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1. |
This Month in Anesthesiology |
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Anesthesiology,
Volume 80,
Issue 5,
1994,
Page 27-27
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ISSN:0003-3022
出版商:OVID
年代:1994
数据来源: OVID
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2. |
Implications for Subspecialty Care of Anesthetized Children |
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Anesthesiology,
Volume 80,
Issue 5,
1994,
Page 969-971
Jeffrey Morray,
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PDF (223KB)
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ISSN:0003-3022
出版商:OVID
年代:1994
数据来源: OVID
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3. |
Ventilation of the Acute Respiratory Distress Syndrome |
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Anesthesiology,
Volume 80,
Issue 5,
1994,
Page 972-975
John Marini,
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PDF (318KB)
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ISSN:0003-3022
出版商:OVID
年代:1994
数据来源: OVID
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4. |
Bradycardia during Anesthesia in InfantsAn Epidemiologic Study |
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Anesthesiology,
Volume 80,
Issue 5,
1994,
Page 976-982
Richard Keenan,
Jay Shapiro,
Francis Kane,
Pippa Simpson,
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摘要:
Background:The frequency and morbidity of bradycardia during anesthesia in infants are not well documented. This study sought to determine the frequency of bradycardia during anesthesia in infants (0 to 1 yr) compared to that in older children, describe causes and morbidity, and identify factors that influence its frequency.Methods:Computerized information abstracted from 7,979 anesthetic records of patients ages 0–4 yr undergoing non-cardiac surgery were examined for the presence or absence of intraoperative bradycardia. To study bradycardia in infants, 4,645 anesthetics in patients aged 0–1 yr were considered. Those with bradycardia to heart rates less than 100 beats/min were examined for causes, morbidity, and treatment of the bradycardia. For analysis of influencing factors, the frequency of bradycardia in infants was related to age, sex, race, ASA physical status, surgical site (body cavity), complexity (major or minor) and duration, type of primary anesthetist, type of supervising anesthesiologist, and anesthetic agents. Logistic regression was used to estimate the significance (P< 0.05) and odds ratios for each.Results:The frequency of bradycardia was 1.27% In the 1st yr of life, but only 0.65% in the third and 0.16% in the 4th yr, a significant difference. Causes of bradycardia in infants included disease or surgery in 35%, the dose of inhalation agent in 35%, and hypoxemia in 22%. Morbidity included hypotension in 30%, asystole or ventricular fibrillation in 10%, and death in 8%. Treatment involved epinephrine in 30% and chest compression in 25%. Associated factors included an ASA physical status of 3–5 (vs.1 or 2) and longer (vw.shorter) surgery. Bradycardia was less than half as likely when the supervising anesthesiologist was a member of the Pediatric Anesthesia Service as with other anesthesiologists (P< 0.001).Conclusions:Bradycardia is more frequent in infants undergoing anesthesia compared to older children and is associated with substantial morbidity. It is more likely in sicker infants undergoing prolonged surgery and less likely when a pediatric anesthesiologist is present.
ISSN:0003-3022
出版商:OVID
年代:1994
数据来源: OVID
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5. |
Effects of Pressure‐controlled with Different IE Ratios Versus Volume‐controlled Ventilation on Respiratory Mechanics, Gas Exchange, and Hemodynamics in Patients with Adult Respiratory Distress Syndrome |
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Anesthesiology,
Volume 80,
Issue 5,
1994,
Page 983-991
Martin Lessard,
Emmanuel Guérot,
Hubert Lorino,
Francois Lemaire,
Laurent Brochard,
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摘要:
Background:Pressure-controlled (PCV) and pressure-controlled inverse ratio ventilation (PCIRV) have been proposed instead of volume-controlled conventional ratio ventilation (VC) with positive end-expiratory pressure (PEEP) for patients with adult respiratory distress syndrome (ARDS). The advantages advocated with the use of PCIRV are to decrease airway pressures and to improve gas exchange. However, most studies did not compare PCIRV and VC while keeping both the level of ventilation and end-expiratory alveolar pressure (total-PEEP) constant.Methods:Nine patients with moderate to severe ARDS (lung injury score 2.83 ± 0.18) had their lungs ventilated with VC, PCV with a conventional ratio (I:E 1:2; PC 1/2), and PCIRV (I: E 2:1 and 3:1; PC 2/1 and PC 3/1, respectively). Ventilator settings were adjusted to keep tidal volume, respiratory rate, Fio2, and total-PEEP constant in every mode. With each mode, a complete set of ventilatory, hemodynamic, and gas exchange parameters was obtained after 30 min.Results:In PC 3/1, the data obtained could not be strictly compared to the other modes because total-PEEP was higher despite external-PEEP being set at zero. For the other modes (VC, PC 1/2, and PC 2/1), despite differences in peak airway pressures, no difference was noted for end-inspiratory and end-expiratory static airway pressures (which better reflect alveolar pressures) nor for lung and respiratory system compliance. Arterial oxygenation deteriorated slightly with PC 2/1 despite a higher mean airway pressure, whereas alveolar ventilation tended to be slightly, but not significantly, improved (lower Paco2). A decrease in systolic and mean arterial pressure also was observed with PC 2/1 without other significant hemodynamic change.Conclusions:In this prospective controlled study, no short-term beneficial effect of PCV or PCIRV could be demonstrated over conventional VC with PEEP in patients with ARDS.
ISSN:0003-3022
出版商:OVID
年代:1994
数据来源: OVID
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6. |
Sympathetic Neural Blockade by Thoracic Epidural Anesthesia Suppresses Renin Release in Response to Arterial Hypotension |
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Anesthesiology,
Volume 80,
Issue 5,
1994,
Page 992-999
Hans-Bernd Hopf,
Rainer Schlaghecke,
Jürgen Peters,
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摘要:
Background:The renin-angiotensin and vasopressin systems, in addition to the sympathetic system, are important backup mechanisms for maintaining arterial blood pressure during circulatory challenges. We tested the hypothesis that preganglionic sympathetic blockade by thoracic epidural anesthesia interferes with the functional integrity of the renin-angiotensin system.Methods:Renin concentrations were assessed in awake non-sedated patients in response to induced arterial hypotension both before and during sympathetic blockade by thoracic epidural anesthesia (n = 10). Heart rate (electrocardiogram) and mean arterial blood pressure (electromanometry) were recorded continuously. Active renin (radioimmunoassay), vasopressin (radioimmunoassay), and osmolality (osmometry) in arterial blood were measured intermittently: (1) at baseline, (2) during a hypotensive challenge (15 min) induced by sodium nitroprusside (titrated to decrease mean arterial blood pressure by at least 25%) with the sympathetic system intact, (3) during recovery, (4) with epidural anesthesia alone (sensory blockade T1-T11), and (5) during a second hypotensive challenge and sympathetic blockade with sodium nitroprusside titrated to the same mean arterial blood pressure as with the sympathetic system intact.Results:With the sympathetic system intact hypotension almost doubled renin concentration (34 ± 32 SD to 60 ± 58 pg ml-1,P= 0.019), while vasopressin concentration remained unchanged. In contrast, during sympathetic blockade and despite identical hypotension (mean arterial blood pressure 68 ± 8vs.67 ± 5 mmHg), renin concentration did not change (35 ± 27vs.35 ± 29 pg ml-1,P= 0.5), whereas vasopressin concentration increased (4.6 ± 2.5 to 13.4 ± 9.4 pg ml-1, P = 0.01). Osmolality remained unchanged.Conclusion:Our results Indicate a key role of renal sympathetic fibers in mediating renin release during hypotension in humans, and that epidural anesthesia interferes with the functional integrity of the renin-anglotensin system.
ISSN:0003-3022
出版商:OVID
年代:1994
数据来源: OVID
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7. |
Endogenous Vasopressin and Renin‐Angiotensin Systems Support Blood Pressure after Epidural Block in Humans |
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Anesthesiology,
Volume 80,
Issue 5,
1994,
Page 1000-1007
H. Carp,
R. Vadhera,
A. Jayaram,
D. Garvey,
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摘要:
Background:Studies in experimental animals show that endogenous Arg-vasopressin (AVP) and the renin-angiotensin system support blood pressure when the sympathetic system is impaired pharmacologically or after epidural anesthesia. However, extrapolation to humans is uncertain. Therefore, we administered an AVP type V1receptor antagonist and an angiotensin-converting enzyme inhibitor to volunteers and measured the effect on blood pressure after epidural anesthesia.Methods:Healthy volunteers in whom epidural catheters were placed were randomly assigned to receive 1.25 mg intravenous enalapril or saline placebo followed by 0.5 mg AVP type V1antagonist β-mercapto-β, β-cyclopentamethylene-proprionyl-o-Met-Tyr-Arg-vasopressin (AVPA) or saline placebo. Finally, 2% lidocaine was injected to obtain a T2 level. Controls received intramuscular lidocaine.Results:Blood pressure did not significantly change after T-2epidural anesthesia in subjects treated with saline placebo, AVPA or enalapril alone (n = 10, for each treatment). In contrast, combined treatment with enalapril and AVPA resulted in a 36 ± 11% decrease in blood pressure after epidural dosing (n = 6). Controls given intramuscular lidocaine, in place of the epidural did not develop hypotension after AVPA and enalapril treatment (n = 10).Conclusions:Endogenous AVP and the renin-anglotensin system play important roles in maintaining blood pressure after epidural anesthesia in healthy subjects.
ISSN:0003-3022
出版商:OVID
年代:1994
数据来源: OVID
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8. |
The Incidence of Pneumocephalus after Supratentorial CraniotomyObservations on the Disappearance of Intracranial Air |
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Anesthesiology,
Volume 80,
Issue 5,
1994,
Page 1008-1012
Daniel Reasoner,
Michael Todd,
Franklin Scamman,
David Warner,
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摘要:
Background:Pneumocephalus occurs in a variety of clinical settings and has important anesthetic implications, particularly if N2O is used. One common cause of pneumocephalus is a craniotomy or craniectomy, and therefore patients undergoing these neurosurgical procedures may be at increased risk for the development of tension pneumocephalus if N2O is used during a subsequent anesthetic. However, because the rate at which a postoperative pneumocephalus resolves has not been well denned, the duration of this risk period is unknown.Methods:Department of Anesthesia billing codes were used to identify all patients undergoing supratentorial craniotomy between 1986 and 1990. This list was cross-indexed with Department of Radiology data to generate a list of patients who had had a computed tomographic scan of the head performed on or after the day of their surgery. From this list, 240 scans were examined for the presence of intracranial air. The magnitude of pneumocephalus, if present, was ranked as large, moderate, small, or trace.Results:Air was seen in all scans obtained in the first 2 postoperative days. Sixty-six percent of these pneumocephali were judged to be moderate or large. The incidence of pneumocephalus decreased to 75% by postoperative day 7. During the 2nd and 3rd postoperative weeks, the incidence of pneumocephalus decreased to 59–6 and 26.3%, respectively. The size of the pneumocephali also decreased. Still, 11.8% of the scans obtained during the 2nd postoperative week had pneumocephali that were judged to be moderate or large.Conclusions:These data indicate that all patients have pneumocephalus immediately after a supratentorial craniotomy. Although the incidence and size of pneumocephali decrease over time, a significant number of patients have an intracranial air collection large enough to put them at risk for complication if N2O is used during a second anesthetic in the first 3 weeks after the first procedure. This information should be considered in the evaluation of the patient and in the selection of anesthetic agents.
ISSN:0003-3022
出版商:OVID
年代:1994
数据来源: OVID
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9. |
Pharmacokinetics of Aprotinin in Preoperative Cardiac Surgical Patients |
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Anesthesiology,
Volume 80,
Issue 5,
1994,
Page 1013-1018
Jerrold Levy,
James Bailey,
Markku Salmenperä,
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摘要:
Background:Aprotinin, a polypeptide protease inhibitor, reduces bleeding and transfusion requirements during cardiac surgery. To investigate aprotinin's pharmacokinetics, we administered therapeutic doses to patients scheduled to undergo cardiac surgery.Methods:Preoperative doses of 500,000 and 1,000,000 kallikrein inhibitor units (KIU) were administered as an infusion over 30 min to 28 patients, and plasma concentrations were measured for 48 h. Aprotinin concentrations were determined using a sandwich-enzyme-linked immunosorbent assay. A three-compartment model was fit to the measured aprotinin concentrations using extended nonlinear least-squares regression.Results:Plasma aprotinin concentrations at the end of the 30-min infusion were 147 ± 61 KIU/ml for the 1,000,000-KIU dose and 60 ± 19 KIU/ml for the 500,000-KIU dose. Elimination clearance was 35.5 ml/min, and volume of distribution at steady state was 26.5 1.Conclusions:A 2,000,000-KIU dose is needed to produce the plasma concentration of 200 KIU/ml associated with kallikrein inhibition. Plasma concentrations in excess of 50 KIU/ml, the concentration required to inhibit plasma, can be achieved by a significantly smaller dose. Based on the derived pharmacokinetic parameters, an infusion model was developed to appropriately administer and maintain effective plasma concentrations of aprotinin, depending on the plasma concentration desired and the target proteases to be inhibited.
ISSN:0003-3022
出版商:OVID
年代:1994
数据来源: OVID
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10. |
Renal Concentrating Function with Prolonged Sevoflurane or Enflurane Anesthesia in Volunteers |
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Anesthesiology,
Volume 80,
Issue 5,
1994,
Page 1019-1025
Edward Frink,
T. Malan,
R. Isner,
Elizabeth Brown,
Scott Morgan,
Burnell Brown,
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摘要:
Background:Sevoflurane, a new inhalational anesthetic, is biotransformed, producing peak plasma inorganic fluoride concentrations that may exceed 50 mm. We evaluated plasma inorganic fluoride concentrations with prolonged (> 9 MAC-h) sevoflurane or enflurane anesthesia in volunteers and compared renal concentrating function with desmopressin testing 1 and 5 days after anesthesia.Methods:Fourteen healthy male volunteers received either enflurane or sevoflurane (1–1.2 MAC) for more than 9 MAC-h. Each volunteer was administered three tests of renal concentrating function, with intranasal desmopressin and urine collections performed 1 week before anesthesia and 1 and 5 days after anesthesia. Venous blood samples were obtained for plasma fluoride concentrations during and after anesthesia. Creatinine clearance was determined by 24-h urine collections 7 days before and 4 days after anesthesia. Urine samples were obtained before and 1, 2, and 5 days after anesthesia for determination of n-acetyl-β-glucosaminidase and creatinine concentrations.Results:Prolonged sevoflurane anesthesia (9.5 MAC-h) did not impair renal concentrating function on day 1 or 5 postanesthesia, as determined by desmopressin testing. Maximal urinary osmolality on day 1 postanesthesla was decreased (< 800 mOsm/kg) in two of seven enflurane-anesthetized volunteers; however, mean results did not differ from the those of the sevoflurane group. Mean peak plasma fluoride ion concentrations were 23 ± 1 μM 6 h postanesthesia for enflurane and 47 ± 3 μM at the end of anesthesia for sevoflurane (P< 0.01). There were no changes in creatinine clearance or urinary n-acetyl-β-glucosaminidase concentration in either anesthetic group.Discussion:Prolonged sevoflurane anesthesia did not impair renal concentrating function, as evaluated with desmopressin testing 1 and 5 days postanesthesia in healthy volunteers. Although with prolonged enflurane anesthesia, mean maximal osmolality values on day 1 postanesthesia did not differ from sevoflurane values, there was evidence in two volunteers at this time point of impairment in renal concentrating function, which normalized 5 days postanesthesia. These results occurred despite a higher peak plasma fluoride ion concentration and greater total inorganic fluoride renal exposure with sevoflurane anesthesia.
ISSN:0003-3022
出版商:OVID
年代:1994
数据来源: OVID
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