An acute myocardial infarction (AMI) occurs due to the occlusion of a coronary artery with a thrombus formation. This event causes necrosis of cardiac tissue and can predispose the patient to the development of multiple dysrhythmias and death. The blood supply to the myocardium is accomplished through arteries that lie on the outside of the heart supplying the various areas of the myocardium. Plaques develop below the intima, the innermost layer of vessels, which then rupture through this layer developing a narrowed passage for the blood supply. Once the plaque is present inside the vessel, a clot forms at the site. This thrombus formation is the critical pathology that creates a situation for ischemia, injury, and necrosis in that particular part of the heart.
Pathophysiology of Acute Myocardial Infarction Coronary Artery Supply
Two major arteries supply the heart with its own blood supply. These are the left and right coronary arteries. These arteries arise from the aortic valve through ostia or openings around the cusps. Each of these arteries then have branches that help to encircle the heart, providing oxygen rich blood to this important organ (Coronary arteries).
Even though the make up of the coronary artery circulation is similar in all patients, there are congenital modifications that do occur. The terms “left dominant” and “right dominant” have to do with the origin of the posterior descending artery (PDA). When this arises from the circumflex branch (LCX) of the left coronary artery (LCA), the patient is said to be “left dominant.” When the PDA develops from the right coronary artery (RCA), it is then known as “right dominant.” Other alterations also occur, such as the source of the sinus node artery. This can arise from the RCA or the circumflex. In the majority of patients, this branch comes off of the RCA. These deviations are important when looking at potential problems that occur when patients develop blockages in certain vessels. Each of these arteries supplies not only different portions of the heart wall, but also distinctive areas within the heart such as the SA and AV node. For instance, when the RCA is obstructed, patients will most often have difficulty with the SA and AV node. See Major Coronary Arteries and Areas Supplied for an explanation of the common areas supplied by each of the major arteries.
Major Coronary Arteries and Areas Supplied
The usual etiology for an AMI is atherosclerotic heart disease. However, there are other reasons for these events to occur. Coronary artery spasms, congenital anomalies, trauma, use of illicit drugs such as cocaine, hyperthyroidism, anemia, aortic dissection, GI bleed syndromes, and carbon monoxide poisoning are a few of the reasons for patients to develop AMIs. Children can also have MIs. Marfan’s syndrome and Kawasaki disease can predispose children to this disease process, as well as inflamed coronary arteries, nephrotic syndrome, and congenital malformations of the LCA. Familial high cholesterol can also influence the development of AMI in young patients.
Acute Coronary Syndrome
Acute coronary syndromes include several aspects of the process of occlusion and possible necrosis of cardiac tissue. The three subcategories of this disease pattern are:
- Unstable Angina
- Non-ST segment elevation myocardial infarction (NSTEMI)
- ST segment elevation myocardial infarction (STEMI)
Angina causes chest pain when there is a decrease in the amount of oxygen available for the heart to function. This can happen because there is an increase in the demand for oxygen (exercise, stress, physical activity) or there is a decrease in the amount of oxygen available (hypoxia). One form of angina is considered to be “stable.” This is when discomfort is noted during exercise, physical activity, or some type of stressful situation. This increase in demand for oxygen is relieved by rest or the use of nitroglycerin. The episodes are very short—from 2 to 15 minutes.
Unstable angina is present when one of three factors exists:
- Chest pain and associated symptoms occur during rest or with minimal physical exertion. This usually lasts for more than 20 to 30 minutes.
- Symptoms that are of new onset but occur due to extremely minimal physical exertion.
- Stable angina symptoms that are now occurring more frequently, are more severe, and lasting for greater periods of time.
Patients with unstable angina are often in a preinfarction stage. Treatment is necessary to prevent them from subsequently infarcting. Follow up studies are important for these patients to properly diagnose and treat this disorder. Another form of unstable angina is called Prinzmetal’s angina. Another term for this is variant angina. Though some patients may have associated atherosclerosis, many do not have this aspect of myocardial vessel disease. In this presentation, coronary arteries spasm thus causing a decrease in the blood supply to the myocardium. An interesting aspect of this type of angina is that it almost always occurs at rest with the prime time for symptomatic pathology occurring between midnight and 8 o’clock in the morning. For these patients, ST segments may be elevated during the time of pain and will return to baseline when the pain has resolved. Episodes may be short but can cause dysrhythmias including ventricular tachycardia and fibrillation leading to sudden death.
When patients present with complaints of “not feeling well,” they may not be able to identify that chest discomfort is a part of their distress. Oftentimes, when asked if they are having chest pain, they will quickly reply “no.” However, on further questioning, the health care provider may be able to ascertain that chest “heaviness” or “tightness” is present that the patient does not qualify as “pain.” Always make sure that these inquiries are made. It is part of the health care professionals “job” to help the patient to verbalize these difficult symptoms. Be sure to let them know that heaviness and tightness in the chest area is indeed pain. The health care professional and the patient must be able to “speak the same language” when it comes to symptoms.
Non-ST Segment Elevation Myocardial Infarction
The name defines it when a patient is diagnosed with non-ST segment myocardial infarction (NSTEMI). This simply means that the ST elevation that is seen with an ST segment elevation myocardial infarction (STEMI) is not present. Some EKG changes that can occur with the NSTEMI are: 1. Transient ST segment depression and 2. T wave inversion that is 1 mm or more. These changes should be seen in at least two contiguous leads. The chief identifying characteristic for this event is that the biomarkers will be increased indicating a leakage of enzymes from damaged cardiac tissue. These EKG changes may occur with unstable angina, but, the biomarkers are not elevated in unstable angina. The frequency of this type of AMI has increased.
ST Segment Elevation Myocardial Infarction
As the name implies, these myocardial infarctions carry the classic ST segment elevation in the leads associated with the damaged myocardium. Biomarkers will also be elevated in this type of AMI. Most of these patients will eventually produce the Q wave, which marks actual necrosis. These patients are candidates for thrombolytic therapy and percutaneous transthoracic coronary angiography and subsequent interventions.
T Wave Changes
The outermost part of the area of infarction involves an area of ischemia or decreased oxygen supply to a particular part of the heart. The T wave is associated with this area. In the early stages of an MI, the T waves can become hyperacute, meaning they are tall and peaked. This then changes to the depressed or inverted T wave which can be present for extended periods of time. This can occur alone or concurrently with the ST segment elevation (T wave inversion, Hyperacute T wave, and Zone of ischemia).
T wave inversion
Hyperacute T wave
It is important to compare the EKG in question with old EKGs. Changes may or may not be occurring. If suspected changes are the same as they were “6 months ago,” they may or may not be important in diagnosing the patient with ischemia at “this particular time.” Also, some patients may actually have inverted T waves that they normally carry. In this case, the T wave may become “normal.” This is called pseudonormalization. The only way to determine this phenomenon is to judge the electrocardiograms side by side.
Zone of ischemia
ST Segment Elevation
ST segment elevation, noted in two contiguous leads, which means the leads look at the same area of the heart, occurs as an indicator of injury. The middle area, lying between the zone of ischemia and the zone of infarction, is the region revealed by this change in the EKG (Zone of injury).
This ST elevation, seen in patients presenting with STEMI, will be observed in the patient evolving to infarction. When ST segment elevation is noted on the EKG, it is not an indicator of necrosis of myocardium. ST changes can occur and stay elevated (>1 mm) for several hours before actual infarction takes place. This is reversible at this time.
These can return to baseline after a period of time or can be a factor in reperfusion of myocardium when thrombolytic therapy or angioplasty is performed. ST segment elevation is an indicator for reperfusion interventions.
This ST segment elevation can occur with other circumstances as well, such as pericarditis, hyperkalemia, a pulmonary embolism, or hypothermia. ST segments that tend to stay elevated for prolonged periods of time could signify an aneurysm that has formed in a ventricle. When elevated ST segments are present, they will vary as to the morphology, but the configuration will usually appear as an upward swing in the ST segment as it merges with T wave (ST segment elevation).
Zone of injury
ST segment elevation
ST segment depression can occur in some MIs, when the leads in which it is present are directly opposite to the true area of infarction. This depression is known as “reciprocal” ST changes. A reciprocal change is actually a mirror image; therefore, these will occur in the opposite leads from where the actual injury is occurring. As an example, if an anterior MI occurs, reciprocal changes will be seen in the inferior leads.
Pathologic Q Wave
The Q wave is seen when necrosis actually occurs in the area. This is the last layer of the zones (Zone of infarction). When necrosis occurs, no depolarization is able to take place. The absence of conduction correlates with a deep negative deflection (below the isoelectric line) on the EKG tracing. The infarction is now in an irreversible stage.
Zone of infarction
Q waves are said to be “pathologic” when they are greater than 0.04 seconds in duration (wider) or the Q wave is one third the overall R wave height (deeper) (Pathologic Q wave). ST segments are usually no longer elevated by the time the Q waves become present in the leads associated with the area of infarction. Q waves can occur within hours of the development of the AMI or may take longer to form. This is something that can remain on the EKG for the patient’s lifetime and is evidence of the infarction forever. This is called a “Q wave” MI.
Pathologic Q wave
Lead aVR normally has a deep and negatively deflected Q wave. It should not be analyzed for the presence of a myocardial infarction. It can be used to help determine that the leads have been correctly placed on the patient. If the negative deflections are not noted, the leads should be rechecked. It could also mean a major change in axis. Children can have normal “pathologic—appearing” Q waves in certain leads including II, III, aVF, V5, and V6. If “pathologic” Q waves are present in this population in other leads, it could reflect cardiac disease processes. Other changes that may be normal for the infant or child are T wave inversion in leads V1, V2, and V3 and long QT intervals in infants under the age of 6 months. Another aspect that is different when attempting to identify the presence of a myocardial infarction is a left bundle branch block. When this is present, it is difficult to recognize any of the normal changes that are typically noted with an AMI.