Thursday, December 30, 2021

ECG Blog #272 (80) — 3 Days of Chest Pain in a 70yo Man

The patient is a man in his 70s — with symptoms for the past 3 days. He presented to the ED with worsening chest pain. His initial ECG is shown in Figure-1.



  • Should you activate the cath lab?
  • How many of the 12 leads manifest abnormal ST-T wave changes?
  • Is the low voltage a relevant finding?

Figure-1: Initial ECG in the ED — obtained from a man in his 70s with 3 days of chest pain.



NOTE: Some readers may prefer at this point to listen to the 4:00-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 these tracings (that appear below ECG MP-80).


Today's ECG Media PEARL #80 (4:00 minutes Audio) — Reviews the ECG finding of Low Voltage (and potential clinical implications of low voltage in the setting of acute MI).



MY Approach to the ECG in Figure-1:

As always — I favor a Systematic Approach for interpretation of every ECG I encounter (This Systematic Approach is reviewed in ECG Blog 205).

  • Rate & Rhythm: The rhythm is sinus at ~70/minute. 
  • Intervals: The PR, QRS and QTc intervals all appear normal.
  • Axis: The frontal plane QRS axis is normal (close to zero degrees — as the QRS complex in lead aVF is nearly isoelectric).
  • Chamber Enlargement: None


PEARL #1: Did YOU note the relatively Low Voltage throughout this tracing? Although strict criteria for low voltage are not quite met in this tracing (ie, the QRS complex in all 6 limb leads is not ≤5 mm — because the R wave in lead I is taller than this). That said — 5 of the 6 limb leads satisfy this low voltage criterion — and all 6 chest leads are of small amplitude!

  • As we are about to contemplate the possibility of acute or recent infarction — it is helpful to be aware of potential causes associated with low voltage.
  • Relevant potential causes of Low Voltage to consider in today's case include: i) Pericardial effusion; ii) Takotsubo cardiomyopathy; and, iii) A large acute (or recent) infarction, that may result in myocardial "stunning" (See the above Audio Pearl and/or ECG Blog #262 for more on this subject).


Continuing My System — Regarding Q-R-S-T Changes:

  • Q Waves — Assessment is challenging because of the small amplitude of the beats in lead III, and especially in lead aVF. That said — a QS wave is seen in at least 2 of the 3 beats in lead III. It looks like an ever-so-tiny initial positive deflection (r wave) is present in the middle beat in this lead. 
  • I find it even more difficult to assess lead aVF for the presence of Q waves — as QRS amplitude is tiny (no more than 2 mm) in this lead. What can be said about lead aVF — is that all 3 of the beats that we see in this lead are notched (ie, fragmented).

PEARL #2: The finding of an isolated QS complex in lead III and/or lead aVF is not diagnostic of previous inferior infarction. 

  • Higher specificity for the occurrence of inferior infarction at some point in time is only obtained when Q waves of a "certain size" (ie, larger and/or wider than normal septal q waves) are seen in all 3 inferior leads (ie, leads III, aVF and also lead II).
  • That said, in my experience — the finding of an isoelectric or predominantly negative QRS complex that is fragmented in one or more inferior leads (as seen in lead aVF in Figure-1) — significantly increases the likelihood that inferior infarction occurred at some point in time.
  • In Figure-1 — there is no Q wave in lead II. As a result — the question of a QS complex in lead III by itself does not reliably predict inferior infarction at some point in time. However, in association with the tiny, notched (fragmented) complex in lead aVF — I'd suspect an inferior infarction may have occurred at some point. Whether this event began 3 days ago (at the time of symptom onset in today's patient) — or whether the inferior infarction is old and unrelated to the ST-T wave changes we are about to assess in the chest leads — can not be determined from this single ECG.



Continuing My System — Regarding R Wave Progression:

The zone of "Transition" — is said to occur where the height of the R wave becomes taller than the depth of the S wave in the chest leads. Transition is normally seen between lead V2-to-V4. Because of common usage — I've retained the term, "R wave progression" as part of my Systematic Approach to 12-lead interpretation — though defining the zone of "transition" provides us with more useful information (See ECG Blog #269 — for full review on R Wave Progression).

  • R Wave Progression: In Figure-1 — R wave progression is "poor", because transition is delayed to between lead V4-to V5.
  • Other than the QS complex in lead V1 — Q waves and/or QS complexes are not seen in other chest leads. That said — the delayed transition is relevant in today's case! This is because the reduced r wave amplitude in anterior leads, and small size of the R waves in leads V5 and V6 — may reflect loss of anterior forces from recent infarction.


Finally — Regarding ST-T Wave Changes:

ST-T wave abnormalities (some subtle — some not subtle) are seen in at least 9 of the 12 leads in today's tracing. For clarity — I've labeled some of these findings in Figure-2:

  • The most remarkable abnormal ST-T wave findings — are the hyperacute T waves in leads V2-thru-V6. It is challenging to define the term, "hyperacute" in reference to T wave appearance. My definition is that in the "right" clinical setting (ie, in a patient with cardiac-sounding chest pain) — 1 or more T waves take on a "hypervoluminous" appearance — in that they appear taller-than-expected given QRS amplitude in the lead being looked at — as well as being "fatter"-at-their-peak and wider-at-their-base than would normally be expected (See ECG Blog #218as well as the Audio Pearl in that post for more on defining hyperacute T waves).
  • The 3 leads in Figure-2 in which T waves are most obviously "hyperacute" — are leads V3V4 and V5. In each of these leads — T waves tower over the small-amplitude R waves. Not only are these T waves much taller than the R waves — but these T waves are clearly "fatter"-at-their-peak and wider-at-their-base than one would expect, given the size of the R waves (and QRS complex) in these respective leads.

PEARL #3: By the concept of "patterns of neighboring leads" — Since the ST-T waves in leads V3, V4 and V5 are so obviously abnormal — the somewhat less obvious ST-T wave changes in neighboring leads V2 and V6 are also most probably abnormal.

  • In lead V6 — although the T wave is not taller than the R wave — this T wave in lead V6 is still much taller-than-one-would-expect given small size of the R wave in this lead.
  • Height of the T wave in lead V2 is not as pronounced as T wave amplitude in lead V3. However, the ST segment "takeoff" is unusually straight (ie, parallel to the slanted RED line in lead V2 of Figure-2). In addition, considering how small the r wave is in lead V2 (ie, 2 mm) — the T wave in this lead is once again "hypervoluminous" (ie, clearly with a much-wider-than-it-should-be base). I would therefore interpret leads V2 and V5 as also being "hyperacute".
  • ST-T wave changes in lead V1 are subtle — but nevertheless "real". Normally in this lead — there is no more than minimal ST elevation. Although the T wave in lead V1 may normally be inverted (PURPLE arrow in Figure-2) — the shape of the ST segment in this lead (ie, coved or "frowny"-configuration, as schematically shown by the curved RED arc) — in association with the ST elevation seen (with respect to the dotted RED line in lead V1 — showing the PR segment baseline) is not a normal finding (especially given obvious ST-T wave abnormalities in the 5 other chest leads)!

Figure-2: I've labeled some of the abnormal ST-T wave changes from Figure-1.

Regarding ST-T wave Changes in the Limb Leads:

  • The ST-T waves in leads IIIII and aVF are all clearly abnormal. ST segments in each of these inferior leads are "scooped", with suggestion of slight ST depression. That said — the most remarkable finding is the terminal T wave positivity in each of these 3 inferior leads (upward-pointing BLUE arrows in Figure-2 — with the most prominent terminally positive T wave being seen in lead II)
  • Depending on the clinical situation (and the stage of evolution during an acute cardiac event) — this finding of terminal T wave positivity in association with ST flattening or depression is clearly abnormal, and may represent the beginning reperfusion changes (ie, the mirror-image of inverting T waves in leads which manifested ST elevation).
  • Without the benefit of a prior (baseline) ECG for comparison — I was uncertain if the ST-T waves in leads I and aVL were abnormal. I thought the apearance of the QRST complex in lead aVR was unremarkable.

PEARL #4: When assessing an ECG for the possibility of acute ischemic heart disease — the more leads that are abnormal, the greater the chance that the abnormalities you identify are realI find it helpful to start with a few leads that obviously show acutely abnormal ST-T wave findings — and then to apply the concept of "patterns of neighboring leads" as I look closely to identify more subtle findings in the remaining leads.

  • As described above in Figure-2 — We have identified definite ST-T wave abnormalities in no less than 9/12 leads. This provides strong support in favor of a recent (or still ongoing) cardiac event.

Putting IAll Together:

The ECG in Figure-2 shows sinus rhythm — low voltage — a question about a QS in lead III (with a tiny, fragmented complex in lead aVF) — poor R wave progression (with low-amplitude R waves until leads V5, V6) — worrisome hyperacute T waves in leads V2-thru-V6 — with apparent reciprocal ST-T wave changes in the inferior leads (including terminal T wave positivity that probably represents upright reperfusion T waves).

  • Given the history of 3 days of symptoms in this older man who finally presented to the ED because of worsening chest pain — I interpreted this tracing as suggesting acute and/or ongoing extensive anterior infarction. Although none of the chest leads manifest J-point ST depression — the disproportionately large chest lead T waves are consistent with a deWinter-like T wave pattern (See ECG Blog #183 for "My Take" on this concept). That said — I wasn't certain about WHEN it was during the patient's 3 days of symptoms that acute infarction took place — or whether perhaps there was an ongoing "stuttering" course with spontaneous opening and closure.
  • The course of acute infarction is not always "all or none". By this I mean — that the "culprit artery" (most likely the proximal or mid-LAD in today's case) — may acutely occlude — then spontaneously reopen — followed by spontaneous reopening and reclosure a number of times until a final state is reached for the "culprit" artery.
  • Regardless of when during the patient's 3 days of symptoms acute coronary occlusion first occurred — the lack of anterior Q waves, in association wth marked hyperacute T wave changes in this patient who presented to the ED for increased symptoms — strongly suggests that there is still a large area of jeopardized myocardium that may benefit from prompt reperfusion. Cardiac cath was clearly indicated to define the anatomy and guide clinical decision-making.



Cardiac cath was performed on the patient in today's case. Not surprisingly, this revealed total occlusion of the mid-LAD (Left Anterior Descending) coronary artery. Minor lesions were found in the LCx (Left Circumflex) and RCA (Right Coronary Artery).

  • This patient subsequently developed arrhythmias — that I discuss as this case is continued in my next ECG Blog #273.



Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23-LINK in Blog #205).
  • ECG Blog #269 — Reviews assessment of R-Wave Progression (with a Video Pearl in this post on the subject).
  • ECG Blog #218 — Reviews of the concept of WHAT is a "Hyperacute" T Wave (Also see the Audio Pearl in this post). 
  • ECG Blog #183 — Reviews a case of deWinter-like T Waves (with the Audio Pearl in this post discussing some variants of the deWinter T wave pattern).
  • ECG Blog #53 — Reviews another case of deWinter T Waves.
  • ECG Blog #258 — Reviews the concept of HOW to "Date" an Infarction (Also see the Audio Pearl in this post).

  • ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "culprit artery". NOTE: The Audio Pearl reviews the concept of why the term "OMI" ( = Occlusion-based MI) should replace the more familiar term STEMI.
  • ECG Blog #262 — Reviews a case of recent acute Infero-Postero MI with group beating from Wenckebach conduction and Low Voltage (with a list of the causes of Low Voltage).
  • The January 24, 2020 post in Dr. Smith's ECG Blog — Reviews a case in which Low Voltage (with progressive reduction in QRS amplitude on serial ECGs) was due to myocardial stunning  (See My Comment at the bottom of the page). 
  • The November 12, 2020 post in Dr. Smith's ECG Blog — Reviews a case in which Low Voltage was seen in a patient with Covid-19 and cardiogenic shock, in which low voltage seemed to precede (? predict) reduced LV function! (See My Comment at the bottom of the page).

Sunday, December 26, 2021

ECG Blog #271 (79) — What is the ST Segment Baseline? (PR or TP segment?)

You are shown the ECG in Figure-1 without the benefit of any history.

  • HOW would you interpret this tracing?
  • Should you activate the cath lab?
  • What would you use as the ST Segment Baseline for assessing ST segment elevation and/or ST depression?

ANSWER: My thoughts on this ECG appear at the bottom of this post, below the following "mini-didactic" on HOW to determine the ST segment baseline.

Figure-1: How would you interpret this ECG without the benefit of any history? (See text).

NOTE: I have updated this content regarding determination of the ST Segment Baseline from ECG Blog #94 that I wrote in 2014 — and I've added the above illustrative clinical case.
  • My revised 3:00 minutes ECG Video (MP-79) on how we define the ST Segment Baseline (ie, whether to use the PR or TP segmentor both?) appears further down in this post!
  • CLICK HERE — to download a PDF summary on assessment of Q Waves and for determining the ST Segment Baseline (from my ECG-2014-ePub).
  • ECG Blog #205 — Reviews my Systematic Approach to 12-Lead ECG Interpretation (including an Audio Pearl).

QRST: Assessing for ST-T Wave Abnormalities
The 1st Step in assessment of ST-T wave Changes is to determine the baseline that you will use — since it is with respect to this baseline that ST segment deviation (either elevation or depression) is judged. Although defining the ST segment baseline is simple in theory — in practice, it can sometimes be extremely challenging. FIRST — Some definitions:
  • The PR segment — is the connecting line that extends from the end of the P wave until the beginning of the QRS complex.
  • The TP baseline — extends from the end of the T wave until the beginning of the next P wave (or if there is no P wave — to the beginning of the next QRS).
  • The J Point — is the point where the end of the QRS joins the beginning of the ST segment (ie, the J-point "joins" the S at the end of the QRS — to the beginning of the ST segment = it "joins" the S's).

The normal ST segment is isoelectric. It lies on the baseline — and, is neither “elevated” nor “depressed” (Figure-2). Although my preference in general is to use the PR segment baseline — the TP baseline may be selected instead.
  • Particular features on a given tracing (such as artifact, the amount of baseline wander or the presence of PR depression) may influence your selection of which baseline to choose — or whether to combine use of PR and TP segments in a given case. 
  • Heart rate is another factor that may influence your choice of which baseline to use (PR, TP or both). For example, sinus tachycardia may shorten the PR interval, as well as reducing duration of the TP segment. Clearly — accurate determination of the true “baseline” for judging ST-T wave deviations will not always be as clear cut as it is in Figure-2.
  • KEY Point: Far more important than whether to select the TP or PR segment as your baseline — is to overview the entire tracing to assess for artifact, baseline wander, or for whatever other particularities about the ECG being looked at that might affect validity of whichever baseline you select.

Figure-2: Overview illustration of ST-T Wave Changes. ST segment deviation (either elevation or depression) — is judged with respect to the PR Segment Baseline (green arrow in Panel A). Alternatively — the TP baseline may be used. Panels B and C show several millimeters (little boxes) of ST Elevation (B) or ST Depression (C). Given how distinct boundaries between P wave, QRS complex and T wave are — it does not matter in this Figure whether one selects the PR or the TP segment as the “baseline”. Panel D shows the J-Point (defined as the point where the end of the QRS  joins the beginning of the ST segment). Note that there is at least 1mm of J-point ST elevation in Panel D. J-point notching as seen here — is very characteristic of Early Repolarization.

Advanced POINT:
On occasion — the presence of an overly large positive or negative P wave may complicate assessment of the PR segment baseline — because of its effect on the Ta (atrial repolarization) wave.
  • My Comment (at the BOTTOM of the page) in the December 9, 2021 post of Dr. Smith's ECG Blog — reviews a case in which giant positive inferior lead P waves resulted in a large negative Ta (atrial repolarization) wave that simulated ST depression.
  • My Comment (at the BOTTOM of the page) in the June 3, 2020 post of Dr. Smith's ECG Blog — reviews a case in which large negative inferior lead P waves resulted in a large positive Ta wave that simulated inferior lead ST elevation.


ECG Media Pearl #79 (3:00 minutes Video) — ECG Blog #271 — Reviews how we define the ST Segment Baseline (ie, whether to use the PR or TP segment — or both?).


Let's return to the case I presented at the beginning of this post.

You were asked to interpret the ECG shown in Figure-1 without the benefit of any history.

QUESTIONS that I Asked: 
  • HOW would you interpret this tracing?
  • What would you use as the ST Segment Baseline for assessing ST segment elevation and/or ST depression?

ANSWER: I note the important ECG findings in today's case below. For clarity — I have labeled the ST segment baselines that I used for determining the amount of ST segment deviation in Figure-3:
  • There is sinus tachycardia at ~110/minute. Regarding intervals — the PR interval looks to be normal. Although the QRS looks a little wide, I measure it to be no more than half a large box in duration (ie, ~0.10 second). The QTc appears prolonged, though it is difficult to precisely measure, and to assess the clinical significance of the QTc here, given the increased rate and marked ST-T wave changes.
  • There is incomplete RBBB (Right Bundle Branch Block) because: i) there is a QR’ pattern in lead V1 (with an rSr’ in lead V2)ii) there are terminal s waves in left-sided leads I and V6andiii) the QRS complex is not wide enough to qualify as “complete” RBBB.
  • The frontal plane axis is difficult to assess — because the QRS complex looks nearly isoelectric in each of the limb leads — and because assessment of axis may be more difficult to determine with right bundle branch conduction abnormalities.
  • Assuming there is normal standardization (We don't see the standardization mark) — there does not appear to be any chamber enlargement.

Figure-3: I have labeled the ECG in Figure-1 to show the ST segment baselines that I used to determine the amount of ST segment deviation in the various leads (See text).

Regarding ST-Wave Changes:
As a result of the incomplete RBBB — QRS morphology in Figure-3 is altered in many leads (ie, leads V1 and V2 with an r' — and most other leads manifesting S waves). As a result — it's more difficult to determine the J-point, which makes assessment of the amount of ST elevation and depression challenging.
  • Note the thin, vertical dotted BLUE lines that I've drawn in Figure-3 in the simultaneously-recorded leads aVR, aVL, aVF; and in V1,V2,V3 — to facilitate identifying the end of QRS complex (and therefore the J-point) in these leads.
  • Diffuse ST segment depression is seen here in no less than 7 leads — and probably 8 leads if the subtle shape of ST depression is counted in lead I (RED horizontal lines serving as the baseline I used to assess ST depression). This ST segment depression is most marked in leads V4 and V5 — but is also prominent in the inferior leads, and in lead V6.
  • ST elevation is most marked in lead aVR — but it is also seen in leads aVL and V1 (BLUE horizontal lines serving as the baseline I used to assess ST elevation).
  • There is minimal ST segment deviation in lead V2 — with this being the one lead in which I cannot determine if there is ST elevation or depression.

KEY Point: As I emphasized above — Opinion is divided as to whether the optimal baseline” for assessing the amount of ST segment elevation or depression should be the PR or Tsegment.
  • In practice, this gets complicated because: i) The PR segment tends to shorten with tachycardia; ii) PR segment depression and/or elevation may sometimes be present (this occurs not only with pericarditis! — but also with other conditions); iii) There may be artifact or baseline wander (due to patient movement, tremor, pain, shortness of breath, etc.); and, iv) In cases like the ECG shown in Figure-3 — the limits of the TP segment are not always clear (ie, the PR and TP baselines are not all the same in each of the leads in Figure-3).
  • My Preference: While I generally favor use of the PR segment as my baseline — I always survey the entire tracing, and often end up using a combination of PR and TP segments in various leads.
  • Disclaimer: I fully acknowledge that others may differ with the baselines I chose in Figure-3 to assess ST segment deviation.

Putting It All Together: 
My clinical impression for the ECG that is shown in Figure-3 — is that there is sinus tachycardia at ~110/minute — incomplete RBBB — with marked and diffuse ST depression in multiple leads (with ST elevation in leads aVR, aVL and V1).
  • This particular ECG pattern is worrisome for coronary disease that may be acute — but which does not localize to any particular anatomic lead area. The underlying pathophysiologic process responsible for this ECG pattern is "supply-demand mismatch". The terminology that I favor to describe these ECG findings is diffuse Subendocardial Ischemia.

PEARL #1: Recognition of the above ECG pattern in which there is diffuse ST segment depression (usually present in at least 7-8 leads) + ST elevation in lead aVR — should immediately suggest the following Differential Diagnosis:
  • Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
  • Subendocardial Ischemia from another Cause (ie, sustained tachyarrhythmia; cardiac arrest; shock/profound hypotension; GI bleeding; anemia; "sick patient"; etc.).

PEARL #2: The ECG pattern seen in Figure-3 does not suggest acute coronary occlusion. There is no anatomic localization to this pattern.
  • This pattern is not consistent with a posterior STEMI — because ST depression is most prominent in the inferior and lateral chest leads (and not in leads V2,V3).
  • In addition to lead aVR showing ST elevation — leads aVL and V1 may also sometimes show slight ST elevation (less marked than in lead aVR) with the pattern of diffuse subendocardial ischemia. We see this in Figure-3.

PEARL #3: For as helpful as stat Echo at the bedside can be in the diagnosis of acute coronary occlusion — we need to remember that there are frequently no wall motion abnormalities when there is diffuse subendocardial ischemia. This is because: iThe epicardium remains functional, since it is only the endocardium that is ischemic; andii) Subendocardial ischemia is diffuse — and therefore does not localize to any particular myocardial region.

PEARL #4: The History is KEY for suggesting whether diffuse coronary ischemia in any given case is likely to be due to severe coronary diseaseor — to one of the other causes that I listed above.
  • For discussion purposes — I intentionally did not give any history for today's case. IF the history for this patient had been new, worrisome chest pain — then prompt cardiac cath would clearly be indicated to define the anatomy. 
  • It turns out that the ECG in today's case was from a patient with depressed mental function from a CNS bleed. As a result, cardiac cath was not performed — since results of a cath would not have altered the unfortunate outcome.

PEARL #5: It's important to remember that CNS catastrophes (stroke, bleed, trauma, tumor, sudden coma, etc.) are notorious for causing among the most abnormal (and sometimes bizarre) ECG findings. 
  • Pseudo-infarct patterns are common with CNS catastrophes — and may manifest Q waves, diffuse ST segment elevation and/or depression — often with a markedly prolonged QTc. The markedly abnormal ECG in today's case could be perfectly consistent with a large CNS bleed.

Related Material of Interest: 
  • CLICK HERE — to download a PDF summary on assessment of Q Waves and the ST Segment Baseline (from my ECG-2014-ePub).

  • ECG Blog #205 — Reviews my Systematic Approach to 12-Lead ECG Interpretation (including an Audio Pearl).

  • ECG Blog #204 — Reviews the ECG diagnosis of Bundle Branch Block (RBBB, LBBB, IVCD).

  • ECG Blog #250 — Reviews another case of diffuse subendocardial ischemia that surprisingly was due to a persistent tachycardia.

  • My Comment (at the BOTTOM of the page) in the May 13, 2020 post of Dr. Smith's ECG Blog — reviews another case of diffuse subendocardial ischemia.

  • My Comment (at the BOTTOM of the page) in the December 9, 2021 post of Dr. Smith's ECG Blog — reviews a case in which giant positive inferior lead P waves resulted in a large negative Ta (atrial repolarization) wave that simulated ST depression.
  • My Comment (at the BOTTOM of the page) in the June 3, 2020 post of Dr. Smith's ECG Blog — reviews a case in which large negative inferior lead P waves resulted in a large positive Ta wave that simulated inferior lead ST elevation.

Wednesday, December 22, 2021

ECG Blog #270 (78) — MI vs Septal Q Waves?

The ECG in Figure-1 is from a patient with chest pain, obtained several hours after cardiac catheterization.

  • Are there Q waves or Q wave "equivalents" in the inferior and anterior leads of ECG #1?
  • What else would YOU say about this tracing?

ANSWER: My thoughts on this ECG appear at the bottom of this post below the following "mini-didactic" on Septal vs Infarction Q waves.

Figure-1: ECG obtained several hours after cath from a patient with chest pain. (Please note that this ECG is from the case presented in the November 20, 2019 post in Dr. Smith's ECG Blog).

NOTE: I have updated this content on pointers related to Q Wave assessment from ECG Blog #94 that I wrote in 2014 — and I've added an illustrative clinical case.
  • My revised 4:30 minutes ECG Video (MP-78) on how we define "Q Waves" — and how to distinguish "normal" septal Q waves from Infarction Q waves appears further down in this post!
  • CLICK HERE — to download a PDF summary on assessment of Q Waves and for determining the ST Segment Baseline (from my ECG-2014-ePub).
  • ECG Blog #205 — Reviews my Systematic Approach to 12-Lead ECG Interpretation (including an Audio Pearl).

Assessing for Q-R-S-T Changes: Looking for Q Waves
Simply stated — a Q wave is defined as the 1st downward deflection of the QRS complex (Figure-2):
  • Small and narrow Q Waves (as seen in Panel A of Figure-2) — are often normally seen in healthy subjects. This is particularly true when such small and narrow q waves are present in one or more of the lateral leads (leads I, aVL; V4,V5,V6) — especially if the clinical scenario and the rest of the ECG appears to be benign.
  • In contrast — large and wide Q Waves (as in Panel B) — are much more likely to indicate that at some point there has been an MI (Myocardial Infarction). The larger and wider the Q waves are — and, the more leads in which they are seen — the more likely it becomes that they indicate prior MI.
  • The 3rd possibility regarding Q waves in seen in Panel C — in which there is an all-negative complex. Because there is no positive deflection (ie, no R wave)  — We are unable to tell if the all-negative deflection that is seen is: i) a Q wave; ii) an S wave; or, iii) some combination of the two. As a "compromise" — this pattern is called a QS complex.
  • NOTE: For communication and clarification purposes — we favor use of large or small-case letters for description of Q waves, depending on whether the Q wave is wide and at least 3 mm ( = 3 little boxes) deep (Figure-2).

Figure-2: Nomenclature for describing Q waves (See text).

Clinical Points Regarding Figure-2:
  • A QS pattern is most commonly seen in one or more of the anterior leads. Depending on other parameters (such as QRS complex width and ST-T wave appearance) — clinical implications of a QS pattern may be similar to clinical implications of a wide Q wave (possible previous infarction) — especially if QS complexes are seen in multiple leads. On the other hand — the presence of one or more QS complexes may be a normal finding (See discussion of R wave progression in ECG Blog #269).

  • PEARL #1: All bets are off!IF QS complexes are seen in a patient with QRS widening from LBBB (Left Bundle Branch Block). In this situation — anterior QS complexes are not only common, but an expected accompaniment of LBBB (See my Review on BBB in ECG Blog #204).

  • Even when large and wide Q waves indicate that prior infarction has taken place (as would be suggested by Panel B) — the mere presence of such Q waves does not tell us anything about the "age" of the infarct (ie, whether it occurred years ago — or fairly recently).
  • To determine IF an MI might be "acute" (ie, beginning within the past few hours — and possibly still ongoing) — We use a combination of: i) History (ie, Is there new-onset chest pain?orIs chest discomfort more of a longterm problem without recent onset?); ii) Serial ECGs (for assessment of ST-T wave changes); iii) Cardiac markers (ie, troponin); and, iv) Other tests (ie, Echo at the bedside, looking for wall motion abnormality during chest painorCardiac Cath, as the definitive test looking for acute coronary occlusion).

  • PEARL #2: While we often think of Q waves as a longstanding marker of prior infarction — it's important to appreciate that Q waves may sometimes develop rapidly (ie, in as little as 1-2 hours after the onset of symptoms). This point emphasizes the importance of the History and comparison with prior tracings for optimal understanding of the meaning Q waves have in any particular case.

  • PEARL #3: And, although deep and wide Q waves often serve as a “marker” of prior infarction — this ECG sign is not without exceptions. Certain conditions (ie, cardiomyopathy) may produce Q waves not due to infarction (See ECG Blog #45). Further complicating assessment of Q waves on ECG — is the clinical reality that infarction-related Q waves do not always persist after the event. With time — Q waves may either decrease in size or disappear entirely. As a result — even small q waves may at times be a “marker” of prior infarction (ie, if a previously large infarction-Q-wave shrunk in size but did not disappear). Awareness of the clinical history and what the patient’s baseline ECG looked like would be needed to know if persistent small q waves in that patient were serving as a marker of prior infarction (assuming lead placement issues and a shift in axis were not the reasons for change in Q wave morphology). 
  • Bottom LINE: The term, "significant" Q wave is potentially misleading — because the size of a Q wave is not necessarily a reliable indicator of infarction. Instead of using this term — I favor describing the location and relative size of Q waves in my Descriptive Analysis — and then correlating clinically (ideally with review of prior tracings for comparison) to determine the likely significance of this finding.


ECG Media Pearl #78 (4:30 minutes Video) — ECG Blog #270 — Reviews how we define, "Q Waves" — and how to distinguish "normal" septal Q waves from Infarction Q waves.


Let's return to the case I presented at the beginning of this post.

The ECG in Figure-1 is from a patient with chest pain, obtained several hours after cardiac catheterization.

QUESTIONS that I Asked: 
  • Are there Q waves or Q wave "equivalents" in the inferior and anterior leads?
  • What else would YOU say about this tracing?

ANSWER: The ECG in today's case was taken from a patient who was found to have multi-vessel coronary disease and an acute inferior infarction. My purpose in selecting this tracing was to focus on the variety of Q-waves and Q-wave "equivalents" that are seen, which I've labeled in Figure-3. Significant ECG findings in this tracing include the following:
  • The rhythm in Figure-3 is sinus bradycardia at ~50/minute. Regarding intervals — the PR interval is upper normal (ie, ~0.20 second) — the QRS in narrow — and the QTc is normal. There is a leftward axis of about -30 degrees (isoelectric QRS in lead II — therefore not negative enough to qualify as LAHB). There is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • Q waves and/or Q wave "equivalents" are seen in multiple leads.
  • Small and narrow q waves are seen in high-lateral leads I and aVL. These q waves look like normal septal q waves (because of their small size and lateral location).
  • I call the QRS complex in lead II a "Q-wave equivalent" — because for all practical purposes, clinical implications are the same as they would be for a legitimate Q wave. Note that there is an ever-so-tiny initial upward deflection to this QRS complex in lead II (RED arrow in lead II) — which is the reason this technically is not a "Q wave", but rather an rsR'S' complex. PEARL #4: In my experience, when the only thing negating the definition of a Q wave is a tiny initial positive deflection in a tracing that otherwise indicates acute infarction — this effectively serves as a marker for infarction.
  • In lead III — there is an rS complex, with a tiny-but-definitely-present initial r wave in this lead (RED arrow in lead III). By itself — this type of complex would not qualify as a "Q wave equivalent" — because unlike what we see in lead II, there is no back-and-forth change between positive and negative deflections.
  • PEARL #5: We need to remember that the ECG is the "net effect" of all ongoing electrical activity. Since the initial QRS deflections of LAHB (Left Anterior HemiBlock) and Inferior Infarction Q waves are oppositely directed — it can be extremely challenging at times to determine IF a patient has inferior lead infarction Q waves — OR — rS inferior lead complexes from LAHB — OR — some combination of the two. Therefore, in Figure-3 — although the QRS in lead II is not predominantly negative enough to qualify as LAHB, it is possible that both inferior MI and LAHB are present (ie, the QRS complexes in both leads III and aVF are very much consistent with LAHB).
  • Because of the slow heart rate — there are only 2 QRS complexes in lead aVF. The 1st QRS complex in this lead shows a definite small-but-present initial r wave, followed by a notched (fragmented) descent of the S wave (RED arrow in lead aVF). However, I do not see any initial positive deflection in the 2nd QRS complex in lead II — which qualifies this complex as a QS in lead aVF.
  • PEARL #6: Regardless of whether true QRS morphology in lead aVF is an rS or QS complex — I call the "slurring" in the initial S wave descent in this lead (RED arrow in lead aVF) as a "Q-wave equivalent" — since in the context of other ECG findings of acute infarction, this "slurring" in an inferior lead serves as a marker for infarction.
  • PEARL #7: Small and narrow q waves are seen in leads V5 and V6 (GREEN arrows in these leads). That said — by the concept of proportionality — these q waves are disproportionately large considering the tiny size of the R wave in leads V5 and V6. Especially in view of associated ST-T wave changes — despite their tiny size — I'd call these "infarction q waves".

Figure-3: I've labeled the initial tracing in today's case (See text).

Regarding R-Wave Progression:
  • There is poor R-Wave Progression (PRWP) in the chest leads of Figure-3 — because Transition is delayed, and does not occur until leads V5-to-V6, if then (ie, the R wave in lead V6 is barely more positive than the S wave in this lead is deep — See ECG Blog #269 for review of R Wave Progression).
  • Note that although it looks as if there is a QS complex in lead V3 (BLUE arrow) — there is actually a small, initial positive deflection (r wave) to the QRS complex in this lead. Since leads V1, V2 and V3 are simultaneously recorded — the vertical dotted BLUE line in Figure-3 defines the onset of the QRS in these 3 leads.
  • PEARL #8: Although lead V3 does not manifest a QS complex — there is "Loss of R-Wave" from lead V2-to-V3 — which in the context of the acute ST-T wave changes, serves as a "Q-wave equivalent" marker of anterior infarction!

Regarding ST-T Wave Changes:
  • Hyperacute T-waves (that are taller, fatter-at-their-peak, and wider-at-their-base than expected) are seen in multiple leads (ie, in the 3 inferior leads — and in all 6 chest leads). Virtually all of these leads show at least slight J-point ST elevation (which attains ~1.5 mm of ST elevation in each of the inferior leads — See ECG Blog #218 for more on Hyperacute T waves).
  • There is ST-T wave depression in high-lateral leads I and aVL in Figure-3. Note the mirror-image opposite relationship for the ST-T wave depression in lead aVL (including 1-1.5 mm of J-point depression) — compared to the shape of the ST elevation and hyperacute T wave in lead III. In the setting of new chest pain — this ECG finding is diagnostic of acute inferior infarction (See ECG Blog #184 for more on this topic).

Putting It All Together:
My goal in writing today's ECG Blog #270 — was to focus on the evaluation of Q waves and Q wave "equivalents" by means of didactic review and an illustrative case. Given the history of chest pain — the ECG in Figure-3 is diagnostic of acute infarction. ECG findings of concern include:
  • Fairly marked sinus bradycardia.
  • Signs of acute inferior infarction — including Q waves or Q wave "equivalents" in leads II and aVF — inferior lead ST elevation and hyperacute T waves — mirror-image opposite ST-T wave depression in lead aVL.
  • Suggestion of acute antero-lateral infarction — including "loss" of R wave (from lead V2-to-V3) — disproportionately large q waves in leads V5 and V6 — hyperacute T waves in all 6 chest leads.

Related Material of Interest: 
  • CLICK HERE — to download a PDF summary on assessment of Q Waves and the ST Segment Baseline (from my ECG-2014-ePub).

  • ECG Blog #205 — Reviews my Systematic Approach to 12-Lead ECG Interpretation (including an Audio Pearl).

  • ECG Blog #269 Reviews assessment of R Wave Progression (including the causes of "Poor" R wave progression).
  • ECG Blog #204 Reviews the ECG diagnosis of Bundle Branch Block (RBBB, LBBB, IVCD).
  • ECG Blog #45 Reviews the unusual ECG findings in this patient with Muscular Dystrophy (which is known for the occurrence of cardiomyopathies).
  • ECG Blog #218 — Reviews what is a Hyperacute T Wave (including the Audio Pearl in this post ).
  • ECG Blog #184 — Reviews the "magical" mirror-image opposite relationship with acute infarction between lead III and lead aVL (including the Audio Pearl in this post).

  • Please note that the ECG shown in Figure-1 of today's case is from the November 20, 2019 post in Dr. Smith's ECG Blog. (This is ECG #5 from my figure in My Comment at the BOTTOM of the page in that Dr. Smith post).