Thursday, June 17, 2021

ECG Blog #234 — What is the Unifying Diagnosis?


The ECG shown in Figure-1 was obtained from a man in his 60s, who presented to the ED (Emergency Department) with shortness of breath.

  • How would you interpret this ECG?
  • Clinically — What would you say about this patient?

 


Figure-1: ECG obtained from a man in his 60s who presented with shortness of breath (See text).


 

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NOTE #1: Some readers may prefer at this point to listen to the 7:20 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-50).

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Today’s ECG Media PEARL #50 (7:20 minutes Audio) — Reviews the ECG diagnosis of RVH (with distinction between pulmonary disease vs RVH).

  • NOTE #2: For an 8-page PDF review of RVH — CLICK HERE (These 8 pages appear below in Figures-3, -4, -5 and -6 in the ADDENDUM below).

 


 

My THOUGHTS on the ECG in Figure-1:

The rhythm is sinus at ~90-95/minute. The PR interval is normal. The QRS is not prolonged. The QTc is at most minimally prolonged. 

  • There is marked RAD (Right Axis Deviation) — as determined by the tiny r wave in lead I with predominantly negative S wave.
  • There is marked RAA (Right Atrial Abnormality) — as diagnosed by the finding of tall, peaked and pointed P waves in each of the inferior leads. In particular, the P wave in lead II is at least 3 mm tall, and as voluminous of a P wave as you are likely to see.

 

PEARL #1 (Beyond the Core): Many clinicians may be tempted to interpret the deep negative component of the P wave in lead V1 as consistent with LAA (Left Atrial Abnormality). However, on occasion — the right atrium may become so enlarged as to "flop over", and be viewed by right-sided lead V1 as manifesting electrical activity moving away from lead V1.

  • True LAA typically produces a rounded deep negative component to the P wave in lead V1. The fact that the negative component to the P wave in lead V1 of Figure-1 is pointed, in association with huge pointed P waves in each of the inferior leads suggests to me the likelihood of an extremely large right atrium, but no LAA.
  • NOTE: For more on review of ECG criteria for RAA and LAA — See ECG Blog #75.

 

Regarding Q-R-S-T Changes:

  • There are tiny q waves in the inferior leads that are unlikely to be of any clinical significance. But the Q wave in lead V1 is significant! (See PEARL #2 below!).
  • Regarding R Wave Progression — There is a predominant R wave in lead V1! (Normally there should be predominantly negativity in this right-sided lead). Of note — R wave amplitude dramatically decreases in size after lead V4 (with no more than tiny r waves + deep, persistent S waves in leads V4-thru-V6).
  • Regarding ST segments and T waves — There is ST segment flattening with slight ST depression in each of the inferior leads, and in leads V1-thru-V4. I'd interpret these ST-T wave changes as suggestive of RV “strain” in both of the lead areas where this finding may be seen ( = the anterior and inferior leads).

 

PEARL #2: The presence of a qR pattern in lead V1 in a patient with longstanding pulmonary disease is a marker of severe pulmonary hypertension, with increased risk of mortality (Waligóra et al: J Electrocardiol — 50(4): 476-483, 2017).

  • Technically — one might call the qR pattern in lead V1 consistent with incomplete RBBB, because terminal S waves are seen in lateral leads I and V6. My preference (given the totality of ECG findings) — is to attribute this qR pattern to severe RVH with pulmonary hypertension, rather than to postulate a conduction defect.

 

Putting It All Together:

I've listed ECG findings suggestive of RVH in Figure-2. Considering the History in today's case ( = a man in his 60s, who presented to the ED with shortness of breath) — the combination of the following ECG findings described above for Figure-1 strongly suggest longstanding, severe RVH with pulmonary hypertension.

  • Marked RAD.
  • Marked RAA.
  • Relatively low voltage in the limb leads (though not strictly qualifying for "low voltage" — since the QRS complex in lead III is clearly more than 5 mm in amplitude).
  • Persistent precordial S waves (with predominant S waves seen in leads V4, V5 and V6).
  • RV "strain" in both the inferior and anterior lead areas.
  • Predominant R wave in lead V1.


Follow-Up in Today's Case: This patient was found to have longstanding severe pulmonary disease with marked pulmonary hypertension and right ventricular dysfunction.

  • For more on Treatment of Heart Failure associated with Pulmonary Hypertension — Please check out my ADDENDUM #2 below (that I added on 6/20/2021).

 

 

Figure-2: ECG findings suggestive of RVH in adults (This subject is the theme of the above 7:20 minute Audio Pearl — and is summarized in Figures-3 through -6 in our Addendum below).


 

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).
  • There is no single ECG criterion 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).
  • 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.
  • Technically there is an S1Q3T3 pattern in ECG #1 (albeit the q wave in lead III is no more than a tiny negative deflection). That said, we need to remember that the finding of an S1Q3T3 pattern is of limited sensitivity and specificity for diagnosing acute PE — and, must be interpreted in the clinical context in which it is found. Although we do not know details of the clinical history in today's case (beyond shortness of breath) — I thought the totality of ECG findings in this tracing (especially the huge size of P waves and the predominant R, wave with qR pattern in lead V1) — favored longstanding RVH with pulmonary hypertension as more likely than acute PE (See ECG Blog #233for more on the S1Q3T3 pattern and ECG diagnosis of acute PE).

 

Final PEARL: The unifying diagosis that explains all of the ECG findings in Figure-1 is severe RVH with pulmonary hypertension. Regardless of whether the shortness of breath in today's case is the result of an exacerbation of this patient's longstanding pulmonary disease and/or superimposed pulmonary embolism — recognition of several (or more) of the ECG findings listed in Figure-2 in a patient with dyspnea should instantly alert you to the fact that you are not dealing with left-sided heart failure, but rather with a patient having severe pulmonary disease.

  • For more on Treatment of Heart Failure associated with Pulmonary Hypertension — Please check out my ADDENDUM #2 below (that I added on 6/20/2021).

 

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Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for making me aware of this case and allowing me to use this tracing.

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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #77 — Reviews ECG criteria for the diagnosis of RVH and RV “Strain”.
  • ECG Blog #75 — Reviews the ECG criteria for the diagnosis of RAA & LAA.
  • ECG Blog #233 — Reviews the ECG diagnosis for acute PE (Pulmonary Embolism).
  • ECG Blog #156 — Reviews a case of Tetralogy of Fallot in an adult (with marked RAA, RVH, pulmonary hypertension).

 

An Example of RVH in a 21yo Woman:

  • See My Comment at the BOTTOM of the page in the September 1, 2020 post on Dr. Smith’s ECG Blog (as I comment in detail on the 1st of the 6 cases that Dr. Smith presents).

 

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ADDENDUM (6/17/2021): I've excerpted below in Figures-3-4-5, and -6, — several pages from my ECG-2014-ePub — that summarize the ECG diagnosis of RVH (Right Ventricular Hypertrophy).

 

 

Figure-3: ECG Criteria for RVH.


 

 

Figure-4: ECG Criteria for RVH (Continued).


 

 

Figure-5: ECG diagnosis of pulmonary disease and RVH in children.


 

 

Figure-6: Example tracings of RVH.



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ADDENDUM #2 (6/20/2021): I did not discuss treatment of this patient — as this was not my personal case (and because my Blog is primarily focused on clinical ECG interpretation).

  • That said — the "Take-Home Points" from today's case are that the cause of this patient's shortness of breath are associated with severe RVH and probable severe Pulmonary Hypertension — and that an ECG like the one in today's case should immediately alert the treating clinicians to the fact that left-sided heart failure is unlikely to be the primary problem.
  • Treatment of acute dyspnea with associated severe pulmonary hypertension is complex — and usually within the realm of the pulmonologist or intensivist. Much depends on the cause of the pulmonary hypertension (about which we do not know in today's case).

 

The following comprehensive articles explore in detail KEY aspects of this condition:






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