Evolution of Acute Myocardial Infarction

Non-STEMI

• ST depression can be seen with acute coronary syndrome, (non-Q non-ST infarction) and can also be seen as a chronic finding in hypertrophy or bundle branch block.
• Drugs such as digitalis can depress the ST segment as well as atrial repolarization waves (Ta waves)
• T wave abnormalities can be seen in over 60 situations, thus the term “nonspecific”. A significant inverted T wave with symmetrical shape is typical of ischemia especially in Leads I and V4-V6. Inverted T waves can be normal in V1-V3, especially in children and woman.

 

ST segment depression may be nonspecific, as well as an important index of myocardial ischemia. ST segment depression may indicate subendocardial (non-Qwave) infarction or may be present as a reciprocal change in leads opposite the are of acute injury. ST segment depression can be seen during anginal attacks or during a positive stress test. Identical ST segment alteration in the lateral as well and inferior leads can be produced by the effects of antiarrhythmic medications, such as digitalis and quinidine. Other conditions such as hypothermia and electrolyte imbalances-principally hyperkalemia or hypokalemia-affect wave forms and segments.

Left ventricular hypertrophy is seen on the lateral leads of the 12-lead ECG as ST segment depression. Such changes over the right precordial leads are slightly more reliable for specific pathologic conditions, present with right ventricular hypertrophy and infarctions of the true posterior wall. ST segment abnormalities may also be a normal variant in up to 20 percent of otherwise healthy females.

T Wave Changes

The T wave contour is susceptible to many extra cardiac factors. T-wave inversion or flattening in nonspecific for ischemic heart disease, but the presence of deep, symmetric T-wave inversion is somewhat more suggestive of the diagnosis of ischemia. T-wave contour is not only affected by many pathologic cardiac conditions but may also be altered by exercise, hyperventilation, food ingestion, smoking or significant electrolyte disturbance.

The normal amplitude for T-wave excursion has never been firmly established. In precordial T-waves the are greater the 10mm in deflection, however, hyperkalemia should be highly suspected. They may also be seen in the right precordial leads in patients with left ventricular hypertrophy. It is because of the considerations the ST segment and T waves should be interpreted only after the QRS has been carefully analyzed.

Symmetrical T-waves inversion is a lead that normally has an upright T wave is an acute sign and may be clinically associated with ischemia. T-wave inversion that is symmetrical and greater than 5mm in depth is called nadir T waves.

Because T-wave inversion may be due to there causes, it is vital the clinician compare clinical history and patient presentation to the changes as they are noted. Cardiac causes of T-wave inversion include:

• Bundle branch block
• Ventricular hypertrophy
• Pericarditis

Noncardiac causes of T-wave inversion include:

• Electrolyte disorders
• Shock
• Positional changes as posture with dyspnea, or patients is seated in the upright rather than supine position.
• Central nervous system disorder such as subarachnoid hemorrhage and stroke.

Acute Coronary Syndrome

ST elevation greater then 1mm in leads may indicate an injury, acute myocardial infarction, paricarditis.

ST elevation (J point elevation) is also a normal variant, but new ST segment elevation is a lead facing a surface of the heart greater then 1mm is an acute sign. ST segment elevation is also known as the current of injury pattern. Again, ST segment elevation greater then 1mm in the limb leads and greater then 2mm in the pericardial leads indicates an evolving AMI until proven otherwise. ST segment elevation is usually evident soon after transmural injury is recognized so that the steps in reperfusion can be implemented as quickly as possible.

ST elevation (J point elevation) is also a normal variant, but new ST segment elevation is a lead facing a surface of the heart greater then 1mm is an acute sign. ST segment elevation is also known as the current of injury pattern. Again, ST segment elevation greater then 1mm in the limb leads and greater then 2mm in the pericardial leads indicates an evolving AMI until proven otherwise. ST segment elevation is usually evident soon after transmural injury is recognized so that the steps in reperfusion can be implemented as quickly as possible.

Recall that myocardial ischemia may be indicated by ST depression in a reciprical leads. It is critical to assess clinical presentation and the ECG in one of the valuable tools in making a diagnosis of ischemia, injury and infarction. The clinician must be vigilant and maintain a high index of suspicion of any patient who presents with chest pain of any description. ST elevation in contiguous leads points to the problem. Reciprical (minor image) ST depression in a lead opposite the surface helps confirm the problem. True reciprocals may not always be present.

 

ST segment elevation related to myocardial injury usually appears convex or coved. Sometimes this is referred to a positive ST segment coving. Following acute infarction, or when resolution of ischemia has taken place, the ST segment usually returns toward baseline; this is usually occurs in the first 72 to 96 hours after damage.

 

To summarize, one of the following criteria is necessary to make the diagnosis of transmural injury.

1. elevation of the origin of the ST segment in 0.004 second past the J point and of greater then or equal to 1mm in two or more limb leads or pericardial leads V4-V6 or greater then or equal to 2mm in two or more pericardial leads V1-V3.

2. Depression of origin of the ST segment at the J point of greater than or equal to 1mm in two leads V1-V3 with ST elevation greater than 1mm in two or more leads V4-V6.

Other cardiac conditions that cause ST segment elevation include. Pericarditis ST elevation is marked by a flat or concave ST segment and usually accompanied by T-wave elevation and depression PR segment. Ventricular Aneurysm ST segment elevation that does not return to baseline over time.

Abnormal U Waves

Prominent U waves suggest hypokalemia and inverted U waves are seen with acute ischemia, hypertrophy, or digitalis.

An abnormal U wav is a frequent mark of ischemic heart disease. It is most often recorded in leads I and II, and in precordial leads V5 and V6. Negative U waves is seen in 10 to 60 percent of patients with AMI, and in up to 30 percent of patients with inferior MI. The appearance of a negative U wave may precede other ECG changes of infarction by up to several hours.

Q Waves

A Q wave should reach 0.04 second wide to suggest infarction. The more the leads showing infarction Q waves, the more secure the diagnoses.

Q waves are absent in most leads in the normal ECG. A word of caution, however; there are small Q waves commonly present in leads I, aVL aVF, V5 and V6. Significant, pathologic Q waves are wide, greater than 0.04 seconds in duration, and a least one-quarter of he amplitude of the entire QRS.

In AMI the foremost changes of the QRS complex is the development of a Q wave. The new Q wave will be seen in those leads that explore the particular area of infarction. Necrotic tissue has no polarity; thus with acute myocardial necrosis, the forces of the depolarization are no longer generated in the damaged areas. The remaining forces of the ventricular depolarization are accentuated, displacing the mean ORS vector in each lead system away from the zone of necrosis. The forces of depolarization will be seen moving away, and a Q wave or negative deflection will be recorded. The lead system closest to the infracted tissue will record the most significant Q waves. At the same time, the reciprocal leads will show initial positive deflection. While the necrotic area is no longer capable of depolarization, contraction, or repolarization, it is still surrounded by area of ischemic myocardium, completely depolarized with each ventricular activation.

 

In the patient that presents with chest pain, a detailed clinical history including history of preset illness, past medical conditions, and family history of risk factors and accurate reporting of the ECG to include ST-T and QRS configuration is necessary. Prompt application of the 12-lead ECG on any patient with chest pain is necessary to ensure the transmission of data, accurate reporting , and diagnosis are available for rapid intervention.

Transmural infarctions (full thickness infarctions) produce Q waves. While the presence of Q waves is the hallmark of infarctions, there is no way to determine whether Q waves represent an evolving event, a recent event, or are a historical sign of old infarction. Thus, a detailed clinical history and accurate reporting of the QRS configuration are critical. A request for previous ECGs for comparison is always advisable.

 

Q waves will persist over time. While they occasional decrease in size, rarely do they resolve completely. Other conditions can produce pathological Q waves, including ventricular hypertrophy, diffuse myocardial disease, and the fascicular blocks.

Absence of Q waves dose not rule out MI. The MI that does not involve all three layers of the heart is called nontransmural and often Q waves are not present in the leads reflecting the infarction.