12-LEAD ECG's - A "Web Brain" for Easy Interpretation

             

  
   

Infarction and Ischemia

One of the most important reasons for obtaining an ECG is to help evaluate the patient who presents with new-onset chest pain.  By doing so we hope to determine:

  • If any acute changes are present.

  • If there is evidence of prior infarction.

Specifically, we want to determine if the patient being evaluated is acutely infarcting or ischemic. If so, what area of the heart is involved, how extensive is the involvement, are other abnormalities present (i.e., AV block, conduction defects, arrhythmias) and most importantly, is the patient a candidate for acute intervention (i.e., with thrombolytic therapy or angioplasty)?

KEY Point

Be aware that as many as 1/3 of all infarcts are "silent" MIs (i.e., not associated with chest pain).  Instead there may be dyspnea, mental status changes, or no symptoms at all. Use of a prior ECG may be invaluable for determining if abnormalities seen on a current tracing are new or old.  To facilitate comparison, fax tracings.

 

Acute Infarction: What are the Changes?

There are 4 principal ECG indicators of acute infarction:

  1. ST segment elevation

  2. T wave inversion

  3. Development of Q waves

  4. Reciprocal ST segment depression.


A and B (figure below right)
show a normal QRS complex before any changes develop.  Note that a small narrow q wave may often be present (as in A) as a normal finding (reflecting normal septal Q waves that are commonly seen in lateral leads).  Q waves of infarction tend to be bigger and wider.

C
shows the "hyperacute" stage, which is the earliest change of Acute MI, in which the T wave becomes broader and peaks (almost as if "trying" to lift the ST segment).  This change may be subtle (and easy
to miss!); it usually is short-lived.

D
shows conventional ST elevation follows (with ST coving/"frowny" shape) and developing Q waves.

E and F
show Q waves becoming bigger, ST elevation is maximal, and T wave inversion begins. T waves evolve as ST segments return to baseline (in F).

G
shows ST-T wave abnormalities resolving (or nearly resolving) but there is persistence of Q waves.



KEY Points regarding the ECG with Acute MI:

  • Not all patients with Acute MI develop ECG changes.  As many as 1/3 do not develop changes, especially if MI occurs in electrically silent areas of the heart.

  • The A thru F sequence in the figure above represents the "typical" evolution of Acute MI. Unfortunately, many patients don't read the textbook!  Variations on this theme are common (i.e., ST depression or T wave inversion may be the only change, Q waves don't always develop, Q waves sometimes resolve with time, etc.).

  • Non-Q wave infarctions may occur.  These tend to be "incomplete" infarctions (often not transmural) and pose a high risk for reinfarction (i.e., "completing" the infarct). Consider early revascularization !

  • Because ECG changes are not always seen with Acute MI, and serum markers (CK-MB, troponin) may initially be negative, a key determinant of whether or not to admit a patient with chest pain to the hospital must be the history.  In general, if in doubt, admit the patient to rule out Acute MI!

  • Acute ECG changes may be subtle (as in the hyperacute). Look for reciprocal changes (ST depression in leads not showing ST elevation) to help determine if ECG findings are acute. (causes of ST depression) Use the concept of "patterns of leads".  For example, if uncertain about whether a Q wave or T wave inversion in lead III or aVF is clinically significant, look at the other inferior lead (which is lead II) to see if these changes are also present (review normal variant Q waves/T inversion).


Coronary Anatomy: Relation to the Site of Infarct

The most common cause of Acute MI is sudden total occlusion of a major coronary artery.

  • Sudden total occlusion of the RCA (Right Coronary Artery) causes acute inferior MI and/or posterior or right ventricular MI (ST elevation in lead V4R helps diagnose RV infarction.). Mobitz I is common with inferior MI (the RCA supplies the AV nodal artery).

  • Sudden occlusion of the Left Main coronary artery leads to sudden death (from massive infarction).

  • Sudden occlusion of the LAD (Left Anterior Descending) artery leads to anterior infarction; bundle branch block/Mobitz II 2° AV block may be seen.

  • Sudden occlusion of the Circumflex artery leads to lateral infarction.  In about 10% of patients this artery (rather than the RCA) also supplies the inferior and posterior walls of the left ventricle.

Note -  Collateral development changes the above patterns.

 

Treatment Goals:

Since the cause of Acute MI is most often sudden total occlusion of a major coronary artery, the goal
of treatment should be to attempt to restore flow as soon as possible to the IRA (Infarct-Related Artery).

Acute angioplasty (with or without stenting) may be preferable if available (only about 20% of US hospitals have this on an emergency basis).  As a result, thrombolytic therapy is the most commonly used method for attempting reperfusion.
 

Regarding Thrombolytic Therapy:

Who Qualifies?

Ideally patients < 75 years old with chest pain and ST elevation who are seen less than 6 hours after symptom onset and who have no contraindications to thrombolysis. Criteria for thrombolysis have been expanded in selected cases to include older patients and those who are seen more than 6 hours after symptom onset.

Who Benefits Most?

Those seen earlier (ideally within 4 hours) & those with larger infarcts (i.e., anterior location/more ST elevation with more reciprocal depression).  Patients who have not yet formed Q waves (or with only small Q waves) are also more likely to benefit (greater chance of reversibility).

 

 12-LEAD ECG's - A "Web Brain" for Easy Interpretation