischemia in a swine model of concomitant brain and lung injury (Table 2 ). In patients, Yoshida et al [ 60 ] demonstrated increased oxygenation and mean arterial pressure (MAP) with decreased atelectasis using P-APRV as compared to LTV ventilation.…”

Intracranial pressure responsiveness to positive end-expiratory pressure in different respiratory mechanics: a preliminary experimental study in pigs

“…The increase of E L was induced by slowly instillation of 0.1 mol/L hydrochloride (4 mL/kg) down the endotracheal tube via a thin suction catheter placed at the level of the carina. This method has been previously reported as creating an animal model with ARDS-like lung injury including lung inflammation, edema, hemorrhage, and variable lung region aeration [ 25 , 26 ]. One hour following hydrochloride administration the model was validated by achieving a pulse oxygen saturation ≤ 90%.…”

“…IH was induced by inflating the intracranial balloon with saline at a rate of 0.5 mL/min until the ICP was constant between 30 and 40 cm H 2 O for > 30 min [ 26 , 27 ].…”