The symptoms of ischemia are also those that are often consistent with an acute coronary syndrome or myocardial infarction. But they're not just chest pain, pressure, heaviness, tightness. There are many things that may be associated with myocardial ischemia that we may not think of. Most of us are familiar with the chest pain with radiation to neck, jaw, shoulder or arm, which is usually on the left side.
Sometimes there's an epigastric location, but that may be difficult to separate from the substernal location and may accompany it. Shortness of breath, nausea, vomiting, sweating are not unusual. Some people only express a sense of profound fatigue or weakness.
Syncope or presyncope can be the only symptom, and that's usually due to some type of an arrhythmia associated with an ischemic myocardium. New EKG changes. Alternatively, the location of the MI may be stated like inferior, lateral or anterior. Cardiac Imaging. Imaging evidence includes echocardiogram, the radioactive nuclide imaging myocardial perfusion , or SPECT. MRI of the heart and CT angiograms, or cardiac cath with angiography, and other modalities can identify wall motion abnormalities, systolic or diastolic dysfunction, changes in ejection fraction.
Extent of infarct is sometimes identified as well as structural abnormalities, perfusion abnormalities of affected coronary arteries and with cardiac cath intracoronary thrombus may be identified.
Troponin levels in suspected myocardial infarction are measured on admission, typically two to four hours after admission, six to eight hours after admission for the third, and occasionally a fourth measurement at 12 hours depending on whether the first three are diagnostic or not.
Troponin I is preferred to troponin T because it's a little more specific and a bit more accurate. For different labs, the reference ranges vary. In the case examples shown in the table below you can see whether or not the levels are elevated and whether they rise or fall. In general, higher troponin levels are associated with more extensive myocardial injury. Keep in mind though that a very high troponin level alone is not diagnostic of a myocardial infarction and must be supported by evidence of acute myocardial ischemia.
In Case 1, there is evidence of acute myocardial injury because the troponin level is very high compared to the URL of 0. If there is also evidence of acute myocardial ischemia symptoms, new EKG changes, cardiac imaging , we have an acute myocardial infarction either Type 1 or Type 2, depending on the cause. The same is true for Case 2 where there is a dramatic fall from a very high level of In Case 3 , the troponin level is elevated but there is a slight fall and then a slight rise occurs followed by another fall that is more or less stable without a clear trend.
This likely represents chronic nonischemic myocardial injury. Case 4 shows only very slightly elevated levels and are rather flat. We don't really know if they are dropping. These might be within the normal range for this patient even though these are above the normal reference range.
How quickly does the troponin level disappear after injury? It can take up to two weeks for the troponin level to return to normal, so a delayed diagnosis of myocardial infarction can still be made.
The above table shows the ischemic and other nonischemic causes of myocardial injury. Ischemic causes of myocardial injury in the setting of acute myocardial ischemia are myocardial infarctions of all types, most commonly Types 1 and 2. If the cause of the myocardial injury is non-ischemic, there is no myocardial infarction. Classically, there are three phases after a coronary artery occlusion :. Myocardial ischemia may be caused by a deficiency in blood supply, such as acute coronary syndrome , coronary spasm or anemia; or caused by an increase of myocardial demand, such as tachycardias or infections.
After occlusion of a coronary artery , ischemia produces delayed repolarization of myocardial cells, causing changes in T wave 1 2. Subendocardium is the most sensitive area to ischemia, and is the first area to suffer oxygen deficiency. Delayed repolarization causes tall T waves peaked Twaves , accompanied by a lengthening of QTc. Subepicardial ischemia transmural ischemia causes a delay in repolarization of the entire myocardium of the affected area, generating negative or flattened T waves on the EKG 1.
If ischemia persists, changes of myocardial injury occur on the electrocardiogram. Injury causes ST segment abnormalities , elevation or depression. Subendocardial injury is usually caused by a partial occlusion of a coronary artery , generating a greater degree of injury in subendocardium more sensitive to ischemia than subepicardium.
When a total occlusion of a coronary artery occurs, a transmural injury appears classically called subepicardial injury , This means that the entire myocardium in the area is affected. The subepicardial injury produces ST segment elevation in leads near the affected regions 2 3. Remember: ST elevation is a sign of acute myocardial infarction and must be treated as soon as possible fibrinolysis or angioplasty. Read ST-segment elevation myocardial infarction Myocardial infarction or necrosis is caused by long-term persistence of ischemia.
It usually appears in the evolution of ST-segment elevation myocardial infarction STEMI , producing death necrosis of myocardial tissue. The infarcted regions are electrically inactive, abnormal Q waves or QS complexes appear in leads near the affected regions.
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