Anesthesia and analgesia
-
Anesthesia and analgesia · Dec 2001
Randomized Controlled Trial Clinical TrialEarly pregnancy does not reduce the C(50) of propofol for loss of consciousness.
Requirements for inhaled anesthetics decrease during pregnancy. There are no published data, however, regarding propofol requirements in these patients. Because propofol is often used for induction of general anesthesia when surgery is necessary in early pregnancy, we investigated whether early pregnancy reduces the requirement of propofol for loss of consciousness using a computer-assisted target-controlled infusion (TCI). Propofol was administered using TCI to provide stable concentrations and to allow equilibration between blood and effect-site (central compartment) concentrations. Randomly selected target concentrations of propofol (1.5-4.5 microg/mL) were administered to both pregnant women (n = 36) who were scheduled for pregnancy termination and nonpregnant women (n = 36) who were scheduled for elective orthopedic or otorhinolaryngologic surgery. The median gestation of the pregnant women was 8 wk (range, 6-12 wk). Venous blood samples for analysis of the serum propofol concentration were taken at 3 min and 8 min after equilibration of the propofol concentration. After a 10-min equilibration period of the predetermined propofol blood concentration, a verbal command to open their eyes was given to the patients twice, accompanied by rubbing of their shoulders. Serum propofol concentrations at which 50% of the patients did not respond to verbal commands (C(50) for loss of consciousness) were determined by logistic regression. There was no significant difference in C(50) +/- SE of propofol for loss of consciousness between the Nonpregnant (2.1 +/- 0.2 microg/mL) and Pregnant (2.0 +/- 0.2 microg/mL) groups. These results indicate that early pregnancy does not decrease the concentration of propofol required for loss of consciousness. ⋯ The C(50) of propofol for loss of consciousness in early pregnancy did not differ from that in nonpregnant women, indicating that there is no need to decrease the propofol concentration for loss of consciousness when inducing general anesthesia for termination of pregnancy.
-
Anesthesia and analgesia · Dec 2001
Clinical Trial Controlled Clinical TrialThe additive pulmonary vasodilatory effects of inhaled prostacyclin and inhaled milrinone in postcardiac surgical patients with pulmonary hypertension.
Selective pulmonary vasodilation is an advantageous therapeutic strategy for cardiac surgical patients with increased pulmonary vascular resistance (PVR) and right ventricular failure. We hypothesized that milrinone, an adenosine-3',5'-cyclic monophosphate (cAMP)-selective phosphodiesterase enzyme (PDE) inhibitor may, when nebulized and inhaled, cause selective pulmonary vasodilation and potentiate the vasodilation by inhaled prostacyclin (iPGI(2)). Consequently, we investigated the hemodynamic effects of inhaled milrinone or the combination iPGI(2) + inhaled milrinone in cardiac surgical patients with postoperative mean pulmonary arterial pressure (MPAP) >25 mm Hg and PVR >200 dynes. s(-1). cm(-5). During mechanical ventilation and using a conventional nebulizing system, 9 patients inhaled incremental concentrations of milrinone (0.25, 0.5 and 1 mg/mL) in subsequent 10-min periods (Study Part 1). In the same manner, 11 patients received iPGI(2) (10 microg/mL) followed by the combination of iPGI(2) (10 microg/mL) and inhaled milrinone (1 mg/mL) (Study Part 2). Inhaled milrinone reduced PVR with a maximal effect (-20%, P < 0.001) at the largest concentration. As compared with iPGI(2) alone, iPGI(2) + inhaled milrinone caused a further and prolonged reduction of PVR (-8%, P < 0.05) and increased stroke volume (+5%, P < 0.05). Systemic vascular resistance or mean arterial pressure was not affected by inhalation of either drug(s). The authors conclude that inhalation of the cAMP-selective PDE-inhibitor milrinone selectively dilates the pulmonary vasculature without systemic effects in cardiac surgical patients with pulmonary hypertension. Furthermore, inhaled milrinone appears to potentiate and prolong the pulmonary selective vasodilatory effect of iPGI(2). Inhaled milrinone alone or combined with iPGI(2) may be an important therapeutic option in the treatment of patients with pulmonary hypertension and right ventricular failure. ⋯ Pulmonary hypertension may cause or aggravate right heart failure. IV vasodilators reduce systemic blood pressure and might thereby further impair coronary perfusion and right heart performance. In the present study of cardiac surgical patients with pulmonary hypertension, selective pulmonary vasodilation without systemic effects was induced by nebulized, inhaled vasodilators.
-
Anesthesia and analgesia · Dec 2001
Comparative StudyRegional anesthesia does not increase the risk of postoperative neuropathy in patients undergoing ulnar nerve transposition.
The use of regional anesthetic techniques in patients with preexisting neuropathies has been widely debated. The possibility of needle- or catheter-induced trauma, local anesthetic toxicity, or neural ischemia during regional blockade may place patients with underlying mechanical, ischemic, or metabolic neurologic derangements at increased risk of progressive neural injury. We evaluated the safety of regional versus general anesthesia in patients with a preexisting ulnar neuropathy undergoing ulnar nerve transposition. All patients (n = 360) who underwent ulnar nerve transposition at the Mayo Clinic from 1985 to 1999 were retrospectively studied. A general anesthetic was performed in 260 (72%) patients. The remaining 100 (28%) patients received an axillary block, including 64 patients in whom an ulnar paresthesia or nerve stimulator motor response was elicited at the time of block placement. Patient characteristics, the severity of preoperative ulnar nerve dysfunction, and surgical variables were similar between groups. Anesthetic technique did not affect neurologic outcome (new or worsening pain, paresthesias, numbness, or motor weakness) immediately after surgery or at 2 or 6 wk after surgery. All six patients in the Axillary Block group who reported new or worsening neurologic symptoms after surgery had received bupivacaine in combination with either an ulnar paresthesia or motor response. By using logistic regression, bupivacaine was identified as an independent risk factor for worsening of ulnar nerve function compared with other local anesthetics. We conclude that axillary blockade is a suitable anesthetic technique for this procedure. ⋯ The use of regional anesthetic techniques in patients with preexisting neuropathies has been widely debated. Theoretical concerns include the risk of progressive nerve damage from direct needle trauma or local anesthetic toxicity. This investigation, however, supports the safety of axillary blockade in patients with preexisting ulnar neuropathy undergoing ulnar nerve transposition.
-
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.