EKG: Acute Myocardial Infarction Patterns

Acute Myocardial Infarction: Areas of Infarction

With Acute Myocardial Infarction, when analyzing the 12-lead EKG, it is easy to determine the areas that are involved in an acute ST segment elevation myocardial infarction. As explained in Chapter 4, different leads look at distinct areas of the heart. When leads are contiguous, that is, particular leads look at specific parts of the heart and changes are seen in two or more “contiguous” leads, this is a key aspect of identifying AMIs and marking its location. Contiguous does not mean that they follow one another in succession rather they look at the same aspect of the heart. Consequently, when categorizing myocardial infarctions, two or more leads are listed which meet the criteria for the precise site of ischemia, injury, or infarction.

It is important to remember that some individuals do have variances in their heart anatomy, so it must be recognized that some variations might exist. However, for the majority of the population, there are particular conclusions that can be drawn for each area. In general, the anatomic areas of infarction are: inferior, anterior, lateral, septal, and posterior. Depending on the vessel occluded, combinations of these can also occur such as an anterolateral or an inferoposterior MI. It is also important to understand that when the health care practitioner is determining the site of an infarction, two separate entities are involved, they are:

  • The artery and its branches that are expected to be supplying the area.
  • The leads that actually “look” at the area.

Types of Myocardial Infarctions describes the artery involved, the leads depicting the area, and common dysrhythmias associated with each type of MI.

Types of Myocardial Infarctions

1

Clinical Alert

Not every MI is going to present as a “pure” type of infarct. Reading EKGs for this problem is not always “black and white.” There are many variances that can occur and individuals can have infarctions in two places in the heart. Therefore, “classic” pictures are not always visualized.

Anterior Myocardial Infarction

Leads indicating a blockage in the anterior portion of the heart are V1, V2, V3, and V4 (Anterior-lateral myocardial infarction). The left coronary artery (LCA) and the left anterior descending artery (LAD) are implicated in an anterior MI. When it occurs in the left main coronary artery, this is often known as the “widow maker.” The left coronary artery also feeds the circumflex. An anterolateral MI which would include blockage to the LAD and the circumflex would include leads I, aVL, V3, V4, V5, and V6. An anteroseptal MI, which indicates damage to the septum, would include the leads V1 and V2. Reciprocal changes would be seen in the inferior leads, II, III, and aVF.

Anterior-lateral myocardial infarction

1

An anterior MI causes major malfunction of the left ventricle leading to left-sided heart failure, decreased cardiac output, and hypotension. Cardiogenic shock is often present. Oxygenated blood is normally delivered to the left ventricle, the septum, and the bundle branches from this location. A variety of dysrhythmias can occur with an anterior MI including atrial fibrillation, atrial flutter, tachydysrhythmias, premature ventricular contractions (PVCs) (due to irritability), and second-degree blocks. Bundle branch blocks are also prevalent. Poor R wave progression may also be present.

Lateral Myocardial Infarction

A lateral MI involves blockage in the circumflex artery. Changes are seen in leads I, aVL, V5, and V6 (Lateral myocardial infarction). This may occur with either an anterior or inferior myocardial infarction. Dysrhythmias linked to this area are AV blocks and PVCs. Reciprocal changes will be seen in the inferior leads II, III, and aVF.

Lateral myocardial infarction

2

Septal Myocardial Infarction

Leads to locate a septal MI in are V1 and V2 (Septal myocardial infarction). R waves can disappear when lack of oxygenated blood is delivered to the areas that are replenished by the left anterior descending artery. This area of infarction may accompany an anterior MI. The bundle of His and the bundle branch blocks are located in this area of delivery as well. This is commonly seen with an anterior myocardial infarction. Dysrhythmias that are commonly seen with this type of myocardial infarction are AV blocks, especially second degree type II and complete (third degree).

Septal myocardial infarction

1

Inferior Myocardial Infarction

The right coronary artery feeds the area concerned with an inferior myocardial infarction through the posterior descending branch. Leads which view the inferior aspect of the left ventricle are II, III, and aVF (Inferior myocardial infarction). Dysrhythmias that are usually seen with this type of MI are bradycardias (from increased parasympathetic activity) such as sinus bradycardia and sinus arrest and AV conduction delays such as first- and second-degree block (type I). PVCs can also occur. In these patients, the Q wave that is usually present throughout life may disappear after a period of time. Reciprocal changes would be seen in the leads representing the lateral aspect of the heart, I, aVL.

Inferior myocardial infarction

1

Clinical Alert

Another aspect of the heart that can be involved is the right ventricle. While most infarctions concern the left ventricle due to the location and branching of the LCA, the right ventricle can be associated with an inferior MI. This occurs when the marginal branch which is derived from the RCA is occluded. If only the right marginal branch is occluded, the infarction site can be isolated to the right ventricle. When it occurs proximal to this branch, symptoms from both the right ventricle and inferior aspect of the heart can occur. A decrease in cardiac output can be realized with the right ventricular infarct because the right ventricle does not pump well diminishing the amount of blood that is returning to the left side of the heart. Another problem with the right ventricular infarct is that blood volume builds up in the right ventricle due to the reduced function of this chamber. These pathophysiologic responses lead the patient to the triad of “classic” symptoms that are associated with this disease process. These are: hypotension (from the decreased cardiac output), jugular venous distention (from the build up of blood in the right ventricle and thus the venous system), and clear lung sounds (left ventricular failure causes pulmonary edema). This triad is not always present in all patients with this problem, however, it is considered to be the characteristic symptoms for right ventricular infarct. A right-sided EKG is necessary to see the ST segment elevation for this type of myocardial infarction. V4R to V6R are the leads that are obtained when this infarct is suspected. Left-sided chest leads are transferred to the right side of the chest for these leads.

Posterior Myocardial Infarction

The posterior aspect of the heart is fed by the RCA and the circumflex. The leads that are noted to be different in this MI are leads V1 and V2. Leads V3, and V4 can also be included in this diagnosis (Posterior myocardial infarction). However, these leads show reciprocal changes, ST segment depression, since these leads reflect the mirror image of the posterior aspect, the anterior part of the heart. Other EKG changes to be seen in these anterior leads are tall R waves. In order to see the ST segment elevation expected with a posterior wall MI, a posterior EKG must be done. This includes leads V7, V8, and V9. These leads are placed on the left side of the back in the following positions: V7—left posterior axillary line, V8—under the tip of the scapula, V9—at the left vertebral column.

Posterior myocardial infarction

1

Another way to look at an EKG to determine if it is a posterior MI is to use the “mirror” test. In this test, turn the EKG upside down and hold it toward a mirror. Look at the EKG in the mirror. This will show the ST segments as being elevated, similar to what would be seen with the posterior leads. Another way is called reversed transillumination. Turn the EKG upside down and backwards to the health care practitioner (so that the back of the EKG is toward the practitioner). Hold it up to a light. The ST “elevation” should now show on leads V1 and V2 (Reversed transillumination and the mirror test).

Reversed transillumination and the mirror test

1

Clinical Alert

When special EKGs are needed to assist in determining the type of myocardial infarction the patient is experiencing, they may be labeled differently in each institution. The terms, “15-lead” and “18-lead” EKGs, can thus mean distinct ideas. Sometimes the terms right-sided EKG (V4R, V5R, V6R) and posterior EKG (V7, V8, V9) are used. Be sure to determine which of these are used in the institution in which the health care professional has chosen to work.

Biomarkers

When patients suffer an MI, certain enzymes are released from the affected cardiac tissue. These biomarkers help to provide significant information regarding the diagnosis of an acute myocardial infarction. These are usually drawn immediately upon arrival to medical assistance and repeated in 6 and 12 hours. The presence of these enzymes is particularly helpful with NSTEMI. “False” elevations can occur with other disease processes.

  • Troponin: Released quickly and stays elevated for longer period of time (up to 5 days).
  • CK-MB: An isoenzyme of creatinine kinase—released within 3 to12 hours with a peak in 24 hours. Returns to normal within 48 to 72 hours.
  • Myoglobin: Released rapidly and may be found in urine soon after initial chest pain.

Symptoms

Patients presenting with angina or an AMI will typically complain of chest pain. It is important to help the patient to understand that “pressure” and “tightness” are “pain.” Always ask the patient if these sensations are present because they may be quick to state that no pain is present. Also, certain populations, especially diabetic patients and the elderly may not experience pain at all. Others may have atypical pain such as sharp, stabbing pains. The pain of an acute MI is present for longer periods of time and more intense than angina.

Clinical Alert

Not every patient with an AMI will portray typical symptoms such as clutching their chest. Everyone responds to pain, crisis, and fear in their own ways. Always be alert to the non-typical patient as well and ask pertinent questions in a quick, effective manner.

Other manifestations that may accompany an AMI are shortness of breath, diaphoresis, dizziness, lightheadedness, palpitations, fatigue, malaise, syncope or near syncope, a feeling of “indigestion,” upper mid epigastric pain, a feeling of “fullness,” radiation of pain to the left arm or shoulder area, jaw or neck pain, or numbness to the left arm or hand. When patients faint due to a bradycardic rhythm, this is known as a “Stokes-Adams” attack.

The patient may appear pale and feel cool or clammy to the touch, and have vital sign changes such as hypotension, tachycardia, bradycardia, increased respiratory rate, and a slight increase in temperature.

Treatment

Treatment for patients with an AMI includes prompt recognition of the problem. Every minute that passes without appropriate treatment allows for additional heart muscle to die. Health care professionals must be alert to symptoms, both specific and vague. Treat dysrhythmias that arise with proper interventions. Be sure to attach monitor patches and obtain an EKG immediately upon arrival. Oxygen should be supplied as per institution policy. Utilize a cardiology consult and transfer the patient if necessary depending on the needs of the patient and the services supplied by the institution.

Clinical Alert

The use of nitroglycerin for chest pain is standard procedure. Always have intravenous access before administering nitroglycerin. Patients can respond to the vasodilatory effects of this medication with negative effects such as hypotension. It is not unusual for blood pressures to drop significantly after either sublingual or spray nitroglycerin. If this occurs, be prepared to administer a small bolus of normal saline to counter the vasodilatory effects. Other side effects include headache and the more uncommon reflex tachycardia. These effects are usually short lived due to the short half-life (2-3 minutes) of this medication. Also ask patients about the use of medications for erectile dysfunction since the combination of these can cause very strong episodes of hypotension. Some of these medications are also now being used or explored for their positive outcomes for females.

Other treatment options for these patients includes the use aspirin or clopidogrel (Plavix), glycoprotein IIb-IIIa inhibitors, beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, thrombolytic medications, percutaneous angiography with stent placement, angioplasty, or atherectomy, coronary artery bypass graft, or the use of a balloon pump.

Conclusion

AMI are a major cause of death and disability in the United States. The most common reason for this event in the adult population is atherosclerotic coronary artery disease. Major points from this chapter include the following:

  • Plaques develop below the intimal layer of coronary arteries and then break through the layer to cause narrowed passages for blood flow.
  • Two major arteries supply blood to the heart—the right and left coronary arteries.
  • Branches from the two main arteries encircle the heart.
  • A “left dominant” individual will have the PDA arise from the circumflex branch of the left coronary artery.
  • A “right dominant” individual will have the PDA arise from the right coronary artery.
  • The usual etiology for a myocardial infarction is atherosclerotic heart disease; however there are other reasons for patients to have an MI.
  • Acute coronary syndrome is divided into unstable angina, NSTEMI, and STEMI.
  • Stable angina occurs with activity and is relieved by rest or the use of nitroglycerin.
  • Unstable angina occurs after very slight exertion or at rest.
  • Prinzmetal’s angina is another form of angina that occurs due to coronary artery spasm and is not associated with activity.
  • NSTEMI is diagnosed initially based on increased levels of biomarkers.
  • STEMI will carry the injury pattern of ST elevation in the affected areas of the heart.
  • An inverted T wave is an indicator of ischemia.
  • In early stages of an AMI, the T wave can be hyperacute.
  • There are three areas of infarcted tissue—the zone of ischemia, the zone of injury, and the zone of infarction.
  • Elevated ST segments do not show actual damage.
  • Reciprocal changes occur in areas opposite of where the actual injury is occurring.
  • Pathologic Q waves indicate infarcted myocardium.
  • A pathologic Q wave is greater than 0.04 seconds in width or one third the overall QRS height.
  • Lead aVR is not used to determine changes associated with myocardial infarctions.
  • Contiguous leads mean that leads look at similar parts of the heart.
  • When determining the site of the infarction, both the arteries involved and the leads that “look” at the area are involved.
  • An anterior MI will show changes in V1, V2, V3, and V4 and involves the left coronary artery (LCA) and the left anterior descending artery (LAD).
  • An infarction of the left coronary artery is called “the widow maker.”
  • A lateral MI involves the circumflex artery and is shown as changes in leads I, aVL, V5, and V6.
  • A septal MI is seen in leads V1 and V2 and involves the LAD.
  • An inferior MI is seen in leads II, III, and aVF and the artery blocked is the posterior descending branch of the right coronary artery.
  • A right ventricular infarct can accompany an inferior MI.
  • A right-sided EKG must be done to see the ST elevation in a right ventricular infarct.
  • The triad of symptoms with a right ventricular infarct is: hypotension, increased jugular venous distention (JVD), and clear lungs.
  • A posterior MI is seen with reciprocal changes in leads V1 and V2.
  • Posterior leads—V7, V8, and V9—must be done to visualize the ST segment elevation in a posterior MI.
  • Biomarkers are enzymes that are released from infarcted tissue and help to make the diagnosis of an acute myocardial infarction.
  • The three biomarkers used in AMI are: troponin, CK-MB, and myoglobin.
  • Patients will usually present with chest pain when an MI is present, but not every patient will actually have chest pain or recognize it as such.
  • Other symptoms that are associated with an MI are: shortness of breath, lightheadedness, dizziness, sweating, syncope or near syncope, “indigestion,” and arm, neck, and jaw pain.
  • Stokes—Adams attack occurs when a patient has a syncopal event due to a slow heart rate.
  • Treatment options for patients with an AMI include: oxygen, nitroglycerin, aspirin, or clopidogrel (Plavix), treating dysrhythmias, beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, thrombolytics, angiography, stents, angioplasty, atherectomy, coronary artery bypass grafting, and balloon pump.

Leave a Reply

Your email address will not be published. Required fields are marked *