Treatment of asthma-related respiratory arrest with endotracheal abuterol (Salbutamol)

1988 ◽  
Vol 17 (4) ◽  
pp. 358-360 ◽  
Author(s):  
P Richard Verbeek ◽  
Annie B Gareau ◽  
Christopher J Rubes
Keyword(s):  
2014 ◽  
Vol 4 (4) ◽  
pp. 514-519
Author(s):  
Mary Ann Sens ◽  
Sarah E. Meyers ◽  
Mark A. Koponen ◽  
Arne H. Graff ◽  
Ryan D. Reynolds ◽  
...  

1996 ◽  
Vol 11 (1) ◽  
pp. 60-62 ◽  
Author(s):  
Christopher E. Kapsner ◽  
David C. Seaberg ◽  
Charles Stengel ◽  
Kaveh Ilkhanipour ◽  
James Menegazzi

AbstractIntroduction:The esophageal detector device (EDD) recently has been found to assess endotracheal (ET) tube placement accurately. This study describes the reliability of the EDD in determining the position of the ET tube in clinical airway situations that are difficult.Methods:This was a prospective, randomized, single-blinded, controlled laboratory investigation. Two airway managers (an emergency-medicine attending physician and a resident) determined ET-tube placement using the EDD in five swine in respiratory arrest. The ET tube was placed in the following clinical airway situations: 1) esophagus; 2) esophagus with 1 liter of air instilled; 3) trachea; 4) trachea with 5 ml/kg water instilled; and 5) right mainstem bronchus. Anatomic location of the tube was verified by thoracotomy of the left side of the chest.Results:There was 100% correlation between the resident and attending physician's use of the EDD. The EDD was 100% accurate in determining tube placement in the esophagus, in the esophagus with 1 liter of air instilled, in the trachea, and in the right mainstem bronchus. The airway managers were only 80% accurate in detecting tracheal intubations when fluid was present.Conclusions:The EDD is an accurate and reliable device for detecting ET-tube placement in most clinical situations. Tube placement in fluid-filled trachea, lungs, or both, which occurs in pulmonary edema and drowning, may not be detected using this device.


2021 ◽  
Vol 77 (18) ◽  
pp. 2742
Author(s):  
Julia J. Lovin ◽  
Tyler Fick ◽  
Edward Hickey ◽  
M. Regina Lantin-Hermoso
Keyword(s):  

1984 ◽  
Vol 75 (5) ◽  
pp. 241-248
Author(s):  
Ibrahim Jawad ◽  
Vithal Kinhal ◽  
Harisios Boudoulas

1997 ◽  
Vol 82 (4) ◽  
pp. 1119-1125 ◽  
Author(s):  
G. S. Supinski ◽  
D. Stofan ◽  
R. Ciufo ◽  
A. Dimarco

Supinski, G. S., D. Stofan, R. Ciufo, and A. DiMarco. N-acetylcysteine administration alters the response to inspiratory loading in oxygen-supplemented rats. J. Appl. Physiol. 82(4): 1119–1125, 1997.—Based on recent studies, it has been suggested that free radicals are elaborated in the respiratory muscles during strenuous contractions and contribute to the development of muscle fatigue. If this theory is correct, then it should be possible to attenuate the development of diaphragm fatigue and/or delay the onset of respiratory failure during loaded breathing by administering a free radical scavenger. The purpose of the present experiment was, therefore, to examine the effect of N-acetylcysteine (NAC), a free radical scavenger and glutathione precursor, on the evolution of respiratory failure in decerebrate unanesthetized rats breathing against a large inspiratory resistive load. We compared the inspiratory volume and pressure generation over time in animals pretreated with either saline or NAC (150 mg/kg) and then loaded until respiratory arrest. After arrest, the diaphragm was excised, and samples were assayed for reduced (GSH) and oxidized glutathione. As a control, we also assessed respiratory function and glutathione concentrations in groups of nonloaded saline- and NAC-treated animals. We found that NAC-treated animals were able to tolerate loading better than the saline-treated group, maintaining higher inspiratory pressures and sustaining higher inspired volumes. Administration of NAC also increased the time that animals could tolerate loading before the development of respiratory arrest. In addition, although saline-treated loaded animals had significant reductions in diaphragmatic GSH levels compared with unloaded controls, the magnitude of this reduction was blunted by NAC administration (i.e., GSH averaged 965 ± 113, 568 ± 83, 907 ± 39, and 784 ± 61 nmol/g for unloaded-saline, loaded-saline, unloaded-NAC, and loaded-NAC groups, P< 0.05, with the value for the loaded-saline group lower than the values for the two unloaded groups; GSH for the loaded-NAC group was not different, however, from unloaded controls). These data demonstrate that administration of NAC, a free radical scavenger, slows the rate of development of respiratory failure during inspiratory resistive loading.


2010 ◽  
Vol 27 (9) ◽  
pp. 846-848
Author(s):  
Sabrina Hoesni ◽  
Karen Tan ◽  
Suzanne Crowe

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