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Benefits of Morphine for Myocardial Infarction Treatment

Pain can activate the sympathetic nervous system and cause diaphoresis, weakness, light-headedness, and palpitations in patients with myocardial infarction. 
Published Online: Jun 23,2016
Jeannette Y. Wick, RPh, MBA, FASCP
Myocardial infarction (MI) is a painful condition with tightness, pressure, or squeezing pain in the chest for approximately 75% of patients who experience it.

This pain often radiates to the arms, jaw, or back. Nitrates bring relief to many patients, but up to one-third of those who experience MI have nitrate-resistant chest pain and receive morphine instead.

Clinicians have used morphine for pain associated with MI since the early 1900s. The drug’s use through today is largely based on the “it’s always been done it this way” school of thought.

However, a 2005 observational study found that MI patients treated with morphine had inferior outcomes than those who didn’t receive morphine. More recently, researchers examined morphine’s use in MI in the June 2016 issue of American Heart Journal. In it, they acknowledged that the 2005 study was followed by a flurry of new questions and studies.

Although some concerns have been identified, few alternatives are available. Treating pain in MI patients is critical, as pain activates the sympathetic nervous system and causes or aggravates diaphoresis, weakness, light-headedness, and palpitations. This, in turn, increases cardiac work load.

As a potent opioid, morphine has seemed to be the ideal analgesic. It has innate hemodynamic effects that are beneficial during MI. It decreases heart rate, blood pressure, and venous return, and it may also stimulate local histamine-mediated processes. Theoretically, this reduces myocardial oxygen demand.

Meperidine causes similar hemodynamic effects, but possible central nervous system excitability or seizures have limited its use. Other opiates may also have harmful adverse effects in patients who have experienced MI. Meanwhile, morphine is associated with vomiting, hypotension, and respiratory depression.  

The study authors also reported that morphine may inhibit and delay oral antiplatelet drug absorption. Rapid platelet inhibition is the cornerstone of treatment in acute coronary syndrome, and any slowing of antiplatelet effect may worsen outcomes.

Unfortunately, these adverse effects are unsubstantiated by prospective, randomized outcomes trials. Although further research is needed, study design will be difficult to structure because of ethical limitations associated with placebo-controlled randomization.

The study authors summarized alternatives to morphine, including acetaminophen for pain measuring less than 7 on a visual analogue scale; alfentanil, which has some limitations; and drugs in the naloxone, naloxagol, and methylnaltrexone family.

The researchers concluded that morphine remains a valuable agent when nitrates, beta-blockers, and expedited reperfusion fail to relieve pain.