Wednesday, January 13, 2021

A 47-year-old man with abdominal pain and heart rates approaching 300 bpm

 Written by Pendell Meyers

A 47-year-old man with known WPW syndrome presented to the ED complaining of left abdominal pain, diarrhea, and chills. He denied palpitations, but is found to have a heart rate of 170 bpm at triage. He states that he occasionally has episodes of tachycardia which usually lasts about 1 hour, which he was instructed to "ride out at home unless they persist."  Other than his heart rate, his other vitals were within normal limits, and the patient did not show any signs of compromised cardiac output or distress.

Here is his initial ECG:

What do you think?

The ECG shows an irregularly irregular polymorphic tachycardia at approximately 186 bpm. Occasional beats are conducted with narrow, normal morphology, but most are conducted aberrantly with a nonspecific intraventricular conduction delay pattern, which is not actually very wide despite the abnormal conduction. While most of the abnormally conducted beats have the same morphology, the morphology becomes more polymorphic when the rate increases, as seen twice during this ECG, with lead V1 best demonstrating significantly different morphology between QRS complexes. Several beats are conducted at approximately 300 msec after the previous beat, which is extremely unlikely to be the result of a normal AV node conduction.

Because it is irregularly irregular, polymorphic, and has R-R intervals approaching less than 300 msec, the diagnosis is atrial fibrillation with WPW (also called pre-excited atrial fibrillation) until proven otherwise.

Here is his baseline ECG:

Sinus rhythm with very short PR interval and subtle delta waves. The QRS morphology matches the most common beats in the presentation ECG above, implying that this is his most common QRS pattern as a result of simultaneous activation via the AV node and accessory pathways.

Although the patient remained clinically stable and never showed any signs of distress or shock, his heart rate gradually accelerated over the course of the next 30 minutes.  He never showed any signs of deterioration, and cardioversion was not attempted. All nodal blockers (BB, CCBs, amiodarone, adenosine) were avoided.

A repeat ECG was performed:

Extremely rapid rates, approaching 260-280 bpm. It is technically polymorphic (again V1 is most clear), although I must say it is slightly less polymorphic than other examples of AF + WPW that I have seen at rates like this. It is also still irregularly irregular, so it must still be AF.

We (Smith and Meyers) believe that the best course of action for this persistent dysrhythmia at a rate of nearly 280 bpm, even if the patient is not clinically unstable, is probably just to perform synchronized cardioversion at this time, without waiting for infusions such as ibutilide or procainamide. Dysrhythmias like this which are persistent at such high rates and polymorphic have a high chance of deterioration into VT/VF. We would give etomidate and perform synchronized cardioversion for this. In my practice, it takes a significant amount of time to actually obtain and administer ibutilide or procainamide. If it recurs after cardioversion, of course an infusion will be required.

In this case, however, electrical cardioversion was not performed and the patient did not deteriorate.

Cardiology advised starting ibutilide (a class III antidysrhythmic medication which blocks K channels, increasing the duration of the refractory period, which inhibits conduction and propagation of dysrhythmias). Procainamide (a class Ia Na channel blocker) would also have been reasonable.

Ibutilide was started, followed by conversion to sinus rhythm approximately 20 minutes later.

Here is his repeat ECG:

Sinus rhythm similar to baseline ECG.

The patient was admitted for observation and treatment of the underlying illness.

Learning Points:

Irregularly irregular polymorphic (usually wide, but not always greater than 120 msec) tachycardia should be assumed to be atrial fibrillation with WPW until proven otherwise.

Adenosine should never be given to any rhythm that is irregular or polymorphic.

Any AV nodal blocker is considered contraindicated in AF with WPW for fear of enhancing conduction through the bypass tract, which theoretically could result in deterioration of the rhythm.

Unstable patients should be cardioverted. For stable patients, procainamide or ibutilide are both accepted pharmacologic agents for this scenario. Synchronized cardioversion with sedation is a reasonable and safe option as well, however it would not be appropriate if the rhythm is intermittently terminating and recurring (because it will simply recur after your cardioversion). Even for seemingly stable patients, the greater the heart rate and more polymorphic the QRS, the more likely the rhythm will deteriorate, and the more appropriate synchronized cardioversion becomes.

Please refer to our tachycardia algorithm (found on our "teaching images" tab:, and/or our EMRAP Corependium chapter on Tachydysrhythmias for more information.

See other examples of this rare rhythm here:

A Clinical Scenario to Recognize- Irregular WCT

Monday, January 11, 2021

A wide complex tachycardia

Submitted by Van Wall M.D., Written by Pendell Meyers

Let's go back to the basics for a common and classic scenario.

A middle-aged patient presents with shortness of breath and palpitations. The patient was stable without signs of low cardiac output or distress. Her ECG is shown below (first see what you think without using the baseline): 

What do you think?

There is a (minimally) wide complex, regular monomorphic tachycardia at a little faster than 150 bpm. I measure the QRS duration at almost exactly 120 ms. The differential would include ventricular tachycardia, any cause of narrow complex regular tachycardia plus added conduction aberrancy (such as a bundle branch block), or other causes of QRS widening like hyperkalemia or sodium channel blockade. Of course, the interpreter should always start by assuming that a wide complex monomorphic tachycardia is due to ventricular tachycardia and/or life threatening hyperkalemia, until proven otherwise.

This demonstrates why it is so important to be able to recognize RBBB, LBBB, and paced rhythms (pacer spikes) so quickly. This ECG has perfect RBBB morphology, one of the rare times that we can be confident that a regular wide complex rhythm is not classic ventricular tachycardia. 

For more discussion on features of SVT vs. VT, see these prior posts:

A prior baseline showing identical RBBB morphology during sinus rhythm would prove this definitively. 

Here is the prior baseline ECG on file:

This shows the same RBBB morphology in sinus rhythm.

They applied Lewis leads to see if they could get a better look at the atrial rhythm:

I can't say that I see clear atrial activity.

They gave 12 mg adenosine (a perfectly reasonable and guideline-endorsed option for any rhythm that is regular and monomorphic, regardless of QRS width):

Flutter waves are revealed.

The rhythm soon returned to 2:1 atrial flutter, of course. The patient was then rate controlled and did well.

Learning Points:

Assume that wide complex regular tachycardia is VT and/or hyperkalemia. Then work backwards and prove that assumption false, if possible. VT is more likely statistically, and the likelihood of VT increases further with age, cardiac pathology, and QRS duration.

Recognizing classic RBBB or LBBB morphology may enable the diagnosis of SVT with aberrancy. This can be basically definite if the morphology is shown to be identical to prior known RBBB or LBBB morphology on baseline ECG.

Adenosine is contraindicated in irregular or polymorphic QRS complex rhythms. It is not contraindicated for wide complex regular monomorphic tachycardia, and is very reasonable in this scenario.

Friday, January 8, 2021

Acute chest pain, ST Depression in V2 and V3, relief with Nitroglycerine, "normal" coronaries, and apical ballooning. Is it takotsubo?

This was submitted by Michael Fischer, one of our outstanding 2nd year EM residents at Hennepin Healthcare.


A previously healthy female in her 40s presented 1 hour after abrupt onset 10/10 crushing chest pain that started while brushing her hair that morning. The pain radiated to her bilateral jaw and right shoulder, and did not seem to be exertional or pleuritic in nature.  


Here is her pre-hospital ECG: 

What do you think?

Smith: V2 and V3 have some minimal ST depression with downsloping.  This is highly suggestive of posterior MI.

This was read by EMS as non-specific. Aspirin 324mg was given by EMS. Nitroglycerin spray x3 was also given which brought her pain down to 3/10 upon arrival to the ED. She was vitally stable with systolic BP of 140s. No cardiac history, not taking any medications, but does have 1st degree relatives with CAD.  


Here is her first ED ECG:

The ST Depression is more pronounced, and has extended to V4

This was interpreted as ST-depression in V2-V4. Additional sublingual nitro was given x2, bringing her pain to 0/10 in her chest, however she still had pain in her jaw.  


Given the abrupt onset of pain, aortic pathology was also a concern. Bedside echocardiography revealed grossly intact left ventricular function, non-dilated aortic root. Suprasternal view of the aorta revealed normal caliber aorta with no obvious dissection flap. Upper extremity pulses were equal. D-dimer was sent as further rule out for dissection.  


A repeat ECG was obtained with her chest pain resolved after nitroglycerin: 

Almost completely resolved

This was interpreted as resolved anterior ST-depression. 


Over the course of the next 30 minutes while labs were pending, her chest pain slowly returned. Her troponin returned at 0.682 ng/mL (upper reference limit of 0.045 ng/mL), D-dimer negative. At this point, interventional cardiology was consulted and recommended medical management with plan for the catheterization lab that afternoon. She remained vitally stable with systolic BP in the 130-140s. She was started on a nitro drip and was heparinized.  


Her chest pain continued to wax and wane on the nitro infusion. She additionally received hydromorphone and ondansetron. Interventional cardiology was consulted again regarding her waxing and waning pain, at which time they took the patient to the catheterization lab.  


Given her rapid improvement on nitro, it was thought that her symptoms could be due to coronary vasospasm given her overall lack of CAD risk factors. Ruptured plaque and coronary dissection remained leading differentials as well.  


Angiogram report: 

Normal coronary arteries.  

Left ventriculogram demonstrated apical ballooning and hypercontractile base consistent with stress-induced cardiomyopathy.  


Takotsubo Cardiomyopathy- The Great Imitator! 

As previously discussed in this blog, Takostubo cardiomyopathy may manifest as T-wave inversion or ST elevation that can mimic a STEMI. This patient’s ECG with anterior ST depression is an atypical ECG presentation in takotsubo, and diagnostic of posterior MI, prompting angiography to rule out acute coronary occlusion.  

On chart review, there was no inciting stressor thought to precede her symptoms. She did well and was discharged on an ACE-inhibitor and beta-blocker. 

Smith comment: This ECG is very unusual for takotsubo.  And although it correlates mostly closely with posterior transmural ischemia (posterior STEMI), it would not be unusual for subendocardial ischemia due to LAD spasm or LAD subtotal thrombosis.  Thus, I am not entirely convinced of takotsubo in this case.  

All management was appropriate.  The cath lab certainly needed activation.  The coronaries were clean.  There was apical ballooning on ventriculogram.  

However, the cath report does not mention whether the LAD wraps around to the inferior wall, and there was no intravascular ultrasound (IVUS) to prove absence of ruptured plaque that does not manifest on plain angiogram (which only shows the lumen of the artery and, unlike IVUS, does not show extraluminal plaque).

Moreover, the onset of chest pain was without inciting event, as usually happens with takotsubo, and was relieved with nitroglycerin, which strongly suggests some element of coronary ischemia.

Thus, we may never know whether this was LAD ACS, LAD spasm, or a very strange sort of takotsubo.

Monday, January 4, 2021

ECG with Aslanger's Pattern. CT Pulmonary Angiogram Reveals LAD Ischemia (Septal Transmural). But this is not Contradictory.

A 52 y.o. male presented with persistent central chest pressure, without radiation, SOB or diaphoresis, which began at rest approximately one hour prior to arrival.   He had never had pain like this before.  He felt slightly nauseous earlier but no vomiting.  He is denying any back pain or abdominal pain.  

An ECG was recorded during pain:

What do you think?

This shows significant ST depression in I, II, and V4-V6, with reciprocal ST Elevation in aVR.  This suggests diffuse subendocardial ischemia.  

However, along with that subendocardial ischemia, there is also STE in lead III with reciprocal ST depression in aVL, and some STE in V1.  These suggest inferior OMI with possible RV involvement.

Both of these patterns together suggest Aslanger's pattern, recently published in J Electrocardiology: A new electrocardiographic pattern indicating inferior myocardial infarction.

This newly recognized ECG pattern is defined as "(1) any STE in III, but not in other inferior leads, (2) STD in any of leads V4 to V6, (but not in V2) with a positive or terminally positive T-wave, (3) ST in lead V1 higher than ST in V2."  

One might argue that this case does not apply because of the ST depression in V2, but 1) V2 is probably misplaced and 2) it is not enough ST depression to negate the rule.

Here, we will ignore lead V2 because it doesn't make any sense at all: the R/S ratio is higher than in either V1 or V3, which suggests misplacement.

Here is an illustration of the ST vector in Aslanger's pattern:

The label of leads II and III are reversed -- Sorry

The right side of the inferior wall manifests ST Elevation, resulting in an ST vector directly to the right. Thus, even though there is inferior OMI, there is no STE in II or aVF, only in III.  Moreover, this means there will be MORE reciprocal STD in lead I than in lead aVL, and this is indeed the case with our ECG above.  If there is also subendocardial ischemia, the ST depression vector remains leftward, with a reciprocal ST Elevation vector also to the right.  With the ST vector all to the right, the only leads with ST Elevation are III, aVR and V1.

Thus, this pattern was associated with simultaneous inferior MI AND diffuse ischemia due to LAD, Left Main, or 3 vessel disease.

HOWEVER, there is yet another entity which could produce this, and it is transmural septal ischemia.  Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), with ADDED STE in III?  

Aslanger added in the limitations in his article: 

"Theoretically, an isolated basal inferoseptal infarction or an acute inferior MI in the presence of previous infarctions that may change the orientation of lesion vector can also cause a similar picture. Lastly, this pattern may represent a chronic change from a previous ischemic insult as seen in a limited number of the patients in the control group".


In diffuse subendocardial ischemia, which when due to ACS, is usually from LAD or Left Main insufficiency, all walls would have a negative vector pointing from the endocardium to the epicardium (positive vector from epicardium to endocardium, the opposite of OMI).  Since there is no ventricular wall at the top ("base") of the heart (there are only atria), then the addition of all those negative vectors points towards the apex; if the entire heart has subendocardial ischemia, then the ST depression vector points towards the apex (II, V5), with a reciprocal STE vector towards aVR (and even V1).   

In Septal STEMI, transmural ischemia of the septum is recorded by the overlying lead V1 as ST Elevation.  aVR is similarly (but not exactly) placed and can show STE.  Lead III is also on the right and might manifest ST Elevation in Septal STEMI.

It is important to remember that the ST depression of subendocardial ischemia does not localize.  Here, the ST depression is in "lateral" leads, but this does not mean there is "lateral" ischemia.  It may either be reciprocal to Septal STEMI, or due to subendocardial ischemia from the LAD insufficiency.

Case Continued

Bedside ultrasound was performed:

This shows an anterior wall motion abnormality, and highly suggests the LAD as the infarct artery.  Often patients with subendocardial ischemia on the ECG do NOT have a wall motion abnormality, which contrasts with patients with OMI/STEMI who always have a wall motion abnormality, at least if the echo is of high enough quality and uses bubble contrast.

The patient was slightly tachypneic and mildly hypoxic in the stabilization room and therefore the physicians obtained a CT pulmonary angiogram as well as aortogram to rule out dissection and PE.

The initial Abbott hs troponin I returned at 52 ng/L (Upper reference limit for males is less than or equal to 34 ng/L).  FYI: 52 ng/L is the threshold for "rule in" by European studies as it has a high positive predictive value in the setting of chest pain.

The D dimer was undetectable, so CTPA was probably unnecessary, but it did have interesting findings:

Top left: conventional CT.  

Top right is colored iodine overlay; Blue areas of myocardium are ischemia.  

Bottom left is plain iodine map.  

Bottom right is low Kilo Electron Volt image which brings out iodine.  See the 2 very dark areas, one in the septum and one near the apex.  Notice that they correlate with blue on the colored spectral CT (blue is ischemia on spectral CT).

These areas of hypoperfusion are in the septum and apexstrongly suggesting LAD ischemia.  In addition, they are indeed transmural!

This CT interpretation was made with moderate certainty

Contrast this CT transmural ischemia here with this CT subendocardial ischemia. 

Below we can see a coronal image of the heart:

Notice the inferior wall (lower part of image) is subtly transmurally darker than the remainder.
If prospectively interpreted in blinded fashion, this is not definitively diagnostic, according to our CT Guru, Gopal Punjabi (
This suggests inferior OMI but is by no means diagnostic.

Case continued

The patient was placed on a nitroglycerin drip and chest pain gradually resolved.  The emergency medicine faculty spoke directly with cardiology faculty and the decision was made to activate the cath lab via "pathway B."  (Our "Pathway A" is for clear STEMI; "Pathway B" is intensive evaluation and discussion for patients who might need the cath lab emergently for possible OMI, but it is not as clear as with STEMI).  The patient was subsequently given 5000 units of heparin, 180 mg of ticagrelor, and defib pads were placed on the patient in the event that he should have a cardiac arrest. 


Culprit Lesion: 90% mid LAD stenosis with evidence of plaque rupture, TIMI III flow on angiography.

Troponin profile:

Unfortunately, they were not measured to peak, which would help determine if this was indeed Septal STEMI or Non-Occlusive Subendocardial Ischemia.

ECG after PCI:

Left axis deviation, but otherwise normal

Formal Echo:

The estimated left ventricular ejection fraction is 71%.

There is no left ventricular wall motion abnormality identified.

So the wall motion has recovered (remember we showed a definite WMA during the ischemia).  Such quick recovery is uncommon in STEMI/OMI unless there is very quick reperfusion.  If this case was indeed OMI, then there was very fast spontaneous reperfusion, as in indicated by the open artery with TIMI III flow.  When reperfusion is not so fast, wall motion recovery may require many days to weeks.  When recovery is delayed, it is often called "myocardial stunning."

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