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.


  1. Can this ECG pattern consistent with Takotsubo Cardiomyopathy?

    1. @ JJ —There are a variety of ECG patterns that might be seen with Takotsubo Cardiomyopathy — so it’s difficult to say that this particular pattern (from today’s ECG) could not be seen … That said — the QTc is not overly prolonged (as it often is with Takotsubo), and the finding of diffuse ST depression with ST elevation in lead aVR that we see here IS suggestive of a distinct clinical entity = diffuse subendocardial ischemia.

      In contrast — I’m more inclined to think of Takotsubo Cardiomyopathy when I see a markedly abnormal ECG that doesn’t quite fit any clinical picture (ie, if ECG findings seem out of proportion to the clinical presentation — or aren’t relatable to a specific anatomic area).

      For more on the ECG presentation of Takotsubo Cardiomyopathy — Please check out Blog #46 ( — especially Figure-3 in the Addendum of that post).