Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is presented of a morbidly obese parturient who had multiple medical problems. She had angina and was receiving nitrate therapy, had insulin-dependent diabetes mellitus, hypertension, asthma and benign intracranial hypertension (pseudotumour cerebri). Lumbar epidural analgesia was chosen for labour and delivery and resulted in an uneventful outcome.
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PMID:Anaesthetic management of a complex morbidly obese parturient. 174 26

The situation of absent pain with silent myocardial ischemia is highly difficult to define. There are probably several reasons for the lack of pain. Partly, nerve ways may be destroyed, partly, myocardial ischemia as peripheral pain stimulus may be to weak and beyond threshold, however, additionally, there are a lot of clues for the participation of endogenous pain modification systems therein. A certain amount of myocardial ischemia is a necessary, but not sufficient precondition for anginal pain. Myocardial ischemia is only felt painfully if the peripheral nociceptive impulse rate is high enough to pass the actual inhibitory pain threshold, and if the nerve ways are intact. It is generally accepted that the endogenous opiate system, to some extent, takes part in the endogenous analgesia system. A range of examinations in recent years hinted at the fact that endorphins are in relation to the absence of pain in silent ischemia. Patients with symptomatic and asymptomatic myocardial ischemia are significantly different in plasma beta-endorphin levels at rest and during physical exercise. A relation between peripheral endogenous opiates and suffering behavior can, at present, only be indicated correlatively. It is likely that the intensive overlaying of the cardiovascular and pain regulating systems is related to the absence of pain in silent myocardial ischemia.
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PMID:Influence of opiate systems in pain transmission during angina pectoris. 196 35

We report on a patient with acute pancreatitis whose pain was resistant to simultaneous administration of morphine, procaine and Buscopan. This episode was complicated by development of hypertension, tachycardia, angina pectoris, ventricular arrhythmias and electrocardiographic modifications. Analgesia was provided by epidural administration of fentanyl and bupivacaine and brought about rapid resolution of all symptoms. The usefulness of epidural analgesia in acute pancreatitis is discussed.
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PMID:[The value of epidural analgesia in acute pancreatitis]. 230 24

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

Evidence suggests that endogenous opioids, particularly the beta-endorphins and met-enkephalins, are closely involved in stress-induced analgesia and nociceptive pain control. Numerous investigations have been conducted to evaluate the role of opioids in silent vs symptomatic myocardial disease. There is good evidence to suggest that patients with asymptomatic ischemia have defective pain perception compared with those with angina; however, the precise role of the endorphin and enkephalin systems in this phenomenon remains to be elucidated. Possible sources for disparate study results include variation in patient populations, insensitive or improperly timed assay techniques, and differences in amount of ischemia.
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PMID:Endorphins and pain perception in silent myocardial ischemia. 296 55

Cardiac nociceptive afferences are mainly transmitted by sympathetic nervous tracts. After passing the ganglion stellatum and neighbouring ganglia, the nerves enter the dorsal horn of the spinal cord at C8-Th9 (especially Th2-Th6). Here the nerve synapses for the first time, mainly to neurons which run up to the thalamus contralaterally by the tractus spinothalamicus. Apart from atypically localised pain (jaw, head, neck), the nervus vagus is rarely involved in transmitting angina pectoris pain. There is no close relation between peripheral pain localisation and localisation of coronary stenosis or myocardial ischemia areas. The localisation of angina pectoris is decided by viscero-somatic summation (convergence-projection-theory). Almost all the ascending tracts of the tractus spinothalamicus with visceral inflow also receive inflow from somatic afferences, from skin areas of the dermatome from the same segment level, and especially from deep somatic structures such as muscle and ligaments (Head's zones). Additional reflex mechanisms, where the efferent part is probably sympathetic, explain transferred effects in the matching dermatome such as hypothermic skin zones, cutaneous hyperalgesia, higher pressure sensitivity of the muscles and occasionally even dystrophic changes. The amount of spinal visceral afferences is relatively small (only 1.5-2.5% of all somatic spinal afferences). The low amount, the pronounced divergence and, compared to converging somatic afferences, the larger receptive fields in the organ explain the diffuse, barely localisable character of angina pectoris pain. Cardiac afferences are tonically and phasically inhibited at spinal and supraspinal levels, especially by descending tracts. This explains why angina pectoris can be missing in spite of pronounced peripheral nociceptive impulse rates. Patients with silent myocardial ischemia have a higher central pain threshold than patients with symptomatic myocardial ischemia. Endogenous opioids are involved in the body's own analgesia system. The beta-endorphin level in the serum rises significantly in many patients during exercise diagnostic tests. Patients with silent myocardial ischemia have higher beta-endorphin levels compared to symptomatic patients at the same exercise level. This can be interpreted as expressing quantitative differences in a superior pain regulation system. Myocardial ischemia is experienced as angina pectoris pain when the peripheral nociceptive impulse rate is so pronounced that the prevailing inhibitory pain threshold can be overcome and when the pain pathways are intact.
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PMID:[Pain perception and peripheral pain localization in angina pectoris]. 306 37

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

Sudden cardiac death (SCD) due to acute myocardial infarction (AMI) is mostly the result of ventricular fibrillation (VP) which is an electrical accident appearing on the basis of electrical instability of the myocardium. In addition to the chronic electrical instability predisposing to ventricular arrhythmias the trigger effect of a precipitating factor also seems necessary which may disrupt the normal sequence of cardiac contractions. In view of this hypothesis the following strategy of therapeutic interventions aimed at preventing SCD from AMI seems to be logical: Prophylactic measures to prevent pathological processes underlying chronic electrical instability of the heart i.e. elimination of identified risk factors of ischemic heart disease. Protection from SCD due to AMI: by using drugs which could, prevent further electrical destabilization as shifts in myocardial and plasma ionic balance, in pH, in pCO2, accumulation of potentially arrhythmogenic metabolites: Inhibit the trigger effect of sudden changes: in hemodynamics, in the autonomic nervous outflow and balance. The general supportive measures include therapeutic interventions which are not directly connected with appearance of lethal arrhythmias but may indirectly contribute to their development as pain, arterial Hb desaturation, deep vein thrombosis. Some of the measures listed above are capable of limiting the size of the developing infarct, a major determinant of the future conditions of life and prognosis of the patient. In the prehospital phase of AMI when two thirds of all coronary deaths occur general supportive measures and drug treatment of life threatening arrhythmias should be applied simultaneously. Sedatives and anxiolytics, furthermore analgetics are widely used. They are however often associated with bradycardia and sometimes with hypotension. This latter is dominant in patients with inferior infarction, showing a parasympathetic hyperactivity, when atropine treatment is needed. Sympathetic hyperactivity responds to analgesia and sedation but beta blockers may be required to reduce increased MVO2. These agents belong to the group of anti-ischemic drugs. The beneficial anti-ischemic action of beta-blockers is mostly due to their negative chronotropic and inotropic effect. A direct metabolic action was shown by use as well as the presence of a positive steal phenomenon in the experimental angina model in dogs. Anti-ischemic action of coronary vasodilators. The most reliable drug for preventing or abolishing anginal attack is still the classic nitroglycerin. On the other hand persantine a potent coronary dilator failed to protect against anginal attack in man.
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PMID:[Pharmacological possibilities for the prevention of complications following myocardial infarction]. 382 Nov 31

During 2588 coronarography examinations conducted over a period of 4 years, assisted circulation was employed in 63 cases to reduce the risks of the examination procedure in particularly debilitated patients. These high risk cases included 48 patients with unstable angina resistant to medical treatment and 45 cases of recent infarcts with complications. Mortality with assisted circulation was very low, in spite of the severe nature of the affections, but the authors use this technique in only a limited number of cases, mainly because of the risk of lower limb ischemia, and the possibility of using intravenous nitroglycerin and analgesia from neuroleptics for examination. For this reason the number of cases examined in this way has dropped from 4% in 1977 to 2% in 1978, though assisted circulation is still employed in certain particularly severe cases of angina, and for infarcts with complications.
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PMID:[Assisted circulation during coronarography: advantages and limitations. A report on 63 cases (author's transl)]. 625 75

Atrial pacing was used for preoperative evaluation of six patients with recent anterior myocardial infarction (MI) (e.g. within 6 weeks) scheduled for abdominal emergency surgery. Central and coronary haemodynamics were used to compare changes in myocardial work and oxygenation with alternations of the non-invasive variables rate pressure product (RPP) (systolic blood pressure X heart rate), triple product (TP) (systolic blood pressure X heart rate X mean pulmonary arteriolar occlusion pressure) and ST-T segments (lead V5). There was good correlation between myocardial oxygen consumption and rate pressure product and triple product during pacing to stable angina pectoris. ST-T-segment depressions were recorded already at moderate chest discomfort and correlated well with a decrease in coronary vascular resistance. Changes in myocardial oxygen consumption induced by combined thoracic epidural analgesia (T3-4 to L1-2) and light general anaesthesia with nitrous oxide and fentanyl were poorly correlated with changes in rate pressure product or triple product. ST-T-segment depressions were recorded on five occasions in four of the patients, all in association with intubation and/or extubation. Only on one of these occasions could RPP or TP have indicated that myocardial oxygen demand exceeded supply. On the other four occasions, it was probable that myocardial ischaemia was induced by transient arterial hypoxaemia. The V5 ST-T-segment was the most sensitive non-invasive variable to monitor. The anaesthetic method was safe in all patients, as judged by good intraoperative cardiovascular stability, low morbidity and absence of intra- or postoperative reinfarction.
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PMID:Invasive analysis of non-invasive indicators of myocardial work and ischaemia during anaesthesia soon after myocardial infarction. 731 77


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