Saturday, January 30, 2021

Chest pain, ST Elevation, and tachycardia in a 40-something woman

A prehospital cath lab activation for STEMI came through with the information that the 40-something woman had chest pain and a pulse of 140.

We were immediately skeptical that the patient had a STEMI because of the high heart rate.  She would have to be in cardiogenic shock with a massive STEMI for that.  Certainly possible, but when the heart rate is so high, be skeptical.

The patient arrived with this ECG:

Here the heart rate is obviously no longer 140
What do you think?

ECG: it certainly appears to be an anterior STEMI, but it is important to realize that right ventricular ischemia from either inferior and RV STEMI or from pulmonary embolism can manifest with STE in V1-V3.

On arrival, she immediately lost pulses. Due to body habitus, an adequate transthoracic echo could not be done.  There was no ventricular fibrillation recorded, but in the rush of action, she did get defibrillated.  Most involved agree there was never any ventricular fibrillation.   

This turned out to be a pulmonary embolism (on autopsy).  

Massive PE can have Right Ventricular ischemia resulting in RV ST Elevation.  When there is sudden loss of pulse but no ventricular fibrillation, then STEMI is an unlikely etiology of arrest.  In this series of 1246 cardiac arrests, 60 of which were from PE, only 3 had ventricular fibrillation.

In contrast, the vast majority of initial rhythms in cardiac arrest from acute coronary syndrome are shockable rhythms, and the vast majority are ventricular fibrillation.

This case was particularly confusing because CPR was very effective: good pulses, good O2 saturations, good arterial line waveform, non low end tidal CO2.  CPR is generally not very effective in pulmonary embolism because of obstruction of the pulmonary vasculature.  Additionally, transesophageal echo (TEE) was placed and did not show a particularly enlarged RV. 

Unfortunately, in spite of administration of 100 mg of tPA, the patient could not be resuscitated.

See this case:

Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation....

Learning Points:

1. When there is chest pain and ST elevation in the right precordial leads, think of pulmonary embolism.

2. When there is extreme sinus tachycardia, ACS becomes less likely unless there is:
  A.  Another simultaneous pathology 
  B.  Pre-existing poor ventricular function or 
  C. Cardiogenic shock caused by the ACS, and confirmed by poor LV function on bedside cardiac echo.

3.  Corollary to Learning point #2.: Cardiac ultrasound and volume assessment is essential to interpreting the ST Elevation on the ECG.

4.  If a patient has cardiac arrest witnessed to be PEA, then ACS is very unlikely to be the etiology.

5.  If a patient is found in PEA after a significant down time, the arrest may have started as ventricular fibrillation and degenerated to PEA.  Such arrests may be due to any etiology.

Thursday, January 28, 2021

Wellens' syndrome: to stent or not? IVUS negative, Symptoms persist, Stress Testing, Instantaneous Wave Free Ratio, and Fractional Flow Reserve.

A 55 y.o. male with no cardiac PMHX presented for 2 weeks of exertional chest pain, worsened on the day prior to presentation.  On the day of presentation, the chest discomfort was particularly intense, and associated with diaphoresis and nausea.  It was resolved (pain free) when the ECG was recorded:

This ECG was read as "nonspecific" by the providers.  
What do you think?

These is classic Wellens' pattern A (biphasic, terminal T-wave inversion), and it is Wellens' syndrome (Angina, resolved -- pain free -- with preserved R-waves and Wellens' pattern A T-waves).  The morphology of these T-waves is very distinct and most T-wave inversion does not fit the pattern.  The pattern manifests a rising ST segment with a sudden fall into the slightly negative T-wave.   If you recognize this pattern, then you are not so dependent on troponin for your diagnosis.  

Wellens' syndrome does not mandate emergent cath lab activation, since the artery is open and the patient is pain free; there is no persistent ongoing ischemia. When the patient was suffering pain prehospital, the artery was occluded, but it spontaneously reperfused (autolysis).  However, the patient is at high risk for re-occlusion at any time and cath lab activation is optimal because this should be considered a transient STEMI in which the ST elevation would have been there had the ECG been recorded during pain.

The initial Abbott high sensitivity troponin I was 60 ng/L (upper reference limit for men = 34 ng/L).

This initial troponin in this context is all but diagnostic of acute MI.  The actual definition of acute MI by the 4th Universal Definition requires a rise and/or fall of troponin.

The 2nd troponin also returned at 60 ng/L.  No rise, no fall.

Often, low or non-dynamic troponins may be explained away by "type 2 MI" or non-MI "myocardial injury" and so this physician did not want to risk such dismissal by an inpatient team.  

He therefore ordered a CT coronary angiogram:

--Calcium score (Agatston method): 0.

Followed by contrast scan:
--LAD: Noncalcified plaque in the proximal LAD, with a linear intravascular filling defect, concerning for dissection with likely severe stenosis.  Appearance is concerning for a severe stenosis. 

In fact, all 4 troponins were at plateau:

So this LAD is completely consistent with LAD thrombosis and Wellens syndrome.

He went to the cath lab within hours: Angiogram result:

Moderate hazy Eccentric plaque in the ostial/proximal LAD assessed via intravascular ultrasound (IVUS), which showed that the lesion on the Proximal LAD had 50% stenosis but without evidence of ruptured plaque.  "The lesion was discrete and eccentric."

LAD: Type III LAD is noted.  The LAD is a large caliber vessel.

Summary: No angiographic significant obstructive disease.

Medical Rx. Aggressive risk factor modification.

In the absence of proven ruptured plaque on IVUS, the interventionalist did not place a stent. This was also because the lesion was very close to the ostium (close to the takeoff from the left main) and thus higher risk.

Subsequent events

He was treated overnight with heparin and nitroglycerine infusions.

ECG the next day:

This shows evolution of Wellens waves to deeper and symmetric (Wellens Pattern B).  In spite of absence of rise and/or fall of troponin, this confirms that there is acute MI here.  In spite of the definition requiring rise and/or fall, any elevated troponin may be called acute MI under the right circumstances.

Cardiology note

EKG showed Wellens' waves, and Coronary CT in ED showed proximal LAD plaque. Flat troponin trend most consistent with unstable angina. He was treated overnight with nitro and heparin drips.  Angio today showed proximal LAD lesion with 50% stenosis, no PCI given TIMI3 flow, lack of rupture on IVUS, and proximity to left main. He does have area of soft plaque, and has continued risk of rupture. Plan is to treat patient medically with dual antiplatelet therapy and high intensity statin, and obtain a stress test.

Strangely, he did not get an echocardiogram.  

The patient was discharged on dual antiplatelet therapy,

He continued having angina for the next month.  He had no further troponins or ECGs.  He was scheduled for a Sestamibi stress test with Regadenoson.  (Regadenoson is an adenosine receptor agonist that is a vasodilator and is used in place of exercise to stress coronary flow)   

This stress test was markedly positive.  It showed: 

1) wall motion abnormalities of the anterior and anteroseptal walls, consistent with LAD ACS.  

2) Inducible and reversible perfusion of these walls, consistent with a flow limiting lesion.  This is in contrast to the angiogram, which only showed 50% stenosis. 

He was taken back to cath lab because of positive stress test.

Culprit Lesion (s): 50% eccentric ostial LAD stenosis, unchanged.

iFR (see below) with pressure transducer in distal LAD 0.94, suggestive of no hemodynamic significance (less than or equal to 0.89 is significant; greater than or equal to 0.90 is not).  

Angiographers note: "Given discrepancy between iFR and regadenoson MPI, FFR was performed; FFR was 0.82 at maximal hyperemia.  While this value is above our traditional threshold for intervention, N Johnson et al. have suggest that a higher threshold should be utilized for LAD or left main disease (0.83 or 0.86, respectively; Johnson, Nils P., et al. "Prognostic value of fractional flow reserve: linking physiologic severity to clinical outcomes." Journal of the American College of Cardiology 64.16 (2014): 1641-1654.)"

"Given these factors and limiting chest pain at cardiac rehab, episode of nocturnal angina, and abnormal MPI, decision was made to proceed with PCI following discussion with the patient."

FFR = Fractional flow reserve.  Requires administration of vasodilators so that vessel distal to lesion is not obstructing flow.  It measures the pressure distal to the lesion, divided by the pressure proximal to the lesion.  Reported in fractions of 1 (e.g., 0.92)

iFR = instantaneous wave-Free Ratio.  Similar, but done during diastole.  "iFR represents a diastolic resting index that allows the assessment of coronary lesions during the phase in the cardiac cycle where microvascular resistance is at its lowest, allowing for increased myocardial perfusion and coronary flow."  Quote is from this article in Circulation: Cardiovascular Interventions: 

Instantaneous Wave-Free Ratio or Fractional Flow Reserve for Hemodynamic Coronary Lesion Assessment?  Yes, Just Do It!

Unlike FFR, iFR does not require administration of vasodilators because hyperemia is not necessary when measuring pressure during the wave-free diastolic period of the cardiac cycle.  iFR is proven to reduce procedure time, patient discomfort and cost compared to FFR.

Learning Points: 

1. First, Recognize Wellens' waves and Wellens' syndrome.

2. Wellens' syndrome implies an unstable lesion.  

3.  It is a truism that, if ACS does not received a stent on the index visit, it is likely to need one later.  See this post"Pay me now, or pay me later"  

4.  Wellens' waves may diagnose LAD ACS in spite of absence of rise and/or fall of troponin.

5. Troponin may plateau in acute MI and not manifest rise and/or fall.

6. Stenting a lesion is complex

7. IVUS may not always adequately characterize a coronary lesion.

8. Multiple modalities may be needed to inform the stenting decision.

9. FFR and iFR are useful in determining the need for stenting. 

Saturday, January 23, 2021

Acute Chest pain which then resolves spontaneously

A 50-something woman presented with sudden onset of left sided chest pain while driving, radiating down left arm, in addition to feeling diaphoretic, dizzy, and lightheaded. 

She presented immediately to the ED and had this ECG recorded:

QTc was 432 ms
What do you think? 

One of our fellows and a resident were worried about the ST Elevation in V3-V5, and but they were uncertain if it was possibly normal variant STE.

They calculated the formula at 21.05, which very strongly suggests acute LAD occlusion.  18.2 is the most accurate cutoff value, but at 19.0 it is very very specific.  21.05 is nearly always an acute LAD occlusion.

See here for everything about the formula and how to use it:

12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

The pain resolved after approximately 30 minutes total, and they did not activate the cath lab.

The first troponin I (Abbott, high sens) returned at 28 ng/L (Upper limit for women = 16 ng/L).  

The 2nd returned at 1332 ng/L, and another ECG was recorded 2.5 hours after the first: 

What do you think?

There is new T-wave inversion in V3-V6, biphasic.  This is Wellens' syndrome (Pattern A), which is indicative of reperfusion, though most Wellens' of the LAD is V2-V4. 

(The only difference from Wellens,' as described by Wellens, is that we were able to record an ECG during pain, and it showed what the true precursor to Wellens' waves is: ST Elevation of acute occlusion.  Wellens did not know at the time that his T-wave pattern was a sign of reperfused but unrecorded STEMI.  This was inferred after studies by Wehrens and also by Doevendans revealed identical T-waves after thrombolytic reperfusion)  

Moreover, this 2nd ECG confirms that the first ECG, recorded with pain, was indeed due to LAD occlusion and that when the pain resolved on its own, that resolution was due to spontaneous reperfusion of the LAD.

She was taken for angiogram shortly thereafter:


60% diffuse Moderate CAD in the distal LAD at an a segment where the vessel appear to have an intra-myocardial course. This could represent atherosclerosis with or without a ruptured plaque but also raises the possibility of spontaneous coronary artery dissection (SCAD).

The LAD is a large caliber vessel.

The LAD has moderate, indeterminate disease in the distal segment of the vessel. 60% diffuse Moderate CAD in the distal LAD at an a segment where the vessel appear to have an intra-myocardial course.

So it is unclear to me whether this is SCAD or myocardial bridging, or both.  There was nothing to be intervened upon (no stent).

See below for posts on these 2 entities (Bridging and SCAD).


Decreased left ventricular systolic performance-mild. The estimated left ventricular ejection fraction is 45-50%.  Regional wall motion abnormality-distal septum anterior and apex.

Third troponin: 1263 ng/L.  Unfortunately, it was not measured to peak. Peak troponin has a rough correlation with infarct size.  Echocardiogram correlates with myocardium at risk, but not with infarct size because myocardium that is "stunned" by ischemia, but not infarcted, may have persistent wall motion abnormalities (WMA) that are not permanent.  In other words, WMA only tell you that the myocardium was ischemic, not whether it is permanently infarcted.

Clinical Course:

The patient was initiated on beta blockers and dual antiplatelet therapy, carvedilol, and lisinopril.  The patient's contraception was discontinued, as hormones are associated with SCAD.  

Cardiac MRI was pursued with patient but she was unable to tolerate this due to anxiety.  Underwent cardiac rehab during course of stay and was cleared for discharge by cardiology with plans for outpatient follow-up and follow-up TTE. 

Learning Points

1. The LAD Occlusion/Normal Variant ST Elevation formula can help you to assess whether ST Elevation is due to ischemia or due to normal variant.

2. ST Elevation in V2-V5 during pain, with subsequent terminal T-wave inversion after pain resolves, is Wellens' syndrome.  An identical pattern can be seen in inferior leads and also in lateral leads after reperfusion. An analogous finding can be seen after reperfusion of the posterior wall.

3. LAD Occlusion can be caused by SCAD, which usually (but not always) does not require stenting.

4. Myocardial Bridging can also result in transient occlusion.

Myocardial Bridging: Tachycardia, fever to 105, and ischemic ST Elevation -- a Bridge too Far

3 posts on Spontaneous Coronary Dissection (SCAD):

Sunday, January 17, 2021

Typical chest pain and hypotension, Activate the Cath lab?

I was texted this ECG with the info that the patient "clinically looked like he was having a myocardial infarction":

What do you think?

There is atrial and ventricular pacing.  Both spikes are best seen in V1 and V2 (as always, if you click on the image, it enlarges).  The QRS is very very wide.  On the image below, I have drawn lines in every lead from the QRS onset (blue) and QRS end (red).  I measure the QRS duration at about 280 ms.  Of course, all ventricular paced rhythm is wide, but not often this wide.  One must always consider hyperkalemia when the QRS is very wide, but the K turned out to not be high.  

Here is the EKG with blue lines at the QRS onset and red lines at QRS end:

Since this was a photo of the ECG, it was not perfectly square, and so that lines are also not perfect.

Beside the pacing and wide QRS, there is no significant concordant ST Elevation, and no excessively discordant ST elevation or depression (in other words, it does not meet the Smith Modified Sgarbossa criteria, even at the 20% ratio).  

There is possible trace STE in III and reciprocal STD in aVL.  

There is Pseudo ST Depression in V2, but as you can see from my lines, that is QRS, not ST segment.

There is also QRS fragmentation (see especially leads II, III, aVF).  This is a good sign of ischemic heart disease, and analogous to Q-waves of MI.  In combination with the very long QRS, my reply to the text message was this:

There is QRS fragmentation, but no evidence of acute OMI or acute ischemia.  The wide QRS and fragmentation suggest that this patient has ischemic cardiomyopathy.   Of course, ischemia, and even OMI, may not manifest on the ECG, whether in the context of paced rhythm or normal conduction.  The patient may have chronically elevated troponins with this cardiomyopathy.

More history was obtained:

A male in his 60s with h/o dialysis, peripheral arterial disease, coronary disease, and sick sinus syndrome with pacemaker complained of onset of chest pain and vomiting.  His systolic blood pressure was in the 80s and he "looked like he was having a heart attack."  After a complete workup, including a bedside POCUS which showed poor ejection fraction, the clinicians were convinced that the patient was having a myocardial infarction, and that was reinforced by their interpretation of the ECG as "showing an inferior MI."

Smith opinion: There is no ECG evidence of acute ischemia.  However, unless another etiology of chest pain and hypotension can be immediately found, one must assume that this is high risk ACS in spite of the absence of ACUTE findings on the ECG.  The patient should be taken for angiogram.  The ECG clearly shows the presence of coronary disease.

They activated the cath lab thinking there was an inferior MI (Smith aside: I do not think this ECG shows inferior MI).  

The cath team decided not to take the patient.  They did not come up with an alternative explanation for the chest pain and hypotension.

Smith comment: I can understand that if a patient presents with chest pain and has no objective evidence of ischemia (EKG or troponin rising/falling), then one might blame it on esophageal reflux.  But hypotension and shock need an explanation.  If you have acute chest pain, ECG and echo evidence of ischemic cardiomyopathy,  low ejection fraction, and no other explanation, then you must rule out a coronary etiology with an angiogram.

Troponins, with discussion:

His troponins later returned: Initial troponin T was 0.088 ng/mL and 2.5 hours later it was 0.091 ng/mL.  

It would not be surprising if this patient had chronically elevated troponins, and indeed at a different hospital on a previous visit, the patient had these serial troponins measured (contemporary, 4th generation, troponin I -- manufacturer unknown):  

Previous visit, Troponin I: 0.124 ng/mL ➡️ 0.127 ng/mL ➡️ 0.129.  

These previous steady state Troponin I further support chronically elevated troponins.  Nevertheless, because troponin I and T are very different and no two assays can be directly compared, we cannot determine whether the troponins on this visit (the present one) are, or are not, more elevated and thus could represent acute on chronic elevation. There is no rise and/or fall, which usually (but not always) indicates that they are chronic (called "chronic myocardial injury," and common in cardiomyopathy).  Sometimes there is an acute rise and the 2 values are measured on either side of a peak and so do not show rise and/or fall.  Furthermore, troponin I and T do NOT correlate well with each other.  Trop I is often a 5-10x larger number than trop T.  Therefore, trop T of 0.088 ng/mL and 0.091 ng/mL might indeed be high compared to the previous visit (which was trop I), but this is uncertain.

Thus, if this is ACS, it is possible that it is acute MI, but if not, it could very well be unstable angina, which still exists even in the era of high sensitivity troponin. See Thelin reference below, with comment, and this blog post: "Unstable Angina still exists", even in the Age of High Sensitivity Troponin


Four hours later, the patient had a ventricular fibrillation arrest and the patient could not be resuscitated.  

In acute coronary syndrome, the ECG frequently does not manifest ischemia. If the patient looked like he was having an MI, and there is no other explanation, especially if he is hypotensive with poor myocardial contractility, then you treat it as such and take the patient to the cath lab.  That is why the ACC/AHA guidelines state that emergent cath lab activation may be necessary in an unstable patient even in the absence of STEMI, and the European guidelines say that many patients need < 2 hour angiogram “even in the absence of EKG or biomarker evidence of infarction.”

Here is a quote from the guidelines at this link:
See page 2367

4.4. Ischemia-Guided Strategy Versus Early Invasive Strategies

See Figure 3 for the management algorithm for ischemia guided versus early invasive strategy.
4.4.1. Early Invasive and Ischemia-Guided Strategies
For definitions of invasive and ischemia-guided strategies, see Table 8.
1. An urgent/immediate invasive strategy (diagnostic angiography with intent to perform revascularization if appropriate based on coronary anatomy) is indicated in patients (men and women¶) with NSTE-ACS who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures).40,42,173,174 (Level of Evidence: A)
2. An early invasive strategy (diagnostic angiography with intent to perform revascularization if appropriate based on coronary anatomy) is indicated in initially stabilized patients with NSTE-ACS (without serious comorbidities or contraindications to such procedures) who have an elevated risk for clinical events (Table 8).40,42,173–177 (Level of Evidence: B)


“Refractory angina should go to the cath lab within 2 hours”
Hemodynamic instability
Electrical instability
Worsening Heart Failure

High Sensitivity Troponins and Unstable Angina

There was no rise and/or fall of troponin in this case, so it does not meet the definition of myocardial infarction.  These troponins were NOT high sensitivity (hs) troponin, but that does not matter.  However, even in the era of hs troponin, unstable angina still exists.  Here I describe one study which used the Roche hs-cTnT assay.

Thelin et. al. Eur Ht J, Acute Card Care 2014; 4(5):403-9

• Initial hs-cTnT among 478 patients presenting with chest pain as the primary symptom

• 160 (33.5%) had initial value below 5 ng/L

• NPV of 100% for NSTEMI (70 NSTEMI; 37 UA)

• NPV of only 94% for any ACS (includes Unstable Angina)

• Sensitivity 91% (80-95)

– Missed 10 of 107 ACS as diagnosed by angiography; 8 PCI

• Clinical judgment and pre-test probability of ACS is critical

More on Fragmented QRS

This paper found that a fragmented QRS in inferior leads is a particular high risk for sudden death: QRS fragmentation and the risk of sudden cardiac death in MADIT II

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."

Recommended Resources