Coronary and left ventricular hemodynamic responses following reversal of flunitrazepam-induced sedation with flumazenil in patients with coronary artery disease

The effects of reversal of flunitrazepam-induced sedation with flumazenil on coronary hemodynamics, myocardial oxygen consumption (MVO2), and left ventricular (LV) performance were investigated, in a double-blind trial, in 12 patients with stable coronary artery disease undergoing cardiac catheteriz...

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Published in:Anesthesiology (Philadelphia) 1991, Vol.74 (1), p.71-76
Main Authors: MARTY, J, NITENBERG, A, PHILIP, I, FOULT, J.-M, JOYON, D, DESMONTS, J.-M
Format: Article
Language:English
Subjects:
Adult
Anesthetics. Neuromuscular blocking agents
Biological and medical sciences
Coronary Circulation - drug effects
Coronary Disease - physiopathology
Diastole - drug effects
Female
Flumazenil - pharmacology
Flunitrazepam - pharmacology
Humans
Male
Medical sciences
Middle Aged
Neuropharmacology
Oxygen Consumption - drug effects
Pharmacology. Drug treatments
Vascular Resistance - drug effects
Ventricular Function, Left - drug effects
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Summary:The effects of reversal of flunitrazepam-induced sedation with flumazenil on coronary hemodynamics, myocardial oxygen consumption (MVO2), and left ventricular (LV) performance were investigated, in a double-blind trial, in 12 patients with stable coronary artery disease undergoing cardiac catheterization. Coronary sinus blood flow was measured by continuous thermodilution. Arterial and coronary sinus blood were analyzed for oxygen and lactate contents. The determinants of LV performance were obtained from the cardiac output measured by thermodilution and from left heart catheterization data. To reverse flunitrazepam-induced sedation, patients were randomly allocated to receive placebo or flumazenil (by increment, up to 1 mg) at the end of procedure. In the placebo group, no significant hemodynamic changes were observed. In the flumazenil group, heart rate, cardiac index, maximum velocity of shortening, and relaxation time constant were not significantly altered. By contrast, mean aortic pressure and LV end-diastolic pressure (baselines: 90 +/- 5 and 7.3 +/- 4.1 mmHg, respectively) increased (9%, P less than 0.05 and 67%, P less than 0.05, respectively) after flumazenil administration, but these changes represented mainly a return toward presedation values. MVO2 and coronary resistance were not significantly altered, whereas CSBF increased slightly (baseline: 119 +/- 20 ml/min; increase 10%, P less than 0.05). No electrocardiographic evidence of myocardial ischemia was observed during the study. These data show that reversal of benzodiazepine effects with flumazenil is not associated with a major alteration of LV systolic function, relaxation, or coronary hemodynamics in patients with coronary artery disease. Nevertheless, it should be cautiously used when LV end-diastolic pressure is increased at the time of its administration.
ISSN:0003-3022
1528-1175
DOI:10.1097/00000542-199101000-00012