Manual versus target-controlled infusion remifentanil administration in spontaneously breathing patients.

BACKGROUND: The combination of propofol-remifentanil for procedural deep sedation in spontaneously breathing patients is characterized by the frequent incidence of side effects, especially respiratory depression. These side effects may be due to either the drug combination or the drug delivery technique. Target-controlled infusion (TCI) might optimize drug delivery. In this prospective, randomized, double-blind study in patients undergoing elective colonoscopy, we thus tried to answer two questions: first, if adding remifentanil to propofol surpasses the disadvantages of the combination of these two products, and second, if administration of remifentanil via TCI decreases the incidence of side effects, compared to manually controlled administration. METHODS: Patients undergoing elective colonoscopy were randomly assigned to receive remifentanil via manually controlled continuous infusion (MCI) (0.125 microg x kg(-1) x min(-1) for 2 min followed by a continuous infusion of 0.05 microg x kg(-1) x min(-1)), TCI remifentanil (1 ng/mL), or placebo (normal saline either as TCI or manual infusion of equivalent rate). All patients received TCI propofol, adjusted to a target concentration level that provided deep sedation in which patients were not responsive to verbal commands, but maintained spontaneous ventilation without assistance. RESULTS: Significantly more patients in the placebo group showed movement, cough and hiccup, which transiently interfered with the examination. There were no clinically significant differences in hemodynamic or recovery variables among all groups. Remifentanil administered via TCI resulted in a decrease in propofol requirements. The incidence of hypopnea and apnea was less frequent when remifentanil was administered via TCI compared to MCI (TCI n = 7, MCI n = 16, P < 0.05). CONCLUSION: The combination of remifentanil and propofol for deep sedation in spontaneously breathing patients, offered better conditions for colonoscopy than propofol used as a single drug. Remifentanil administered via TCI resulted in a decrease in propofol dosing and in a lower incidence in apnea and respiratory depression (TCI n = 7, MCI n = 16, P < 0.05), compared to manually controlled administration of remifentanil.

Remifentanil used to supplement propofol does not improve quality of sedation during spontaneous respiration.

STUDY OBJECTIVE: To evaluate whether the use of remifentanil to supplement propofol during spontaneous respiration confers any benefits in terms of quality of sedation and recovery, or in terms of reduction in propofol requirements. DESIGN: Prospective, randomized, double-blind study. SETTING: University hospital. PATIENTS: 50 ambulatory adult ASA physical status I and II patients scheduled for total colonoscopy. INTERVENTIONS: Patients were randomized to receive either propofol alone or propofol plus remifentanil 0.1 microg/kg/min, while independently maintaining spontaneous respiration. MEASUREMENTS: Cardiovascular and respiratory variables were measured before induction and at 1-minute intervals thereafter. Recovery from anesthesia was assessed using simple verbal commands and the Steward Post Recovery Score. Patient satisfaction was measured with a visual analog scale. Computer simulation was used to calculate the effect-site concentrations of propofol and remifentanil. MAIN RESULTS: The depressant effects on blood pressure and respiratory function were significantly higher when propofol and remifentanil were combined. Although the addition of remifentanil resulted in a decrease of propofol usage, recovery of anesthesia was faster and patient satisfaction was higher when using propofol alone. CONCLUSIONS: The addition of remifentanil to propofol during spontaneous ventilation offered no benefits compared with the use of propofol alone.

Vascular hyporesponsiveness in the mesenteric artery of anaesthetized rats with cirrhosis and portal hypertension: an in-vivo study.

INTRODUCTION: Cirrhosis is complicated by splanchnic vasodilation. Nitric oxide (NO) and prostacyclin contribute to this. Vascular hyporesponsiveness has been reported, but the underlying pathophysiological mechanisms are unclear. OBJECTIVE: This in-vivo study examined the contribution of NO and prostacyclin to the development of vascular hyporesponsiveness in the mesenteric circulation of animals with cirrhosis and portal hypertension. METHODS: Rats underwent common bile duct ligation (CBDL) (n = 11), partial portal vein ligation (PPVL) (n = 12) and sham-operation (sham) (n = 11). Blood flow in the mesenteric artery (MBF) was measured during intramesenteric infusion of endothelium-dependent (acetylcholine) and endothelium-independent vasodilators (deta-NONOate, pinacidil) and a vasoconstrictor (L-phenylephrine). The measurements were repeated after systemic infusion of L-NAME (NO synthase inhibition) and indomethacin (cyclo-oxygenase inhibition). RESULTS: The MBF response to acetylcholine was significantly lower in CBDL and tended to be lower in PPVL than in sham. L-NAME and indomethacin significantly decreased the MBF response to acetylcholine in all groups. The hyporeactivity to acetylcholine in CBDL and PPVL was maintained after L-NAME and indomethacin. The MBF response to pinacidil, deta-NONOate and phenylephrine, before and after NO synthase and cyclo-oxygenase inhibition, was lower in CBDL and PPVL than in sham. CONCLUSION: This is the first in-vivo study demonstrating an impaired response to endothelium-dependent and endothelium-independent vasodilators as well as vasoconstrictors in the mesenteric artery of animals with cirrhosis and portal hypertension. The generalised hyporeactivity suggests an abnormality on the vascular smooth muscle cell level. The hyporesponsiveness persisted after combined NO synthase and cyclo-oxygenase inhibition.