Conclusion: Rate Related VS Primary ST-T Changes


This is the conclusion to our previous case, RATE RELATED VS PRIMARY ST-T CHANGES“. Check it out before you read this final portion.


This was the initial 12 lead ECG obtained by EMS prior ED arrival:

Scan_20140922 (5)There is an irregularly irregular tachycardia with no signs of P waves, which the Lifepak 15 determined to be Atrial Fibrillation with Rapid Ventricular Response (RVR), however, V1 also appears to have the presence of Flutter waves, so the possibility of A-flutter is present. There is evidence of subendocardial ischemia, seen as generalized ST segment depression and slight ST segment elevation in aVR. There are also signs of Left Ventricular Hypertrophy (LVH). There is normal frontal axis with good R wave proggression.

Remember there are multiple things that can cause an irregularly irregular rhythm, not just A-Fib, such as:

  • Wandering Atrial Pacemaker
  • Multifocal Atrial Tachycardia
  • A-Flutter with variant conduction
  • Premature impulses

Although this patient presented with Chest Pain and considered unstable by “ACLS guidelines”, no other changes where noted by field personnel, and Syncronized Cardioversion was not performed. This patient was placed on O2 at 15 Lpm via Non-rebreather mask, peripheral IV access obtained and given 324mg ASA.

This was the first 12 lead ECG obtained in the ED:

final ed 1

The ST segment depression is evolving in both precordial leads (V3-6) and frontal plane (limb leads), however the rhythm remains irregularly irregular.


Now, lets get to the main question: Are these primary ST segment changes, meaning, due to ischemia (occlusion/vasospasm), or are these rate related changes?

All of these are possibilities, when we take into consideration, age, medical history, signs and symptoms and other risk factors. Certainly, Left Main Coronary occlusion, Multi-vessel or 3  vesssel diesease and Proximal LAD occlusion, can cause these generalized ST segment changes when there is partial blood flow reduction to all these areas, however, most likely, there is no complete occlusion, as this would lead to infarction causing ST segment elevation over time, and most of these cases do not survive. It is just tough to accurately determine the cause with this rate.

The patient was treated with 20mg Diltiazem followed by 10mg over 1 hr,  .25mg Digoxin followed and a total of 10 mg Morphine for chest pain with overall resolution of both rhythm and pain.

For further on Digoxin, click on the link:  Understanding Digoxin

This is the post-treatment 12 lead ECG:

Scan_20140922There is a sinus rhythm with minimal LVH voltage criteria, supported by Left Atrial Enlargement or Abnormality (LAE or LAA). The R wave progression has not changed, but the ST segment depression has resolved.

All Primary ECG changes have resolved after rate reduction and no coronary artery abnormalities were found during angiography.


 Elevated heart rates have been found to increase Myocardial Oxygen Consumption (MvO2) progressing to cardiac ischemia, reducing Cardiac Output, exacerbate other complications such as Congestive Heart Failure and increasing discordant ST segment elevation in LBBBs among other findings.





  • Anonymous says:

    I am wondering why all these cardiac patients in the discussions still receive oxygen so frequently? My guidelines state only administer if <94% to achieve 94% or above unless they have COPD. My understanding is this guideline is based upon evidence of high flow 02 causing coronary vasoconstriction therefore increasing ischemia. So what's the deal, why so much 02 all the time!?

  • Anonymous2 says:

    It is misconstrued that medics are titrating oxygen to prevent exacerbating ischemia from vasoconstriction…too much oxygen consumption demands more work on damaged tissue not allowing for it to heal causes more damage….same concept is used for induced hypothermia after cardiac arrest…this example is of oxygen deprived heart not yet damaged…it was hard to see but I didn’t see ST elevation

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