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Biomedical subjects

N T Smith

Publications and source records attributed to N T Smith.

At least 55 records · Page 3Linked to original sources

'Catatonia' produced by alfentanil is reversed by methylnaloxonium microinjections into the brain.

Alfentanil, a short-acting and powerful analgesic, when injected peripherally to rats (0.5 mg/kg) produced a catatonic state characterized by a rigid akinesia. The present study was designed to explore the neuroanatomical location of the opiate receptors mediating the alfentanil induced catatonia. The catatonic effect of alfentanil was measured using a bar test and depression of locomotor activity in rats tested in photocell cages during an active nocturnal phase of their cycle. Methylnaloxonium HCl (MN), a quaternary derivative of naloxone which does not readily cross the blood-brain barrier, injected into the lateral ventricle significantly reduced the catatonia at doses of 0.125-2.0 micrograms as measured in both the locomotor and bar test. MN perfusion of similar doses directly into the nucleus raphe pontis, but not in the caudate nucleus significantly antagonized the catatonia. These data complement results on alfentanil-induced muscular rigidity (Blasco et al., see companion paper) where EMG indices of rigidity in rats were reversed by microinjections of low doses of MN (0.125 and 0.5 microgram) in the nucleus raphe pontis, but not the caudate nucleus even at a high dose (4.0 micrograms). Together these results suggest that the region of the nucleus raphe pontis is an important neural substrate for opiate-induced muscular rigidity, and that the catatonic state produced by opiates depends on more diffuse opiate receptor activation of which one important component may be the nucleus raphe pontis.

Alfentanil↗

The effect of muscle movement on the electroencephalogram during anesthesia with alfentanil.

Using aperiodic analysis, we examined the impact on the electroencephalogram (EEG) of muscle activity from opiate-induced rigidity with alfentanil. We compared two groups of patients, one receiving alfentanil with neuromuscular blocking agents and the other group receiving no relaxants. The alfentanil-induced muscle rigidity exerted a noticeable effect on the EEG, with a moderate effect on total power at 1 Hz; a marked effect on the total number of waves, cumulative percent power at 3 Hz, and average power at 17 to 19 Hz; and a striking effect on F90, the frequency below which 90% of the power resides. The presence of electromyographic (EMG) noise in the EEG consistently altered the variables derived from the EEG, so that anesthetic depth appeared less than it actually was. This was true in spite of the fact that we gave slightly more alfentanil in the group not receiving a relaxant. Although the observed muscle activity was greater than that usually seen clinically, and may have differed qualitatively, the results do serve as a warning that muscle noise can interfere with the EEG. Currently, there is no computerized technique that will reject or account for this noise, and we must depend on observation to recognize the EMG patterns within the EEG, either with the raw recording or with a detailed analysis (such as aperiodic analysis), and to compensate for this noise if possible. Techniques that average the EEG or that present a single number have difficulty providing this information. These results do not detract from the usefulness of the EMG contained in EEG recordings as a supplementary or complementary indicator of anesthetic lightness.

Alfentanil↗

Physiology of alfentanil-induced rigidity.

The authors investigated the hemodynamic, metabolic, electroencephalographic (EEG), and electromyographic (EMG) characteristics of narcotic-induced rigidity during induction of anesthesia with alfentanil (175 micrograms/kg) in 10 patients. Thiopental (4 mg/kg) was administered to a ten-patient control group. Rigidity was quantified in eight muscle groups (sternocleidomastoid, deltoid, biceps, forearm flexors, intercostal, rectus abdominus, vastus medialis/lateralis, and gastrocnemius). Marked rigidity was observed in all muscle groups in all patients receiving alfentanil and in none receiving thiopental. Central venous pressure increased with onset of rigidity, while mean arterial pressure and cardiac index remained unchanged. Manual ventilation was extremely difficult during alfentanil-induced rigidity. Arterial oxygen tension decreased more rapidly during rigidity than during the same time interval in the control group, while patients experiencing rigidity were more acidotic, as reflected by greater increases in base deficit. The EEG demonstrated an anesthetic state without seizure activity. The immediate increase in central venous pressure with the onset of rigidity, along with occasional simultaneous parallel variations in central venous pressure and the EMG, strongly suggest a mechanical mechanism for the change in central venous pressure. The metabolic changes during rigidity may be partly related to the absence of the normal cardiovascular reflexes that are reported to occur during voluntary isometric muscle contractions. A neurochemical mechanism of narcotic-induced rigidity is briefly reviewed.

Alfentanil↗

A comparison of morphine, fentanyl, and sufentanil anesthesia for cardiac surgery: induction, emergence, and extubation.

We compared anesthetic doses of three popular opiates, morphine (n = 10), fentanyl (n = 9), and sufentanil (n = 9) in patients undergoing cardiac surgery. Opiate administration after induction was based upon EEG and cardiovascular signs of the depth of anesthesia. Total doses were morphine, 4.4 +/- 0.71 mg/kg, fentanyl, 95.4 +/- 9.9 micrograms/kg, and sufentanil, 18.9 +/- 2.2 micrograms/kg. Comparisons among opiates included times for induction of anesthesia, return of consciousness, return of spontaneous ventilation, return of adequate cardiovascular status, and extubation. The following times (mean and SEM) were significantly (P less than 0.05) shorter for sufentanil than for fentanyl or morphine: induction (15 +/- 2.3 min, 5.9 +/- 0.7 min, and 3.0 +/- 0.2 min for morphine, fentanyl, and sufentanil, respectively); return of consciousness (morphine 109.7 +/- 34.4 min, fentanyl 62.3 +/- 17.9 min, sufentanil 17 +/- 8.7 min); return of acceptable and stable cardiovascular status (morphine 587.3 +/- 139.3 min, fentanyl 537.9 +/- 144.8 min, sufentanil 173.7 +/- 56.8 min); and extubation (morphine 1121.3 +/- 61.8 min, fentanyl 1005.7 +/- 77.7 min, sufentanil 533.3 +/- 67.8 min). We conclude that sufentanil administered in the dosage range of 19 micrograms/kg allows more rapid induction, earlier emergence from anesthesia, and faster extubation of patients than either morphine or fentanyl.

Adult↗

Availability of intraarterial pressure waveforms from catheter-manometer systems during surgery.

We determined how often and for how long usable pressure waveforms were unavailable from a radial intraarterial pressure cannula during anesthesia and surgery in 41 patients. During cardiac surgery with a continuous flush system, usable arterial pressure was unavailable 8.7% of the time. It was unavailable 9.1% of the time during noncardiac surgical procedures with a continuous flush system, and 14.7% of the time in system without continuous flush. Thus, the use of a continuous flush device improves intraarterial pressure availability. Artifact is the principal contributor to unavailability, followed by flushing and blood sampling. With rare exceptions the use of a Riva-Rocci cuff for occasional return-to-flow maneuvers on the same arm as the intraarterial cannula reduces intraarterial pressure availability only slightly, certainly not enough to detract from its usefulness in providing an estimation of systolic pressure during intraarterial pressure monitoring.

Aged↗

Evaluation of two prototype devices producing noninvasive, pulsatile, calibrated blood pressure measurement from a finger.

We evaluated two prototype instruments that measure pulsatile blood pressure continuously and noninvasively and compared the mean arterial pressure obtained from these devices with that obtained invasively in 17 male surgical patients. Each prototype consisted of an infrared photoplethysmograph mounted inside a finger cuff. The cuff was connected to a pressure control valve, which rapidly changed the cuff pressure so as to maintain a null pressure difference across the finger arterial wall. The resultant cuff pressure rapidly tracked the pulsatile intraarterial pressure. The prototypes reproduced absolute pressure, as well as pressure changes, accurately and linearly over a wide range of mean arterial pressures (from 2 to 164 mm Hg), with an average offset error of 0.8 mm Hg (SD +/- 3.8; range, -4.6 to 7.9), a mean scatter error of 5.3 mm Hg (range, 3.6 to 8.6), a mean regression slope of 0.97 (range, 0.79 to 1.22) and a mean correlation coefficient of the regression of 0.96 (range, 0.89 to 0.98). Both prototypes worked satisfactorily on all 17 patients, but not all the time on all patients. In 7 patients, probable arterial spasm prevented measurement of finger blood pressure 12.1% of the time, or 5.4% of the time for all patients. Ninety-six percent of the lost samples occurred with prototype 2, suggesting an instrument-related cause, rather than one related to the principle itself. The prototypes were simple to use and were almost free from artifact. Continuous monitoring for up to 7 hours on a single finger caused no harm to the finger.

Aged↗

An electroencephalographic comparison of alfentanil with other narcotics and with thiopental.

Using aperiodic analysis, we compared the EEG produced by alfentanil with the EEGs produced by two other opiates--fentanyl and sufentanil--on the one hand and with the EEG produced by a barbiturate--thiopental--on the other hand. Alfentanil and thiopental were injected over 1 minute; fentanyl and sufentanil were injected over 10 to 15 minutes. From the aperiodic analysis we derived up to seven single-number variables computed over 30- or 60-second epochs. All the opiates induced EEGs that were qualitatively similar to each other, although the maximum or minimum values tended to be greater and the time course more rapid with alfentanil than with the other two opiates. This finding may have been related to the fact that we injected relatively more alfentanil and administered it more rapidly. The EEGs produced by alfentanil and thiopental differed markedly, both qualitatively and quantitatively. The total power at 1 Hz and cumulative power at 3 Hz went to higher peak values with alfentanil, the latter tending to decrease with thiopental. The total number of waves per epoch went to lower peak values with alfentanil; there was little change with thiopental. The frequency below which 90% of the power resides went to considerably lower peak values with alfentanil than with thiopental. Finally, total power at 10 to 12 Hz (alpha waves) and average power at 17 to 19 Hz (beta waves) went to very high peak values with thiopental, but decreased with alfentanil.(ABSTRACT TRUNCATED AT 250 WORDS)

Alfentanil↗

EEGs during high-dose fentanyl-, sufentanil-, or morphine-oxygen anesthesia.

In 49 patients undergoing open-heart surgery we compared the electroencephalographic (EEG) effects of high-dose morphine, fentanyl, or sufentanil with O2, using two computerized analysis and display techniques: a period analysis (the Klein method) and an aperiodic analysis (the Neurometrics monitor). During fentanyl or sufentanil anesthesia, both techniques revealed a general decrease in frequency, shown by the aperiodic analysis primarily as a marked increase in the very low frequency range: an increase in the 1-Hz bin (TP1, in muv2) from 2.80 X 10(4) +/- 3.20 X 10(4) (SD) to 45.1 X 10(4) +/- 27.2 X 10(4) for fentanyl and from 3.11 X 10(4) +/- 2.83 X 10(4) to 52.8 X 10(4) for sufentanil. The cumulative percent power at 3 Hz (CP3) increased from 27.2 +/- 6.8 to 83.0 +/- 11.0 for fentanyl and from 22.7 +/- 5.2 to 85.1 +/- 10.4 for sufentanil, while the frequency at 90% cumulative percent power (F90, in Hz) decreased from 17.8 +/- 2.9 to 7.9 +/- 2.8 for fentanyl and 16.4 +/- 5.2 to 5.6 +/- 4.3 for sufentanil. The changes with morphine were less obvious, with some attenuation of high-frequency power shown by the Klein method, and an increase from 24.1 +/- 8.6 to 59.3 +/- 20.7 with CP3, but no change in TP1. Low-frequency power with the period analysis and TP1 with the aperiodic analysis decreased between laryngoscopy and the incisions with fentanyl and sufentanil.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Automatic control in anesthesia: a comparison in performance between the anesthetist and the machine.

This report is divided into two parts. First, we developed two new servo control systems by modifying an existing one. The original system was designed to control inspired halothane concentration using mean arterial pressure; the two new systems were designed to control inspired halothane concentration using end-tidal concentration or to control mean arterial pressure using the automated infusion of nitroprusside. Second, we compared the performance of experienced physician and nurse anesthetists (nine, six, and six experiments, respectively). The experiments incorporated a standardized testing sequence of two changes in desired blood pressure (set point) and two pharmacologically induced disturbances in blood pressure (perturbations). The scoring was designed to examine how fast blood pressure changed (90% response time), how far past the set point it went (overshoot), how long it took to eliminate most of the fluctuations in blood pressure (settling time), and the degree of fluctuation of blood pressure after settling (stability). Given three systems to be tested, there were (3 X 14) 42 possible mean scores for the machine and 42 for the anesthetists. The machine scored better than the anesthetists in 38 out of 42 of the mean scores; the differences were statistically significant in 19 out of 42 scores. The wide scatter in performances of the anesthetists prevented the achievement of significance in nine cases with large differences between means. Thus when the scores from the three systems were combined to achieve a larger n value, the machine outperformed the anesthetist in 12 out of 14 scores.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗

Anesthesia in septorhinoplasty. Effects of halothane vs nitrous oxide narcotic on bleeding.

The effects of halothane and nitrous oxide narcotic anesthesia on bleeding were studied. Coagulation parameters were examined preoperatively and a half hour after induction. There were no notable changes with either anesthetic technique, and there were no substantial differences between the two anesthesias. A clinical comparison of bleeding, surgical exposure, blood pressure, and duration of surgery also was made. The two anesthetic techniques tested had no notable differences in the previously mentioned parameters on septorhinoplasty.

Adult↗

Digital and sampled-data control of arterial blood pressure during halothane anesthesia.

A control system that maintains mean arterial pressure (MAP) at a desired level by automatically controlling halothane input has been developed. The control system is a discrete, digital type and is implemented with a small desk-top programmable calculator. Essentially, if MAP decreases, the inspired concentration of halothane will decrease; if MAP increases, the system will compensate by increasing inspired halothane concentration. The control system was tested in two ways: with a hybrid computer model of uptake and distribution of halothane and with dog experiments. The results indicate that (a) the model can be used to predict the response of the animal-anesthesia machine control system, and (b) the proposed algorithm is successful in controlling one anesthetic agent with one physiologic variable.

Anesthesiology↗

Anaesthesia for electroconvulsive therapy: a psychiatric viewpoint.

Brief general anaesthesia has added to the safety and comfort of electroconvulsive therapy (ECT). While usually a simple procedure, there are several areas in which ECT differs from other procedures requiring brief anaesthesia. These differences call for even more collaboration between psychiatrist and anaesthetist than is customary. This review details the areas where the anaesthetic management may affect the outcome of ECT for both an individual treatment and a treatment series. These include the patient evaluation, the patient preparation, the sequence and doses of anaesthetic agents, and the recovery period. Because each patient receives a series of treatments, an optimum regimen from both the psychiatric and anaesthetic standpoints can ultimately be achieved.

Anesthesia↗

Interactions among ventilation, the circulation, and the uptake and distribution of halothane--use of a hybrid computer multiple model: I. The basic model.

The authors describe an 18-compartment hybrid computer multiple model of the uptake and distribution of halothane. This model uses 88 equations and 124 parameter settings. Three submodels are incorporated into the basic model: 1) The mass transport of halothane is simulated on the digital portion of the hybrid computer. 2) A breath-by-breath pulmonary model with two compartments describes air pressure-flow relations in the airway system. 3) A beat-to-beat cardiovascular model with 15 compartments describes in detail blood pressure-flow relations. In addition, a baroreceptor-heart rate loop is included: an increase in arterial pressure causes a decrease in heart rate. The slope of the baroreceptor response is progressively decreased by halothane until at 2 per cent there is no response. The model of halothane uptake and distribution is separate from the blood and air pressure-flow models, but is, in effect, driven by them. Myocardial "contractility" (stroke volume) and certain regional vascular resistances can be affected by the concentration of halothane in one or any proportion of any combination of three compartments: arterial blood (arteriolar concentrations), cerebral gray matter, or myocardial. In turn, these factors significantly affect the uptake and distribution of halothane. The responses to three steady-state concentration, as well as to a step change in concentration from 0 to 2 per cent, were examined. Twenty-four outputs were recorded, including halothane concentrations in ten compartments; myocardial "contractility"; left and right ventricular and right atrial pressures; cardiac output; stroke volume, R-R interval; and blood flows in six regions. Two variables--alveolar concentration of halothane and arterial blood pressure--were recorded during a step change of 0 to 5 per cent. The model describes the appropriate steady-state and dynamic cardiovascular responses to halothane. It also demonstrates the complex interrelationships among caridac output, regional blood flow distribution, and the uptake and distribution of halothane. During step change in halothane concentration, most of the responses occur early, a phenomenon also seen in man and goats. Thus, the model is useful not only for representing organ and tissue halothane concentrations, but also for gaining new insights into cardiovascular alterations produced by rapidly changing concentrations of halothane and into the complex interactions between the circulation and the uptake and distribution of halothane.

Anesthesia, Inhalation↗

Interactions among ventilation, the circulation, and the uptake and distribution of halothane--use of a hybrid computer multiple model: II. Spontaneous vs. controlled ventilation, and the effects of CO2.

The authors have described a basic hybrid computer multiple model of the circulation, ventilation, and uptake and distribution of halothane in a companion paper. A multiple model consists of two or more submodels, each of which is complete in itself and could operate independently. In a multiple model, however, each submodel interacts with the others. The present paper describes the addition of a CO2-control loop (submodel), through which the partial pressure of CO2 modulates ventilation, as well a myocardial "contractility," arterial pressure, cardiac output, and regional vascular resistances. The concentration of halothane modifies these CO2-induced modulations. The CO2- and halothane-induced changes in ventilation and circulation in turn modify the uptake and distribution of halothane. Thus, a complex set of interrelationships among the submodels and compartments exists.

Anesthesia, Inhalation↗

Psychological functioning after halothane or enflurane anesthesia.

Halothane and enflurane anesthesia were administered without surgery to young volunteer subjects who were compared with unanesthetized control subjects. All subjects were tested for intellectual function, visual-motor coordination, and personality characteristics, and they were asked to complete a symptom checklist on three occasions: before anesthesia, 2 days after anesthesia, and 2 weeks after anesthesia. Except for slight temporary effects in a few individuals, anesthesia altered neither intellectual or visual-motor measures nor personality characteristics. Although both anesthetics induced a number of symptoms persisting for 2 days after anesthesia, malaise was clearly greater following halothane than enflurane. Halothane was specifically associated with difficulty in remembering things, difficulty in concentrating, faintness or dizziness, and having to do things slowly to do them right. These symptoms were absent at the 2-week test.

Enflurane↗

Contribution of asynergic contraction to halothane-induced myocardial depression.

We investigated the possibility that myocardial asynergy (dyscoordinate contraction) is a contributing mechanism to the impairment of cardiac function produced by halothane. Coronary cineangiograms were performed in seven dogs, awake and at 1, 2, and 3 MAC halothane. The relative motions between four arterial bifurcations (six segments) were plotted as an indication of changing ventricular dimensions. To quantitate ventricular asynergy, we calculated anisotropy (AI) and asynchrony (AS), the coefficient of variation of mean shortening (S-) and of mean time to half shortening (T-50), respectively, of the six segments. From these a myocardial performance index (MPI) was derived: MPI = S-/AI + T-50 + AS. In general, S- and MPI decreased with increasing halothane concentration. Anisotropy showed a trend, although usually insignificant, toward increasing, while AS did not change. These observations have two implications. First, asynergy of contraction contributes little, if anything, to halothane-induced impairment of myocardial performance. Second, changes in measurements of intact cardiac performance, such as dP/dtmax, may be reasonably valid during halothane, provided loading conditions are taken into account.

Anesthesia, Inhalation↗

The "D circle": closed-circuit operation of the Bain circuit.

A method of converting a Mapleson D (Bain) circuit to closed-circuit operation is presented, utilizing a laboratory air pump and a Waters carbon dioxide absorber canister to recirculate exhaled gas. The elimination of carbon dioxide from the circuit was studied and found to be adequate. The circuit would allow the use of low fresh gas flows for the maintenance of anaesthesia without the danger of carbon dioxide rebreathing. We suggest that such a circuit could provide appropriate conditions of gas humidity and temperature for endotracheal anaesthesia, while realizing the advantage of a circulator in mask anaesthesia is possible. Further design considerations for a "D circle" breathing system for clinical use are discussed.

Anesthesiology↗