Thursday, April 28, 2022

A man in his 40s with RUQ abdominal pain

Submitted and written by Lucas Goss MD, edits by Meyers and Smith

A man in his 40’s with only past medical history of tobacco use presented with sharp RUQ abdominal pain that's worse with exertion and associated with nausea and diaphoresis. On arrival the provider noted him to be ill-appearing. His vitals are shown below, and on exam he had cool extremities and RUQ abdominal tenderness. 

HR 108

RR 24

BP 106/85

SpO2 88%

Initial ECG:

What do you think?

My interpretation:

Sinus tachycardia

Normal QRS

No HyperK

Normal QT


In V1-V4 (however most notable in V2 and V3) there are small R waves followed by large S waves with associated convex upward ST elevation followed by deep symmetric T wave inversions. Additionally there are symmetric T wave inversions in the inferior leads. These findings, in conjunction with tachycardia, hypoxemia, RUQ pain, and shortness of breath is quite specific for acute right heart strain, with the most common cause being acute PE.


Smith comment: This ECG is all but pathognomonic for pulmonary embolism.  The heart rate is 116: the easiest way to identify this ECG as “probably not ACS” is the tachycardia.  ANY time I see tachycardia I doubt ACS as the etiology of the ST-T abnormalities (see abstract we wrote at the bottom).  It is easy to recognize.  This is a rule which is easy for even an ECG novice to apply, unlike T-wave morphology etc.  

Neither 1. hypoxia nor 2. tachycardia occur in ACS UNLESS there is 1. pulmonary edema due to cardiogenic shock or 2. low stroke volume due to cardiogenic shock.  Wellens syndrome does NOT cause cardiogenic shock since the artery is open.  Bedside echo of course can tell you immediately about the stroke volume.  Thus, Wellens' T-waves are not associated with tachycardia or hypoxia UNLESS there is a 2nd simultaneous pathology.

See our abstract on tachycardia in ACS at the bottom.


His initial high sensitivity troponin I returned at 754 ng/L (URL for men 20 ng/L). The provider treating this patient was instead concerned for Wellens Syndrome (LAD reperfusion) and Cardiology was consulted. Other labs returned and showed mild elevation of AST and ALT along with an elevated BNP. When cardiology evaluated the patient he had significant RUQ tenderness and they were concerned for an intra-abdominal process somehow contributing to his increased troponin (as if by "demand ischemia"). Due to significant abdominal pain a CT of the abdomen and pelvis was performed. In the meantime a repeat troponin returned at 671 ng/L.

Repeat ECG: 

As you can see, his ECG is essentially unchanged. 


Why is the ECG and clinical picture not suggestive of reperfusion T waves in the anterior leads (Wellens Syndrome)? 

  • When there are T wave inversions in the precordial leads, then T wave inversions in lead III are much more likely to be due to PE rather than ACS. 

  • The patient’s symptoms are not resolved at the time of the ECG, rather they continue to get worse. In Wellens (LAD reperfusion), you'd expect the patient’s symptoms to be largely resolved or at least significantly improved.

  • Additionally he has mild hypoxia with clear lungs. This is not as typical for a large anterior MI in cardiogenic shock, where you’d expect pulmonary edema. Rather, this patient has a chest x-ray with clear lungs, symptoms of hepatic congestion/RV failure (RUQ pain, elevated liver enzymes), and tachycardia (usually not present in OMI unless cardiogenic shock is present) which all point towards acute RV failure.  

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

Back to our case:

His CT of the abdomen and pelvis returned, and did not demonstrate any acute intra-abdominal process, however luckily did catch extensive bilateral pulmonary emboli. 

A CTA of the chest was then performed. from Lucas Robert on Vimeo.

CT Read: Large bilateral pulmonary emboli with elevated RV/LV ratio

A formal echo was also performed that demonstrated a severely dilated RV with hypokinesis of the free wall and preserved apical function (McConnell sign) consistent with acute right heart strain. He also was found to have a PFO with a right-left shunt. 

Fortunately, the patient remained hemodynamically stable and was determined to have a severe-submassive PE. He was started on heparin and admitted to the ICU. Ultimately, he never required thrombolysis or other advanced therapies. He had a lower extremity ultrasound that demonstrated bilateral DVTs with portions of chronic thrombosis. He had an uneventful hospital course otherwise and was discharged home. 

As you can see, it’s critical to apply these ECG findings to the right clinical context and use bedside echocardiography to aid in diagnosis. 

It can sometimes be hard to tell the difference between anterior reperfusion T waves, anterior and inferior reperfusion T-waves in the case of a wrap-around LAD,  and acute right heart strain as seen in this case. However, using the clinical picture, history of symptoms, and bedside echo can help differentiate the two. Additionally, remember that simultaneous TWI in III and anterior leads is more likely PE than ACS, as demonstrated in Kosuge et al. 

More importantly, anterior reperfusion and PE simply look different on the ECG, in ways that I have a hard time describing in words, but just has to be visually memorized.

Below you can compare cases of acute right heart strain to cases of anterior reperfusion.

Here are some cases of PE with acute right heart strain:

Compare our patient’s ECG with these examples of anterior reperfusion:

You can see that in these examples of anterior reperfusion, the T waves are largely upright in leads III and aVF. Additionally, reperfusion T waves often extend into the lateral leads (depending on the area of the vessel that was previously occluded). This is compared to acute right heart strain where findings are often most maximal in the leads representing the RV (V2 and V3, sometimes out to V4). 

Learning Points:

Tachycardia does not occur with Wellens and is unusual in ACS, unless the ACS is so severe that it results in cardiogenic shock, or unless there is another simultaneous pathology.

Hypoxia does not occur with Wellens and is unusual in ACS, unless the ACS is so severe that it results in cardiogenic shock with pulmonary edema (B-lines on ultrasound), or unless there is another simultaneous pathology.

All you have to do is memorize the shapes of these squiggly lines and you can instantly diagnose some of the most important PEs. You can avoid several hours delay to diagnosis, avoid the confusion of thinking this could be Wellens, etc. Sometimes the ECG is the more specific than the physical exam, sometimes not. If you can recognize when the ECG unlocks the understanding of the case, patients will benefit.

Although the ECG is not sensitive for any PE (especially those without right heart strain), the findings of symmetric t-wave inversions (most notably in V2 and V3) with associated T wave inversions in lead III and AVF, with the morphology shown above, can be specific for acute right heart strain. 

Apply the ECG to the clinical context of the patient and use your bedside ultrasound if you are unable to distinguish this pattern from Wellens. The ultrasound is also very different between the two pathologies.

Wellens ECG findings are different from findings of acute right heart strain. In Wellens, there are usually no T-wave inversions in leads III and aVF and findings often extend out to the lateral leads. Again, this is in contrast to acute right heart strain where findings are often maximal in lead V2 and V3. 

See Also:

A woman in her 50s with shortness of breath

A crashing patient with an abnormal ECG that you must recognize

A man in his 40s with a highly specific ECG

Chest pain, ST Elevation, and tachycardia in a 40-something woman

Repost: Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3

A young woman with altered mental status and hypotension

An elderly woman transferred to you for chest pain, shortness of breath, and positive troponin - does she need the cath lab now?

A 30-something woman with chest pain and h/o pulmonary hypertension due to chronic pulmonary emboli

A 30-something with 8 hours of chest pain and an elevated troponin

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

Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis?

Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis

Answer: pulmonary embolism. Now another, with ultrasound....

This is a quiz. The ECG is nearly pathognomonic. Answer at bottom.

Chest Pain, SOB, anterior T-wave inversion, positive troponin

Anterior T wave inversion due to Pulmonary Embolism

Collapse, pulse present, ECG shows inferior OMI. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest")

The Negative Predictive Value of Tachycardia for Type I MI in Hemodynamically Stable Patients with Chest Pain.
Lee DH.  Sandoval Y.  Apple FS.  Ives S.  Smith SW.  The Negative Predictive Value of Tachycardia for Type I MI in Hemodynamically Stable Patients with Chest Pain.  Academic Emergency Medicine. 25 (S1): S253. 

Patients with type 1 myocardial infarction with normal left ventricular function that are hemodynamically stable do not usually manifest with sinus tachycardia. The goal of the present analysis was to examine whether the presence of tachycardia identified patients unlikely to have type 1 myocardial infarction.

This was a secondary post-hoc analysis of a prospective, observational data study of 1927 consecutive ED patients over 4 months who had at least 1 contemporary troponin I (cTnI) resulted.  

Inclusion criteria were chest pain, at least 2 serial cTnI in 24 hours, sinus rhythm, and at least 1 ECG. 

Exclusion criteria were age less than 18, SBP less than 100 mmHg, echocardiogram with EF less than 50%, STEMI, pregnancy, and trauma.

All cases with at least one elevated cTnI were adjudicated into specific MI type (or no MI) by two clinicians who reviewed all medical records. Patients were stratified according to presence or absence of type I MI, and of heart rate (HR) of less than 99 bpm, and less than 120 bpm on presenting ECG. All ECGs were coded by an expert clinician as having ST-elevation, ST-depression, T-wave inversion [ST/T abnormalities, (ST/T-A)], or none of the above.

877 patients were included, of whom 135 had HR greater than 99 bpm (742 less than or = to 99 bpm) and 23 had HR greater than 120 bpm (854 less than or equal to 120 bpm).  Of the 877, 58 (6.6%) had type I MI and 819 did not; 4 of 58 (6.9%) with type I MI, and 131 of 819 (16.0%) without, had HR greater than 99 (P=0.02).  The negative predictive value (NPV) of HR less than 99 for type I MI was 97.04% (95%CI 92.6-98.8) and the negative likelihood ratio [(-)LR] was 0.43 (95%CI 0.17-1.12).  23 had HR greater than 120 bpm (854 ≤ 120 bpm); 0/23 with HR greater than 120 bpm had type 1 MI.  The NPV of HR less than 100 bpm for type I MI among those with ST/T-A was the same as in those without, at 92.0% (95%CI 74.7.6-97.8).  Of 23 patients with HR greater than 120 bpm, 4 had ST/T-A.  See Table for diagnostic utility.


In hemodynamically stable patients with chest pain, sinus tachycardia aids in the identification of patients unlikely to have type I MI, especially in those with HR greater than 120 bpm.


MY Comment by KEN GRAUER, MD (4/28/2020):


Insightful case presented by Drs. Goss and Meyers highlighting the importance of recognizing the ECG signs of acute PE. I focus my comments on further dissecting some of these "tell-tale" ECG features.

  • The "theme" of today's case was "pattern recognition". Like the ECG diagnosis of RVH (Right Ventricular Hypertrophy) — ECG recognition of the "pattern" suggestive of acute PE is not made on the basis of any single ECG finding.
  • Instead — in a patient with a History and Exam potentially consistent with the diagnosis — it is the constellation of ECG findings that when present, strongly suggests acute PE until proven otherwise. 

As per Drs. Goss and Meyers — the ECG pattern of acute PE is one that we need to recognize within seconds of seeing it!

  • For clarity — I've reproduced the initial ECG in today's case in Figure-1. I've added at the bottom of this Figure the Table that I showed in My Comment from the March 28, 2022 post of Dr. Smith's ECG Blog.

Figure-1: Assessment of the initial ECG in today's case for features suggestive of acute PE (See text).

Did Today's Patient "Read the Textbook?"
To emphasize — There is no single ECG finding that is diagnostic of acute PE. Instead, the diagnosis may be suggested by the presence of at least several of the ECG findings in Figure-1 when they occur in the "right" clinical setting.
  • Most patients do not "read the textbook" before they have their event. Today's patient was no exception — as clinical "context" was needed to interpret a number of the ECG findings that I highlighted with BLUE arrows.
  • FIRST — Although today's patient did not complain of acute dyspnea — this "ill-appearing" 40-year old man was tachycardic (108/minute) — tachypneic (24/minute) and hypoxemic (SpO2 = 88%) — so his presentation was clearly "potentially consistent" with acute PE.

  • Sinus Tachycardia: While not absolutely essential for the diagnosis, a rapid heart rate (usually to at least 90/minute) is a common and expected finding in patients with hemodynamically significant acute PE. The heart rate in today’s case is consistent with this at ~115/minute.

  • RV (Right VentricularStrain: Recognition of the ECG picture of RV "strain" is one of the most important ECG indicators of acute hemodynamically significant PE. Unfortunately, this sign remains all-too-often unappreciated and misinterpreted as coronary ischemia. RV “strain” manifests as ST depression and/or T wave inversion that typically occurs in the anterior leads (V1,V2,V3) — and/or in the inferior leads (II,III,aVF). In ECG #1 — the ST segment coving with deep, symmetric T wave inversion in anterior leads is perfectly consistent with the ECG picture of acute "RV strain". While inferior lead changes are not nearly as marked — the T wave is inverted in leads III and aVF, with a hint of inversion also in lead II.

  • S1Q3T3: In my experience, it is rare (if ever) that the isolated finding of an S1Q3T3 pattern will make the diagnosis of a new significant PE. That said, this ECG sign may be extremely helpful IF seen in association with other ECG evidence of acute PE. NOTE: Technically — an S1Q3T3 sign is not present in ECG #1 — because there is a small-but-present initial positive deflection (r wave) in lead III. Clinical implications of an S1Q3T3 pattern have only been validated if all 3 components are present ( = an S wave in lead I — a Q wave in lead III — and T wave inversion in lead III).
  • That said — despite the lack of a "true" S1Q3T3 sign — the deeper-than-expected S wave in lead I and the rSR' complex that we do see in lead III both add support to the ECG impression of acute RV "strain". The nearly isoelectric (if not slightly negative) QRS complex in lead I, in association with nearly isoelectric QRS complexes in most other limb leads result in an indeterminate frontal plane axis, that is one of the findings associated with acute RV "strain".
  • Complete or incomplete RBBB is another ECG finding associated with acute PE. Lead III is a right-sided lead (with an electrical viewpoint of +120 degrees in the frontal plane). As a result — the finding of an rSR' complex in lead III (instead of in lead V1) serves as a surrogate form of incomplete RBBB, especially given the narrow S waves in lateral leads I and V6, and the terminal notch (instead of an R' complex) in lead V1.
  • ECG findings in Figure-1 that are not present in today's tracing — include RAA, a predominant R wave in lead V1, ST elevation in lead aVR, and atrial fibrillation.
  • The final ECG finding that is at least suggested — is persistence of precordial S waves through to lead V6 (albeit the s wave in lead V6 is small).

BOTTOM LINE Regarding ECG #1: Fitting the "theme" of today's case ( = pattern recognition) — the moment I saw the sinus tachycardia and ST coving with deep, symmetric T wave inversion in leads V1-thru-V4 — I thought, "acute RV strain" until proven otherwise"
  • Strengthening my impression of acute PE was the clinical presentation (ie, "ill-appearing patient", tachycardia, tachypnea, hypoxemia) — plus several more subtle additional ECG findings that "in context" further supported this diagnosis. These included — the deep S in lead I (with indeterminate frontal plane axis) — the suggestion of RV "strain" that is also present in the inferior leads — the surrogate IRBBB pattern in lead III — and persistence of S waves in the precordial leads (albeit the S wave in lead V6 was not overly deep).

Final PEARL: The ECG is far less likely to help in the diagnosis of relatively small (ie, subsegmental) PEs that are not hemodynamically significant — and which are often only discovered on Chest CT performed on patients with less convincing symptoms. This is probably a “good thing” — since evidence is lacking that treatment of incidentally discovered, non-hemodynamically significant subsegmental PEs is beneficial (and it certainly is not without potential for harm). Perhaps it is a “benefit-in-disguise” that the ECG is unlikely assist in detection of relatively smaller pulmonary emboli.
  • By the time you see significant hypoxemia, tachycardia and clear indication of acute RV "strain" on ECG (as in today's case) — you are almost certainly dealing with a hemodynamically significant PE in need of prompt diagnosis and treatment!

Tuesday, April 26, 2022

RBBB and LAFB: Is there a "concordance" of the ST segment in inferior leads? Is the ST depression in V3 due to RBBB only?

This ECG was texted to me.  

I later received this clinical history: The patient in his 60s with h/o COPD had presented with 2 days of dyspnea without any chest pain.  He was not hypoxic.  He also had abdominal discomfort and vomiting.

What do you think?

There is a very atypical RBBB + LAFB.  It lacks the typical rSR' in V1-V3.  The first R-wave is taller than the 2nd R-wave in V1 (abnormal).  There is no R'-wave in V2 and V3.  

The providers thought that there was "concordant ST depression" in inferior leads -- however, this apparent inferior STD is a mimic!  What may appear to be ST depression is really a negative notch in the QRS.   Below I have indicated the end of the QRS by drawing lines at the end of the QRS in all leads:

The lines mark the end of the QRS
Notice that the "concordant ST depression" is really a negative notch at the end of the QRS.

My response was that it is "not an ischemic ECG."  

I was convinced by the RBBB + LAFB with very high voltage that the repolarization abnormalities were all secondary to the abnormal depolarization.  There is only 1 mm of ST depression in lead V3, and that is an acceptable amount of ST depression when it is discordant to the R'-wave.  

The problem is that there is no R'wave!!  So this was a mistake on my part.

The ST depression in V3 comes after a single upright R-wave, NOT after an R'-wave.  

See this typical RBBB here, in which there is ST depression in V1-V3 but it follows an R'-wave:
Notice that there is up to 1 mm of normal ST depression following the R'-wave in V1-V3

Unbeknownst to me, there was a previous ECG in the chart from 9 months prior:
A definite change in the ST segment in V3 and T-waves in V4-V6 is now obvious

Case Progression

Cardiology was contacted.  The initial troponin returned at 9,800 ng/L, consistent with subacute MI.  The patient was treated for Non-OMI (Non-STEMI with open artery).

Serial troponins downtrended.

Next AM, this was recorded. 
ST depression in V3 persists.  There is some change in T-waves

It is very similar.  Here are precordial leads side-by-side:

                                 First ECG                                                                    Next AM

There is new T-wave inversion in V5 and V6, suggesting reperfusion of a lateral OMI

An formal echo was done:

Normal left ventricular sized and function; estimated LVEF is 56%.

Basal inferolateral and inferior segments are akinetic.

This is a new wall motion abnormality; a previous echo was normal

Translation: there is a new posterior wall motion abnormality.  This ST depression in V3 represented a subacute OMI supplying the posterior wall.

At 36 hours, this was recorded:

ST segment in V3 mostly normalized
T-wave is more upright in V2, and more inverted in V4-V6.

An angiogram was done on day 3:

--Severe distal small (one vessel) disease involving the small LPL1 with an apparent filling defect.

--Vessel is less than 1 mm in diameter and flow improved with IC TNG.

--Otherwise, mild Plaque no angiographically significant obstructive coronary artery disease 

--Based on lesion of filling defect there is high suspicion for thromboembolic occlusion secondary to a proximal atrial fibrillation versus proximal coronary plaque rupture, thought to be less likely.

This confirms OMI to the posterior wall


There was indeed OMI of a very small vessel.  It may have been due to an embolism.  No matter the etiology, it did manifest on the ECG and was easily, but mistakenly, attributed to RBBB and high voltage.

Learning Points:

1.  ST depression is only normal following an R'-wave in V1-V3.  If there is no R'-wave, then ST depression should be considered ischemic.

2.  Make sure you identify the end of the QRS in any BBB before attributing deviations to the ST segment.

3.  Always compare with a previous ECG if one is available.

Comment by KEN GRAUER, MD (4/26/2022):
Interesting case for discussion — regarding the ECG that was sent to Dr. Smith for his interpretation. I wanted to present another perspective regarding how I approached this initial ECG in today’s case.

I have previously reviewed my approach to the ECG diagnosis of RBBB (See My Comment at the bottom of the page in the July 1, 2019 post in Dr. Smith’s ECG Blog). The reasons this approach allows me to diagnose the type of conduction defect in less than 5 seconds are that: i) You only have to look at 3 leads (ie, left-sided leads I and V6 — and right-sided lead V1)andii) Assuming you've ruled out VT, WPW, hyperkalemia and other toxicity as the cause of QRS widening — there are for practical purposes, only 3 possible answers (ie, RBBBLBBB or IVCD).

  • RBBB (Right Bundle Branch Block) — is defined as a supraventricular rhythm in which the QRS complex is wide — and — QRS morphology in the KEY leads is consistent with RBBB (ie, an rsR' pattern or it's "equivalent" in right-sided lead V1 — and an R wave with a wide terminal S wave in left-sided leads I and V6).

  • NOTE: For those interested in my user-friendly approach that allows ECG diagnosis of the type of conduction defect within seconds — Please check out my 13-minute ECG Video and downloadable PDF at the bottom of this page.

I focus my comments on the initial ECG in today's case. For clarity — I have reproduced this tracing in the bottom panel of Figure-1
  • As per Dr. Smith — ECG #1 (Bottom panel in Figure-1) — manifests a sinus rhythm with QRS widening due to a bifascicular block ( = RBBB/LAHB)

  • With a typical RBBB pattern (in which there are no other potentially confounding factors) — QRS morphology in right-sided lead V1 should manifest a triphasic rsR’ or rSR’ pattern, in which: i) There is an initial positive deflection, in the form of a small, slender r wave; ii) This initial r wave deflection is then followed by an S wave that descends below the baseline; andiii) There is a terminal R’ (taller right “rabbit ear” deflection) — in which this R’ is slender and taller than initial positive r deflection.

The above said — it is common to see other QRS morphologies in lead V1 that are still consistent with RBBB despite not manifesting the typical triphasic rsR' or rSR' pattern.
  • In a normal ECG — the QRS complex in an adult will be predominantly negative in right-sided lead V1. This is because left ventricular mass predominates over right ventricular mass in an adult — such that the depolarization vector is primarily directed to the left (or away from lead V1 — which is why a deep S wave is normally seen in lead V1).
  • IF the rhythm is supraventricular — and — the QRS complex is wide and predominantly positive in right-sided lead V1 (ie, similar to any of the QRS patterns shown in the upper panel of Figure-1) — then RBBB may still be present despite the absence of a triphasic rsR' or rSR' pattern in lead V1 — as long as a wide terminal S wave is present in left-sided leads (ie, in leads I and V6).
  • Reasons why the typical triphasic (rsR'; taller right rabbit ear) complex in lead V1 may be lost in some patients with RBBB include scarring (cardiomyopathyand/or infarction (which will often be suggested by a qR in lead V1 and/or V2).

MY Thoughts on Today's Initial ECG:
The rhythm in ECG #1 is sinus. The PR interval is normal. The QRS complex is wide. The diagnosis of RBBB is confirmed by the finding of a predominantly positive QRS complex in lead V1 (consistent with one of the RBBB "Equivalent" Patterns shown in Figure-1) — in association with the presence of wide terminal S waves in both leads I and V6.
  • LAHB (Left Anterior HemiBlock) is diagnosed in addition to RBBB — by the predominant negativity in the initial descent of the S wave in each of the inferior leads.
  • There is excessive fragmentation in a number of QRS complexes in this tracing (ie, in the upslope of the S wave in leads II, III, aVF — and in the slurred R waves in leads aVR and V1). This amount of fragmentation often implies "scar" and/or prior infarction.
  • Q waves are present in leads aVL and V2. The Q wave in lead V2 is definitely not normal (RED arrow in this lead in Figure-1) — since as described above, an initial positive deflection is normally seen in lead V1 (and usually also in lead V2) with a "typical" RBBB. While not definitive — this small Q wave in lead V2 may be a marker of anterior infarction having occurred at some point in time.
  • The Q wave in lead aVL may or may not be significant (RED arrow in this lead). While true that normal septal q waves are commonly seen in one or more lateral leads (due to the left-to-right vector of septal depolarization, that does not change direction with RBBB) — I thought the Q wave in lead aVL in ECG #1 was slightly more prominent than expected for a septal q wave.
  • As I reviewed in My Comment in the July 1, 2019 post — typical RBBB or LBBB both alter the sequence of ventricular depolarization and repolarization in a predictable fashion in the KEY leads. With regard to the expected ST-T wave changes with simple RBBB — we should expect to see the ST segment and T wave in leads I, V1 and V6 oppositely directed to the last QRS deflection in that lead. This is precisely what we see in ECG #1 — in that the upright T wave in leads I and V6 is oppositely directed to the wide terminal S wave — and the depressed ST-T wave in lead V1 is oppositely directed to the all positive RR' complex that we see in lead V1.

KEY Point: In Figure-1 — there are other chest leads in ECG #1 that do not manifest the ST-T wave appearance expected if the only thing going on is simple RBBB.
  • Lead V2 is indeed unusual in manifesting a huge positive R wave (over 30 mm tall). Assuming the chest lead V2 electrode is correctly placed — the small Q wave in this lead is abnormal. The ST segment in this lead is also unusual and probably abnormal — in that rather than initial downsloping (as is seen for the ST segment in lead V1) — the slightly depressed ST segment in lead V2 is upsloping!
  • As emphasized earlier — there may normally be some ST-T wave depression in right-sided lead V1 with RBBB. But when the only thing going on is RBBB — then the relative amount of this ST-T wave depression should progressively decrease as one moves across the precordium. This is not what we see in lead V3 — in which the amount of J-point ST depression has again increased (relative to lead V2) — and the shape of the ST segment is now clearly coved (similar to the curved RED line in this lead) — followed by a deepening of symmetric T wave inversion. This is not what should be seen with simple RBBB.
  • The T wave remains inverted in lead V4 (BLUE arrow) — which again should not be expected with simple RBBB.

In the Limb Leads:
It is common to see some T wave inversion in leads III and aVF when the QRS is predominantly negative. The T wave in lead II is less likely to be inverted unless there is ischemia.
  • That said — the shape of the ST segment prior to developing symmetric T wave inversion in not only leads III and aVF — but also in lead II — is coved (similar to the curved RED lines in these leads). This is not a normal appearance for the ST-T wave in the inferior leads with simple LAHB.

BOTTOM LINE: No history was provided at the time I first saw the initial tracing in today's case. The ECG shows sinus rhythm with bifascicular block (ie, RBBB/LAHB) of uncertain age.
  • I did not think the above-described ST-T wave changes suggested acute coronary occlusion.
  • Depending on the prior ECG and the past and present medical History — I thought ECG #1 could reflect ischemia and/or recent infarction.
  • Given the bifascicular block — the QRS fragmentation in no less than 5 leads —the potentially significant Q waves in leads aVL and V2 — and ST-T wave abnormalities in multiple leads that looked to be more than just RBBB and LAHB — I suspected that at the least, this patient had significant underlying heart disease.

Figure-1: TOP — QRS morphology of RBBB "Equivalent" Patterns. BOTTOM — I've labeled the initial ECG in today's case.


ECG Media Pearl #22 (13:15 minutes Video) — Reviews a user-friendly approach that allows diagnosis of the Bundle Branch Blocks in less than 5 seconds.

  • CLICK HERE to download a PDF of this 12-page file on the ECG diagnosis of BBB (from Grauer K: ECG-2014-ePub).

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