Myocardial Infarction Immediate Treatment – Mnemonic:
Myocardial infarction or acute myocardial infarction (AMI) is the medical term for an incident commonly known as a heart attack. Myocardial infarction happens when blood supply to the hear stops flowing properly to part of the heart and since the oxygen supply to that part of the heart is now insufficient, it leads to heart muscle injury. This is usually because of one of the coronary arteries that supplies blood to the heart develops a blockage due to an unstable buildup of white blood cells, cholesterol and fat. The event occurs suddenly, hence the term “acute”.
- Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium, where it may mimic heartburn.
- Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include
- Diaphoresis (an excessive form of sweating)
- Increased Age,
- Hypercholesterolemia (high cholesterol levels),
- Family history of Coronary artery disease (CAD),
- Diabetes Mellitus,
- Tobacco use,
- Male > Females
- Postmenopausal female > Premenopausal female
- Electrocardiogram (ECG): will show ST segment elevation and T-wave changes; Possible new arrhythmia, Left Bundle Branch Block (LBBB), or Q-wave changes.
- Serial Cardiac Enzymes:
- Changes in enzymes in the initial 24 hours after Myocardial Infarction are helpful for making a diagnosis of acute infarction. Enzymes are measured every 8 hours in the first 24 hours after presentation (total of 3 sets)
- Creatine phosphokinase myocardial fraction (CPK-MB) increases 2-12 hours post Myocardial Infarction, and it peaks in 12-40 hours and declines in 24-72 hours. This can also be measured for diagnosis of recurrent Myocardial Infarction that might occur after 3 days of initial Myocardial Infarction.
- Lactase dehydrogenase (LDH) increases in 6-24 hours and peaks in 3-6 days (this is rarely used for diagnosis)
- Troponin-I increases in 3 hours, Peaks in 6 hours, and gradually decreases over 7 days. This is the most sensitive enzyme in diagnosing Myocardial Infarction.
- Morphine (pain control can decrease cardiac oxygen demand)
The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, mainly smoking cessation, regular exercise, a sensible diet for those with heart disease, and limitation of alcohol intake. People are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:
- Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction.
- Beta blocker therapy such as metoprolol or carvedilol should be commenced. These have been particularly beneficial in high-risk patients such as those with left ventriculardysfunction and/or continuing cardiac ischaemia. β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.
- ACE inhibitor therapy should be commenced 24–48 hours post-MI in hemodynamically stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post-MI.
- Statin therapy has been shown to reduce mortality and morbidity post-MI. The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other (“pleiotropic”) effects that may prevent myocardial infarction in addition to their effects on blood lipids.
- The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above. Spironolactone is another option that is sometimes preferable to eplerenone due to cost.
- Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease. In high-risk people there is no clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids. And they may increase risk in some groups.
- Giving heparin to people with heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of minor bleeding.
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