Hypotensive and Tachycardic in Clinic: A Quick Ticket to the ED and Lewis Leads

This was contributed by one of our fine interns, Aaron Robinson.

A 40-something male cancer patient presented to clinic for a routine follow up and stated he was feeling “tired.” He was just finishing a course of antibiotics for bacteremia. 

His BP was found to be 60 systolic with a heart rate in the 170s.  He was moved to the Emergency Department.

He appeared ill, but was not acutely in distress. He showed signs of volume depletion.

His initial ECG is shown below. What do you see?
Initial ECG: This is a regular narrow complex tachycardia at a rate of 157 BPM. 

There is no obvious atrial activity prior to the QRS. There seems to be some perturbation of the T wave (inverted retrograde P-waves, seen in PSVT) in the inferior leads making SVT very likely. 

Smith comment: The differential of regular narrow complex tachycardia at a rate of 157 is: 
1. sinus tach
2. paroxysmal SVT (PSVT, due to AVNRT or WPW)
3. atrial flutter with 2:1 conduction, and 
4. very rarely, junctional tachycardia. 

You can see what appear to be small negative waves after nearly every QRS.  This would indicate PSVT  When you become accustomed to seeing these, you can readily recognized them as retrograde P-waves.

We have seen many instances in which sinus tachycardia was misdiagnosed as SVT.  Here is one:

A Relatively Narrow Complex Tachycardia at a Rate of 180.

So if you're uncertain whether these are retrograde P-waves, and are wondering if you are missing sinus tachycardia, and the patient is stable (as here), you can try Lewis leads to see if sinus P-waves appear.  

It takes about 30 seconds to align Lewis leads and then switch to lead I to see the result.

Aaron continues: Bedside cardiac US demonstrated a hyperdynamic and tachycardic heart with IVC variation with each breath, suggesting volume depletion, as we initially suspected. 

Fluid resuscitation was started but the rate stayed between 160 and 170. 

Smith comment: assessing response to volume repletion is a great way to confirm sinus tach.  Sinus is an automatic rhythm with varying rate, where re-entrant rhythms such as PSVT are always at a constant rate.  If the rate slowly drifts down, this confirms sinus.  If the rate does not change, you have not confirmed a non-sinus rhythm, but you have made it far more likely.

Aaron continues:  The physicians then re-arranged the limb leads of the 12-lead ECG in the Lewis Leads pattern, in order to better identify P-waves, or lack thereof.   

Smith comment: it is much easier to use the monitor leads for Lewis lead placement than to use the 12-lead.   

For a quick review on Lewis Lead Placement, check out this post.

  1. Place the Right Arm electrode on the patient's manubrium.
  2. Place the Left Arm electrode on the 5th intercostal space, right sternal border.
  3. Place the Left Leg electrode on the right lower costal margin.
  4. Monitor Lead I.
Aaron continues: The 12-lead ECG using Lewis Leads is below. What do you see?  Remember, look at Lead I. In this example, Lead II is helpful too.
In this ECG, retrograde atrial activity is more obvious in the Lewis Leads.  Do you notice anything weird about the P-waves? They are upright, with 2 humps! The Lewis Leads were reversed on this 12-lead EKG, such that retrograde P-waves appeared upright.  

Just as importantly, the Lewis leads did not uncover normal upright P-waves in front of the QRS.  Thus, Lewis leads did not reveal sinus rhythm; at the same time, they did confirm retrograde P-waves, but because the leads were reversed, it was somewhat confusing!   

Regardless, this Lewis Lead ECG helped the physicians confirm the diagnosis of SVT with retrograde P waves.

The patient was given 6mg adenosine and converted to a rate in the 110’s. His post-adenosine ECG is below.
Normal sinus rhythm

Learning Points:
1.     The most important takeaway from this case is that you should use Lewis Leads on the monitor, not on the 12-lead EKG (even though limb leads on the 12-lead will suffice). You will be able to have a live view of the appropriate leads on the monitor. You don’t need all 12 leads!
2.     Lewis Leads can help to ascertain atrial activity by focusing the electrodes on the atria.
3.     Be mindful of lead reversal. If something doesn’t make sense, consider reversed leads. Check out this LITFL page for a quick summary on lead reversal. In our case, it caused the P waves to be upright, not negative like we expected. 

Here is another very nice case using Lewis leads:

Wide Complex Tachycardia. What is the Diagnosis?

Are these Wellens’ waves?

This ECG was sent to me by one of my residents, who was puzzled by it:

This ECG is from a 21 yo M with PMH of poly-substance abuse.  He presented with nausea and vomiting after drinking the night before.  He denied any chest pain or shortness of breath.  He has no other significant medical history he does not take any medications.

This one was read by the computer as "Acute STEMI" (!!)
What do you think?
My resident thought this looked like Wellens' pattern in lead V2

Some hours later, this was recorded:
Now there is resolution of the inverted T-wave in V2

Electrolytes were normal.

My response:

I looked at the ECGs before reading anything.

The one read as acute STEMI was clearly early repol to me.  

What particularly confuses one would be the T-wave inversion in V2.  However, also notice that there is an rSr' in both V1 and V2.  Notice that in the second ECG, these are gone and the T-wave inversion is not present.  Both of these findings (rSr' and T-wave inversion in lead V2) are seen if V1 and V2 are recorded too high on the chest, which is a very common recording error, but not well known among physicians.  The second ECG is normalized.  I strongly suspect that they were not recorded with the leads in the same position.  Or the patient was lying down for the first one and sitting up for the second, which changes the position of the heart in the chest.

I showed this to Brooks Walsh, see below.  He added this important aspect:

There is one complication: normally, the P-wave in V1 is biphasic.  When the leads are placed too high, the P-wave in V1 is all negative, because all atrial depolarization is moving down, away from the highly placed leads.

In this case, there are all upright P-waves in V1 in both ECGs.  But look also at limb leads: the P-wave is inverted!  Thus, in this case, there is an ectopic atrial rhythm, not sinus rhythm.  This ectopic atrial rhythm accounts for the upright P-waves in V1 and V2, even though the leads were placed too high.

In other words, if you depend on P-wave morphology in lead V1 to tell you if the leads are placed too high, you would be misled!

Learning Points:

1. rSr' in lead V1 is often a result of leads placed too high

2. this also results in T-wave inversion in lead V2.

3. this should also result in an all negative P-wave in V1, unless there is a co-existing ectopic atrial rhythm, as in this case.

My friend, co-author and frequent blog poster, Brooks Walsh, just wrote a great article on this topic.

Here it is:

Syncope, History of Coronary Disease, and ST Elevation: Should Medics Activate the Cath Lab?

A 60-something male had a syncopal episode.  911 was called.   The patient had no complaint of chest pain or shortness of breath. A prehospital ECG was recorded:

Limb leads
Precordial Leads
There is ST Elevation in V1-V3, and in aVL, with reciprocal ST depression in II, III, and aVF.
There is also some ST depression in V5 and V6, and ST elevation in aVR.
What do you think?

The medics interpreted the ST elevation, with reciprocal ST depression, as STEMI, and activated the cath lab.

Note that you cannot see the entire QRS on the prehospital ECG.  The R-waves in leads II and III are cut off.  The S-waves in V1-V3 are cut off.  There is likely to be very high voltage that is cut off.

It is important to remember that not all ST elevation with reciprocal ST depression is a manifestation of STEMI.   LVH, LBBB, and WPW can all have ST Elevation with reciprocal ST depression. Especially LVH.

On arrival, I looked at the ECG and immediately knew it was a false positive due to LVH.

An ECG was recorded in the ED:
This confirms high voltage. QRS is 118 ms.
There is no evidence of STEMI.
All ST deviation is a result of LVH with secondary repolarization abnormalities
These are secondary to abnormal depolarization due to LVH, with high voltage.
These are expected ST-T abnormalities given the high voltage abnormal QRS.
They are not "primary" ST-T abnormalities of ischemia.

This ECG has similarities to Left Bundle Branch Block (LBBB), but it is NOT LBBB because the QRS is not long enough and there is not enough delay from onset of the QRS to peak of R-wave in lateral leads.  Q-waves in V5 and V6, and absence of monophasic R-wave in aVL also argue against LBBB.  See more on LBBB and LVH at the bottom of the post.

The cath lab was de-activated.

There was further history:

The patient had not anything to eat or drink all day long and felt subjectively dehydrated. He had been walking much of the day, then went to the bathroom and after urinating became light headed and fell w/ brief loss of consciousness.

There was never any chest pain or dyspnea.

He had a history of CABG and ischemic cardiomyopathy.

A repeat ECG 3 hours later was not different.


The troponins were slightly positive, peaking at 0.52 ng/mL (not consistent with STEMI).  Cr. was elevated, consistent with dehydration.

Echo showed:

Decreased left ventricular systolic performance, moderately-severe, EF about 35%, with LV enlargement.
Asynchronous interventricular septal motion consistent with left bundle branch block (although the ECG did not show LBBB).
Regional wall motion abnormality-distal septum and apex.
Evidence for dilated left ventricle with regional dysfunction in the LAD distribution. 
Markedly dysynchronous septal motion consistent with LBBB.

Thus, there is echo evidence of myocardial infarction (new or old), thought to be old.  Syncope could have been vasovagal (neurocardiogenic, triggered by dehydration), but with poor LV function, it could also have been due to ventricular tachycardia.  Acute type I MI is much less likely.  Troponin elevation is probably due to type II MI: underperfusion in the setting of chronic coronary disease.

The patient refused further investigations and was discharged.

Learning Points:

1. Syncope alone is an uncommon presentation of STEMI.  Any ECG finding with ST elevation should be approached with skepticism if there is no chest pain or chest discomfort.

Corollary: It should be very unusual for medics to activate the cath lab for syncope alone, without chest pain, as any associated ST Elevation is likely to be a false positive.

2. LVH is a common cause of false positive ST elevation, and often has reciprocal ST depression.

LBBB has recently been re-defined:

Strauss DG, Selvester RH, Wagner GS. Defining left bundle branch block in the era of cardiac resynchronization therapy. Am J Cardiol. 2011;107(6):927–34.

Here is a quote from the abstract: 

"Three key studies over the past 65 years have suggested that 1/3 of patients diagnosed with LBBB by conventional electrocardiographic criteria may not have true complete LBBB, but likely have a combination of left ventricular hypertrophy and left anterior fascicular block. On the basis of additional insights from computer simulations, the investigators propose stricter criteria for complete LBBB that include a QRS duration ≥140 ms for men and ≥130 ms for women, along with mid-QRS notching or slurring in ≥2 contiguous leads. Further studies are needed to reinvestigate the electrocardiographic criteria for complete LBBB and the implications of these criteria for selecting patients for CRT." 

One more very short article with full text: 

Int Cardiovasc Res J. 7(2):39-40.LBBB: State of the Art Criteria.