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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical effects of a propofol-alfentanil association were studied in fifteen patients ASA II (mean age 50.1 +/- 14.1) anaesthetized for E.N.T. endoscopy after informed consent. All the patients received an intramuscular premedication with 0.10 to 0.15 mg.kg-1 midazolam. Propofol 2.5 mg.kg-1 was injected in a peripheral venous line with alfentanil 10 micrograms.kg-1, followed by continuous automatic injection of propofol at a dose of 5 to 10 mg.kg.h-1 and alfentanil 5 micrograms.kg-1 given just before suspension. After induction and during maintenance of anaesthesia, the patients were allowed to breathe oxygen spontaneously O2 assisted when apneic. The following variables were studied before induction (to), after induction (t1), during suspension (t2) and when stopping the infusion (t3): haemodynamic parameters using an invasive method and blood gases. Statistical analysis was performed using the Student's test for paired samples. Surgical conditions and anaesthetic quality were good with early recovery of consciousness and return of all reflexes. After an initial period of cardio vascular depression, the haemodynamic parameters did not vary much during the anaesthesia and propofol-alfentanil appeared to limit considerably the hypertension due to laryngoscopy. However, there was a moderate degree of hypercapnia (p less than 0.001) in most patients, giving evidence of some respiratory depression and possibly a greater depth of anaesthesia than desirable. Indeed, the doses of alfentanil required seemed to be more important with propofol because of a probably interference between the two drugs; the doses of these drugs should therefore be modified according to the length of surgery.
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PMID:[Circulatory and respiratory repercussions to direct suspension laryngoscopy in the adult: value of a propofol-alfentanil combination]. 249 72

The hemodynamic modifications during anesthesia induction with etomidat or thiopentalum, with and without pretreatment with fentanyl, were studied in 60 ASA I-II patients. The patients were randomly divided into six subgroups, as a function of the induction agent (etomidat, 0.15 mg/kg, or thiopentalum, 3 mg/kg) and of the pretreatment used (fentanyl, 5 micrograms/kg, or 0.9% 1 ml/kg saline solution). Systolic, diastolic ATs and pulse were followed and measured during induction and after tracheal intubation. During induction the presence or absence of the thoracic rigidity, after fentanyl administration, and also the appearance of myoclonias and of local pain after etomidat injection were noted. Measurement of hemodynamic constants showed, in the control subgroups unprotected by fentanyl, that AT and pulse frequency increase following laryngoscopy and intubation irrespective of the induction agent used. Association of thiopentalum with fentanyl influenced partially tachycardia and postintubation hypertension. Administration of 5 micrograms/kg fentanyl prevented the SAT and pulse modifications but not the DAT variation. Association of 10 micrograms/kg fentanyl ensured a complete protective effect versus the tracheal intubation but, it led, first, to a SAT decrease by intensification of the myocardial depressing effect of the barbiturate. On the other hand, use of fentanyl as induction adjuvant with etomidat ensured the blockage of the pressure response to intubation, with hemodynamic stability during anesthesia induction, irrespective of the dose of fentanyl injected. Thoracic rigidity and the side effects generated by etomidate were absent.
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PMID:[The effect of fentanyl as an adjuvant to etomidate and thiopental on the hemodynamic response to the induction of anesthesia and endotracheal intubation]. 253 39

Hypertension after carotid endarterectomy has a variable incidence ranging up to 56%. Blood pressure (BP) control is essential due to possible increased risk of morbidity from neurologic deficits or cardiovascular complications. This study evaluated intravenous labetalol for control of hypertension after carotid endarterectomy. Sixty ASA II-IV patients were studied; 20 developed BP high enough for treatment with labetalol. The anesthetic technique was standardized. Labetalol was administered at the conclusion of surgery as a 20-mg bolus over two minutes followed by 40 mg every 10 minutes until the desired BP was achieved (BP less than or equal to 10% above average preoperative BP or less than 150 mmHg, systolic) or 300 mg had been given. The mean total dose of labetalol was 42.0 +/- 33.0 mg (mean +/- SD) and mean time to reach the desired BP was 16.2 +/- 21.4 minutes. Systolic, diastolic, mean arterial pressure and heart rate significantly decreased after labetalol treatment and remained so for the remainder of the 180-minute study period. There was no hypotension, bradycardia, evidence of myocardial ischemia or central nervous system dysfunction present with labetalol treatment. Blood samples were obtained for determination of plasma renin activity, epinephrine, and norepinephrine in 10 patients who developed hypertension and received labetalol, and 10 patients who did not develop hypertension. In the patients developing hypertension, there was a significant elevation in epinephrine just before treatment, that decreased by 30 minutes after treatment. Norepinephrine levels became significantly elevated five minutes after labetalol treatment in the group with hypertension and remained elevated for 120 minutes. Concomitantly, there was a significantly lower plasma renin activity seen in this group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous labetalol for the treatment of hypertension after carotid endarterectomy. 257 2

We reviewed 212 patients whom we consulted before elective surgery concerning their indications of operation and anesthetic risks for the last 18 month periods. Patients' ages were between 6 months to 89 years old, and 46% of the patients consulted were over 60 years of age. Main medical problems related to anesthetic risks included cardiovascular problems (36% of patients), respiratory problems (14%), the abnormality of metabolism or endocrine (8%), hepatic dysfunction (8%), and so on. Most of the patients with ischemic heart disease, hypertension, dysrhythmia, or dysfunction of respiratory system, were over 60 years of age. Those with diabetes mellitus, dysfunction of liver or kidney, or anemia were over 40 years of age. Those with convulsion or congenital heart disease were under 19 years of age. In attempting anesthetic evaluations, patients were assessed according to ASA physical status classification; class I (3%), class II (56%), class III (36%), class IV (5%). Although there was no patient who had intraoperative cardiac arrest or death related to anesthesia, postoperative mortality within 3 months were 19% for ASA class III patients and 60% for class IV. And all ASA IV patients who received their operation died postoperatively. In patients who were classified as ASA III or IV, we feel it is better to add more detailed classification such as Goldman's classification in addition to physical status classification of ASA for preanesthetic assessments of patients, because the majority of patients were elderly with life-threatening complications of cardiovascular and/or respiratory systems.
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PMID:[An analysis and evaluation of anesthetic consultations for patients undergoing elective surgery]. 261 94

Regional anesthesia is often preferred over general anesthesia for patients with cardiovascular disease because of presumed decreased risk of perioperative myocardial ischemia. However, few studies have addressed this issue directly. To determine whether the type of anesthesia is independently associated with myocardial ischemia, records of 134 patients undergoing peripheral vascular grafting under general or regional anesthesia were examined. There were no significant differences preoperatively between groups in ASA class, age, sex, or prevalence of angina, diabetes, or hypertension. Twelve patients developed myocardial ischemia or infarction within 7 days of operation; 11 of these 12 patients had received regional anesthesia (p less than 0.015). The association between anesthetic approach and perioperative myocardial ischemia or infarction remained after adjustment for preoperative factors associated with ischemia or with type of anesthesia. General anesthesia does not appear to be associated with increased risk of myocardial ischemia, and stringent recommendations to avoid it in this population may be unfounded. A clinical trial is needed to define more clearly the risks and benefits of different types of anesthesia in high-risk patients.
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PMID:Regional versus general anesthesia in high-risk surgical patients: the need for a clinical trial. 227 Nov 99

Stressful surgical stimuli, such as endotracheal intubation, surgical incision, organ manipulation and emergence from anesthesia, elicit adrenergic responses that precipitate transient but intense increases in heart rate and blood pressure. Although this response is well tolerated in healthy patients, patients with ischemic heart disease are at significant risk of myocardial ischemia and infarction owing to the sudden increase in myocardial oxygen demand. Parenteral beta blockers are effective in blunting this adrenergic response, but the duration of action of these agents is long-lasting and the degree of beta blockade is often difficult to predict. Further, long-acting parenteral beta blockers may cause adverse effects, the reversal of which presents a difficult clinical problem in patients with ischemic heart disease. The availability of esmolol, an ultrashort-acting parenteral beta-adrenergic antagonist with a half-life of 9 minutes, brings obvious advantages to the perioperative management of hypertension and tachycardia. With esmolol treatment, the difficulties of therapy with long-lasting beta blockers are avoided. Also, to blunt the adrenergic response, the anesthesiologist will have an alternative to increasing the depth of anesthesia, which can accentuate cardiovascular depression and prolong awakening and postoperative respiratory depression. Clinical studies performed during the perioperative period reveal that esmolol is safe and effective in this setting. Esmolol has been shown to be safe and efficacious in patients in ASA classifications I through IV and patients undergoing carotid endarterectomy and coronary artery bypass surgery. The pharmacokinetic profile, rapid onset and elimination half-life make this agent particularly well suited to treat the very intense but transient adrenergic responses to surgical stress in patients undergoing cardiac and noncardiac surgery.
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PMID:Perioperative use of esmolol. 286 50

The accepted correct procedure for treating occlusive arterial diseases includes surgical disobstruction, CL as well as PTA. Combined non-surgical strategies are effective in about 60% of these patients. However, a high risk of rethrombosis despite from the prophylaxis with anticoagulants like heparin or antiplatelet drugs like ASA is proven, especially in patients with multi-segmental stenosis as well as in patients with extensive narrowing of the arteries. In these cases primary lesions (endangitis obliterans) or secondary lesions of the endothelium cause local depletion of plasminogen in the endothelium. Independent of the method used for reopening the vessel in these patients, a significant progression of the vessel disease and a high rethrombosis rate during longterm follow-up is observed. These results lead us to apply plasminogen locally to decrease the rate of rethrombosis. In patients suffering from stage III-IV (La Fontaine) including patients with multi-segmental stenosis as well as extended narrowing of the artery, PTA in combination with CL was performed. The catheter was placed as near as possible to the thrombus. In some cases the 'fibrinolyticum' could be injected directly into the thrombus. In these cases a bolus of 4,000 U/ml was locally infused, otherwise 1.0-1.5 million U urokinase per 24 hrs. were locally infused with heparin. In 28% (22 patients) no sufficient clinical response occurred using this combined therapy and plasminogen was applied locally. The following criteria supported our decision to include the patients in this study: 1. Insufficient response occurring after 12-24 hrs. of local infusion. 2. Following 6 bolus injections no reopening of the vessel occured within 60 minutes or the clinical response was insufficient due to rethrombosis. 3. Insufficient effects of lysis therapy after 2 hours and contraindication for a systemic fibrinolytic therapy (e.g. hypertension, age, etc.). 1,000 U plasminogen per ml were infused locally or 2,000 U up to 5,000 U plasminogen (in 5 to 10 ml 0.9% saline) were infused slowly (2-4 minutes infusion time) into the catheter in these patients 10 minutes after unsuccessful treatment with local urokinase therapy. Five minutes after administering plasminogen local intraarterial fibrinolytic therapy with urokinase was continued. No severe side effects due to this therapy were observed, although some patients suffered from acute pains in the peripheral segments of the arteries occurring immediately after infusion of plasminogen. In 16 of 22 patients a complete recanalization occurred and in 3 patients a satisfying clinical improvement was observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effectiveness of intraarterial plasminogen application in combination with percutaneous transluminal angioplasty (PTA) or catheter assisted lysis (CL) in patients with chronic peripheral occlusive disease of the lower limbs (POL). 296 85

Using probit analysis, dose-response curves for induction of anesthesia with midazolam or ketamine were constructed in ASA class III and IV patients premedicated with morphine, 0.1 mg/kg, and glycopyrrolate, 4 micrograms/kg. For ketamine, ED50 values for abolition of the response to verbal commands, eyelash stimulation, and painful stimulation were 0.9, 1.3, and 1.3 mg/kg, respectively; corresponding ED95 values were 1.6, 2.3, and 4.3 mg/kg, which are within the range of clinically recommended doses. For midazolam, ED50 values for verbal commands, eyelash stimulation, and painful stimulation were 0.19, 0.24, and 0.36 mg/kg, significantly greater than those previously reported for unpremedicated ASA class I and II patients. The corresponding ED95 values, 0.35, 0.43, and 1.04 mg/kg exceed previously reported values and are appreciably greater than the doses used in most previous studies of midazolam induction. Midazolam decreased systolic blood pressure slightly but significantly (from 138 +/- 4 to 128 +/- 4 mm Hg, mean +/- SEM, P less than 0.005), while diastolic blood pressure and heart rate remained unchanged. In contrast, ketamine increased systolic blood pressure (from 141 +/- 4 to 164 +/- 5 mm Hg, P less than 0.005), diastolic blood pressure (from 71 +/- 3 to 88 +/- 4 mm Hg, P less than 0.005), and heart rate (from 84 +/- 2 to 102 +/- 4 beats/min, P less than 0.005). On the basis of these data, we conclude that in ASA class III and IV patients, midazolam induction allows for hemodynamic stability and avoids the significant tachycardia and hypertension associated with equipotent doses of ketamine.
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PMID:Induction dose-response curves for midazolam and ketamine in premedicated ASA class III and IV patients. 316 Feb 64

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 (0.1 mg.kg-1) 90-120 min prior to arrival to the operating room. Group 2 (n = 40) received clonidine po approximately 5 micrograms.kg-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 0.01) 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 0.01) following laryngoscopy and tracheal intubation, and significantly reduced intraoperative cardiovascular lability and anesthetic requirement for isoflurane (P less than 0.05) and for fentanyl (P less than .001). In patients managed with LA, intraoperative systolic (P less than 0.01) and diastolic BP and HR variability (P less than 0.05) were significantly lower in patients receiving clonidine as compared to controls. Intraoperatively, a significantly higher incidence of hypertension (P less than 0.01) and tachycardia (P less than 0.05) 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 0.01). Thus, clonidine may represent a useful adjunct in the management of the aged patient in the setting of ophthalmic surgery.
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PMID:Anesthesia for ophthalmic surgery in the elderly: the effects of clonidine on intraocular pressure, perioperative hemodynamics, and anesthetic requirement. 328 31

A controlled, randomized, double blind assessment of the efficacy of meptazinol 3 mg kg-1 in reducing the circulatory responses to tracheal intubation was carried out in 20 ASA class I patients. After thiopentone 4 mg kg-1, meptazinol 3 mg kg-1 (ten patients) or saline (ten patients), and suxamethonium 1.5 mg kg-1 tracheal intubation was carried out, and the changes in pulse rate and arterial blood pressure compared between the groups and with control values. Significance was assessed at the 5% level (Student's t-test and paired t-test). Patients who received saline exhibited a rise in pulse rate, significant 1 and 2 min after intubation, and a significant rise in mean arterial pressure for 5 min after intubation. Patients who received meptazinol exhibited no significant rise in pulse rate, but a significant fall in pulse rate occurred from 5 min onwards. Mean arterial pressure rose significantly for 4 min after intubation but the rise was significantly less than that seen in the saline group. Suppression of spontaneous ventilation or movement in 50% of the group lasted for 7 min and 9 min after induction of anaesthesia in the control group and meptazinol treated group respectively. Meptazinol 3 mg kg-1 modifies the circulatory responses to tracheal intubation, preventing the tachycardia and reducing the hypertension, and causes a short delay in the onset of spontaneous respiration or movement.
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PMID:[Reduction of circulatory reactions to intratracheal intubation--the effect of meptazinol]. 353 65


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