scholarly journals Frequency and Risk Factors for Reverse Triggering in Pediatric ARDS During Synchronized Intermittent Mandatory Ventilation

2020 ◽  
Author(s):  
Tatsutoshi Shimatani ◽  
Benjamin Yoon ◽  
Miyako Kyogoku ◽  
Michihito Kyo ◽  
Shinichiro Ohshimo ◽  
...  

Abstract [BACKGROUND] Reverse triggering (RT) occurs when respiratory effort begins after a mandatory breath is initiated by the ventilator. RT may exacerbate ventilator-induced lung injury and lead to breath stacking. We sought to describe the frequency and risk factors for RT amongst ARDS patients and identify risk factors for breath-stacking. [METHODS] Secondary analysis of physiologic data from children on Synchronized Intermittent Mandatory pressure control ventilation enrolled in a single center RCT for ARDS. When children had a spontaneous effort on esophageal manometry, waveforms were recorded and independently analyzed by two investigators to identify RT. [RESULTS] We included 81,990 breaths from 100 patient-days and 36 patients. Overall, 2.46% of breaths were RTs, occurring in 15/36 patients (41.6%). Higher tidal volume and a minimal difference between neural respiratory rate and set ventilator rate were independently associated with RT (p = 0.001) in multivariable modeling. Breath stacking occurred in 534 (26.5%) of 2017 RT breaths, and 14 (93.3%) of 15 RT patients. In multivariable modeling, breath stacking was more likely to occur when total airway delta pressure (Peak Inspiratory Pressure-PEEP) at the time patient effort began, Peak Inspiratory Pressure, PEEP, and Delta Pressure were lower, and when patient effort started well after the ventilator initiated breath (higher phase angle) (all p < 0.05). Together these parameters were highly predictive of breath stacking (AUC 0.979). [CONCLUSIONS] Patients with higher tidal volume and who have a set ventilator rate close to their spontaneous respiratory rate are more likely to have RT, which results in breath stacking over 25% of the time. Trial registration: NIH/NHLBI R01HL124666, Clinical Trials.gov NCT03266016, Registered 29 August 2017, https://clinicaltrials.gov/ct2/show/NCT03266016

2006 ◽  
Vol 82 (4) ◽  
pp. 279-283 ◽  
Author(s):  
Jefferson G. Resende ◽  
Carlos A. M. Zaconeta ◽  
Antônio C. P. Ferreira ◽  
César A. M. Silva ◽  
Marcelo P. Rodrigues ◽  
...  

2019 ◽  
Vol 126 (4) ◽  
pp. 863-869 ◽  
Author(s):  
Maximilian Pinkham ◽  
Russel Burgess ◽  
Toby Mündel ◽  
Stanislav Tatkov

Nasal high flow (NHF) is an emerging therapy for respiratory support, but knowledge of the mechanisms and applications is limited. It was previously observed that NHF reduces the tidal volume but does not affect the respiratory rate during sleep. The authors hypothesized that the decrease in tidal volume during NHF is due to a reduction in carbon dioxide (CO2) rebreathing from dead space. In nine healthy males, ventilation was measured during sleep using calibrated respiratory inductance plethysmography (RIP). Carbogen gas mixture was entrained into 30 l/min of NHF to obtain three levels of inspired CO2: 0.04% (room air), 1%, and 3%. NHF with room air reduced tidal volume by 81 ml, SD 25 ( P < 0.0001) from a baseline of 415 ml, SD 114, but did not change respiratory rate; tissue CO2 and O2 remained stable, indicating that gas exchange had been maintained. CO2 entrainment increased tidal volume close to baseline with 1% CO2 and greater than baseline with 3% CO2 by 155 ml, SD 79 ( P = 0.0004), without affecting the respiratory rate. It was calculated that 30 l/min of NHF reduced the rebreathing of CO2 from anatomical dead space by 45%, which is equivalent to the 20% reduction in tidal volume that was observed. The study proves that the reduction in tidal volume in response to NHF during sleep is due to the reduced rebreathing of CO2. Entrainment of CO2 into the NHF can be used to control ventilation during sleep. NEW & NOTEWORTHY The findings in healthy volunteers during sleep show that nasal high flow (NHF) with a rate of 30 l/min reduces the rebreathing of CO2 from anatomical dead space by 45%, resulting in a reduced minute ventilation, while gas exchange is maintained. Entrainment of CO2 into the NHF can be used to control ventilation during sleep.


2006 ◽  
Vol 0 (0) ◽  
Author(s):  
Jefferson G. Resende ◽  
Cristiane G. Menezes ◽  
Ana M. C. Paula ◽  
Antônio C. P. Ferreira ◽  
Carlos A. M. Zaconeta ◽  
...  

2000 ◽  
Vol 48 (5) ◽  
pp. 766
Author(s):  
Byung O Jeong ◽  
Youn Suck Koh ◽  
Tae Sun Shim ◽  
Sang Do Lee ◽  
Woo Sung Kim ◽  
...  

1985 ◽  
Vol 63 (4) ◽  
pp. 552-555 ◽  
Author(s):  
Kevin R. Cooper ◽  
Peter A. Boswell ◽  
Sung C. Choi

✓ Thirty-three patients with severe head trauma were studied to determine whether the use of positive end-expiratory pressure (PEEP) would cause an increase in intracranial pressure (ICP). Changes in ICP induced by PEEP were then correlated with a panel of physiological variables to try to explain these changes. Mean ICP increased from 13.2 ± 7.7 mm Hg (± standard deviation) to 14.5 ± 7.5 mm Hg (p < 0.005) due to 10 cm H2O PEEP, but the eight patients with elevated baseline ICP experienced no significant increase. Cardiac output and venous admixture (Qs/Qt) declined significantly, while central venous pressure, peak inspiratory pressure, functional residual capacity, and arterial pCO2 increased significantly due to PEEP. Blood pressure and cerebral perfusion pressure were unchanged. The change in ICP due to PEEP correlated significantly with a combination of cardiac output, peak inspiratory pressure, Qs/Qt, and changes in blood pressure and arterial pCO2 due to PEEP, indicating that the effect of PEEP on ICP could be largely explained by its effect on hemodynamic and respiratory variables. No patient deteriorated clinically due to PEEP. It is concluded that 10 cm H2O PEEP increases ICP slightly via its effect on other physiological variables, but that this small increase in ICP is clinically inconsequential.


CHEST Journal ◽  
1989 ◽  
Vol 95 (5) ◽  
pp. 1081-1088 ◽  
Author(s):  
David C. Lain ◽  
Robert DiBenedetto ◽  
Stephen L. Morris ◽  
An Van Nguyen ◽  
Robert Saulters ◽  
...  

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