Anesthesia and analgesia
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Anesthesia and analgesia · Nov 2002
Case ReportsCardiac arrest from tension pneumopericardium in a premature infant.
This case report describes a rare and potentially fatal anesthetic complication. It occurred during the care of a small premature infant as a result of improper use of medical equipment.
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Anesthesia and analgesia · Nov 2002
Clinical TrialDoes the choice of electrocardiography lead affect the efficacy of the T-wave criterion for detecting intravascular injection of an epinephrine test dose?
Accidental intravascular injection of an epinephrine-containing test dose decreases the T-wave amplitude of a Lead II electrocardiogram (EKG) with 100% sensitivity and specificity on the basis of the T-wave criterion (positive if there is a > or =25% decrease in amplitude). We designed this study to test whether the choice of EKG lead would affect the efficacy of the simulated intravascular test dose in anesthetized patients. After an 8-h fast and no premedication, 35 healthy patients were anesthetized with end-tidal 2% sevoflurane and nitrous oxide after endotracheal intubation. When hemodynamic stability was obtained, all subjects received 3 mL of normal saline IV, followed 4 min later by 1.5% lidocaine 3 mL plus 15 microg of epinephrine (1:200,000) IV. Heart rate, systolic blood pressure, Leads II (n = 35) and V(5) (n = 35), and either Lead I (n = 17) or III (n = 18), whichever had the greater T-wave amplitude, were continuously recorded for 4 min after the saline and test-dose injections. An IV test dose produced significant increases in heart rate and systolic blood pressure and produced decreases in the T-wave amplitude of all EKG leads studied in all subjects, whereas IV saline elicited no changes in these variables. The maximum percentage decreases in T-wave amplitude of Leads II, I, III, and V(5) were -87% +/- 13%, -88% +/- 8%, -94% +/- 15%, and -86% +/- 16%, respectively (mean +/- SD; P > 0.05). There was no significant difference in temporal changes in T-wave amplitude among the 4 leads, and sensitivity and specificity were 100% on the basis of the T-wave criterion, irrespective of the lead examined. Our results indicate that Leads II, I, III, and V(5) of the EKG are equally effective for detecting intravascular injection of the epinephrine-containing test dose in sevoflurane-anesthetized adults. ⋯ To determine whether an epidural catheter is in a blood vessel, an epidural test dose containing 15 microg of epinephrine is used. We found that decreases in the T-wave amplitude of Leads I, II, III, and V(5) of the electrocardiogram were equally sensitive and specific for detecting intravascular injection of the test dose in sevoflurane-anesthetized adult patients.
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Anesthesia and analgesia · Nov 2002
Clinical TrialLumbar plexus posterior approach: a catheter placement description using electrical nerve stimulation.
The authors describe a modified technique of posterior approach to the lumbar plexus in the psoas compartment which allows nerve stimulation for the location of the plexus and catheter placement for extended-duration surgery and postoperative patient-controlled regional analgesia. A frequent incidence of total lumbar plexus block was observed.
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Anesthesia and analgesia · Nov 2002
Isoflurane does not produce a second window of preconditioning against myocardial infarction in vivo.
The administration of a volatile anesthetic shortly before a prolonged ischemic episode exerts protective effects against myocardial infarction similar to those of ischemic preconditioning. A second window of preconditioning (SWOP) against myocardial infarction can also be elicited by brief episodes of ischemia when this occurs 24 h before prolonged coronary artery occlusion. Whether remote exposure to a volatile anesthetic also causes delayed myocardial protection is unknown. We tested the hypothesis that the administration of isoflurane 24 h before ischemia produces a SWOP against infarction. Barbiturate-anesthetized dogs (n = 25) were instrumented for measurement of hemodynamics, including aortic and left ventricular (LV) pressures and LV +dP/dt(max), and subjected to a 60-min left anterior descending coronary artery occlusion followed by 3 h of reperfusion. Myocardial infarct size and coronary collateral blood flow were assessed with triphenyltetrazolium chloride staining and radioactive microspheres, respectively. Two groups of dogs received 1.0 minimum alveolar anesthetic concentration isoflurane for 30 min or 6 h that was discontinued 30 min (acute) or 24 h (delayed) before ischemia and reperfusion, respectively. A control group of dogs did not receive isoflurane. Infarct size was 27% +/- 3% of the LV area at risk in the absence of pretreatment with isoflurane. Acute, but not remote, administration of isoflurane reduced infarct size (12% +/- 1% and 31% +/- 3%, respectively). No differences in hemodynamics or transmural myocardial perfusion during or after occlusion were observed between groups. The results indicate that isoflurane does not produce a SWOP when administered 24 h before prolonged myocardial ischemia in vivo. ⋯ Isoflurane mimics the beneficial effects of ischemic preconditioning by protecting myocardium against infarction when it is administered shortly before a prolonged ischemic episode. However, unlike ischemic preconditioning, isoflurane does not produce a second window of protection 24 h after administration in dogs.