Abstract
The haemodynamic responses following induction of anaesthesia with ketamine and midazolam have not been determined previously. Twenty adult patients for elective myocardial revascularization were randomized to two regimens for induction of anaesthesia. Patients in Group I received ketamine, 2 mg·kg−1, and midazolam, 0.2 mg·kg−1 and those in Group II received ketamine, 2 mg·kg−1, and midazolam, 0.4 mg·kg−1. Measurements were recorded at baseline, 1 min postinduction, and at one, three, five and ten minutes after tracheal intubation. Tachycardia and hypertension (>20% increases from awake baseline values) were treated with esmolol, 250 μg·kg−1. There were 11 patients in Group I and nine patients in Group II. There were no significant intergroup differences in demographic or haemodynamic variables. Both groups had decreases (P<0.05), in stroke volume, pulmonary capillary wedge pressure, and right ventricular end-diastolic volume at multiple study intervals following anaesthetic induction. None of these changes required clinical intervention. Five patients (all in Group Il) had hypertensive responses to tracheal intubation. Preoperative hypertension (mean arterial pressure ≥100 mmHg) was a predictor (P<0.05) of a hypertensive response to intubation, independent of the midazolam dose. Intravenous ketamine and midazolam was associated with a high incidence (25%) of haemodynamic responses to tracheal intubation. The higher dose of midazolam did not provide any haemodynamic advantage.
Résumé
La réponse hémodynamique après induction de l’anesthésie avec kétamine et midazolam n’a pas été déterminée à date. Vingt patients adultes, pour une chirurgie de revascularisation myocardique, furent randomisés en deux groupes. Le groupe I a reçu de la kétamine 2 mg·kg−1, et du midazolam 0,2 mg·kg−1 alors que le groupe II a reçu de la kétamine 2 mg·kg−1 et du midazolam 0,4 mg·kg−1. Les mesures furent enregistrées avant l’induction, une minute post-inductiion, et à trois, cinq et dix minutes après l’intubation trachéale. La tachycardie et l’hypertension (>20% des valeurs de base après induction) furent traitées avec de l’esmolol, 250 μg·kg−1. Il y avait Il patients dans le groupe I et neuf patients dans le groupe II. Il n’y avait aucune différence significative entre les groupes dans les données démographiques et les variables hémodynamiques. Les deux groupes avaient une diminution significative (P<0,05) dans le volume d’éjection, la pression capillaire pulmonaire bloquée, le volume en fin de diastole du ventricule droit aux différents intervalles de l’étude après induction de l’anesthésie. Aucun de ces changements n’a requis une intervention clinique. Cinq patients (tous du groupe II) ont présenté une hypertension lors de l’intubation. L’hypertension préopératoire (pression artérielle moyenne ≥ 100 mmHg) pouvant prédire (P<0,05) la réponse hypertensive lors de l’intubation et indépendamment de la dose de midazolam. L’administration intraveineuse de kétamine et de midazolam fut associée à une inducence élevée (25%) de réponse hémodynamique lors de l’intubation. La dose élevée de midazolam n’a pas fourni d’avantage hémodynamique.
Article PDF
Similar content being viewed by others
References
Reich DL, Silvay G. Ketamine: an update of the first twenty-five years of clinical experience. Can J Anaesth 1989; 36: 186–97.
White PF, Way WL, Trevor AJ. Ketamine—its pharmacology and therapeutic uses. Anesthesiology 1982; 56: 119–36.
Ivankovich AD, Miletich DJ, Reimann C et al. Cardiovascular effects of centrally administered ketamine in goats. Anesth Analg 1974; 53: 924–33.
Lundy PM, Lockwood PA, Thompson G, Frew R. Differential effects of ketamine isomers on neuronal and extraneuronal catecholamine uptake mechanisms. Anesthesiology 1986; 64: 359–63.
White PF. Comparative evaluation of intravenous agents for rapid sequence induction—thiopental, ketamine and midazolam. Anesthesiology 1982; 57: 279–84.
Cartwright PD, Pingel SM. Midazolam and diazepam in ketamine anaesthesia. Anaesthesia 1984; 59: 439–42.
Toft P, Romer U. Comparison of midazolam and diazepam to supplement total intravenous anaesthesia with ketamine for endoscopy. Can J Anaesth 1987; 34: 466–9.
Tuman KJ, McCarthy RJ, Ivankovich AD. Perioperative hemodynamics using midazolam-ketamine for cardiac surgery. Anesth Analg 1988; 67: S238.
Kaplan JA. Hemodynamic monitoring.In: Kaplan JA (Ed.). Cardiac Anesthesia, 2nd ed., Orlando: Grune & Stratton, 1987: 179–225.
Dhainaut J-F, Brunet F, Monsallier JF et al. Bedside evaluation of right ventricular performance using a rapid computerized thermodilution method. Crit Care Med 1987; 15: 148–52.
Tuman KJ, Keane D, Spiess BD et al. Effect of high dose fentanyl on fluid and vasopressor requirements after cardiac surgery. Journal of Cardiothoracic Anesthesia 1988; 2: 419–29.
Bedford RF, Feinstein B. Hospital admission blood pressure: a predictor for hypertension following endotracheal intubation. Anesth Analg 1980; 59: 367–70.
Stone JG, Föex P, Sear JW et al. Myocardial ischemia in untreated hypertensive patients: effect of a single small oral dose of a beta-adrenergic blocking agent. Anesthesiology 1988; 68: 495–500.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Marlow, R., Reich, D.L., Neustein, S. et al. Haemodynamic response to induction of anaesthesia with ketamine/midazolam. Can J Anaesth 38, 844–848 (1991). https://doi.org/10.1007/BF03036958
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF03036958