Morphine myocardial infarction

Relief of pain associated with a myocardial infarction (morphine)... 

Morphine produces venous and arteriolar dilation, which may result in orthostatic hypotension. Hypovolemic patients are more susceptible to morphine-induced hypotension. Morphine is often considered the opioid of choice to treat pain associated with myocardial infarction, as it decreases myocardial oxygen demand. 

Q87 Morph ine should not be used for pain relief in myocardial infarction. Morphine may induce hypotension as a side-effect. 

Opioids such as diamorphine, pethidine, and pentazocine strongly inhibit gastric emptying and greatly reduce the absorption rate of paracetamol. Codeine, however, has no significant effect on paracetamol absorption. Morphine and diamorphine have been shown to reduce the absorption of antiarrhyth-mics such as mexiletine in patients with myocardial infarction. 

Most of the contraindications specific to pentazocine stem from its excitatory effects. Other contraindications are similar to those for morphine. Pentazocine is contraindicated in patients with myocardial infarction because it increases heart rate and cardiac load. Similarly, it is contraindicated in epileptic patients because it decreases seizure threshold. In addition, in head trauma patients, it can increase intracranial pressure and brain injury. Pentazocine use in patients with psychoses is contraindicated because of its psychotomimetic side effects. 

Butorphanol tartrate is a weak partial p-receptor agonist, 3.5-5 times as potent as morphine. The incidence of psychotomimetic effects is relatively low. The recommended doses are 1-4 mg intramuscularly every 3-4 h or 0.5-2 mg intravenously. Respiratory depression produced by butorphanol 2 mg IV is similar to that of 10 mg morphine. However, there is a ceiling effect for respiratory depression, and near-maximum depression occurs after 4 mg in normal adults. In healthy volunteers, butorphanol 0.03-0.06 mg-kg-1 produces no significant cardiovascular changes. However, in patients with cardiac disease, progressive increases in cardiac index and pulmonary artery pressure occur, and butorphanol should be avoided in patients with recent myocardial infarction. Butorphanol is metabolised mainly in the liver to inactive metabolites. The terminal half-life is 2.5-3.5 h. 

Acute severe pain after trauma (accidents), myocardial infarction, etc. and life-threatening pulmonary edema requiring inhibition of the respiratory center. For these indications, administration of morphine (intravenously or subcutaneously) in suf cient amounts is appropriate. With short-term use, development of tolerance or dependence is of no concern. 

Intrabiliaiy pressure may rise substantially after morphine (as much as 10 times in 10 minutes), due to spasm of the sphincter of Oddi. Sometimes biliary colic is made worse by morphine, presumably in a patient in whom the dose happens to be adequate to increase intrabiliary pressvue, but insufficient to produce more than slight analgesia. In patients who have had a cholecystectomy this can produce a syndrome sufficiently like a myocardial infarction to cause diagnostic confusion. Naloxone may give dramatic symptomatic relief, as may glyceryl trinitrate. Another result of this action of morphine is to dam back the pancreatic juice and so cause a rise in the serum amylase concentration. Morphine is therefore best avoided in pancreatitis but buprenorphine has less of this effect. 

Adverse cardiac effects due to morphine are rare. They comprise inappropriate heart rate responses to hypotension, rather than conduction defects. They are not especially associated with inferior myocardial infarction, as was previously thought (SED-11,142) (14). 

Morphine hydrochloride Use in palliative care, pain relief in respect of suspected myocardial infarction or for relief of acute or severe pain after trauma, including in either case postoperative pain relief Rectal... 

Endogenous opioid peptides are increased in myocardial ischemia. Their effect is mediated through presynaptic and postsynaptic mechanisms. Opioids limit the release of stimulating catecholamines by its presynaptic action while opioid receptor agonists act via Gi -linked pathways postsynaptically and alter myocardial channel activity and intracellular activities of protein kinases. Table 1. Figure 10. Blockade of 5 and x-opioid receptors reduced the tolerance of the isolated rabbit heart to ischemia and reperfusion.105 Furthermore, blockade of 8-opioid receptor abrogated the ischemic preconditioning mediated cardioprotective effect while activation of 8-opioid receptor by morphine decreased infarct size and apoptosis in a rabbit model of coronary occlusion and reperfusion.106... 

Little information exists about how a patient s drug therapy influences the informed consent process. For example, can a patient who has had several doses of intravenous morphine give consent to participate in an acute myocardial infarction protocol Sedated patients may not understand adequately what they are being told therefore, they cannot make up their minds freely. As another example, how informed can patients be who are experiencing blurred vision from atropine Does drug exposure influence continued participation or future consent If there are any doubts, a family member, guardian, or patient advocate should be involved in the informed consent process. 

Therapeutic doses of morphine have minimal effects on blood pressure, cardiac rate, or cardiac rhythm when patients are supine however, morphine does produce venous and arteriolar vessel dilatation, and orthostatic hypotension may result. Hypovolemic patients are more susceptible to morphine-induced cardiovascular changes (e.g., decreases in blood pressure). Because morphine prompts a decrease in myocardial oxygen demand in ischemic cardiac patients, it is often considered the drug of choice when using opioids to treat pain associated with myocardial infarction. 

Effects on the myocardium are not significant in normal individuals. In patients with coronary artery disease but no acute medical problems, 8-15 mg morphine administered intravenously produces a decrease in oxygen consumption, left ventricular end-diastolic pressure, and cardiac work effects on cardiac index usually are slight. In patients with acute myocardial infarction, the cardiovascular responses to morphine may be more variable than in normal subjects, and hypotension may be more pronounced. 

Morphine may exert its well-known therapeutic effect in the treatment of angina pectoris and acute myocardial infarction by decreasing preload, inotropy, and chronotropy, thus favorably altering determinants of myocardial consumption and helping to relieve ischemia. Morphine... 

Butorphanol tartrate (stadol) is better suited for the relief of acute than chronic pain. Because of its side effects on the heart, it is less useful than morphine or meperidine in patients with congestive heart failure or myocardial infarction. The usual dose is 1-4 mg of the tartrate given intramuscularly or 0.5-2 mg given intravenously every 3-4 hours. A nasal formulation (STADOLNS) is available and has proven to be effective. 

The client is complaining of severe chest pain radiating down the left arm and is nauseated and diaphoretic. The HCP suspects the client is having a myocardial infarction (Ml) and has ordered morphine sulfate (MS), a narcotic analgesic, for the pain. Which intervention should the nurse implement ... 

The absorption of mexiletine is reduced following myocardial infarction, and very markedly reduced and delayed if diamorphine or morphine is used concurrently. A higher loading dose may be needed if oral mexiletine is required during the first few hours following a myocardial infarction. 

A pharmacokinetic study showed that the mean plasma levels of mexiletine (400 mg orally followed by 200 mg 2 hours later) in the first 3 hours were more than 50% lower in 6 patients who had suffered a myocardial infarction and who had been given diamorphine 5 to 10 mg or morphine lOto 15 mg than in 4 patients who had not been given opioids. In addition, the AUCo.8 was 38.6% lower in those who had received opioids. ... 

Morphine has hypotensive effects, increasing peripheral vascular capacity and decreasing blood pressure, which may be mediated through adenosine. For this reason, as well as its analgesic properties, intravenous morphine has been given for myocardial infarction, although it is not a part of the current standard of treatment. 

Medical pain morphine is the drug of choice for the relief of pain due to myocardial infarction. Relief of ischemic pain decreases sympathetic nervous system activity thus reducing myocardial oxygen demand. Morphine is used in patients with acute pulmonary edema for its cardiovascular effects and to decrease air hunger. Morphine can be used to treat the pain of sickle cell disease with crisis. Morphine can be used to treat the pain of Guillain-Barre syndrome, osteoarthritis and obstetric pain. Morphine s sedative effects can be utilized in the intubated and ventilated patient. 

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