פוסט זה זמין גם ב:
עברית
http://orcid.org/0000-0002-3607-5181Jonathan L Kwong1, Ian R Drennan2,3, Linda Turner4,
Sheldon Cheskes3,4 Correspondence to Dr Jonathan L Kwong, Division of Emergency Medicine, University of Toronto Faculty of Medicine, Toronto M8W 3S2, Canada; jon.kwong@mail.utoronto.ca
Abstract![](data:image/svg+xml,%3Csvg%20xmlns='http://www.w3.org/2000/svg'%20viewBox='0%200%20134%2050'%3E%3C/svg%3E)
Background Predefibrillation end-tidal CO2 (ETCO2) may predict defibrillation success and could guide defibrillation timing in ventricular fibrillation (VF) cardiac arrest. This relationship has only been studied using advanced airways. Our aim was to evaluate this relationship using both basic (bag–valve–mask (BVM)) and advanced airways (supraglottic airways and endotracheal tubes).
Methods Prehospital patient records and defibrillator files were abstracted for patients with out-of-hospital cardiac arrest in Ontario, Canada, with initial VF cardiac rhythms between 1 January 2018, and 31 December 2019. Analyses assessed the relationship between each predefibrillation ETCO2 reading and defibrillation outcomes at the subsequent 2 min pulse check (ie, VF, asystole, pulseless electrical activity (PEA) or return of spontaneous circulation (ROSC)), accounting for airway types used during resuscitation. Multivariable logistic regression evaluated the association between the first documented predefibrillation ETCO2 and postshock VF termination or ROSC.
Results Of 269 cases abstracted, 153 had predefibrillation ETCO2 measurements and were included in the study. Among these cases, 904 shocks were delivered and 44.4% (n=401) had predefibrillation ETCO2 measured. The first ETCO2 reading was more often from BVM (n=134) than advanced airways (n=19). ETCO2 readings were lower when measured through BVM versus advanced airways (30.5 mm Hg (4.06 kPa) (±14.4 mm Hg (1.92 kPa)) vs 42.1 mm Hg (5.61 kPa) (±22.5 mm Hg (3.00 kPa)), adjANOVA p<0.01). Of all shocks with ETCO2 reading (n=401), no difference in preshock ETCO2 was found for subsequent shocks that resulted in persistent VF (32.2 mm Hg (4.29 kPa) (±15.8 mm Hg (2.11 kPa))), PEA (32.8 mm Hg (4.37 kPa) (±17.1 mm Hg (2.30 kPa))), asystole (32.4 mm Hg (4.32 kPa) (±20.6 mm Hg (2.75 kPa))) or ROSC (32.5 mm Hg (4.33 kPa) (±15.3 mm Hg (2.04 kPa))), analysis of variance p=0.99. In the multivariate analysis using the initial predefibrillation ETCO2, there was no association with VF termination on the subsequent shock (adjusted OR (adjOR) 0.99, 95% CI 0.97 to 1.02, p=0.57) or ROSC (adjOR 1.00, 95% CI 0.97 to 1.03, p=0.94) when evaluated as a continuous or categorical variable.
Conclusion Predefibrillation ETCO2 measurement is not associated with VF termination or ROSC when basic and advanced airways are included in the analysis. The role of predefibrillation ETCO2 requires careful consideration of the type of airway used during resuscitation.