Increasing Sweep Gas Flow Reduces Respiratory Drive and Dyspnea in Nonintubated Venoarterial Extracorporeal Membrane Oxygenation Patients: A Pilot Study

Author:

Bureau Côme1ORCID,Schmidt Matthieu2,Chommeloux Juliette3,Rivals Isabelle4,Similowski Thomas5,Hékimian Guillaume6,Luyt Charles-Edouard7,Niérat Marie-Cécile8,Dangers Laurence9,Dres Martin10,Combes Alain11,Morélot-Panzini Capucine12,Demoule Alexandre13

Affiliation:

1. 1Sorbonne Université, Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche S1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France; Assistance Publique–Hôpitaux de Paris Sorbonne Université, Pitié-Salpêtrière Hospital, Médecine Intensive–Réanimation Unit, Paris, France.

2. 2Sorbonne Université, RESPIRE, Institut National de la Santé et de la Recherche Médicale, UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, Paris, France; Médecine Intensive–Réanimation Unit, Cardiologie Institute, Assistance Publique–Hôpitaux de Paris Sorbonne Université, Pitié–Salpêtrière Hospital, Paris, France.

3. 3Sorbonne Université, RESPIRE, Institut National de la Santé et de la Recherche Médicale, UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, Paris, France; Médecine Intensive–Réanimation Unit, Cardiologie Institute, Assistance Publique–Hôpitaux de Paris Sorbonne Université, Hôpital Pitié–Salpêtrière, Paris, France.

4. 4Sorbonne Université, Institut National de la Santé et de la Recherche Médicale, UMRS 1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France; Equipe de Statistique Appliquée, ESPCI Paris, Pitié Salpêtrière Research University, UMRS 1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France.

5. 5Sorbonne Université, Institut National de la Santé et de la Recherche Médicale, UMRS 1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France; Assistance Publique–Hôpitaux de Paris University Hospital Group, Assistance Publique–Hôpitaux de Paris Sorbonne Université, Pitié-Salpêtrière, Paris, France.

6. 6Sorbonne Université, RESPIRE, Institut National de la Santé et de la Recherche Médicale, UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, Paris, France; Médecine Intensive–Réanimation Unit, Cardiologie Institute, Assistance Publique–Hôpitaux de Paris Sorbonne Université, Pitié–Salpêtrière Hospital, Paris, France.

7. 7Sorbonne Université, RESPIRE, Institut National de la Santé et de la Recherche Médicale, UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, Paris, France; Médecine Intensive–Réanimation Unit, Cardiologie Institute, Assistance Publique–Hôpitaux de Paris Sorbonne Université, Pitié–Salpêtrière Hospital, Paris, France.

8. 8Sorbonne Université, Institut National de la Santé et de la Recherche Médicale, UMRS 1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France.

9. 9Sorbonne Université, Institut National de la Santé et de la Recherche Médicale, UMRS 1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France; Assistance Publique–Hôpitaux de Paris Sorbonne Université, Pitié-Salpêtrière, Médecine Intensive–Réanimation Unit, Paris, France.

10. 10Sorbonne Université, Institut National de la Santé et de la Recherche Médicale, UMRS 1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France; Assistance Publique–Hôpitaux de Paris, Sorbonne Université, Pitié-Salpêtrière Hospital, Médecine Intensive–Réanimation Unit, F-75013, Paris, France.

11. 11Sorbonne Université, RESPIRE, Institut National de la Santé et de la Recherche Médicale, UMRS_1166-ICAN, Institute of Cardiometabolism and Nutrition, Paris, France; Médecine Intensive–Réanimation Unit, Institut de Cardiologie, Assistance Publique–Hôpitaux de Paris Sorbonne, Pitié–Salpêtrière Hospital, Paris, France.

12. 12Sorbonne Université, Institut National de la Santé et de la Recherche Médicale, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France; Assistance Publique–Hôpitaux de Paris Groupe Hospitalier Universitaire, Assistance Publique–Hôpitaux de Paris Sorbonne Université, Site Pitié-Salpêtrière, Service de Pneumologie, Paris, France.

13. 13Sorbonne Université, Institut National de la Santé et de la Recherche Médicale, UMRS1158 Neurophysiologie Respiratoire Expérimentale et Clinique, Paris, France; Assistance Publique–Hôpitaux de Paris Sorbonne Université, Pitié-Salpêtrière Hospital, Médecine Intensive–Réanimation Unit, Paris, France.

Abstract

Background Data on assessment and management of dyspnea in patients on venoarterial extracorporeal membrane oxygenation (ECMO) for cardiogenic shock are lacking. The hypothesis was that increasing sweep gas flow through the venoarterial extracorporeal membrane oxygenator may decrease dyspnea in nonintubated venoarterial ECMO patients exhibiting clinically significant dyspnea, with a parallel reduction in respiratory drive. Methods Nonintubated, spontaneously breathing, supine patients on venoarterial ECMO for cardiogenic shock who presented with a dyspnea visual analog scale (VAS) score of greater than or equal to 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 the dyspnea-VAS and the Multidimensional Dyspnea Profile. The respiratory drive was assessed by the electromyographic activity of the alae nasi and parasternal muscles. Results A total of 21 patients were included in the study. Upon inclusion, median dyspnea-VAS was 50 (interquartile range, 45 to 60) mm, and sweep gas flow was 1.0 l/min (0.5 to 2.0). An increase in sweep gas flow significantly decreased dyspnea-VAS (50 [45 to 60] at baseline vs. 20 [10 to 30] at 6 l/min; P < 0.001). The decrease in dyspnea was greater for the sensory component of dyspnea (−50% [−43 to −75]) than for the affective and emotional components (−17% [−0 to −25] and −12% [−0 to −17]; P < 0.001). An increase in sweep gas flow significantly decreased electromyographic activity of the alae nasi and parasternal muscles (−23% [−36 to −10] and −20 [−41 to −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 to −0.87), between the respiratory drive and the sensory component of dyspnea (r = 0.29; 95% CI, 0.13 to 0.44) between the respiratory drive and the affective component of dyspnea (r = 0.29; 95% CI, 0.02 to 0.54) and between the sweep gas flow and the alae nasi and parasternal (r = −0.31; 95% CI, −0.44 to −0.22; and r = −0.25; 95% CI, −0.44 to −0.16). Conclusions In critically ill patients with venoarterial ECMO, an increase in sweep gas flow through the oxygenation membrane decreases dyspnea, possibly mediated by a decrease in respiratory drive. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Publisher

Ovid Technologies (Wolters Kluwer Health)

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