Cardiovascular Effects of Increasing Positive End-Expiratory Pressure in A Model of Left Ventricular Cardiogenic Shock in Female Pigs.


Journal

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

Informations de publication

Date de publication:
26 Aug 2024
Historique:
medline: 26 8 2024
pubmed: 26 8 2024
entrez: 26 8 2024
Statut: aheadofprint

Résumé

Cardiogenic shock (CS) presents a medical challenge with limited treatment options. Positive end-expiratory pressure (PEEP) during mechanical ventilation has been linked with clinical benefits in patients with CS. We investigated if increasing PEEP levels could unload the left ventricle (LV) in CS in a large animal model of LV-CS. LV-CS was induced in 26 female pigs (60 kg) by microsphere injections into the left main coronary artery. In one study protocol PEEP was increased (5, 10, and 15 cmH2O) and then reverted (15, 10, 5 cmH2O) in 3-minute intervals. In another protocol PEEP increments with higher granularity were conducted through 3-minute intervals (5, 8, 10, 13, and 15 cmH2O). Hemodynamic measurements were performed at all PEEP levels during the healthy state and LV-CS with LV pressure-volume loops. The primary endpoint was pressure-volume area (PVA). Secondary endpoints included other mechano-energetic parameters and estimates of LV preload and afterload. Cardiac output (CO) decreased significantly in LV-CS from 4.5±1.0 L/min to 3.1±0.9 L/min (P<0.001). Increasing PEEP resulted in lower PVA, demonstrating a 36±3% decrease in the healthy state (P<0.001) and 18±3% in LV-CS (P<0.001) at PEEP 15 cmH2O. These effects were highly reversible when PEEP was returned to 5 cmH2O. While mean arterial pressure declined with higher PEEP, CO remained preserved during LV-CS (P=0.339). Increasing PEEP caused reductions in key measures of LV preload and afterload during LV-CS. Right ventricular stroke work index was decreased with increased PEEP. Despite a minor increase in heart rate (HR) at PEEP levels of 15 cmH2O (71 bpm vs. 75 bpm, p<0.05), total mechanical power expenditure (PVA normalized to HR) decreased at higher PEEP. Applying higher PEEP levels reduced PVA, preserving CO while decreasing MAP. PEEP could be a viable LV unloading strategy if titrated optimally during LV-CS.

Sections du résumé

BACKGROUND BACKGROUND
Cardiogenic shock (CS) presents a medical challenge with limited treatment options. Positive end-expiratory pressure (PEEP) during mechanical ventilation has been linked with clinical benefits in patients with CS. We investigated if increasing PEEP levels could unload the left ventricle (LV) in CS in a large animal model of LV-CS.
METHODS METHODS
LV-CS was induced in 26 female pigs (60 kg) by microsphere injections into the left main coronary artery. In one study protocol PEEP was increased (5, 10, and 15 cmH2O) and then reverted (15, 10, 5 cmH2O) in 3-minute intervals. In another protocol PEEP increments with higher granularity were conducted through 3-minute intervals (5, 8, 10, 13, and 15 cmH2O). Hemodynamic measurements were performed at all PEEP levels during the healthy state and LV-CS with LV pressure-volume loops. The primary endpoint was pressure-volume area (PVA). Secondary endpoints included other mechano-energetic parameters and estimates of LV preload and afterload.
RESULTS RESULTS
Cardiac output (CO) decreased significantly in LV-CS from 4.5±1.0 L/min to 3.1±0.9 L/min (P<0.001). Increasing PEEP resulted in lower PVA, demonstrating a 36±3% decrease in the healthy state (P<0.001) and 18±3% in LV-CS (P<0.001) at PEEP 15 cmH2O. These effects were highly reversible when PEEP was returned to 5 cmH2O. While mean arterial pressure declined with higher PEEP, CO remained preserved during LV-CS (P=0.339). Increasing PEEP caused reductions in key measures of LV preload and afterload during LV-CS. Right ventricular stroke work index was decreased with increased PEEP. Despite a minor increase in heart rate (HR) at PEEP levels of 15 cmH2O (71 bpm vs. 75 bpm, p<0.05), total mechanical power expenditure (PVA normalized to HR) decreased at higher PEEP.
CONCLUSIONS CONCLUSIONS
Applying higher PEEP levels reduced PVA, preserving CO while decreasing MAP. PEEP could be a viable LV unloading strategy if titrated optimally during LV-CS.

Identifiants

pubmed: 39186681
pii: 141929
doi: 10.1097/ALN.0000000000005201
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Society of Anesthesiologists.

Déclaration de conflit d'intérêts

Conflicts of interest: Henrik Wiggers has been the principal or a sub-investigator in studies involving the following pharmaceutical companies: MSD, Bayer, Daiichi-Sankyo, Novartis, Novo Nordisk, Sanofi-Aventis, and Pfizer. The other authors have no conflicts of interest to report.

Auteurs

Oskar Kjærgaard Hørsdal (OK)

Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.

Kasper Lykke Wethelund (KL)

Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.

Nigopan Gopalasingam (N)

Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.

Mads Dam Lyhne (MD)

Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Department of Anesthesiology and Intensive Care, Aarhus University Hospital, Aarhus, Denmark.

Mark Stoltenberg Ellegaard (MS)

Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Department of Anesthesiology and Intensive Care, Aarhus University Hospital, Aarhus, Denmark.

Ole Kristian Møller-Helgestad (OK)

Department of Clinical Pharmacology, Aalborg University Hospital, Aalborg, Denmark.

Hanne Berg Ravn (HB)

Department of Anaesthesiology and Intensive Care, Odense University Hospital, Odense, Denmark.
Department of Clinical Research, University of Southern Denmark, Odense, Denmark.

Henrik Wiggers (H)

Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.

Steffen Christensen (S)

Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Department of Anesthesiology and Intensive Care, Aarhus University Hospital, Aarhus, Denmark.

Kristoffer Berg-Hansen (K)

Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.

Classifications MeSH