Wednesday, June 7, 2023

ECG Blog #383 — Is this Coronary Disease?


Please NOTE: 

  • After today — No new ECG Blog posts for 2-to-3 weeks ...
  •     — I will also not be prompt in replying to emails ...


All material on this ECG Blog site remains open!

  • The INDEX tab (in the upper right of each page) — has linked Contents, listed by subject. So IF you are looking for ECG material — There is plenty on this web site!

  • IF you scroll down a little on the right-hand column of this blog — You'll see a lot of icons. These include links to my Audio Pearls (more than 50 of them) — my Video Pearls (18 of them)My Comments in Dr. Smith's ECG Blog (more than 500 of them! — scroll to the bottom of each blog post to find them) — and more than 80 detailed Laddergrams.

THANK YOU all for your interest & support!
— I'll be back! —


ECG Blog #383 — Is this Coronary Disease?


The ECG in Figure-1 — was obtained from a previously healthy 70-year old man who presented to the ED (Emergency Department) with new CP (Chest Pain).
  • How would YOU interpret this tracing?

  • Should you activate the cath lab? (ie, Is the ST elevation in lead V1 — in association with the ST-T wave changes in lateral chest leads suggestive of Precordial "Swirl" from proximal LAD occlusion, as discussed in ECG Blog #380)?

Figure-1: The initial ECG in today's case.

MY Thoughts on the Initial ECG:
I thought ECG #1 was both fascinating and a bit bizarre ...
  • The rhythm overall looks to be a fairly regular sinus rhythm with a PAC — although P waves in lead II are extremely small. P waves are probably best seen in lead V2, which is unusual for sinus rhythm — so possibly this is an ectopic atrial rhythm.
  • Intervals overall (PR, QRS, QTc) appear to be normal. That said — lack of a well defined P wave in lead II makes assessment of the PR interval difficult — and — the QRS looks a little wide in lead V3, albeit QRS duration does not appear to exceed 0.10 second in any particular lead.
  • The frontal plane axis is slightly leftward (ie, the QRS being more negative than positive in lead aVF) — but not leftward enough to qualify for LAHB (ie, the QRS in lead II is not predominantly negative).

Regarding Chamber Enlargement:
  • There is marked LVH! As shown in Figure-2 by coloring of the QRS complexes in leads V4,V5,V6 — there is abundant overlap, with marked increase in QRS amplitude in these leads (ie, the RED-colored R wave in lead V5 = 27 mm — and the GREEN-colored R wave in lead V6 = 25 mm).

Regarding Q-R-S-T Changes:
  • There is a small Q wave in lead aVL — and a very large Q wave in lead V1.
  • Regarding R Wave Progression Transition is early! That is, a predominant R wave is already seen by lead V2.
  • There is marked J-point ST depression (of ≥3 mm in leads V5,V6 — with lesser degrees of ST depression in 4 limb leads and leads V3,V4). ST segments are downsloping — terminating in symmetric T wave inversion that is deep in the inferior and lateral chest leads.
  • There are 2 mm of ST elevation in lead V1 — with ST segment coving and a hint of elevation in neighboring lead V2.

Putting It All Together:
As noted — I found today's tracing fascinating, but a bit bizarre!
  • What we know — is that the rhythm in ECG #1 is fairly regular and supraventricular (probably sinus with a PAC — albeit upright P waves are not clearly seen in lead II)
  • There is marked LVH — with dominant R waves in each of the lateral chest leads. ST-T waves.
  • There are profound ST-T wave changes. Part of the ST depression with deep T wave inversion in the lateral chest leads clearly reflects LV "strain" from the marked LVH — but despite the very large QRS amplitudes, this ST-T wave appearance looks disproportionate, suggesting at least a component of ischemia.
  • The above said — LVH and ischemic coronary disease does not explain the ST-T wave depression in the inferior leads (BLUE arrows in leads II,III,aVF) — that is much more commonly seen as a sign of acute RV "strain".
  • However — ECG #1 is not especially suggestive of RVH. Tall, peaked and pointed inferior P waves of RAA (Right Atrial Abnormality) are not seen — although this might be the result of a non-sinus rhythm (ie, As noted earlier — a clearly defined upright sinus P wave is not seen in lead II). There is no rightward axis — and no predominant R wave in lead V1. The persistent S wave in lead V6 that attains 13 mm is deeper than is normally seen — but by itself, this does not satisfy criteria for RVH.

And then — there is the Qr' pattern in lead V1 with ST elevation:
  • The Qr' pattern in lead V1 with ST elevation was the most challenging part of today's tracing for me to explain.

 I like my ECGs to "tell a story". By this I mean that all ECG findings over serial tracings and the course of the patient's evaluation make sense when correlated clinically to the history and physical exam.

  • The Qr' in lead V1 does not look like simple RBBB conduction. The QRS is not wide enough for a complete RBBB — and, lateral limb leads I and aVL both lack terminal S waves.
  • I've previously discussed the interesting correlation of a qR pattern in lead V1 in patients with RVH — as strongly suggesting associated pulmonary hypertension (See ECG Blog #234 and Blog #248). However, today's case lacks a dominant R wave in lead V1 — and lacks other ECG evidence of clear RVH.
  • Then there is the significant ST elevation we see in lead V1 ... But limitation of this ST elevation to a single lead is not consistent with any distribution of a STEMI.
  • And then — IF we "forget" about the initial Q wave in lead V1, and instead just focus on the r' with upward sloping ST elevation — Doesn't the shape of this r' followed by upward sloping ST elevation with an upright T wave resemble the saddleback of a Brugada-2 ECG pattern (See ECG Blog #238 — for review of Brugada patterns and Phenocopy).
  • Finally — there is the bizarre-looking initial positive "hump" just before the Q wave in lead V1. I had no idea what this represents, given that this small positive "hump" occurs before the QRS (The vertical dotted BLUE line in Figure-2 marks the beginning of the QRS) — yet after the onset of the clearly seen P wave in lead V2.

  • BOTTOM Line: I could not come up with any logical "story" that would correlate all ECG findings of today's tracing with the limited history I was given of "new CP". I would not be at all surprised if prompt cardiac cath was performed — since the patient did present with new CP — and there is marked ST-T depression on this ECG — but I felt sure that "something else" must be going on.

Figure-2: I've labeled key findings from Figure-1 (See text).

The CASE Continues:
The bizarre appearance of the QRST complex in lead V1 was not the result of any lead misplacement (Repeat ECGs verifying placement were similar).
  • never got to see a prior tracing — which could have been extremely insightful explaining how this current tracing compared to this patient's baseline ECG.

  • Cardiac Cath showed patent coronary arteries!
  • An Echo on this patient was revealing! It showed reduced LV function — significant concentric LVH — a dilated left atrium — severe aortic stenosis (seemingly in need of prompt valve replacement) — and at least moderate pulmonary hypertension, with resultant moderate pulmonary regurgitation.

  • The plan was to proceed as soon as possible with aortic valve replacement. Unfortunately — the patient abruptly developed hypoxemia, followed by cardiac arrest with PEA. He could not be resuscitated.

PEARL #2: Although always difficult to retrospectively "look back" after a patient dies, trying to better understand events that happened — doing so is immensely helpful in learning from the experience in the hope of optimizing future care.
  • Apparently while waiting on the hospital floor for the decision regarding optimal aortic replacement — the patient took one of his sublingual NTG (nitroglycerin) tablets. As may happen with critical AS (Aortic Stenosis) — the vasodilating effect of NTG may further reduce systolic pressure. It was thought that this action precipitated the patient's desaturation, and led to his cardiac arrest.
  • In patients with severe valvular disease (such as this patient's critical AS) — the finding of significant pulmonary hypertension (as was found on this patient's Echo) — often indicates a decompensated state, in which left ventricular and left atrial compensation is no longer able to prevent backward transmission (to the pulmonary circuit) of elevated left atrial pressure. A point may be reached in which even with valve replacement — pulmonary hypertension persists, which serves as a marker for a poor longterm prognosis (Maeder et alFrontiers in Cardiovasc Med 5(40):1-15, 2018)

ECG Findings in Today's Tracing Now Make Sense!
In view of the knowledge that cardiac cath revealed no significant coronary disease — and Echo indicated critical aortic stenosis with reduced LV function and significant pulmonary hypertension — the ECG findings in today's tracing now make sense!
  • Severe AS is a common cause of marked LVH with LV "strain" on ECG. This explains the marked increased in QRS amplitude in the lateral chest leads — as well as some of the ST-T wave depression in these leads.
  • Whereas excessive ST-T wave depression in the lateral chest leads probably reflects a superimposed ischemic component to this patient's marked LVH — the inferior lead T wave inversion (BLUE arrows in leads II,III,aVF of Figure-2) is consistent with RV "strain".
  • In the context of RV "strain" — the Qr' pattern in lead V1 most probably reflects this patient's significant pulmonary hypertension (See ECG Blog #248).

  • I suspect that the saddleback ST elevation that we see isolated to lead V1 may reflect a Brugada-2 Phenocopy pattern (See ECG Blog #238) in this hemodynamically decompensated patient.
  • Perhaps the small positive "hump" that appears just before the QRS complex in lead V1 reflects a similar phenomenon as can be seen with the Spiked Helmet Sign — in which with conditions of excessive endogenous catecholamines (as may occur with hemodynamically compromised patients) — there may be some elevation of the isoelectric line that begins before the QRS complex (See ECG Blog #310).


"Take Home" Lessons from Today's Case:
This is not a simple case! As I emphasized — This complex ECG did not initially make sense to me until I learned more about the clinical history. 
  • The most important "Take-Home" Points about today's case — are not about these complex ECG findings — but rather to highlight the need to clinically correlate ECG findings. Many ECGs "tell a story" — and recognizing: i) That despite this patient's presentation of new chest pain (and despite the deep ST-T wave depression in lateral chest leads)this was not ACS (it was not an Acute Coronary Syndrome); ii) There is marked LVH; and, iii) That the inferior lead T wave inversion and Qr' with ST elevation in lead V1 point to RV "strain" with pulmonary hypertension — which in association with this patient's critical aortic stenosis explain the principal pathology. This patient needed prompt aortic valve replacement. Although this was recognized by the treating health care team — the patient unfortunately expired before this could be accomplished. 


Acknowledgment: My appreciation to 林柏志 (from Taiwan) for making me aware of this case and allowing me to use this tracing.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 

  • ECG Blog #380 — Reviews what is "Precordial Swirl" (LOTS of links to blog posts on various aspects of acute OMI/ischemia).

  • ECG Blog #234 — and ECG Blog #248 — Review of ECG diagnosis of RVH and the qR Pattern for recognition of Pulmonary Hypertension.
  • 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).

  • ECG Blog #310 — Reviews the Spiked Helmet Sign! (Catecholamine excess).

  • ECG Blog #238 — Reviews Brugada Patterns and Phenocopy.


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).
  • ECG Blog #245 — Reviews assessment of LVH on ECG.
  • ECG Blog #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
  • ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.

  • ECG Blog #75 — Reviews "My Take" on the ECG Diagnosis of LAA & RAA. 
  • ECG Blog #234 — Reviews "My Take" on the ECG Diagnosis of RVH.
  • The November 4, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews 3 ECG Clues for rapid recognition of erroneous lead V1,V2 placement. 
  • The March 31, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates the potentially misleading effect the pre-hospital ECG may have in patients with LVH (ie, by cutting off S wave voltage in the anterior leads).
  • The March 29, 2019 post in Dr. Smith's ECG Blog — My Comment regarding Tracing A (at the bottom of the page) illustrates how LVH is a common mimic of acute ischemia. 
  • The December 27, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates a case with anterior ST elevation from LVH that may falsely suggest acute anterior infarction.


No comments:

Post a Comment