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

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

A total of 243 patients who had reversible ischemic attacks (RIA) were submitted to clinical trial to determine whether dipyridamole (400 mg/day) (D) or aspirin (100 mg/48 hours) + dipyridamole (300 mg/day) (ASA + D) would produce significant reduction in the subsequent occurrence of RIA and completed stroke. One hundred and fifteen were selected for Group ASA + D and 71 were treated with dipyridamole only. The treatment groups were similar in relation to age, sex, risk factors, duration and presumed vascular territory of RIA, incidence of alterations of arterial supra-aortic trunks, cerebral infarct (CT scan), and platelet function. Patients were followed for a mean time of 21 months. At the end of the study, 21.7% of the ASA + D group and 19.7% in the D group had suffered new episodes of RIA or completed stroke (p = 0.88). Frequency of stroke (reversible ischemic neurologic deficit or completed stroke) was 7.8% in the ASA + D patients and 9.8% in the D patients (p = 0.83). Subgroup analysis did not show significant differences either. It is concluded that ASA + D has no significantly greater beneficial effect than that observed with D alone in the secondary prevention of atherothrombotic cerebral ischemia. However, a statistical Type II error cannot be excluded by the reduced number of recurrences.
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PMID:Low-dose acetylsalicylic acid (ASA) plus dipyridamole versus dipyridamole alone in the prevention of stroke in patients with reversible ischemic attacks. 332 18

Cardiopulmonary baroreceptors located primarily on the low-pressure side of the circulation sense slight reductions in cardiac filling pressures and elicit sustained peripheral vasoconstriction. Because most inhalation and many intravenous anesthetics attenuate arterial baroreflex function, the low-pressure baroreflex may serve a major role in maintaining blood pressure during intraoperative hypovolemia. To activate the low-pressure baroreflex, progressive nonhypotensive reductions in central venous pressure were produced with graded applications of lower body negative pressure (LBNP, -5, -10, -15 mm Hg) in 18 ASA class I patients before elective surgery. This produced linear reductions in stroke volume as determined by impedance cardiography and cardiac output. Cardiopulmonary baroreflex-mediated increases in total and forearm vascular resistance assisted in maintaining stable blood pressure. After ten patients were anesthetized with fentanyl (12.5 micrograms/kg) and diazepam (0.25 mg/kg) and an additional eight received these agents plus supplemental N2O (70%), reflex vasoconstrictor responses to LBNP were not attenuated and, therefore, blood pressure continued to be well maintained despite substantial reductions in cardiac filling pressures. Thus, these anesthetic regimens preserved vasoconstrictor responses mediated by cardiopulmonary baroreflexes. This promoted cardiovascular stability that may be particularly beneficial in patients with cerebral, cardiovascular, or renal disease undergoing surgical procedures with potential for rapid blood loss.
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PMID:Fentanyl-diazepam anesthesia with or without N2O does not attenuate cardiopulmonary baroreflex-mediated vasoconstrictor responses to controlled hypovolemia in humans. 337 9

The combination of two-dimensional and pulsed Doppler echocardiography was used to measure determinants of cardiac function in 20 ASA physical status I infants and small children (9 days-32 months of age) during equipotent halothane (n = 10) or isoflurane (n = 10) anesthesia in oxygen. Five sets of cardiovascular data were recorded in each patient. In the awake, unmedicated state prior to induction, at three different anesthetic levels, 0.75, 1.0, and 1.25 MAC (corrected for age) and a final measurement repeated at 1.25 MAC after the intravenous infusion of 15 ml X kg-1 of Lactated Ringers solution. The study was completed prior to intubation and surgery. Results are expressed as mean +/- SEM. Isoflurane and halothane decreased mean blood pressure from the awake level (isoflurane 76.6 +/- 2.3 to 60.6 +/- 3.1 mm, halothane 72.2 +/- 3.9 to 60.6 +/- 3.1 mm at 1.25 MAC). Isoflurane increased heart rate at all anesthetic levels (128.7 +/- 4.2 to 142.5 +/- 6.0 beats/min at 0.75 MAC). Halothane decreased heart rate at 1.25 MAC (124.6 +/- 4.6 to 119.4 +/- 3.5 beats/min). Isoflurane and halothane decreased cardiac index at 1.25 MAC. Stroke volume index decreased at 1.0 and 1.25 MAC with both isoflurane (36.9 +/- 3.8 to 30.2 +/- 3.5 ml/m2) and halothane (32.7 +/- 2.5 to 28.9 +/- 2.5 ml/m2). Ejection fractions also decreased significantly at 1.0 and 1.25 MAC in both groups of patients (22 +/- 6% at 1.25 MAC halothane and 28 +/- 8% at 1.25 MAC isoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulsed Doppler and two-dimensional echocardiography: comparison of halothane and isoflurane on cardiac function in infants and small children. 360 47

Acute respiratory acidosis results in increases in cardiac output and in systemic and pulmonary arterial blood pressures. The aim of this investigation was to determine if isoflurane modifies these effects. Nine patients (ASA II or III) scheduled for major surgery took part in the investigation. After the induction of general anesthesia, CO2 was added to the inspiratory gas mixture. After 15 min, ventilation with addition of CO2 (PaCO2 8-9 kPa) isoflurane (3%) was added. Hemodynamic measurements were made to study the effects of acute hypercapnia and the effects of isoflurane during hypercapnia. The addition of carbon dioxide resulted in increases in cardiac output, systemic and pulmonary arterial blood pressures, and right and left ventricular stroke work. The addition of isoflurane during hypercapnia decreased systemic arterial blood pressure, but pulmonary arterial blood pressure was unaffected, cardiac output and stroke volume did not change, and left but not right ventricular stroke work decreased. In conclusion, acute pulmonary hypertension induced by hypercapnia was not affected by isoflurane but, despite increased right ventricular stroke work, there were no signs of right ventricular failure.
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PMID:Circulatory effects of isoflurane during acute hypercapnia. 368 95

The effects of halothane anesthesia on cardiopulmonary (low pressure) baroreflex control of peripheral resistance were studied in 10 ASA class I young men. Graded (-5, -7.5, -10, -12.5 mmHg) lower body negative pressure (LBNP) was used to produce progressive decreases in thoracic blood volume and central venous pressure. These stimuli activate reflexes from cardiopulmonary baroreceptors. Volunteers were studied while awake and during 1 MAC (0.75%) and 1.25 MAC (0.93%) halothane anesthesia. Hetastarch (6%) in 0.9% normal saline was infused into patients before baseline recordings were initiated. Blood pressure, stroke volume, cardiac output, and systemic and forearm vascular resistance decreased and forearm blood flow increased during halothane anesthesia. In awake subjects, LBNP did not alter heart rate or blood pressure, but stroke volume and cardiac output decreased. Blood pressure was maintained by cardiopulmonary baroreflex-mediated increases in peripheral resistance. In anesthetized subjects, decreases in stroke volume and cardiac output during LBNP were similar to awake responses, however, hypotension occurred because reflex resistance increases were markedly attenuated. The authors conclude that halothane anesthesia blunts cardiopulmonary baroreflex resistance responses provoked by mild decreases in thoracic blood volume in humans.
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PMID:Halothane anesthesia attenuates cardiopulmonary baroreflex control of peripheral resistance in humans. 406 21

Fifty-seven patients with cervical bruits and abnormal ocular pneumoplethysmography but without symptoms were followed prospectively. Mean follow-up was 32 months and all patients were followed for at least 1 year. Twenty-nine patients consented to join a randomized study comparing treatment with aspirin, close follow-up, and no intervention unless symptoms developed [( NI: ASA] n = 14) versus intervention with arteriography and prophylactic surgery [( I: A/S] n = 15). Among patients who refused randomization, 14 were treated with NI: ASA and 14 with I: A/S. Endpoints for analysis included all unfavorable outcomes related to both management plans and included stroke, death of stroke, major angiographic and perioperative complications, asymptomatic carotid occlusion, and recurrent carotid artery stenosis. In both the randomized and nonrandomized portions of the study unfavorable outcomes were more frequent in patients treated with I: A/S, and by combining the results of both studies a significant difference was observed (N: ASA - 3.6% versus I: A/S - 31%; X:2 = 4.78; p less than 0.05). Among patients treated with NI: ASA, a single minor stroke occurred without warning. In patients from all groups who underwent arteriography, advanced carotid stenosis was found in 78% (mean percent diameter stenosis = 72% +/- 2%; mean residual lumen = 1.3 +/- 0.1 mm). We conclude that, despite the probability of underlying severe carotid stenosis, most patients with cervical bruit and abnormal ocular pneumoplethysmography but without symptoms are appropriately managed without intervention unless symptoms develop.
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PMID:Asymptomatic cervical bruit and abnormal ocular pneumoplethysmography: a prospective study comparing two approaches to management. 638 88

Isoflurane was used in 10 ASA I or II female patients, undergoing hysterectomy. It was given at a constant inspired concentration of 1.3% in a 50% N2O/50% O2 mixture, after induction of anaesthesia using etomidate (0.3 mg kg-1) and intubation following pancuronium (0.1 mg kg-1). No analgesic supplement was given. The patients were hyperventilated minimally (PaCO2 4.7-5.3 kPa). At standardized times (before induction, after induction, 5', 25', 50' and 75' min after surgical incision, awake and awake +60'), cardiovascular (blood pressure, cardiac output, stroke volume, heart rate), respiratory (blood gases), metabolic (oxygen consumption, blood glucose) and hormonal (noradrenaline, adrenaline, cortisol, prolactin) changes were measured. Blood pressure changes were very moderate (mean values were lower than before induction), but heart rate was increased significantly. Decreases in stroke volume and changes in cardiac output were not significant. Oxygen consumption was decreased below basal values during surgery. Blood glucose levels increased significantly in the course of surgery and remained raised postoperatively. Adrenaline and noradrenaline levels increased significantly. At each examination time, cortisol levels were decreased significantly. Prolactin levels had decreased significantly 75 mins after incision and remained low 60 mins after awakening.
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PMID:Cardiovascular, metabolic and hormonal changes during isoflurane N2O anaesthesia. 644 92

Systemic circulatory responses to atracurium (0.2 and 0.4 mg/kg) were studied in 15 healthy (ASA I or II) adult patients during enflurane (1.0 to 1.25% inspired) and nitrous oxide (70% inspired) anesthesia. All patients were premedicated with intramuscular morphine (10-15 mg) and glycopyrrolate (0.2 mg). Compared with control measurements during enflurane-nitrous oxide anesthesia, heart rate, cardiac and stroke index, central venous pressure, and systemic mean arterial pressure remained unchanged at 2, 5, and 10 min after administration of both doses of atracurium. Systemic vascular resistance was minimally decreased (7% compared to control) (0.01 less than P less than 0.05) at 10 min following both doses of atracurium. No patient demonstrated a decrease in systemic mean arterial pressure greater than 6 mmHg. The authors conclude that atracurium in doses which produce adequate skeletal muscle relaxation during steady-state enflurane anesthesia produces no clinically significant alteration in hemodynamic variables.
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PMID:Systemic vascular responses to atracurium during enflurane-nitrous-oxide anesthesia in humans. 668 16

Attempts at prevention of arterial thrombosis with platelet inhibitors have been the subject of a number of major trials in recent years. These trials were prompted by earlier observations that aspirin takers seemed to fare better after acute myocardial infarction and were further stimulated by the recent growth of knowledge about the role of vascular and platelet prostaglandins. The trials have sought to establish that aspirin (ASA), sulphinpyrazone and dipyridamole may prevent thrombosis in the form of recurrence of transient ischaemic attack (TIA) and stroke or reduce the recurrence rate and mortality after acute myocardial infarction. No single trial has provided conclusive evidence although there is a strong suggestion of some benefit from ASA. With further understanding of PG metabolism and the effects of inhibitors new approaches are likely to emerge in the near future.
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PMID:Anti platelet agents for strokes and myocardial infarction: a critical appraisal of recent clinical trials. 703 73


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