Another post written by Pendell Meyers, with edits from Dr. Smith:
A male in his late 40s presented with nausea, vomiting, and epigastric abdominal pain of several hours duration. An ECG was recorded from triage:
The ventricular rate is 160 bpm and regular with narrow complex. Rhythm differential is therefore sinus tachycardia, SVT (AVRT, AVNRT, etc), or atrial flutter. There is clear ST elevation present in V4-V6, as well as II, III, and aVF. No clear reciprocal changes in aVL, however with this distribution you could consider a very rare case in which high lateral STE cancels out reciprocal STD.
Because of many prior examples of this phenomenon on this blog, this ECG was immediately recognized by two separate physicians who reviewed this ECG shortly after his presentation. The cath lab was not activated. Rather, they started to treat the patient's atrial flutter (as well as the underlying cause of his pain and vomiting).
Atrial flutter causes undulating of the baseline, frequently simulating ST elevations and depressions.
See these other cases where atrial flutter mimicked ST elevations or depressions:
If this diagnosis did not come easily to you, here is how they knew:
Here are some general principles:
First, STEMI generally does not cause tachycardia unless there is cardiogenic shock.
While normal heart rate has zero predictive abilities for ACS, a rapid heart rate in ACS means there is compensation for low stroke volume (low ejection fraction). This should be readily evident on bedside echo. If there is normal or hyperdynamic function, then there is something else going on.
Second, tachycardia often distorts the ST segment, mimicking STEMI.
Third, demand ischemia (type 2 MI) can have such severe ischemia that it results in ischemic ST elevation that is NOT due to ACS. So you have to identify and treat that other problem (dysrhythmia? bleeding? dehydration? sepsis? PE?) first and then re-evaluate.
Fourth, the ST elevation may not really be the ST segment, as in this case.
What the physicians saw:
With a regular narrow complex tachycardia at 160 bpm, you should immediately begin trying to differentiate ST vs. SVT. vs. atrial flutter. Go to the bedside and watch the rate and the monitor. SVT and atrial flutter generally will show constant rate, whereas sinus tachycardia will float up and down. In atrial flutter, you will occasionally glimpse a single dropped beat in the rhythm (brief 3:1 instead of 2:1), exposing a tiny flutter wave for just an instant that you may see on the monitor. Vagal maneuvers such as the REVERT maneuver offer a quick and feasible diagnostic maneuver at bedside. Lewis leads are another option.
Look closely at the ECG. In general lead V1 and the inferior leads will show the clearest evidence of atrial flutter. In atrial flutter, the P-waves in V1 are often fully upright, which cannot happen in sinus rhythm (sinus rhythm always has a negative component due to left atrial depolarization because the impulse from the SA node must travel away from V1 to reach the left atrium). Atrial flutter typically has fully upright P-waves in V1, as here.
Furthermore, you must train your eyes using these examples to be able to "subtract the QRS complexes out", and see what pattern emerges without them. Below are some close-ups using different methods to explain this.
A repeat ECG is slightly more obvious, but still 2:1 conduction throughout:
The treating physicians were convinced of atrial flutter. They were about to give diltiazem when the patient had an episode of severe vomiting, and a rhythm change was noted with each bout of vomiting, so this ECG was recorded:
Increased vagal tone to the AV node in the setting of vomiting is likely responsible for this brief increased AV block. Clearly the diagnosis of atrial flutter is confirmed in leads V4-V6 during the break in the rhythm.
The patient received several rounds of diltiazem IV pushes, but continued to have 2:1 flutter, and ultimately required a diltiazem drip. On the drip another ECG was recorded:
Initial troponin I was barely elevated at 0.03 ng/mL (0.01 is considered "elevated" for our assay). Potassium was 3.1 mEq/L.
CT scan confirmed the clinical suspicion of small bowel obstruction. The atrial flutter was treated by treating the underlying causes of bowel obstruction, repleting electrolytes, and temporizing with AV nodal blockade. Repeat troponins were all unchanged at 0.03. The patient did well.
Learning Points:
1) Atrial flutter can mimic ST elevations or depressions.
2) Atrial flutter can be determined based on a combination of ECG and bedside clinical characteristics, as well as bedside diagnostic maneuvers such as Lewis leads, vagal maneuvers, and adenosine.
3) When there is apparent ST elevation in a patient with tachycardia, look for other causes than ACS.
A male in his late 40s presented with nausea, vomiting, and epigastric abdominal pain of several hours duration. An ECG was recorded from triage:
 | |
|
The ventricular rate is 160 bpm and regular with narrow complex. Rhythm differential is therefore sinus tachycardia, SVT (AVRT, AVNRT, etc), or atrial flutter. There is clear ST elevation present in V4-V6, as well as II, III, and aVF. No clear reciprocal changes in aVL, however with this distribution you could consider a very rare case in which high lateral STE cancels out reciprocal STD.
Because of many prior examples of this phenomenon on this blog, this ECG was immediately recognized by two separate physicians who reviewed this ECG shortly after his presentation. The cath lab was not activated. Rather, they started to treat the patient's atrial flutter (as well as the underlying cause of his pain and vomiting).
Atrial flutter causes undulating of the baseline, frequently simulating ST elevations and depressions.
See these other cases where atrial flutter mimicked ST elevations or depressions:
Is this inferor STEMI?
Atrial Flutter with Inferior STEMI?
If this diagnosis did not come easily to you, here is how they knew:
Here are some general principles:
First, STEMI generally does not cause tachycardia unless there is cardiogenic shock.
While normal heart rate has zero predictive abilities for ACS, a rapid heart rate in ACS means there is compensation for low stroke volume (low ejection fraction). This should be readily evident on bedside echo. If there is normal or hyperdynamic function, then there is something else going on.
Second, tachycardia often distorts the ST segment, mimicking STEMI.
Third, demand ischemia (type 2 MI) can have such severe ischemia that it results in ischemic ST elevation that is NOT due to ACS. So you have to identify and treat that other problem (dysrhythmia? bleeding? dehydration? sepsis? PE?) first and then re-evaluate.
Fourth, the ST elevation may not really be the ST segment, as in this case.
What the physicians saw:
With a regular narrow complex tachycardia at 160 bpm, you should immediately begin trying to differentiate ST vs. SVT. vs. atrial flutter. Go to the bedside and watch the rate and the monitor. SVT and atrial flutter generally will show constant rate, whereas sinus tachycardia will float up and down. In atrial flutter, you will occasionally glimpse a single dropped beat in the rhythm (brief 3:1 instead of 2:1), exposing a tiny flutter wave for just an instant that you may see on the monitor. Vagal maneuvers such as the REVERT maneuver offer a quick and feasible diagnostic maneuver at bedside. Lewis leads are another option.
Look closely at the ECG. In general lead V1 and the inferior leads will show the clearest evidence of atrial flutter. In atrial flutter, the P-waves in V1 are often fully upright, which cannot happen in sinus rhythm (sinus rhythm always has a negative component due to left atrial depolarization because the impulse from the SA node must travel away from V1 to reach the left atrium). Atrial flutter typically has fully upright P-waves in V1, as here.
 |
| Fully upright P-waves in V1. |
Furthermore, you must train your eyes using these examples to be able to "subtract the QRS complexes out", and see what pattern emerges without them. Below are some close-ups using different methods to explain this.
 |
| Red arrows indicate flutter waves at exactly twice the ventricular rate. |
 |
| QRS complexes have been removed and replaced with a line showing what would be consistent with flutter waves. The influence of the superimposed T-waves cannot be edited out, and this is the only reason the flutter waves do not appear perfectly symmetric after the QRS (as they do in the ECG later in the case). |
A repeat ECG is slightly more obvious, but still 2:1 conduction throughout:
The treating physicians were convinced of atrial flutter. They were about to give diltiazem when the patient had an episode of severe vomiting, and a rhythm change was noted with each bout of vomiting, so this ECG was recorded:
Increased vagal tone to the AV node in the setting of vomiting is likely responsible for this brief increased AV block. Clearly the diagnosis of atrial flutter is confirmed in leads V4-V6 during the break in the rhythm.
The patient received several rounds of diltiazem IV pushes, but continued to have 2:1 flutter, and ultimately required a diltiazem drip. On the drip another ECG was recorded:
 |
| Atrial flutter with variable AV block. |
Initial troponin I was barely elevated at 0.03 ng/mL (0.01 is considered "elevated" for our assay). Potassium was 3.1 mEq/L.
CT scan confirmed the clinical suspicion of small bowel obstruction. The atrial flutter was treated by treating the underlying causes of bowel obstruction, repleting electrolytes, and temporizing with AV nodal blockade. Repeat troponins were all unchanged at 0.03. The patient did well.
Learning Points:
1) Atrial flutter can mimic ST elevations or depressions.
2) Atrial flutter can be determined based on a combination of ECG and bedside clinical characteristics, as well as bedside diagnostic maneuvers such as Lewis leads, vagal maneuvers, and adenosine.
3) When there is apparent ST elevation in a patient with tachycardia, look for other causes than ACS.
Steve,
ReplyDeleteExcellent case and very well-presented! Kudos to the physicians who recognized this for what it is. In my boot camps participants have asked if an occlusion involving the SA nodal artery could cause atrial flutter during an MI. I have never seen an example, though atrial fibrillation does occur at times with SA nodal artery involvement Have you ever seen or heard of such a case?
Jerry,
DeleteI don't think I have seen such a case.
Thanks for the comments!
Steve
How does small bowel obstruction causes atrial flutter?..
ReplyDeleteWell, it doesn't cause atrial flutter, and there may be no relation, just coincidence. More likely, the vomiting caused a hyperadrenergic state which initiated atrial flutter.
DeleteDr. Smith,
ReplyDeleteIn lead V1 (in the first 12 lead), would you considers those small upright waves before the QRS to be P-waves?
The idea is that they APPEAR to be P-waves, but are really flutter waves. To actually be a P-wave, the impulse should originate in the sinus node. But it doesn't. And if it originates in the sinus node, the wave should be biphasic, not fully upright. That is how you can very easily recognize this as flutter.
Delete