scholarly journals Tidal Volume Dependence on the Ventilatory Frequency and Alveolar Compliance in HFOV

Author(s):  
M. Rožánek ◽  
Z. Horáková ◽  
B. Padertová ◽  
J. Ráfl ◽  
K. Roubík
1977 ◽  
Vol 52 (3) ◽  
pp. 269-275 ◽  
Author(s):  
J. R. A. Rigg ◽  
E. M. Inman ◽  
N. A. Saunders ◽  
S. R. Leeder ◽  
N. L. Jones

1. The effect of mental arithmetic tasks on ventilation, breathing pattern, oxygen intake and carbon dioxide output was studied during air breathing and carbon dioxide rebreathing in healthy subjects. 2. Ventilation and breathing frequency increased significantly on performance of the task during 4 min air breathing and 4 min rebreathing; tidal volume was unchanged. The slopes of the ventilatory, frequency and tidal volume responses to carbon dioxide changed little during task performance. 3. During 15 min air breathing, oxygen intake was unchanged with task performance. Carbon dioxide output increased significantly with task performance, as a result of wash-out of carbon dioxide from body stores by the increased ventilation. 4. Mental arithmetic had no effect on the coefficients of variation of the slope and position variables of the ventilatory, frequency and tidal volume responses to carbon dioxide. It is concluded that task performance does not improve the reproducibility of these responses.


1984 ◽  
Vol 45 (C8) ◽  
pp. C8-57-C8-60 ◽  
Author(s):  
M. Hanfland ◽  
K. Syassen ◽  
N. E. Christensen

2010 ◽  
Vol 4 (1) ◽  
pp. 27-36
Author(s):  
Ming-Jui Hung ◽  
Ming-Yow Hung ◽  
Wen-Jin Cherng ◽  
Li-Fu Li

Abstract Background: Positive pressure ventilation with large tidal volumes has been shown to cause lung injury via the serine/threonine kinase-protein kinase B (Akt) and endothelial nitric oxide synthase (eNOS)-pathways. However, the effects of high tidal volume (VT) ventilation on the heart are unclear. Objectives: Evaluate the effect of VT ventilation on the cardiac vascular permeability and intracellular Akt and eNOS signaling pathway. Methods: C57BL/6 and Akt knock-out (heterozygotes, +/−) mice were exposed to high VT (30 mL/kg) mechanical ventilation with room air for one and/or five hours. Results: High VT ventilation increased cardiac microvascular permeability and eNOS phosphorylation in a timedependent manner. Serum cardiac troponin I was increased after one hour of high VT ventilation. Cardiac Akt phosphorylation was accentuated after one hour and attenuated after five hours of high VT ventilation. Pharmacological inhibition of Akt with LY294002 and high VT ventilation of Akt+/− mice attenuated cardiac Akt phosphorylation, but not eNOS phosphorylation. Conclusion: High VT ventilation increased cardiac myocardial injury, microvascular permeability, and eNOS phosphorylation. Involvement of cardiac Akt in high VT ventilation was transient.


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