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

The 'chain-of-survival' concept has gained general acceptance in the care of cardiac arrest victims. Most standards and guidelines for cardiopulmonary resuscitation, however, focus on the initial links in the chain. We consider appropriate in-hospital care for the survivors a logical extension of the chain of survival. In recent years extensive research activity has probed the pathophysiology and pharmacology of postischemic reperfusion. The present review discusses the current understanding of mechanisms for cerebral damage following global ischemia. Promising pharmacological principles for protection or resuscitation from cerebral ischemia are reviewed. None of them are considered ready for clinical application. Clinical guidelines are proposed, based on the reviewed data and previously published clinical observations. Cornerstones of the proposed brain-oriented intensive care protocol are: (1) hemodynamic monitoring and meticulous treatment of circulatory disturbances, (2) controlled ventilation providing normoventilation and normoxia to all comatose patients, (3) avoiding hyperglycemia and hyperthermia in comatose patients, (4) adequate analgesia and sedation, tempered by the understanding that oversedation impedes neurological evaluation without promoting recovery. An accurate prognosis can usually be made 48-72 h after resuscitation. This permits reevaluation and assignment to an appropriate level of continued hospital care.
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PMID:Brain-oriented intensive care after resuscitation from cardiac arrest. 829 Aug 16

Recent data suggest that postbypass and postoperative myocardial ischemia are related to adverse cardiac outcome following myocardial revascularization. Therapeutic trials to suppress postoperative ischemia are warranted. Because anesthetics can suppress a variety of physiologic responses to stress as well as myocardial ischemia intraoperatively, we examined whether use of intensive analgesia in the stressful postoperative period could decrease postoperative ischemia. In 106 patients undergoing elective myocardial revascularization, we standardized the anesthetic prior to bypass (sufentanil 5-10 micrograms/kg [induction] and 4.2-6.0 micrograms.kg-1.h-1 [infusion] supplemented with up to 0.5 mg/kg of diazepam). During bypass, patients were randomly assigned to receive either morphine sulfate (group M, n = 54, up to 2 mg/kg) or sufentanil (group S, n = 52, 1 microgram/kg and 1 microgram.kg-1.h-1). In the intensive care unit (ICU), group M received low-dose analgesia (morphine sulfate 1-10 mg intravenously every 30 min, average dose = 2.2 +/- 2.1 mg/h), while group S continued to receive intensive analgesia (infusion of sufentanil at 1 microgram.kg-1.h-1). Both groups received supplemental midazolam in the ICU (group M = 1.1 +/- 1.1 mg/h; group S = 0.6 +/- 0.6 mg/h; P = 0.01). All analgesic and sedative-hypnotic medications were discontinued at 18 hours following myocardial revascularization. Using continuous two-channel electrocardiographic (ECG) monitoring (CC5 and CM5), we documented and characterized ECG changes consistent with ischemia during the preoperative, intraoperative (pre- and postbypass), and postoperative (on- and off-treatment) periods. The total ECG monitoring time was 8,486 h, averaging 81 h per patient. During the prebypass (anesthetic control) period, groups M and S had a similar incidence, but group S episodes were more severe: maximum ST-segment change (median), S versus M: -1.8 mm versus -1.4 mm (P = 0.04). During the postbypass period, both groups had a similar incidence of ischemia, but episodes in group S were less severe: maximum ST-segment change, S versus M: -1.8 mm versus -2.7 mm (P = 0.0005). During the ICU-on-therapy period, the incidence of ischemic episodes was less in group S patients, and the severity was less: area-under-the-ST-time curve, S versus M: -21 mm.min versus -161 mm.min (P = 0.05). After discontinuation of the drug regimen in the ICU, the incidence and severity of ischemic episodes was similar. The incidence of hypotension, hypertension, and tachycardia was similar in both groups in both the intraoperative and ICU periods.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Postoperative myocardial ischemia. Therapeutic trials using intensive analgesia following surgery. The Study of Perioperative Ischemia (SPI) Research Group. 153 42

Hemodynamic changes were studied during two different anesthetic techniques in 54 patients undergoing coronary artery bypass grafting (CABG). All patients had normal to moderately impaired left ventricular function and were randomly assigned to two groups. In 27 patients, high thoracic epidural analgesia (TEA) with bupivacaine 0.375% plus sufentanil 1:200,000 (ie, 5 micrograms/mL) was used in combination with general anesthesia with midazolam/N2O; in the other 27 patients, general anesthesia (GA) with midazolam and sufentanil was used. After induction of epidural analgesia, heart rate and mean arterial pressure (MAP) decreased. Changes in cardiac index, systemic vascular resistance, and pulmonary capillary wedge pressure were not observed, whereas the stroke volume index increased significantly. After induction of intravenous anesthesia MAP decreased (20%) in both groups. During the pre-bypass period, metaraminol was used in 7 of 27 patients in the GA group and in 5 of 27 patients in the TEA group to treat hypotension. Inotopic drugs were used in 5 patients in the GA group and in none in the TEA group to treat a low CO. Ten GA patients and 4 TEA patients developed hypertension after sternal spread and the GA patients required more nitroprusside. Four GA patients developed electrocardiographic evidence of prebypass ischemia and, therefore, more nitroglycerin was needed for treating myocardial ischemia. More sodium nitroprusside was needed in the GA group during cardiopulmonary bypass (CPB) and the post-bypass period to treat hypertension with a high SVR. In conclusion, hemodynamic stability was more pronounced in the TEA than the GA group before and after CPB.
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PMID:Coronary artery bypass grafting using two different anesthetic techniques: Part I: Hemodynamic results. 847 38

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

The significance of ischemia-producing intravenous regional anesthesia (IVRA) was investigated using isotonic saline for injection. The possible analgesic effect of morphine was tested by injecting 40 ml morphine hydrochloride 0.01% for IVRA. Analgesia was evaluated subjectively by measuring the thresholds (warmth and pain) to laser stimulation and objectively by measuring the brain potentials (amplitude and latency) evoked by brief laser stimuli. Morphine and saline produced total pain alleviation after 30 minutes of IVRA. A control study was performed in which 40 ml lidocaine 0.5% and 40 ml prilocaine 0.5% were used for IVRA. This caused an inhibition of the laser-induced pain after 5-10 minutes. After the deflation of the cuff, the thresholds and the brain potentials recovered rapidly. No differences in the efficacy of lidocaine or prilocaine were observed. It is concluded that 30 minutes of tourniquet application is sufficient to cause analgesia and that morphine does not provide more adequate analgesia than saline when used for IVRA.
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PMID:Laser-induced pain for quantitative comparison of intravenous regional anesthesia using saline, morphine, lidocaine, or prilocaine. 207 83

The possible options for the management of acute pain are quite numerous and continue to expand as our understanding of the mechanisms of pain becomes increasing sophisticated. Many of the options discussed have been available for years, and their present underutilization may be a reflection of the lack of emphasis on the importance of management of acute pain. An illustration of this would be our present ritual of prescribing narcotics postoperatively, a longstanding, but unfortunately inadequate practice. Because of poor selection and scheduling of doses, postoperative analgesia is typically a less than satisfactory experience for many patients convalescing in a hospital following surgery. The clinician should of course be guided by the clinical situation itself in order to determine what modality or combination of modalities may be appropriate for pain management. Certain techniques, such as continuous local anesthetic infusions, may warrant an escalated level of monitoring and ancillary care. Other techniques, such as the infiltration of a wound with local anesthetic or the addition of a nonsteroidal anti-inflammatory agent to a regimen of mild oral narcotics are so simple that excluding them from patient care is almost callous and inconsiderate. Attention to the mechanisms of pain that may be present in a given situation, whether it be muscle spasm, ischemia, inflammation, edema, or nerve injury, may guide the clinician toward a more rational approach in managing that pain.
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PMID:Non-narcotic modalities for the management of acute pain. 218 13

Parenterally administered narcotic analgesics are a critically important part of therapy for the patient with acute myocardial ischemic syndromes. These agents are very effective and, when used with appropriate caution and monitoring, are also generally safe. They not only relieve the sensation of severe pain but also reduce the effective and physiologic reaction to pain and thus reduce patient anxiety. Because these agents all depress respiratory drive to some degree in the doses used for adequate analgesia, close attention to respiratory status is mandatory. In patients with underlying pulmonary disease or significant congestive heart failure, this monitoring should be even more intensive and include arterial blood gas measurements and preparations for possible narcotic antagonist administration and ventilatory assistance. With regard to the hemodynamic changes produced by these agents, several important points are worth noting. It must be remembered that the conclusions regarding hemodynamic effects of these agents are derived from studies involving patient groups that were generally hemodynamically stable, usually pain-free, and almost always at least several hours following acute presentation. Thus, the hemodynamic effects of these agents may be quite different in patients with active pain during a period of acute ischemia, or in patients that are hemodynamically unstable. Hemodynamic studies during these acute settings, however, are extremely difficult to perform because the patient's acute distress mandates rapid administration of an analgesic agent prior to the institution of invasive monitoring. With these cautions relating to data interpretation in mind, it is still possible to make certain recommendations regarding the use of analgesic therapy in acute MI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analgesic therapy in acute myocardial infarction. 290 10

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

Since the mid-1970s, evidence has accumulated that cholecystokinin (CCK) has a role as a neuromodulator or neurotransmitter in the central nervous system as well as in the periphery. CCK has been shown to have a variety of effects on gastrointestinal functions and is one of the main candidates for a role as a peripheral negative feedback signal to stop feeding behavior. CCK produces satiety not only in animals but also in man: it reduces appetite and activation arising from the preparation of a meal and inhibits intake of liquid and solid food in both lean and obese subjects. The closely related peptide caerulein has similar effects. The site of action of peripherally administered CCK seems to be on an abdominal organ innervated by gastric vagal branches and relayed to the brain by afferent vagal fibres, since selective gastric vagotomy blocks the satiety effect, but pharmacological antagonism of vagal motor effects or lesions of the ventromedial hypothalamus do not. CCK also may have a role in the regulation of pain perception. In mice, CCK and caerulein were shown to produce a decrement in response to noxious stimulation after peripheral and central administration. In man, caerulein was demonstrated to relieve pain originating from biliary and renal colic as well as from cancer and ischemia. A series of studies in healthy man revealed that caerulein also alleviates experimentally induced cutaneous pain. Data from animal studies suggest that CCK-like peptides not only are able to produce analgesic effects on their own, but also are involved in the modulation of opioid systems mediating analgesia. Further study of these effects of CCK should elucidate the regulatory connections between the life-sustaining functions of feeding and pain sensation.
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PMID:Effects of cholecystokinin and caerulein on human eating behavior and pain sensation: a review. 308 29

In a placebo-controlled, double-blind study we evaluated the ability of a single 50 mg oral dose of nalmefene to block the effects of intravenous opioid challenge (2 micrograms/kg fentanyl). Fentanyl-induced respiratory depression (CO2 responsiveness), analgesia (tourniquet ischemia), and subjective effects were totally blocked for 48 hours and showed only minimal breakthrough 72 hours after nalmefene. Plasma concentration-time data for nalmefene indicate good oral bioavailability and a prolonged terminal elimination phase (mean t1/2 11.1 hours). These findings suggest that nalmefene could provide prolonged effectiveness in limiting emergence of opioid effects during addiction therapy.
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PMID:Prolonged blockade of opioid effect with oral nalmefene. 353 70


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