ECG Blog #545 — Is the Rhythm VT?

The ECG in Figure-1 was obtained from a 60-something year old man — who presented with a history of recurrent palpitations over the past several years. He was hemodynamically stable with this rhythm.

• Prior to the onset of these episodes of palpitations — the patient had been healthy without medical problems.

• Of note — the patient recently developed ankle edema with progressively increasing dyspnea on exertion.

QUESTIONS:

• How would you interpret the rhythm in Figure-1? 
• What clinical entity is suggested by the above history?

  

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on Today's CASE:

As frequently reviewed on this ECG Blog — I favor the Ps,Qs,3R Approach for assessment of tachycardias (See ECG Blog #185 — for review of this system).

• The rhythm in Figure-1 is Regular at a Rate of ~150/minute.
• The QRS is wide (ie, ≥0.12 second).

Regarding the 4th and 5th parameters of the Ps, Qs and 3Rs:

• P waves are absent — which by definition means there is no Relation between P waves with neighboring QRS complexes (since there are no P waves).

Impression: The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~150/minute.  

• Statistically in an adult of a certain age — We start with the reality that 80-90% of regular WCT rhythms without sinus P waves will turn out to be VT. Therefore — Assume VT until proven otherwise. Treat the patient accordingly.
• That said, since this patient is hemodynamically stable — You have at least a moment in time to look closer at the rhythm for features that might increase (or decrease) your diagnostic likelihood of an 80-90% chance that the rhythm is VT.

As illustrated in last week's ECG Blog #544 — Among the most time-efficient and helpful ECG features that I look for are the following:  

• The frontal plane axis during the WCT rhythm. 
• Other potential signs of atrial activity.
• QRS morphology.

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Looking Closer at Figure-1 ...

In today's case — neither the frontal plane axis nor searching for signs of atrial activity help to provide an answer:

• Although the frontal plane axis during the WCT rhythm is markedly leftward — the axis does not satisfy my definition of an "extreme" axis (because the QRS is not entirely negative in either lead I or lead aVF). Instead — a small-but-definitely-present upright initial positive deflection (r wave) is present in lead aVF. As a result — assessment of the frontal plane axis is not sufficiently discriminating to be helpful.
• I see no clear indication of atrial activity in Figure-1. This feature is therefore of no assistance for determining the etiology of today's rhythm.

QRS Morphology during the WCT:

This leaves us with assessing QRS morphology in our hope to increase statistical likelihood beyond the 80-90% likelihood that we start with by simply knowing that today's rhythm is a regular WCT without clear sign of sinus P waves.

• As emphasized in ECG Blog #211 — the chance that a WCT rhythm will turn out to be supraventricular will significantly increase IF — we can demonstrate that QRS morphology is typical for one of the known forms of conduction block (ie, RBBB, LBBB, LAHB or LPHB; or RBBB with one of these hemiblocks).

PEARL #1: The entity of fascicular VT marks an exception to the general rule that when a regular WCT resembles a bifascicular block — that the rhythm is likely to be supraventricular. The reason for this — is that by definition, “fascicular VT” will resemble one of the hemiblock forms (ie, either RBBB/LAHB or RBBB/LPHB). 

• The KEY to recognizing that a regular WCT rhythm that bears a certain resemblance to an rbbb conduction pattern (with either marked left or right axis deviation) is unlikely to represent a supraventricular rhythm — is that there are some features that are atypical for rbbb conduction with either LAHB or LPHB.
• To Emphasize: QRS morphology is not a perfect science. Even in the best of hands — nothing is perfect (ie, It is always possible that prior scarring from cardiomyopathy or previous infarction will result in a markedly abnormal baseline tracing during sinus rhythm).
• This leaves us with the clinical reality that much of the time — we'll need to begin our treatment of a regular WCT before we know for certain what the etiology of the rhythm is. That said — I find it helpful to be aware of the relative probability for VT vs some type of SVT rhythm before I contemplate therapeutic options for treatment.

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Take another LOOK at today’s initial ECG:

I've reproduced today's initial ECG in Figure-2. 

• Does QRS morphology during the WCT rhythm in Figure-2 look like one of the known forms of conduction block?

  

Figure-2: I've reproduced today's initial ECG. 

Answer:

YES — Today's initial ECG that is shown in Figure-2 does resemble the RBBB/LAHB form of bifascicular block. That said, as I suggest below in Figure-3 — there are some atypical features:

• PEARL #2: Although the possibility of rbbb conduction is suggested by the all upright QRS in lead V1 — a triphasic rsR' morphology is lacking (ie, in which there is an s wave that descends below the baseline with a terminal taller right "rabbit ear" R’ wave in lead V1). 
• As discussed in detail in ECG Blog #211 — whereas not all patients with RBBB necessarily manifest a classic triphasic rsR' morphology — the finding of an entirely upright monophasic R wave that we see in lead V1 of Figure-3 could be either the result of supraventricular rbbb conduction or this could be VT. Therefore — the resemblance that we see in lead V1 to rbbb conduction is not helpful in distinguishing between SVT vs VT.
• PEARL #3: The other characteristic feature of rbbb conduction is the presence of a wide terminal s wave in lateral leads I and V6. And although in Figure-3 we do see a terminal s wave in both leads I and V6 (the YELLOW arrows in these leads) — this terminal s wave is narrow in lead I and tiny in lead V6.
• PEARL #4: The typical appearance of lahb conduction — is for there to be rS waves (with predominant negativity) in each of the inferior leads. And although there are initial r waves in leads II,III,aVF — these initial r waves are extremely small in leads II and aVF (YELLOW arrows in these leads) — which is not the typical picture for QRS morphology with lahb conduction.
• PEARL #5: The initial vector of depolarization tends to be fast with supraventricular conduction (because electrical activity once it reaches the ventricles — begins within the His-Purkinje system). In contrast — the slope of the initial depolarization vector tends to be slower with VT (because electrical activity begins away from the conduction system — from within ventricular myocardium). 
• Instead of a more vertical upslope — the R wave in lead I rises at a slower rate than I'd expect with supraventricular conduction (BLUE arrow in this lead).
• PEARL #6: An insensitive, but highly specific morphologic feature to be aware of when assessing a WCT rhythm — is that IF there is either global positivity or global negativity in all 6 chest leads (ie, Leads V1-thru-V6 being either all positive or all negative) — then the etiology of the rhythm is almost certain to be VT.
• There would be global positivity in leads V1-thru-V6 in Figure-3 — if it were not for tiny intermittent s waves in lead V2; and in leads V4,V5,V6. These tiny s waves reduce specificity of this finding for VT (albeit the nearly all positive chest lead QRS morphology remains highly suspicious for VT).

Bottom Line: While fully acknowledging that QRS morphology is not definitive for either VT or a supraventricular etiology in today's initial ECG — the above atypical features made me strongly suspect left posterior fascicular VT as the diagnosis.

Figure-3: I've labeled key features regarding QRS morphology.

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The CASE Continues:

The patient was treated for presumed VT with IV Amiodarone, but without success. Electrical cardioversion was applied, which transientlly converted the rhythm — only to result in recurrence of the regular WCT moments later. 

• The patient's condition deteriorated requiring intubation.
• Persistence of the regular WCT led to marked hypotension with cardiogenic shock.
• Finally — overdrive pacing successfully converted the WCT. The resultant rhythm is shown in the bottom tracing in Figure-4.

QUESTIONS:

• Does the repeat ECG recorded after successful overdrive pacing shed light on the etiology of today's initial ECG?
• Going back to the history that we were given at the beginning of today's case (ie, that this 60-something patient had been having recurrent palpitations over a period of years — with recent development of ankle edema and increasing dyspnea on exertion) — What clinical entity is suggested?

Figure-4: Comparison between today's initial ECG — and the repeat ECG recorded after successful overdrive pacing.

CASE Conclusion:

The "good news" is that this patient improved greatly after overdrive pacing successfully converted the WCT rhythm.

• The repeat ECG in Figure-4 — shows restoration of sinus rhythm. The remarkable finding is that QRS morphology in sinus rhythm is almost identical during the WCT and during sinus rhythm.
• ECG #2 shows a sinus rhythm at a rate just over 60/minute.
• There is bifascicular block (RBBB/LAHB).
• There is LVH (R wave in lead aVL ≥12 mm; R wave >18 mm in lead V6).
• ST-T waves do not look acute (The inverted T waves in the inferior leads are not necessarily abnormal given the predominantly negative QRS complexes in these leads — and chest lead ST-T wave changes are most likely secondary to the RBBB and to LVH).

• PEARL #8: Cases like today keep us humble! Despite strong suggestion from QRS morphology that today's WCT rhythm was fascicular VT — the finding of nearly identical QRS morphology in the repeat ECG after overdrive pacing tells us that the rhythm in ECG #1 was a reentrant SVT rhythm (and not fascicular VT). 
• This highlights the importance of being aware that "atypical" QRS morphology during a regular WCT rhythm may occasionally be the result of a markedly abnormal baseine ECG (and not VT).

PEARL #9: The patient's history of frequent episodes of recurrent palpitations over a period of years (ie, with recent development of ankle edema and worsening dyspnea on exertion) suggests development of TICM (Tachycardia-Induced CardioMyopathy). Over time, this so depressed LV function as to result in progressively increasing heart failure (See Nerheim et al: — Circulation 110(3):247-252, 2004 — and — Huizar et al: JACC 73(18):2328-2344, 2019 — for more on TICM).

• Although TICM typically takes weeks (or longer) to develop after exposure to a persistent tachyarrhythmia — it's important to be aware that TICM may develop in as little as 3 days!
• Fortunately — the depressed LV function that occurs with TICM is usually reversible after rate control is achieved (ideally with conversion to sinus rhythm). Return to normal LV function may be surprisingly fast (within days to a few weeks).  A majority of patients recover within 6 months.
• Unfortunately, if the tachyarrhythmia recurs — deterioration of LV function tends to be rapid. As a result — longterm monitoring of the patient's heart rate is essential.

Final Disposition: Today's patient was referred to EP Cardiology. EP study revealed the etiology of today's WCT rhythm to be recurrent AVNRT with dual AV nodal pathways. Ablation of the extra pathway resulted in "cure" of the patient's arrhythmia.

• Normal LV function returned soon after resolution of the arrhythmia. This rapid response to treatment proved that the patient's heart failure was indeed the result of TICM.

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Acknowledgment: My appreciation to Mohammed Elsisi (from Benha City, Egypt) — for allowing me to use this case and this tracing.

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For Additional Review:

• See ECG Blog #489 — for insightful review of another case that illustrates my approach to a patient with suspected fascicular VT.

 

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ECG Blog #544 — Caused by an Acute MI?

The ECG in Figure-1 was obtained from a man in his 60s — who presented to the ED (Emergency Department) for "palpitations". He was hemodynamically stable with this rhythm.

• The patient overall had previously been healthy without a known cardiac history.
• The above said — he is a heavy smoker, and has been on a number of psychoactive medications.

QUESTIONS:

• How would you interpret the rhythm in Figure-1? 
• How certain are you of your diagnosis?
• How should you treat the patient?

Figure-1: The initial ECG in today's case — obtained from a hemodynamically stable patient with "palpitations". (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts:

The ECG in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at ~170/minute, without clear sign of sinus P waves. As per the many cases of regular WCT rhythms that we've seen in this ECG Blog:

• Statistically — 80-90% of regular WCT rhythms without sinus P waves will turn out to be VT. Therefore — Assume VT until proven otherwise. Treat the patient accordingly.
• That said, since this patient is hemodynamically stable — You have at least a moment in time to look closer at the rhythm for features that might increase (or decrease) your diagnostic certainty from an initial statistical likelihood of 80-90% VT.

Among the ECG features I look for are:  

• The frontal plane axis.
• Signs of atrial activity.
• QRS morphology during the WCT rhythm.

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The Frontal Plane Axis:

The finding of an extreme frontal plane axis during a WCT is highly predictive of VT. The KEY for applying this criterion — is to appreciate how we define "extreme". The definition I favor is driven by seeking a highly specific diagnostic criterion, which if satisfied — will strongly predict VT as the etiology.

• As a result — my definition of an "extreme" frontal plane axis — is that the QRS complex must be entirely negative in either lead I and/or in lead aVF.
• As highlighted in Figure-2 — there is indeed a marked right axis in ECG #1, as the small-amplitude QRS in lead I is predominantly negative.
• That said — the QRS in lead I is not all negative, because a small-but-definitely-present initial positive deflection (r wave) is seen in this lead.
• Bottom Line: The marked right axis in Figure-2 favors VT. However, because the QRS is not all negative in lead I — the descriminatory value of a right-but-not-extreme axis is significantly reduced. Therefore, the rightward axis in ECG #1 is of limited diagnostic value, and does not prove VT.

Signs of Atrial Activity:

Although we don't see sinus P waves in ECG #1 — there do appear to be retrograde P waves, as highlighted in Figure-2 by the YELLOW arrows that produce a notching seen just after the QRS complex in each of the 3 inferior leads.

• That said — these retrograde P waves appear to occur after each QRS complex in the inferior leads. Since both reentry SVT rhythms (AVNRT, AVRT) and VT may manifest 1:1 VA conduction as we see here — the finding of retrograde P waves in ECG #1 does not prove VT.

QRS Morphology during the WCT:

This leaves me with assessing QRS morphology in my hope to increase statistical likelihood beyond the 80-90% likelihood that we start with by simply knowing that today's rhythm is a regular WCT without clear sign of sinus P waves. 

• The "good news" — is that assessment of QRS morphology may help greatly to narrow down the likelihood that a given WCT rhythm is either VT or an SVT (SupraVentricular Tachycardia) with preexisting BBB (Bundle Branch Block) or aberrant conduction (See ECG Blog #196 for details).
• As emphasized in ECG Blog #211 — the chances of a WCT rhythm being supraventricular increase significantly IF — QRS morphology is consistent with one of the known forms of conduction block (ie, RBBB, LBBB, LAHB or LPHB; or RBBB with one of these hemiblocks).

Take another LOOK at today’s initial ECG:

• Does QRS morphology during the WCT rhythm look like one of the known forms of conduction block?

Figure-2: I've labeled key features from Figure-1.

ANSWER:

• As seen in Figure-2 — QRS morphology during the WCT rhythm in today’s initial ECG does not in the least resemble RBBB conduction. This is because the QRS is all negative in lead V1, as well as in other anterior leads.
• QRS morphology also does not resemble LBBB conduction — because the QRS is predominantly negative in the lateral limb leads ( = leads I and aVL).
• As shown in Figure-2 — the frontal plane axis is rightward (ie, as determined by predominant negativity of the QRS in lead I). This immediately rules out LAHB conduction which requires a markedly leftward frontal plane axis. LPHB conduction is also unlikely — because the typical qR morphology in the inferior leads is lacking (ie, monophasic R waves without an initial q wave are seen in leads II,III,aVF).

Instead, if anything — QRS morphology is most consistent with RVOT VT (Right Ventricular Outflow Track Ventricular Tachycardia):

• As noted in ECG Blog #525 — QRS morphology of RVOT is characterized by a pattern resembling LBBB conduction in the chest leads — with a rightward axis in the frontal plane.
• There clearly is a rightward frontal plane axis in Figure-2.
• Most cases of RVOT VT manifest a QRS with predominant negativity for the first 3 or 4 chest leads — after which a predominantly positive R wave develops. Although transition to a predominantly positive R wave is delayed in Figure-2 — it does finally develop by lead V6. Thus, although R wave progression is a bit atypical for RVOT VT — the QRS morphology that we see in Figure-2 still could be consistent with RVOT VT if an all positive R wave develops by lead V7 or V8.

Bottom Line: QRS morphology in Figure-2 is most consistent with some form of VT. 

• As discussed in ECG Blog #525 and in the ADDENDUM at the bottom of this page — the clinical relevance of determining whether or not an ischemic form of VT is present vs RVOT VT — is that initial treatment considerations may differ. That said, because QRS morphology does not resemble any known form of conduction block — the odds are strongly in favor of some form of VT.

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Today's CASE Continues . . .

As stated in the introduction of today's case — the patient was hemodynamically stable in association with today's initial ECG. The decision was made to electrically cardiovert the patient. 

• Editorial Note: There is often more than a single way to treat a given patient. As reviewed in the ADDENDUM below — Once you identify a regular WCT rhythm as fascicular VT, and know that the patient is likely to have idiopathic VT (ie, VT in the absence of underlying heart disease) — IV Verapamil becomes the treatment of choice with the best chance for medical conversion to sinus rhythm. That said — the lack of an upright R wave in anterior leads tells us this is not a fascicular VT, so Verapamil is not indicated (and if anything — would seem contraindicated because of its vasodilating and negative inotropic effect).
• Given the age and history of today's patient (who is a longterm male smoker in his 60s, who is also on a number of psychoactive medications) — it becomes less likely that the rhythm in Figure-2 represents an outflow track form of idiopathic VT. This is especially true given the presence of QS complexes in leads V1-thru-V5, with transition only beginning between leads V5-to-V6. I therefore would not opt for Adenosine in this patient.
• Since the patient remained hemodynamically stable in association with today's WCT rhythm — either an antiarrhythmic (such as IV Amiodarone) or going straight to synchronized electrical cardioversion are the options I would favor.

The repeat ECG recorded after cardioversion is shown in the bottom tracing in Figure-3.

QUESTION:

• Does the post-cardioversion ECG suggest that the cause of this patient's VT was an acute MI?

Figure-3: Comparison between today's initial ECG — and the repeat ECG recorded after synchronized electrical cardioversion.

My Thoughts:

The "good news" — is that synchronized cardioversion successfully converted the patient to sinus rhythm, albeit with a bradycardia at a rate just under 50/minute.

• Diffuse notching of the P wave suggests an intra-atrial conduction disturbance — although the upright P wave with constant PR interval confirms sinus rhythm.
• The QRS is at most, no more than minimally widened (between 0.10-0.11 second). However the all-upright QRS in lead V1 is distinctly abnormal. Whether this is the result of an incomplete RBBB (somewhat widened terminal S waves are seen in lateral leads I and V6) — left septal fascicular block (an uncommon phenomenon — but one that can produce prominent anterior forces) — RVH (given the not overly wide, all upright QRS in lead V1) — or some combination of these factors, is uncertain from this single post-cardioversion tracing.
• However, the most remarkable finding in ECG #2 — is the diffuse T wave inversion, that is especially deep in the anterior leads (BLUE arrows in Figure-3).

Impression: Again, the "good news" is that this patient is no longer in the regular WCT rhythm that he presented with! Comparison between the 2 tracings in Figure-3 shows a dramatic change in QRS morphology after conversion to sinus rhythm. This strongly supports our suspicion that today's initial ECG was indeed VT.

• Questions remain regarding this previously healthy 60s man given his smoking history, longterm use of a number of psychoactive medications, and the ECG abnormalities on his post-cardioversion tracing (intra-atrial block; Tall R in lead V1 of uncertain etiology; and diffuse T wave inversion). 
• Because of the diffuse T wave inversion in ECG #2 — We cannot rule out the possibility of an acute MI as the cause of this patient's episode of VT. 
• The above said — We need to remember the common phenomenon known as Cardiac Memory following an episode of sustained VT.

Additional Follow-Up:

• Cardiac Echo showed mild-to-moderate reduction in ejection fraction, with a hypokinetic apical area. There was no indication of RVH.
• Serial Troponins were all negative for infarction.

Cardiac Memory:

The fascinating phenomenon of CM (Cardiac Memory) — may be seen following a period of prolonged altered ventricular activation from an episode of sustained VT, cardiac pacing, WPW-related WCT rhythms, or SVT with QRS widening (Gunaseelan et al: J Emerg, Trauma, Shock 13(4), 2020 — and — Viskin et al: Circulation 146:1170-1181, 2022).

• Although the precise causative mechanism is uncertain — the thought is that a sustained tachycardia with QRS widening will be associated with oppositely-directed abnormal T waves. With conversion to normal sinus rhythm — there is an abrupt "correction" of QRS morphology. The T waves ultimately will also "correct" — but there may sometimes be a transient stage of "memory" (usually lasting only hours — but sometimes persisting for up to a few days) in which T waves "remember" the vector of abnormal QRS morphology that was present during the WCT rhythm.
• As might be imagined — distinction between acute ischemia and/or infarction vs a benign "memory" effect may at times be difficult!
• 
  
• KEY Point: Cardiac catheterization is not necessarily be needed to prove a “memory” effect if T wave inversion resolves in timely fashion, Troponins are negative, normal LV function resumes and the patient returns to their pre-arrhythmia asymptomatic state.
• 
  
• In today's case — the fact that serial Troponins were all negative supports the likelihood that the diffuse T wave inversion in ECG #2 represents a benign "memory" effect.
• That said — the patient's Echo did show abnormal LV function and the post-conversion ECG is not "normal". As a result — further evaluation is in order.

CASE Conclusion:

Unfortunately — We lack follow-up in this case ... As a result — I can only report planned management in this case. This included:

• Ongoing obvservation with serial ECGs — to see if the diffuse T wave inversion persisted or resolved in timely fashion (ie, Resolution of diffuse T wave inversion within a few hours in association with negative serial Troponins — would strongly support the likelihood of "Memory" ).
• Careful review of this patient's medical record — including comparison with prior ECGs to see if the bradycardia, intra-atrial block, and tall R wave in lead V1 were present beforehand.
• Potentially cardiac catheterization — depending on results of other follow-up.
• Referral to EP cardiology for study and potential ablation given the persistent VT episode that brought the patient into the hospital.
• Coordination between cardiology and psychiatry teams regarding optimal use of psychoactive medications so as to minimize future arrhythmia risk.
• Encouragement of smoking cessation ...

P.S.: On the Proarrhythmic Risk of Psychoactive Drugs ...

The list of medications that may potentially exacerbate arrhythmias is huge (Tisdale et al — Circulation 142(15):e214-233, 2020). This is especially true regarding the use of psychoactive medications — such that in a patient like the 60s man in today's case who had been taking "a number of psychoactive agents" — specifics of names, dose, and duration of treatment for all psychoactive medications being taken is essential — after which a need for balance between severity of the arrhythmia vs the need for continued psychoactive drug use must be arrived at (Sicouri and Antzelevitch — Arrhythmia & Electrophysiology Rev 7(3):199-209, 2018).

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Acknowledgment: My appreciation to Mohammed Elsisi (from Benha City, Egypt) — for allowing me to use this case and this tracing.

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ADDENDUM (8/29/2026):

• Below — More on idiopathic VT:

Figure-4: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? 

— WHY do we care? Special attention to the 2 most common forms 

= RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

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ECG Blog #543 — A 24-Hour Holter was Done ...

The ECG in Figure-1 was obtained from a previously healthy elderly woman — who presented with dizzyness and fatigue, but no CP (Chest Pain).

• Details of the timing of this patient's symptoms with respect to when the ECG in Figure-1 was recorded are uncertain.

QUESTIONS:

With the above history in mind: 

• How do YOU interpret today's initial ECG?
• Clinically — What would you do?

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

My Thoughts:

The ECG in Figure-1 shows sinus bradycardia at a rate of ~50/minute.

• The QRS is narrow — the PR interval is normal — and the QTc is probably not increased given the slow rate. 
• There may be small U waves in the mid-chest leads (which sometimes occurs in association with bradycardia).
• There is a slight leftward axis — though not negative enough to qualify as LAHB (The QRS is slightly more negative than positive in lead aVF — but mainly positive in lead aVL — which puts the axis at about -15 degrees).
• There may be voltage for LVH (Hard to say for sure if the R in aVL ≥12 mm — given overlap of this R wave in aVL with the S wave in lead aVR).

Regarding Q-R-S-T Wave Changes:

• The narrow Q waves in leads I,aVL are probably not abnormal given fairly tall R wave amplitude in these leads.
• R wave progression — looks normal, with transition (where the R wave becomes taller than the S wave is deep) occurring normally beween leads V2-V3.
• There are subtle ST-T wave abnormalities in a number of leads. As shown in lead III and in leads V1,V2,V3 — there is ST segment coving but really no elevation, followed by T wave inversion (the RED arrows in these leads).
• BLUE question marks in a number of other leads highlight ST-T wave segments of uncertain significance — especially given the different ST-T wave appearance between the only 2 complexes that we see in leads aVL and aVF — and our inability to fully see the ST-T wave of the 2nd complex in leads V4,V5,V6 (? what is real vs artifact?). That said — there appears to at least be ST segment flattening in lead II, with slight ST depression in leads V4,V5,V6.

Impression: In view of the brief history we are given, but without "being there" — it's hard to know what to think of the above described ECG changes shown in Figure-2.

• It is clearly possible that this elderly woman at some point in time (possibly recently) — had inferior and anterior infarction. That said — the lack of a history of preceding chest pain (and uncertainty about the time of this elderly patient's "dizzyness and fatigue" ) — make it difficult to know whether she may have had a "silent" MI with "chest pain equivalent" symptoms? And if so — when this may have happened? (See ECG Blog #228 — for more on "Silent" MI).
• Without a preceding history of CP that then resolved — this case does not fit criteria for "Wellens' Syndrome". That said — ECG #1 certainly could be the result of infero-antero infarction at some point in time, possibly recent (See ECG Blog #320 and ECG Blog #350 — for more on what Wellens Syndrome is, and what it is not).

Figure-2: I've labeled ECG findings in the initial ECG.

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The CASE Continues:

This elderly woman up until now had not sought out medical care. She lived alone and functioned completely independently. Although she reported dizziness and fatigue as the reason for her emergency visit — the medical care provider who treated the patient thought she looked remarkably well. As a result — ACS (Acute Coronary Syndrome) was not considered:

• Of note, the patient did not have medical insurance, and she had financial limitation. As a result — she did not want an extensive diagnostic work-up, especially given that she felt good enough to return to her independent living situation at home. 
• Troponin was not ordered.
• Instead, a 24-hour ambulatory Holter monitor was placed — and the patient went home. Follow-up was scheduled for her to return the next day.

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The Patient's Holter Monitor . . .

As you think about the challenging limitations for managing this case — what follows below in Figures-3 -thru-9 are non-sequential rhythm strips from this patient's 24-hour ambulatory Holter moniter that was reviewed the next day.

• NOTE: Each of the 6 non-sequential Holter rhythm strips that are shown below manifest 6 leads — including 1 limb lead (lead aVF) — and 5 chest leads (leads V1-thru-V5).
• As you review these 6-lead rhythm strips — Keep in mind that the only symptoms this elderly woman reported was some "dizzyness" and "mild fatigue" — but no chest pain. The 24 hour ambulatory Holter was started several hours after this woman had been evaluated. She still had no chest pain.
• For ease of comparison in Figure-3 — I've reproduced this patient's initial ECG that was shown above in Figure-2.

Figure-3: Comparison between the initial ECG — and Holter-A, recorded several hours later after the patient had returned home (at 11:16 pm — while the patient was sleeping).

My Thoughts on Holter-A:

Keeping in mind the inevitable slight differences in lead placement with 6-lead Holter monitoring vs lead placement with the patient's 12-lead ECG — I did not perceive there to be any significant change between these 2 tracings in Figure-3.

13 Minutes Later ...

Figure-4: Holter-B — recorded just 13 minutes later (at 11:29 pm) while the patient was still sleeping.

Subsequent Recordings during Sleep ...

Figure-5: Holter-C — recorded ~2 hours after Holter-B (at 1:23 am). The ST elevation that began in Holter-B has now progressed — with development of prominent Q waves in leads V2,V3,V4 — and extensive hyperacute ST-T waves. The patient still asleep ...  

Figure-6: Holter-D — recorded at 7:30 am the next morning.

Figure-7: A closer look at Holter-D — in which I've labeled regular-occurring P waves that are unrelated and "march through" neighboring QRS complexes ==> complete AV Block. These RED arrow P waves are not from the SA Node (as these P waves are no longer upright in lead aVF). The vertical RED line marks the end point of the now widened QRS complex in these 6 simultaneously-recorded leads. The ST segment begins to the right of this vertical RED line, and still shows obvious ST elevation in the lateral chest leads.

Figure-8: 10 minutes after Holter D — We now see a markedly widened agonal rhythm without atrial activity.

Figure-9: 12 minutes later a flat line is seen ...

Editorial Comment:

Today's case is difficult. This elderly woman who lived alone — died at home in her sleep. These Holter tracings were only retrieved afterward.

• Presumably — the initial ECG in Figure-2 did represent recent LAD occlusion and infarction in the form of a "silent" MI in this elderly woman who presented with minimal "CP-equivalent" symptoms ( = some dizzyness and fatigue) — but who otherwise looked good and wanted to go home.
• Presumably, the reason this patient's initial ECG did not show acute ST elevation — is that some time after LAD occlusion, there was spontaneous reperfusion of her MI, with resolution of what must have been ST elevation several hours earlier. The RED arrows in leads III; V1,V2,V3 — as well as the Blue question marks in her initial ECG (in Figure-2) clearly represented reperfusion T waves.
• 
  
• I have "been there". As a family medicine Attending and faculty physician for 30 years — we would periodically see elderly patients present a day or more after they had symptoms, with an ECG similar to that shown in Figure-2. While hospitalization for a day or two to ensure nothing active is still ongoing would be ideal in such cases (and depending on case specifics — serial tracings, Troponins and in some instances cardiac catheterization would all ideally be done) — that is not always the path chosen by these older patients who decide (with full informed consent) that they simply want to return home.

I have also "been there" in the eerie situation of interpreting a Holter monitor recording on a patient admitted to the hospital and seemingly doing well on a telemetry-monitored floor — while all of a sudden as I'm interpreting the Holter — I see sudden slowing of the heart rate on sequential rhythm strips that reveal progressive evolution to VFib and cardiac arrest.

• At that point — I ran upstairs to the patient's room, only to find a full complement of health care providers in the midst of what turned out to be an unsuccessful resuscitation effort on the patient whose Holter I had been in the middle of interpreting ...
• These are tough cases. We go back and ask ourselves what could have been done differently to avoid the patient's unexpected demise? We don't necessarily come up with answers — but the soul-searching retrospection is an essential component of our need to draw meaning from these tragic occurrences that we painfully hope to learn from.
• P.S.: I found the literature sadly lacking in examples of Holters serendipitously recorded during the evolution of an acute cardiac event. While realistically impossible to avoid all future episodes of this kind — We need to learn from such cases. (See Watanabe et al — Heart Rhythm 8:18-25, 2014 and Nikolic et al — Circulation 66(1):218-225, 1982).

Final "Take-Aways" ...

• Be aware of the multiple subtle appearances that an ECG may have following recent infarction. Look for the reperfusion T waves of spontaneous reperfusion. Depending on when during the course of evolution the ECG is recorded — there may be "pseudo-normalization" — in which an ECG captured in between the phase of resolving ST elevation on the way to developing reperfusion T waves — the ECG may look relatively "normal" (See ECG Blog #467).
• The patient's symptoms may be subtle (as in the Audio Pearl on "Silent MI" in ECG Blog #228). Be especially attuned for subtle symptoms that may reflect recent infarction in older patients.
• Correlate the timing of the presence and relative severity of patient symptoms to the timing of each ECG that is recorded. Learning that symptoms may have decreased several hours later (at the time the ECG you are looking at was recorded) — clues us in to the need to appreciate subtle findings on that ECG that may be important.
• Realize that no matter how diligent we may be — unexpected events as occurred in today's case sometimes happen ...

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Acknowledgment: My appreciation to Passang Jinpa (from Guayaquil, Ecuador) — for allowing me to use this case and this tracing.

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pful ...