Objectives: The benefits of spontaneous breathing over muscle paralysis have been proven mainly in mild lung injury; no one has yet evaluated the effects of spontaneous breathing in severe lung injury. We investigated the effects of spontaneous breathing in two different severities of lung injury compared with muscle paralysis.
Design: Prospective, randomized, animal study.
Setting: University animal research laboratory.
Subjects: Twenty-eight New Zealand white rabbits.
Interventions: Rabbits were randomly divided into the mild lung injury (surfactant depletion) group or severe lung injury (surfactant depletion followed by injurious mechanical ventilation) group and ventilated with 4-hr low tidal volume ventilation with spontaneous breathing or without spontaneous breathing (prevented by a neuromuscular blocking agent). Inspiratory pressure was adjusted to control tidal volume to 5–7 mL/kg, maintaining a plateau pressure less than 30 cm H2O. Dynamic CT was used to evaluate changes in lung aeration and the regional distribution of tidal volume.
Measurements and Results: In mild lung injury, spontaneous breathing improved oxygenation and lung aeration by redistribution of tidal volume to dependent lung regions. However, in severe lung injury, spontaneous breathing caused a significant increase in atelectasis with cyclic collapse. Because of the severity of lung injury, this group had higher plateau pressure and more excessive spontaneous breathing effort, resulting in the highest transpulmonary pressure and the highest driving pressure. Although no improvements in lung aeration were observed, muscle paralysis with severe lung injury resulted in better oxygenation, more even tidal ventilation, and less histological lung injury.
Conclusions: In animals with mild lung injury, spontaneous breathing was beneficial to lung recruitment; however, in animals with severe lung injury, spontaneous breathing could worsen lung injury, and muscle paralysis might be more protective for injured lungs by preventing injuriously high transpulmonary pressure and high driving pressure.
1 Laboratório de Pneumologia LIM09, Faculdade de Medicina da University of São Paulo, São Paulo, Brazil.
2 Department of Anesthesiology and Intensive Care Medicine, Osaka University Graduate School of Medicine, Suita, Japan.
3 Department of Pathology, School of Allied Health Sciences, Osaka University Graduate School of Medicine, Suita, Japan.
*See also p. 685.
This study was performed at Osaka University Graduate School of Medicine, Suita, Japan.
Dr. Yoshida has received grant support form Fukuda Foundation for Medical Technology, Tokibo CO, Newport Medical Instruments Inc, and Osaka University Scholarship for Short-term Overseas Research 2012. Dr. Uchiyama has received governmental funding. Dr. Fujino has received grant support and support for travel from a governmental fund. The remaining authors have not disclosed any potential conflicts of interest.
Address requests for reprints to: Takeshi Yoshida, MD, Department of Anesthesiology and Intensive Care Medicine, Osaka University Graduate School of Medicine, 2-15 Yamadaoka, Suita, Osaka, 565-0871, Japan. E-mail: firstname.lastname@example.org or email@example.com