Arrhythmia? Ischemia? Both? Electricity, drugs, lytics, cath lab? You decide.

Written by Pendell Meyers with edits by Steve Smith

A male in his 60s presented with off and on shortness of breath and chest pressure over the past few days. He was hypertensive and tachycardic, with mildly increased work of breathing. Here is his initial ECG:

What do you think? What will you do for this patient? How many problems does he have?

When the team saw this ECG, we obviously noticed the large STE in the inferior leads, with STD in V1-V5, I, and aVL, and STE in V6. However we also noticed that the rhythm is rapid, regular, and narrow, with no P-waves, at a rate of approximately 200 bpm, and therefore not sinus rhythm in this patient in his 60s. The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenic shock" is not applicable outside of sinus rhythm. The rhythm differential for narrow, regular, and tachycardic is sinus rhythm, SVT (encompassing AVNRT, AVRT, atrial tach, etc), and atrial flutter (another supraventricular rhythm which is usually considered separately from SVTs). Therefore this patient is either in some form of SVT or atrial flutter. 

Atrial flutter, when regular, must be conducting at 1:1, 2:1, 3:1, etc. 

If 1:1, a regular ventricular rate of 200 as the result of atrial flutter would require a flutter rate of 200, and that is too slow for flutter (unless the patient is taking a type I antidysrhythmic such as flecainide, which slows atrial conduction and flutter rate). Atrial flutter in the absence of modifying medications is generally from 240-360 bpm. Furthermore, most old adult AV nodes cannot conduct at 200 bpm.

If 2:1, this would require a flutter rate of 400 bpm. This is far too fast for flutter. 

The most common case of atrial flutter results in a ventricular rate of approximately 150 bpm, due to the average size of the atria and the normal rate of atrial conduction (resulting in an atrial rate of approximately 300 bpm), combined with the typical capacity of the AV node to conduct (usually 2:1 block in the setting of an atrial rhythm going 300 bpm).

So we asked the patient if he had any new medications recently. 

He said, "I just started taking flecainide last week." Chart review confirmed that he had been started on flecainide for atrial fibrillation.

This new information makes the diagnosis of atrial flutter far more likely: first, atrial fibrillation and flutter are closely associated and, second, this makes a flutter rate of 200 bpm (with 1:1 conduction) quite likely.

Back to the interpretation of the ECG: Does the rhythm matter to you in this case? If so, why?

The rhythm does matter! For many reasons, including these:

1) The flutter waves of atrial flutter are well known to mimic ST deviations, as well as hide true ischemic ST deviations from the reviewer. In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished.

2) Tachycardia to this degree can cause ST segment changes in several ways. First, there can simply be diffuse ST depressions (which obligates reciprocal STE in aVR) associated with tachycardia which are not indicative of ischemia. Second, the increased demand created by extreme tachycardia may exceed the ability of the coronary arteries to supply sufficient blood (due to preexisting three vessel or left main disease, with or without ACS). In this case, there is diffuse ischemic ST depression of subendocardial ischemia, of course with accompanying reciprocal STE in aVR. Finally, if a region of the myocardium supplied by a severely flow limiting (but not necessarilly fully occluded) lesion suddenly undergoes massively increased demand due to acute tachycardia, the supply/demand mismatch may be so great that the tissue undergoes acute transmural ischemia, both subendocardial and subepicardial, which may result in infarction (just as in the case of classic thrombotic Occlusion MI). This case represents the same physiologic event as OMI in terms of the result on the myocardium, therefore with identical ECG features, however there may not be ACS!

So you do care what the rhythm is, and you should be wondering:

Am I being fooled into seeing ST elevations due to possible flutter waves?

Is that an obvious STEMI underneath that rhythm?

If I fix the rhythm will the ST changes resolve?

Is he even stable enough to attempt changing his rhythm? Is he unstable enough to warrant cardioversion? Do ischemic changes on ECG mean unequivocally that the rhythm is "unstable" and therefore mandate electrical cardioversion?

His vitals were: 

BP 176/92

HR 202

SpO2 98%

RR 20

Exam: Mild increased work of breathing. Mildly sweaty. Fatigued-appearing but mentating perfectly. Clear lungs. Perfused extremities.

What would you do and in what order?

Our bedside assessment of the situation was this: 

The patient did not appear critically ill or acutely unstable to us. He did not appear to be actively decompensating in front of us. We felt that we had a few seconds to think about our next move. During this time, we activated the cath lab. We believed that the ST deviations on the presentation ECG were far out of proportion and not morphologically consistent with only flutter waves mimicking STE - we thought there was truly a visible current of injury present. But we recognized that the injury pattern may be either due to OMI, or secondary to the extreme rate combined with a preexisting lesion (type II STEMI). Either way, the rhythm must be dealt with first, because it is exacerbating either form of ischemia and can be treated more rapidly than an occlusion. In the best case scenario, all ST segment deviations may cease after a few minutes of normal heart rate, making Occlusion MI less likely. Conversely, if there truly is OMI underlying the rhythm, normalization of the rhythm will expedite its discovery and management.

We discussed several pharmacologic and electrical options. We first gave adenosine 6mg. There was a temporary break in the rhythm, but artifact prevented seeing any uncovered flutter waves at this moment, then the rate immediately jumped back up to 202 bpm. 

Next we gave 15mg diltiazem IV push, which should slow AV conduction and clearly reveal the flutter waves (or, if PSVT, which is unlikely, it will convert it). Diltiazem is not terribly effective for conversion of atrial flutter to sinus, so this should not be an expected result. Approximately 1 minute later, the rhythm broke from 202 bpm into this:

The rhythm has converted to sinus! (Again, not an expected outcome with diltiazem). There is still a clear signal of focal transmural ischemia in the inferior and posterior walls. Despite the fact that the magnitude/proportionality of the ST segment changes has improved, it is difficult to distinguish the relative component of decreased rate. If you're having an OMI of the inferior and posterior walls, it makes sense that the ECG changes would be more pronounced at higher heart rates because there is even more mismatch between supply and demand. Not to mention that tachycardia makes essentially all ECG findings more dramatic, regardless of whether there is ischemia or not. 

It also takes a while for ischemia and ST segments to resolve - wait a while and repeat it, just like you would post-ROSC! 

Here is his baseline on file for comparison:

Normal ECG, complete with some normal STE in V4-V6.

The lower heart rate was maintained, as were the ST segment changes above, over the next 10 minutes in the resuscitation room. His symptoms improved with decreased heart rate, but did not fully go away.

He was taken to the cath lab.

They found the following CAD:

LAD prox 70%
LAD mid 80%
LAD distal 90%
Circumflex mid 95%
RCA prox 70%
RCA mid 90%

It seems that the angiographers identified two culprit lesions:

1) mid LCX: TIMI 3 flow initially, still 3 after intervention, thrombus present

2) mid RCA, TIMI 3 flow initially, still 3 after intervention, thrombus present

Both lesions were stented. 

Serial troponin T measurements rose from zero to 2.80 ng/mL over the next 10 hours. 

Here is the ECG after intervention:

Persistent STE in III and aVF, with persistent STD in V2-V5. However, there is terminal T-wave inversion in the inferior leads and large upright T-wave morphology in the anterior leads, signifying the changes of successful reperfusion rather than ongoing transmural ischemia.

Flecainide was discontinued. The patient did well. Although we are not electrophysiologists, we are under the impression that it is standard, or at least common,  when a patient starts flecainide to also start the patient on oral diltiazem in case the patient develops atrial flutter. We asked the patient about this, and he stated that his doctor told him to start taking flecainide in place of his atenolol. He was not instructed to take any calcium channel blocker or beta blocker with the flecainide. Perhaps this event could have been avoided. We also asked one of our electrophysiologists who states that patients should not be started on flecainide without first ruling out CAD, to prevent situations like this. 

With the report of thrombotic lesions and the magnitude of troponin rise, as well as classic ECG changes that persisted beyond correction of the tachycardia, it is possible that this patient did indeed suffer Occlusion MI or its equivalent, simultaneously with his 1:1 atrial flutter. But this is not definite because the angiogram was not done at the same time as the ECG changes suggesting OMI. 

On the other hand, it is still possible that there was actually no ACS at all. Anyone with severe preexisting stenoses with a heart rate of 200 bpm will have the same ECG and troponin findings from start to finish. Sometimes what appears to be thrombus on angiogram is not actually thrombus.

Learning Points:

Acute arrhythmias such as SVT, rapid AF, and atrial flutter may coexist and/or be caused by ischemia, or vice versa.

The ECG cannot differentiate the various etiologies of acute transmural ischemia - the myocardial cells do not know the reason for their acute lack of blood supply, they simply report that they are dying imminently. The same is true for diffuse subendocardial ischemia. You must figure this out clinically.

Flecainide slows the rate of conduction, sometimes causing an atrial rate of 200 bpm and therefore allowing 1:1 conduction with adverse results.

Sometimes you must correct the rhythm to see what lies underneath.

See these other cases:

Atrial fibrillation with rapid ventricular response with ECG injury pattern

Tachycardia and ST Elevation.

Is this inferor STEMI?

Atrial Flutter with Inferior STEMI?

What is the Diagnosis?

Atrial Flutter Mimicking ST Depression

Inferolateral ST elevation, vomiting, and elevated troponin

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My Comment by KEN GRAUER, MD (11/26/2018):

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Excellent discussion by Drs. Meyers and Smith — in which they have covered numerous aspects of this case in superb detail! I limit my comments to a number of academic and semantic concepts relating to the arrhythmia in this case:

What is an “SVT”?

There are some semantics to the term, “SVT” = SupraVentricular Tachycardia. Supraventricular rhythms are defined as arising at or above the AV node, ergo “supra” (or above) the ventricles. When the rate of such rhythms is ≥100/minute — the rhythm qualifies as an “SVT”.

• SVT is a generic, all-encompassing term that includes any rhythm arising at or above the AV node, with an average rate of ≥100/minute. This technically includes not only reentry SVT rhythms (ie, AVNRT, AVRT) and atrial tachycardia — but also atrial fibrillation (if the average rate is fast enough) — atrial flutter — MAT — junctional tachycardia — and even sinus tachycardia, among others.
• Awareness of this semantic distinction is important in communication — since clinicians all-to-often associate the term “SVT” with different meanings. Just as we need to specify what we mean when we say a patient is “lethargic” — we should clarify what we mean when we use the term SVT.
• One instance in which the generic term, “SVT” is uniquely suited — is when the rhythm in question is an, “SVT of Uncertain Etiology”. This is the situation for the initial tracing in this case (ECG #1 = TOP tracing in Figure-1). The rhythm is an “SVT” — because the QRS complex is narrow and the rate is fast. Since the rhythm is regular — the differential includes sinus tachycardia, atrial flutter, atrial tachycardia, and reentry forms of SVT.

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Figure-1: TOP ( = ECG #1) — Initial ECG in this case. BOTTOM ( = ECG #2) — The resultant rhythm after IV Diltiazem (See text). 

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What is the Rhythm in ECG #1?

As per Dr. Meyers, awareness that this patient had just been started on Flecainide for treatment of AFib, but without concomitant use of an AV nodal blocking agent — greatly increases the likelihood that the SVT rhythm in ECG #1 is the result of a proarrhythmic effect of Flecainide (ie, conversion of AFib to AFlutter with 1:1 AV conduction).

• Without the knowledge that Flecainide was started — I would have guessed the rhythm in ECG #1 was AVNRT.
• As emphasized by Dr. Meyers — administration of IV Diltiazem usually does not result in prompt conversion of AFlutter. Instead — this drug typically slows the ventricular response, which generally reveals flutter waves if AFlutter is the underlying rhythm. In those instances in which Diltiazem does convert AFlutter to sinus rhythm — it tends not to do so abruptly. Unfortunately — the KEY rhythm strip in this case (ie, moment-to-moment monitoring immediately on administering IV Diltiazem) is missing. I suspect availability of this telemetry information would have confirmed the diagnosis of AFlutter with 1:1 AV conduction. That said, without such monitoring — we can only presume the diagnosis is Flecainide-induced AFlutter with 1:1 AV conduction.

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What is the Rhythm in ECG #2?

As per Dr. Meyers — administration of IV Diltiazem converts the SVT rhythm seen in ECG #1 to a supraventricular rhythm, albeit the rate is still tachycardic at ~115/minute.

• Rather than sinus rhythm — I suspect the rhythm in ECG #2 is a low atrial rhythm. That’s because we do not see an upright P wave in lead II. Although difficult to assess due to baseline artifact — positive P waves are seen in both leads I and aVL of ECG #2, and it appears that a tiny-amplitude negative P wave is seen in lead III. Clinically, this still counts as “chemical conversion” from AFlutter to an atrial mechanism — although persistence of tachycardia in ECG #2 (at a rate of ~115/minute) raises of the question of whether this could be an ectopic atrial tachycardia ... Restoration of sinus rhythm after PCI (the 4th ECG shown above in this case) resolves the issue of what the rhythm in ECG #2 might have been.
• Assuming there is no dextrocardia or lead misplacement — sinus rhythm is defined by the presence of a conducting upright P wave in lead II. Note that an upright P wave is seen in lead II of this patient’s baseline tracing, as well as in the post-intervention tracing ( = the 3rd and 4th ECGs shown above in this case).

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Final Semantic Point:

As has been emphasized — the most common ventricular rate for untreated AFlutter is ~150/minute (usual rate range ~140-160/minute). This is because under normal circumstances, there will be 2:1 AV conduction when the AV node is confronted with 300 atrial impulses/minute.

• Rather than 2:1 AV “block” — the term, 2:1 AV “conduction” is preferred. Use of the term, “block” implies pathology. Instead, it is a physiologic function of the AV node to limit the number of flutter impulses conducted to the ventricles, since perfusion will be better with a ventricular response of ~150/minute compared to 1:1 conduction with a ventricular rate of 300/minute.

Our THANKS again to Drs. Meyers and Smith for this superb discussion!