Thursday, March 29, 2018

I saw this ECG only after the patient was discharged....

I was reading ECGs on the computer system when this one came up:
What do you think?

There is apparent ST elevation in III, with reciprocal ST depression in aVL.  At first glance, it looks like an inferior STEMI.

It also has a wavy pattern reminiscent of hypokalemia.  See these cases:

Prehospital Ventricular Fibrillation in a Young Woman. What is the Diagnosis?

But it looks very bizarre.  And I knew why. 

I looked to see what the patients symptoms were, and she was a 30-something woman with symptoms listed as "chest burning."

Then I saw that..... It was I who had seen and discharged this patient! 

It turns out she had complained to me only of cough and SOB, and had an asthma exacerbation, and we (I and an advanced practice provider) had treated her for an asthma exacerbation.  Her chest burning was only during coughing.  I had not known that she had an ECG recorded in triage.

The computer diagnosis was "Non-specific ST-T abnormality."   We immediately show all ECGs to faculty physicians in triage, but somehow this one did not get seen.

It had not occurred to me that she needed an ECG, and so I had not looked to see if she had had one.

The advance practice provider who was primarily responsible for the patient had not noticed the ECG abnormality.

So look at the ECG closely:

The 2 most bizarre leads are leads I and III.  aVR, aVL, and aVF also have ST-T abnormalities.

But lead II is completely normal.

How is this possible?

Only if there is artifact of one electrode, specifically the left arm electrode.

This diagram shows how limb leads are produced from the 3 electrodes:
Leads I - III are calculated like this:
Lead I: voltage difference between right arm and left arm electrode
Lead II: voltage difference between right arm and left leg electrodes
Lead III: voltage difference between left arm and left leg electrodes.

The augmented leads are calculated like this:
 aVR: from right arm electrode + average of left arm and left leg
aVL: left arm electrode + average of right arm and left leg
aVF: left leg electrode + average of right arm and left arm.

Notice that:
Lead II does not depend on the left arm electrode.
All other leads do depend on the left arm electrode.

Since, lead II is completely normal, there was a problem with the left arm electrode.

I was 99% certain that these ECG abnormalities were entirely due artifact.  But I wanted to be 100% certain, so we tried to call the patient back.  She said she would return, but she did not.

See this recent case:  Bizarre (Hyperacute??) T-waves

Tuesday, March 27, 2018

Do you want to be interrupted to view what the computer calls normal or nonspecific ECGs? 2 cases at once!

Two Cases

Male Patient

I was handed this ECG of a 40-something male patient.  It was recorded at triage.  The chief complaint was "chest pain."
The computer interpretation was "Nonspecific"
What do you think?

Female Patient

At the exact same time, I was viewing the computer queue of unconfirmed ECGs (read by computer but not yet overread by physician) and saw this one from a 40-something woman, about whom I knew nothing:
The computer interpretation was: "Normal ECG"
What do you think?

Male Patient: When I saw the first one, on a 40-something male, I knew it was a new inferior MI (minimal STE in III with reciprocal STD in aVL, without another explanation), but it looked like it might be subacute or reperfused because the T-wave is inverted in lead III and reciprocally upright in aVL.

Female patient: When I saw the 2nd one, I immediately suspected hyperacute inferior MI.


1. The inferior T-waves are too large
2. There is T-wave inversion in aVL
3. There is T-wave inversion in V2, suggestive of posterior MI

I looked in the EHR to find the patient, saw she was in triage, and went to locate her there.  She was sitting quietly in the waiting room.  She stated she had one hour of chest tightness.

I brought her by wheelchair to the ED to a room and recorded this ECG 15 minutes after the first one:
This time the computer called it: "Moderate ST depression."
Of course, it is actually clearly an acute inferior MI, even though (as is so frequent) it does not meet "STEMI criteria."
I activated the cath lab and brought her to our stabilization room.
I called the cardiologists to tell them that we have 2 acute MIs in the ED.

Male patient: I went back to the room of the first patient and he stated that he had been having chest pain on and off for 3 days.  He stated that it had never completely resolved but was constant, with waxing and waning, for the entire 72 hours.  At the moment I was talking with him it seemed to be on the waning end of the spectrum.  This "waning" corresponded with the inverted T-wave in lead III (inverted T-waves are signs of reperfusion -- this is Wellens' of the inferior wall).  The artery was probably open and so his MI was less acute than the woman's.

This is called"Acuteness" of the ECG of MI.

Female patient: I went to tend to the this woman, whose T-waves were upright and hyperacute, and made sure everything was set for the cath lab.

Male patient: Then I returned to the man and he was up out of bed, standing next to the bed and leaning on it, looking ill, holding his chest and stating that he had "terrible gas".

This alarmed me, so I brought him to the stabilization room as well, and recorded this ECG:
Now the inferior T-waves are upright (pseudonormalization) and there is more ST elevation and more reciprocal ST depression in aVL.  Plus ST depression in precordial leads.  
Thus, his artery had re-occluded and this explained why he had suddenly become more ill.

The female patient had just gone to the cath lab, and on that particular day we could not do 2 patients at once, so we gave him aspirin, heparin, ticagrelor and eptifibatide, as well as IV NTG for BP 160/100 (I did not suspect RV MI, though it would be optimal to record a right sided ECG).

His pain started to improve and we suspected that he was reperfusing.  So we recorded another ECG:
The T-wave in III is inverted again, though there is still quite a bit of STE.

The first ECG change after reperfusion is terminal T-wave inversion.
Later, the ST segments resolve. 

A bit later, all pain was resolved, and this ECG was recorded (this is a right sided ECG; that is to say, V1-V6 are V1R-V6R):
Limb leads are nearly identical to the first one.
ST elevation is now resolved.
(The artery is reperfused)
There is no evidence of right ventricular MI, but this means nothing by itself: even if the RV were involved, it would likely not manifest STE after reperfusion.

The cath lab was now open and he went for angiogram.  Here it is:
Obvious mid-RCA severe stenosis, but there is flow (reperfusion, spontaneous, autolysis)

Female patient:

She had a 2nd Obtuse Marginal occlusion (Left dominant, off the circumflex!).  It was actually a dissection, not an atherosclerotic plaque rupture.  Here is her post reperfusion ECG:
Nearly normalized

And the next morning:
Truly normalized T-waves.
Reperfusion early and without T-wave inversion!

Learning Points

1. Again, a "Normal ECG," as read by the computer algorithm in triage, would miss an acute MI.

2. One subtle finding may be normal variant (e.g., large inferior T-waves), but the combination of subtle findings makes the ECG diagnostic (add T-wave inversion in aVL and V2)

3. Acute coronary occlusion frequently presents with subtle ECG findings.  (We will give a systematic explanation of this when we publish our OMI Manifesto -- soon)

4. Inverted T-waves in MI are due to reperfusion or long duration.

5.  When such T-waves suddenly become upright, it is due to re-occlusion (this is often called "pseudonormalization" of the T-wave)

6.  All else being equal, the patient with the upright T-waves in the affected area of infarct is the one who has the persistently occluded artery and needs to have priority in going to the cath lab.

7.  Adjunctive anti-thrombotic, anti-platelet, and anti-ischemic therapy makes early spontaneous reperfusion more likely.

Saturday, March 24, 2018

You have two hours to save this patient's life

Written by Pendell Meyers, edits by Steve Smith

A female in her 60s with history of CAD s/p PCI and CABG, alcohol abuse, and recurrent pancreatitis presented at 14:55 complaining of sudden onset epigastric pain. Initial vital signs were heart rate 44 bpm, respiratory rate 16, BP 143/67, SpO2 96% on room air. On initial exam she was in mild distress and complaining of severe nausea.

Here is her initial ECG:
What do you think?

There is decreased ECG quality due to baseline movement. Despite this, there are clearly hyperacute T-waves in lead III with reciprocal negative hyperacute T-waves in aVL (and lead I) with likely a small amount of STD in aVL. This is diagnostic of acute transmural inferior acute MI, with the most likely etiology being acute coronary occlusion. There is clear STD in V2 indicative of posterior involvement. Sinus bradycardia despite critical illness also points toward inferior acute coronary occlusion (as the SA and AV node are generally supplied by the same vessel as the inferior wall).

Here are two immediate repeat ECGs performed in efforts to get less baseline wander and artifact:

The same findings are evident throughout, but with baseline movement obscuring various sections. There is even a very small amount of STE present in III on the third ECG.

The emergency physicians activated the cath lab. Apparently this decision was made only on perceived STE in lead III on the last of the ECGs above.

This happened to have been the 6th emergent cath lab activation called by the ED within the past 4 hours (!). The cardiologist came to bedside and deactivated the cath lab. His opinion was that the ECGs did not meet STEMI criteria, that she was probably not suffering from ACS given her pain was epigastric and he interpreted the physical exam as showing epigastric tenderness to palpation.

Initial labs returned showing a first troponin negative.

At approximately 15:30, the nurse called for a physician to bedside because the patients blood pressure dropped to 89 systolic and she became lightheaded.

Here is the repeat ECG at that time:
Massive STD V1-V5, maximal in V2-V3, diagnostic of posterior acute MI. Interestingly, the inferior hyperacute T-waves are no longer present. There is obligatory STE in aVR generated by the large amounts of STD elsewhere.  

ST Elevation in aVR in the setting of inferior MI should also tip you off to possible right ventricular MI (RV MI) and to the need for a right sided ECG. In fact, it is a good idea to do a right sided ECG in every inferior MI, as there is no finding that is 100% sensitive for RV MI on the standard 12-lead ECG.

A possible explanation is that the thrombus in the proximal segment of the vessel supplying the inferior wall may have embolized distally and occluded the portion supplying only the posterior wall. The problem with this hypothesis is that occlusion of the proximal part of the vessel should also have caused posterior ischemia at that time. It is possible that the first ECGs were too early to detect this posterior ischemia. This theory is not provable without cath, but is an anatomic possibility. We do not have records to indicate if her native RCA is patent, or what graft supplies the inferior wall if applicable.

Based on this ECG, the cath lab was reactivated with concern for posterior acute coronary occlusion.

The cardiologist came back and this time took the patient immediately to the cath lab. However, the cath lab was occupied by at least one of the prior 5 "STEMI activations" from earlier in the day, thus there was a delay in which the patient was kept in the cath holding area.

At approximately 1600, the patient acutely decompensated even further. She was rushed into the cath lab, where she lost her pulses just as she was placed on the cath lab table, suffering PEA arrest. ACLS was initiated. The notes state that a transvenous pacemaker was attempted but "never entered her heart" for unclear reasons. No left heart cath was performed. I cannot find an explanation as to why this patient was not an ECMO candidate. She was pronounced around 1700.

It is overwhelmingly likely that this patient died from acute coronary occlusion, but I do not have an angiogram to prove it. Autopsy was not performed.

Learning Points:

1) You must advocate for your patients, as "subtle" findings such as hyperacute T-waves are simply not yet recognized by a wide range of providers as an early finding of acute coronary occlusion (the event for which "STEMI" is a very poor surrogate term)

2) Repeat ECGs are important.

3) Bradycardia in the setting of any critical illness must prompt immediate consideration of hyperkalemia, acute coronary occlusion (usually inferior), and primary rhythm disturbance, among other less common and less reversible causes.

4) This patient, and many others with similar initial ECGs, is an unfortunate victim of a broken paradigm for acute MI management: STEMI vs. NSTEMI. This is a false dichotomy that inspires ignorance to anything except the ST segments. The "STEMI criteria" seem to have been one of the barriers to emergent catheterization which was not overcome in this case, ultimately leading to the patient's death. It is very likely that this patient could have been saved in the two hours from initial ECG to cardiac arrest.

Tuesday, March 20, 2018

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?

Friday, March 16, 2018

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:

Wednesday, March 14, 2018

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.

Monday, March 12, 2018

A crashing patient with an abnormal ECG that you must recognize

Written by Pendell Meyers, with edits from Steve Smith

Let's consider this nearly pathognomonic ECG without the clinical context (because sometimes the clinical context will not be as easy as in this case).
What is the answer?

This ECG is diagnostic of hemodynamically significant acute right heart strain. Notice I did not say "pulmonary embolism," because any form of severe acute right heart strain may produce this ECG. This includes, but is not limited to, PE, asthma/COPD exacerbation, hypoxic vasoconstriction from pneumonia, acute pulmonary hypertension exacerbation.  It has even been seen anecdotally in acute cessation or discontinuation of continuous IV pulmonary vasodilator.

The findings include sinus tachycardia, characteristic QRS morphology most diagnostic in V3 with a small R wave followed by a very large S wave with a convex upward ST segment morphology, ST segment strain morphology in the inferior and anterior leads leading to deep symmetric T-wave inversion.

Why is it not Wellens??? (Wellens pattern is a term which refers to coronary reperfusion morphology in the anterior leads)

The best answer is because the entire gestalt of the ECG shows acute right heart strain instead, and just does not look like Wellens after you've seen Wellens hundreds of times. It is true that the morphology of the T-wave inversions can be very similar in anterior reperfusion syndrome (Wellens). It is also true that anterior and inferior T-wave inversion could be consistent with reperfusion of a type III wraparound LAD occlusion, despite the fact that Kosuge et al showed that T-wave inversion in lead III is much more likely to be PE than ACS if your differential contains nothing else.  However, in reperfusion (Wellens'), the symptoms are resolved at the time of the ECG.  Thus, it is critical to compare the ECG with the symptomatic state of the patient!  

Differences of Pulmonary Embolism T-waves from Wellens' T-waves:
1. Wellens' is a syndrome of a painless period following an anginal (chest pain) event.  Coronary reperfusion changes on ECG should be accompanied by significant reduction or resolution of symptoms. In this case we have a crashing patient while T-wave inversion is ongoing!

2. Acute coronary occlusion (especially during reperfusion) is very rarely accompanied by tachycardia.  When there is tachycardia, the patient is in cardiogenic shock with very poor LV function on bedside echo.

3. The T-waves simply look different in Wellens'.  Here is an example of Wellens'.  We hope you can see the difference:

See these cases for more examples: 

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

Please notice in particular the morphology in V2-V3, as I believe this is particularly helpful to describe as evidence of acute right heart strain, including:

- Generally much bigger S-wave than R-wave
- Usually either isoelectric J-point or some small J-point elevation followed by convex upward ST segment elevation rollercoastering into T-wave inversion
- Usually some ST segment depression in the more lateral leads V4-V6 and the inferior leads, also with T-wave inversion
- Please note that these QRS characteristics will not apply in the not-uncommon scenario that the patient develops acute RBBB because of the strain on the RV

Here are the blown up images of V2-V3 from several of the cases on this blog with acute right heart strain (all but one of which was due to pulmonary embolism, and the other was due to acute severe asthma exacerbation)

Now that we've learned the lesson, let's watch this very interesting case play out:

A female in her 40s with history of HTN and obesity presented with progressively worsening dyspnea with mild exertion, and now with dyspnea at rest over the past 4 days. She also complained of generalized weakness, lightheadedness, diaphoresis, chest pain, and cough. On initial exam she appeared acutely ill, with initial vitals showing tachycardia, hypoxia, and borderline hypotension.

Here is her initial ECG, followed by her repeat ECG approximately 15 minutes later:

Bedside echo was done.  This one is from a previous case on this blog,  but is similar to this patient:

This shows impressively obvious right heart strain.  The LV is small (underfilled) with good function. 

She was appropriately anticoagulated immediately with heparin before going to CT scan.
There are filling defects in both main pulmonary arteries. The pulmonary artery trunk is dilated at 35mm per radiology report.

Filling defects are seen to extend to bilateral lobar, interloper, and segmental branches diffusely throughout both lungs. This is a very large clot burden. Radiology commented that the inter ventricular septum is bowed towards the left ventricle, suggestive of right heart strain.

Troponin T returned elevated at 0.12 ng/mL. NT pro BP returned at 10,676 pg/mL.

Despite heparin and supportive care, the patients mental status and blood pressure worsened. She was diagnosed with massive PE and given intravenous tPA with rapid improvement in hemodynamics and mental status.

She had an uneventful ICU course and improved steadily over the course of a week. She was discharged and did well.

Here is her ECG on day 2 after much improvement in hemodynamics and oxygenation:
Tachycardia has resolved. ST and T-wave abnormalities evolving appropriately.

Here is her ECG on day 4:
Almost entirely back to normal.

 Learning Points:

1) The history and exam will not always be this obvious, yet in cases this severe, the ECG findings often are obvious if you know what to look for.

2) The cells of the right ventricle do not know why they are having such a hard time when they report their acute strain on the ECG. Whether it's a PE or a severe asthma attack, the cellular physiology of these cells is acutely the same. Therefore the ECG is also indistinguishable between acute right heart strain etiologies.

3) Reperfusion T-wave inversion should be present in the pain free state. These T-wave inversions in the anterior and inferior leads during pain are likely to be due to acute right heart strain from PE.

Primer on the ECG in Pulmonary Embolism:
These are findings of acute right heart strain, and could be seen in any condition which results in a rapid rise in pulmonary artery pressure. This includes hypoxia because of "pulmonary hypoxic vasoconstriction" 

The ECG is not sensitive for PE, but when there are findings such as S1Q3T3 or anterior T-wave inversions, or new RBBB, then they have a (+) likelihood ratio and the S1Q3T3, or even just the T3, may help to differentiate Wellens' from PE. 

Stein et al. found normal ECGs in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE.  Today, however, that number would be higher because we diagnose more of the submassive PEs that have minimal symptoms.

This is a paper worth readingMarchik et al. studied ECG findings of PE in 6049 patients, 354 of whom had PE.  They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. 

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS.  In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

Witting et al. looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls.  This does not contradict the conclusions of Kosuge et al. that when T-wave inversions in the right precordial leads and in lead III are indeed present, then PE may indeed by more common.  In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrari found that anterior T-wave inversions were the most common ECG finding in massive PE. 

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