Femoral nerve "sheath" for inguinal paravascular lumbar plexus block is not found in human cadavers.

STUDY OBJECTIVE: To determine if a femoral nerve sheath capable of conveying local anesthetic to the lumbar plexus and the obturator nerve exists in human cadavers. DESIGN: Injection of methylene blue dye into the femoral nerves of human cadavers followed by dissection and observation of dye distribution. SETTING: University medical center pathology department autopsy room. PATIENTS: Six fresh adult cadavers about to undergo postmortem examination. INTERVENTIONS: Both femoral nerves of six fresh cadavers were injected with either 20 ml or 40 ml of dye. The abdomen was opened and distribution of the dye was observed. MEASUREMENTS AND MAIN RESULTS: In all of the cadavers studied there was no evidence of a femoral nerve sheath capable of conveying methylene blue dye to the lumbar plexus. Both 20 ml and 40 ml of dye injected into the femoral nerve failed to reach the lumbar plexus or the obturator nerve. When 40 ml of dye was injected it always stained the femoral nerves, it usually stained the lateral femoral cutaneous nerves, but it never stained the obturator nerves. CONCLUSIONS: A femoral nerve sheath capable of conveying a solution to the cadaver lumbar plexus does not exist in human cadavers. Dye injected into the cadaver femoral nerve does not reach either the lumbar plexus or the obturator nerve. When 40 ml of methylene blue dye is injected into the cadaver femoral nerve, some dye usually diffuses under the iliacus muscle fascia to the lateral femoral cutaneous nerve. This study indicates that in patients the "3-in-1 block" always blocks the femoral nerve, it usually blocks the lateral femoral cutaneous nerve, but it probably does not block the lumbar plexus or the obturator nerve.

The effects of large-dose flumazenil on midazolam-induced ventilatory depression.

Flumazenil, a benzodiazepine antagonist, clearly reverses midazolam-induced sedation; reversal of ventilatory depression has not been as well demonstrated. Thirty-two subjects completed this randomized, double-blind, placebo-controlled study investigating the dose-response relationship and duration of flumazenil's effects on ventilatory depression and hypnosis induced by a continuous midazolam infusion. A computer-controlled infusion of midazolam was used to titrate the predicted midazolam plasma concentration to a level at which subjects were unresponsive to verbal commands and then to maintain that concentration. Measurements of ventilation and hypnosis were repeated at predetermined intervals: before midazolam administration, before test drug (flumazenil [1, 3, or 10 mg] or placebo), and 5, 30, 60, 120, and 180 min after test drug administration. Ventilation and tidal volume were measured during an isocapnic hyperoxia clamp at a PETCO2 of 46 mm Hg (VE46 and VT46, respectively). A pseudo-rebreathing technique was used to measure the hypercapnic ventilatory response (HCVR) slope and ventilation intercept at a PETCO2 of 58 mm Hg (VE58). Midazolam reduced VE46, VT46, and VE58, as well as hypnosis scores, in all test drug groups. The reduction in HCVR slope, however, was significant only when all 32 subjects were considered in aggregate. All three doses of flumazenil reversed hypnosis and also reversed the reduction in VE46 and VT46 within 5 min. The reduction in VE58, however, was reversed less consistently. Flumazenil's effect on VE46 and VT46 lasted at least 30 min after 1 mg and at least 60 min after 3 mg, paralleling the effect of these doses on hypnosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Permanent tracheostomy for expired air collection in conscious dogs.

To facilitate continuous collection of exhaled air in conscious unmedicated dogs, a surgical technique of permanent tracheostomy was developed. Small portions of cartilagenous rings were dissected from the trachea creating a stoma approximately 0.5 x 2 cm. The tracheal mucosa and cut cartilage was secured to the dermis in such as manner that skin covered sternohyoid muscle covered the permanent tracheostomy when not in use. This allowed the dog to use its upper respiratory tract more effectively, preventing the frequent complication of tracheobronchitis and pneumonia. This procedure resulted in a maintenance-free stoma that did not require a high humidity environment or special care.

Increasing myocardial oxygen demand during prolonged halothane anesthesia in dogs.

The effect of prolonged halothane anesthesia on myocardial oxygen uptake and coronary blood flow is unknown. This 5.5-hr study was undertaken to determine whether myocardial changes occur in dogs during prolonged steady-state halothane anesthesia. Hourly data were collected beginning 1.5 hr after induction of steady-state anesthesia. When compared to values obtained at 1.5 hr of halothane anesthesia, no significant myocardial changes were observed during the initial 3.5 hr. However, after 4.5 hr, mean arterial blood pressure increased 14% (P less than 0.01), coronary sinus flow increased 22% (P less than 0.05), and myocardial oxygen uptake increased 19% (P less than 0.05). At 5.5 hr mean arterial pressure was 18% (P less than 0.01), coronary sinus flow 31% (P less than 0.01), and myocardial oxygen uptake 21% (P less than 0.05) above levels measured at 1.5 hr. At 5.5 hr whole body oxygen uptake was 6% (P less than 0.01) above the 1.5 hr value. Cardiac output, heart rate, and systemic and coronary vascular resistances did not change significantly. This study demonstrates that duration of anesthesia is an important factor in determining the metabolic oxygen requirements of the heart. During prolonged anesthesia, the increase in myocardial oxygen demands may have an unfavorable effect on the myocardial oxygen supply-demand relationship.