Wednesday, August 18, 2021

ECG Blog #245 — Heart Failure. An Acute Event?

The ECG in Figure-1 was obtained from a 65-year old man with longstanding hypertension. He presented to the ED (Emergency Department) with an exacerbation of HF (Heart Failure). No chest pain. No prior tracing was available.



  • Is there evidence of MI (Myocardial Infarction) in Figure-1?
  • IF so — Are you concerned about a "new" or "old" MI?


Figure-1: ECG obtained from a 65-year old man with hypertension and a heart failure exacerbation. No chest pain. How would you interpret his ECG?



NOTE: Some readers may prefer at this point to listen to the 9:10-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-59).



Today's ECG Media PEARL #59 (9:10 minutes Audio) — Reviews the ECG diagnosis of LVH (and its impact clinically with both chronic and acute cardiac disorders).

  • Please see the Addendum below for Figures-3 and -4 that illustrate and summarize voltage and other criteria for ECG diagnosis of LVH and LV "strain".
  • For additional detail on the ECG diagnosis of LVH  Please see ECG Blog #73.



MY Sequential Thoughts on the ECG in Figure-1:

As always — I favor the use of a Systematic Approach (which I review in ECG Blog #205):

  • Rate & Rhythm: The P wave is upright in lead II — so the rhythm in Figure-1 is sinus. The rate is regular at 70/minute.
  • Intervals (PR/QRS/QTc): All intervals are normal (ie, the PR interval is not more than 1 large box — the QRS not more than half a large box — and the QTc is clearly less than than half the R-R interval).
  • Axis: The frontal plane axis is normal at about +70 degrees (ie, greater positivity in lead aVF compared to lead I — with slight negativity of the QRS in lead aVL).


Chamber Enlargement: My "system" entails sequentially asking myself if ECG criteria for enlargement are present for each of the 4 cardiac chambers (as reviewed in ECG Blog #75 for RAA/LAA — and in ECG Blog #234 for RVH):

  • Is there RAA (Right Atrial Abnormality)? — No, since the P wave in the inferior leads is not abnormally tall and peaked.
  • Is there LAA (Left Atrial Abnormality)? — Probably, as the negative component of the P wave in lead V1 looks to be widened (See PEARL #1 below).
  • Is there RVH (Right Ventricular Hypertrophy)? — No (There is no right axis — no RAA — no tall R wave in lead V1 — no RV "strain" — and no persistent S waves in lateral chest leads).
  • Is there LVH (Left Ventricular Hypertrophy)?  Yes! (Discussed in detail below! )


PEARL #1: As emphasized in ECG Blog #75 — the ECG is neither sensitive nor specific for assessing atrial enlargement. Moreover — expert interpreters often fail to agree regarding the presence of atrial enlargement on ECG. As a result — I generally undercall this ECG finding unless clear criteria are met. Bottom Line: IF you really need to know about atrial dimensions — then Echocardiography is far more accurate. That said — there are subtle signs that suggest LAA is present in Figure-1:

  • The clinical history in today's case does suggest a high prevalence likelihood for LAA — because this patient has longstanding hypertension, and he presents with an exacerbation of his heart failure (both conditions that predispose to LAA).
  • As we'll see momentarily, there is definite ECG evidence of LVH (which is often seen when there is LAA).
  • The most reliable ECG criterion for LAA is the presence of a negative P wave component in lead V1 that is deeper and/or wider than normal. The physiologic reason for this finding — is that it reflects increased atrial electrical activity moving away from right-sided lead V1 (or toward the left atrium). Although the P wave in lead V1 is of low amplitude in Figure-1 — it clearly seems that duration of this terminal negative P wave component is prolonged. 
  • NOTE: While true that a common cause of a negative P wave component in lead V1 is erroneous placement of the V1 and V2 electrodes too high on the chest — I do not think lead misplacement is the cause of P wave negativity in Figure-1 because: i) QRS morphology in leads aVR, V1 and V2 is not at all similar (as it usually is when leads V1, V2 are placed too high on the chest); and, ii) The shape of P waves in leads aVR, V1 and V2 is very different in these leads. While too-high lead placement of lead V1 may produce P wave negativity in this lead — it would not be expected to prolong duration of the negative P wave. Therefore — the finding of a widened and negative P wave component in lead V1 that is not seen in lead V2, and which is not suggestive of too-high placement of the V1 electrode, further supports LAA as the cause of this finding. (For review of how to quickly recognize lead V1,V2 misplacement — Please see My Comment at the bottom of the page in the November 4, 2018 post in Dr. Smith's ECG Blog).


PEARL #2: There is definite ECG evidence of LVH in Figure-1.

  • As was the case for LAA — the clinical history in today's case also suggests a high prevalence likelihood for LVH in this patient with longstanding hypertension and heart failure, even before you look at his ECG.
  • Several of the voltage criteria for LVH are easily satisfied in this 65-year old man (See Figure-3 in the Addendum below). These include: i) Deepest S in V1,V2 + tallest R in V5,V6 ≥35 mm (Figure-2); ii) Tall R wave ≥25 mm in lead V5; and, iii) Tall R wave ≥18 mm in lead V6.
  • As I'll discuss momentarily (below) — ST-T wave changes consistent with repolarization changes of LV "strain" are present.


PEARL #3: Did YOU notice that S wave amplitude is cut off in lead V3? R wave amplitude is also cut off in lead V4.

  • We have no idea how deep the S wave in lead V3 or the R wave in lead V4 would be IF QRS amplitude in these leads would not have been cut off.
  • It is extremely likely that additional voltage criteria for LVH (from Figure-3) would have been satisfied IF this ECG would have been recorded at half-standardization to enable us to capture full dimensions of the QRS complex in these leads.
  • KEY Point: While ECG criteria for LVH are considered "satisfied" when any one of the voltage criteria are met — the more voltage criteria fulfilled (and the greater the amount that voltage limits are exceeded), the greater the probability (and the more the likely severity) there is for true chamber enlargement. 

Figure-2: I've labeled a number of the ECG findings from Figure-1. Among these, I've outlined in RED the limits of the QRS complex in lead V5, which partially overlaps with the S wave in lead V4 (See text).


Returning to the ECG in today's case for completion of our Systematic Approach — We conclude our assessment with a look at Q-R-S-T Changes:

  • Q Waves — There is a deep and wide Q wave in lead aVL (RED arrow in Figure-2). There is also a tiny q wave in lead I.
  • R Wave Progression — is normal. A definite initial positive deflection (r wave) is already seen in lead V2 — with transition (where the R wave in the chest leads becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.


Regarding ST-T Wave Changes:

  • There is J-point ST depression in multiple leads — as shown by appearance of ST segments below the dotted RED lines in leads II, III, aVF; and in V4, V5, and V6.
  • The shape of these depressed ST segments is abnormal, in that it is coved (ie, "frowny"-configuration) — as is schematically illustrated by the light BLUE drawings in lead V5 of Figure-2.
  • There is deep, symmetric T wave inversion in each of these leads with ST depression, as well as in lead V3.
  • In addition to the Q wave in lead aVL that was noted above — there is slight-but-real ST elevation in this lead (as shown by appearance of the ST segment in aVL above the dotted BLUE line in this lead).


Today's ECG: Putting It All Together

In the absence of a prior ECG for comparison — interpretation of today's ECG is challenging. MThoughts There is sinus rhythm with marked LVH and probable LAA. The Q wave in lead aVL may indicate previous infarction of uncertain age. The diffuse J-point ST depression, with ST segment coving and deep, symmetric T wave inversion in multiple leads is consistent with LV "strain" and/or ischemia that may be acute. Urge clinical correlation.

  • The reality is — that definitive interpretation of today's ECG is simply not possible from this single tracing. More information (ie, finding a prior ECG on this patient for comparison — serial ECGs in the ED — serial troponins — consideration of stat Echo looking for a localized wall motion abnormality, etc.) will be needed for accurate assessment of the clinical picture.
  • PEARL #4: The reason I wrote LV "strain" and/or ischemia above for my interpretation — is that on occasion, the finding of either LV "strain" or ischemic-looking ST-T wave changes may mask the other! When this happens — it may be difficult (if not impossible) to distinguish between marked LVH (ie, from longstanding hypertension and/or cardiomyopathy) — vs LVH in a patient who also has acute ischemia/ongoing infarction. 
  • The "good news" — is that acute OMI ( = Occlusion-based Myocardial Infarction) does not seem to be occurring. The only lead that shows ST elevation is lead aVL — but a deep and wide Q wave has already formed, and the shape of the elevated ST segment in lead aVL (within the RED oval in Figure-2) does not suggest acute OMI. Additional support against acute OMI — is the absence of chest pain.
  • KEY Point: As a result of the previous bullet — it would seem that the cath lab does not have to be activated at this point! Instead — optimal management would consist of treating this patient's acute heart failure exacerbation — with careful follow-up, as more information is obtained. Even if troponins turn out to be positive — in the absence of chest pain and acute ST elevation, acute intervention would not be needed.




Related ECG Blog Posts to Today’s Case: 

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

  • 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, 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.



ADDENDUM (8/18/2021): I've added below in Figure-3 and Figure-4 additional material to facilitate ECG diagnosis of LVH and LV "strain".


Figure-3: The voltage and other criteria I favor for ECG diagnosis of LVH (Please see ECG Blog #73 for additional details).


Figure-4: ST-T wave appearance of normal (A) — vs "strain" (C) or a strain "equivalent" pattern (B) — vs ischemia (D). (Please see ECG Blog #73 for additional details).

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