Tuesday, September 1, 2020

21 year old woman with CP, SOB, then syncope, and with ST depression with T-wave inversion in V1-V3

You can see that I (Smith) have too much time on my hands now, as it is a beautiful Saturday afternoon and I am laid up, non-weight bearing for 6 weeks after knee surgery:


Case 1.

A 21 year woman developed SOB, CP and epigastric pain while running for a bus, then had syncope.  She was brought by ambulance.  Medics report that when they arrived she was awake but ashen and cyanotic, and they could not obtain a blood pressure.

On arrival to the ED she was alert and asymptomatic, and she had a BP of 100/60 and a normal exam.

She reported one previous episode of syncope 3 months prior.  She had been to another ED at that time, but sent home without further diagnosis.  It is uncertain whether she had an ECG recorded then or not, and, if so, what the interpretation was.

Here is her ED ECG:
Sinus tachycardia.
T-wave inversions in V1-V4, and lead III.
What do you think?














Residents were worried about pulmonary embolism, which is very reasonable.  However, I immediately recognized that this ECG represented a chronic condition, not an acute one.

What is this chronic condition?   





There are large R-waves in the right precordium (V1-V3) and a deep S-wave in lead I.  The axis is slightly greater than 90 degrees, perhaps 95-100. This is diagnostic of right ventricular hypertrophy (RVH).  

The large R-wave and high RS ratio in V1 tell us that this is chronic RV hypertrophy, not just acute RV strain.  

The ST depression and negative T-waves are the expected abnormal repolarization in the setting of abnormal depolarization -- these too are typical of RVH. These do not imply any acute ischemia.

We did get a d dimer and it was negative and we admitted her to the hospital on a monitor.  Troponins were mildly elevated, with rise and fall.  This would be a type 2 MI of the right ventricle due to hypotension.


She was admitted to the hospital and found on echo and right sided catheterization to have significant right ventricular hypertrophy, pulmonary hypertension with pulmonary artery pressures of 80/26 mmHg, a patent foramen ovale with some right to left shunting.  (Normal pulmonary MAP = 15 mmHg and elevated is MAP above 25 or systolic above 35 mmHg.)  The right to left shunting implies there would be some element of cyanotic heart disease -- I do not have the O2 saturations available.

She was diagnosed with primary pulmonary hypertension.

Syncope

You can read a lot about syncope here, including about the ECG in syncope: 

Emergency Department Syncope Workup: After H and P, ECG is the Only Test Required for Every Patient.....



Here is recently published data on the ECG in syncope:

Here is the paper
ECG in Canadian Syncope Risk Score was derived (full text): 
https://www.cmaj.ca/content/cmaj/188/12/E289.full.pdf

And validated (abstract only):
https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2763181

These tables are from the derivation.

These are univariate ECG predictors of adverse events:
Notice that Right Ventricular Hypertrophy (RVH) is not here, nor is Axis greater than 90

Multivariate analysis -- these 3 ECG findings were independent risk factors for serious adverse events:


Here are all the independent variables found in the derivation:
Would our patient be classified as high risk?
Yes, but only if we recognized that the clinical presentation is "cardiac syncope," which is obvious given the symptoms of 1) exertion 2) CP and SOB and 3) prehospital BP.
 
In this study, except for troponin elevation, Gestalt was the best predictor.
The article does not specify the QT correction method

Why is right ventricular hypertrophy (RVH) not found in this large study of syncope?  Probably because it is not common enough to be identified in a general syncope study.  Not every high risk factor will be identified in such studies, but it is obvious that RVH is a dangerous condition and that, if identified on ECG, needs further workup.  

Why were so few ECG findings predictive?

Because most abnormal ECG findings were considered adverse outcomes in their own right and not evaluated as predictors!!


Why does pulmonary hypertension cause syncope?

The RV normally functions at low pressure, MAP about 15, or 20/12.  Unlike the LV, which is under high pressure during systole, and therefore is perfused during diastole, the RV can be perfused during the entire cardiac cycle.  Her resting pulmonary pressure is 80/26, and so her RV can only perfuse during diastole. 

In addition, the RV is usually thin-walled with high compliance, and is able to expand the free wall when there is increased preload.

With a stiff RV, any sudden increase in RV pressure leads to both RV ischemia (and resulting RV dysfunction, with some degree of pump failure), decreased RV output, and thus decreased LV filling (lowered diastolic filling pressure due to poor RV output, and decreased LV size due to septal bulging).  All of this means decreased LV stroke volume. 

Also, high RV pressure may result in tricuspid regurgitation, further diminishing RV output.

What causes an increase in RV pressure?  Anything which increases RV preload or afterload, especially exertion, can trigger the above cascade.

Fortunately for her, this was transient.  Severe cases of RV overload can spiral downward into death.

RV failure is a complicated topic. Here is a great article (full text) on RV failure diagnosis and management in the ED, from Annals of EM, by Susan Wilcox: https://emcrit.org/wp-content/uploads/2016/03/Pulm-HTN-Wilcox.pdf 



Case 2.
Here is another case of RV hypertrophy, diagnosed in the ED by ECG:

This 23 year old presented to the Emergency Department with pharyngitis, but in review of systems also complained of dyspnea on exertion.  (Review of systems actually made a difference!).

This ECG was recorded:



The wide complex (QRS 155 ms) may distract your attention from the rhythm, which is simply sinus. There are massive S-waves in lateral leads, with an extreme right axis deviation (180 or -180, same thing). There are massive R' waves of RBBB in the right precordial leads.   The combination of wide S-wave in V5 and V6, and large R' wave in lead V1 is diagnostic of RBBB.  RBBB normally has a large R'-wave, but when more than 15 mm, it is suggestive of additional RV hypertrophy.  Here the R'-wave in V1 is 65 mm !!  

So this is diagnostic of massive Right ventricular hypertrophy. One might be concerned for ischemia because of the large amount of ST depression and T wave inversion in V1-V3. Some discordant (in the opposite direction of a high voltage or bundle branch block QRS) ST depression and T inversion is usually found at baseline in RBBB, but this is more than usual. However, the voltage is also more than usual. The ratio of the ST depression to QRS voltage is about 4mm to 60 mm, or 0.067, which is normal. The troponin was mildly elevated due to demand ischemia of the RV.

Further history, only obtained after the ECG, revealed congenital pulmonic stenosis which was dilated at age 7 days. The patient did not have further followup since then! 

Echocardiogram revealed an estimated peak systolic pulmonary pressure of 127 mmHg with RV enlargement and severe hypertrophy.



Case 3:
The ECG can help you to differentiate acute PE from RV hypertrophy.  Click the link to see this amazing case with a bedside cardiac echo showing large RV, but the ECG tells you it is chronic:


Chronic Right Ventricular Hypertrophy, or Acute Right Heart Strain? The ECG Helps Make the Diagnosis.




Case 4.
Knowing what RV hypertrophy looks like can also reassure you.

A 30-something woman with known history of pulmonary hypertension due to chronic pulmonary emboli presented with 12 hours of substernal chest pain.

Here was her ED ECG:


This precordial T-wave inversion is typical of right ventricular hypertrophy (RVH).  However, most other features of RVH are not present.  There is an incomplete RBBB, which does support RVH.  But there is no right axis deviation (axis is however borderline at 83 degrees, nearly vertical.  There is no large R-wave in V1.  However, these findings are not sensitive enough for RVH to rule it out.

The T-wave morphology, along with the known history of pulmonary hypertension, should alert you to look for a previous ECG.

I saw this and thought immediately that this was probably her baseline EKG.  We looked for old ones, and indeed previous ECGs were identical.

The patient ruled out for both PE and MI while in the ED, and could be discharged.  This was her baseline ECG.  Our diagnosis was gastroesophageal reflux.


2 ECGs: RVH mimics ACS
Unless you know what RVH looks like:

Case 5

55 year old woman with chest pain and precordial T-wave Inversions

This one does have right axis deviation and a large R-wave in V1




Case 6
A 50-something male with Dyspnea
This one also has slight right axis deviation and a large R-wave in V1


===================================
MY Comment by KEN GRAUER, MD (9/1/2020):
===================================
In my experience — one of the most commonly overlooked diagnoses in the area of 12-lead ECG interpretation is longstanding RVH in an adult. The consequences of missing this diagnosis are potentially life-threatening — as emphasized above by Dr. Smith in 6 illustrative case studies.
  • In the hope of enhancing recognition of advanced RVH and pulmonary hypertension on ECG — I’d like to delve deeper into the 1st Case presented. For clarity — I’ve reproduced in Figure-1 this 1st ECG shown above in Case 1.
  • For those wanting a refresher on recognition of ECG criteria for RVH CLICK HERE  and for recognition of RAA — CLICK HERE.

Figure-1: The ECG shown above in Case 1 (See text).



As noted in Figure-1 — the history associated with this tracing is that of a 21-year old woman who presented with dyspnea, chest discomfort and exertional syncope.
  • QUESTION: HOW MANY findings can YOU identify on ECG #1 that support the diagnosis of RVH and pulmonary hypertension?
  • HINT: If you come up with less than 7 supportive ECG findings — You may want to take another look at ECG #1 (and/or the links I provide above).

My THOUGHTS on ECG #1: The rhythm is sinus tachycardia at a rate just over 100/minute. ECG findings in favor of RVH include the following:
  • A vertical frontal plane axis (slightly more positive than +90 degrees — given slightly more negativity of the QRS in lead I and clearly more net positivity for the QRS in lead III than in lead II).
  • RAA (as diagnosed by the finding of tall, peaked and pointed P waves in the inferior leads — which are ≥2.5 mm tall in lead II).
  • There is a predominant R wave in right-sided lead V1 (Normally there should be predominantly negativity in this right-sided lead).
  • There is ST-T wave depression suggestive of RV “strain” in both of the lead areas where this finding may be seen ( = the anterior and inferior leads).
  • There is persistence of sizeable S waves across the precordium (ie, the finding of fairly deep S waves in leads V5 and V6 suggests significant forces away from these left-sided leads — which in this tracing means there is probably an increase in right-sided forces).

Additional PEARLS in ECG #1 in Support of RVH:
  • There are S waves in the 3 standard limb leads ( = leads I, II, III) — which is a finding seen in pulmonary disease.
  • Although most of the time the diagnosis of RAA is made by the finding of tall, peaked and pointed P waves in the inferior leads — sometimes the only clue to RAA that you will see is the presence of overly peaked and pointed P waves in one or more anterior leads (most impressive here in lead V2).
  • In the setting of RVH with a predominant R wave in lead V1 — the finding of a Q wave in lead V1 (ie, a qR pattern, as seen in ECG #1) strongly suggests there is pulmonary hypertension.
  • NOTE #1: Technically there is an S1Q3T3 in ECG #1 — but we need to remember that this finding is of limited sensitivity and specificity for diagnosing acute PE and must be interpreted in the clinical context in which it is found. As per Dr. Smith — the clinical context in Case 1 overwhelming favors interpreting ECG findings in this tracing as supporting longstanding RVH + pulmonary hypertension (and not acute PE).

Additional PEARLS Regarding the ECG Diagnosis of RVH:
  • Detection of RVH in adults by ECG criteria is often exceedingly difficult. This is because the left ventricle is normally so much larger and thicker than the right ventricle — that it masks even moderate increases in RV chamber size. As a result, many patients with RVH will not be identified IF assessment of chamber enlargement is limited to obtaining an ECG (an Echo will often be needed to know for sure).
  • In contrast to adults — ECG diagnosis of RVH is often surprisingly EASY in children with congenital heart disease (because the relative size of the RV compared to the LV is not nearly as different in infants and young children as it is in adults).
  • KEY POINT — By the time you see a predominant R wave in lead V1 of an adult — the extent of RVH is usually marked (ie, the patient almost always has end-stage pulmonary disease and/or pulmonary hypertension).
  • NOTE #2: There is no single ECG criteria that by itself can reliably diagnose RVH. Instead, a combination of ECG findings is needed — especially when seen in a likely clinical setting (ie, COPD, long-term asthma, right-sided heart failure, pulmonary hypertension).
  • NOTE #3: There is only 1 condition in medicine that produces right atrial enlargement without also producing RVH. That condition is tricuspid stenosis, which is rare. Therefore, the ECG finding of RAA that is not the result of slender body habitus — often provides an important indirect clue to the presence of RVH.

FINAL Thought on Case 1: Retrospectively looking back at Case 1 — Considering the young age of this patient and the severity of her symptoms on presentation (ie, exertional syncope is alarming!) — the combination of ECG findings described above should prompt suspicion of primary pulmonary hypertension within the few seconds it takes to recognize the predominant R wave in lead V1 + RAA + inferior and anterior lead RV “strain”.
  • The history in this case of dyspnea, chest discomfort and exertional syncope in a young woman is typical for primary pulmonary hypertension.
  • The number of diagnostic entities that are likely to present de novo in a young adult female who manifests such ECG markers of longstanding severe RVH + pulmonary hypertension as we see in ECG #1 is limited.


8 comments:

  1. Hello Dr. Smith and Dr. Grauer,

    apart from the ECG findings typical of RVH, isn't there also a very long QT with U waves in the first ECG? If so, how do you explain that?

    Thanks!

    ReplyDelete
    Replies
    1. @ Giacomo — I think it is hard to know what a prolonged QTc in this patient means given the rapid rate and RV “strain”. I think it’s difficult in this tracing ( = my opinion) to distinguish a biphasic T wave from a U wave (I thought we were primarily seeing biphasic T waves … but hard to be certain). It wasn’t my case — and there is no mention of serum K+ & Mg++ — but electrolyte disturbance could be a contributing factor. So, you ARE correct that the QTc might be prolonged (I would not call it “very” prolonged given the heart rate) — and electrolyte disturbance could be contributing. All that said — the “THEME” of this tracing is severe RVH + pulmonary hypertension — and that’s where I’d focus my attention ( in addition to checking serum lytes). THANKS for your comment!

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  2. What's the best way to differentiate between RVH and posterior MI?

    ReplyDelete
    Replies
    1. @ PM — Good question! If posterior MI is acute — there will almost always be associated acute inferior lead changes (because the RCA commonly supplies both the inferior and posterior walls of the LV). However — with RVH — there should be (as I emphasize in my comment above) — additional signs — and THAT is what we see in ECG #1 (RAA, RV strain in inferior and anterior leads, qR in lead V1, persistent lateral precordial S waves, S waves in leads I,II,III).

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  3. Why can't this be RBBB instead of being RVH?

    ReplyDelete
    Replies
    1. Hello MG. I will assume you are talking about ECG #1 in my Figure-1 (from Case 1). You ask an EXCELLENT question!

      FIRST — It is true that there is some overlap between certain cases of RVH that manifest with a predominant R wave in lead V1 and RBBB. And sometimes — both conditions may be present. That said I believe the “theme” in ECG #1 is RVH, RVH, RVH + Pulmonary Hypertension.

      This clearly isn’t complete RBBB — because the QRS complex is not wide (at most, I measure 0.10 second duration). And this ECG lacks the terminal WIDE S waves that should be seen in leads I and V6 when there is complete RBBB.

      Everything about this case says, “RVH + Pulmonary H.T.”. The clinical presentation is very typical for primary pulmonary hypertension in a young woman — and the qR in V1 suggests pulmonary hypertension (it lacks the initial small positive deflection that is usually found when there is incomplete or complete RBBB). Supportive findings of RVH include all of the things I mentioned above in My Comment (Tall R in V1; RAA; S waves in I,II,III & persisting through to V6; RV “strain” in inferior and anterior leads).

      The above said — it IS true that I can’t rule out in addition to RVH, that there may also be incomplete RBBB (because there ARE terminal narrow s waves in I and V6 + an R’ in V1) — but the predominance of RVH features suggest to me that there is no conduction defect.

      Again — there ARE cases in which distinction from these 2 entities is clearly more difficult.

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  4. Excellent cases. Nothing to add except an anecdote. My very first night as a first-year internal medicine resident was ER duty (no EM residencies back then). A young woman around 20 y/o came in complaining of a headache. I noted a BP around 180/110 and asked her about neuro symptoms and did a thorough neuro exam, after which I gave her some medicine for her hypertension expecting that to relieve her headache. A few minutes later a nurse came and got me, telling me that the patient was turning blue and getting short of breath. I rushed back to see her. I put her on O2 with no improvement. I had no idea what was happening. Fortunately for me, there was an older, much more experienced internist in the ER seeing one of his own patients and I enlisted his help. After telling him what had happened, he immediately listened to her chest. I remember wondering why he was listening to her chest when she obviously had a neuro problem. Then he asked her, "Do you have any heart problems?" and she answered, "Yes. I have a patent ductus arteriosus." He had her pull her knees up tightly on her chest and then told me that the O2 would start to help in a few minutes (which it did). I learned so many lessons that night - the importance of a complete history and physical exam, the need to look for a cause of hypertension in a very young person and a thorough, first-hand understanding of Eisenmenger's Syndrome. I had not thought about that night for years until I read this post. Thanks!

    Jerry W. Jones, MD FACEP FAAEM
    https://medicusofhouston.com

    ReplyDelete
    Replies
    1. THANKS so much Jerry. Your comment reminds me of my anecdote related to this post — being awakened in the middle of the night for what I thought was the umpteenth case of LV failure/acute pulmonary edema — only to find that instead of severe LVH, the ECG showed severe RVH with RV stain ... — which highlighted to me how being able to recognize that uncommon case of severe RVH on ECG could totally change the management approach. THANKS again for your comment! — :)

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