Anesthesia and analgesia
-
Anesthesia and analgesia · Mar 2003
Postcardiac surgery complications: association of acute renal dysfunction and atrial fibrillation.
Postoperative creatinine increase is associated with adverse outcome after cardiac surgery. Although postoperative stroke and renal dysfunction are associated after cardiac surgery, suggesting a common systemic insult, a similar assessment of atrial fibrillation and renal dysfunction has not been performed. Therefore, we tested the hypothesis that patients with new-onset atrial fibrillation complicating coronary bypass surgery have a greater postoperative creatinine increase. Data were obtained for 453 elective coronary bypass surgery patients with no history of atrial fibrillation. Multivariate regression analyses of factors associated with peak fractional change in creatinine demonstrated a two-way interaction between age and atrial fibrillation (variable estimate, -1.1; P = 0.002). Similar results were obtained in a secondary multivariate model analyzing factors associated with peak postoperative creatinine (variable estimate, -0.01; P = 0.04). We confirmed our hypothesis that patients with new-onset atrial fibrillation are more likely to have acute renal dysfunction after cardiac surgery. The association of atrial fibrillation and creatinine increase diminishes with advancing age. These data are consistent with a common pathophysiology that contributes in an age-dependent fashion to the etiology of both acute renal dysfunction and atrial fibrillation after coronary bypass surgery. ⋯ We found an independent association between new-onset atrial fibrillation and postoperative creatinine increase that is influenced by age. The degree to which atrial fibrillation is associated with postoperative creatinine increase diminishes with advancing age. This interaction suggests that a common etiology for these two complications may be more important in younger patients.
-
Anesthesia and analgesia · Mar 2003
Clinical TrialAn evaluation of the supraclavicular plumb-bob technique for brachial plexus block by magnetic resonance imaging.
Partly based on magnetic resonance imaging studies, the "plumb-bob" approach for brachial plexus block was designed to minimize the risk of pneumothorax. Nevertheless, the risk of pneumothorax has remained a concern. We analyzed magnetic resonance images from 10 volunteers to determine whether the risk of pneumothorax was decreased with this method. The recommended initial needle direction is anteroposterior through the junction between the lateral-most part of the sternocleidomastoid muscle and the superior edge of the clavicle. If the initial placement is not successful, the brachial plexus may be sought in sectors 20 degrees -30 degrees cephalad or caudad to the anteroposterior line in a sagittal plane through the insertion point. We found that the anteroposterior line reached the pleura in 6 of 10 volunteers without prior contact with the subclavian artery or the brachial plexus, but always with contact with the subclavian vein. To reach the middle of the brachial plexus, a mean cephalad redirection of the simulated needle by 21 degrees was required (range from 41 degrees cephalad to 15 degrees caudad in one case). We conclude that the risk of contacting the pleura and the subclavian vessels may be reduced by initially directing the needle 45 degrees cephalad instead of anteroposterior. If the brachial plexus is not contacted, the angle should be gradually reduced. ⋯ In magnetic resonance images of volunteers, simulated needle passes with the "plumb-bob" approach to the supraclavicular brachial plexus block were analyzed for precision and risk profile. To avoid needle contact with the lung, the subclavian vein, and the subclavian artery, our results suggest a change in the method's initial needle direction.
-
Anesthesia and analgesia · Mar 2003
Inclusion of turnover time does not influence identification of surgical services that over- and underutilize allocated block time.
Allocation of operating room (OR) block time is an ongoing challenge for OR managers. In this study, we sought to determine whether inclusion or exclusion of turnover time in comparisons of block utilization would identify different surgical services as under- or overused. For a 13-mo period, we evaluated data extracted from the OR information system of a large academic medical center. During that time period, 15 surgical services performed 12,245 surgical procedures. Allocated block hours, number of first cases performed, total number of cases, and average case durations were determined. The average turnover time for each service was determined by a manual, case-by-case review of data from 1 mo. Raw utilization (RU; case durations only) and adjusted utilization (AU; case duration plus turnover time) were calculated for each service. Turnover time was credited to the service performing surgery after room turnover. Case du-ration was limited to surgeries performed during resource hours. Two indices of utilization (i.e., the usage rate of the service divided by the overall use of all ORs in the suite) were used to compare services: the RU or AU Index (RUI or AUI). Outliers were services with indices that were >1.15 or <0.85. The RUI identified three services as underutilizers and one service as an overutilizer. Using the AUI, the same outliers were identified, and no new services were identified. Examining the changes in index (between AUI and RUI), the percentage of to-follow cases highly correlated with changes in index (r(2) = 0.60); the average turnover time did not (r(2) = 0.002). Inclusion of turnover time did not change the services that were identified as under- and overutilizer. ⋯ Turnover time is difficult to determine from existing operating room information systems. This study determined the use of block time with and without turnover time for each surgical service in a large academic hospital. Turnover time did not change identification of surgical services that over- (one service) or underused (three services) allocated block time.
-
Anesthesia and analgesia · Mar 2003
Carbon monoxide production from sevoflurane breakdown: modeling of exposures under clinical conditions.
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. ⋯ 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.
-
Anesthesia and analgesia · Mar 2003
GABA(A) receptor blockade antagonizes the immobilizing action of propofol but not ketamine or isoflurane in a dose-related manner.
The enhancing action of propofol on gamma-amino-n-butyric acid subtype A (GABA(A)) receptors purportedly underlies its anesthetic effects. However, a recent study found that a GABA(A) antagonist did not alter the capacity of propofol to depress the righting reflex. We examined whether the noncompetitive GABA(A) antagonist picrotoxin and the competitive GABA(A) antagonist gabazine affected a different anesthetic response, immobility in response to a noxious stimulus (a tail clamp in rats), produced by propofol. This effect was compared with that seen with ketamine and isoflurane. Picrotoxin increased the 50% effective dose (ED(50)) for propofol by approximately 379%; gabazine increased it by 362%, and both antagonists acted in a dose-related manner with no apparent ceiling effect (i.e., no limit). Picrotoxin maximally increased the ED(50) for ketamine by approximately 40%-50%, whereas gabazine increased it by 50%-60%. The isoflurane minimum alveolar anesthetic concentration increased by approximately 60% with the picrotoxin and 70% with the gabazine infusion. The ED(50) for propofol was also antagonized by strychnine, a non-GABAergic glycine receptor antagonist and convulsant, to determine whether excitation of the central nervous system by a non-GABAergic mechanism could account for the increases in propofol ED(50) observed. Because strychnine only increased the immobilizing ED(50) of propofol by approximately 50%, GABA(A) receptor antagonism accounted for the results seen with picrotoxin and gabazine. We conclude that GABA(A) antagonism can influence the ED(50) for immobility of propofol and the non-GABAergic anesthetic ketamine, although to a different degree, reflecting physiologic antagonism for ketamine (i.e., an indirect effect via a modulatory effect on the neural circuitry underlying immobility) versus physiologic and pharmacologic antagonism for propofol (i.e., a direct effect by antagonism of propofol's mechanism of action). This study also suggests that the immobilizing action of isoflurane probably does not involve the GABA(A) receptor because antagonism of GABA(A) receptors for animals anesthetized with isoflurane produces results quantitatively and qualitatively similar to ketamine and markedly different from propofol. ⋯ IV picrotoxin and gabazine antagonized the immobilizing action of propofol in a dose-related manner, whereas antagonism of the immobilizing action of ketamine and isoflurane was similar, smaller than for propofol, and not dose-related. These results are consistent with a role for gamma-amino-n-butyric acid subtype A receptors in mediating propofol anesthesia but not ketamine or isoflurane anesthesia.