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Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study

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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.

in: J CLIN MONIT COMPUT, Jahrgang 36, Nr. 2, 04.2022, S. 341-347.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Saugel, B, Bebert, E-J, Briesenick, L, Hoppe, P, Greiwe, G, Yang, D, Ma, C, Mascha, EJ, Sessler, DI & Rogge, DE 2022, 'Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study', J CLIN MONIT COMPUT, Jg. 36, Nr. 2, S. 341-347. https://doi.org/10.1007/s10877-021-00653-9

APA

Saugel, B., Bebert, E-J., Briesenick, L., Hoppe, P., Greiwe, G., Yang, D., Ma, C., Mascha, E. J., Sessler, D. I., & Rogge, D. E. (2022). Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study. J CLIN MONIT COMPUT, 36(2), 341-347. https://doi.org/10.1007/s10877-021-00653-9

Vancouver

Saugel B, Bebert E-J, Briesenick L, Hoppe P, Greiwe G, Yang D et al. Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study. J CLIN MONIT COMPUT. 2022 Apr;36(2):341-347. https://doi.org/10.1007/s10877-021-00653-9

Bibtex

@article{bf3dfb467b7e43acb3b685b8e08c1d7b,
title = "Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study",
abstract = "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*m2 (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.",
author = "Bernd Saugel and Elisa-Johanna Bebert and Luisa Briesenick and Phillip Hoppe and Gillis Greiwe and Dongsheng Yang and Chao Ma and Mascha, {Edward J} and Sessler, {Daniel I} and Rogge, {Dorothea E}",
year = "2022",
month = apr,
doi = "10.1007/s10877-021-00653-9",
language = "English",
volume = "36",
pages = "341--347",
journal = "J CLIN MONIT COMPUT",
issn = "1387-1307",
publisher = "Springer Netherlands",
number = "2",

}

RIS

TY - JOUR

T1 - Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study

AU - Saugel, Bernd

AU - Bebert, Elisa-Johanna

AU - Briesenick, Luisa

AU - Hoppe, Phillip

AU - Greiwe, Gillis

AU - Yang, Dongsheng

AU - Ma, Chao

AU - Mascha, Edward J

AU - Sessler, Daniel I

AU - Rogge, Dorothea E

PY - 2022/4

Y1 - 2022/4

N2 - 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*m2 (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.

AB - 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*m2 (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.

U2 - 10.1007/s10877-021-00653-9

DO - 10.1007/s10877-021-00653-9

M3 - SCORING: Journal article

C2 - 33523352

VL - 36

SP - 341

EP - 347

JO - J CLIN MONIT COMPUT

JF - J CLIN MONIT COMPUT

SN - 1387-1307

IS - 2

ER -