Updated: Apr 4
Firefighter / Paramedic
Acute Care Nurse Practitioner
Expert commentary provided by Dr. Ken Grauer
An 82 y/o Male called 911 for sudden onset dizziness while at rest. Upon arrival he was found alert and oriented, and without gross distress. He denied difficulty breathing, epigastric pain, or chest discomfort.
RR 14 (non-labored)
SpO2 95 RA
Physical exam revealed slight pallor and diaphoresis. Auscultation of breath sounds did not yield any evidence of wheezing, crackles, or diminished fields. He reported a history of ischemic cardiomyopathy with coronary stent placement approximately 10 years prior, but could not recall the specific artery involved.
Attached is the first ECG.
My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. There is, indeed, appreciable J-point elevation in this lead with a demonstrably robust T wave, and when paired with its respective QRS – incorporating the art of proportionality – one can certainly make the case that it is a hyperacute T wave.
But there is more to reconcile here. First, the QRS is wide. The computer measures its duration at 130ms. I find it to be slightly less than this – around 120ms, specifically. There is LBBB-like morphology in V1, aVL, and Lead I – and Leads I and aVL, in particular, reveal q-waves, as well as T waves that are concordant with the QRS. This is atypical as the rule of discordance mandates that these T waves should be directed opposite the primary QRS.
Furthermore, V5 and V6 display rS patterns to suggest a delayed transitional zone directed leftward as the result of cardiac dilation in the presence of ischemic heart disease.
Additional findings include a patently leftward frontal plane axis, an intriniscoid deflection (i.e., R wave peak time) of 50ms in aVL, and a deep S-wave in Lead III – all of which to suggest, with limited sensitivity, that LVH has culpability in the findings. [1, 2]
The most clinically useful definition to account for this entire constellation is intraventricular conduction delay.
But something just didn’t look right to me, specifically the QRS-T manifestation in V1 and V2. I glanced over at the patient’s chest and noticed that these respective leads had been placed far too high, almost subclavicular in location. V1 and V2 were reconfigured to the appropriate precordial zone and a second ECG was captured.
The QRS voltage in V1 and V2 is no longer attenuated, and V2, specifically, now shows a fully reconstituted S-wave, thus eliminating the prospect of TQRSD. There is an adjusted equilibration of the QRS-T proportionality, as well, but keep in mind – this remains an abnormal ECG! The T waves are still somewhat bulky amidst a modestly straightened ST segment. In fact, I resulted an ST/S ratio of 0.23 in V2 (Smith modified Sgarbossa), a value that should cause any clinician to take pause in the setting of LBBB-like morphology. Given such findings, serial ECG’s are prudent to consider, and carry significant impact moving forward, which has been demonstrated in previous posts.
Anecdotally, had there been symptoms unequivocally consistent with ACS then one could justifiably make the case for a potential D1 occlusion. As previously addressed – there exists positive T wave concordance in Leads I and aVL, and the ST/T of V2 is noteworthy. Subtracting TQRSD from the differential diagnosis should not establish a false sense of security. Rather, correct lead placement permits a shift in focus to other areas of concern that may pose hazard downstream, and must be equally surveilled extensively.
The patient verbalized complete resolution of symptoms, and the skin was noted to be warm, pink, and dry. He denied any chest discomfort, or difficulty breathing. He requested transport to the hospital out of an abundance of caution, and all subsequent serial ECG’s showed no changes from Figure 1-2, shown above. The respective hospital course was unremarkable.
Figure 1-2. Is it LBBB, or LAFB?
From Dr. Ken Grauer
I’ll preface this by saying that IF you were to ask 10 expert cardiologists — I bet you’d get at least 5 different answers! That’s because in my experience, there is NO universal agreement on terminology for this type of tracing! So, when I first began teaching ECGs and writing my books (in the early 1980s) — I decided to synthesize my impressions of the literature into what I felt (e.g. my opinion) was the most user-friendly and time-efficient and still as-accurate-as-anything-else-I-have-ever-seen-out-there Approach.
I measure 0.12 for QRS duration. Looks like LBBB in the limb leads (though you should never “normally” see a q in I or aVL with simple LBBB). In the setting of “LBBB-like” — then “LAHB” doesn’t make sense (better to say, “left-axis”). I agree with IVCD as the best terminology to call this — because chest leads look nothing like LBBB (and QRS amplitude DECREASES in V6 !!! — which is strange. In addition — with LBBB (or LBBB-like) conduction defects — the ST-T wave should be OPPOSITELY directed to the last QRS deflection in leads I, aVL — and it is upright here.
Now since there is “IVCD” as the reason for QRS widening — to say in addition there is “LAHB” to me is a contradiction in terms — because that would make for 2 different “conduction defects”. Therefore, my preference would be to describe this type of supraventricular QRS morphology as “IVCD with LAD (left axis deviation)”. It COULD BE — that those q waves in I, aVL indicate prior infarction — and it could be that the loss of QRS amplitude in lateral chest leads also represents prior anterior infarction — but I could not say that for certain based on this single ECG …
All of that said — with full AWARENESS that it becomes MORE difficult to assess ST-T wave morphology of any coduction defect for ischemia — I thought the slight-but-real J-point ST elevation with ST segment straightening in lead V1, and what looks to be disproportionate J-point ST elevation (given modest depth of the S wave) in lead V2, in which the ST segment takeoff is STRAIGHT — were ABNORMAL findings! Whether this represents a potential acute cardiac event would depend on the history, comparison with prior tracings and serial tracings.
Finally — the upright (albeit small amplitude) T wave in high lateral leads I and aVL is NOT a “typical” finding with simple LBBB-like tracings — so that might also represent a new or old ST-T wave abnormality … So, CLINICAL CORRELATION would be essential for optimal interpretation.
LAHB tends to widen QRS duration by 0.01-0.02 at most, when this is the only factor operative. There is more than that degree of widening here …
There is not uniform agreement among experts as to what constitutes a “wide” QRS. Many use ≥0.12 second. I have over the past 4 decades favored >0.10 second — for MANY reasons. Not the least of these, is that VT on occasion in an adult can manifest a QRS duration of 0.11 second (ie, with a pure fascicular VT) — so How can you NOT count 0.11 second as the beginning of “wide”? Isn’t VT ALWAYS “wide”? I realize some may disagree with me (and insist on 0.12 second as the definition of “wide”) — but in addition to me standing by my definition — my definition serves the additional purpose of making it EASY to tell IF you have QRS “widening” or not regardless of how clear or unclear the little boxes in the ECG grid paper are. HALF of a large box on ECG paper = 1/2 of 0.20 second = 0.10 second. So ALL you have to do is find the widest QRS on the tracing — pick a complex that begins or ends on a HEAVY grid line — and then IF the QRS duration is clearly MORE than HALF a large box in duration — then by MY definition, the QRS is WIDE (ie, >0.10 second). This method has worked for me for 40+ years — and it takes only SECONDS to tell if the QRS is “wide” or not.
The literature I have seen requires ≥0.12 second for both LBBB and RBBB. But in my opinion, this does not make sense. IF you have typical RBBB morphology ( = rsR’ or equivalent in V1 and wide terminal S waves in I and V6) — then 0.11 should (in my opinion) qualify as “complete” RBBB. After all, the RV is MUCH smaller than the LV — so if the right bundle branch is blocked — it should NOT take nearly as long to depolarize the LV as when the much, much larger left bundle branch in the much, much larger LV is blocked …. Similarly — if you have a pure hemiblock, it should NOT widen the QRS by more than a little bit (ie, 0.01-0.02 second, at most!).
Regardless of how much QRS duration is on today’s tracing — the QRS in today’s tracing LOOKS WIDE! This simply does NOT “look” like a simple LAHB.
Before I began writing my ECG books (35+ years ago) — I asked numerous cardiologists for their interpretations of various tracings — and in doing so, I learned about intra-observer variability among experts, which is considerable. The MOST variation in these excellent cardiologists’ interpretations was in defining what truly is “IVCD”. In my experience — there is simply NO consensus on the ECG diagnosis of IVCD. But HOW ELSE can you classify today’s tracing? It is NOT a simple LAHB pattern. It is neither typical LBBB nor typical RBBB. So my approach for a time-efficient, user-friendly approach to the diagnosis of IVCD allows recognition of this heterogeneous entity in seconds (with equal accuracy to ANY system any expert can come up with) — IF the QRS is wide, and does not resemble a pure hemiblock or RBBB or LBBB — then this satisfies my definition of IVCD (and ALL you need is a “little bit” of QRS widening = ≥0.11 second) for there to be IVCD.
A 75 y/o Male called 911 in the early morning hours after suddenly awakening with crushing chest discomfort. He was found diaphoretic and uncomfortable, and verbalizing a prior history of myocardial infarction and that, furthermore, the acute symptoms were identical to that which had been associated with RCA stent placement 4 years prior.
A 12 Lead ECG was immediately acquired.
The V1 / V2 leads were appropriately placed in this circumstance, and dedicated followers of the Smith ECG Blog will instantly recognize the problem at hand. This ECG shows legitimate TQRSD in V2, a finding that is 100% specific for LAD occlusion when differentiating Early Repolarization.  Corroborating evidence is the reciprocal change of downward sloping ST segments in II/III/aVF with down-up signature T waves. Although wavering baseline is apparent, V5 and V6 nonetheless manifest subtle flattened ST-segment depression.
ASA 324mg was administered while a STEMI activation was simultaneously transmitted to the nearest PCI center. Enroute the patient verbalized symptom alleviation and a second ECG was captured.
V4 / V5 / V6 = V4R / V8 / V9, respectively
Specific to V2, there is reconstitution of the S-wave – however, not secondary to relocation of the respective lead to its proper space, but rather as a sign of reperfusion! Additionally, the T waves in V2 and V3 (previously hyperacute) have now “deflated” with concomitant manifestation of subtle terminal T wave inversion. There is dramatic resolution of the ST/T characteristics in II/III/aVF. And one additional feature – the T wave amplitude in Leads I and aVL (Figure 2-2) have both lessened. As a testament to the power of serial ECG’s, make a juxtaposition of these very leads between Figures 2-1 and 2-2. You will see that they were initially ischemic, by definition, because of the subsequent voltage attenuation.
A 99% LAD occlusion was stented.
These two cases show the value of accurate lead placement and how it makes the difference in appropriate trajectory of care, or misdiagnosis with unnecessary utilization of resources. The most common finding of V1 / V2 malposition is P wave inversion, and rSr’ QRS with T wave inversion, potentially leading clinicians to suspect Brugada pattern, for example, when no such entity exists.  Another spurious finding is a QS pattern that mimics Anterior MI, and in the acute setting this may elicit compulsory urge to pursue invasive coronary intervention that is entirely unwarranted. 
In my personal experience, malposition of V1 and V2 is more prevalent than the ubiquitous RA / LA limb lead reversal. In addition to accurate diagnosis, attention to these details promotes professional rapport with our specialist colleagues. Below is a refresher on appropriate precordial lead placement. 
A more robust examination of lead malposition can be found at the Emergency Medicine Cases website by the great Dr. Jesse McLaren.
Also, do not miss Dr. Grauer's great explanations on --
 Ravi, S., et al. (2013). Diagnosis of left ventricular hypertrophy in the presence of left anterior fascicular block: A reexamination of the 2009 AHA/ACC/HRS guidelines. Annals of Noninvasive Electrocardiology, 18(1), 21-28.
 Surawicz, B. & Knilans, T. K. (2008). Chapter 6: Other Intraventricular Conduction Disturbances. Chou’s Electrocardiography in Clinical Practice, 6th ed. 108-123.
 Smith, S. W., et al. (2016). Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization. American Journal of Emergency Medicine, 34(11), 2182-2185.
 Baranchuk, A, et al. (2015). Differential diagnosis of rSr’ pattern in leads V1-V2: Comprehensive review and proposed algorithm. Annals of Noninvasive Electrocardiology, 20(1), 7-17.
 Walsh, B. (2018). Misplacing V1 and V2 can have clinical consequences. American Journal of Emergency Medicine, 36, 865-870.
 Goldberger, A. L, et al. (2018). Chapter 4: ECG leads. Goldberger’s Clinical Electrocardiography: A Simplified Approach, 9th ed. 21-31.