ECG Blog #207 (ECG MP-24) — The ECG Computer Report: Friend or Foe?

You are asked to interpret the ECG shown in Figure-1, obtained from a 52-year-old woman. Unfortunately, no additional information is available to you.

• The Computer Report interpreted this tracing as, “Sinus rhythm; Nonspecific T wave abnormality; Abnormal ECG”.

QUESTIONS:

• Do you agree with the computer report?
• How would YOU interpret this ECG?
• Is there anything to be concerned about on this ECG?

 

Figure-1: ECG obtained on a 52-year-old woman. No history available. Is there anything to be concerned about? (See text).

 

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NOTE #1: Some readers may prefer at this point to listen to the 9:00 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-24).

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Today’s ECG Media PEARL #24 (9:00 minutes Audio) — Review on the Pros and Cons of the Computerized ECG Report.

 

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NOTE #2: Written summary of “My Take” on Optimal Use of the ECG Computer Interpretations appears below in the Addendum (in Figure-2 and Figure-3).

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COMMENT: This case brings up the issue of how best to use (or not use) the Computerized ECG Report. Like it or not — virtually all ECG systems in modern offices, clinics, urgent care centers and hospitals make use of a computerized ECG report. How best should the ECG interpretation be used?

• NOTE: Regardless of whether you love or hate the computerized ECG interpretation — it is part of the medical record. Therefore — IF you disagree with what it says, you should cross out those computer statements that you feel are wrong.

 

MY Approach to the ECG in Figure-1:

As I’ve emphasized previously — it is always challenging when you are given a tracing to interpret without the benefit of any history. This is the situation in today’s case. I would recommend proceeding as follows:

• PEARL #1 — Do not look at the computer report until after you have completely interpreted the ECG in Figure-1. (My rational for emphasizing this point is explained in full in the above Audio Pearl #24).
• The rhythm in Figure-1 is regular at just under 100/minute. The QRS complex is narrow in all leads. P waves are present and upright in lead II, with a constant and normal PR interval — so the rhythm is sinus at a relatively fast rate.
• All intervals (PR, QRS, QTc) and the axis are normal.
• There is no chamber enlargement. (NOTE: I did not call LAA = Left Atrial Abnormality — because the negative component to the P wave in lead V1 is not deep — and I think the reason the P wave looks “notched” in inferior leads is the baseline artifact).
• Several leads show some fine baseline artifact. This makes it difficult to appreciate if there is (or is not) a QS for the very small-amplitude complex in lead III. Other than this — there are no Q waves.
• R wave progression is fairly normal, albeit transition (where the R wave becomes taller than the S wave is deep) is slightly delayed until lead V4-to-V5. 
• NONE of the above descriptive findings are of concern. However, assessment of ST-T wave appearance for the ECG in Figure-1 is of concern (See below).

 

Assessment of ST-T waves:

• Looking at all 3 inferior leads in Figure-1 together — raises concern that the T waves (especially in leads III and aVF) may be hyperacute. 
• PEARL #2: The "definition" as to what constitutes a "hyperacute" T wave is sometimes admittedly elusive, and dependent on interpreter experience + the clinical context (See ECG Blog #193 for full discussion of this subject). That said — Consider the possibility of “hyperacute” T waves when you see T waves that are disproportionately tall and/or fatter-at-their-peak or wider-at-their-base than should be expected given R wave and S wave amplitude in that lead. The more leads in a given lead area that show hyperacute changes — the greater the concern for acute OMI (Occlusion-based MI).
• In Figure-1 — QRS amplitude in leads III and aVF is admittedly tiny, and this makes it that much more difficult to assess what constitutes “larger-than-expected”. That said — T wave amplitude in lead III actually exceeds QRS amplitude in this lead — and the T wave is clearly more “voluminous” than one would normally expect. While not as obvious in lead aVF — the T wave in this 2nd inferior lead also looks more “voluminous” than might be expected. That said — the 3rd inferior lead ( = lead II) does not look overly abnormal.
• PEARL #3: Despite a lack of ST elevation in lead III, and a lack of J-point ST depression in lead aVL — there does appear to be that “magical” mirror-image opposite picture for the shape of reciprocal changes for the T waves in leads III and aVF (See ECG Blog #184 for full discussion of this subject). This finding should significantly increase your concern about possible ongoing or recent OMI.
• There is subtle-but-real T wave inversion in lead I. Given the absence of voltage criteria for LVH — I felt this subtle, shallow T inversion in lead I supports concern about reciprocal high-lateral ST depression.
• There is some nonspecific ST-T wave flattening in most of the chest leads — but this does not look acute.

 

BOTTOM LINE: The KEY point is that we need some History in order to know what to do with this tracing. 

• Finding a prior ECG on this patient could prove invaluable — because it is possible that the ECG changes we see in Figure-1 are old.
• In the absence of a prior ECG on this patient — IF the clinical history suggested new or recent symptoms for possible coronary disease — then the ECG in Figure-1 could represent an acute or recent event!
• An acute or recent event would be far less likely if this patient had no new or recent symptoms — which places the onus on us to find out the clinical history!
• Although the computer did recognize that the ECG in Figure-1 is abnormal and shows “T wave abnormality” — the computer failed to recognize the possibility of a recent or acute ongoing cardiac event. Hopefully the clinicians caring for this patient did not depend solely on the computer interpretation at the time they decided on management of this patient. 

 

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Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #193 — Discusses the concept of using the term, “OMI” ( = Occlusion-based MI) instead of STEMI — and — reviews the ECG findings to look for when your patient with chest discomfort does not manifest frank STEMI-criteria ST elevation on ECG.
• ECG Blog #184 — Reviews the “magical” mirror-image OMI relationship to look for between leads III and aVL.

 

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My Publications on Computerized ECG Interpretation include the following:

• Grauer K: Chapter 21 — Does the Computer Know Better? — from Grauer K: Practical Guide to ECG Interpretation (2nd Edition) — Mosby, St. Louis, 1998, pp 374-379.
• Grauer K, Kravitz L, Ariet M, Curry RW, Nelson WP, Marriott HJL: Potential Benefits of a Computer ECG Interpretation System for Primary Care Physicians in a Community Hospital. J Am Bd Fam Prac 1:17-24, 1989.
• Grauer K, Kravitz L, Curry RW, Ariet M: Computerized Electrocardiogram Interpretations: Are They Useful for the Family Physician? J Fam Prac 24:39-43, 1987.
• Grauer K, Curry RW: Chapter 11: Use of Computerized ECG Interpretation Programs — from Clinical Electrocardiography (Grauer & Curry) — Blackwell Scientific Publications, Boston, 1992, pp 418-425.

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ADDENDUM (3/23/2021): In the following 2 Figures — I review “My Take” on the Pros and Cons of the Computerized ECG Report (Section 13, contained in Figure-2 and -3 — is excerpted from Grauer K: ECG-2014-ePub, KG/EKG Press).

 

 

Figure-2: “My Take” on the Pros & Cons of Computerized ECG Interpretations (Please listen to my 9-minute ECG Audio Pearl above, in this post = ECG MP-24).

 

Figure-3: Example of hyperacute T waves missed by the Computer Report.

ECG Blog #206 — How Many Conduction Defects?

The 12-lead ECG and long lead II rhythm strip shown in Figure-1 was obtained from a 60-something woman, who presented with presyncope. Basic blood work was unremarkable (normal electrolytes).

• HOW would you interpret this ECG?
• WHAT treatment is indicated? Why?

 

Figure-1: 12-lead ECG and long Lead II rhythm strip, obtained from a 60-something woman with presyncope (See text).

 

  

MY Approach to the Rhythm in Figure-1:

This is a highly challenging tracing! I made the following initial observations:

• There is group beating, in the form of alternating short-long cycles with similar (but not identical) R-R interval durations for the shorter cycles (ie, beats #1-2; 3-4; 5-6; 7-8) — and for the longer cycles (ie, beats #2-3; 4-5; 6-7).
• There are fairly (but not completely) regular P waves which are upright in lead II — so the underlying rhythm appears to be some form of sinus arrhythmia.
• The QRS is wide (at least 0.12 second in duration). As is best seen in the long lead II rhythm strip — QRS morphology alternates every-other-beat.

 

PEARL #1: The simple step of labeling P waves in a complex arrhythmia often makes it much easier to appreciate what is going on (RED arrows in Figure-2).

• Setting my calipers at the P-P interval suggested between any 2 consecutive P waves facilitates “walking out” the atrial rhythm (thereby confirming the underlying sinus mechanism).

 

Figure-2: I’ve added RED arrows to Figure-1 in order to highlight the underlying regular atrial rhythm (See text).

  

PEARL #2: It is common to see slight variation in the atrial rate when there is 2nd- or 3rd-degree AV block. This phenomenon is known as ventriculophasic sinus arrhythmia — and is thought to be due to better perfusion, with resultant slight shortening of the P-P interval for those P waves that “sandwich” a QRS complex — and slight lengthening of P-P intervals that do not contain a QRS between them.

 

PEARL #3: The finding of an underlying sinus mechanism (in this case, ventriculophasic sinus arrhythmia) — and group beating should immediately suggest the possibility of AV Wenckebach ( = Mobitz I, 2nd-degree AV block) for the rhythm we see in Figure-2. 

• The diagnosis of AV Wenckebach can be confirmed in today’s case by the following additional observations: i) The same PR interval terminates each of the pauses in this rhythm (ie, a PR interval of ~0.16 second is seen before beats #1, 3, 5 and 7); ii) The PR interval then increases by a comparable amount for the 2nd beat in each of the groups (ie, the same PR interval of ~0.24 second is seen before beats #2, 4, 6 and 8); and, iii) The 3rd P wave in each group is non-conducted.
• Therefore — there is 2nd-Degree AV Block, Mobitz Type I (AV Wenckebach) with 3:2 AV conduction (ie, with 3 P waves in each group, of which only 2 of these P waves are conducted).

 

LADDERGRAM:

The easiest way to illustrate this form of 2nd-degree AV block, is by drawing a laddergram (Figure-3). 

• NOTE: For review on how to read (and draw) laddergrams — See ECG Blog #188).   

 

Figure-3: Laddergram illustration of the Mobitz I, 2nd-degree AV block with 3:2 AV conduction, as described above in today’s case (See text).

 

Today’s Case Continued:

There is more to today’s case! We still need to explain WHY morphology of the QRS complex consistently changes from one beat-to-the-next (Figure-4).

• Look at lead V1 in Figure-4. Although QRS morphology is different for the 2 beats seen in this lead (corresponding to beats #5 and 6 in Figure-4) — both of these QRS complexes seen in lead V1 are consistent with RBBB (ie, an rsR’ pattern with QRS widening). That RBBB is present in Figure-4 is confirmed by the presence of wide, terminal S waves in lateral leads I and aVL.
• KEY Point: The fact that we have a simultaneously-obtained long lead II rhythm strip at the bottom of the 12-lead ECG in Figure-4 is invaluable in today’s case for clarifying which beats in each of the 12 leads correspond to which of the 2 QRS morphologies.
• QRS morphology in the KEY leads for the Bifascicular Blocks was reviewed ECG Blog #205. For clarity, I’ve added a visual reminder at the top of Figure-4 showing how to identify the 2 forms of bifascicular block ( = RBBB/LAHB and RBBB/LPHB).
• LOOK in Figure-4 at QRS morphology for beat #1 in simultaneously-recorded leads I, II and III. The qRS pattern in lead I, with wide terminal S wave in this lead is consistent with RBBB. In association with RBBB — the predominantly negative QRS in leads II and III for beat #1 is consistent with LAHB (Left Anterior HemiBlock). Therefore, beat #1 conducts with a RBBB/LAHB pattern of bifascicular block.
• Now LOOK at beat #2 in simultaneously-recorded leads I, II and III. There is still a wide terminal S wave in lead I, consistent with RBBB. But note how steep the initial (ie, straight) portion of S wave descent is in lead I. Coincident with this — note the change in QRS morphology in leads II and III for beat #2, which now manifest a qR pattern consistent with LPHB (Left Posterior HemiBlock). Beat #2 therefore conducts with a RBBB/LPHB pattern of bifascicular block.
• Applying these observations to the changing QRS morphology that we see occurring every-other-beat in the long lead II rhythm strip — we can deduce that there is a pattern of alternating hemiblock, in which odd-numbered beats (ie, beats #1,3,5,7) all manifest RBBB/LAHB conduction — and even-numbered beats (ie, beats #2,4,6,8) manifest RBBB/LPHB conduction.

 

Figure-4: The rhythm in today’s case manifests RBBB with alternating hemiblock conduction (See text).

LADDERGRAM with Events in the 3 Major Conduction Fascicles:

To better illustrate the complex alternating conduction pattern in today’s case — I schematically represent in Figure-5 the events that occur in the Ventricular Tier for the 3 major conduction fascicles, each of which is color-coded.

• RBBB is present for all beats on this tracing. This block in conduction through the right bundle branch is represented by the PURPLE lines with butt ends in the Ventricular Tier for all 8 beats in Figure 5.
• As previously noted — odd-numbered beats (ie, beats #1,3,5,7) are conducted with a RBBB/LAHB pattern of bifascicular block. This means that after passing through the AV Node and the Bundle of His — conduction through the ventricles occurs over the intact Left Posterior Hemifascicle (RED arrows within the Ventricular Tier for beats #1,3,5,7).
• In contrast — even-numbered beats (ie, beats #2,4,6,8) are conducted with a RBBB/LPHB pattern of bifascicular block. This means that after passing through the AV Node and the Bundle of His — conduction through the ventricles occurs over the intact Left Anterior Hemifascicle (light BLUE arrows within the Ventricular Tier for beats #2,4,6,8).

 

Figure-5: Schematic representation of events in the 3 major conduction fascicles (See text).

BOTTOM LINE: It should be evident that this 60-something woman who presented with presyncope has severe conduction system:

• The underlying rhythm is a ventriculophasic sinus arrhythmia. Because of frequent non-conducted beats — the overall ventricular rate is slow.
• There is abnormal ST-T wave inversion in leads I, aVL and V2, with some ST-T wave flattening elsewhere. Whether or not this represents ischemia of recent origin is difficult to determine given the bradycardia and conduction defects.
• There is 2nd-Degree AV Block, Mobitz Type I (with 3:2 AV conduction).
• There is complete RBBB.
• There is alternating Hemiblock (with the pattern of bifascicular block shifting from one-beat-to-the-next from RBBB/LAHB to RBBB/LPHB).

 

Follow-Up to this Case: A dual chamber pacemaker was implanted in this patient given her symptoms occurring in association with severe conduction system disease.

 

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #186 – When to suspect Mobitz I 
• ECG Blog #62 — Mobitz I vs Mobitz II 2nd-degree AV block.
• ECG Blog #164 — Review of another case with step-by-step analysis of Mobitz I. 
• ECG Blog #188 — How to Read (and Draw) Laddergrams.
• ECG Blog #205 — Review of the Bifascicular Blocks.
• ECG Blog #130 — Alternating Bundle Branch Block (RBBB/LBBB).
• ECG Blog #232 — For more on Bigeminal Rhythms (when the 1st beat in each pair is sinus-conducted).

 

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• Acknowledgment: My appreciation to Ser Barsa (from Yerevan, Armenia) and to J.B. (from the UK) for the case and this tracing.

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ECG Blog #205 — What is Trifascicular Block?

HOW would you interpret the ECG shown in Figure-1? Unfortunately — there is no history available to assist you.

• QUESTION: There are 7 ECG findings that should be noted. How many of them did YOU identify?

 

Figure-1: There are 7 ECG findings that should be noted in this tracing. HOW many of the 7 did you identify?

 

 

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NOTE #1: Some readers may prefer at this point to listen to the 7:40 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-23).

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 Today’s ECG Media PEARL #23 (7:40 minutes Audio) — A user-friendly Systematic Approach to 12-Lead ECG Interpretation.

 

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NOTE #2: Written summary of my Systematic Approach to 12-Lead ECG Interpretation appears below in the Addendum (in Figures-2 through Figure-4).

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MY Approach to this Tracing:

The BEST way to avoid overlooking important ECG findings — is to use a Systematic Approach. This is especially true for interpreting tracings when the QRS complex is wide.

• PEARL #1: Regardless of the system you use — it’s important to assess intervals at an early point in the process. This is because IF the QRS complex is wide — then criteria for assessing the QTc, Axis, Chamber Enlargement and Ischemia/Infarction will all change! Therefore, as soon as you recognize QRS widening — STOP and Figure Out WHY the QRS is wide before going further in your assessment.

 

The 6 KEY Parameters in my Systematic Approach:

• Rate & Rhythm: The P wave is upright in lead II — so the rhythm in Figure-1 is sinus. Although we are not provided with a long-lead rhythm strip — it should still be apparent that the R-R interval is varying enough to qualify as sinus arrhythmia, here with bradycardia (heart rate varying between ~50-60/minute). 
• Intervals (PR/QRS/QTc): The PR interval is clearly prolonged (ie, to ~0.32 second) — so there is 1st-Degree AV Block.
• Continuing with Intervals — the QRS complex in Figure-1 is wide (I measure between 0.12-0.13 second). As noted in Pearl #1 (above) — as soon as you recognize QRS widening — STOP and Figure Out WHY the QRS is wide before going further in your assessment.

 

WHY is the QRS Complex Wide?

As discussed in detail in ECG Blog #204 — once you confirm that the rhythm is supraventricular — the reason for QRS widening can be most time-efficiently determined by focusing attention on the 3 KEY Leads (ie, leads I, V1 and V6). 

• Lead V1 — shows an rSR’ complex that is completely typical for RBBB (Right Bundle Branch Block), in that the initial r wave is small and thin — the S wave that follows descends below the baseline — and the terminal R’ is tall and thin (ie, taller right “rabbit ear”).
• Leads I and V6 — confirm the diagnosis of RBBB, because they each manifest a wide terminal S wave.

 

 

Returning to our Systematic Approach:

Assessment of the remaining parameters in our Systematic Approach is made with awareness that there is complete RBBB.

• QTc: The remaining interval to assess is the QTc. Bundle branch block per se may prolong the QTc. That said — the longest QT that I measure in Figure-1 looks to be less than 450 msec, which considering the bradycardia and conduction defect is not prolonged. (Visually — the QT interval is decidedly less than half the R-R interval, so almost certainly not prolonged in Figure-1).

AXIS — The “meaning” of axis is altered in RBBB. This is because of the zig-zag direction of electrical activity due to this conduction defect. That is — the initial left-to-right vector of septal depolarization is preserved (since the conduction defect with RBBB is on the right side of the septum) — which is followed by depolarization of the unblocked LV (during which time the wave of depolarization travels back to the left)— and finally, return rightward, as the “blocked” RV is the last part of the heart to depolarize. 

• Clinically — the only thing we care about regarding the axis with RBBB is whether there is: i) RBBB + LAHB; ii) RBBB + LPHB; or, iii) RBBB without any hemiblock. In Figure-1, in addition to RBBB — the QRS complex is predominantly negative in lead II. Therefore — there is bifascicular block (ie, RBBB + LAHB).

 

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NOTE: For visual review of the Bifascicular Blocks with RBBB — Begin at 9:20 minutes in my Media Pearl #21 in ECG Blog #203).

• I have excerpted a written summary from my ECG-2014-ePUb on the ECG diagnosis of the bifascicular blocks. This appears below in the Addendum (in Figure-5 through Figure-7).
• To download a PDF of Figures-5, 6, 7 — CLICK HERE. 

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Chamber Enlargement: There is no RAA, LAA or RVH. There is LVH. 

• Criteria for atrial abnormality are unaffected by bundle branch block. However, because RBBB and LBBB alter the sequence of both ventricular depolarization and ventricular repolarization — voltage criteria and ST-T wave changes of LV or RV “strain” will be more difficult to identify.
• That said — because the LV depolarizes unopposed with RBBB (since RV depolarization is delayed by this conduction defect) — the effect of RBBB on ECG diagnosis of LVH may not be marked. How much of an effect RBBB may have on ECG diagnosis of LVH may be difficult to predict. So, realizing that data and definitive answers are lacking — the dramatically increased voltage that we see in Figure-1 for the R wave in lead aVL (ie, ~15 mm), in association with an ST-T wave appearance in this lead that looks typical for LV “strain” suggests at least probable LVH.
• Figure-4 in the Addendum below shows the voltage criteria I favor for ECG diagnosis of LVH. The caveat — is that voltage criteria in Figure-4 are based on normal QRS duration.
• P.S. — LAHB on occasion has also been known to alter QRS amplitude on ECG in a way that may make recognition of LVH problematic. Bottom Line: IF one truly needs to know whether or not there is LVH — an Echo will be needed.

 

Q-R-S-T Changes:

• Q Waves are seen in both high lateral leads in Figure-1 (ie, in leads I and aVL). Although the Q in lead I is small — the Q wave in lead aVL is both deeper and wider than expected for a normal septal q wave. This abnormal Q wave should be noted in the written interpretation — and, it should be noted that this Q wave in lead aVL may reflect prior lateral infarction.
• R Wave Progression — is less relevant in this tracing, since the presence of RBBB by definition results in a predominant R wave in lead V1.

 

PEARL #2: There are primary ST-T Wave Changes in at least leads V1 and V2. As discussed in detail in ECG Blog #204 — the normal response of ST-T waves in the 3 KEY lead with BBB is to be oppositely directed to the last QRS deflection.

• If anything — the ST segment in lead V1 may be slightly elevated. It normally should be depressed (ie, opposite to the last QRS deflection, which is the positive R’ in this lead). The T wave in lead V1 is clearly abnormal — as the normal ST-T wave response with RBBB in lead V1 should be at least some ST depression.
• It is difficult to predict for “how many leads” the expected ST depression with RBBB should last — but the surprisingly tall and peaked T wave in lead V2 is clearly not a normal response.
• We’ve already noted the shape of the ST-T wave depression in lead aVL — which looks very much like LV “strain”. Other leads in Figure-1 show nonspecific flattening of the ST segment and reduced T wave amplitude. Therefore — the 2 leads in this tracing of most concern regarding ST-T wave appearance are leads V1 and V2.

 

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ANSWER to the Question We Posed at the Beginning of this Case:

The 7 ECG Findings that should be noted in Today’s Tracing are:

• Sinus bradycardia and arrhythmia.
• RBBB.
• LAHB.
• 1st-Degree AV Block.
• LVH (with ST-T wave changes consistent with LV “strain”).
• An abnormal Q wave in lead aVL (with a smaller Q in lead I).
• Primary ST-T wave changes, at least in leads V1 and V2.

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Putting It All Together: It is always challenging to have to interpret ECGs in the absence of any clinical history. That said — I was often confronted with this situation as the faculty member charged with official interpretation of ECGs for multiple providers in our clinic, regarding numerous patients I knew nothing about.

• It should be obvious that the patient in today’s case has significant underlying heart disease, given probable LVH (with LV “strain”) — possible prior infarction (the abnormal Q in lead aVL) — and bradycardia + 3 additional indicators of conduction system disease (ie, 1st-degree AV block — RBBB — LAHB).
• That said — despite the primary T wave abnormalities in leads V1 and V2 — my “hunch” is that the changes we see are probably not acute (since other than the changes in leads V1 and V2 — ST-T wave changes in the other 10 leads do not look new). 
• BOTTOM LINE: Clinical correlation on this patient will be needed for deciding appropriate management. Finding a prior tracing on this patient would be invaluable for determining which of the above ECG findings are likely to be new vs old. And, IF there was a history of syncope or presyncope — this would be especially concerning given bradycardia + 3 conduction system defects. A recent history of chest pain would also be of great concern — since the ECG findings on today's tracing could be consistent with recent infarction. Clinical correlation is essential.

 

 

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Is There Tri-Fascicular Block?

The term, “trifascicular” block — implies impaired conduction in all 3 of the major conduction fascicles: i) the right bundle branch; ii) the left anterior hemifascicle; and, iii) the left posterior hemifascicle.

• The term, “trifascicular block” is no longer recommended (Surawicz et al, JACC: Vol. 53, No. 11, pp 976-981, 2009). This is because of “the great variation in anatomy and pathology producing this pattern” — as well as the fact that one will usually not be able to make a definitive diagnosis of trifascicular block from the surface ECG. We simply can not tell IF PR interval prolongation in a patient with bifascicular block (as occurs in Figure-1) is due to AV nodal disease or disease in the remaining conducting fascicle.
• Rarely, one may be able to diagnose involvement in all 3 conduction fascicles — if for example, there is RBBB and LAHB that alternates with LPHB. But even in this circumstance — current recommendations favor clarity in description by avoiding the term “trifascicular block”, and instead noting each of the conduction defects that are present (ie, in Figure-1 — this is 1st-degree AV block + RBBB + LAHB).

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Relevant ECG Blog Posts to Today’s Case: 

• ECG Blog #203 — Reviews the ECG diagnosis of Axis and Hemiblocks.
• ECG Blog #204 — Review of my user-friendly Approach to the ECG diagnosis of BBB.
• ECG Blog #73 — “My Take” on the ECG diagnosis of LVH.
• ECG Blog #185 — Use of a Systematic Approach to Rhythm Interpretation. 

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ADDENDUM (3/18/2021): In the following 3 Figures — I outline the Systematic Approach that I favor (in Figures-2 and -3) — and my preferred criteria for the ECG diagnosis of LVH (Figure-4).

 

 

Figure-2: The Systematic Approach that I favor. Review of the first 4 parameters in Descriptive Analysis (Rate; Rhythm; Intervals; Axis). NOTE: IF the QRS complex is wide — then STOP and find out WHY the QRS is wide before proceding to assessment of Axis, Chamber Enlargement and QRST Changes. This is because IF the QRS is wide because of BBB (Bundle Branch Block) — criteria for axis, hypertrophy, and ST-T wave changes will be different when there is BBB or IVCD! To emphasize, IF the QRS is wide — this is the ONE time that I depart from the sequence in Figures-2 and -3 (P.S. IF the QRS is wide — Make sure that the rhythm is not VT. If the rhythm is sinus — ECG Blog #204 reviews how to determine if RBBB, LBBB or IVCD is present).

 

Figure-3: The Systematic Approach that I favor (Continued). Review of the last 2 parameters in Descriptive Analysis (Chamber Enlargement; Looking for Q-R-S-T Changes) — and then formulating your Clinical Impression.

 

Figure-4: Simplified Criteria for ECG Diagnosis of LVH (Full discussion of this topic can be found in ECG Blog #73).

 

Figure-5: RBBB/LAHB — RBBB/LPHB.

 

Figure-6: RBBB/LPHB (cont.) — ECG examples of bifascicular block.

 

Figure-7: Trifascicular Block? — Isolated LPHB vs marked RAD.