A "minidose" of 4 mg bupivacaine in combination with 20 microg fentanyl provides spinal anesthesia for surgical repair of hip fracture in the elderly. The minidose combination caused dramatically less hypotension than 10 mg bupivacaine and nearly eliminated the need for vasopressor support of blood pressure.

The syndrome of transient neurologic symptoms (TNS) after spinal lidocaine has been presumed to be a manifestation of local anesthetic neurotoxicity. Although TNS is not associated with either lidocaine concentration or dose, its incidence has never been examined with very small doses of spinal lidocaine. One hundred ten adult ASA physical status I and II patients presenting for arthroscopic surgery of the knee were randomly assigned to receive spinal anesthesia with either 1% hypobaric lidocaine 50 mg (Group L50) or 1% hypobaric lidocaine 20 mg + 25 microg fentanyl (Group L20/F25). Hemodynamic data, block height and regression, and time to first micturition and discharge were recorded. Follow-up phone calls were made by a blinded researcher at 48-72 h using a standardized questionnaire. Both groups had a median peak cephalad block level of T10. Lidocaine 50 mg was associated with a greater decrease in systolic blood pressure and a greater need for ephedrine. Time until block regression to the S2 dermatome (80 vs. 110 min) and outpatient time to void (130 vs 162 min) and discharge (145 vs. 180 min) were faster in the L20/F25 group. Complaints of TNS were found in 32.7% of the patients in the L50 group and in 3.6% of the patients in the L20/F25 group. We conclude that spinal anesthesia with lidocaine 20 mg + fentanyl 25 microg provided adequate anesthesia with greater hemodynamic stability and faster recovery than spinal anesthesia with lidocaine 50 mg. The incidence of TNS after spinal lidocaine 20 mg + fentanyl 25 microg was significantly less than that after spinal lidocaine 50 mg.

Increased LF power reflects sympathetic cardiac activation. As the LF range accounts for regulation of blood pressure and baroreflex, several mechanisms may explain this activation. This in turn may predispose patients who suffer from cardiac disease to higher risk of developing ventricular arrhythmias, besides the possible adverse hemodynamic consequences of PPP.

No abstract