The effect of propofol-sufentanil intravenous anesthesia on systemic and cerebral circulation, cerebral autoregulation and CO2 reactivity – a case-series
O efeito da anestesia intravenosa com propofol-sufentanil na circulação sistêmica e cerebral, autorregulação cerebral e reatividade ao CO2 : uma série de casos
Marianna Juhász, Dénes Páll, Béla Fülesdi, Levente Molnár, Tamás Végh, Csilla Molnár
Abstract
Background and objectives
The aim of our study was to assess systemic and cerebral hemodynamic changes as well as cerebral CO2-reactivity during propofol anesthesia.
Methods
27 patients undergoing general anesthesia were enrolled. Anesthesia was maintained using the Target-Controlled Infusion (TCI) method according to the Schnider model, effect site propofol concentration of 4 μg.mL-1. Ventilatory settings (respiratory rate and tidal volume) were adjusted to reach and maintain 40, 35 and 30 mmHg EtCO2 for 5-minutes, respectively. At the end of each period, transcranial Doppler and hemodynamic parameters using applanation tonometry were recorded.
Results
Systemic mean arterial pressure significantly decreased during anesthetic induction and remained unchanged during the entire study period. Central aortic and peripherial pulse pressure did not change significantly during anesthetic induction and maintenance, whereas augmentation index as marker of arterial stiffness significantly decreased during the anesthetic induction and remained stable at the time points when target CO2 levels were reached. Both cerebral autoregulation and cerebral CO2-reactivity was maintained during propofol anesthesia.
Conclusions
Propofol at clinically administered doses using the Total Intravenous Anesthesia (TIVA/TCI) technique decreases systemic blood pressure, but does not affect static cerebral autoregulation, flow-metabolism coupling and cerebrovascular CO2 reactivity. According to our measurements, propofol may exert its systemic hemodynamic effect through venodilation.
Trial registration
The study was registered at http://www.clinicaltrials.gov, identifier: NCT02203097, registration date: July 29, 2014.
Keywords
Resumo
Justificativa e objetivos: O objetivo do nosso estudo foi avaliar as alterações hemodinâmicas sistêmicas e cerebrais, bem como a reatividade cerebral de CO2 durante a anestesia com propofol. Métodos: 27 pacientes submetidos à anestesia geral foram incluídos. A manutenção da anestesia foi realizada pelo método de Infusão Controlada-Alvo (TCI) de acordo com o modelo Schnider, concentração de propofol no local de efeito de 4 g.mL-1. As configurações ventilatórias (frequência respiratória e volume corrente) foram ajustadas para atingir e manter 40, 35 e 30 mmHg de EtCO2 por 5 minutos, respectivamente. Ao final de cada período, o Doppler transcraniano e os parâmetros hemodinâmicos por meio da tonometria de aplanação foram registrados. Resultados: A pressão arterial média sistêmica diminuiu significativamente durante a indução anestésica e permaneceu inalterada durante todo o período do estudo. A pressão de pulso aórtica central e periférica não mudou significativamente durante a indução e manutenção anestésica, enquanto o índice de aumento como marcador de rigidez arterial diminuiu significativamente durante a indução anestésica e permaneceu estável nos momentos em que os níveis-alvo de CO2 foram atingidos. Tanto a autorregulação cerebral quanto a reatividade cerebral de CO2 foram mantidas durante a anestesia com propofol. Conclusões: O propofol em doses administradas clinicamente pela técnica de anestesia intravenosa total (TIVA / TCI) diminui a pressão arterial sistêmica, mas não afeta a autorregulação cerebral estática, o acoplamento do metabolismo do fluxo e a reatividade cerebrovascular de CO2. De acordo com nossas medições, o propofol pode exercer seu efeito hemodinâmico sistêmico por meio da venodilatação.
Palavras-chave
References
1 K. Schmieder, W. Schregel, M. Engelhardt, et al. Cerebral vascular reactivity response to anaesthetic induction with propofol in patients with intracranial space-occupying lesions and vascular malformations Eur J Anaesthesiol, 20 (2003), pp. 457-460
2 A.R. Absalom, V. Mani, T. De Smet, et al. Pharmacokinetic models for propofol - defining and illuminating the devil in the detail Br J Anaesth, 103 (2009), pp. 26-37
3 F. de Wit, A.L. van Vliet, R.B. de Wilde, et al. The effect of propofol on haemodynamics: cardiac output, venous return, mean systemic filling pressure, and vascular resistances Br J Anaesth, 116 (2016), pp. 784-789
4 M. Juhász, L. Molnár, B. Fülesdi, et al. Effect of sevoflurane on systemic and cerebral circulation, cerebral autoregulation and CO(2) reactivity BMC Anesthesiol, 19 (2019), p. 109
5 A. Conti, D.G. Iacopino, V. Fodale, et al. Cerebral haemodynamic changes during propofol-remifentanil or sevoflurane anaesthesia: transcranial Doppler study under bispectral index monitoring Br J Anaesth, 97 (2006), pp. 333-339
6 P. Sárkány, S. Lengyel, R. Nemes, et al. Non-invasive pulse wave analysis for monitoring the cardiovascular effects of CO2 pneumoperitoneum during laparoscopic cholecystectomy--a prospective case-series study BMC Anesthesiol, 14 (2014), p. 98
7 C. Leve, A. Hong, S. Millasseau, et al. Influence of noninvasive central blood pressure devices for afterload monitoring with aortic velocity-pressure Loop in anesthetized patients Blood Press Monit, 25 (2020), pp. 184-194
8 G. Settakis, A. Lengyel, C. Molnár, et al. Transcranial doppler study of the cerebral hemodynamic changes during breath-holding and hyperventilation tests J Neuroimaging, 12 (2002), pp. 252-258
9 M. Muzi, R.A. Berens, J.P. Kampine, et al. Venodilation contributes to propofol-mediated hypotension in humans Anesth Analg, 74 (1992), pp. 877-883
10 S. Hoka, K. Yamaura, T. Takenaka, et al. Propofol-induced increase in vascular capacitance is due to inhibition of sympathetic vasoconstrictive activity Anesthesiology, 89 (1998), pp. 1495-1500
11 A. Dagal, A.M. Lam Cerebral autoregulation and anesthesia Curr Opin Anaesthesiol, 22 (2009), pp. 547-552
12 A. Möller Petrun, M. Kamenik Bispectral index-guided induction of general anaesthesia in patients undergoing major abdominal surgery using propofol or etomidate: a double-blind, randomized, clinical trial Br J Anaesth, 110 (2013), pp. 388-396
13 C.S. Goodchild, J.M. Serrao Propofol-induced cardiovascular depression: science and art Br J Anaesth, 115 (2015), pp. 641-642
14 X.X. Song, B.W. Yu Anesthetic effects of propofol in the healthy human brain: functional imaging evidence J Anesth, 29 (2015), pp. 279-288
15 A. Vandesteene, V. Trempont, E. Engelman, et al. Effect of propofol on cerebral blood flow and metabolism in man Anaesthesia, 43 Suppl (1988), pp. 42-43
16 K.K. Kaisti, L. Metsähonkala, M. Teräs, et al. Effects of surgical levels of propofol and sevoflurane anesthesia on cerebral blood flow in healthy subjects studied with positron emission tomography Anesthesiology, 96 (2002), pp. 1358-1370
17 G.F. Jansen, B.H. van Praagh, M.B. Kedaria, et al. Jugular bulb oxygen saturation during propofol and isoflurane/nitrous oxide anesthesia in patients undergoing brain tumor surgery Anesth Analg, 89 (1999), pp. 358-363
18 F. Grüne, S. Kazmaier, R.J. Stolker, et al. Carbon dioxide induced changes in cerebral blood flow and flow velocity: role of cerebrovascular resistance and effective cerebral perfusion pressure J Cereb Blood Flow Metab., 35 (2015), pp. 1470-1477
19 R. Mariappan, J. Mehta, J. Chui, et al. Cerebrovascular reactivity to carbon dioxide under anesthesia: a qualitative systematic review J Neurosurg Anesthesiol, 27 (2015), pp. 123-135
20 A. Nakagomi, T. Shoji, S. Okada, et al. Validity of the augmentation index and pulse pressure amplification as determined by the SphygmoCor XCEL device: a comparison with invasive measurements Hypertens Res, 41 (2018), pp. 27-32
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