scholarly journals Inspiratory time and tidal volume during intermittent positive pressure ventilation.

1985 ◽  
Vol 60 (3) ◽  
pp. 259-261 ◽  
Author(s):  
D Field ◽  
A D Milner ◽  
I E Hopkin
1995 ◽  
Vol 79 (1) ◽  
pp. 176-185 ◽  
Author(s):  
V. Jounieaux ◽  
G. Aubert ◽  
M. Dury ◽  
P. Delguste ◽  
D. O. Rodenstein

We have recently observed obstructive apneas during nasal intermittent positive-pressure ventilation (nIPPV) and suggested that they were due to hypocapnia-induced glottic closure. To confirm this hypothesis, we studied seven healthy subjects and submitted them to nIPPV while their glottis was continuously monitored through a fiber-optic bronchoscope. During wakefulness, we measured breath by breath the widest inspiratory angle formed by the vocal cords at the anterior commissure along with several other indexes. Mechanical ventilation was progressively increased up to 30 l/min. In the absence of diaphragmatic activity, increases in delivered minute ventilation resulted in progressive narrowing of the vocal cords, with an increase in inspiratory resistance and a progressive reduction in the percentage of the delivered tidal volume effectively reaching the lungs. Adding CO2 to the inspired gas led to partial widening of the glottis in two of three subjects. Moreover, activation of the diaphragmatic muscle was always associated with a significant inspiratory abduction of the vocal cords. Sporadically, complete adduction of the vocal cords was directly responsible for obstructive laryngeal apneas and cyclic changes in the glottic aperture resulted in waxing and waning of tidal volume. We conclude that in awake humans passive ventilation with nIPPV results in vocal cord adduction that depends partly on hypocapnia, but our results suggest that other factors may also influence glottic width.


1989 ◽  
Vol 7 (4) ◽  
pp. 223-229 ◽  
Author(s):  
Mark C. Mammel ◽  
Stephen J. Boros ◽  
Dennis R. Bing ◽  
Keith K. Holloman ◽  
John R. Connett

1995 ◽  
Vol 79 (1) ◽  
pp. 186-193 ◽  
Author(s):  
V. Jounieaux ◽  
G. Aubert ◽  
M. Dury ◽  
P. Delguste ◽  
D. O. Rodenstein

We have previously observed that, in normal awake subjects passively hyperventilated with intermittent positive-pressure ventilation delivered through nasal access (nIPPV), the glottis could interfere with the ventilation. We report on data obtained in the same subjects during stable sleep. In all cases, the glottis was continuously observed through a fiber-optic bronchoscope, and other indexes were also continuously recorded. Mechanical ventilation was progressively increased up to 30 l/min. We have observed during passive nIPPV in stable sleep that increases in delivered minute ventilation (VEd) resulted in progressive narrowing of the glottic aperture, with increases in inspiratory resistance and progressive reductions in the percentage of the delivered tidal volume effectively reaching the lungs. For a given level of VEd, comparisons showed that the glottis was significantly narrower during sleep than during wakefulness and that the glottis was significantly narrower during stage 2 than during stages 3/4 non-rapid-eye-movement sleep. Moreover, when CO2 is added to the inspired air, glottic aperture increased in five of nine trials without changes in sleep stage. We also observed a significant negative correlation between glottic width and the VED, independent of the CO2 level. We conclude that during nIPPV glottis narrowing results in a decrease in the proportion of the delivered tidal volume reaching the lungs.


2018 ◽  
Vol 87 (5) ◽  
pp. 263-270
Author(s):  
A. J. H. C. Michielsen ◽  
A. Binetti ◽  
J. Brunsting ◽  
F. Gasthuys ◽  
S. Schauvliege

An eight-year-old Thoroughbred mare was presented with acute colic symptoms. Clinical and ultrasonographic examination revealed a suspicion of diaphragmatic hernia, which was confirmed during an emergency midline laparotomy performed the same day. Patients with diaphragmatic hernia pose a challenge for the surgeon and the anesthesiologist, because of the disturbed function of the diaphragm and the displacement of the abdominal organs into the thoracic cavity. Achieving optimal ventilation and oxygenation without causing damage to the lungs is not simple. In this case, assisted-controlled, intermittent positive pressure ventilation with a low tidal volume, low pressure and relatively high respiratory rate was applied. Alongside the difficulties during ventilation, the patient was cardiovascularly compromised. Due to the extent and position of the hernia, euthanasia was performed after obtaining the owner’s consent during surgery.


2019 ◽  
Vol 39 (5) ◽  
pp. 723-729 ◽  
Author(s):  
David N. Matlock ◽  
Shasha Bai ◽  
Michael D. Weisner ◽  
Norman Comtois ◽  
Jennifer Beck ◽  
...  

1975 ◽  
Vol 3 (4) ◽  
pp. 284-294 ◽  
Author(s):  
N. Abrahams ◽  
G. C. Fisk ◽  
A. E. Churches ◽  
J. Loughman ◽  
J. B. Vonwiller ◽  
...  

Instrument errors that can occur when pneumotachography is used during Intermittent Positive Pressure Ventilation (IPPV) have been described previously (Kafer 1973). Our efforts to eliminate these errors led to the discovery of further inaccuracies, which appear to be due to the design of the differential pressure transducers used with the pneumotachograph head. A system was used in which a sine-wave pump delivered a constant tidal volume to a dummy lung, the tidal volume being measured by means of a pneumotachograph. Using Grass, Statham and Devices differential pressure transducers, the volume recorded as leaving the dummy lung was consistently greater than that recorded as entering, and changing the pneumatic polarity of the differential pressure transducer produced large differences in the recorded volume. In some cases the error was greater than the volume being measured. There would seem to be several causes of such errors. The Sanborn 270 differential pressure transducer and the Greer micromanometer appeared to be free of these artifacts. The results of this study throw into doubt much previously published work using pneumotachography during IPPV.


2017 ◽  
Vol 62 (4) ◽  
pp. 334
Author(s):  
K. PAVLIDOU (Κ. ΠΑΥΛΙΔΟΥ) ◽  
I. SAVVAS (Ι. ΣΑΒΒΑΣ) ◽  
T. ANAGNOSTOU (Τ. ΑΝΑΓΝΩΣΤΟΥ)

Mechanical ventilation is the process of supporting respiration by manual or mechanical means. When normal breathing is inefficient or has stopped, mechanical ventilation is life-saving and should be applied at once. The ventilator increases the patient's ventilation by inflating the lungs with oxygen or a mixture of air and oxygen. Ventilators play an important role in the anaesthetic management of patients, as well as in the treatment of patients in the ICU. However, there are differences between the anaesthetic ventilators and the ventilators in ICU. The main indication for mechanical ventilation is difficulty in ventilation and/or oxygenation of the patient because of any respiratory or other disease. The aims of mechanical ventilation are to supply adequate oxygen to patients with a limited vital capacity, to treat ventilatory failure, to reduce dyspnoea and to facilitate rest of fatigued breathing muscles. Depression of the central nervous system function is a pre-requirement for mechanical ventilation. Some times, opioids or muscle relaxants can be used in order to depress patient's breathing. Mechanical ventilation can be applied using many different modes: assisted ventilation, controlled ventilation, continuous positive pressure ventilation, intermittent positive pressure ventilation and jet ventilation. Furthermore, there are different types of automatic ventilators built to provide positive pressure ventilation in anaesthetized or heavily sedated or comatose patients: manual ventilators (Ambu-bag), volumecontrolled ventilators with pressure cycling, volume-controlled ventilators with time cycling and pressure-controlled ventilators. In veterinary practice, the ventilator should be portable, compact and easy to operate. The controls on most anaesthetic ventilators include settings for tidal volume, inspiratory time, inspiratory pressure, respiratory rate and inspiration: expiration (I:E) ratio. The initial settings should be between 10-20 ml/kg for tidal volume, 12-30 cmH2 0 for the inspiratory pressure and 8-15 breaths/min for the respiratory rate. Mechanical ventilation is a very important part of treatment in the ICU, but many problems may arise during application of mechanical ventilation in critically ill patients. All connections should be checked in advance and periodically for mechanical problems like leaks. Moreover, complications like lung injury, pneumonia, pneumothorax, myopathy and respiratory failure can occur during the course of mechanical ventilation causing difficulty in weaning.


Author(s):  
Bayane Sabsabi ◽  
Ava Harrison ◽  
Laura Banfield ◽  
Amit Mukerji

Objective The study aimed to systematically review and analyze the impact of nasal intermittent positive pressure ventilation (NIPPV) versus continuous positive airway pressure (CPAP) on apnea of prematurity (AOP) in preterm neonates. Study Design In this systematic review and meta-analysis, experimental studies enrolling preterm infants comparing NIPPV (synchronized, nonsynchronized, and bi-level) and CPAP (all types) were searched in multiple databases and screened for the assessment of AOP. Primary outcome was AOP frequency per hour (as defined by authors of included studies). Results Out of 4,980 articles identified, 18 studies were included with eight studies contributing to the primary outcome. All studies had a high risk of bias, with significant heterogeneity in definition and measurement of AOP. There was no difference in AOPs per hour between NIPPV versus CPAP (weighted mean difference = −0.19; 95% confidence interval [CI]: −0.76 to 0.37; eight studies, 456 patients). However, in a post hoc analysis evaluating the presence of any AOP (over varying time periods), the pooled odds ratio (OR) was lower with NIPPV (OR: 0.46; 95% CI: 0.32–0.67; 10 studies, 872 patients). Conclusion NIPPV was not associated with decrease in AOP frequency, although demonstrated lower odds of developing any AOP. However, definite recommendations cannot be made based on the quality of the published evidence. Key Points


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