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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nociceptive effect of conventional and morphine-prolonged epidural analgesia (MPEA) has been compared in 60 patients with acute myocardial infarction (AMI). In 30 patients of the test group pain was relieved with MPEA used during 7 days, while in 30 control patients analgesia was performed with the intravenous administration of morphine or fentanyl, or neuroleptanalgesia was used. MPEA was shown to produce a more prompt and reliable anesthetic effect, thus improving the clinical course of AMI. As regards all the parameters, the effect of MPEA was higher compared to conventional analgesia techniques.
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PMID:[The use of prolonged epidural analgesia with morphine for relief of the pain syndrome in patients with acute myocardial infarct]. 176 59

The effect of conventional and prolonged epidural analgesia (PEA) with morphine on the clinical course and the size of the focus of necrosis was studied and compared in 60 patients with acute myocardial infarction. In the basic group (n = 30), analgesia was carried out for 7 days with the aid of PEA. In the control group (n = 30), analgesia was performed by intravenous injection of morphine. In both the groups, the clinical course ant the size of the focus of myocardial necrosis were estimated (precordial cartography and detection of creatine phosphokinase made in series). PEA was established to bring about complete analgesia rapidly and safely, which in turn favours noticeable limitation of the focus of necrosis and amelioration of the clinical course of acute myocardial infarction. The effect produced by PEA was considerably higher in all the parameters as compared to that attained with conventional analgesia.
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PMID:[The effect of prolonged morphine epidural analgesia on the clinical course and size of the necrotic area in patients with an acute myocardial infarct]. 180 97

Acute myocardial infarction is potentially a highly treatable disease. Immediate interventions are directed to decreasing tissue hypoxia with oxygen and improving bloodflow to ischemic myocardium using nitrates and thrombolytic agents. Cardiac workload should be reduced by eliminating endogenous catecholamine release with analgesia and sedation, and beta blockade in patients without CHF to decrease heart rate and myocardial oxygen demand. Treatment of the complications of AMI include dysrhythmia prophylaxis, monitoring and specific therapy. Treatment of pump failure includes using vasodilators, vasopressors and positive inotropic agents. Early recognition and timely initiation of appropriate therapy should be every physician's goal.
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PMID:Update: drug therapy for acute myocardial infarction. 187 27

The treatment of pain in the acute phase of a suspected acute myocardial infarction is often insufficient and has remained unchanged during recent years. The introduction of substances with a potential to limit the infarct size, such as thrombolysis and beta-blockade, have, however, decreased the requirement for narcotic analgesics (which are still the drugs of choice in many hospitals). Knowledge is still lacking regarding the duration of pain relief, the time between drug administration and pain relief, and optimal doses for various analgesics. Future research should aim at the development of drugs with a more rapid onset of action, less side effects and more complete analgesia.
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PMID:Analgesia in myocardial infarction. 256 84

Using a model of local myocardial ischaemia in the dog, the authors studied the electrostabilizing effect of a combination of the benzodiazepine midazolam (Dormicum Hoffman--La Roche) and the strong narcotic analgesic drug Fentanyl (Richter). The electrostabilizing effect was assessed using the method of ventricular fibrillation threshold (VFT) measurement. The same increase in the fibrillation threshold as that induced by the administration of midazolam or fentanyl alone was achieved by a combination of both drugs given, however, in reduced doses. The electrostabilizing effect of benzodiazepines and potent analgesics is enhanced by their simultaneous administration. At the same time, the adverse side effects observed on the administration of fentanyl alone (bradycardias, hypotension, cardiac blockade) due to the prevalence of parasympathetic drive, are reduced. Simultaneous administration of a benzodiazepine and an analgesic has become a modern technique, in anaesthesiology, so-called analgosedation. Experiments have shown the technique, in addition to the generally recognized analgesia, sedation and anxiolysis, exerts electrostabilizing effects on the myocardium damaged by ischaemia. The authors therefore recommend analgosedation in the drug treatment of acute myocardial infarction.
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PMID:The electrostabilizing effect of a combination of midazolam and fentanyl: an experimental study in the dog. 261 72

The authors analyze the efficacy of their method of prolonged analgesia in acute myocardial infarction. A comparison of the clinical efficacy of epidural analgesia with obsidan and local anesthetics hemodynamic effects of epidural and intravenous administration of obsidan indicates that use of the new method of analgesia ensures adequate anesthesia, provides an improvement of the clinical course of the disease and has no adverse effects on the circulation.
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PMID:[Epidural analgesia with obzidan in the acute period of myocardial infarct]. 262 62

Twenty patients with moderate or severe pain of suspected myocardial infarction received nalbuphine 50 mg intravenously as analgesia in 2 divided doses of 30 mg and 20 mg with 10 mg metoclopramide and were observed for 2 hours. Eighteen patients received nalbuphine outside hospital. The median time from onset of pain to treatment was 73 minutes. Within 30 minutes of the drug's administration 90% of all patients reported satisfactory pain relief (grade 0 or 1). For those with definite myocardial infarction 83% reported satisfactory pain relief at 30 minutes. There were no significant adverse cardiorespiratory effects observed or serious side-effects reported. Nalbuphine is effective and safe when used in this higher dose, although no additional analgesic effect was demonstrated when compared with lower established doses used early in acute myocardial infarction.
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PMID:High dose nalbuphine in early acute myocardial infarction. 271 14

The effect of high thoracic epidural anaesthesia with intermittent epidural bolus injections of bupivacaine (2.5 or 5 mg ml-1) was studied in 28 patients with unstable angina pectoris. The majority of the patients had a history of previous acute myocardial infarction(s) and/or angina pectoris and severe coronary artery disease. All patients were treated with nitroglycerin infusion for greater than 24 h and were included in the study if they had chest pain, not caused by acute myocardial infarction, at bed rest or recurrent anginal pain at rest greater than 2 days after infarction. 4.4 +/- 0.3 ml of bupivacaine induced a blockade of the upper seven sympathetic segments (Th1-7) for 98 +/- 9 min. Heart rate decreased significantly from 70 +/- 3 to 64 +/- 3 beats min-1 while blood pressure was unaffected by thoracic epidural anaesthesia. In 27 patients (96%) the anaesthesia induced complete analgesia. Nitroglycerin infusion was discontinued definitely within 3 h in 26 patients (93%) and pain was thereafter controlled by means of thoracic epidural anaesthesia as the sole treatment in 23 patients (82%) and as the major treatment in 25 patients (89%). Twenty-one patients (75%) were fully mobilized and stabilized. Treatment with thoracic epidural anaesthesia lasted for 6.0 +/- 1.1 days. The number of daily epidural injections decreased significantly with time from 2.7 +/- 0.3 the first day to 0.9 +/- 0.3 the fourth day (P less than 0.01, n = 19). Two patients developed acute myocardial infarction during the anaesthesia treatment period, and one of these patients died.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thoracic epidural anaesthesia in patients with unstable angina pectoris. 275 7

Recently, more attention has been focused on the detection and treatment of silent myocardial ischaemia. Electrocardiographic signs of exercise-induced asymptomatic myocardial ischaemia are very common findings among survivors of acute myocardial infarction. From data of our population we found that silent exercise-induced ischaemia is present in 15-20% of all patients, and that about half of the patients with exercise-induced ST-segment depression were free of symptoms. Ergometric data at the ischaemic threshold are similar between asymptomatic and symptomatic patients while the presence of symptoms is more frequent in patients who were also symptomatic before the myocardial infarction. During the training period, the majority of the 'silent' patients remained asymptomatic, 23% developed effort angina, and 9% developed angina at rest. Training monitoring may be helpful in identifying the variability of symptoms. Physical training, in particular an intermittent programme, increased the work-load at which the ECG ischaemic signs appeared. Among the possible mechanisms responsible for exercise-induced silent ischaemia, a different pain tolerance and control of analgesia may be ascribed to explain the absence of pain, perhaps also determined by different endogenous beta-endorphin levels.
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PMID:Silent ischaemia in post-myocardial infarction patients submitted to physical training. 324 37

The epidemiology and etiology, pathophysiology, diagnosis, clinical presentation, complications, and treatment of acute myocardial infarction (AMI) are reviewed. Major risk factors for AMI include age, sex (men greater than women), family history, race, hyperlipidemia, hypertension, cigarette smoking, diabetes mellitus, and diet. AMI occurs when there is a prolonged decrease in oxygen supply to the myocardium caused by coronary thrombosis or coronary vascular spasm. Traditional drug treatment of uncomplicated AMI includes oxygen, laxatives, and analgesics. For analgesia, narcotic agonists are generally preferred, although intravenous nitroglycerin is of value for both reducing infarct size and relieving pain. Fibrinolytic therapy is also indicated in these patients. Low-dose heparin should be initiated on admission to the hospital. Beta-adrenergic blocking agents have proven useful in reducing the incidence of ventricular fibrillation and sudden death. Antiplatelet agents may also be used to decrease long-term mortality. Recent studies have focused on reduction of infarct size using agents such as beta blockers, calcium-channel blockers, nitroglycerin, and thrombolytics. Revascularization procedures are required in some patients to re-establish adequate coronary perfusion. Most patients who survive AMI initially have a relatively uncomplicated clinical course. An increasing number of therapeutic interventions are available for acute and chronic treatment of AMI.
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PMID:Current concepts in clinical therapeutics: acute myocardial infarction. 352 26


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