Abstract:
RATIONALE:End-tidal CO2 (EtCO2) is used to monitor cardiopulmonary resuscitation (CPR), but it can be affected by intrathoracic airway closure. Chest compressions induce oscillations in expired CO2, and this could reflect variable degrees of airway patency. OBJECTIVES:To understand the impact of airway closure during CPR, and the relationship between the capnogram shape, airway closure, and delivered ventilation. METHODS:This study had three parts: 1) a clinical study analyzing capnograms after intubation in patients with out-of-hospital cardiac arrest receiving continuous chest compressions, 2) a bench model, and 3) experiments with human cadavers. For 2 and 3, a constant CO2 flow was added in the lung to simulate CO2 production. Capnograms similar to clinical recordings were obtained and different ventilator settings tested. EtCO2 was compared with alveolar CO2 (bench). An airway opening index was used to quantify chest compression-induced expired CO2 oscillations in all three clinical and experimental settings. MEASUREMENTS AND MAIN RESULTS:A total of 89 patients were analyzed (mean age, 69 ± 15 yr; 23% female; 12% of hospital admission survival): capnograms exhibited various degrees of oscillations, quantified by the opening index. CO2 value varied considerably across oscillations related to consecutive chest compressions. In bench and cadavers, similar capnograms were reproduced with different degrees of airway closure. Differences in airway patency were associated with huge changes in delivered ventilation. The opening index and delivered ventilation increased with positive end-expiratory pressure, without affecting intrathoracic pressure. Maximal EtCO2 recorded between ventilator breaths reflected alveolar CO2 (bench). CONCLUSIONS:During chest compressions, intrathoracic airway patency greatly affects the delivered ventilation. The expired CO2 signal can reflect CPR effectiveness but is also dependent on airway patency. The maximal EtCO2 recorded between consecutive ventilator breaths best reflects alveolar CO2.
journal_name
Am J Respir Crit Care Medauthors
Grieco DL,J Brochard L,Drouet A,Telias I,Delisle S,Bronchti G,Ricard C,Rigollot M,Badat B,Ouellet P,Charbonney E,Mancebo J,Mercat A,Savary D,Richard JMdoi
10.1164/rccm.201806-1111OCsubject
Has Abstractpub_date
2019-03-15 00:00:00pages
728-737issue
6eissn
1073-449Xissn
1535-4970journal_volume
199pub_type
杂志文章abstract:RATIONALE:The development of host-targeted, prophylactic, and therapeutic interventions against tuberculosis requires a better understanding of the immune mechanisms that determine the outcome of infection with Mycobacterium tuberculosis. OBJECTIVES:To identify T-cell-dependent mechanisms that are protective in tuberc...
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