Showing papers in "Anesthesiology in 1988"
TL;DR: It is concluded that CT scan lung density and oxygen exchange efficiency are correlated; the main effect of augmenting PEEP is to recruit perfused alveolar units that were previously collapsed.
Abstract: Twenty-two patients with acute respiratory failure underwent lung computed tomography (CT) and physiological measurements at 5, 10, and 15 cm H2O positive end-expiratory pressure (PEEP) to investigate the relationship between morphology and function. Lung densities were primarily concentrated in the dependent regions. From the frequency distribution of CT numbers (difference in x-ray attenuation between water and lung) and lung gas volume measurements the authors obtained a quantitative estimate of normally inflated, poorly inflated, and non-inflated lung tissue weight. This estimated average lung weight was increased twofold above normal and excess lung weight correlated with the mean pulmonary artery pressure (P less than 0.01). Venous admixture correlated with the non-inflated tissue mass (P less than 0.01). Increasing PEEP caused progressive clearing of radiographic densities and increased the mass of normally inflated tissue (anatomic recruitment), while reducing venous admixture. The cardiac index decreased after increasing PEEP while oxygen delivery was unchanged. The authors conclude that CT scan lung density and oxygen exchange efficiency are correlated; the main effect of augmenting PEEP is to recruit perfused alveolar units that were previously collapsed.
593 citations
TL;DR: An anesthesia simulation environment that provides a re-creation of the anesthesiologist's task environment in a real operating room is described and it is suggested that anesthesia simulation can be accomplished at nominal expense and has major potential for training, continuing education, certification, and research.
Abstract: Simulation is used extensively in industries that involve routine, but risky activities. The authors describe an anesthesia simulation environment that provides a re-creation of the anesthesiologist's task environment in a real operating room. The system provides appropriate inputs to standard monitoring equipment in common use during anesthesia, including ECG (with arrhythmias); invasive systemic arterial, pulmonary arterial, and central venous pressures (all coupled to ECG arrhythmias); automated cuff blood pressure; pulse oximetry; mass spectrometry; breathing circuit spirometry; and oxygen analysis. An intubation/thorax mannequin allows tracheal intubation and tube manipulation, and provides for simulation of occlusion, malposition, or disconnection of the tracheal tube, as well as regurgitation of gastric contents. The simulation is comprehensive in that it is "hands-on" and requires actual performance of most interventions using actual equipment. The simulation is conducted by a systems operator and a simulation director; the latter also acts in the roles of surgeon and circulating nurse. The simulator outputs are determined by a "script" that defines the consequences of routine anesthetic actions and pre-established critical incidents. Decisions about timing and override of the script are made by the simulation director. This control system offers maximum flexibility while maintaining clinical realism. The simulator experiences were judged as highly realistic by 21 subjects. Limitations in this version have centered on the mannequin (e.g., no patient movement, minimal or confusing physical signs) and will be addressed in future versions of the system. The authors suggest that anesthesia simulation can be accomplished at nominal expense and has major potential for training, continuing education, certification, and research.
495 citations
TL;DR: Nine of the 15 patients with severe chronic obstructive pulmonary disease and cardiovascular disease were weaned successfully from mechanical ventilation with unchanged PAOP, and transmural pulmonary artery occlusion pressure markedly increased, mandating a reinstitution of MV.
Abstract: The authors studied the hemodynamic effects of rapidly weaning from mechanical ventilation (MV) 15 patients with severe chronic obstructive pulmonary disease (COPD) and cardiovascular disease who were recovering from acute cardiopulmonary decompensation. In each patient, 10 min of spontaneous ventilation (SV) with supplemental oxygen resulted in reducing the mean esophageal pressure (X +/- SD, + 5 +/- 3 to -2 +/- 2.5 mmHg, P less than .01) and increasing cardiac index (CI) 3.2 +/- 0.9 to 4.3 +/- 1.3 1/min/M2, P less than .001), systemic blood pressure (BP 77 +/- 12 to 90 +/- 11 mmHg, P less than .001), heart rate (HR 97 +/- 12 to 112 +/- 16 beats/min, P less than .001), and, most importantly, transmural pulmonary artery occlusion pressure markedly increased (PAOPtm 8 +/- 5 to 25 +/- 13 mmHg, P less than .001), mandating a reinstitution of MV. In four patients with left ventricular (LV) catheters, the PAOP correlated with the LV end-diastolic pressure during both MV and SV. Gated blood pool imaging showed SV increased the LV end-diastolic volume index (65 +/- 24 to 83 +/- 32/M2, P less than .002) with LV ejection fraction unchanged. Patients were treated for a mean of 10 days with diuretics, resulting in a reduction of blood volume (4.55 +/- 0.9 1 to 3.56 +/- 0.55 1) and body weight (-5 kg, P less than .001). Subsequently, nine of the 15 patients were weaned successfully from mechanical ventilation with unchanged PAOP.
488 citations
443 citations
TL;DR: In this paper, a preliminary review of 900 closed insurance claims for major anesthetic mishaps was conducted to determine whether recurring patterns of management may have contributed to the occurrence or outcome of these anesthetic misbehavior.
Abstract: Fourteen cases of sudden cardiac arrest in healthy patients who received spinal anesthesia were discovered in a preliminary review of 900 closed insurance claims for major anesthetic mishaps. All patients were resuscitated from the intraoperative cardiac arrest, but six suffered such severe neurologic injury that they died in hospital. Of the eight survivors, only one exhibited sufficient neurologic recovery to allow independence in daily self-care. In view of the unexpected nature of the cardiac arrests, as well as the ultimate severity of injury, these cases were analyzed in detail to determine whether there were recurring patterns of management that may have contributed to the occurrence or outcome of these anesthetic mishaps. Two patterns were identified. The first was the intraoperative use of sufficient sedation to produce a comfortable-appearing, sleep-like state in which there was no spontaneous verbalization. Cyanosis frequently heralded the onset of cardiac arrest in patients exhibiting this degree of sedation, suggesting that unappreciated respiratory insufficiency may have played an important role. The second pattern appeared to be an inadequate appreciation of the interaction between sympathetic blockade during high spinal anesthesia and the mechanisms of cardiopulmonary resuscitation. Prompt augmentation of central venous filing through the use of a potent alpha-agonist and positional change might have improved organ perfusion, shortened the duration of cardiac arrest, and lessened the degree of neurologic damage.
429 citations
TL;DR: This clinical study demonstrates the feasibility of performing pharmacokinetic and pharmacodynamic analyses when complex infusion and bolus regimens are used for administering iv anesthetics.
Abstract: The pharmacokinetic and pharmacodynamic properties of propofol were studied in 50 surgical patients. Propofol was administered as a bolus dose, 2 mg/kg iv, followed by a variable-rate infusion, 0-20 mg/min, and intermittent supplemental boluses, 10-20 mg iv, as part of a general anesthetic technique that included nitrous oxide, meperidine, and muscle relaxants. For a majority of the patients (n = 30), the pharmacokinetics of propofol were best described by a two-compartment model. The propofol mean total body clearance rate was 2.09 +/- 0.65 1/min (mean +/- SD), the volume of distribution at steady state was 159 +/- 57 l, and the elimination half-life was 116 +/- 34 min. Elderly patients (patients older than 60 yr vs. those younger than 60 yr) had significantly decreased clearance rates (1.58 +/- 0.42 vs. 2.19 +/- 0.64 l/min), whereas women (vs. men) had greater clearance rates (33 +/- 8 vs. 26 +/- 7 l.kg-1.min-1) and volumes of distribution (2.50 +/- 0.81 vs. 2.05 +/- 0.65 l/kg). Patients undergoing major (intraabdominal) surgery had longer elimination half-life values (136 +/- 40 vs. 108 +/- 29 min). Patients required an average blood propofol concentration of 4.05 +/- 1.01 micrograms/ml for major surgery and 2.97 +/- 1.07 micrograms/ml for nonmajor surgery. Blood propofol concentrations at which 50% of patients (EC50) were awake and oriented after surgery were 1.07 and 0.95 microgram/ml, respectively. Psychomotor performance returned to baseline at blood propofol concentrations of 0.38-0.43 microgram/ml (EC50). This clinical study demonstrates the feasibility of performing pharmacokinetic and pharmacodynamic analyses when complex infusion and bolus regimens are used for administering iv anesthetics.
419 citations
TL;DR: Mivacurium may offer increased versatility in providing clinical muscle relaxation in a variety of situations, and further studies seem appropriate.
Abstract: Mivacurium chloride (BW B1090U), a bis-benzylisoquinolinium diester compound, was found to undergo hydrolysis in vitro by purified human plasma cholinesterase in a pH-stat titrator at 88% of the rate of succinylcholine at pH 7.4, 37 degrees C and 5 microM substrate concentration. In 72 consenting ASA Physical Status I-II patients receiving nitrous oxide/oxygen-narcotic-thiopental anesthesia, the neuromuscular blocking effect of mivacurium was assessed following bolus doses from 0.03 to 0.30 mg/kg, as well as during and following continuous infusions from 35 to 324 min in length. The calculated ED95 for inhibition of adductor pollicis twitch evoked at 0.15 Hz was 0.08 mg/kg. At 0.1 mg/kg, 96% block developed, onset to maximum block required 3.8 +/- 0.5 min, and recovery to 95% twitch height occurred 24.5 +/- 1.6 (SE) min after injection. At 0.25 mg/kg, onset was 2.3 +/- 0.3 min; 95% recovery developed within 30.4 +/- 2.2 min, an increase in duration of action of only 24% versus 150% higher dosage. Comparative recovery indices from 5 to 95% or from 25 to 75% twitch heights did not differ significantly among all dosage groups from 0.1 to 0.3 mg/kg (range 12.9 to 14.7 and 6.6 to 7.2 min, respectively). In 38 patients who received mivacurium by continuous infusion (duration 88.1 +/- 7.1/47.1 min, SE/SD) for maintenance of 95 +/- 4% twitch inhibition, the mean 5-95% and 25-75% recovery indices after discontinuation of infusion were 14.4 +/- 0.6 and 6.5 +/- 0.3 min (P greater than 0.5 vs. all single bolus doses). The train-of-four (T4) ratio, within 2.6 +/- 0.5 min after 95% twitch recovery following bolus doses, averaged 79.5 +/- 1.8% (n = 32). Similarly, after discontinuation of infusions, the T4 ratio reached 73.4 +/- 1.9% within 3.4 +/- 1.9 min after 95% twitch recovery (n = 33). Antagonism of residual block was seldom indicated, but, to test ease of reversal, eight patients electively received neostigmine (0.06 mg/kg) with atropine (0.03 mg/kg) at 67 to 93 (76.6 +/- 3.5) % block. Twitch returned to 95% of control within 4.5 to 9.5 (6.3 +/- 0.5) min after neostigmine. Mivacurium may offer increased versatility in providing clinical muscle relaxation in a variety of situations. Further studies seem appropriate.
367 citations
TL;DR: It is concluded that mild hypertension, when untereated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beat-adrenergic blocking agent, given with premedication, can significantly reduce that risk.
Abstract: In a non-double-blind, prospective, randomized study, the intra-operative electrocardiograms of 128 mildly hypertensive surgical patients were examined in order to determine the incidence of myocardial ischemia during anesthesia. No patient had been receiving chronic antihypertensive therapy prior to the study, but a single small oral dose of a beta-adrenergic blocking agent (labetalol, atenolol, or oxprenolol) was given to 89 of them along with premedication. Forty-four per cent of the untreated control patients and 61% of the patients pretreated with a beta-adrenergic blocking agent had normal preoperative electrocardiograms and no risk factors for coronary artery disease other than hypertension (this difference between groups was not statistically significant). During tracheal intubation and/or emergence from anesthesia, a brief, self-limited episode of myocardial ischemia was detected in 11 of 39 untreated control patients, and in two of 89 patients pretreated with a beta-adrenergic blocking agent (P less than 0.001). Tachycardia always accompanied the ischemic events, but a conspicuous increase in blood pressure did not. The authors conclude that mild hypertension, when untreated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beta-adrenergic blocking agent, given with pre-medication, can significantly reduce that risk.
354 citations
342 citations
TL;DR: It is hoped that future studies in experimental animals, careful psychophysical testing and microneurographic recordings in chronic pain patients, will lead to a better understanding of the pathophysiology of pain.
Abstract: In the last two decades, considerable advances have been made in our understanding of the mechanisms of pain. Studies correlating subjective magnitude estimations of pain in man with activity in single nerve fibers in experimental animals, and microneurographic recordings in awake humans, have provided convincing evidence for the role of specific nociceptors and labelled lines for signalling pain sensation in the normal skin. The response properties of the different types of nociceptive afferents, both myelinated and unmyelinated, from skin, muscle, and joints make them ideal candidates for signalling pain sensations. Cutaneous inflammation from any cause results in hyperalgesia. Cutaneous hyperalgesia at the site of an injury, i.e., primary hyperalgesia, can be explained by sensitization of nociceptors. This sensitization is likely due to local release of chemical mediators in the inflamed area. The metabolites of arachidonic acid (eicasonoids) and bradykinin appear to play an important role in the sensitization of nociceptors. Similar inflammation-induced changes in response properties of fine articular afferents might explain the pain of acute arthritis. The neuropeptide substance P released from primary afferents may also play an important role in the pathogenesis of arthritis. The mechanism of hyperalgesia in the region surrounding the injury, i.e., secondary hyperalgesia, is less well understood, and probably results from changes both in the peripheral and central nervous systems. While considerable advances have been made in our understanding of the mechanisms of acute pain, the pathophysiology of most chronic pain states is still unclear. We hope that future studies in experimental animals, and careful psychophysical testing and microneurographic recordings in chronic pain patients, will lead to a better understanding of the pathophysiology of pain.
316 citations
TL;DR: Propofol phnrmacokinetics and protein binding of propofol following a single intravenous bolus dose were not markedly affected by uncomplicated cirrhosis of the liver.
Abstract: The pharmacokinetics and protein binding of propofol were studied in ten patients with cirrhosis and in ten control patients undergoing elective surgery. All patients received 2.5 mg.kg-1 propofol as an intravenous bolus injection for the induction of anesthesia. Whole blood propofol concentrations were measured at intervals up to 12 h, using a high-performance liquid chromatography (HPLC) technique. Propofol protein binding was estimated by equilibrium dialysis 10 min after injection of propofol. Individual propofol profiles for all patients were best described by a three-compartment open mammillary model. Rapid and slow propofol distribution half-times were observed, followed by an elimination phase with a half-time of 4-5 h. Propofol total body clearance was reduced (1.99 +/- 0.68 l.min-1) in the patients with cirrhosis but did not differ significantly from that in the control patients (2.30 +/- 0.61 l.min-1). The apparent volume of distribution at steady state (Vdss) was similar in the two groups. No significant difference in elimination half-life was observed between the two groups. Propofol was extensively bound (mean: 97-98%) to the plasma protein of both cirrhotic and control groups. This study shows that propofol pharmacokinetics and protein binding of propofol following a single intravenous bolus dose were not markedly affected by uncomplicated cirrhosis of the liver.
TL;DR: Previous recommendations for the routine use of a V5 lead (either uni- or bipolar) in all patients at risk for ischemia are confirmed, and it is confirmed that V4 is more sensitive than lead II, and should be considered as a second choice.
Abstract: Based primarily on results obtained during exercise treadmill testing, electrocardiographic (ECG) leads II and V5 are the suggested optimal leads for detecting intraoperative myocardial ischemia. However, these recommendations have not been validated in this setting using all 12 ECG leads. Accordingly, the authors studied 105 patients with known or suspected coronary artery disease (CAD) undergoing noncardiac surgery with general anesthesia by continuously recording the 12-lead ECG intraoperatively in all patients. The average duration of monitoring was 8.2 +/- 2.7 h (mean +/- SD). Ischemic episodes (i.e., greater than or equal to 1-mm horizontal or downsloping ST depression, greater than or equal to 1.5-mm slowly upsloping ST depression or greater than or equal to 1.5-mm ST elevation in a non-Q wave lead) occurred in 25 patients (24%). Out of 51 ischemic episodes, 45 involved ST depression alone, and the remaining six involved both ST depression and elevation. ST segment changes occurred in a single lead only in 14 episodes, while multiple leads were involved in 37 episodes. Lead sensitivity was estimated assuming that all ST segment changes were true positive responses. Sensitivity using a single lead was greatest in V5 (75%) and V4 (61%), and intermediate in II, V3, and V6 (33%, 24%, and 37%, respectively). The remaining seven leads demonstrated very low sensitivity (2-14%) or exhibited no ischemic changes (I and a VL). Combining leads V4 and V5 increased sensitivity to 90%, while the standard clinical combination, II and V5, was only 80% sensitive. Sensitivity increased to 96% by combining II, V4, and V5. The further addition of V2 and V3 (five leads) increased sensitivity to 100%. This study confirms previous recommendations for the routine use of a V5 lead (either uni- or bipolar) in all patients at risk for ischemia. V4 is more sensitive than lead II, and should be considered as a second choice. However, lead II, superior for detection of atrial dysrhythmias, is more easily obtained with conventional monitors. The use of all three would appear to be the optimal arrangement for most clinical needs, and is recommended if the clinician has the capability.
TL;DR: It is demonstrated that halothane and isoflurane produce marked improvement in the recovery of segment function following a transient ischemic episode, and volatile anesthetics may attenuate postischemic left ventricular dysfunction occurring intraoperatively and enhance recovery of regional wall motion abnormalities during reperfusion.
Abstract: Following brief periods (5-15 min) of total coronary artery occlusion and subsequent reperfusion, despite an absence of tissue necrosis, a decrement in contractile function of the postischemic myocardium may nevertheless be present for prolonged periods. This has been termed "stunned" myocardium to differentiate the condition from ischemia or infarction. Because the influence of volatile anesthetics on the recovery of postischemic, reperfused myocardium has yet to be studied, the purpose of this investigation was to compare the effects of halothane and isoflurane on systemic and regional hemodynamics following a brief coronary artery occlusion and reperfusion. Nine groups comprising 79 experiments were completed in 42 chronically instrumented dogs. In awake, unsedated dogs a 15-min coronary artery occlusion resulted in paradoxical systolic lengthening in the ischemic zone. Following reperfusion active systolic shortening slowly returned toward control levels but remained approximately 50% depressed from control at 5 h. In contrast, dogs anesthetized with halothane or isoflurane (2% inspired concentration) demonstrated complete recovery of function 3-5 h following reperfusion. Because the anesthetics directly depressed contractile function, additional experiments were conducted in which a 15-minute coronary artery occlusion was produced during volatile anesthesia; however, each animal was allowed to emerge from the anesthetized state at the onset of reperfusion. Similar results were obtained in these experiments, demonstrating total recovery of contractile function within 3-5 h following reperfusion. Thus, despite comparable degrees of contractile dysfunction during coronary artery occlusion in awake and anesthetized dogs, the present results demonstrate that halothane and isoflurane produce marked improvement in the recovery of segment function following a transient ischemic episode. Therefore, volatile anesthetics may attenuate postischemic left ventricular dysfunction occurring intraoperatively and enhance recovery of regional wall motion abnormalities during reperfusion.
TL;DR: Central postsynaptic alpha2 adrenergic receptors mediate a significant part of the reduction of anesthetic requirements caused by dexmedetomidine, with no apparent involvement of either opiate or A1 adenosine receptors.
Abstract: The effect of 4(5)-[1-(2,3-dimethylphenyl)ethyl]imidazole (medetomidine), the alpha 2 adrenergic agonist, on anesthetic requirements was investigated in rats anesthetized with halothane. Halothane MAC was determined before and after either dexmedetomidine (d-enantiomer) or levomedetomidine (l-enantiomer) 10, 30, and 100 micrograms/kg or vehicle ip. There was a dose-dependent decrease in MAC with the d-, but not the l-, stereoisomer. At the highest dose of dexmedetomidine (100 micrograms/kg), halothane could be discontinued for up to 30 min with no response to tail clamping. To determine whether alpha 2 adrenoreceptors mediated this effect of dexmedetomidine on MAC, cohorts of rats were pretreated with idazoxan, 10 mg/kg ip, a highly selective alpha 2 antagonist. This completely prevented the reduction of MAC caused by dexmedetomidine. To determine whether the reduction of MAC caused by dexmedetomidine was mediated in part through either opiate or adenosine receptors, groups of rats were pretreated with either naltrexone, 5 mg/kg ip, an opiate antagonist, or 8-phenyltheophylline, 2.5 mg/kg ip, an A1 adenosine antagonist. These two pretreatments did not alter the reduction of MAC by dexmedetomidine. To determine whether postsynaptic mechanisms mediate the anesthetic effect of dexmedetomidine, rats were depleted of central catecholamine stores with either n-(2-chloroethyl)-n-ethyl-2-bromobenzylamine (DSP-4) or reserpine and alpha-methyl-para-tyrosine and MAC was determined before and after each dose of dexmedetomidine. While the catecholamine-depleted rats had a lower basal MAC than the vehicle controls, there was still a profound reduction in halothane MAC after administration of dexmedetomidine. The reduction of MAC by dexmedetomidine was blocked with idazoxan in the catecholamine depleted rats.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: In agreement with sevoflurane's low blood/gas partition coefficient (0.6), the rate of rise of alveolar concentration toward that inspired (FA/FI) for sev of lurane was significantly faster than that for either halothane or isoflureane.
Abstract: The anesthetic requirements for sevoflurane, isoflurane, and halothane were determined in mongrel dogs. The MACs (minimum alveolar concentration) of sevoflurane, isoflurane, and halothane were 2.36 +/- 0.46% (n = 18), 1.39 +/- 0.25% (n = 10), and 0.89 +/- 0.20% (n = 12), respectively (mean +/- SD). In agreement with sevoflurane's low blood/gas partition coefficient (0.6), the rate of rise of alveolar concentration toward that inspired (FA/FI) for sevoflurane was significantly faster than that for either halothane or isoflurane. Thirty seconds after breathing a constant inspired concentration FA/FI was 0.75 for sevoflurane, which was 2.96 times higher than that with halothane (0.25 +/- 0.02) and 1.29 times higher than that with isoflurane (0.6 +/- 0.05). Induction with sevoflurane was smooth, with no struggling nor excessive salivation.
TL;DR: Outcome data suggest that there are potential advantages and disadvantages of both the sitting and horizontal positions without supporting a significantly increased morbidity or mortality associated with either position.
Abstract: Controversy continues to surround the use of the sitting position for neurosurgical procedures This retrospective review of 579 posterior fossa craniectomies performed over a 4-yr period from 1981 through 1984 examines outcome following these procedures performed with the patients in cither the sit
TL;DR: CABG patients have frequent preoperative episodes of myocardial ischemia, most of which are silent, and anesthesia and surgery do not worsen the prcoperative ischemic pattern, which concludes that ECG changes suggestive of my Cardiac Infarction fequently follow CABG surgery.
Abstract: Previous studies investigating the incidence of myocardial ischemia in patients undergoing coronary-artery bypass grafting (CABG) surgery have not considered the potential significance of the preoperative myocardial ischemia and infarction. Accordingly, the authors compared the frequency and severit
TL;DR: Clonidine was more effective than diazcpam as a premedicaltion in elderly patients scheduled for elective ophthalmic surgery under general anesthesia (GA) and local anesthesia (LA) and significantly reduced intraoperative cardio vascular lability and anesthetic requirement for isoflurane and fentanyl.
Abstract: The effects of clonidine on intraocular pressure and perioperative cardiovascular variables were studied by a randomized double blind design in 80 elderly patients (ASA physical status I-III) scheduled for elective ophthalmic surgery under general anesthesia (GA) and local anesthesia (LA) Group 1 (n = 40), the control group, received diazepam po (01 mgkg-1) 90-120 min prior to arrival to the operating room Group 2 (n = 40) received clonidine po approximately 5 microgramskg-1 po at the same time Each group was divided into subgroups of 20 patients each to be managed with GA (GA subset) or LA (LA subset) Ninety to 120 minutes after the premedication, a large decrease in IOP from 20 +/- 3 to 12 +/- 3 mmHg (P less than 001) and a small but significant reduction of both systolic and diastolic BP and HR were observed in patients receiving clonidine, while no changes occurred in controls In the patients managed with GA, clonidine effectively prevented IOP rise and attenuated the associated cardiovascular response (P less than 001) following laryngoscopy and tracheal intubation, and significantly reduced intraoperative cardiovascular lability and anesthetic requirement for isoflurane (P less than 005) and for fentanyl (P less than 001) In patients managed with LA, intraoperative systolic (P less than 001) and diastolic BP and HR variability (P less than 005) were significantly lower in patients receiving clonidine as compared to controls Intraoperatively, a significantly higher incidence of hypertension (P less than 001) and tachycardia (P less than 005) were respectively observed in the LA subset and GA subset of the controls when contrasted with the corresponding subset of those receiving clonidine Moreover, clonidine was more effective than diazepam as a premedication; in fact, satisfactory intraoperative sedation and cardiovascular stability were observed in 85% of the patients who received clonidine, and in 50% of those patients who did not receive clonidine (P less than 001) Thus, clonidine may represent a useful adjunct in the management of the aged patient in the setting of ophthalmic surgery
TL;DR: Results showed that the greater neuromuscular blocking potency of pancuronium and vecuronium is lost after removal of one or both of the acetylcholine moieties, and it is suggested that a nondepolarizing equivalent of suxamethonium, when discovered, may necessarily be a drug of relatively low potency.
Abstract: The hypothesis that the neuromuscular blocking potency of pancuronium and vecuronium depends on the two acetylcholine moieties present at positions 3 and 17 was tested in cats by examining the neuromuscular profile of several desacetoxy analogues. Blockade of sciatic nerve-induced contraction of the tibialis and soleus muscles, as well as the effects on vagal-induced bradycardia and on sympathetically induced contractions of the nictitating membrane, were studied. The bis-desacetoxy analogue of pancuronium (ORG 7931) was one-fifth as potent as the parent compound as a neuromuscular blocking drug and as a vagolytic agent, but the neuromuscular block was faster in onset and shorter in duration than that produced by pancuronium. The desacetoxy analogues of vecuronium (ORG 8730 and ORG 8764) also were less potent neuromuscular blocking drugs, and, in addition, produced more vagal block than did vecuronium itself. The neuromuscular block produced by these desacetoxy analogues was of more rapid onset and shorter duration than that produced by vecuronium. The results thus showed that the greater neuromuscular blocking potency of pancuronium and vecuronium is lost after removal of one or both of the acetylcholine moieties. An analysis of the relationship between neuromuscular blocking dose and duration of action revealed that it was reciprocal, and it is suggested that a nondepolarizing equivalent of suxamethonium, when discovered, may necessarily be a drug of relatively low potency.
TL;DR: It is concluded that propofol-Nitrous oxide compares favorably to thiopental-isoflurane-nitrous oxide for maintenance of anesthesia during short outpatient procedures, however, for major abdominal operations, prop ofol anesthesia does not appear to offer any clinically significant advantages over a standard inhalational anesthetic technique.
Abstract: One hundred and twenty patients undergoing elective operations were randomly assigned to receive anesthesia with either thiopental, 4 mg/kg-isoflurane, 0.2-3%-nitrous oxide, 60-70% (control) or propofol, 2 mg/kg-propofol infusion, 1-20 mg/min-nitrous oxide, 60-70% (propofol). Although anesthetic conditions were similar during the operation, differences were noted in the recovery characteristics. For non-major (superficial) surgical procedures, the times to awakening, responsiveness, orientation, and ambulation were significantly shorter in the propofol group (4 +/- 3, 5 +/- 4, 6 +/- 4, and 104 +/- 36 min) than in the control group (8 +/- 7, 9 +/- 7, 11 +/- 9, and 142 +/- 61 min, respectively). In addition, less nausea and vomiting (20 vs. 45%) and significantly less psychomotor impairment was noted in the non-major propofol (vs. control) group. Following major abdominal operations, recovery characteristics did not differ between propofol and control groups. Delayed emergence (greater than 20 min), significant psychometric impairment, and a high overall incidence of postoperative side effects (55-60%) were noted in both drug treatment groups. The authors conclude that propofol-nitrous oxide compares favorably to thiopental-isoflurane-nitrous oxide for maintenance of anesthesia during short outpatient procedures. However, for major abdominal operations, propofol anesthesia does not appear to offer any clinically significant advantages over a standard inhalational anesthetic technique.
TL;DR: The pharmacokinetics of caudal bupivacaine in infants are characterized by Cmax of total drug similar to those observed in adults after epidural injection, and the free fraction is increased at least until 6 months of life.
Abstract: Pharmacokinetics and protein binding of bupivacaine were studied after caudal injection of 2.5 mg/kg in 13 ASA PS 1 infants (1-6 months of age) scheduled for elective hernia repair. Blood was sampled at frequent intervals from 5 min to 600 min in all but one patients. Additional samples were taken at 720 and 840 min in five patients. Bupivacaine concentration was measured using gas chromatography. Protein binding was measured using ultrafiltration. Peak serum concentrations ranged between 0.55 and 1.93 micrograms/ml. The time to reach the peak ranged from 10 to 60 min. Terminal half-life (T1/2 beta) was 7.7 +/- 2.4h (mean +/- SD), the volume of distribution (Vss) was 3.9 +/- 2.01.kg, and the total body clearance (CL) was 7.1 +/- 3.2 ml.min.kg-1. The free fraction was markedly increased (0.16 +/- 0.07) when compared with published adult values, and showed a highly significant negative correlation with age. Alpha 1 acid glycoprotein measured in the same infants correlated significantly with age. In conclusion, pharmacokinetics of caudal bupivacaine in infants are characterized by Cmax of total drug similar to those observed in adults after epidural injection. The free fraction is increased at least until 6 months of life. This suggests caution in the use of bupivacaine in infants until we understand the clinical significance of this increased free fraction.
TL;DR: The data suggest that the effects of sev ofluranc on cerebral blood flow, cerebral metabolic rate for oxygen, intracranial pressure, and the electroencephalogram are indistinguishable from those of equivalent concentrations of isoflurane in the rabbit.
Abstract: The effects of 0.5 and 1.0 MAC end-tidal concentrations of sevo-flurane on intracranial pressure, cerebral metabolic rate for oxygen, cerebral blood flow, and the electroencephalogram were compared to those of equi-MAC concentrations of isoflurane in rabbits anesthetized with morphine-nitrous oxide. At 1.0 MAC end-tidal level, both sevoflurane and isoflurane caused a significant reduction in cerebral metabolic rate for oxygen of about 50%. Neither anesthetic caused a significant change in global cerebral blood flow or cortical cerebral blood flow during either 0.5 or 1.0 MAC administration. However, both sevoflurane and isoflurane caused small but significant increases in intracranial pressure during 0.5 MAC and 1.0 MAC administration. The electroencephalogram of animals anesthetized with 1.0 MAC of either anesthetic demonstrated a burst suppression pattern with no evidence of spike or seizure activity. The data suggest that the effects of sevofluranc on cerebral blood flow, cerebral metabolic rate for oxygen, intracranial pressure, and the electroencephalogram are indistinguishable from those of equivalent concentrations of isoflurane in the rabbit.
TL;DR: In situations when packed red cells are used for major blood replacement, clotting factors in the form of FFP may not be necessary to maintain the PT or PTT at accepted normal levels.
Abstract: A greater proportion of blood replacement needs are being met by packed red cell concentrates rather than whole blood in situations of major blood loss. Twelve patients, who required major blood replacement during elective surgery, were studied to determine the changes in coagulation when packed red cells were used to replace major blood loss. In addition, the coagulation abnormalities present at the time an observer noted excessive bleeding were determined. Prior to blood product replacement and after the estimated loss of each 0.3 blood volume, coagulation tests were obtained including prothrombin time (PT), partial thromboplastin time (aPTT), platelet count, thrombin time (TT), fibrinogen levels, and assays of coagulation Factors V, VIII, and IX. Coagulation tests were repeated when clinical hemostasis was judged inadequate by the anesthesiologist and attending surgeon. Significant decreases in platelet count, fibrinogen levels, and Factor V, VIII, and IX levels occurred as increasing blood volumes were replaced. Increases in PT and aPTT above control occurred in nine of the 12 patients prior to replacement of 1 blood volume; none of the nine patients had increased clinical bleeding. In four of seven patients who had blood replacement of greater than 1 blood volume, increased clinical bleeding was noted by the observer. Platelet counts were less than 100,000/mm3 in each of these four patients, and a platelet concentrate obtained by pheresis of a single donor was administered. In two of the four patients platelet counts increased, but clinical bleeding did not resolve.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: The results support the proposal that NMDA receptor-mediated events may contribute to neuronal damage in selectively vulnerable regions of the central nervous system after ischemia and suggest that ketamine administered over an increasing length of time in the postischemic period provided significant protection.
Abstract: The neuroprotective activity of two systemically administered N-methyl-D-aspartate (NMDA) receptor antagonists, ketamine and MK-801, were investigated in a long-term recovery model of near-complete forebrain ischemia in the rat. Doses of each drug were chosen on the basis of the known degree and time course of NMDA antagonism seen in vivo after their systemic administration. Ketamine, administered at a dose of 20 mg.kg-1 iv, either immediately before or shortly after the 10-min ischemic period, failed to lessen neuronal damage in the selectively vulnerable hippocampal CA1 region. Increasing doses of ketamine administered over an increasing length of time in the postischemic period, however, did provide significant protection. MK-801 0.25 or 0.5 mg.kg-1 iv administered before ischemia also resulted in significant protection. The results support the proposal that NMDA receptor-mediated events may contribute to neuronal damage in selectively vulnerable regions of the central nervous system after ischemia.
TL;DR: The authors conclude that, despite optimal hemodynamic control, ischemia will still occur in 30% of patients with coronary artery disease; preoperative adminsitration of beta adrenergic blocking drugs effectively prevents most tachycardia-related ischemIA by keeping heart rate below the ischemian threshold.
Abstract: To examine the role of chronic calcium entry blocking drug administration on perioperative myocardial ischemia and, specifically, the frequency of hemodynamically unrelated ischemia, the authors studied 444 patients undergoing coronary artery bypass operations. Before induction of anesthesia, 119 pa