Cargando…
Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study
It remains unclear whether reduced myocardial contractility, venous dilation with decreased venous return, or arterial dilation with reduced systemic vascular resistance contribute most to hypotension after induction of general anesthesia. We sought to assess the relative contribution of various hem...
Autores principales: | , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Netherlands
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9122881/ https://www.ncbi.nlm.nih.gov/pubmed/33523352 http://dx.doi.org/10.1007/s10877-021-00653-9 |
_version_ | 1784711439680798720 |
---|---|
author | Saugel, Bernd Bebert, Elisa-Johanna Briesenick, Luisa Hoppe, Phillip Greiwe, Gillis Yang, Dongsheng Ma, Chao Mascha, Edward J. Sessler, Daniel I. Rogge, Dorothea E. |
author_facet | Saugel, Bernd Bebert, Elisa-Johanna Briesenick, Luisa Hoppe, Phillip Greiwe, Gillis Yang, Dongsheng Ma, Chao Mascha, Edward J. Sessler, Daniel I. Rogge, Dorothea E. |
author_sort | Saugel, Bernd |
collection | PubMed |
description | It remains unclear whether reduced myocardial contractility, venous dilation with decreased venous return, or arterial dilation with reduced systemic vascular resistance contribute most to hypotension after induction of general anesthesia. We sought to assess the relative contribution of various hemodynamic mechanisms to hypotension after induction of general anesthesia with sufentanil, propofol, and rocuronium. In this prospective observational study, we continuously recorded hemodynamic variables during anesthetic induction using a finger-cuff method in 92 non-cardiac surgery patients. After sufentanil administration, there was no clinically important change in arterial pressure, but heart rate increased from baseline by 11 (99.89% confidence interval: 7 to 16) bpm (P < 0.001). After administration of propofol, mean arterial pressure decreased by 23 (17 to 28) mmHg and systemic vascular resistance index decreased by 565 (419 to 712) dyn*s*cm(−5)*m(2) (P values < 0.001). Mean arterial pressure was < 65 mmHg in 27 patients (29%). After propofol administration, heart rate returned to baseline, and stroke volume index and cardiac index remained stable. After tracheal intubation, there were no clinically important differences compared to baseline in heart rate, stroke volume index, and cardiac index, but arterial pressure and systemic vascular resistance index remained markedly decreased. Anesthetic induction with sufentanil, propofol, and rocuronium reduced arterial pressure and systemic vascular resistance index. Heart rate, stroke volume index, and cardiac index remained stable. Post-induction hypotension therefore appears to result from arterial dilation with reduced systemic vascular resistance rather than venous dilation or reduced myocardial contractility. SUPPLEMENTARY INFORMATION: The online version of this article (10.1007/s10877-021-00653-9) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-9122881 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Netherlands |
record_format | MEDLINE/PubMed |
spelling | pubmed-91228812022-05-22 Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study Saugel, Bernd Bebert, Elisa-Johanna Briesenick, Luisa Hoppe, Phillip Greiwe, Gillis Yang, Dongsheng Ma, Chao Mascha, Edward J. Sessler, Daniel I. Rogge, Dorothea E. J Clin Monit Comput Original Research It remains unclear whether reduced myocardial contractility, venous dilation with decreased venous return, or arterial dilation with reduced systemic vascular resistance contribute most to hypotension after induction of general anesthesia. We sought to assess the relative contribution of various hemodynamic mechanisms to hypotension after induction of general anesthesia with sufentanil, propofol, and rocuronium. In this prospective observational study, we continuously recorded hemodynamic variables during anesthetic induction using a finger-cuff method in 92 non-cardiac surgery patients. After sufentanil administration, there was no clinically important change in arterial pressure, but heart rate increased from baseline by 11 (99.89% confidence interval: 7 to 16) bpm (P < 0.001). After administration of propofol, mean arterial pressure decreased by 23 (17 to 28) mmHg and systemic vascular resistance index decreased by 565 (419 to 712) dyn*s*cm(−5)*m(2) (P values < 0.001). Mean arterial pressure was < 65 mmHg in 27 patients (29%). After propofol administration, heart rate returned to baseline, and stroke volume index and cardiac index remained stable. After tracheal intubation, there were no clinically important differences compared to baseline in heart rate, stroke volume index, and cardiac index, but arterial pressure and systemic vascular resistance index remained markedly decreased. Anesthetic induction with sufentanil, propofol, and rocuronium reduced arterial pressure and systemic vascular resistance index. Heart rate, stroke volume index, and cardiac index remained stable. Post-induction hypotension therefore appears to result from arterial dilation with reduced systemic vascular resistance rather than venous dilation or reduced myocardial contractility. SUPPLEMENTARY INFORMATION: The online version of this article (10.1007/s10877-021-00653-9) contains supplementary material, which is available to authorized users. Springer Netherlands 2021-02-01 2022 /pmc/articles/PMC9122881/ /pubmed/33523352 http://dx.doi.org/10.1007/s10877-021-00653-9 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Original Research Saugel, Bernd Bebert, Elisa-Johanna Briesenick, Luisa Hoppe, Phillip Greiwe, Gillis Yang, Dongsheng Ma, Chao Mascha, Edward J. Sessler, Daniel I. Rogge, Dorothea E. Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study |
title | Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study |
title_full | Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study |
title_fullStr | Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study |
title_full_unstemmed | Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study |
title_short | Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study |
title_sort | mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9122881/ https://www.ncbi.nlm.nih.gov/pubmed/33523352 http://dx.doi.org/10.1007/s10877-021-00653-9 |
work_keys_str_mv | AT saugelbernd mechanismscontributingtohypotensionafteranestheticinductionwithsufentanilpropofolandrocuroniumaprospectiveobservationalstudy AT bebertelisajohanna mechanismscontributingtohypotensionafteranestheticinductionwithsufentanilpropofolandrocuroniumaprospectiveobservationalstudy AT briesenickluisa mechanismscontributingtohypotensionafteranestheticinductionwithsufentanilpropofolandrocuroniumaprospectiveobservationalstudy AT hoppephillip mechanismscontributingtohypotensionafteranestheticinductionwithsufentanilpropofolandrocuroniumaprospectiveobservationalstudy AT greiwegillis mechanismscontributingtohypotensionafteranestheticinductionwithsufentanilpropofolandrocuroniumaprospectiveobservationalstudy AT yangdongsheng mechanismscontributingtohypotensionafteranestheticinductionwithsufentanilpropofolandrocuroniumaprospectiveobservationalstudy AT machao mechanismscontributingtohypotensionafteranestheticinductionwithsufentanilpropofolandrocuroniumaprospectiveobservationalstudy AT maschaedwardj mechanismscontributingtohypotensionafteranestheticinductionwithsufentanilpropofolandrocuroniumaprospectiveobservationalstudy AT sesslerdanieli mechanismscontributingtohypotensionafteranestheticinductionwithsufentanilpropofolandrocuroniumaprospectiveobservationalstudy AT roggedorotheae mechanismscontributingtohypotensionafteranestheticinductionwithsufentanilpropofolandrocuroniumaprospectiveobservationalstudy |