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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Under study were thirty patients of ASA class I-II scheduled for lower abdominal and lower extremities surgery. Premedication included intramuscular injection of pethidine, atropine and prochlorperazine. Epidural anesthesia was accomplished with 12-15 ml 2% lidocaine with epinephrine (1:80,000). Thirty minutes later, when blood pressure returned to control value, patients were put to sleep by 2 mg/kg propofol and the sleep was maintained with continuous infusion of propofol at a rate of 6 mg/kg/h. Infusion rate was adjusted when necessary. Patients breathed room air spontaneously through the whole course of anesthesia. The results showed that all patients fell to sleep within 28.3 +/- 2.7 s after intravenous injection of propofol 2 mg/kg. Sleeping dose was satisfactorily achieved using a mean infusion rate of 6.1 +/- 1.7 mg/kg/h. The mean time from the end of the infusion of propofol to opening of the eyes on command and telling the correct date of birth were 7.9 +/- 2.8 min and 9.9 +/- 3.8 min respectively. Two minutes after injection, there were significant decrease in systolic pressure, diastolic pressure, cardiac output, and stroke volume with a mean of 17.9 +/- 3.8%, 18.8 +/- 3.3%, 7.6 +/- 0.5% and 11.1 +/- 1.9% respectively. Two patients (7%) developed apnea after 2 mg/kg propofol which was considered to be the most serious side effect. Propofol infusion had to be stopped in 13% patients due to a 30% fall of arterial blood pressure during maintenance. In the recovery stage, no other complications were noted except one patient who felt dizziness. Propofol, used as the supplementary sedative, provides satisfactory result for surgery under epidural anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intravenous propofol as a supplement in epidural anesthesia]. 175 43

In 40 patients, the cardiovascular effects of low- and high-dose propofol anesthesia (single bolus of 1.5 mg/kg in group A, 2.5 mg/kg in group C) were examined and compared with those of low- and high-dose thiopental (4 mg/kg in group B, 6.5 mg/kg in group D) (n = 10 patients per group). After induction of anesthesia with etomidate, all patients were ventilated with 70% nitrous oxide in oxygen. Peripheral arterial systolic blood pressure (SAP) and transesophageal echocardiographic short-axis measurements were used to calculate the end-systolic pressure-volume relationship (E) as an index of global myocardial contractility. In all groups SAP decreased significantly below baseline levels for the duration of the measurements (15 min after drug administration), except for the lower dose of thiopental, where SAP returned to baseline values within 10 min. Propofol at a dose of 1.5 mg/kg significantly decreased cardiac output (CO) (from 5.1 +/- 0.25 [mean +/- SEM] to 4.2 +/- 0.23 L/min), stroke volume (SV) (from 64 +/- 3 to 56 +/- 3.6 mL), and the slope of E (from 71 +/- 3.5 to 65 +/- 4.2 mm Hg/mL) until 4 min after drug administration. The higher dose of propofol significantly decreased CO (from 5.1 +/- 0.29 to 4.1 +/- 0.26 L/min), SV (from 64 +/- 3 to 52 +/- 4.6 mL), and the slope of E (from 71 +/- 3.6 to 62 +/- 3.7 mm Hg/mL) until 10 min after drug administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiodynamic effects of propofol in comparison with thiopental: assessment with a transesophageal echocardiographic approach. 173 85

Propofol, in both its new oil-in-water emulsion and the former cremophor-EL solution, is known to produce significant decreases in arterial blood pressure. The aim of this study was to obtain a precise hemodynamic profile of anesthesia induction with propofol under conditions of daily routine (additional 70% nitrous oxide) and to evaluate the influence of (1) premedication with lormetazepam and (2) additional i.v. injection of fentanyl. Forty patients (ASA classes I and II) were randomly assigned to one of four groups (A, B, C, and D). Anesthesia was induced with a sleep dose of propofol (mean: 2.4 mg/kg) and the patient was ventilated with 30% O2 and 70% N2O via a face mask. In groups B and D, 3 micrograms/kg fentanyl were injected immediately prior to propofol injection. Patients in groups A and B received no premedication. Patients in groups C and D received 2 mg lormetazepam on the evening prior to the anesthetic and 1 mg 2 h prior to the anesthetic orally. The following parameters were determined immediately prior to induction of anesthesia and 1, 3, 5, 8, and 10 min after the start of the propofol injection: heart rate (HR), mean arterial blood pressure (MAP), mean pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary occlusion pressure (POP), cardiac output (CO), stroke volume (SV), and systemic vascular resistance (SVR). In all four groups a slight decrease in HR and SVR occurred while a marked decrease in arterial blood pressure (SAP, MAP, DAP) and cardiac output was seen. PAP and preload pressures showed no significant changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamics under propofol-nitrous oxide anesthesia: effects of premedication with lormetazepam and of additional fentanyl]. 289 30

Using gated radionuclide ventriculography and invasive cardiac monitoring, the effects of propofol alone and in combination with fentanyl on left ventricular (LV) volumes and function were investigated in 10 ASA III, unpremedicated patients (51-75 years) with coronary artery disease (NYHA II-III). Anesthesia was induced with propofol (2 mg/kg) followed by an infusion (100 micrograms.kg-1.min-1). Vecuronium (0.05 mg/kg) was administered and ventilation (FIO2, 1.0) was manually controlled via a face mask (FECO2, 4-5%). Data acquisitions were serially obtained over 15 minutes after the bolus IV injection of propofol and 5 minutes after the injection of fentanyl (5 micrograms/kg). Propofol induced a rapid decrease (15%) in mean arterial pressure (MAP) exclusively related to a decrease in cardiac index (CI), without reduction in indexed systemic vascular resistances (SVRI). Despite the decrease in MAP, heart rate did not change. The decrease in CI was associated with a lower preload. After the addition of fentanyl, MAP decreased significantly (35%) below the last set of propofol measurements. The decrease in MAP was associated with a reduction in CI and SVRI. Fentanyl was also associated with a significant decrease in heart rate (16%) resulting in a decrease in CI, whereas stroke index and end diastolic volume did not change. Neither global ejection fraction (EF) nor end systolic volume changed significantly at any time, nor were there changes in the ECG or in regional ejection fractions (REF). The absence of changes in REF was consistent with lack of wall motion abnormalities of the left ventricle. Propofol alone and in combination with fentanyl does not alter LV performance in patients with good LV function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular function during propofol and fentanyl anesthesia in patients with coronary artery disease: assessment with a radionuclide approach. 326 23

Propofol, a rapid and short-acting i.v. anesthetic, was associated with the risk of anaphylactic reactions in its original cremophor-EL formulation. It has been reformulated in a soybean emulsion with satisfactory anesthetic properties. A former study of hemodynamic changes after i.v. induction with propofol, thiopental, methohexital, etomidate, and midazolam in patients with coronary artery disease demonstrated that in comparison to other induction agents propofol depressed systolic and diastolic arterial pressures more severely, compromising coronary perfusion. In the present investigation left ventricular parameters as well as hemodynamic effects during extracorporeal circulation (ECC) were studied in comparison to midazolam during opiate analgesia. Methods. Hemodynamic effects of 2 mg/kg body weight propofol as compared to 0.15 mg/kg midazolam were studied in 34 patients during coronary artery surgery before cannulation of the large vessels (measurement of left ventricular parameters) or during ECC (measurement of arterial perfusion pressure and oxygenator volume). Results (see Table 1, Figs. 1 and 2). Propofol decreased systolic and diastolic pressures (-27%, -22%) more than midazolam (-10%, -9%). Cardiac index and stroke volume index were diminished following both drugs (propofol: -14%, -9%; midazolam: -15%, -11%); total systemic resistance was reduced significantly by propofol (-22%). Dp/dtmax was compromised more markedly by propofol (-24%) than by midazolam (-18%), but there was no significant difference.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamic action profile of propofol in comparison with midazolam. A study in coronary surgical patients]. 350 Dec 52

We have compared the haemodynamic effects of a sedative dose of propofol with placebo (vehicle of propofol) in a randomized, double-blind study in 20 patients immediately after coronary artery bypass grafting (CABG). During a continuous infusion of a mixture of fentanyl and pancuronium, each patient was given in a crossover design, a loading dose of propofol 0.5 mg kg-1 and vehicle over 5 min followed by a continuous infusion of propofol 20 micrograms kg-1 min-1 and vehicle, respectively, for 55 min. Administration of propofol caused a significant decrease in mean arterial pressure (mean change from pre-drug values to those during drug infusion: -15.4% vs +1.3% with placebo; P < 0.001), mean pulmonary artery pressure (-6.5% vs +5.8%; P < 0.001), systemic vascular resistance (-13.8% vs -0.6%; P < 0.05), pulmonary vascular resistance (-2.0% vs +9.0%; P < 0.05), cardiac output (-2.4% vs +2.6%; P < 0.05) and pulmonary artery occlusion pressure (-8.0% vs +1.4%; P < 0.05). Propofol did not affect heart rate, but it tended to decrease stroke volume (P = 0.102). These data suggest that, during the recovery phase from CABG surgery, a short-term infusion of a sedative dose of propofol decreases systemic and pulmonary arterial pressure by decreasing systemic and pulmonary vascular resistance, respectively, and cardiac output. The decrease in cardiac output appeared to be caused mainly by a decrease in stroke volume.
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PMID:Haemodynamic effects of propofol infusion for sedation after coronary artery surgery. 766 68

The hemodynamic effects of propofol-fentanyl and isoflurane-fentanyl anesthesia during the prebypass period were compared in 42 patients undergoing coronary artery bypass grafting (CABG) and 22 patients undergoing valve replacement (VR) for stenotic lesions. Anesthesia was induced with fentanyl, 25 micrograms/kg, and pancuronium, 0.1 mg/kg, and was maintained with a propofol infusion commenced at 4 mg/kg/h (range 1 to 10 mg/kg/h) or with isoflurane commenced at 1% (range 0 to 2%). Additional fentanyl, 7.5 micrograms/kg, was given before sternotomy. Hemodynamic measurements were made before induction of anesthesia and at various times in the prebypass period. In the VR group, there were no significant differences between the two anesthetics in any hemodynamic variables during the study. Significant decreases (P < 0.05) in mean arterial pressure (MAP 14%), left ventricular stroke work index (LVSWI 29%), and stroke volume index (SVI 24%) occurred after 15 minutes of propofol anesthesia in the CABG group. With isoflurane MAP was well maintained with reductions in LVSWI and SVI of 22% and 20%, respectively. Isoflurane was, however, associated with a significant increase in heart rate (HR) in the CABG group (P < 0.05), whereas no significant change in HR occurred in CABG or VR patients receiving propofol. With both techniques there were no significant changes in right-sided or left-sided filling pressures or in systemic vascular resistance index in the CABG or VR groups, except for a decrease in pulmonary artery occlusion pressure in the propofol VR group and isoflurane CABG group at the time of aortic cannulation. Propofol produced similar hemodynamic changes in the CABG and VR groups. Both anesthetic techniques caused myocardial depression and effectively controlled the autonomic responses to sternotomy in both groups. The study suggests that propofol-fentanyl anesthesia is an acceptable technique for CABG surgery and for VR in patients with stenotic valvular heart disease.
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PMID:Propofol-fentanyl anesthesia: a comparison with isoflurane-fentanyl anesthesia in coronary artery bypass grafting and valve replacement surgery. 806 Dec 62

The hemodynamic effects of a propofol infusion adjusted to achieve and maintain a burst-suppression pattern [episodes of depressed background activity (electrical silence) more than 4 s alternating with a high-voltage slow activity], were studied in 10 patients without cardiorespiratory disease undergoing elective neurosurgical interventions. Propofol infusion was started after a bolus dose of 1 mg/kg at a rate of 20 mg.kg-1 x h-1, reduced after 30 min to 15 mg.kg-1 x h-1, and terminated after 60 min (1926 +/- 346 mg cumulative propofol dose, maximal serum concentration 9.2 +/- 2.9 micrograms/dL; mean +/- SD). Hemodynamic data and arterial blood samples were collected during a sedated, resting control period, and then every 15 min during drug infusion. Lactated Ringer's solution was infused at a rate sufficient to maintain pulmonary capillary wedge pressure at or above control levels (20-30 mL.kg-1 x h-1). Burst-suppression pattern in the electroencephalogram was achieved after 15.7 +/- 3.2 min and maintained until 10.9 +/- 2.6 min after the propofol infusion was terminated. Significant decreases (% of control, Friedman and Wilcoxon Wilcox test, P < 0.05) were found in heart rate (19%), mean arterial pressure (20%), cardiac index (23%), and left ventricular stroke work index (26%). No adverse consequences were caused by the propofol or crystalloid infusion. The results demonstrate that doses of propofol sufficient to silence the electroencephalogram are associated with venodilating and myocardial depressant properties. However, propofol can be administered with minimal hemodynamic risk in healthy patients when cardiac filling pressures are maintained by intravenous fluid administration.
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PMID:Electroencephalographic burst suppression by propofol infusion in humans: hemodynamic consequences. 831 24

Cardiac arrhythmia can be a serious complication during general anesthesia. On the other hand, there is a need for general anesthesia of patients suffering from cardiac arrhythmias and using antiarrhythmic drugs. The aim of the present experiments was to establish the way in which procainamide, N-acetyl-procainamide, verapamil and propranolol influence hemodynamic parameters of rabbits during propofol anesthesia. The experiments were performed on rabbits. Heart rate was counted from ECG. Blood pressure was measured directly in the carotid artery. Cardiac output, stroke volume, and total peripheral resistance were estimated using the method of human Cr51 albumin dilution. Hepatic blood flow was estimated after single injection of 99mTc/Sn Hepida. Renal blood flow was estimated after a single injection of 125J-hippurate. Propofol decreases renal and hepatic blood flows, decreases blood pressure and peripheral vascular resistance. Propranolol given alone or in combination with propofol decreases hepatic blood flow. The administration of antiarrhythmic drugs during propofol anesthesia decreases renal blood flow. Propofol decreases blood pressure in rabbits as a result of decreased peripheral vascular resistance. It also decreased RBF and HBF. Disadvantages of interactions of propofol and antiarrhythmic drugs concern mainly with RBF and HBF. Propranolol (given alone or in combination with propofol) strongly decreases HBF. NAPA given during P anesthesia exerts a weaker effect on HBF. The administration of antiarrhythmic drugs during propofol anesthesia decreases RBF. The strongest disadvantageous action is exerted by propranolol, the slightest one--by verapamil.
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PMID:The influence of selected antiarrhythmic drugs on the hemodynamic parameters in rabbits during anesthesia. Part I. Propofol anesthesia. 868 87

Three patients with intractable thalamic pain unresponsive to a range of previous treatments received a course of six bilateral electroconvulsive therapy (ECT) treatments over 2 weeks. There was no evidence of any improvement in the intensity of the pain, pain relief or mood as measured on visual analogue scales and with standard measures. Propofol was used as the anaesthetic induction agent. Two patients showed wide changes in blood pressure during ECT but all three patients showed prompt recovery. In the light of the negative findings of this study and those of a previous study of the use of unilateral ECT in similar patients it is concluded that ECT is not an effective treatment for post-stroke thalamic pain.
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PMID:Does electroconvulsive therapy (ECT) have any role in the management of intractable thalamic pain? 1129 32


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