A 50 year old man with sudden altered mental status and inferior STE. Would you give lytics? Yes, but not because of the ECG!

Submitted by Alex Bracey, written by Pendell Meyers

A man in his 50s was hunting with a friend when he suddenly "fell out" (similar to syncope), but then did not return to baseline, and instead had persistent altered mental status. His friend was able to get him into the truck and drive him to a nearby community hospital (non-PCI center). 

When he arrived, his mental status had deteriorated further, to the point that he was quickly intubated on arrival. After intubation, vital signs were all within normal limits. He was quickly rushed to the CT scanner and a noncontrast head CT was completely normal.

Side note: The differential of sudden persistent loss of consciousness with adequate hemodynamics is relatively short: seizure, intracranial hemorrhage, basilar artery occlusion. After a negative noncontrast head CT the next step is looking for a hyperdense basilar artery sign AND to perform a CT cerebral angiogram).

An ECG was recorded quickly on return to the ED:

(sorry for poor quality, cannot get originals)

What do you think?

There is a narrow complex regular rhythm at a rate of approximately 120 bpm. There is the appearance of STE in inferior leads II, III, and aVF (with STD in aVR), but this is entirely due to flutter waves which are only seen in those leads. 

Also, the atrial flutter in this case is relatively slow like in many other cases we've shown. Normal atrial size and conduction rate typically results in a flutter circuit of about 300 bpm, with 2:1 conduction causing resultant ventricular rate of about 150 bpm. Here the flutter rate is approximately 240 bpm, with ventricular rate around 120 bpm. This implies a large atrium, slowed conduction (due to, for instance, Na channel blocking agents), or both.

We have shown countless examples of this same phenomenon (atrial flutter mimicking inferior STE or STD). We have also shown several cases in which atrial flutter hides true, active ischemia.

Christmas Eve Special Gift!! Prehospital Cath Lab Activation: What do you think?

Global ST depression with ST elevation in aVR - what is the cause?

Is this inferor STEMI?

Tachycardia and ST Elevation.

Atrial Flutter with Inferior STEMI?

Atrial Flutter Mimicking ST Depression

What is the Diagnosis?

Inferolateral ST elevation, vomiting, and elevated troponin

The treating team did not identify the flutter waves and they became worried about possible "STEMI" (despite the unusual clinical scenario). They called their transfer center cardiologist on call, who reviewed the case on the phone with them, as well as the ECG. The EM provider asked if the cardiologist thought it was a "STEMI." The cardiologist also did not see atrial flutter, and advised giving thrombolytics for perceived "inferior STEMI."

The patient received thrombolytics and then was transferred to the PCI referral center. 

On arrival to the PCI center's Emergency Department, the receiving team recorded an ECG on arrival:

Persistent atrial flutter, however this time the QRS occurs on a slightly different portion of the flutter wave. In my opinion this makes the flutter waves slightly easier to recognize in this ECG.

Atrial flutter was recognized at this time. On arrival, apparently the patients mental status was improved compared to his initial presentation, because he was noticed to be pulling at his tube and gagging, requiring sedation.

The case was reviewed by the receiving team who had concerns for acute stroke or other cause of acute altered mental status. 

A CT angiogram of the head and neck was performed which showed a basilar artery thrombus which was concerning for brainstem stroke as the inciting cause. There was again no intracranial hemorrhage. Serial troponins were negative. 

The patient was admitted for stroke management. No obvious adverse events were attributed to the thrombolytics. Long-term outcome is unknown.

Thus, it seems that two mistakes may have inadvertently led accidentally to the appropriate administration of thrombolytics!! They mistook atrial flutter for STEMI, and did not recognize the clinical presentation of basilar artery occlusion. Correct, but for the wrong reason!

So the answer to the title of this post is: "Yes, I have a patient with a devastating stroke, and I do not have neurointerventional capabilities, so I will give thrombolytics!"

Discussion

Flutter waves are well known to mimic ST deviations, as well as to hide true ischemic ST deviations from the interpreter. In many cases of flutter waves mimicking ST deviations, the expert electrocardiographer can see the morphology of the flutter waves as the cause of apparent STE or STD. Likewise, in some cases of ischemia concealed by flutter waves, the ischemia can be seen despite the flutter waves, whereas in other cases the dysrhythmia must be terminated before the ischemia can be clearly distinguished. 

Even when flutter waves conceal true ST segment deviations, the cause and effect relationship may be unclear. Tachycardia to this degree can cause ST segment changes in several ways. First, there can simply be diffuse STD (which obligates reciprocal STE in aVR) associated with tachycardia, which are not even necessarily 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 STD of subendocardial ischemia, of course with accompanying reciprocal STE in aVR. Finally, if a region of the myocardium supplied y a severely flow-limiting (but not necessarily 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, ACS may not even be present.