Anaesthesiology intensive therapy · 2020
The effect of intravenous lidocaine on hemodynamic response to endotracheal intubation during sufentanil-based induction of anaesthesia.
СтатьяРандомизированное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Zou Yi, Kong Gaoyin, Wei Lai, Ling Yingzi, Tang Yixun, Zhang Le, Huang Qian
Аннотация
INTRODUCTION: Endotracheal intubation (ETI) can cause a cardiovascular response. The aim of the present study was to investigate the effect of intravenous lidocaine on the hemodynamic response to ETI during sufentanil-based induction of anaesthesia.
MATERIAL AND METHODS: Ninety patients aged 18-65 years were recruited, induction of anaesthesia was initiated by sufentanil, midazolam, cisatracurium, and propofol, the patients were randomized to three groups: Group L1 received 1 mg/kg-1 of lidocaine, Group L1.5 received 1.5 mg kg-1 of lidocaine, Group S received an equal volume of normal saline (NS). Lidocaine or NS was administered in a bolus 2 min before ETI. Systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), and heart rate (HR) were recorded at four time points: before anaesthetic induction, 1 min after lidocaine administration, immediately after ETI, 5 min after ETI. The incidences of hypotension, hypertension, bradycardia, and tachycardia were also recorded.
RESULTS: The SAP, DAP, MAP, and HR at baseline were not significantly different among the three groups (P = 0.620, P = 0.575, P = 0.433, P = 0.537, respectively). Immediately after ETI, the SAP in Group L1 was significantly lower than Group S (P = 0.024), while the DAP, MAP, and HR were comparable among the three groups at the same time points (P > 0.05). There were no significant differences in the incidences of hypotension, hypertension, bradycardia and tachycardia among the three groups (P > 0.200).
CONCLUSIONS: Intravenous lidocaine could attenuate the increase of blood pressure but not HR after ETI during sufentanil-based induction of anaesthesia without increased incidence of side-effects.
MATERIAL AND METHODS: Ninety patients aged 18-65 years were recruited, induction of anaesthesia was initiated by sufentanil, midazolam, cisatracurium, and propofol, the patients were randomized to three groups: Group L1 received 1 mg/kg-1 of lidocaine, Group L1.5 received 1.5 mg kg-1 of lidocaine, Group S received an equal volume of normal saline (NS). Lidocaine or NS was administered in a bolus 2 min before ETI. Systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), and heart rate (HR) were recorded at four time points: before anaesthetic induction, 1 min after lidocaine administration, immediately after ETI, 5 min after ETI. The incidences of hypotension, hypertension, bradycardia, and tachycardia were also recorded.
RESULTS: The SAP, DAP, MAP, and HR at baseline were not significantly different among the three groups (P = 0.620, P = 0.575, P = 0.433, P = 0.537, respectively). Immediately after ETI, the SAP in Group L1 was significantly lower than Group S (P = 0.024), while the DAP, MAP, and HR were comparable among the three groups at the same time points (P > 0.05). There were no significant differences in the incidences of hypotension, hypertension, bradycardia and tachycardia among the three groups (P > 0.200).
CONCLUSIONS: Intravenous lidocaine could attenuate the increase of blood pressure but not HR after ETI during sufentanil-based induction of anaesthesia without increased incidence of side-effects.