Anesthesia and analgesia
-
Anesthesia and analgesia · Dec 2001
Case ReportsThe use of a "reverse" axis (axillary-interscalene) block in a patient presenting with fractures of the left shoulder and elbow.
A patient presented for surgery to repair a fractured left shoulder and elbow and requested regional anesthesia. Most upper extremity operations require a single brachial plexus nerve block. The position of the two fractures however required the use of two separate approaches, an interscalene and an axillary approach.
-
Anesthesia and analgesia · Dec 2001
Case ReportsHemostatic analysis of a patient with hereditary angioedema undergoing coronary artery bypass grafting.
Hereditary angioedema is a disease associated with acute complement-mediated inflammation and swelling of the airway and other vital organs. This case describes the impact of hereditary angioedema and cardiopulmonary bypass on hemostasis as assessed by thrombelastography.
-
Anesthesia and analgesia · Dec 2001
The predictive value of ventricular fibrillation electrocardiogram signal frequency and amplitude variables in patients with out-of-hospital cardiac arrest.
We evaluated ventricular fibrillation frequency and amplitude variables to predict successful countershock, defined as pulse-generating electrical activity. We also elucidated whether bystander cardiopulmonary resuscitation (CPR) influences these electrocardiogram (ECG) variables. In 89 patients with out-of-hospital cardiac arrest, ECG recordings of 594 countershock attempts were collected and analyzed retrospectively. By using fast Fourier transformation analysis of the ventricular fibrillation ECG signal in the frequency range 0.333-15 Hz (median [range]), median frequency, dominant frequency, spectral edge frequency, and amplitude were as follows: 4.4 (2.4-7.5) Hz, 4.0 (0.7-7.0) Hz, 7.7 (3.7-13.7) Hz, and 0.94 (0.24-1.95) mV, respectively, before successful countershock (n = 59). These values were 3.8 (0.8-7.7) Hz (P = 0.0002), 3.0 (0.3-9.7) Hz (P < 0.0001), 7.3 (2.0-14.0) Hz (P < 0.05), and 0.53 (0.03-3.03) mV (P < 0.0001), respectively, before unsuccessful countershock (n = 535). In patients in whom bystander CPR was performed (n = 51), ventricular fibrillation frequency and amplitude before the first defibrillation attempt were higher than in patients without bystander CPR (n = 38) (median frequency, 4.4 [2.4-7.5] vs 3.7 [1.8-5.3] Hz, P < 0.0001; dominant frequency, 3.8 [0.9-7.7] vs 2.6 [0.8-5.9] Hz, P < 0.0001; spectral edge frequency, 8.4 [4.8-12.9] vs 7.2 [3.9-12.1] Hz, P < 0.05; amplitude, 0.79 [0.06-4.72] vs 0.67 [0.16-2.29] mV, P = 0.0647). Receiver operating characteristic curves demonstrate that successful countershocks will be best discriminated from unsuccessful countershocks by ventricular fibrillation amplitude (3000-ms epoch). At 73% sensitivity, a specificity of 67% was obtained with this variable. ⋯ In patients with out-of-hospital cardiac arrest, successful countershocks will be best discriminated from unsuccessful countershocks by ventricular fibrillation amplitude (3000-ms epoch). At 73% sensitivity, a specificity of 67% was obtained with this variable.
-
Anesthesia and analgesia · Dec 2001
Comparative StudyThe comparative electrophysiologic and hemodynamic effects of a large dose of ropivacaine and bupivacaine in anesthetized and ventilated piglets.
Ropivacaine is less potent and less toxic than bupivacaine. We administered these two local anesthetics in a cardiac electrophysiologic model of sodium thiopental-anesthetized and ventilated piglets. After assessing the stability of the model, bupivacaine (4 mg/kg) and ropivacaine (6 mg/kg) were given IV in two groups (n = 7) of piglets. No alteration in biological variables was reported throughout the study. Bupivacaine and ropivacaine similarly decreased mean aortic pressure from 99 +/- 22 to 49 +/- 31 mm Hg and from 87 +/- 17 to 58 +/- 28 mm Hg, respectively, and decreased the peak of the first derivative of left ventricular pressure from 1979 +/- 95 to 689 +/- 482 mm Hg/s and from 1963 +/- 92 to 744 +/- 403 mm Hg/s, respectively. Left ventricular end-diastolic pressure was similarly increased from 6 +/- 5 to 9 +/- 5 mm Hg and from 6 +/- 4 to 12 +/- 4 mm Hg, respectively. Bupivacaine and ropivacaine similarly lengthened the cardiac cycle length (R-R; from 479 +/- 139 to 706 +/- 228 ms and from 451 +/- 87 to 666 +/- 194 ms, respectively), atria His (from 71 +/- 15 to 113 +/- 53 ms and from 64 +/- 6 to 86 +/- 10 ms, respectively), and QTc (QTc = QT x R-R(-0.5), Bazett formula; from 380 +/- 71 to 502 +/- 86 ms and from 361 +/- 33 to 440 +/- 56 ms, respectively) intervals. Bupivacaine altered to a greater extent the PQ (the onset of the P wave to the Q wave of the QRS complex) (from 97 +/- 20 to 211 +/- 60 ms versus from 91 +/- 8 to 145 +/- 38 ms, P < 0.05), QRS (from 58 +/- 3 to 149 +/- 34 ms versus from 60 +/- 5 to 101 +/- 17 ms, P < 0.05), and His ventricle interval (from 25 +/- 4 to 105 +/- 30 ms vs from 25 +/- 4 to 60 +/- 30 ms, P < 0.05) than ropivacaine. A 6 mg/kg ropivacaine dose induced similar hemodynamic alterations as 4 mg/kg bupivacaine. However, bupivacaine altered the variables of ventricular conduction (QRS and His ventricle) to a greater extent. ⋯ A 6 mg/kg ropivacaine dose induced similar hemodynamic alterations as 4 mg/kg bupivacaine. However, bupivacaine altered the variables of ventricular conduction (QRS and His ventricle) to a greater extent.
-
Anesthesia and analgesia · Dec 2001
The involvement of the mu-opioid receptor in ketamine-induced respiratory depression and antinociception.
N-methyl-D-aspartate receptor antagonism probably accounts for most of ketamine's anesthetic effects; its analgesic properties are mediated partly via N-methyl-D-aspartate and partly via opioid receptors. We assessed the involvement of the mu-opioid receptor in S(+) ketamine-induced respiratory depression and antinociception by performing dose-response curves in exon 2 mu-opioid receptor knockout mice (MOR(-/-)) and their wild-type littermates (WT). The ventilatory response to increases in inspired CO(2) was measured with whole body plethysmography. Two antinociceptive assays were used: the tail-immersion test and the hotplate test. S(+) ketamine (0, 10, 100, and 200 mg/kg intraperitoneally) caused a dose-dependent respiratory depression in both genotypes, with greater depression observed in WT relative to MOR(-/-) mice. At 200 mg/kg, S(+) ketamine reduced the slope of the hypercapnic ventilatory response by 93% +/- 15% and 49% +/- 6% in WT and MOR(-/-) mice, respectively (P < 0.001). In both genotypes, S(+) ketamine produced a dose-dependent increase in latencies in the hotplate test, with latencies in MOR(-/-) mice smaller compared with those in WT animals (P < 0.05). In contrast to WT mice, MOR(-/-) mice displayed no ketamine-induced antinociception in the tail-immersion test. These results indicate that at supraspinal sites S(+) ketamine interacts with the mu-opioid system. This interaction contributes significantly to S(+) ketamine-induced respiratory depression and supraspinal antinociception. ⋯ The involvement of the mu-opioid receptor system in S(+) ketamine-induced respiratory depression and spinal and supraspinal analgesia was demonstrated by performing experiments in mice lacking the mu-opioid receptor and in mice with intact mu-opioid receptors.