Abstract
Purpose
Rapid increase in inspired isoflurane concentration increases heart rate and arterial blood pressure. To investigate whether the responses to isoflurane were elicited from stimulation of lower airway and/or lungs, haemodynamic responses to isoflurane administered after tracheal intubation were measured with or without endotracheal or intravenous administration of lidocaine.
Methods
Seventy-two ASA physical status I patients, aged 21–50 yr, were randomly allocated to one of four groups. After tracheal intubation, anaesthesia was maintained with oxygen 100% and isoflurane 1.0% with controlled ventilation. After stabilization for 15 min, the isoflurane concentration was rapidly increased to 3.0% in three groups. An endotracheal lidocaine group received pretreatment with endotracheal 0.4 ml lidocaine 8% spray, an intravenous lidocaine group received pretreatment of 32 mg lidocaineiv, and an isoflurane 3% group received not pretreatment. In a control group, inspired isoflurane concentration was maintained at 1.0%. Heart rate, systolic blood pressure and end-tidal isoflurane concentration were measured every minute for 10 min.
Results
The rapid increase in isoflurane concentration increased heart rate (25 ± 12% increase from baseline; P < 0.05) but the increase was reduced by endotracheal lidocaine (9 ± 9%), but not by intravenous lidocaine (22 ± 13%). The plasma concentration of lidocaine was lower in the endotracheal lidocaine group (0.4 ± 0.3 μg·ml−1) than in theiv lidocaine group ( 1.5 ± 0.2 μg·ml−1).
Conclusion
The isoflurane-induced tachycardia is reduced by pre-treatment with endotracheal lidocaine.
Résumé
Objectif
Un accroissement rapide de la concentration d’isoflurane inspiré augmente la fréquence cardiaque et la tension artérielle. C’est afin d’évaluer si les réactions à l’isoflurane sont déclenchées par la stimulation des voies aériennes inférieures et/ou des poumons, que nous avons mesuré les réponses hémodynamiques à l’isoflurane, administré après l’intubation, avec ou sans administration endotrachéale ou intraveineuse de lidocaïne.
Méthode
Soixante-douze patients ASA, d’état physique I, âgés de 21 à 50 ans, ont été répartis au hasard en quatre groupes. Après l’intubation, l’anesthésie a été maintenue avec 100 % d’oxygène et de l’isoflurane 1,0 % sous ventilation contrôlée. Suivant une stabilisation de 15 min, la concentration d’isoflurane a été rapidement augmenté à 3,0 % dans trois groupes. Un groupe sous lidocaïne endotrachéale a reçu un prétraitement comprenant 0,4 ml de lidocaïne 8 % en pulvérisation endotrachéale, un groupe sous lidocaïne intraveineuse a reçu 32 mg de lidocaïneiv et un groupe sous isoflurane 3% n’a reçu aucun prétraitement. Dans un groupe témoin, la concentration d’isoflurane inspiré a été maintenue à 1,0 %. La fréquence cardiaque, la tension artérielle systolique et la concentration d’isoflurane de fin d’expiration ont été mesurées à chaque minute pendant 10 min.
Résultats
Laccroissement rapide de la concentration d’isoflurane a augmenté la fréquence cardiaque (25 ± 12 % d’augmentation par rapport à la mesure de base;P < 0,05) mais cet accroissement a été réduit par la lidocaïne endotrachéale (9 ± 9 %), et non par la lidocaïne intraveineuse (22 ± 13 %). La concentration plasmatique de lidocaïne était plus faible dans le groupe de lidocaïne endotrachéale (0,4 ± 0,3 μ·ml−1) que dans le groupe de lidocaïneiv (1,5 ± 0,2 μg·ml−1).
Conclusion
La tachycardie induite par l’isoflurane est réduite par le prétraitement avec de la lidocaïne endotrachéale.
Article PDF
Similar content being viewed by others
Avoid common mistakes on your manuscript.
References
Eger EI II. Isoflurane: a review. Anesthesiology 1981; 55: 559–76.
Kotrly KJ, Eben TJ, Vucins E, Igler FO, Barney JA, Kampine JP. Baroreceptor reflex control of heart rate during isoflurane anesthesia in humans. Anesthesiology 1984; 60: 173–9.
Skovsted P, Sapthavichaikul S. The effects of isoflurane on arterial pressure, pulse rate, autonomic nervous activity, and barostatic reflexes. Can Anaesth Soc J 1977; 24: 304–14.
Yli-Hankala A, Randell T, Seppälä T, Lindgren L. Increases in hemodynamic variables and catecholamine levels after rapid increase in isoflurane concentration. Anesthesiology 1993; 78: 266–71.
Ishikawa T, Nishino T, Hiraga K. Immediate responses of arterial blood pressure and heart rate to sudden inhalation of high concentrations of isoflurane in normotensive and hypertensive patients. Anesth Analg 1993;77: 1022–5.
Nishino T, Tanaka- A, Ishikawa T, Hiraga K. Respiratory, laryngeal, and tracheal responses to nasal insufflation of volatile anesthetics in anesthetized humans. Anesthesiology 1991; 75: 441–4.
Tanaka S, Tsuchida H, Namba H, Namiki A. Clonidine and lidocaine inhibition of isofluraneinduced tachycardia in humans. Anesthesiology 1994; 81: 1341–9.
Tomori Z, Widdicombe JG. Muscular, bronchomotor and cardiovascular reflexes elicited by mechanical stimulation of the respiratory tract. J Physiol Lond 1969; 200: 25–19.
Himes RS Jr, DiFazio CA, Burney RG. Effects of lidocaine on the anesthetic requirements for nitrous oxide and halothane. Anesthesiology 1977; 47: 437–40.
Coleridge HM, Coleridge JCG, Luck JC, Norman J. The effect of four volatile anaesthetic agents on the impulse activity of two types of pulmonary receptor. Br J Anaesth 1968; 40: 484–92.
Paintal AS. Mechanism of stimulation of type J pulmonary receptors. J Physiol Lond 1969; 203: 511–32.
Warde D, Nagi H, Raflery S. Respiratory complications and hypoxic episodes during inhalation induction with isoflurane in children. Br J Anaesth 1991; 66: 327–30.
Weiskopf RB, Eger EI II, Daniel M, Noorani M. Cardiovascular stimulation induced by rapid increases in desflurane concentration in humans results from activation of tracheopulmonary and systemic receptors. Anesthesiology 1995; 83: 1173–8.
Gormley WP, Murry JM, Trinick TR. Intravenous lidocaine does not attenuate the cardiovascular and catecholamine response to a rapid increase in desflurane concentration. Anesth Analg 1996; 82: 358–61.
Bunting HE, Kelly MC, Milligan KR. Effect of nebulized lignocaine on airway irritation and haemodynamic changes during induction of anaesthesia with desflurane. Br J Anaesth 1995; 75: 631–3.
Weiskoph RB, Moore MA, Eger EI II, et al. Rapid increase in desflurane concentration is associated with greater transient cardiovascular stimulation than with rapid increase in isoflurane concentration in humans. Anesthesiology 1994; 80: 1035–45.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Takakura, K., Sugiura, Y., Takeuchi, K. et al. Endotracheal administration of lidocaine inhibits isofluraneinduced tachycardia. Can J Anaesth 45, 1181–1185 (1998). https://doi.org/10.1007/BF03012460
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF03012460