ST elevation myocardial infarction analgesic therapy
| Myocardial infarction | |
| ICD-10 | I21-I22 |
|---|---|
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
| Cardiology Network |
 Discuss ST elevation myocardial infarction analgesic therapy further in the WikiDoc Cardiology Network |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor: Cafer Zorkun, M.D., Ph.D. [2]
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Overview
Although, the recommendation for morphine induced pain relief has been reduced to a Class IIa recommendation for patient with unstable angina pectoris (UA) and Non ST Elevation Myocardial Infarction (NSTEMI), the use of opiate analgesics (e.g. morphine) remains a Class I recommendation for patients with STEMI.
Analgesic agents that are contraindicated in STEMI
In contrast to morphine and aspirin, cyclooxygenase-2 (COX-2) inhibitors and other non steroidal anti inflammatory drugs should be discontinued immediately in the setting of STEMI in so far as they inhibit aspirin and because they have been associated with an increased risk of cardiovascular events. [1] [2] Non-steroidal anti-inflammatory drugs (NSAIDs) bind to a serine residue and thereby block aspirin's access cyclooxygenase-1, through interference with the prostaglanin system they may worsen hypertension or congestive heart failure. In a non-randomized analysis from the EXTRACT trial, administration of a NSAID within 7 days of enrollment was associated with a higher incidence of 30-day death or nonfatal recurrent MI (15.9% vs. 10.8%, p < 0.001).
Mechanism of Benefit
The mechanisms of benefit of morphine sulfate include the following:
- Reduction in the hyperadrenergic state that accompanies vessel occlusion which in turn:
- Reduces the pulse and thereby reduces oxygen consumption
- Reduces the systolic blood pressure (afterload) and thereby reduces cardiac workload
- Increases the threshold for ventricular fibrillation
- Reduces metabolic demands and therefore cardiac workload
- Reduces the work of breathing
- Reduces preload and pulmonary capillary wedge pressure
Clinical Trial Data
While there is no large scale clinical trial data demonstrating an improvement in mortality or other hard endpoints associated with analgesic administration, analgesic agents do relieve anxiety and apprehension, both of which can heighten pain perception. Morphine may reduce the pulmonary capillary wedge pressure and make breathing easier improving the patient's quality of life.
Dosing
Morphine sulfate (2 to 4 mg IV with increments of 2 to 8 mg IV repeated at 5- to 15-minute intervals)
Side Effects
Adverse effects can be seen in patients with morphine sensitivity.
- Hypotension: Hypotension can be minimized by keeping the patient supine. If the systolic blood pressure drops below 100 mm Hg, then the lower extremities can be elevated.
- Vagomimetic Effects such as Bradycardia: Morphine can heighten vagal tone, and administration of a vagolytic agent such as intravenous atropine in doses of 0.5- to 1.5-mg doses intravenously may be helpful in reducing the excessive vagomimetic effects of morphine. The administration of atropine should be reserved for those patients in whom bradycardia or hypotension are present.
- Respiratory Depression: Respiratory rate and depth should be monitored. The narcotic reversing agent naloxone, 0.1 to 0.2 mg intravenously, can be given initially if indicated and repeated after 15 minutes if necessary.
- Nausea and Vomiting: May be treated with phenothiazines.
Guidelines (DO NOT EDIT)
Class I
1. Morphine sulfate (2 to 4 mg IV with increments of 2 to 8 mg IV repeated at 5- to 15-minute intervals) is the analgesic of choice for management of pain associated with STEMI. Class I (Level of Evidence: C)
2. Patients routinely taking NSAIDs (except for aspirin), both nonselective as well as COX-2 selective agents, before STEMI should have those agents discontinued at the time of presentation with STEMI because of the increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture associated with their use. Class I (Level of Evidence: C)[3]
References
- ↑ C. Michael Gibson, Yuri B. Pride, Philip E. Aylward, Jacques J. Col, Shaun G. Goodman, Dietrich Gulba, Mijo Bergovec, Vijayalakshmi Kunadian, Cafer Zorkun, Jacqueline L. Buros, Sabina A. Murphy and Elliott M. Antman.Association of non-steroidal anti-inflammatory drugs with outcomes in patients with ST-segment elevation myocardial infarction treated with fibrinolytic therapy: an ExTRACT-TIMI 25 analysis. DOI10.1007/s11239-008-0264-4.
- ↑ Gaziano JM, Gibson CM (2006). "Potential for drug-drug interactions in patients taking analgesics for mild-to-moderate pain and low-dose aspirin for cardioprotection". Am. J. Cardiol. 97 (9A): 23–9. doi:10.1016/j.amjcard.2006.02.020. PMID 16675319. Unknown parameter
|month=ignored (help) - ↑ Antman EM, Hand M, Armstrong PW; et al. (2008). "2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee". Circulation. 117 (2): 296–329. doi:10.1161/CIRCULATIONAHA.107.188209. PMID 18071078. Unknown parameter
|month=ignored (help)