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November 1996
Desflurane-mediated neurocirculatory activation in humans
Muzi M, Lopatka CW, Ebert TJ;
Anesthesiology
[ see abstract below ]
Desflurane can produce sympathetic activation. This study seeks to
identify the threshold for this response and whether the threshold is
affected by the rate of change of desflurane or the concentration.
Return to the Current Literature Review Front Page, or read the abstract:
ABSTRACT
Background
Rapid increases in the inspired concentration of desflurane have been associated with sympathetic activation, tachycardia, hypertension, and in select cases, myocardial ischemia. The current study examined the effects of the rate of change of the desflurane concentration on the sympathetic and hemodynamic responses to desflurane and sought to determine whether a finite concentration (end-tidal) of desflurane consistently initiated these responses.
Methods
After Institutional Review Board approval, 23 healthy mate volunteers were instrumented for electrocardiograms (heart rate (HR)), intraarterial blood pressure, and peroneal nerve microneurography (sympathetic nerve activity (SNA)). Subjects were given propofol (2.5 mg/kg) and vecuronium (0.15 mg/kg), and their lungs were mechanically ventilated for 30 min at a minimum alveolar concentration of 0.5 MAC with either desflurane or isoflurane (random assignment).
The end-tidal concentration was increased at either 1% per min (n = 7) or 0.5% per min (n = 7) for desflurane or 0.16% per min (n = 9) for isoflurane(MAC-multiple comparable to 1% per min desflurane group) until 1.5 MAC was reached. HR, blood pressure, and SNA were averaged over 1-min segments from 0.5 to 1.5 MAC levels.
Results
Awake neurocirculatory variables did not differ among the three groups. At 0.5 MAC, blood pressure had decreased (12-15%) and HR increased (12-20%) similarly in both groups. SNA decreased 77% in the isoflurane group but was not significantly changed in the desflurane groups. In the des-flurane groups, the threshold (end-tidal concentration associated with a 10% increase in the measured variable) ranged between 4% and 10% for HR and between 4% and 7.7% for SNA.
In the isoflurane group, the threshold occurred between 1.0% and 1.6% for HR and between 0.7% and 1.3% for SNA. The rate of change did not affect the threshold concentration or the peak HR increase in the desflurane groups. In contrast, SNA responses to desflurane were directly proportional to the rate of change.
Conclusions
There was no consistent threshold for the neurocirculatory-y activation associated with desflurane, and the HR and SNA thresholds generally were less than 1 MAC. The HR increase associated with desflurane was not rate- or concentration-dependent. in contrast, SNA responses were proportional to the rate of change and tile concentration of desflurane.
(Key words: Anesthetics, volatile: desflurane; isoflurane. Measurement techniques: microneurography. Sympathetic nervous system: blood pressure; heart rate.)
Received from the Department of Anesthesiology, The Medical College of Wisconsin and VA Medical Center, Milwaukee, Wisconsin. Submitted for publication June 26, 1995. Accepted for publication December 22, 1995. Supported by National Institutes of Health grant RO1, a VA Merit Award (to T.J.E.) and a FAER Award (to M.M.)
Address correspondence to Dr. Ebert: Department of Anesthesiology, VA Medical Center, II 2A, 5000 West National Avenue, Milwaukee, Wisconsin 53295.
Anesthesiology, V 84, No 5, May 1996
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