Sunday, June 27, 2021

ECG Blog #237 (52) — A 70-Year Old with Dizziness


The ECG shown in Figure-1 was obtained from a patient in his 70s — who presented to the ED (Emergency Department) with dizziness.

  • How would you interpret this ECG?
  • And — Is there Complete AV Block?
  • In addition to the interesting rhythm — there are at least 4 other ECG findings that should be commented on. How many of these other findings do you recognize?

 

Figure-1: ECG obtained from a patient with dizziness (See text).


 

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NOTE: Some readers may prefer at this point to refer to ECG Media PEARL #52 ( = the Video Pearl that appears in ECG Blog #236) — before reading My Thoughts regarding the ECG in Figure-1. This 15-minute ECG Video reviews the types of 2nd-degree AV blocks (as opposed to 3rd-degree AV block).

  • For those wanting review on HOW to read (and/or drawLaddergrams — Please check out my 5-minute ECG Video and other material in ECG Blog #188.

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My THOUGHTS on the ECG in Figure-1:

As usual — I find it best to begin by assessing the cardiac rhythm. For clarity — I've added colored arrows in Figure-2, in which I label atrial activity. My sequential thought process for interpreting this tracing was the following:

  • RED arrows in Figure-2 indicate P waves we can definitely see.
  • PINK arrows highlight places where P waves would need to be found IF the atrial rhythm is regular. Although T waves in many of the leads on this 12-lead tracing look more peaked than expected — it is not possible to prove that P waves are hiding under the PINK arrows from this single tracing alone. That said — by far, the most likely explanation for atrial activity is that the atrial rhythm is regular! (It is far less likely for there to be SA node exit block after every third P wave).
  • The QRS is wide (I measure 3 little boxes = 0.12 second in several leads). QRS morphology is consistent with RBBB (Right Bundle Branch Block) because: i) there is a widened and predominantly upright QRS complex in right-sided lead V1; and, ii) there are wide, terminal S waves in lateral leads I and V6.
  • QRS morphology is also consistent with LAHB (Left Anterior HemiBlock) because there is predominant negativity in each of the inferior leads. Therefore — there is bifascicular block (ie, RBBB + LAHB).
  • The PR interval preceding each QRS complex in the long lead II rhythm strip is constant. Therefore — Every third P wave is conducting! Since each QRS complex in this tracing is conducted — the rhythm can not possibly be complete AV block. Instead, the rhythm in Figure-2 represents a "high-grade" form of 2nd-degree Ablock (ie, "high-grade" — because 2 out of every 3 P waves within each group fail to conduct, despite having adequate opportunity to do so).
  • There is marked bradycardia! The atrial rate is approximately 110/minute. Since only 1 out of every 3 P waves is conducted — the ventricular rate is 1/3 the atrial rate, or between ~35-40/minute.



Figure-2: I've labeled atrial activity from Figure-1 with colored arrows (See text).



PEARLs regarding the Rhythm in Figure-2:

The rhythm in Figure-2 most probably represents the Mobitz II form of 2nd-degree AV block because: iConsecutive P waves in each grouping fail to conduct — and that is far less common with Mobitz I 2nd-degree AV block; ii) The QRS complex is wide with morphology consistent with bifascicular block (ie, RBBB/LAHB— whereas the QRS complex most often is narrow with Mobitz I; andiii) It is much more common to see a normal (or relatively normal) PR interval for conducted beats when the rhythm is Mobitz II — because the principal conduction problem lies below the AV node (whereas a long PR interval is a common accompaniment of Mobitz I, in which the level of AV block is at the AV node).

  • That said — we can not conclusively prove that the rhythm in this tracing is Mobitz II, because we never see 2 P waves in a row that conduct with the same PR interval. Therefore, we have not proven that the PR interval would not increase if given a chance to do so.
  • Regardless of whether the conduction disturbance in Figure-2 represents Mobitz II or not — consistent failure of consecutive P waves to conduct (which results in marked bradycardia) suggests that unless a "fixable cause" (ie, medication effect, acute ischemia) is found — that a pacemaker will be needed in this symptomatic patient in his 70s.

 

ECG Findings that Should be Commented On:

ECG findings that should be specifically noted on the interpretation of this tracing include several that we have already mentioned — which are:

  • High-grade 2nd-degree AV block, with resultant marked bradycardia.
  • Complete RBBB.
  • LAHB (thereforebifascicular block = RBBB/LAHB).

 

Additional ECG findings that should be specifically noted include:

  • The Q wave in lead V1 — which suggests anteroseptal MI has occurred at some point in time (ie, Simple RBBB should manifest an rSR' complex in lead V1 — but without any Q wave).
  • Low voltage. While not satisfying strict criteria for low voltage (ie, No R wave exceeding 5 mm in any limb lead) — overall voltage in the 12 leads of this tracing appears reduced. The clinical significance of this uncertain from the information available.
  • Flattening of the ST segment in multiple leads (ie, in leads I, II, III; aVL, aVF; V2-thru-V6) — and — taller-than-expected T waves in leads V2-thru-V5. While some of the increase in T wave amplitude could be the result of the hidden P waves — in association with the diffuse ST segment flattening and the Q wave in lead V1, these subtle findings could reflect a recent event — which could be the reason for this patient's severe conduction disturbance!

 

 

LADDERGRAM of Today's Case:

My laddergram for today's case is straightforward (Figure-3):

  • One out of every 3 P waves in each grouping is conducted to the ventricles.
  • Since I suspect the conduction disturbance represents the Mobitz II form of 2nd-degree AV block — I did not draw a progressive increase in conduction time within the AV nodal tier, but instead showed simple failed conduction for 2 out of every 3 P waves.

 

 

Figure-3: I've labeled P waves that I saw in Figure-1 with colored arrows (See text).
 


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Acknowledgment: My appreciation to Neeraj Sonewane (from Nagpur, India) for allowing me to use this tracing.

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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #236 — Reviews the Types of 2nd-Degree AV Block (as opposed to 3rd-degree AV block). 
  • ECG Blog #188 — Reviews the essentials for reading (and/or drawingLaddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts. 
  • ECG Blog #203 — Reviews the ECG diagnosis of Axis and Hemiblocks (therefore Bifascicular Blocks) — Check out the 12-minute ECG Video (MP-21) in this post.





Thursday, June 24, 2021

ECG Blog #236 (52): The 2nd-Degree AV Blocks (VIDEO)


My GOAL in today's ECG Blog #236 is to clarify by means of a 15-minute ECG Video — the 2nd-Degree AV Blocks, of which there are 3 Types:
  • Mobitz I ( = AV Wenckebach).
  • Mobitz II.
  • 2nd-Degree AV Block with 2:1 AV conduction.


This 15-minute ECG Video (Media PEARL #52) — Reviews the 3 Types of 2nd-Degree AV Blockplus — the hard-to-define term of "high-grade" AV block. I supplement this material with the following 2 PDF handouts.
  • Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks (This is a free download).
  • Section 20 (54 pages = the "long" Answer) from my ACLS-2013-Arrhythmias Expanded Version provides detailed discussion of WHAT the AV Blocks are — and what they are not! (This is a free download).

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For MORE on Diagnosis of ABlocks/AV Dissociation:
  • ECG Media Pearl #4 (4:30 minutes Audio— The ABlocks & WHEN to Suspect Mobitz I (1/21/2021) — See ECG Blog #186 —
  • ECG Media Pearl #(12:00 minutes Video ECG Blog #189 — What type of AV Block? Detailed analysis of this challenging arrhythmia (including ECG Video with step-by-step analysis of this complex ladderegram(1/30/2021).
  • ECG Media Pearl #8 (8:20 minutes Video) — ECG Blog #191 — Distinguishing between AV Dissociation vs Complete AV Block (2/6/2021 — updated on 6/24/2021).
  • ECG Media Pearl #9 (5:40 minutes Video) — ECG Blog #192 — Reviews the 3 Causes of AV Dissociation (2/9/2021).
  • ECG Media Pearl #12 (6:40 minutes Audio) — ECG Blog #195 — Reviews the phenomenon known as isorhythmic AV Dissociation (in which the atrial and junctional [or ventricular] rate is virtually equal, but P waves are not conducting to the ventricles(2/17/2021).
  • ECG Media Pearl #19 (5:00 minutes Audio) — ECG Blog #202 — A few quick things to look at that allow you to rule out complete AV Block within seconds! (3/10/2021).
  • ECG Media Pearl #41 (4:00 minutes Audio) — ECG Blog #224 — Reviews HOW to recognize within seconds (!!!) a Mobitz I ( AV Wenckebach) 2nd-degree AV Block when there is ongoing Inferior STEMI (5/15/2021).
  • ECG Media Pearl #42 (11:00 minutes Video) — ECG Blog #226 — Reviews this case of a recent Inferior MI with dual-level AV Wenckebach (5/21/2021).



Sunday, June 20, 2021

ECG Blog #235 (51) — Is There Complete AV Block?


The ECG shown in Figure-1 was obtained from a patient with dizziness.

  • How would you interpret this ECG?
  • And — Is there Complete AV Block?

 

Figure-1: ECG obtained from a patient with dizziness (See text).


 

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NOTE: Some readers may prefer at this point to listen to the 8:25 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-51).

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Today’s ECG Media PEARL #51 (8:25 minutes Audio) — Reviews my thoughts on "Some Simple Steps to Help Interpret Complex Rhythms".

 

 

 

My THOUGHTS on the ECG in Figure-1:

This is a challenging tracing to interpret. A long lead rhythm strip is shown at the bottom of the 12-lead ECG. Note that neither the rhythm strip, nor the 12 leads in the ECG were recorded simultaneously — which complicates interpretation. That said — My sequential thought process for interpreting the rhythm was as follows:

  • Most of the beats in Figure-1 are wide. Because recordings for each of the 12 leads in the ECG are of such short duration — We are totally dependent on the long lead V4 rhythm strip for determining the rhythm.
  • The QRS for the first 5 beats in the rhythm strip are wide. The R-R interval is regular, and just over 6 large boxes in duration (which corresponds to a rate just under 50/minute).
  • Beats #6, 7 and 8 have a narrow QRS complex. There appears to be at least some conduction — because these last 3 beats are each preceded by a P wave with a constant (and normal) PR interval.
  • A number of other P waves are seen on this tracing — many of which do not appear related to neighboring QRS complexes. This suggests some degree of AV block.

 

PEARL #1: Note that beat #6 occurs earlier-than-expected, considering the longer R-R interval between beats #1-thru-5. This strongly suggests that beat #6 is conducted, especially since it is preceded by a P wave with a normal PR (that is shorter than any of the PR intervals seen for the first 5 beats on the tracing).

  • Since the PR interval preceding beats #7 and 8 is identical to the PR interval preceding beat #6 — we can presume that beats #7 and 8 are also conducted.

 

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At this point in my interpretation — I needed to find the rest of the P waves.

 

QUESTION: Is the atrial rhythm in the long lead V4 rhythm strip of Figure-1 regular?

  • HINT: Use calipers!

 

 


ANSWER: I've labeled the P waves that I saw in Figure-1 with colored arrows (Figure-2).

  • RED arrows highlight P waves that I am certain about.
  • Setting my calipers to the P-P interval suggested by 2 consecutive P waves that I was certain about (ie, the 2 P waves just before and just after either beat #6 or beat #7) — I "walked out" where we would look for additional P waves IF the atrial rhythm was regular.
  • PINK arrows show tiny deflections that most likely represent hidden P waves.
  • The WHITE arrow shows where the remaining P wave would fall if the atrial rhythm was regular.


Figure-2: I've labeled P waves that I saw in Figure-1 with colored arrows (See text).


  

PEARL #2: The KEY to diagnosis of the various forms of AV block is to establish IF the atrial rhythm is regular, and if so — what relation there is (if any) between P waves and neighboring QRS complexes.

  • RED arrows in Figure-2 indicate that regular P waves are definitely seen throughout most of the long V4 rhythm strip.
  • While it is possible for there to be a "sudden development" of SA node exit block — it would seem far more likely that the tiny "extra deflections" suggested under the PINK arrows are also P waves.
  • There is no way to verify that a P wave occurs under the WHITE arrow — because the expected place where an on-time P wave would occur could be totally hidden within the QRS complex of beat #2. That said — Common things are common — and by far, the most likely scenario is that P waves in the long lead V4 are regular.

 

PEARL #3: Advanced rhythm interpretation entails working out theories based on logical assumptions — and then checking out these assumptions as more information is gathered. At this point in my interpretation — I strongly suspected (but could not yet prove) that the underlying atrial rhythm was regular.

  • 2 ways to "check out" one's theories are: i) To see if your theory allows a logical explanation of the rhythm; andii) To seek out additional monitoring on the patient which then does allow you to prove your theory.

 

My Proposed Laddergram for the Rhythm in Figure-2:

The most logical explanation for the rhythm in Figure-2 — is high-grade 2nd-degree AV block. For clarity (working on the assumption of a regular atrial rhythm) — I've labeled all P waves with letters in Figure-3:

  • The first 5 beats in the long lead V4 rhythm strip of Figure-3 look like complete AV block — because the QRS is wide, the ventricular rhythm is regular — and there appears to be complete AV dissociation (ie, the PR interval before these first 5 beats is constantly changing as P waves "march through" these first 5 QRS complexes).
  • The reason for QRS widening is a slightly accelerated ventricular escape focus (at a rate just under 50/minute — whereas 20-40/minute is the usual rate of an idioventricuar escape rhythm).
  • That said — the rhythm is not complete AV block — because the last 3 beats in this tracing are conducted, as indicated by: i) Earlier-than-expected occurrence of beat #6; andii) The constant and normal PR interval preceding beats #6, 7 and 8, that now manifest a normal (narrow) QRS complex.

 

Figure-3: My proposed laddergram for the rhythm in the long lead V4 (See text).


Bottom Line: I interpreted the rhythm in Figure-3 as showing "high-grade" 2nd-Degree AV Block. None of the earlier P waves in this tracing conduct — despite adequate opportunity for P waves a, c, e and g to conduct.

  • Therefore, there is complete AV dissociation early on in this tracing — but when P waves occur at "just the right moment" (as they do for P waves ik and m) — there is conduction! These last 3 beats conduct with 2:1 AV block.
  • The fact that when P waves do conduct, the PR interval is normal — suggests a lower level (and therefore more serious conduction disturbance) for this AV block (ie, below the AV node, within the bundle of His). This patient will almost certainly need a permanent pacemaker.


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The Case Continues:

Additional rhythm strips were recorded on this patient. These additional non-continuous lead V4 rhythm strips are shown in Figure-4.

 

Figure-4: Rhythm A was previously shown in the long lead V4 of Figure-3. Rhythms BC and D are additional non-continuous rhythm strips recorded on this patient.


QUESTION: Do these additional rhythm strips confirm my previous assumptions? (ie, that the underlying atrial rhythm is regular — and that there is high-grade but not complete AV block?).

  • HINT: Use calipers!

 

 

 


ANSWER: I interpreted the additional rhythm strips shown in rhythms BC and D as supporting my prior assumptions — which I explain in Figure-5:

  • RED arrows highlight selected P waves in these tracings. Note that beat #8 in C — and beat #1 in D both manifest that same normal PR interval as did conducted beats #6, 7 and 8 in A.
  • Beats #2-thru-7 in B — beats #1-thru-7 in C — and beats #3-thru-7 in D all show additional episodes transient complete AV dissociation with a slightly accelerated ventricular escape rhythm.
  • Final proof that the narrow QRS complexes in these tracings are being conducted — is forthcoming from the Fusion beats that we see (ie, beat #1 in B — and beat #2 in D).
  • The laddergram in Figure-5 is drawn from Rhythm D. Note depiction of the Fusion beat (ie, beat #2 in D) — that manifests a QRS complex and T wave intermediate in morphology between conducted beat #1 and ventricular beats #2-thru-7.

 

Bottom Line: The rhythm in today's case is "high-grade" 2nd-Degree AV Block — which almost certainly arises from an infrahiscian level. The patient will need a permanent pacemaker.

 

 

Figure-5: I've labeled Figure-4. Rhythm A was previously shown in the long lead V4 of Figure-3. Rhythms BC and D are additional non-continuous rhythm strips recorded on this patient. The laddergram is drawn from Rhythm D.


 

 


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Acknowledgment: My appreciation to Dr. Prabhakar Deshpande (from Nagpur, India) for allowing me to use this tracing — and to Dr. Mehul for making me aware of this case.

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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #185 — Reviews my Systematic Approach to Rhythm Interpretation using the “Ps, Qs & 3R Approach”.
  • ECG Blog #188 — Reviews the essentials for reading (and/or drawingLaddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts.

  • ECG Blog #191 — Reviews distinction between AV Dissociation vs Complete AV Block.
  • ECG Blog #192 — Reviews the 3 Causes of AV Dissociation.
  • ECG Blog #186 — Reviews some basics on AV Blocks, and WHEN to suspect Mobitz I ( = AV Wenckebach) 2nd-degree AV Block. 
  • ECG Blog 189 — More on determining What TYPE of AV Block is present?

  • ECG Blog #133 — Illustrates use of Fusion beats and AV Dissociation in the diagnosis of VT.
  • ECG Blog #128 — Reviews the concept of Fusion Beats. 
  • ECG Blog #129 — Late-cycle (End-diastolic) AIVR and Fusion beats in diagnosis of ventricular beats.




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ADDENDUM (6/21/2021): I received a comment today on this tracing from David Richley, who is well known to most ECG enthusiasts who frequent any of the many ECG internet forums. Dave always offers the most astute commentary on complex arrhythmia interpretation. NOTE: What follows below goes way beyond-the-core! But for those readers who love complex arrhythmia diagnosis — I think you'll find what follows is compulsive!

  • As often happens — Dave's comment "sent me back to the drawing board". I had noticed in Figure-3 that the PR interval had been progressively shortening during the ventricular escape rhythm until finally, with beat #6 — P wave i was able to conduct. But prior to Dave's comment — I had no idea as to why this was so.
  • I would amend Dave's comment (that I show below) to clarify that by the RP interval (which he calculates for us in his Figure-6) — he is actually referring to the interval between the preceding ventricular escape beat — and the onset of the 2nd P wave within that R-R interval.
  • BOTTOM LINE: I went "back to the drawing board" and postulated retrograde conduction out of the ventricular escape rhythm (dotted butt-end lines that I drew into the AV Nodal Tier in my Figure-7). Being meticulous in drawing these dotted lines all at precisely the same length and angle — it becomes apparent (as per Dave)that the "degree" of AV block does not change — but because of the changing relation of dissociated P waves during the period of AV dissociation — P wave i happens to fall at "just the right moment" to enable conduction with 2:1 AV block.
  • Final PEARL: The original reason this ECG was sent to me, was to inquire if I thought there was complete AV block. Dave's theory proves that the degree of AV block was never complete — because when P waves occur "at just the right moment" (ie, beginning with beat #6) — they can and do conduct to the ventricles (albeit with 2:1 AV block). NONE of this changes the fact that this patient has severe conduction system disease — and needs a permanent pacemaker. But it does make for a captivating discussion!
  • Final THOUGHT: Go back to Figure-4. Rhythm A is the rhythm that I show again in my Figure-7. But take another look at Rhythm C in Figure-4. You'll note beat #8 in C is conducted. And, exactly as per Dave's comment — note that during the prior 7 beats in which there is complete AV dissociation and a ventricular escape rhythm — that the PR interval preceding beats #2-thru-7 progressively decreases (because of progressive increase in the RP interval — which is why beat #8 is able to conduct!).

 


Figure-6: Submitted by David Richley, in which he calculated successive RP intervals.



Figure-7: My revised laddergram for Figure-3. The dotted lines within the AV Nodal Tier represent RP-dependent conduction (See Comment by David Richley below).

 

BELOW is the COMMENT I Received Today from David Richley:

This is a fascinating ECG and I agree completely with your analysis. I'd like to make some additional points. I think the ECG provides a good example of what Marriott termed "RP-dependent conduction".

  • It might be puzzling that there is a transition from complete AV dissociation to 2:1 block. Why should this happen? Is there a sudden "improvement" in the functioning of the conduction system?  The reason for the AV dissociation and ventricular escape rhythm for the first 5 beats — is that none of the atrial impulses occurs at such a time that they can conduct — the conduction system is refractory. 
  • However, during this period — because of the AV dissociation — the RP interval is increasing beat by beat. When the RP interval reaches 920 ms (just before beat 6)the conduction system has had sufficient time to recover — and beat 6 is a conducted (or capture) beat
  • Subsequent RP intervals of about 1140 ms obviously mean that alternate P waves will then conduct, so there is 2:1 block. 
  • KEY: The important point is that there is no change in the status of the conduction system during this rhythm strip! Instead, it is the timing of the P waves in relation to the preceding QRS (and the failure of the escape rhythm to reassert itself) — that explain the apparent change in conductivity. This tracing illustrates beautifully why you can not diagnose complete AV block with confidence from a short section of ECG.







Thursday, June 17, 2021

ECG Blog #234 (50) — 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: