Increasing sweep gas flow reduces respiratory drive and dyspnea in non-intubated veno-arterial ECMO patients - a pilot study.


Journal

Anesthesiology
ISSN: 1528-1175
Titre abrégé: Anesthesiology
Pays: United States
ID NLM: 1300217

Informations de publication

Date de publication:
04 Mar 2024
Historique:
medline: 4 3 2024
pubmed: 4 3 2024
entrez: 4 3 2024
Statut: aheadofprint

Résumé

Data on assessment and management of dyspnea in patients on veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for cardiogenic shock are lacking. We hypothesized that increasing sweep gas flow through the VA-ECMO oxygenator may decrease dyspnea in non-intubated VA-ECMO patients exhibiting clinically significant dyspnea, with a parallel reduction in respiratory drive. Non-intubated, spontaneously breathing, supine patients on VA-ECMO for cardiogenic shock who presented with a visual analog dyspnea scale (dyspnea-VAS) ≥ 40/100 mm were included. Sweep gas flow was increased up to +6 L/min by three steps of +2 L/min each. Dyspnea was assessed with dyspnea-VAS and Multidimensional Dyspnea Profile. The respiratory drive was assessed by the electromyographic activity of the alae nasi and parasternal muscles. We included 21 patients. On inclusion, median dyspnea-VAS was 50 ([interquartile range] 45-60) mm and sweep gas flow was 1.0 L/min (0.5-2.0). An increase in sweep gas flow significantly decreased dyspnea-VAS (50[45-60] at baseline vs 20[10-30] at 6L/min; p<0.001). The decrease in dyspnea was greater for the sensory component of dyspnea (-50%[43-75]) than for the affective and emotional components (-17%[0-25] and -12%[0-17], p<0.001). An increase in sweep gas flow significantly decreased electromyographic activity of the alae nasi and parasternal muscles (-23%[36-10] and -20[41-0], p<0.001). There was a significant correlation between the sweep gas flow and the dyspnea-VAS (r=-0.91 95%CI[-0.94, -0.87]), between the respiratory drive and the sensory component of dyspnea (r=0.29 95%CI[0.13, 0.44]), between the respiratory drive and the affective component of dyspnea (r=0.29 95%CI[0.02, 0.54]) and between the sweep gas flow and the alae nasi and parasternal (r=-0.31 95%CI[-0.44, -0.22] and r=-0.25 95%CI[-0.44, -0.16]). In critically ill patients with VA-ECMO, an increase in sweep gas flow through the oxygenation membrane decreases dyspnea, possibly mediated by a decrease in respiratory drive.

Sections du résumé

BACKGROUND. UNASSIGNED
Data on assessment and management of dyspnea in patients on veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for cardiogenic shock are lacking. We hypothesized that increasing sweep gas flow through the VA-ECMO oxygenator may decrease dyspnea in non-intubated VA-ECMO patients exhibiting clinically significant dyspnea, with a parallel reduction in respiratory drive.
METHODS. UNASSIGNED
Non-intubated, spontaneously breathing, supine patients on VA-ECMO for cardiogenic shock who presented with a visual analog dyspnea scale (dyspnea-VAS) ≥ 40/100 mm were included. Sweep gas flow was increased up to +6 L/min by three steps of +2 L/min each. Dyspnea was assessed with dyspnea-VAS and Multidimensional Dyspnea Profile. The respiratory drive was assessed by the electromyographic activity of the alae nasi and parasternal muscles.
RESULTS. UNASSIGNED
We included 21 patients. On inclusion, median dyspnea-VAS was 50 ([interquartile range] 45-60) mm and sweep gas flow was 1.0 L/min (0.5-2.0). An increase in sweep gas flow significantly decreased dyspnea-VAS (50[45-60] at baseline vs 20[10-30] at 6L/min; p<0.001). The decrease in dyspnea was greater for the sensory component of dyspnea (-50%[43-75]) than for the affective and emotional components (-17%[0-25] and -12%[0-17], p<0.001). An increase in sweep gas flow significantly decreased electromyographic activity of the alae nasi and parasternal muscles (-23%[36-10] and -20[41-0], p<0.001). There was a significant correlation between the sweep gas flow and the dyspnea-VAS (r=-0.91 95%CI[-0.94, -0.87]), between the respiratory drive and the sensory component of dyspnea (r=0.29 95%CI[0.13, 0.44]), between the respiratory drive and the affective component of dyspnea (r=0.29 95%CI[0.02, 0.54]) and between the sweep gas flow and the alae nasi and parasternal (r=-0.31 95%CI[-0.44, -0.22] and r=-0.25 95%CI[-0.44, -0.16]).
CONCLUSION. UNASSIGNED
In critically ill patients with VA-ECMO, an increase in sweep gas flow through the oxygenation membrane decreases dyspnea, possibly mediated by a decrease in respiratory drive.

Identifiants

pubmed: 38436930
pii: 139862
doi: 10.1097/ALN.0000000000004962
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 American Society of Anesthesiologists. All Rights Reserved.

Déclaration de conflit d'intérêts

Conflicts of Interest: Dr. Alexandre Demoule reports personal fees from Medtronic, grants, personal fees and non-financial support from Philips, personal fees from Baxter, personal fees from Hamilton, personal fees and non-financial support from Fisher & Paykel, grants from the French Ministry of Health, personal fees from Getinge, grants and personal fees from Respinor, grants and non-financial support from Lungpacer, unrelated to the work submitted. Dr. Thomas Similowski reports, over the last 3 years, 1) personal fees for consulting and teaching activities from ADEP Assistance, AstraZeneca France, Chiesi France, KPL consulting, Lungpacer Inc., OSO-AI, TEVA France, Vitalaire, and 2) as a member of the board of a research association, unrestricted grants from Covidien, Lungpacer, Maquet, and Philips, all unrelated to the present work. Dr. Similowski is listed as inventor on issued patents (WO2008006963A3, WO2012004534A1, WO2013164462A1) describing EEG responses to experimental and clinical dyspnea to identify and alleviate dyspnea in noncommunicative patients. Dr. Martin Dres declares having received personal fees and grants from Lungpacer unrelated to the work submitted. Dr. Matthieu Schmidt reports receiving personal fees from Getinge, Drager, and Xenios, outside the submitted work. Dr. Alain Combes reports receiving personal fees from Getinge, Baxter, Xenios, outside the submitted work. Dr. Charles-Edouard Luyt receiving personal fees from AdvanzPharma and Merck, outside of the submitted work. Drs. Côme Bureau, Juliette Chommeloux, Guillaume Hékimian, Marie-Cécile Niérat, Laurence Dangers, Capucine Morélot-Panzini and Isabelle Rivals have no conflicts of interest related to this work.

Auteurs

Côme Bureau (C)

Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, F-75005 Paris, France.
AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, Service de Médecine Intensive - Réanimation (Département "R3S"), F-75013, Paris, France.

Matthieu Schmidt (M)

Sorbonne Université, GRC 30, RESPIRE, INSERM, UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, F-75013 PARIS, France.
Service de médecine intensive-réanimation, Institut de Cardiologie, APHP Sorbonne Université Hôpital Pitié-Salpêtrière, F-75013 PARIS, France.

Juliette Chommeloux (J)

Sorbonne Université, GRC 30, RESPIRE, INSERM, UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, F-75013 PARIS, France.
Service de médecine intensive-réanimation, Institut de Cardiologie, APHP Sorbonne Université Hôpital Pitié-Salpêtrière, F-75013 PARIS, France.

Isabelle Rivals (I)

Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, F-75005 Paris, France.
Equipe de Statistique Appliquée, ESPCI Paris, PSL Research University , UMRS 1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France.

Thomas Similowski (T)

Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, F-75005 Paris, France.
AP-HP, Groupe Hospitalier Universitaire APHP-Sorbonne Université, site Pitié-Salpêtrière, Département R3S, F-75013 Paris, France.

Guillaume Hékimian (G)

Sorbonne Université, GRC 30, RESPIRE, INSERM, UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, F-75013 PARIS, France.
Service de médecine intensive-réanimation, Institut de Cardiologie, APHP Sorbonne Université Hôpital Pitié-Salpêtrière, F-75013 PARIS, France.

Charles-Edouard Luyt (CE)

Sorbonne Université, GRC 30, RESPIRE, INSERM, UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, F-75013 PARIS, France.
Service de médecine intensive-réanimation, Institut de Cardiologie, APHP Sorbonne Université Hôpital Pitié-Salpêtrière, F-75013 PARIS, France.

Marie-Cécile Niérat (MC)

Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, F-75005 Paris, France.

Laurence Dangers (L)

Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, F-75005 Paris, France.
AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, Service de Médecine Intensive - Réanimation (Département "R3S"), F-75013, Paris, France.

Martin Dres (M)

Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, F-75005 Paris, France.
AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, Service de Médecine Intensive - Réanimation (Département "R3S"), F-75013, Paris, France.

Alain Combes (A)

Sorbonne Université, GRC 30, RESPIRE, INSERM, UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, F-75013 PARIS, France.
Service de médecine intensive-réanimation, Institut de Cardiologie, APHP Sorbonne Université Hôpital Pitié-Salpêtrière, F-75013 PARIS, France.

Capucine Morélot-Panzini (C)

Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, F-75005 Paris, France.
AP-HP, Groupe Hospitalier Universitaire APHP-Sorbonne Université, site Pitié-Salpêtrière, Service de Pneumologie (Département R3S), F-75013 Paris, France.

Alexandre Demoule (A)

Sorbonne Université, INSERM, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, F-75005 Paris, France.
AP-HP. Sorbonne Université, Hôpital Pitié-Salpêtrière, Service de Médecine Intensive - Réanimation (Département "R3S"), F-75013, Paris, France.

Classifications MeSH