PubMed Health⌕ Search

Biomedical subjects

S B Backman

Publications and source records attributed to S B Backman.

At least 19 recordsLinked to original sources
PubMed2006

The management of severe emergence agitation using droperidol.

Emergence agitation can occur following recovery from general anaesthesia. The patient may exhibit aggressive behaviour, disorientation, agitation and restlessness. Untreated, this complication may result in significant morbidity. We report two cases where droperidol was successfully used in the management of severe emergence agitation. In the first case, droperidol was administered to prevent the occurrence of postoperative agitation in a patient known to suffer from this condition following previous general anaesthetics. In the second case, droperidol was used to treat emergence agitation in a morbidly obese patient with a difficult airway who was aggressive and difficult to restrain. Both of these patients remained calm and co-operative, with stable cardio-respiratory parameters, following the administration of droperidol and showed no further signs of agitation. We suggest that droperidol is an effective medication that may be used to prevent and treat severe emergence agitation due to its rapid sedative effect and minimal cardio-respiratory depression.

Adjuvants, Anesthesia↗
PubMed2003

Antagonism of sevoflurane anaesthesia by physostigmine: effects on the auditory steady-state response and bispectral index.

BACKGROUND: Physostigmine, a centrally acting anticholinesterase, antagonizes the hypnotic effect of propofol, as shown by the return of consciousness (response to commands) or wakefulness (spontaneous eye-opening without response to commands) and by recovery of auditory evoked potentials (40 Hz auditory steady-state response (ASSR)) and the bispectral index (BIS). We measured the effects of physostigmine on the hypnotic effect of inhaled volatile anaesthetics, using sevoflurane as the representative agent. METHODS: Eight healthy volunteers received sevoflurane adjusted to produce loss of consciousness. Physostigmine (plus glycopyrrolate) was given while the end-tidal concentration of sevoflurane was kept constant. RESULTS: Loss of consciousness was accompanied by a significant (P<0.02) decrease in ASSR amplitude (to 21% of awake value) and BIS (to 70% of awake value). Five subjects had return of consciousness or wakefulness after physostigmine. The others showed no behavioural change. Physostigmine caused a significant increase of the mean ASSR amplitude from 0.11 (SD 0.04) to 0.17 (0.06) microV (P<0.05). The BIS also increased, from 66 (12) to 74 (12), but the difference was not significant. CONCLUSIONS: Physostigmine can antagonize, at least partially, the hypnotic effect of sevoflurane and changes in arousal after physostigmine are shown by ASSR measurements. However, the antagonism is not as clear or reliable as with propofol.

Adolescent↗
PubMed2000

Liver transplantation in a Jehovah's Witness with ankylosing spondylitis.

PURPOSE: Orthotopic liver transplantation is typically associated with large volume blood loss. Technological and pharmacological advances permit liver transplantation in patients who formerly were not candidates for this surgery because of strict limitations on blood product administration. We describe a liver transplant in a Jehovah's Witness with ankylosing spondylitis. CLINICAL FEATURE: A 49-yr-old Jehovah's Witness with ankylosing spondylitis and end stage liver disease secondary to sclerosing cholangitis underwent orthotopic liver transplantation. Recombinant human erythropoietin (4,000 IU sc every two days for four weeks, then 4,000 IU sc every week) established a normal hemoglobin concentration preoperatively (> 140 g x L(-1) compared with 120 g x L(-1) baseline). Intraoperatively, strategies for reducing risk of blood product transfusion included avoidance of hypothermia (T>35 degrees C), minimal blood sampling (four 1 ml samples), normovolemic hemodilution (two units), administration of Aprotinin (2 million units bolus dose followed by infusion of 500,000 u x hr(-1)), and return of blood (1,500 ml) scavenged from the operative field. Estimated blood loss was 2,200 mi. The preoperative and postoperative hemoglobin concentration was 147 g x L(-1) (hematocrit 0.45) and 123 g x L(-1) (hematocrit 0.37), respectively. No blood products were required and he was discharged three weeks postoperatively without complication. CONCLUSION: Technological and pharmacological advances allow patients to undergo surgery traditionally associated with large volume blood loss with reduced risk of blood product administration.

Blood Loss, Surgical↗
PubMed2000

Foreign body aspiration following unconventional use of a metered dose inhaler.

PURPOSE: Aspiration of a foreign body may be life-threatening. This report describes laryngeal obstruction after inhalation of a piece of a Turbuhaler which resulted from a patient tampering with the device. CLINICAL FEATURES: A 27-yr-old man disassembled a Turbuhaler and inadvertently aspirated a plastic dispensing medication disc (22 mm diameter) while attempting to inhale the remnant terbutaline sulfate which accumulated on it. Although the patient was hoarse, he was not in acute respiratory distress. X-ray revealed the disc lodged in the larynx below the vocal cords. The patient was immediately transferred to an operating theatre, and a drying agent (glycopyrrolate), judicious sedation (midazolam and fentanyl) and O2 were administered. The airway was anesthetized with lidocaine 4% delivered using high-flow O2 through an atomizer. Direct laryngoscopy revealed a partially obstructed view of the disc lodged distal to the vocal cords which was inaccessible for retrieval. Loss of consciousness was subsequently induced by spontaneous mask ventilation with sevoflurane (in O2). The airway was visualized using a suspension laryngoscope and the foreign body was removed with grasping forceps. The patient was awakened, transferred to the ICU and given 4 mg decadron i.v. every eight hours (two doses). Laryngoscopy prior to discharge indicated good mobility of the vocal cords and normal glottic structure. CONCLUSION: Aspiration of a foreign body is a potentially life-threatening situation requiring coordination between anesthesiologist, surgeon, and nursing staff. Anesthetic goals include avoidance of upper airway obstruction and maintenance of adequate ventilation while the foreign body is retrieved. Provisions must be made for tracheostomy if these goals cannot be realized.

Adult↗
PubMed2000

Auditory steady-state response and bispectral index for assessing level of consciousness during propofol sedation and hypnosis.

UNLABELLED: We assessed the effect of propofol on the auditory steady-state response (ASSR), bispectral (BIS) index, and level of consciousness in two experiments. In Experiment 1, propofol was infused in 11 subjects to obtain effect-site concentrations of 1, 2, 3, and 4 microg/mL. The ASSR and BIS index were recorded during baseline and at each concentration. The ASSR was evoked by monaural stimuli. Propofol caused a concentration-dependent decrease of the ASSR and BIS index values (r(2) = 0.76 and 0.93, respectively; P<0.0001). The prediction probability for loss of consciousness was 0.89, 0.96, and 0.94 for ASSR, BIS, and arterial blood concentration of propofol, respectively. In Experiment 2, we compared the effects of binaural versus monaural stimulus delivery on the ASSR in six subjects during awake baseline and propofol-induced unconsciousness. During baseline, the ASSR amplitude with binaural stimulation (0.47+/-0.13 microV, mean +/- SD) was significantly (P<0.002) larger than with monaural stimulation (0.35+/-0.11 microV). During unconsciousness, the amplitude was 0.09+/-0.09 microV with monaural and 0.06+/-0.04 microV with binaural stimulation (NS). The prediction probability for loss of consciousness was 0.97 (0.04 SE) for monaural and 1.00 (0.00 SE) for binaural delivery. We conclude that the ASSR and BIS index are attenuated in a concentration-dependent manner by propofol and provide a useful measure of its sedative and hypnotic effect. BIS was easier to use and slightly more sensitive. The ASSR should be recorded with binaural stimulation. The ASSR and BIS index are both useful for assessing the level of consciousness during sedation and hypnosis with propofol. However, the BIS index was simpler to use and provided a more sensitive measure of sedation. IMPLICATIONS: We have compared two methods for predicting whether the amount of propofol given to a human subject is sufficient to cause unconsciousness, defined as failure to respond to a simple verbal command. The two methods studied are the auditory steady-state response, which measures the electrical response of the brain to sound, and the bispectral index, which is a number derived from the electroencephalogram. The results showed that both methods are very good predictors of the level of consciousness; however, bispectral was easier to use.

Adolescent↗
PubMed2000

Physostigmine reverses propofol-induced unconsciousness and attenuation of the auditory steady state response and bispectral index in human volunteers.

BACKGROUND: It is postulated that alteration of central cholinergic transmission plays an important role in the mechanism by which anesthetics produce unconsciousness. The authors investigated the effect of altering central cholinergic transmission, by physostigmine and scopolamine, on unconsciousness produced by propofol. METHODS: Propofol was administered to American Society of Anesthesiologists physical status 1 (n = 17) volunteers with use of a computer-controlled infusion pump at increasing concentrations until unconsciousness resulted (inability to respond to verbal commands, abolition of spontaneous movement). Central nervous system function was assessed by use of the Auditory Steady State Response (ASSR) and Bispectral Index (BIS) analysis of electrooculogram. During continuous administration of propofol, reversal of unconsciousness produced by physostigmine (28 microgram/kg) and block of this reversal by scopolamine (8.6 microgram/kg) were evaluated. RESULTS: Propofol produced unconsciousness at a plasma concentration of 3.2 +/- 0.8 (+/- SD) microgram/ml (n = 17). Unconsciousness was associated with reductions in ASSR (0.10 +/- 0.08 microV [awake baseline 0.32 +/- 0.18 microV], P < 0.001) and BIS (55.7 +/- 8.8 [awake baseline 92.4 +/- 3.9], P < 0.001). Physostigmine restored consciousness in 9 of 11 subjects, with concomitant increases in ASSR (0.38 +/- 0.17 microV, P < 0.01) and BIS (75.3 +/- 8.3, P < 0.001). In all subjects (n = 6) scopolamine blocked the physostigmine-induced reversal of unconsciousness and the increase of the ASSR and BIS (ASSR and BIS during propofol-induced unconsciousness: 0.09 +/- 0.09 microV and 58.2 +/- 7.5, respectively; ASSR and BIS after physostigmine administration: 0.08 +/- 0.06 microV and 56.8 +/- 6.7, respectively, NS). CONCLUSIONS: These findings suggest that the unconsciousness produced by propofol is mediated at least in part via interruption of central cholinergic muscarinic transmission.

Adolescent↗
PubMed1999

Brain mechanisms of propofol-induced loss of consciousness in humans: a positron emission tomographic study.

In the present study, we used positron emission tomography to investigate changes in regional cerebral blood flow (rCBF) during a general anesthetic infusion set to produce a gradual transition from the awake state to unconsciousness. Five right-handed human volunteers participated in the study. They were given propofol with a computer-controlled infusion pump to achieve three stable levels of plasma concentrations corresponding to mild sedation, deep sedation, and unconsciousness, the latter defined as unresponsiveness to verbal commands. During awake baseline and each of the three levels of sedation, two scans were acquired after injection of an H215O bolus. Global as well as regional CBF were determined and correlated with propofol concentrations. In addition, blood flow changes in the thalamus were correlated with those of the entire scanned volume to determine areas of coordinated changes. In addition to a generalized decrease in global CBF, large regional decreases in CBF occurred bilaterally in the medial thalamus, the cuneus and precuneus, and the posterior cingulate, orbitofrontal, and right angular gyri. Furthermore, a significant covariation between the thalamic and midbrain blood flow changes was observed, suggesting a close functional relationship between the two structures. We suggest that, at the concentrations attained, propofol preferentially decreases rCBF in brain regions previously implicated in the regulation of arousal, performance of associative functions, and autonomic control. Our data support the hypothesis that anesthetics induce behavioral changes via a preferential, concentration-dependent effect on specific neuronal networks rather than through a nonspecific, generalized effect on the brain.

Adult↗
PubMed1999

Organization of the sympathetic innervation of the forelimb resistance vessels in the cat.

UNLABELLED: Detailed information on the outflow pathway of sympathetic vasoconstrictor fibers to the upper extremity is lacking. We studied the organization of the sympathetic innervation of the forelimb resistance vessels and of the sinoatrial (SA) node in the decerebrated, artificially respirated cat. The distal portion of sectioned individual rami T1-8 and the sympathetic chain immediately caudal to T8 on the right side were electrically stimulated while the right forelimb perfusion pressure (forelimb perfused at constant flow) and heart rate were recorded. Increases in perfusion pressure were evoked by stimulation of T2-8 (maximal response T7: 55 +/- 2.3 mm Hg). Responses were still evoked by stimulation of the sympathetic chain immediately caudal to T8 (44 +/- 15 mm Hg). Increases in heart rate were evoked by the stimulation of more rostral rami (T1-5; maximal response T3: 55.2 +/- 8 bpm). These vasoconstrictor and cardioacceleratory responses were blocked by the cholinergic antagonists hexamethonium and scopolamine. Sectioning of the vertebral nerve and the T1 ramus abolished the vasoconstrictor response. Stimulation of the vertebral nerve and of the proximal portion of the sectioned T1 ramus increased perfusion pressure (69 +/- 9 and 34 +/- 14 mm Hg, respectively), which was unaffected by ganglionic cholinergic block. These data suggest that forelimb resistance vessel control is subserved by sympathetic preganglionic neurons located mainly in the middle to caudal thoracic spinal segments. Some of the postganglionic axons subserving vasomotor function course through the T1 ramus, in addition to the vertebral nerve. IMPLICATIONS: Forelimb vasculature is controlled by sympathetic preganglionic neurons located in middle to caudal thoracic spinal segments and by postganglionic axons carried in the T1 ramus and vertebral nerve. This helps to provide the anatomical substrate of interruption of sympathetic outflow to the upper extremity produced by major conduction anesthesia of the stellate ganglion or spinal cord.

Anesthesia, Conduction↗
PubMed1998

Synaptic inhibitory effects of edrophonium on sympathetic ganglionic transmission.

PURPOSE: To evaluate the effect of edrophonium on synaptic transmission in the superior cervical ganglion. METHODS: In anaesthetized rats the effect of edrophonium on synaptic transmission was studied in vitro by testing whether it blocks the compound action potential recorded from postganglionic fibres evoked by stimulation of preganglionic axons. The superior cervical ganglion was excised and the cervical sympathetic trunk and internal carotid nerve were used for stimulating and recording, respectively. Drugs superfused included edrophonium (0.1-500 microM), neostigmine (0.1-10 microM), and muscarinic M1 and M2 antagonists pirenzepine and AFDX-116 (200 nM-10 microM), respectively. To evaluate a presynaptic action, the effect of edrophonium on basal and high-K+ (35 mM) evoked release of [3H]ACh from the superior cervical ganglion was studied in vitro. To evaluate a postsynaptic action, edrophonium's effect on postganglionic nerve discharge in response to arterial injection of ACh (100 micrograms) into the superior cervical ganglion was determined in vivo. RESULTS: Edrophonium (10-500 microM) decreased the compound action potential amplitude (ED50 163.5 microM). A decrease was not produced by neostigmine, nor was it reversed by pirenzepine or AFDX-116. Edrophonium blocked postganglionic cell firing in response to exogenously administered ACh. Although edrophonium did not affect basal or high-K+ evoked ACh release, when the evoked increase was calculated as a multiple of the basal release, it caused approximately a 30% (P < 0.005) reduction. CONCLUSIONS: Edrophonium blocks ganglionic cholinergic transmission postsynaptically and, possibly, presynaptically. The mechanism(s) by which this occurs does not appear to involve inhibition of cholinesterase, or activation of M1 or M2 receptor subtypes.

Acetylcholinesterase↗
PubMed1998

Effect of isoflurane on the auditory steady-state response and on consciousness in human volunteers.

BACKGROUND: The auditory steady state response (ASSR) is a sustained electrical response of the brain to auditory stimuli delivered at fast rates (30-50 responses/s). The aim of this study was to evaluate the effect of 0.26-0.50% isoflurane on the ASSR and on consciousness, defined as responsiveness to verbal commands. METHODS: Ten volunteers (21-31 yr) participated. Isoflurane was administered at three stable, end-tidal concentrations: 0.26%, 0.38%, and 0.50%. The ASSR in response to 18,000 stimuli (500-Hz tonebursts, 10 ms, 82-dB, the right ear, 35-45 bursts/s) was recorded from the vertex with reference to the right mastoid. Recordings were made during baseline, at each isoflurane concentration, and during recovery. RESULTS: The mean (SD) ASSR amplitudes were 0.32 (0.23) microV during baseline, 0.24 (0.17) microV during 0.26% isoflurane, 0.09 (0.05) microV during 0.38% isoflurane, 0.04 (0.03) microV during 0.50% isoflurane, and 0.29 (0.33) microV during recovery. The amplitude during baseline and recovery was larger than during 0.38% and 0.50% isoflurane (P < 0.001). The amplitude at 0.26% was larger than at the other concentrations (P < 0.025). The logarithm of the ASSR amplitude was related linearly to the concentration of isoflurane (r = 0.85; P < 0.0001). The prediction probability (Pk) for loss of consciousness was 0.95 for both ASSR and measured isoflurane concentration. An ASSR amplitude < 0.07 microV was always associated with unconsciousness. CONCLUSIONS: The ASSR is attenuated in a concentration-dependent manner by isoflurane. Suppression of consciousness and maximal attenuation of ASSR occur in the same isoflurane concentration range. Profound attenuation of ASSR appears to reflect unconsciousness, defined as unresponsiveness to verbal commands.

Acoustic Stimulation↗
PubMed1997

Protamine-induced hypotension and bradycardia in a cardiac transplant patient.

PURPOSE: The potential for functional reinnervation of the transplanted heart in man is controversial. We report the sudden onset of bradycardia in a cardiac transplant patient following a period of hypotension subsequent to the administration of protamine. Possible mechanisms underlying this response, including reinnervation of the transplanted heart, are assessed. CLINICAL FEATURES: Eight weeks after cardiac transplantation, a patient returned to hospital for a left femoral-tibial artery bypass vein graft. The patient was anaesthetized using general anaesthesia. Upon completion of the procedure, protamine was administered to reverse the heparin-induced anticoagulation. Although administration of a 5.0 mg "test-dose" appeared to be without cardiovascular effect, after an additional 20.0 mg, blood pressure decreased from 98/52 to 62/40 mmHg. After blood pressure reached its nadir, heart rate decreased precipitously from 57 to 29 beats.min-1. CONCLUSIONS: This report demonstrates that heart rate can change considerably in patients who have undergone cardiac transplantation. It is argued that the change in heart rate observed in the present report cannot be explained by reinnervation of the transplanted heart, as the patient had undergone transplantation only eight weeks previously. Rather, we suggest that the change was mediated by mechanisms intrinsic to the transplanted heart and extrinsic to the CNS.

Bradycardia↗
PubMed1997

Bradycardia produced by pyridostigmine and physostigmine.

PURPOSE: The bradycardia produced by pyridostigmine and physostigmine in an animal model of acute cardiac denervation was examined according to its relation to cholinesterase inhibition and sensitivity to block by cholinergic receptor antagonists. METHODS: Cats were anaesthetised, vagotomised and propranolol-treated. Heart rate was continuously recorded. Erythrocyte cholinesterase activity of arterial blood was measured using a radiometric technique. Nicotinic and muscarinic M1 receptors were blocked with hexamethonium and pirenzepine, respectively. M2 receptors were blocked with gallamine, pancuronium and AFDX-116. RESULTS: With pyridostigmine and physostigmine the dose-response relationship for the decrease in heart rate (ED50 1.05 +/- 0.25 and 0.198 +/- 0.03 mg.kg-1, respectively) was shifted to the right of that for the inhibition of cholinesterase activity (ED50 0.094 +/- 0.03 and 0.032 +/- 0.01 mg.kg-1, respectively). The decrease in cholinesterase activity reached a plateau at a cumulative dose of 0.56 +/- 0.08 and 0.32 +/- 0.08 mg.kg-1, respectively. In contrast, there did not appear to be a plateau in the bradycardic effect. The bradycardia produced by pyridostigmine and physostigmine was blocked by hexamethonium (ED50 10 +/- 1.3 and 15.3 +/- 2.4 mg.kg-1, respectively), pirenzepine (ED50 68 +/- 16 and 138 +/- 32 micrograms.kg-1, respectively), gallamine (56 +/- 11 and 67 +/- 17 micrograms.kg-1, respectively), pancuronium (32 +/- 10 and 30 +/- 4 micrograms.kg-1, respectively), and AFDX-116 (31 +/- 4 and 28 +/- 4 micrograms.kg-1, respectively). CONCLUSION: The bradycardia produced by reversible anticholinesterase drugs containing a carbamyl group is not clearly related to the degree of cholinesterase activity, and has a low sensitivity to nicotinic and muscarinic M1 and a high sensitivity to muscarinic M2 receptor antagonists.

Animals↗
PubMed1997

Heart rate changes in cardiac transplant patients and in the denervated cat heart after edrophonium.

PURPOSE: The effect of edrophonium on heart rate in cardiac transplant patients and in an animal model of acute cardiac denervation were studied, to evaluate the functional state of the peripheral parasympathetic pathway following cardiac denervation. METHODS: Edrophonium was studied in patients with normally innervated hearts (controls) and in cardiac transplants. Edrophonium was also studied in vagotomized, beta-blocked cats. In Group I animals, the vagus nerve was not stimulated. In Groups 2 & 3 the right vagus nerve was electrically stimulated to produce approximately 20% and 40% reductions in baseline heart rate, respectively. RESULTS: Maximum heart rate reduction in transplants (7.3 +/- 0.8 beats.min-1 with 0.6 +/- 0.08 mg.kg-1) was less than in controls (13.3 +/- 1.6 beats.min-1 with 0.4 + 0.05 mg.kg-1, P < 0.01). In Group I animals heart rate decreased maximally by 20.9 +/- 2.5 beats.min-1 with 9.0 +/- 1.9 mg.kg-1. In Groups 2 and 3, with doses < 1.5 mg.kg-1, reductions in heart rate were greater than in Group I and maximum reductions were obtained with lower doses (Group 2: maximum reduction by 20.3 +/- 2.8 beats.min-1 with 1.3 +/- 0.1 mg.kg-1; Group 3:22.6 +/- 4.0 beats.min-1 with 0.8 +/- 0.2 mg.kg-1, P < 0.001). Doses > 1.5 mg.kg-1 in Groups 2 and 3 produced increases in heart rate. CONCLUSION: Edrophonium produced bradycardia in cardiac transplants suggesting spontaneous release of acetylcholine from parasympathetic postganglionic neurons in the transplanted heart. The magnitude of the bradycardia was less in transplant than in control patients. Findings from animal studies suggest that the reduction in transplants can be attributed to diminution or absence of tonic cardiac parasympathetic drive. At high doses, edrophonium may interfere with parasympathetic neuron activation.

Acetylcholine↗
PubMed1996

Neostigmine decreases heart rate in heart transplant patients.

PURPOSE: This study evaluated the effect of neostigmine on heart rate in cardiac transplant patients. METHODS: Neostigmine (2.5-50 micrograms.kg-1) was administered to ASA 1 or 2 patients with normally innervated hearts (controls), and to patients who had undergone recent (< six months before study) or remote (> six months before study) cardiac transplantation. RESULTS: Baseline heart rate was 66 +/- 3 beats.min-1 in controls (n = 10, mean +/- SEM), which was slower than that observed in recently (95 +/- 4 beats.min-1, n = 15, P < 0.001) and in remotely (88 +/- 3 beats.min-1, n = 16, P < 0.001) transplanted patients. Neostigmine produced a dose-dependent decrease in heart rate in all patients. Controls were the most sensitive to neostigmine, with a 10% decrease in heart rate produced by an estimated dose of 5.0 +/- 1.0 micrograms.kg-1. The recently transplanted group was the least sensitive, with the maximum dose producing only an 8.3 +/- 0.9% reduction. The response to neostigmine of the remotely transplanted patients was variable. The estimated dose to produce a 10% decrease in heart rate in this group was 24 +/- 6 micrograms.kg-1 which was greater than that for controls (P = 0.008). Administration of atropine (1.2 mg) reversed the neostigmine-induced bradycardia in all three groups. Reversal of the bradycardia consisted of a transient peak increase in heart rate in controls to 145 +/- 6% of baseline, a value which was greater than that observed in recent (103 +/- 1%, P < 0.001) and in remote (109 +/- 3%, P < 0.001) transplants. CONCLUSIONS: Neostigmine produces a dose-dependent bradycardia in heart transplant patients. Some remotely transplanted patients may be particularly sensitive to the bradycardic effects of neostigmine.

Cholinesterase Inhibitors↗