Joshua Satalin, BA
Research Scientist
SUNY Upstate Medical University
Syracuse, New York, United States
Disclosure information not submitted.
Sarah Blair
Research Scientist
SUNY Upstate Medical University
Syracuse, NY
Disclosure information not submitted.
Penny Andrews, RN
Registered Nurse
University of Maryland, United States
Disclosure information not submitted.
Nader Habashi, MD
Professor
R. Adams Cowley Shock Trauma Center
Baltimore, United States
Disclosure information not submitted.
Louis Gatto, PhD
Professor
SUNY Upstate Medical University, United States
Disclosure information not submitted.
Jason Bates, PhD
Professor
University of Vermont, United States
Disclosure information not submitted.
Gary Nieman, BA
Professor
SUNY Upstate Medical University, United States
Disclosure information not submitted.
Michaela Kollisch-Singule, MD
Assistant Professor
SUNY Upstate Medical University, United States
Disclosure information not submitted.
Title: THE ROLE OF STATIC AND DYNAMIC STRAIN ON VENTILATOR-INDUCED LUNG INJURY
Introduction: Improperly set mechanical ventilation can have adverse effects on healthy and injured lungs by causing injurious levels of both static and dynamic tissue strain leading to a ventilator-induced lung injury (VILI). We hypothesized that dynamic strain (DS) and static strain (SS) individually would lead to pulmonary injury, but that a combination of both would synergistically worsen this injury. Four combinations of DS and SS were generated using the Airway Pressure Release Ventilation (APRV) mode. The Time Controlled Adaptive Ventilation (TCAVä) method has previously been shown to be lung-protective and was used to prevent both DS and SS.
Methods: Yorkshire pigs were anesthetized, instrumented, and lung injury was induced by bronchoscopic instillation of 3% Tween into the dependent lung lobes. The animals were placed on APRV with an inspiratory duration (THigh) of 4.0s and an expiratory pressure (PLow) of 0cmH2O. They were randomized to varying inspiratory pressures (PHigh) and expiratory durations (TLow) set to induce high dynamic strain, high static strain, both, or neither: DS (n=10: P<sub>High 28cmH2O, TLow set to terminate expiratory flow at 25% of peak expiratory flow [TPEF]); SS (n=10: P<sub>High 40cmH2O, 75% TPEF); DS+SS (n=10: P<sub>High 40cmH2O, 25% TPEF); Non-DS/SS (TCAVä Method) (n=10: P<sub>High 28cmH2O, 75% TPEF). Hemodynamic and pulmonary parameters were measured following injury and hourly for 6 hours.
Results: Following injury, the non-DS/SS group had a significantly higher PaO2/FiO2 ratio at T6 (437 ± 49 mmHg) compared to the DS+SS group (226 ± 41 mmHg) (p< 0.05), whereas DS (333 ± 105 mmHg) and SS (377 ± 43 mmHg) had a milder injury as compared with DS+SS (p< 0.05). The DS+SS group had the highest driving pressure at T6 (35.5 ± 0.4 cmH2O) compared to DS (25.1 ± 0.2 mmHg) and SS (22.9 ± 0.7 mmHg) while the non-DS/SS had the lowest (16.4 ± 0.25 cmH2O) (p< 0.001).
Conclusions: Elevated SS and DS individually caused mild lung injury, but when applied simultaneously, resulted in significantly higher driving pressures and lung injury as shown by the decline in P/F ratio. The combination of DS and SS causes VILI but DS and SS independently may not be sufficient for VILI to develop.
Funded R01HL142702 and W81XWH2010696