Anesthetic Depth Defined Using Multiple Noxious Stimuli during Isoflurane/Oxygen Anesthesia: II. Hemodynamic Responses

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The hemodynamic effects of isoflurane have been studied extensively. However, most data are obtained from volunteers or patients in the absence of surgical stimulation. The hemodynamic responses to various stimulation patterns of different intensity have not been evaluated.


In 26 patients, the ability of isoflurane to suppress motor and hemodynamic reactions in response to noxious stimulations of variable degree (trapezius squeeze, tetanic stimulation, laryngoscopy, skin incision, and laryngoscopy plus intubation) was evaluated by measuring arterial blood pressure and heart rate before and after stimulation.


At concentrations that inhibited motor response to these stimuli in 50% of all patients, systolic blood pressure increased by 9 (trapezius squeeze), 15 (tetanic stimulation), 23 (laryngoscopy), 35 (skin incision) and 49 (intubation) mmHg, and heart rate by 5 (trapezius squeeze), 15 (tetanic stimulation), 17 (laryngoscopy), 36 (skin incision), and 36 (intubation) min-1 compared to the prestimulation values. An analysis using multiple regression showed that blood pressure response was influenced most by the type of stimulation followed by the concomitantly occurring motor reaction, the anesthesia time, and least by the isoflurane concentration per se. A high isoflurane concentration had no influence on the magnitude of blood pressure or heart rate increase to stimulation, but it decreased the prestimulation blood pressure and slightly increased the prestimulation heart rate. Heart rate responses were less consistent than those of blood pressure.


Isoflurane used as a sole agent is unable to suppress hemodynamic reactions (blood pressure and heart rate) to painful stimuli. A “normal” blood pressure following stimulation can be achieved only if prestimulation blood pressure is depressed to levels that may be clinically unacceptable. The lack of motor response is not an accurate predictor of the ability of an agent to depress hemodynamic reaction.

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