This ECG shows a common manifestation with inferior wall M.I., BRADYCARDIA.  We see the signs of acute inferior wall M.I. in the inferior leads:  II, III, and aVF all have ST segment elevation.  There almost appear to be pathological Q waves in Leads III and aVF.  There are still VERY tiny r waves, and the downward deflections are not wide, but should full-blown Q waves develop in these leads, they would signify necrosis in the area.  A repeat ECG would certainly be warranted. 

Another sign that there is an inferior wall STEMI is the ST segment depression in Leads I and aVL, which are reciprocal to Lead III.  ST depression can have many meanings, but when it is localized in the leads which are opposite ST elevation, it is reciprocal.  There is also ST depression in Leads V1 and V2.  These leads are reciprocal to the POSTERIOR wall, otherwise known as the upper part of the inferior wall.  If an inferior wall M.I. is large enough, it can produce ST elevation in the posterior leads (not performed in this case), and ST depression in the anterior leads, especially V1, V2, and V3. 

The rhythm is a marked sinus bradycardia, at just under 40 beats per minute.  Sinus bradycardia is very common in inferior wall M.I., because the inferior wall and the sinus node are usually both supplied by the right coronary artery.  AV blocks can also occur because the AV node is also supplied by the RCA in most people. 

It is important to remember that bradycardia does not always need to be treated.  In patients with acute M.I., a well-tolerated bradycardia may actually be beneficial to the injured heart, reducing supply/demand ischemia.  A well-tolerated bradycardia is a rate that does not produce low blood pressure and poor peripheral perfusion.  Some people tolerate rates in the 40’s quite well.  If the patient shows signs of poor perfusion: low BP, decreased mentation, pallor, shortness of breath, the rate should be cautiously increased with medication or electronic pacing.  

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.   

This ECG shows two obvious abnormalities, right bundle branch block AND inferior wall M.I.  It is also a good teaching example of how the terminal wave of RBBB can be mistaken for the ST elevation of M.I.

First, check this ECG to see if it meets the criteria for right bundle branch block:

1)  The QRS will be wide. That is, it will be greater than or equal to .12 seconds (120 ms).  In this case, the QRS is 134 ms.

2)  The rhythm will be supraventricular.  Supraventricular rhythms originate from above the ventricles.  This ECG has P waves before each QRS.  Even though the rhythm is irregular, slowing down during this recorded period, it is a sinus rhythm.

3)  The QRS will have a terminal wave after the "normal" part of the QRS.  This represents the right ventricle depolarizing late.  It is very easily seen in V1, which normally has an rS pattern, and with RBBB has an rSR' pattern, making it appear upright.  V6 and Lead I will show this terminal wave as a wide little s wave.

As mentioned, there is also an acute inferior wall M.I. here.  The ST segment elevation in Leads II, III, and aVF are actually quite subtle.  The flat top of the ST segments gives them away as abnormal, along with the associated ST elevations in V5 and V6, and the reciprocal ST depressions in V1 through V3.  Normally, in IWMI, there will be reciprocal ST depressions in Leads I and aVL, but the elevations they are reflecting are very subtle, and so, therefore, are the depressions. 

The tricky thing about this ECG is that you must look carefully at the inferior wall leads to see the true ST elevation, which, as mentioned, is subtle.  The RBBB terminal wave of the QRS complexes in Leads III and aVF is upright, and is often mistaken for ST elevation.  Remember, ST segments are smooth from the end of the QRS to the peak of the T wave.  See the detail illustration.

This ECG is suitable for your classes from beginner level (rate variation in sinus rhythm) through advanced (clinical significance of RBBB in acute M.I.).  It also offers an example of reciprocal ST changes, and of a situation where the inferior leads II, III, and aVF are related to the low lateral leads V5 and V6 by a shared blood supply.

If you are an ECG instructor, it is important that you address the subject of artifact on the ECG.  Artifact has many causes, and it is important eliminate it whenever possible.  We should strive for the "cleanest" ECG possible.  As you can see in this example, the presence of artifact has caused the machine's computer rhythm interpretation to be incorrect.  The noisy baseline has caused the computer to call this rhythm "atrial fibrillation", but we clearly see P waves in all leads, especially in Lead II.  We recognize these P waves as authentic because they are regular, they  all look alike, and they have the same relationship to the QRS complexes each cycle (PR interval is the same).  

The patient is suffering a very large M.I., showing as ST segment elevation in Leads II, III, aVF, with slight elevation in V5 and V6.  In addition, Leads V1 through V3 have definite  ST depression, indicating extension of the inferior wall injury up the posterior wall of the heart.  There has been quite a bit of discussion lately in the literature about whether to call this a "posterior" M.I, or "high lateral", or just "inferior".  Semantics aside, the involvement of so many leads tells us that this  is a large M.I.  The patient was in the Emergency Dept. complaining of chest pain.

It is fortunate that the artifact did not affect our ability to see the ST elevation, but it could have.  And, of course, we would not want to treat this patient's "atrial fib" based on the machine interpretation.  But, it is always prudent to try to get rid of artifact.  In this example, Lead III has no artifact, so it could be assumed that the right arm electrode is the culprit, as Lead III does not utilize the RA electrode, and the other leads do.  

Troubleshoot for the cause of the artifact, and then retake the ECG.  Some common causes of baseline  artifact of this nature include:  patient movement, loose electrode, dried electrode, something touching the electrode, faulty or broken lead wire, and poor skin contact due to substances on the skin.  The electrodes should be fresh from the package, and applied to skin that is clean and dry.  The patient should be encouraged to relax and hold still (not so easy for a patient in distress).  Others at the bedside should avoid touching or manipulating the limbs of the patient during acquisition of the ECG data.  This only takes about 10 seconds.  I have seen artifact many times when a patient's blood was being drawn during the ECG, and the patient was squeezing his fist for the phlebotomist.