Sympathetic and vascular consequences from remifentanil in humans.

UNLABELLED: We explored the possible mechanisms of hypotension during the administration of sedation-analgesia doses of remifentanil in young (ASA physical status I) volunteers (n = 24). Cardiorespiratory and sympathetic variables were collected at baseline and at plasma concentrations of remifentanil (2 and 4 ng/mL). Monitoring included electrocardiogram, heart rate (HR), direct blood pressure, muscle sympathetic nerve activity, and forearm blood flow (FBF). A cold pressor test (1-min hand immersion in ice water) quantified analgesia effectiveness (visual analog scale, 0-100). Visual analog scale to the cold pressor test (62 at baseline) decreased to 27 and 18 during remifentanil infusions. Respiratory rate decreased and end-tidal carbon dioxide (ETCO(2)) increased with increasing doses of remifentanil; HR, direct blood pressure, muscle sympathetic nerve activity, SpO(2) remained unchanged, but FBF increased compared with placebo. In a second study (n = 7), timed respiration was used to maintain ETCO(2) during remifentanil, but FBF still increased. In a third study (n = 11), direct effects of remifentanil on vascular tone were determined with progressive infusions from 1 to 100 micro g/h into the brachial artery; FBF increased significantly from 3.5 to 4.3 mL/min per 100 mL of tissue (approximately 13%-18% increase). Sedative doses of remifentanil resulted in analgesia but no changes in neurocirculatory end-points except FBF. Direct effects of remifentanil on regional vascular tone may play a role in promoting hypotension. IMPLICATIONS: Remifentanil occasionally has been associated with hypotension, the mechanism of which is unclear. This study found that remifentanil directly causes the forearm arterial vasculature to dilate.

Carbon monoxide production from sevoflurane breakdown: modeling of exposures under clinical conditions.

UNLABELLED: Isoflurane, enflurane, sevoflurane, and especially desflurane produce carbon monoxide (CO) during reaction with desiccated absorbents. Of these, sevoflurane is the least studied. We investigated the dependence of CO production from sevoflurane on absorbent temperature, minute ventilation (VE), and fresh gas flow rates. We measured absorbent temperature and in vitro CO concentrations when desiccated Baralyme reacted with 1 minimum alveolar anesthetic concentration of (2.1%) sevoflurane at 2.3-, 5.0-, and 10.0-L VE. Mathematical modeling of carboxyhemoglobin concentrations was performed using an existing iterative method. Rapid breakdown of sevoflurane prevented the attainment of 1 minimum alveolar anesthetic concentration with low fresh gas flow rates. CO concentrations increased with VE and with absorbent temperatures exceeding 80 degrees C, but concentrations decreased with higher fresh gas flow rates. Average CO concentrations were 150 and 600 ppm at 2.3- and 5.0-L VE; however, at 10 L, over 11,000 ppm of CO were produced followed by an explosion and fire. Methanol and formaldehyde were present and may have contributed to the flammable mixture but were not quantitated. Mathematical modeling of exposures indicates that in average cases, only patients < or =25 kg, or severely anemic patients, are at risk of carboxyhemoglobin concentrations >10% during the first 60 min of anesthesia. IMPLICATIONS: Sevoflurane breakdown in desiccated absorbents is expected to result in only mild carbon monoxide (CO) exposure. Completely dry absorbent and high minute ventilation rates may degrade sevoflurane to extremely large CO concentrations. Serious CO poisoning or spontaneous ignition of flammable gases within the breathing circuit are possible in extreme circumstances.