This ECG is from a 65-year-old woman who presented to the Emergency Department with a complaint of chest pain.  We have no other clinical information. 

There are several subtle, but real, abnormalities on the ECG that should be evaluated in conjuction with her clinical situation.  This is a good ECG to discuss with your more advanced students who have mastered recognition of blatant ST elevation M.I. (STEMI).  But, let’s start with what is NORMAL here. 

NORMAL FEATURES        The normal findings are:  normal sinus rhythm at about 68 bpm.  The rhythm is regular without ectopy. The intervals are within normal limits.  The frontal plane axis is normal. The T waves are all upright. 

ABNORMAL FEATURES         There is subtle ST segment elevation in Leads V1 through V3, and in I and aVL.  The shape of the ST segments is concave upward, or normal.  In a young, asymptomatic patient, we probably would not be at all concerned about this amount of ST elevation.  However, this is an older patient with chest pain. In the chest leads, the R wave progression is interrupted, as the QRS goes abruptly from negative to positive in Lead V3.  This could be due to loss of r waves ( pathological Q waves forming) in V1 and V2 lead placement, or something else. 

This ECG is a good example of an inferior wall M.I. that was confirmed and treated in the cath lab.

The ST segments are elevated in Leads II, III, and aVF, but the amount of elevation may look subtle to some.   When the amount of elevation seems small, what other signs can help us recognize acute ST-elevation M.I.? 

PATIENT HISTORY AND PRESENTATION   This patient had acute chest pain, and was over the age of 50. We do not know his past medical history. His chest pain was described as substernal and epigastric, radiating to his back.  He had nausea and diaphoresis.  His past medical history is unknown, but it would be significant if he had a history of coronary artery disease, past M.I., smoking, metabolic syndrome, strong family history of heart disease, etc.

ST SEGMENT ELEVATION DISTRIBUTION   In acute STEMI, the elevation will be seen in “related leads”. That is, the leads that are affected will reflect a region of the heart that is supplied by the same artery. Some M.I.s are larger than others, affecting more leads, because some obstructions are more proximal than others in the artery.  This ECG shows STE in the inferior wall leads:  II, III, and aVF.  The culprit artery for this patient was the right coronary artery, which supplies the inferior and posterior wall of the left ventricle, the right ventricle, and the right atrium in the majority of people.

RECIPROCAL ST DEPRESSION   Finding reciprocal ST depression in the leads that are OPPOSITE the affected leads is a very reliable sign to confirm that the STEs are due to an acute M.I.  In fact, often the reciprocal depression is “stronger” or easier to see than the elevation.  It is important to teach your students how the standard leads are oriented to the heart, so they will recognize the 12-Lead ECG as a “map” of the heart.  The reciprocal ST depression in this ECG is seen in Leads aVL and I (subtle), which are across the frontal plane from Lead III.   We also note reciprocal ST depression in the precordial leads, especially notable in Leads V1 through V3.  This can reflect the injured area extending up the back of the heart from the inferior wall (posterior wall).  The R waves in V2 and V3 are a bit higher than normally expected, which could indicate a reciprocal view of pathological Q waves on the posterior wall.  Print the ECG out on paper, turn it upside down, and look at V2 and V3 through the back.  V2 and V3 will look like a “classic” STEMI.  This should be approximately the view you would get from additional posterior leads.

This ECG was obtained from a patient who suffered an obstruction of the circumflex coronary artery.  Unfortunately, he was in the approximately 15-18% of the population in whom the circumflex artery is dominant.  That means that it connects with the posterior descending artery, perfusing not only the lateral wall of the left ventricle, but also the posterior and inferior walls.  In this case, the obstruction is in the midportion of the artery, and the high lateral wall is spared.  The large number of leads with ST elevation indicate the large amount of myocardium affected.  Leads II, III, and aVF have ST elevation, as do Leads V3 through V6.  Lead aVL has reciprocal ST depression. The T waves in the affected leads are "hyperacute", or taller than normal.  This is usually an early change in acute M.I., and disappears after the onset of ST elevation.

It is not always easy to determine from the ECG that the circumflex artery is the culprit artery, rather than the right coronary artery, which perfuses the inferior wall in the majority of people.  Some clues are:  Lead III has ST elevation equal to that of Lead II, the low lateral wall (V5 and V6) are affected, and aVL has reciprocal depression but Lead I does not.

This is a very large M.I., due to the dominance of the circumflex artery.  The patient did not survive, in spite of aggressive treatment.

This ECG is from an 80-year-old woman who had an acute inferior wall M.I. with a second-degree AV block.
 
Some people incorrectly call ALL second-degree AV blocks that are conducting 2:1 "Type II".  This is incorrect, as Mobitz Type I can also conduct with a 2:1 ratio.  The progressive prolongation of the PR interval will not be seen with a 2:1 conduction ratio, because there are not two PR intervals in a row.

This is a good example of a Type I, or Wenckebach, block which is initially conducting 2:1.  At the end of the ECG, two consecutive p waves conduct, showing the "progressively-prolonging PR interval" hallmark of a Type I block. Type I blocks are supraHisian - at the level of the AV node - and generally not life-threatening.  Blocks that are conducting 2:1 present a danger, however, in the effect they have on the rate.  Whatever the underlying rhythm is, the 2:1 block will cut the rate in half!  This patient has an underlying sinus tachycardia at 106, so her block has caused a rate of 53.  In light of her acute M.I., that rate is probably preferable to the sinus tach. This patient’s BP remained stable, and she did not require pacing. 

The ST signs of acute M.I. are rather subtle here. Note the "coving upward" shape in Lead III, and the reciprocal depressions in I, aVL, V1, and V2.  Type I blocks are common in inferior wall M.I., since the AV node and the inferior wall often share a blood supply - the right coronary artery. 

While the print quality of this ECG is not the best, it is a great teaching ECG because it starts out with 2:1 conduction, then at the end of the strip, proves itself to be a Wenckebach block.