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.

Several Wide Complex Rhythms in One Patient. Test yourself: Will You See What I Did Not See?

This time I'm going to tell you that the case is mine because the mistakes were mine.  I sat down to write one narrative, but as I looked at all the ECGs, I realized that some of my rhythm analyses were wrong and had to write a different narrative.

Now it all looks so clear and obvious when I'm sitting down without a sick patient in front of me.

But, to test yourself, I'm going to let you look at the ECGs before I explain them:

1.  Presenting ECG in a dialysis patient feeling weak:

 2. His previous ECG:

 What treatment would you give?



















3. This happened after immediately giving Calcium:

 4. This was present after about 11 g of calcium gluconate:

 5.  Then when we though all was stable, lots of calcium in, and K was shifted, we saw this:

So here is the story:

A patient with a history of diabetes and renal failure, on dialysis, was found with a very rapid heart rate.  He was awake and responsive.  Here is the rhythm on the monitor:

There is a wide complex tachycardia.  It is difficult to diagnose without a 12-lead ECG.

  A 12-lead was obtained rapidly:

There are no P-waves.  There is a wide complex very similar to LBBB, but quite wide at 161 milliseconds.  However, the initial part of the QRS is rapid - the onset of the R-wave in right precordial leads to the nadir of the S-wave is only 60 ms, and the R-wave itself is approximately 25 ms.  Therefore this appears to be supraventricular tachycardia with aberrancy.
(It did not occur to me at the time that it might be extremely slow atrial flutter with 1:1 block, which is what I now believe it was).  
 

 There was an recent ECG for comparison:

This has very slow atrial flutter (flutter rate about 204) with 2:1 block and a PVC every 4th beat.  There is a wide complex at 135 ms, which also appears to be LBBB and has a similar morphology to the presenting ECG above.  It should have occurred to me at this point that he was still in atrial flutter, but was with a faster and more regular ventricular response due to a slower flutter rate (slower because of hyperK) that could conduct 1:1 (very rapid)!

Thus, the presenting ECG appeared to me to be SVT with LBBB that is wider than baseline.  A wide QRS is due hyperkalemia until proven otherwise, especially if it is very wide (most LBBB is not wider than 160 ms), and particularly/especially in a dialysis patient.

I considered using adenosine was but thought it prudent to start with calcium, so we gave 3 g of calcium gluconate immediately into a rapidly accessed external jugular vein.

He converted to what we thought was atrial fibrillation with RVR, (but was, in retrospect, atrial flutter with variable block) and the same wide complex.  Unfortunately, there is no image of this.

Shortly thereafter, this is what happened:

Ventricular Tachycardia

The patient continued to be responsive and have a pulse.

He went in and out of this VT rhythm spontaneously as we gave successive 3 g doses of calcium gluconate over the next 20 minutes.  This 12-lead was captured during one of the many episodes:

This QRS at 338 milliseconds duration cannot be anything but VT

Each time we gave calcium, the VT converted and stabilized for several minutes.  Dialysis was prepared.  The patient was also given intramuscular terbutaline, 2 doses of insulin and D50, bicarbonate (in spite of the risk of fluid overload), and albuterol by nebulization.

FYI--lowering of K by use of beta-2 adrenergic agonists.

--0.5 mg of IV albuterol reduces K by about 1.2 mEq/L. 

-- A 20 mg neb (most are 2.5 mg) lowers it by about 1.0 mEq/L.  

--A 10 mg neb lowers it by about 0.6 mEq/L.

-- I give 0.25 mg of IM terbutaline to an adult, but only if it is critical, and add nebulized albuterol also.  I've never given it IV, as I'm a bit reluctant to risk the cardiac irritability.

K returned at 7.5 mEq/L, repeat was 6.7 mEq/L

He seemed to stabilize in this rhythm with a much narrower QRS:

Initially I saw this on the monitor and thought it was a conversion from PSVT to atrial fibrillation.  But, looking at it again, it is obviously a very slow atrial flutter at a rate of 168, with alternating block, 1:1 or 1:2, and a resulting ventricular rate of 114.

 Shortly thereafter, he was seen to be in this rhythm:

There is a relatively narrow complex (not bizarrely wide).  There are no clear P-waves.  The rate was 171.

 On the rhythm monitor only, no P-waves could be seen and this was thought to possibly be recurrent PSVT (though of course it is very slow atrial flutter with 1:1 block, as I can see now).  6 mg of adenosine was given without effect.

Then, 12 mg, of adenosine were given rapid push.

This was the result:

Recurrent VT (which had been recurring many times in this case)

Pulses were still intact.  More calcium was given.  The patient was intubated also.

The patient went back into this rhythm:

Same "SVT" as before.  (Really, it is slow flutter with 1:1 block)

A 12-lead was obtained:

There appear to be P-waves in V1.  They are upright, which suggests atrial flutter.  We know the previous atrial flutter rate was 168 (close to 171), so this is now atrial flutter with 1:1 conduction.

I (erroneously) thought the patient was in sinus tachycardia.  Then the question then was "why is this patient in sinus tach?"  A bedside ultrasound showed very poor EF and it appeared to be cardiogenic shock.  BP was  recorded as 214/143 by cuff, so afterload reduction was going to be started.  An arterial line was placed and the real BP was 80/50.  No afterload reduction was done!!

Dialysis was ready and he went for emergent dialysis.  Shortly thereafter, his AV node began to block some of the flutter impulses, and the ventricular response slowed.  This was recorded less than 2 hours later.

Slow atrial flutter with 2:1 block, PVCs, and a narrower LBBB.  K was normalizing.

Why was the flutter rate so slow?   It is uncertain.  He was on no Na channel blocking agents.  But hyperkalemia will slow atrial flutter.  Thus, his initial atrial flutter was much slower than baseline (160 vs. 204), but after treatment for hyperkalemia, the rate was 170.  At either rate, 160 or 170, the flutter is slow enough to conduct 1:1 and result in a very fast ventricular rate.

Slowest possible Atrial Flutter Rate

Our electrophysiologist says he has mapped atrial flutter as slow as 140.  This was new to me.  I did not consider atrial flutter because it was so slow.  K. Wang has an ECG with the flutter rate (not ventricular rate) at 150 in a patient taking Procainamide.

The Paradox: although the calcium was necessary to treat the VT, it also allowed the flutter rate to increase.  This sometimes improved the situation and sometimes made it worse:

1) the AV node could not conduct that fast and so there was alternating 1:1 and 2:1 block, resulting in a SLOWER ventricular rate.
2) sometimes, the AV node could conduct all beats and the ventricular rate went FASTER, at 170, leading to hypotension


Outcome:

The patient dialyzed and electrically stabilized and did well

Diagnoses:

1. HyperK

2. Atrial flutter with variable block and aberrancy due to pre-existing LBBB (or IVCD) with extra widening due to superimposed hyperkalemia.
3. Ventricular Tachycardia due to hyperkalemia

Lessons:

1. Always think of HyperK
2. Remember Calcium, D50 and insulin, Beta-2 agonists, and Bicarb (?)
3. SVT includes atrial flutter, and its rate can be as slow as 140!