Wednesday, April 27, 2022

ECG Blog #301 — 40yo Man: VT vs Aberrancy?

The ECG in Figure-1 was sent to me for my interpretation. It was obtained from a previously healthy 40-ish year old man — who presented to the ED (Emergency Department) with “palpitations”. He was hemodynamically stable.


  • What is the rhythm: VT vs Aberrancy?

Figure-1: 12-lead ECG and long lead II rhythm strip obtained for a 40-ish year old man with palpitations.

MY Thoughts on the ECG in Figure-1:

We are told that the patient in today’s case is hemodynamically stable with the rhythm in Figure-1. Therefore, by definition — we have at least a moment in time to contemplate the rhythm without need for immediate cardioversion. By the Ps, Qs, 3R Approach (which I review in ECG Blog #185):
  • The rhythm for ECG #1 is rapid and Regular — at a Rate of ~190/minute (Use of the Every-Other-Beat Method to estimate this heart rate is explained below in the legend to Figure-2)
  • The QRS complex is wide
  • I do not see any evidence of atrial activity (ie, there are no P wavesand therefore no "Relation" between atrial and ventricular activity).

  • IMPRESSION: In this hemodynamically stable 40-ish year old man — use of the Ps, Qs, 3Rs allows us to describe the ECG in Figure-1 as a regular WCT ( = Wide-Complex Tachycardia) rhythm at ~190/minute, without clear sign of atrial activity. Before going further — it is well to remember the differential diagnosis of a regular WCT of uncertain etiology (Figure-2).

Figure-2: This is my LIST #1: Causes of a Regular WCT (Wide-Complex Tachycardia) of Uncertain Etiology (ie, without clear sign of sinus P waves).

KEY POINTS Regarding the Above Differential Diagnosis:

  • My reason for repeating VT no less than 8 times in Figure-2 before listing another possibility — is to emphasize that statistical odds that a regular WCT rhythm without clear sign of atrial activity will turn out to be VT begin at ~80%. As per ECG Blog #196 — these odds increase to ≥90% if the patient is of a "certain age" (ie, middle-aged and beyond) and has underlying heart disease. As a result — Assume VT until proven otherwise!

  • PEARL #1: Because of the above "statistical odds" — When assessing a hemodynamically stable patient in a regular WCT rhythm without P waves — our "mindset" should be that we need to prove that the rhythm is not VT, rather than the other way around.
  • That said — 90% is not 100% — so there will be cases in which a regular WCT rhythm will turn out to be supraventricular. We simply need to approach our differential diagnosis with the "starting point" of assuming a regular WCT rhythm without sinus P waves is VT until proven otherwise.

In Today's Case:  — I Did Not Think the Rhythm was VT:
Despite the above statistical odds in favor of VT — Figure-3 illustrates why I did not think ECG #1 was VT.
  • PEARL #2: Although far from perfect — QRS morphology can be helpful for distinguishing between supraventricular vs ventricular rhythms. Many supraventricular rhythms resemble some form of known conduction defect (ie, RBBB, LBBB, LAHB, LPHB, or RBBB with either LAHB or LPBH)
  • In contrast — ventricular rhythms are less likely to resemble any known form of conduction defect (because these rhythms originate in the ventricles, usually from a site not in contact with the conduction system).
  • Of course — Exceptions to the above generalities clearly exist! (ie, Fascicular VT resembles RBBB with a hemiblock — whereas some SVT rhythms may not resemble any known conduction defect IF the preexisting ECG during sinus rhythm showed an unusual form of IVCD)
  • BUT — IF a completely typical QRS morphology for RBBB is present in each of the 3 KEY leads ( = left-sided leads I, V6 — and right-sided lead V1)then a supraventricular etiology is highly likely. This is precisely what we see in Figure-3 because: i) A very typical RBBB conduction pattern (rsR') is seen in right-sided lead V1, in the form a small, initial positive deflection (r wave) — followed by an s wave that descends below the baseline — and ending in a "taller right rabbit ear" with a slender and tall R' complex; ii) Left-sided lead I is consistent with LPHB conduction (rS) — in that a slender initial r wave is followed by a very steep descent to a wide terminal S wave; and, iii) Left-sided lead V6 also manifests a triphasic (qRS) pattern (the opposite of the rsR' pattern in lead V1) — with wide terminal S wave that is highly characteristic of RBBB conduction.

Figure-3: I’ve outlined in RED a QRS complex in each of the 3 KEY leads to highlight the very typical QRS morphology of RBBB conduction (See text). In lead aVF — I illustrate application of the Every-Other-Beat Method for rapid estimation of heart rate (this method discussed in full in ECG Blog #210). It takes a little more than 3 large boxes (RED numbers in lead aVF) — to record 2 beats (BLUE numbers). If it would have taken exactly 3 large boxes to record 2 beats — then 1/2 the rate would have been 300 ÷ 3 = 100/minute. This means that 1/2 of the rate is a little bit slower than 100/minute — which means that the ventricular rate is ~190/minute.

PEARL #3: There is a tendency to simplify the differential diagnosis of a regular WCT rhythm down to 2 entities: VT vs "aberrant" conduction
  • As shown above in LIST #1 (Figure-2) — this simplification overlooks the possibility that the reason for QRS widening in a WCT rhythm could be that the QRS complex was already widened at a time when the patient was in sinus rhythm (ie, as would be the case if there was a preexisting BBB). Unless a prior ECG on the patient is available — there may be no way to know IF the reason for QRS widening in a supraventricular tachycardia is: i) A rate-related conduction defect (ie, "aberrant" conduction); or, ii) A preexisting conduction defect on the baseline tracing.

  • LIST #1 also serves to remind us that in addition to VT and SVT with either preexisting BBB or aberrant conduction — other potential reasons why a tachycardia might manifest QRS widening include: i) A WPW-related tachyarrhythmia that travels first down the Accessory Pathway (anterograde); ii) Hyperkalemia; and/or, iii) Some other toxic effect that results in QRS widening.

PEARL #4: IF our assessment of QRS morphology in Figure-3 is correct — then the WCT rhythm in this tracing will be a regular SVT (SupraVentricular Tachycardia) at ~190/minute, without clear sign of atrial activity. As discussed in the Audio Pearl (ECG-MP-64) in the ADDENDUM below — my LIST #2 that I favor for the differential diagnosis of a regular SVT rhythm consists of Causes:

  • Sinus Tachycardia (Sinus Tach).
  • Atrial Flutter (AFlutter).
  • Reentry SVT (ie, AVNRT or AVRT).
  • Atrial Tachycardia (ATach).

Of these 4 Causes — the least common in my experience is Atrial Tachycardia (ATach)Consideration of the heart rate may provide an important clue to the etiology of a regular SVT without clear sign of atrial activity.

  • In a supine adult (ie, an adult who has not just exercised) — it is not common for sinus tachycardia to exceed ~170/minute. This is not to say that you will never see sinus tachycardia this fast in a non-exercising adult — but rather to suggest that the very rapid heart rate in today’s case (ie, ~190/minute) makes sinus tachycardia much less likely.
  • Untreated AFlutter most commonly presents with 2:1 AV conduction, in which the atrial rate of flutter is close to 300/minute (ie, ~250-to-350/minute range) — and the ventricular rate close to half that, or ~150/minute (ie, ~130-to-160/minute range). The ventricular rate of ~190/minute in today's case would imply an atrial rate of 190 X 2 = 380/minute, which is much faster than the usual atrial rate for AFlutter.
  • From these points — it can be seen that when the rate of a regular SVT rhythm is not more than 150-160/minute — any of the entities on the SVT LIST could be operative. However, when the ventricular rate is greater than ~170/minute (as it is in Figure-3— then a reentry SVT rhythm becomes much more likely!

PEARL #5: Practically speaking — IF the rhythm in Figure-3 turned out to be VT — it would probably be a Fascicular VT. Appreciation of this fact has important clinical implications.
  • As emphasized in ECG Blog #197 — Approximately 10% of all VT rhythms fall into the category of Idiopathic VT rhythms, in which VT occurs in the absence of underlying structural heart disease.
  • Idiopathic VT is more likely to be seen in a previously healthy, younger adult population — which fits the profile of the patient in today's case.
  • Fascicular VT is one of the 2 most common forms of idiopathic VT. Morphologically — the QRS complex in Fascicular VT (as implied in its name) tends to resemble a RBBB pattern with either left anterior or left posterior hemiblock (ie, a "hemi-fascicular" block pattern).
  • Fascicular VT responds surprisingly well to IV Verapamil. On occasion — it may also respond to Adenosine, but IV Verapamil is the drug of choice for known Fascicular VT. In contrast — Verapamil is contraindicated for treatment of scar-related or ischemic VT.

  • BOTTOM LINE: I thought the rhythm in today's case was most likely to be a reentry SVT rhythm — because of the highly suggestive QRS morphology (as shown in Figure-3) that is perfectly consistent with typical RBBB conduction. But if it turned out that this rhythm was VT — its resemblance to RBBB/LPHB conduction would strongly suggest a Fascicular VT. As a result — IV Verapamil would have been my drug of choice, since this drug is 1st-line treatment for both reentry SVT rhythms and Fascicular VT.
  • IV Adenosine that was used in today's case was a perfectly suitable alternative — because this drug is generally safe — it is highly effective in terminating reentry SVT rhythms — and on occasion, it also may convert Fascicular VT.


The patient in today's case was treated with IV Adenosine. The 2-lead rhythm strip in Figure-4 shows the result of such treatment.

  • Was IV Adenosine effective in converting the rhythm?
  • What was the cause of QRS widening in the initial tracing?

Figure-4: Comparison of the initial ECG in today's case — with a 2-lead rhythm strip obtained after administration of IV Adenosine (See text).

Unfortunately — I do not have a 12-lead ECG to show after administration of IV Adenosine. That said — even though I would have greatly preferred a lead V1 (rather than lead V2) rhythm strip — I believe ECG #2 in Figure-4 confirms my impression that the regular WCT rhythm in the initial tracing was supraventricular (in the form of a reentry SVT rhythm), in which the reason for QRS widening was preexisting bundle branch block.
  • Even though we do not have a left-sided monitoring lead (ie, lead I or V6) — and we do not have a lead V1 monitoring lead — the post-Adenosine tracing ( = ECG #2) shows conversion to sinus rhythm with persistent QRS widening and a QRS morphology in leads II and V2 that is virtually identical to the QRS morphology in these same leads during the WCT!

  • P.S.: To emphasize that IV Adenosine works rapidly — with antiarrhythmic effect usually complete with 1-2 minutes after administration. It's BEST to run a continuous hard-copy rhythm strip during the entire ~2-minute period after Adenosine administration — since the etiology of the arrhythmia will usually be evident during the process of conversion to sinus rhythm.

Acknowledgment: My appreciation to M Shah (from Srinagar, India) for the case and this tracing.





Relevant ECG Blog Posts to Today's Case:

  • ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
  • ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm.

  • ECG Blog #220 — Reviews in detail the differentiation in "List #1" for the causes of a Regular WCT ( = Wide-Complex Tachycardia).

  • ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm. 
  • ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 

  • ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
  • ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the video ECG Media Pearl #21 in this blog post.

  • ECG Blog #211 — Reviews in detail WHY Aberrant Conduction occurs (and why RBBB aberration is the most common form).

  • ECG Blog #250 — Reviews in detail the differential in "List #2" for the causes of a Regular SVT ( = SupraVentricular Tachycardia).


ADDENDUM #2 (5/3/2022):

My appreciation to JJ for their comment — in which they bring up the point that "some kind of electrical alternans can be seen in leads V3,V4". 

I agree. I review the subject of Electrical Alternans in ECG Blog #83 — in which I emphasize the definition of this phenomenon = "a beat-to-beat variation in any one or more parts of the ECG recording — that may occur with every-other-beat — or with some other recurring ratio (3:1, 4:1, etc.)."

  • Leads V3,V4 do show variation in the height of the R wave — not strictly every-other-beat — but indeed with a recurring ratio.
  • The finding of electrical alternans is most common with reentry SVT rhythms (especially when there is an accessory pathway) — but on rare occasions, this phenomenon has been reported in monomorphic VT. So seeing electrical alternas supports (but does not prove) a supraventricular etiology.

My appreciation again to JJ for their observation!


ADDENDUM #1 (4/22/2022):

I've added below from previous Blog posts a series of educational material regarding assessment of the Regular WCT — and the basics of Aberrant Conduction.


Figure-5: Use of the "3 Simple Rules" for distinction between SVT vs VT (taken from ECG Blog #196).

Figure-6: Use of lead V1 for assessing QRS morphology during a WCT rhythm (taken from ECG Blog #196).


ECG Media PEARL #28 (4:45 minutes Video) — Reviews WHY some early beats and some SVT rhythms are conducted with Aberration (and why the most common form of aberrant conduction manifests RBBB morphology).

  • CLICK HERE — to download a PDF of this 6-page file on Aberrant Conduction. 

ECG Media PEARL #64 (10:50 minutes Audio) — Reviews my LIST #2: Common Causes of a Regular SVT Rhythm.


Saturday, April 23, 2022

ECG Blog #300 — Why Does It Happen at Night?

The ECG in Figure-1 was obtained from a 50-year old man who developed chest pain after becoming emotionally upset. As his workplace was close to his physician's office — this ECG was obtained within ~5 minutes of the event.
  • How would YOU interpret the ECG in Figure-1?
  • How might you explain that the patient reports 3 recent similar episodes — with chest pain spontaneously resolving each time within 15 minutes?

Figure-1: ECG obtained from a 50-year old man within minutes of developing chest pain after becoming emotional upset.

MY Thoughts on the ECG in Figure-1:
The rhythm is sinus at ~90-95/minute. There is a PVC (in the middle of the tracing — between the lead switch from leads aVR,aVL,aVF — to leads V1,V2,V3).
  • Regarding Intervals — The PR interval is normal. The QRS is narrow. However — the QTc looks prolonged (especially in leads V2, V3).
  • The frontal plane Axis is normal (about 0 degrees — as the QRS is isoelectric in lead aVF).
  • Regarding Chamber Enlargement — QRS amplitude appears increased in the lateral chest leads (although as we'll see in a moment — this does not necessarily reflect LVH).

Regarding Q-R-S-T Changes:
  • There are small and narrow Q waves in each of the lateral leads (ie, leads I, aVL, V5,V6). These are of uncertain significance.
  • R Wave Progression shows normal Transition in the mid-chest lead area — but there is a strange loss of voltage for the tiny QRS complex in lead V3.
  • The most remarkable finding in ECG #1 — are the tall, peaked T waves in leads V2-thru-V6 (especially marked in leads V2, V3, V4). There is also J-point ST elevation in leads V1-thru-V4 (attaining 2-2.5 mm in amplitude in leads V2 and V3). ST segments are flat but not depressed in each of the inferior leads.

The PVC and markedly tall, peaked T waves in multiple chest leads with at least 2 mm of ST elevation in leads V2,V3 in this patient with new-onset chest pain — strongly suggest acute LAD (Left Anterior Descending) occlusion until proven otherwise.

The CASE Continues:
Immediately after ECG #1 was recorded — the patient said, "My chest pain is less. It will go away by itself. I have had clusters of such pains that usually occur between 5-to-6 am in the morning".
  • Supplemental History: The patient is a heavy smoker (2 packs per day). His medical history is otherwise negative. Negative family history.
  • The initial Troponin came back negative.
  • The patient refused medication — so neither nitroglycerin nor analgesics were given. Over the next ~10 minutes — his chest pain completely resolved, at which time ECG #2 was obtained (Middle tracing in Figure-2).
  • The patient stabilized. ECG #3 was obtained about 3 hours after the initial ECG (Bottom tracing in Figure-2). Throughout this time — the patient remained without chest pain.

  • Given the above sequence of events — HOW would you interpret the serial ECGs shown in Figure-2?
  • Based on the above history — WHAT is the likely diagnosis? 
  • What do you think cardiac catheterization showed?

Figure-2: The patient's chest pain resolved quickly. He was pain-free at the time ECG #2 was obtained. He remained pain-free over the next few hours — at which time ECG #3 was obtained (See text).

MY Thoughts on the History and Serial ECGs:
The extreme ST-T wave changes seen in the chest leads of the initial ECG improved dramatically in the ECG obtained just 17-minutes later.
  • As emphasized in the History provided above — the patient was well familiar with the sequence of events in which stress or emotional distress — or simply the early morning hours, brings on a short-lived episode of severe chest pain that he knows will spontaneously resolve minutes later.

  • KEY Clinical Point: The initial ECG ( = ECG #1 in Figure-2) was obtained during this episode of severe chest pain. Minutes later, the chest pain was less — and it was essentially gone at the time ECG #2 was obtained. While several of the mid-chest leads in ECG #2 still manifest somewhat larger-than-expected T waves — the improvement from ECG #1 is obvious.

  • ECG #3 (done ~3 hours after ECG #1) — shows further reduction in T wave amplitude. There is no longer any ST elevation. Instead — leads V3-thru-V6 show 0.5-1.0 mm of ST depression.

Further FOLLOW-UP to Today's CASE:
  • Serum Troponin never became elevated.
  • Cardiac catheterization revealed normal coronary arteries! (Figure 3).
  • Acute MI was ruled out. The patient was discharged with a diagnosis of Prinzmetal Angina.

Figure-3: Cardiac catherization of the patient in today's case was completely normal — without any significant narrowing — and with normal left ventricular function.

Prinzmetal Angina:
The entity known as Prinzmetal Angina (also known as "vasospastic" or "variant" angina) — is a syndrome of recurrent chest pain episodes that occur at rest in association with transient ST-T wave changes (either ST elevation and/or depression). I summarize below KEY points from the following sources — (Ziccardi and Hatcher: StatPearls-NCBI Bookshelf- 7/31/2021) — (Bayés de Luna et al: Ann Noninvasive Electrocardiol 19:442-453, 2014 Consensus Paper) — and — (Ghadri et al: Q J Med 107:375-377, 2014).
  • Charcteristic Features of Prinzmetal Angina — are that: i) Chest pain episodes spontaneously resolve (usually within 5-15 minutes without treatment!); and, ii) Chest pain episodes often occur in clusters over consecutive (or nearly consecutive) days. Fortunately — chest pain episodes resolve faster if short-acting nitrates are promptly given. 
  • There is often a circadian pattern to symptoms — in that episodes most often occur between midnight and the early morning hours. In any given patient — episodes often occur at about the same time during the day or night.

  • Approximately 50% of patients with Prinzmetal Angina have normal coronary arteries on cath. Most of the remainder have nonobstructive coronary lesions (ie, less than 50% vessel narrowing).
  • ECG changes may include ST elevation with/without reciprocal ST depression — which may (or may not) be followed by reperfusion ST changes (ie, T wave inversionSee Below!).
  • Prompt recognition of this entity is important because potentially life-threatening malignant arrhythmias (including VT/VFib, high-grade AV block) may occur. Myocardial infarction is not common (because episodes most often spontaneously resolve within 15 minutes) — but acute MI can occur.

  • The mechanism of Prinzmetal Angina is uncertain — though the end result appears to be diffuse or localized coronary spasm, perhaps precipitated by sympathetic hyperactivity (with or without vagal tone withdrawal) — by reduced nitric oxide synthase with endothelial dysfunction — and/or by genetic predisposition. Coronary vessel hyperreactivity may be precipitated by development of underlying coronary narrowing — OR — "pure" vasospastic angina may be seen in patients with totally normal coronary arteries.

  • Among potential "trigger" factors of anginal episodes include drugs (cocaine, amphetamine, mariuana) — especially if associated with cigarette smoking! Other potential precipitating factors include cold exposure and exercise in a small percentage of patients. That said — there need not necessarily be any triggering factor.
  • Other "vasospastic" disorders (ie, Raynaud phenomenon, typical migraine) may be associated in patients with Prinzmetal Angina.

  • The average age of presentation for patients with Prinzmetal Angina is in an adult between 40-50 years of age. But it does present in other age groups.

  • Standard Treatment of Prinzmetal "Vasospastic" Angina incudes Nitrates (short and/or longterm — with the caution that longterm nitrates may lead to tolerance) — longterm Calcium Channel Blockers (ie, debate persists as to which ones are best) —  plus emphasis on complete smoking cessation! 
  • Additional treatment measures more recently considered include Nicorandil (a nitrate and K-channel activator with coronary vasodilatory properties) — and Fluvastatin (seems to benefit some patients with vasospastic angina by improving endothelial function).
  • Among the Drugs to Avoid include ß-Blockers (which may cause unopposed alpha-receptor agonism) — alpha-agonists (ie, Oxymetazoline, Pseudoephedrine) — Sumatriptan (a serotonin receptor agonist used for acute treatment of migraine — which works by promoting vasoconstriction).

  • NOTE: The diagnosis of Prinzmetal Angina may be difficult — especially because of its usual nocturnal occurrence — with spontaneous resolution of symptoms and ECG changes within minutes! (ie, often before an ECG can be done). For this reason — awareness of the above clinical features and of the expected array of ECG changes that I describe below is essential for recognition of this entity!

  • The "GOOD" News — the occurrence of Prinzmetal Angina is much less frequent than in years past (probably because of increased efficacy of antianginal measures and less smoking in the general population). In addition — the longterm efficacy of Calcium Channel Blockers has resulted in much improved symptom control with reduced morbidity in most patients (especially in those who quit smoking).
  • Editorial Comment: I remember special attention being devoted in my medical training to making us aware of this entity. That said, while some component of coronary spasm clearly occurs in a percentage of patients with coronary disease — Prinzmetal Angina in its "pure" form as described above (as was seen in today's patient) is not a common disorder.

Characteristic ECG Features of Prinzmetal Angina:
Most patients with Prinzmetal Angina have a relatively normal baseline ECG, with at most nonspecific ST-T wave abnormalities. I synthesize below the KEY ECG Features to look for in Prinzmetal patients, as detailed in the 2014 international Consensus Paper by Bayés de Luna et al:
  • The most common initial ECG change — is development of tall, symmetrical and usually peaked T waves — accompanied by a modest increase in the QTc.
  • On occasion — negative U waves may be seen.
  • T wave peaking is typically followed by progressive ST elevation. This ST elevation usually lasts less than 5 minutes — after which there is gradual return to a more normal (or minimally peaked) T wave. The patient's chest pain typically corresponds to the period of maximum ST elevation.

  • Some patients manifest reciprocal ST depression during the period of ST elevation. When this happens — it suggests regional (rather than diffuse) coronary vasospasm.

  • Of interest — R wave amplitude tends to increase — while S wave amplitude tends to decrease (if not disappear) during the phase of ST elevation.

  • There is often upsloping of the T-Q segment (or the T-P baseline) during the phase of ST elevation.
  • Occasional patients may manifest alternans (from one beat-to-the-next) of the elevated ST segment or upsloping T-Q segment.
  • During the resolution stage of ST elevation — T wave inversion may be seen, which can be deep and similar to Wellens' Syndrome ECG changes (ie, presumably reflecting evolution of reperfusion T waves).

  • PVCs including short episodes of NSVT (Non-Sustained Ventricular Tachycardia) — are common during the period of chest pain and ST elevation. Fortunatelysustained VT/VFib are uncommon. Occasional patients may manifest ventricular arrhythmias (ie, AIVR) during the reperfusion stage.

  • NOTE: While ST elevation (and other ECG abnormalities) most often occur in association with chest pain episodes — coronary spasm can be "silent" (without chest pain) in up to 20% of cases. This may account for unexplained sudden death due to ischemia in these patients without any "warning" system.

Looking CLOSER at Serial ECGs in Today's CASE:
Let's now apply the above Consensus Paper description of the KEY ECG features to look for in serial ECGs of a patient with Prinzmetal Angina. 
  • In Figure-4 — I again show the initial ECG ( = ECG #1) — and ECG #3, obtained ~3 hours after resolution of this patient's chest pain. 
  • To this, I have added ECG #4 — done 3 days later. The patient had remained pain-free during this time. MI was ruled out — and the cardiac catheterization showed normal coronary arteries.

Figure-4: Comparison of the initial ECG (obtained during the episode of chest pain) — with the follow-up ECG done 3 hours later — and a final ECG done 3 days later (See text).

Review of Serial ECG Changes in Figure-4:
As we emphasized in discussion of Figure-1 — the initial ECG in today's case (TOP tracing in Figure-4) is remarkable for the tall, peaked T waves in leads V2-thru-V6 (especially marked in leads V2, V3, V4). There is also J-point ST elevation in leads V1-thru-V4 (attaining 2-2.5 mm in amplitude in leads V2 and V3). ST segments are flat but not depressed in each of the inferior leads.
  • These ECG changes were obtained during an episode of chest pain in this patient with Prinzmetal Angina.
  • Additional findings in ECG #1 (consistent with Prinzmetal Angina) include the following: i) A PVC; ii) Loss of S wave amplitude (with near disappearance of the S wave in lead V3); iii) Increased R wave amplitude (seen in the lateral chest leads, in which there is overlap of R wave amplitude into neighboring leads); iv) Upsloping of the T-P baseline (best seen in leads V2, V3, beginning just after the T wave returns to baseline); and, v) Localization of these ST-T wave changes to the chest leads (suggesting regional rather than diffuse coronary spasm).

ECG #3 — was obtained 3 hours after ECG #1. The patient's episode of chest pain was short-lived — and he remained pain-free at the time ECG #3 was obtained.
  • Apart from shallow T wave inversion in lead III — limb lead appearance is unchanged from the initial ECG.
  • In contrast — chest lead T waves are all now normal in size. There is no longer any ST elevation. Instead, leads V3-thru-V6 now show 0.5-1.0 mm of ST depression.
  • The S wave in lead V3 has been reestablished. There is no longer upsloping of the T-P baseline. Lateral chest lead R wave amplitude remains increased.

ECG #4 — was obtained 3 days later. The patient remained pain-free throughout this time. He was discharged from the hospital.
  • There has been essentially no change in limb lead appearance.
  • R wave amplitude has decreased dramatically since ECG #3. Significant S waves are now present through to lead V6.
  • There is no longer any ST depression.
  • The upright T waves that were seen in the chest leads of ECG #3 — have now evolved into a biphasic (positive-negative) small-amplitude T wave. Presumably, this is a reperfusion change.

Acknowledgment: My appreciation to Klanseng Ng (from Kluang, Malaysia) for the case and this tracing.

Additional Relevant Material to Today's Case:
  • See ECG Blog #205 — Reviews my Systematic Approach to 12-Lead ECG Interpretation.

  • ECG Blog #183 — Reviews the concept of deWinter T-Waves (with reproduction of the illustrative Figure from the original deWinter NEJM manuscript). 
  • ECG Blog #222 — Reviews the concept of Dynamic ST-T wave changes, in the context of a detailed clinical case. 
  • ECG Blog #260 — Reviews another case that illustrates the concept of "dynamic" ST-T wave changes.

  • ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
  • ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 

  • ECG Blog #193 — Reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culpritartery.

  • ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.

  • ECG Blog #115 — Shows an example of how drastically the ECG may change in as little as 8 minutes.

  • The July 31, 2018 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case provides an excellent example of dynamic ST-T wave changes on serial tracings (that I illustrate in My Comment) in a patient with an ongoing acutely evolving infarction.