Brian L. Partridge

MAC of sevoflurane in humans and the New Zealand white rabbit

The minimum alveolar concentration of sevoflurane necessary to prevent movement in 50 per cent of patients (MAC) was determined to be 2.05 per cent in 20 adult surgical patients. Because this value was higher than the only other experimentally determined human MAC value for sevoflurane (1.71 per cent), MAC was also determined in New Zealand white rabbits. Comparisons of the MAC ratios of sevoflurane to other volatile anaesthetics in both the human and the rabbit suggest that the human MAC value we obtained for sevoflurane is consistent with experimental determinations of MAC of other volatile anaesthetics in humans.RésuméLa concentration alvéolaire minimale du sévoflurane nécessaire afin de prévenir les mouvements dans 50 per cent des patients (MAC) a été déterminée à 2.05 per cent chez 20 patients adultes subissant une chirurgie. Etant donné que cette valeur était plus élevée que celle obtenue expérimentalement chez les humains avec le sévoflurane (1.71 per cent), le MAC a aussi a été déterminé chez les lapins blanc de la Nouvelle-Zélande. Des comparaisons des rapports de MAC entre le sévoflurane et ďautres agents anesthésiques volatiles tant chez ľhumain que chez le lapin suggèrent que les valeurs du MA C qu’on a obtenues chez ľhumain avec le sévoflurane sont comparables avec celles déterminées expérimentalement pour ďautres agents anesthésiques volatiles chez ľhomme.

Intraoperative monitoring of tibialis anterior muscle motor evoked responses to transcranial electrical stimulation during partial neuromuscular blockade.

We studied the feasibility of recording motor evoked responses to transcranial electrical stimulation (tce-MERs) during partial neuromuscular blockade (NMB). In 11 patients, compound muscle action potentials were recorded from the tibialis anterior muscle in response to transcranial electrical stimulation during various levels of vecuronium-induced NMB. The level of NMB was assessed by accelerometry of the adductor pollicis muscle after train-of-four stimulation of the ulnar nerve. The compound muscle action potential was also recorded from the tibialis anterior muscle after direct stimulation of the peroneal nerve (M-response) as an alternative means of assessing the degree of NMB. In all patients, tce-MERs could be recorded reliably during anesthesia with N2O and a continuous infusion of sufentanil (0.5 micrograms.kg-1.h-1). An intact train-of-four was present in all patients, and the amplitude of the first twitch was recorded and designated as the control value. Before administration of vecuronium, the M-response amplitude was 9.6 +/- 3.6 (mean +/- SD) mV, and the tce-MER amplitude was 1.21 +/- 0.66 mV. Although administration of vecuronium (0.05 mg/kg) resulted in loss of the mechanical adductor pollicis response in 8 of the 11 patients, the M-response and the tce-MER remained recordable. Subsequently, during an infusion of vecuronium, adjusted to maintain one or two mechanical responses to train-of-four stimulation, the average M-response to peroneal nerve stimulation was 5.2 +/- 2.5 mV (53% of the control value), and tce-MER amplitude was 0.59 +/- 0.36 mV (59% of the control value).(ABSTRACT TRUNCATED AT 250 WORDS)

Use of Pulse Oximetry as a Noninvasive Indicator of Intravascular Volume Status

The use of pulse oximetery as a noninvasive method to assess intravascular volume status is described. Pulse oximeters providing a continuous display of the pulse waveform offer a new method of estimating relative volume status during positive-pressure ventilation. Like intraarterial pressure tracings, the peaks of the pulse waveform demonstrate increased variation in response to positive-pressure ventilation when a patient becomes hypovolemic. Pulse oximeter waveform tracings were compared with central venous pressure and intraarterial pressure tracings in 12 patients undergoing major operative procedures. A significant correlation (r = 0.61) was seen between pulse waveform variation and systolic pressure variation, which has previously been shown to be a sensitive indicator of hypovolemia. When data from individual patients were analyzed separately, the correlation between pulse waveform variation and systolic pressure variation was as high as 0.88.The use of pulse oximetery as a noninvasive method to assess intravascular volume status is described. Pulse oximeters providing a continuous display of the pulse waveform offer a new method of estimating relative volume status during positive-pressure ventilation. Like intraarterial pressure tracings, the peaks of the pulse waveform demonstrate increased variation in response to positive-pressure ventilation when a patient becomes hypovolemic. Pulse oximeter waveform tracings were compared with central venous pressure and intraarterial pressure tracings in 12 patients undergoing major operative procedures. A significant correlation (r = 0.61) was seen between pulse waveform variation and systolic pressure variation, which has previously been shown to be a sensitive indicator of hypovolemia. When data from individual patients were analyzed separately, the correlation between pulse waveform variation and systolic pressure variation was as high as 0.88.

Prevention of the cardiovascular and neuroendocrine response to electroconvulsive therapy: I. Effectiveness of pretreatment regimens on hemodynamics.

Electroconvulsive therapy (ECT) under anesthesia is associated with hypertension and tachycardia. The cardiovascular effects of ECT were studied after pretreatment of 10 patients with esmolol (1.0 mg/kg), fentanyl (1.5 μg/kg), labetalol (0.3 mg/kg), lidocaine (1.0 mg/kg), and saline solution (control), using a double-blind, randomized block-design. Each patient received all five pretreatment regimens over the course of five ECT sessions. During control studies, arterial blood pressure and heart rate increased significantly in all patients after ECT (P < 0.05 and P < 0.01, respectively). The rate-pressure product increased by an average of 336% ± 14% (P < 0.01). There were appreciable individual differences in the cardiovascular response to ECT, independent of pretreatment (P < 0.01). Pretreatment with esmolol and labetalol significantly reduced the hemodynamic response to ECT, compared with fentanyl, lidocaine, or saline solution (P < 0.05). Esmolol attenuated arterial blood pressure to a larger extent than did labetalol (P < 0.05). Compared with saline solution (control), pretreatment with labetalol, fentanyl, or lidocaine significantly reduced seizure duration (P < 0.05) and increased the frequency with which a second electrical stimulus was required. In contrast, esmolol pretreatment did not significantly affect seizure duration. Esmolol (1 mg/kg), administered 1 min before induction of anesthesia, produced significant amelioration of the cardiovascular response to ECT with minimal effect on seizure duration.

Prevention of the cardiovascular and neuroendocrine response to electroconvulsive therapy: II. Effects of pretreatment regimens on catecholamines, ACTH, vasopressin, and cortisol.

The neuroendocrine response to electroconvulsive therapy (ECT) was assessed in four patients after pretreatment with esmolol (1.0 mg/kg), fentanyl (1.5 mu;g/kg), labetalol (0.3 mg/kg), and saline solution (control). Each patient received each drug pretreatment using a double-blind, randomized study block-design. During each of the five studies, blood samples were obtained from each patient before anesthetic induction, before ECT shock, and at 1, 5, 10, and 30 min after seizure. Samples were subsequently analyzed for epinephrine, norepinephrine, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), and cortisol. Electroconvulsive therapy after saline pretreatment resulted in a 3-fold and 15-fold increase in norepinephrine and epinephrine levels, respectively (P < 0.05). The ACTH and cortisol levels gradually increased over 30 min, peaking at values that were two to three times the control values (P < 0.05). The AVP levels increased significantly after induction of ECT (P < 0.005) and remained higher than control levels at 5, 10, and 30 min. The effect of pretreatments varied. Pretreatment with esmolol and fentanyl resulted in significant attenuation of the norepinephrine peak after seizure (P < 0.05). Only esmolol significantly attenuated ECT-induced epinephrine secretion, whereas fentanyl pretreatment significantly reduced release of ACTH after ECT. No pretreatment significantly affected the elevated AVP or cortisol levels seen on emergence or up to 30 min after treatment. The ability of esmolol pretreatment to attenuate serum catecholamine release after ECT is consistent with its ability to block the cardiovascular responses to ECT.

Three's a crowd? PredictingEigenmannia's responses to multiple jamming

SummaryWe have studied Jamming Avoidance Responses (JARs) ofEigenmannia in the presence of more than one interfering signal. Experiments were performed on intact as well as curarized specimens, whose silenced electric organ discharge (EOD) was replaced by a sine wave,S1 of frequency,F1. Sine waves,S2 andS3, with respective frequencies,F2 andF3, mimicked EODs of two potential neighbors. Much as in the case of a single interfering signal,S2 (Heiligenberg and Bastian, 1980), the presentation of two interfering signals,S2 andS3, results in modulations of phase,H(t), and amplitude, ¦S¦(t), of the animals contaminated EOD or its substitute,S1, and these modulations drive the JAR. The plots ofH and ¦S¦, as variables in a two-dimensional state-plane, yield graphs in the manner of Lissajous Figures whose shape depends upon the relative intensities, ¦S2¦/¦S1¦ and ¦S3¦/¦S1¦, and the differences in frequencies,ΔF2=F2−F1 andΔF3=F3-F1, of the two stimuli,S2 andS3 (Figs. 1 to 5). On the basis of such graphs, JARs to multiple stimuli can be predicted (Figs. 5 to 7) by a line integration algorithm (Fig. 9) originally developed for the single stimulus case (Heiligenberg and Bastian, 1980). This model, which should predict JARs to any number of interfering stimuli, assumes that the effect of an entire graph is the integral of incremental contributions by line segments which constitute this graph, with the effect of a single line segment depending upon its location and orientation within the state-plane. As a consequence of this mechanism, the animal most strongly avoids the frequency vicinity of the strongest and thus most detrimental stimulus without the necessity of identifying intensities and frequencies of any stimuli in the jamming regime.

Life-threatening effects of intravascular absorption of PGF2 alpha during therapeutic termination of pregnancy.

A case of inadvertent intravascular injection of PGF2alpha during induction of labor by intraamniotic injection for fetal demise involving alternating extreme hypotension and hypertension is described. The woman was a 29-year old in late 2nd trimester with oligohydramnios but no other related history. She was given epidural anesthesia 7.5 mg midazolam and 5 mg morphine S04 for anxiety. Because of oligohydramnios 300 ml Ringers lactate was instilled to dilute the PG. A test dose of 1 mg PGF2alpha was tolerated well. 80 g urea and 20 mg PGF2alpha were injected over 10 minutes. A few minutes later contractions began followed by complaints of burning on face and chest and dyspnea. Oxygen was given by mask. Systolic pressure fell to 70 mm by cuff; peripheral pulses could not be palpated but the patient remained alert and oriented. She was given 35 mg ephedrine and increased iv fluids. She remained dyspneic her extremities became mottled and she complained of chest pressure severe headache and severe breast tenderness. Blood pressure rose to 220/135 mm Hg; pulse to 95 and respiratory rate to 44. Pulse oximetry detectable at the earlobe only was 94% saturation. After 50 mg labetalol blood pressure fell to 134/77 but symptoms remained. For 2 hours blood pressure swung between 76/50 and 225/125 until delivery of the fetus. An arterial line could not be started because of extreme vasoconstriction. Central venous pressure was 13 cm H20. After artificial rupture of the membranes and removal of remaining PG blood pressure stabilized. Delivery was accomplished without incident. The symptoms and labile blood pressure were considered to be due to intravascular injection of PGF2alpha caused by repeated bolus injection at each uterine contraction. In case of PG induction for fetal demise it is recommended that anesthesiologists be prepared to treat intravascular collapse hypertension and bronchoconstriction.

MAC OF SEVOFLURANE IN HUMANS AND THE NEW ZEALAND WHITE RABBIT

The minimum alveolar concentration of sevoflurane necessary to prevent movement in 50 per cent of patients (MAC) was determined to be 2.05 per cent in 20 adult surgical patients. Because this value was higher than the only other experimentally determined human MAC value for sevoflurane (1.71 per cent), MAC was also determined in New Zealand white rabbits. Comparisons of the MAC ratios of sevoflurane to other volatile anaesthetics in both the human and the rabbit suggest that the human MAC value we obtained for sevoflurane is consistent with experimental determinations of MAC of other volatile anaesthetics in humans.