Cardiogenic shock with wide complex tachycardia and poor LV function in a young woman

A 30-something woman presented with CP and SOB.  She was hypoxic and intubated.  She had very poor LV systolic function on bedside echo.  There were no B-lines and the RV was normal.

The following ECG was recorded:
Wide complex regular tachycardia at a rate of 140, no P-waves
What do you think?
What do you want to do?

This ECG was texted to me on my iPhone without any clinical information, with the question: "VT or SVT with aberrancy?"

Here was my response:

"Tough one, as they always are.  Looks like SVT with LBBB (LBBB morphology strongly supports SVT).  Lead  aVR is all negative.  I am going to say SVT and I would try adenosine."

Alternatively, it is sinus tachycardia with LBBB and P-waves are not visible.  Always consider Lewis leads when this is a possibility, as they are likely to exaggerate and uncover otherwise hidden P-waves.

Further analysis, with magnification of V2 and V3:
This is typical LBBB morphology.

When VT has its origin in the RV, it can have an LBBB-like morphology, but there are differences.  Except in the case of fascicular VT, VT starts in the myocardium (not in conducting tissue) and therefore the initial part of the QRS is not rapid (it is slow).   Thus, when it is VT with LBBB morphology, the onset of the LBBB-like QRS is more prolonged. 

Thus, if it were VT
1) the R-wave in right precordial leads would typically be greater than 30 ms.
Here it is about 20 ms

2) the onset of the R-wave to the nadir of the S-wave would be greater than 70 ms.  In fact, it would usually be greater than 100 ms.
Here it is about 60 ms

Thus, this is very likely SVT with aberrancy (or with baseline LBBB), and the SVT is possibly sinus tachycardia with P-waves that can't be discerned.

If the rate varies over time, sinus becomes more likely.

If it is paroxysmal SVT, Adenosine may convert it.

All ECG findings aside, severely decreased LV systolic function does make VT more likely.  But these ECG findings are pretty convincing.

Case Continued

The physians thought they were dealing with ventricular tachycardia (VT)
--Cardioversion at 200 J biphasic was attempted without success.
--K was slightly low, so K and Mg were given.
--Amiodarone was given, 150 mg x 2.
--Cardioversion x 3 was apparently unsuccessful

    Comment: Cardioversion would usually be effective whether SVT or VT.  The question in my mind would be this: was the patient converted to sinus tachycardia (still with LBBB), at a similar rate, such that it that looked nearly identical to the SVT and the providers were unaware that the cardioversion actually worked?

--Lidocaine was given, after which patient became hypotensive.
--CXR showed pulmonary edema.
--Cardiac function on echo was very poor, prompting initiation of chest compressions.
--After 3 minutes of CPR, and 1 mg of Epi, there was ROSC with hypertension and improved cardiac function.
--The wide complex continued, but rate was down to 120, suggesting that the rhythm had indeed converted to sinus tach, but there was uncertainty as to the presence of P-waves at this point.
--A trans-esophageal echo (TEE) probe was placed by the emergency physicians in the ED.  This revealed coordinated atrial followed by ventricular contraction at a rate of 120, suggesting sinus tachycardia.  (Not proving it, as SVT could have atrial before ventricular contraction)

The patient remained in cardiogenic shock due to severely decreased LV systolic function.  The remainder of the management is beyond the scope of this blog.

Later in the day, this ECG was recorded:
Sinus with LBBB.
So the LBBB is definitely baseline.  This is the same morphology that she had while in tachycardia, proving that the rhythm was supraventricular.

The patient recovered neurologically, but with a persistently very low ejection fraction (20%, due to new cardiomyopathy).  She also had very frequent ventricular ectopy, with short runs of VT.    In order to protect against dysrhythmic sudden death, she was discharged on a "Life Vest". (2)

The diagnosis in retrospect was SVT with aberrancy in the setting of severe cardiomyopathy and acute decompensated heart failure, with later runs of ventricular tachycardia.

Learning Points:

1. If it looks just like LBBB or RBBB, it is probably supraventricular.

2. In a regular wide complex tachycardia, use adenosine if you think it is SVT.  If you're wrong and it is VT, adenosine is safe.

3. VT can have a morphology similar to LBBB, but in VT the initial part of the QRS should be prolonged, such that the septal R-wave is wider than 30 ms and/or the onset of the R- to nadir of the S-wave is greater than 70 ms.(1)

4. In a critically ill intubated patient in shock, ED transesophageal echo (TEE) can help to guide management in many ways.  It can especially help to continuously monitor LV function during a resuscitation.  In this case it also helped to verify sinus tachycardia.

5.  A "Life Vest" (Wearable External Cardioverter Defibrillator) can be used for those who only temporarily need such a device, or as a bridge to a later implantable defibrillator (see full text article below for details, if interested).

References with links to full text

1.  Wellens Hein JJ.  Ventricular tachycardia: diagnosis of broad QRS complex tachycardia.  Heart 2001;86:579–585

2.  Zishiri ET.  Chung MK.  The Role of the Wearable Cardioverter-Defibrillator in Contemporary Clinical Practice.   The Journal of Innovations in Cardiac Rhythm Management.  May 2011.

Chest pain and Concordant ST Depression in a patient with aortic valve and previously normal angiogram

60-something presents with acute onset of chest pain.

His pain was accompanied by shortness of breath.  It awoke him from sleep.

Here is the prehospital ECG:
What do you think?

The rhythm appears to be atrial fibrillation.  There are no pacing spikes and the morphology is not right for a paced rhythm.  There is a wide complex that appears to be RBBB + LAFB.  There is excessive ST depression in V1 and V2.  Where normally RBBB would manifest a large R'-wave in V3, the lead may have been placed to far lateral and, instead, there is an S-wave.   In RBBB, a lead with a prominent S-wave, as is normal in V5 and V6, should not have ST Elevation or Depression.  This is all but diagnostic of posterior STEMI.

Then we see V4-V6 which have very broad, wide, "bulky" T-waves.  These by themselves are all but diagnostic for lateral hyperacute T-waves.

When you put the posterior and lateral together, it spells an occlusion of the circumflex territory.

The medics were concerned for STEMI but not certain enough to activate the cath lab, but did give ASA and NTG x 3, and the pain diminshed from 10/10 to 6/10.

On arrival, this ECG was recorded:
What do you think?

The same thoughts apply here.  The concordant ST depression in V3 is all but diagnostic of posterior STEMI.

There was a previous ECG available from one week prior:
This one is paced, with appropriate ST segments, though the concordant T-waves are slightly unusual

So what is going on?

The patient had a normal angiogram 1.5 years ago.  Could he have an acute STEMI now?

The cardiologist on call did not think so.  He suggested looking for other etiologies of chest pain.

The INR returned at 1.8.

The initial troponin I returned at 0.011 ng/L (normal: LoD = 0.010, 99% = 0.030).  This "negative troponin" seems to support the cardiologist, no?

A nitroglycerine drip was started but had to be stopped for hypotension.

Another ECG was recorded 30 minutes later:

Now there is the typical R'-wave in V3 and the concordant ST depression is in V4.
It still looks like a STEMI.

The pain pretty much fully dissipated.

The patient was treated medically, and a 2 hour troponin returned positive at 0.30 ng/mL.  4 hours into his stay, a third troponin returned at 23.5 ng/mL (quite high, and typical of a STEMI), at which time this ECG was recorded:
ST changes are much less pronounced.
This suggests reperfusion, either by lysis of thrombus or through collaterals.

Angiogram showed a lesion in the 2nd obtuse marginal off the circumflex.  Interestingly, at this point it was only 90% occlusive with TIMI-2 flow (this explains the relief of pain).  It could not be aspirated.  Presumably, it was 100% occlusive during pain.

Peak troponin 33.6 ng/mL

The impression was that this was an embolus from the aortic valve or from left atrial appendage (due to atrial fibrillation).

Echocardiogram: Previous echo EF = 56%; Now = 50%

TEE (Transesophageal echo): showed a thrombus on the mechanical aortic valve.

Myocardial infarction with previously normal coronary arteries.

I could not find any studies that looked at patients who had a previous normal angiogram and present with what appears to be acute coronary syndrome.

But there are at least several studies of patients with STEMI who normal coronary arteries at the time of the event.

This one has a nice figure showing the etiologies:

Myocardial infarction with normal coronary arteries: a conundrum with multiple aetiologies and variable prognosis: an update

Note that "concealed atherosclerosis" is one of them.
Even if there is no previous atherosclerotic stenosis on a standard angiogram, there can be significant occult atherosclerosis.  Most atherosclerotic lesions are "extraluminal" and can only be see with intravascular ultrasound or with CT coronary angiogram.  These lesions are very prone to ulcerate and thrombose.

The observed prevalence of normal coronary angiography in patients presenting with acute chest pain and ST elevations was 2.6%. Most of these cases were misdiagnoses, not infarctions. A normal angiogram during a biochemically confirmed infarction is extremely rare (0.7%) and was not seen during the ongoing symptoms of ischemia.

This is the best study I could find:

In this large study of 5767 NSTEMI patients, 88% of patients with acute coronary syndrome had significant CAD (any stenosis greater than or equal to 50%), 6% had mild CAD (any stenosis of 0% to ≤50%), and 6% had no CAD (no stenosis identified).  This shows that even patients with no angiographic coronary stenosis can have unseen extraluminal plaque that ruptures and causes thrombosis and ACS.

Here is a great review in the New England Journal of Medicine:

Mechanisms of Acute Coronary Syndromes and Their Implications for Therapy. 
New Engl J Med 368(21): 2004-2013; may 23, 2013; 

Quote from article:

"Surprisingly, serial angiographic studies have revealed that the plaque at the site of the culprit lesion of a future acute myocardial infarction often does not cause stenosis that, as seen on the antecedent angiogram, is sufficiently severe to limit flow. Angiographic monitoring of responses to thrombolytic therapy has shown that after lysis of the offending thrombus, the underlying stenosis is often not the cause of the critical stenosis of the artery. In a prospective angiographic study involving patients undergoing percutaneous intervention for coronary artery disease, only half the subsequent events arose from lesions with sufficient stenosis to have warranted intervention at the time of revascularization. (CT) angiography, which permits evaluation of the arterial wall (not just the lumen), has shown that the characteristics of plaque associated with acute coronary syndromes include low attenuation (i.e., little or no calcification) and outward expansion of the artery wall, a process that tends to accommodate the growth of plaque while minimizing luminal encroachment.6-8  Intravascular ultrasonography has shown that in acute coronary syndromes, the culprits often lie proximal to the sites of maximal stenosis — the traditional targets of revascularization therapies."

Learning Points

1. A previous normal angiogram decreases the probability that any event is due to ACS, but by no means eliminates it.

2. Acute coronary occlusion may be due to other etiologies than ACS, such as embolism.  Coronay embolism is an indication for PCI.  The embolus can often be aspirated or broken up with the wire.

3. Learn the ECG features of coronary occlusion in the setting of RBBB