Long-term negative pressure ventilation

2002 ◽  
Vol 8 (4) ◽  
pp. 545-557 ◽  
Author(s):  
A CORRADO ◽  
M GORINI
2019 ◽  
Vol 8 (4) ◽  
pp. 562
Author(s):  
Hung-Yu Huang ◽  
Chun-Yu Lo ◽  
Lan-Yan Yang ◽  
Fu-Tsai Chung ◽  
Te-Fang Sheng ◽  
...  

Negative pressure ventilation (NPV), when used as an adjuvant to pulmonary rehabilitation, improves lung function, increases exercise capacity, and reduces exacerbations. The aim of this study was to determine whether maintenance NPV improves long-term clinical outcomes and reduces mortality in patients with chronic obstructive pulmonary disease (COPD). Between 2003 and 2009, 341 patients were treated for COPD either with or without hospital-based NPV. We measured forced expiratory volume in one second (FEV1), 6-min walking distance (6MWD), and oxygen saturation by pulse oximetry (SpO2) during a 6-min walk test (6MWT) every 3–6 months. Desaturation (D) during the 6MWT was defined as a reduction in SpO2 of ≥10% from baseline. The NPV group had a better survival outcome than the Non-NPV group. The 8-year survival probabilities for the NPV and Non-NPV groups were 60% and 20%, respectively (p < 0.01). Baseline desaturation was a significant risk factor for death, and the risk of death increased with desaturation severity (SpO2 80~89: hazard ratios (HR) 2.7, 95% confidence interval (CI) 1.4–5.3; SpO2 < 80: HR 3.1, 95% CI 1.3–7.4). The NPV group had a slower decline in lung function and 6MWD. The NPV + D and Non-NPV+D had a threefold and fourfold increase in the risks of all-cause mortality compared with the NPV-ND, respectively. Maintenance non-invasive NPV reduced long-term mortality in COPD patients. The desaturating COPD patients had an increased mortality risk compared with non-desaturating COPD patients.


CHEST Journal ◽  
1994 ◽  
Vol 105 (1) ◽  
pp. 95-99 ◽  
Author(s):  
Antonio Corrado ◽  
Eduardo De Paola ◽  
Andrea Messori ◽  
Giovanni Bruscoli ◽  
Sandra Nutini

1991 ◽  
Vol 144 (2) ◽  
pp. 390-394 ◽  
Author(s):  
Enrique Fernandez ◽  
Paltiel Weiner ◽  
Ephraim Meltzer ◽  
Mary M. Lutz ◽  
David B. Badish ◽  
...  

2018 ◽  
Vol 37 (4) ◽  
pp. 520-530 ◽  
Author(s):  
Nader S. Aboelnazar ◽  
Sayed Himmat ◽  
Sanaz Hatami ◽  
Christopher W. White ◽  
Mohamad S. Burhani ◽  
...  

1981 ◽  
Vol 50 (1) ◽  
pp. 149-161 ◽  
Author(s):  
A. I. Pack ◽  
R. G. DeLaney ◽  
A. P. Fishman

Studies were conducted in anesthetized paralyzed dogs using a cycle-triggered constant-flow ventilator, which ventilated the animal in phase with the recorded phrenic neural activity. Intermittently tests were performed in which the animal was ventilated with a different airflow for a single breath. Increased airflows, within the range generated during spontaneous breathing, caused an increased rate of rise of the moving average phrenic neurogram and a shortening of the duration of the nerve burst. The magnitude of the increase in the rate of rise of the neurogram was related to the level of inspiratory airflow. Tests with brief pulses of airflow showed that an increase in the rate of rise of the phrenic neurogram could be produced without inflating the lung above the resting tidal volume of the animal. Similar results were obtained with negative-pressure ventilation and the effects were abolished by vagotomy. This vagally mediated augmentation of phrenic neural output may accelerate the inspiratory volume change in the lung during spontaneous breathing at hyperpneic levels.


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