Respiratory Drive in Acute Respiratory Failure

急性呼吸衰竭中的呼吸驱动

基本信息

  • 批准号:
    10637245
  • 负责人:
  • 金额:
    $ 75.05万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2023
  • 资助国家:
    美国
  • 起止时间:
    2023-05-01 至 2028-04-30
  • 项目状态:
    未结题

项目摘要

PROJECT SUMMARY/ABSTRACT Acute respiratory failure (ARF) requiring invasive ventilation occurs in one-third of intensive care unit (ICU) patients and is associated with a high risk of death. Ventilation-induced lung injury (VILI) is a modifiable determinant of ARF outcomes that develops when the at-risk lung experiences excessive global or regional stress/strain. VILI may result from excessive forces applied by the ventilator and/or respiratory muscles. Optimizing ventilator titration has been studied extensively, while far less is known about the contribution of spontaneous breathing effort to VILI in ARF. High respiratory drive can cause injuriously high tidal volumes, increasing global stress/strain either with synchronous effort or breath stacking dyssynchrony depending on ventilator mode. High drive also causes temporally heterogeneous insufflation, increasing intra-tidal regional strain for a given tidal volume. Both patterns of respiratory drive-related increase in stress/strain worsen lung injury in preclinical models and have been observed in patients with ARF, but whether they contribute clinically meaningful lung injury in patients is unclear. Extremes of drive, high or low, also may cause clinically relevant diaphragm injury. High drive risks load-induced injury, particularly in flow-limited ventilator modes or certain patient-ventilator dyssynchronies in which inspiratory support ends prematurely relative to patient effort. Low drive risks diaphragm disuse atrophy, proven to occur in some patients within a few days on the ventilator. Causes of drive heterogeneity in ARF are not well established. Chemoreceptor, mechanoreceptor, and cortical inputs (e.g. pain, anxiety) are well established modulators of respiratory drive, but they alone do not fully explain drive heterogeneity in ARF. Although deep sedation often suppresses respiratory drive in healthy individuals, we recently found that sedation depth and respiratory drive are not well correlated in ARF. Many patients exhibit high drive refractory to deep sedation, while in others even light sedation can completely eliminate drive. Our preliminary data suggest differences in systemic inflammation might explain this drive heterogeneity. This research will deepen understanding of mechanisms underlying drive heterogeneity and its relationship with clinical outcomes in patients with ARF. Our overall hypothesis is that systemic inflammation is a key determinant of respiratory drive, extremes of which cause clinically important lung and diaphragm injury. We will assemble a prospective two-hospital, multi-ICU cohort in whom respiratory mechanics and serum biomarkers are ascertained serially. Aim 1 evaluates circulating inflammatory markers as a potential contributor to drive heterogeneity. Aim 2 determines mechanisms by which extremes of respiratory drive may contribute to lung and diaphragm injury. Aim 3 evaluates the relationship between respiratory drive and time to extubation. Findings from this work will inform development of a precision ventilation strategy, incorporating respiratory drive to optimize lung and diaphragm protection, for evaluation in a future clinical trial.
项目总结/文摘

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

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Jeremy R. Beitler其他文献

Monitoring esophageal pressure
  • DOI:
    10.1007/s00134-024-07401-y
  • 发表时间:
    2024-04-11
  • 期刊:
  • 影响因子:
    21.200
  • 作者:
    Lise Piquilloud;Jeremy R. Beitler;François M. Beloncle
  • 通讯作者:
    François M. Beloncle
Inhaled sedation versus propofol in respiratory failure in the ICU (INSPiRE-ICU2): study protocol for a multicenter randomized controlled trial
  • DOI:
    10.1186/s13063-025-08791-0
  • 发表时间:
    2025-03-31
  • 期刊:
  • 影响因子:
    2.000
  • 作者:
    Brian O’Gara;Alexis L. Serra;Joshua A. Englert;Alisha Sachdev;Robert L. Owens;Steven Y. Chang;Pauline K. Park;Daniel Talmor;Ida Sverud;Peter Sackey;Jeremy R. Beitler
  • 通讯作者:
    Jeremy R. Beitler
Volatile anesthetics for ICU sedation: the future of critical care or niche therapy?
  • DOI:
    10.1007/s00134-022-06842-7
  • 发表时间:
    2022-09-03
  • 期刊:
  • 影响因子:
    21.200
  • 作者:
    Jeremy R. Beitler;Daniel Talmor
  • 通讯作者:
    Daniel Talmor
Respiratory drive in the acute respiratory distress syndrome: pathophysiology, monitoring, and therapeutic interventions
  • DOI:
    10.1007/s00134-020-05942-6
  • 发表时间:
    2020-02-03
  • 期刊:
  • 影响因子:
    21.200
  • 作者:
    Elena Spinelli;Tommaso Mauri;Jeremy R. Beitler;Antonio Pesenti;Daniel Brodie
  • 通讯作者:
    Daniel Brodie
Lung-protective sedation: moving toward a new paradigm of precision sedation
  • DOI:
    10.1007/s00134-022-06901-z
  • 发表时间:
    2022-10-14
  • 期刊:
  • 影响因子:
    21.200
  • 作者:
    Elias Baedorf Kassis;Jeremy R. Beitler;Daniel Talmor
  • 通讯作者:
    Daniel Talmor

Jeremy R. Beitler的其他文献

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{{ truncateString('Jeremy R. Beitler', 18)}}的其他基金

1/2: PREcision VENTilation to attenuate Ventilation-Induced Lung Injury (PREVENT VILI)
1/2:精确通气以减轻通气引起的肺损伤(预防 VILI)
  • 批准号:
    10738958
  • 财政年份:
    2023
  • 资助金额:
    $ 75.05万
  • 项目类别:
Measuring lung stress to identify occult ventilation-induced lung injury in ARDS
测量肺应激以识别 ARDS 患者隐匿性通气引起的肺损伤
  • 批准号:
    9918972
  • 财政年份:
    2019
  • 资助金额:
    $ 75.05万
  • 项目类别:

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    10739060
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    2023
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    $ 75.05万
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利用现有数据的多级分析加强急性呼吸衰竭的实施科学
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    2023
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确定急性呼吸衰竭和脓毒症患者在 ICU 与病房分诊后导致结局差异的患者亚组和护理流程
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