EXTRA COPY — ECG Blog #544: Caused by an Acute MI? — EXTRA COPY

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 — 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 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 Verapamil in this patient.
• Given that 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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EXTRA COPY — ECG Blog #546: I was sent this Tracing ...— EXTRA COPY

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Figure-1: XXXX (To improve visualization — I've digitized the original ECG using PMcardio).

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Figure-2: XXXX

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) and M Shah (from Srinagar, India) — for allowing me to use this case and this tracing.
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THE CASE:

60Y man with CKD history, feels dizziness. A challenging ECG tracing shared for discusson. Thanks to M Shah asking me this one.

 

GREAT case! I don't have time now to draw a laddergram — but I walk thru step-by-step laddergrams in a similar case in my ECG Blog #256 (https://tinyurl.com/KG-Blog-256 ). The mechanism is almost certain to be ESCAPE-CAPTURE with Echo beats that for the most part conduct.

So I will ask 林柏志 and M Shah both for PERMISSION for me to use this case as a future ECG Blog (on which I will draw laddergrams. PLEASE LET ME KNOW if I can use this case!

Otherwise — I'd LOVE to know clinical follow-up — because this 60yo with dizziness DOES have subtle ST segment flattening with taller-than-expected T waves in leads V2,V3 + deeper-than-expected T inversion for simple RBBB conduction in V1 — so I wonder IF recent/acute posterior OMI may be responsible for the bradycardia here with junctional escape?

So — the KEY to this fascinating rhythm is the single sinus conducted beat ( = beat #2 — with the point marked "X" telling us what a "normal" T wave should look like. And while I cannot rule out the possibility of multiple PACs — this looks much more like ALL YELLOW arrows indicate retrograde conduction from junctional escape beats #1,3,6,8,9 and 11).

Beats #3, 4, 6 and 9 then "turn around" such that these "echo beats" on the way back to the atrium are able to ALSO conduct forward to produce echo beats #4,5,7 and 10 (with beat #7 conducting with incomplete rbbb and beat #10 with complete rbbb aberration).

So the underlying rhythm here is sinus bradycardia — which leads to junctional escape — which leads to the retrograde P wave conduction — with my suspicion of need to rule out recent/acute post. OMI as the cause.

Isn't this fascinating? — :)

EXTRA COPY - VT Criteria - EXTRA COPY

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Figure-1: XXXX (To improve visualization — I've digitized the original ECG using PMcardio).

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Figure-2: XXXX

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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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Mohammed Elsisi <mohammedelsisi18@gmail.com>  (EMAIL on 7/14/2026)

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—   ­VT Criteria ... ­—

 

 

Acknowledgment: My appreciation to Mohammed Elsisi (from Cairo, Egypt) for the case and these tracings.

 

This tracing was obtained from a 60 y male pt with free medical hx apart from recurrent palpitation over last 5y, who recently become short of breath & exoerience progreesive ll swelling & presented to the ER. 

Pt was received 2 amp amiodarone with no effect, sync dc shocks also convert rhythm transiently on monitor then rapidly return to this tachy. 

My differential is : 

1)LPF VT

2)Aberrant AFL rhythm is strictly ~150bpm

3)aberrant svt 

Woth this incessant rhythm causes tachycardia induced cardiomyopathy. 

What do u think? 

MY REPLY:

Hi Mohammed.

 

I agree that this regular WCT ( = Wide-Complex Tachycardia) looks like LPF VT!

• The QRS is wide; the rhythm is regular without clear sign of sinus P waves.
• This does NOT look like aberrant conduction.Lead V1 does not show the triphasic rsR’ that characterizes aberrant conduction — and note that the QRS stays predominantly positive for ALL 6 chest leads (which does not generally happen when there is RBBB conduction). In the limb leads — the R in lead I is slow rising, and there is no more than a tiny r wave in the inferior leads — so QRS morphology is atypical for rbbb/lahb conuction.
• Verapamil (not Amiodarone) is the drug of choice for a hemodynamically stable patient with Fascicular VT. Given frequent recurrence of this rhythm — I’d refer to EP for confirmation and then ablation.
• See ECG Blog #489 — for review of a case.

 

Hope the above is helpful! Let me know if you get follow-up!

 

: ) Ken

 

MOHAMMED REPLY:

Thanks ken, as i mentioned  before pt was admitted to ccu d was intubated due to cardiogenic shock d respiratory distress rhythm was incessant & resistant to dc shock. 

D over drive pacing done with succeessful conversion to sinus rhythm with morphology strictly the same during tacharrhythmia. 

Pt hemodynamics improvwd d was successfully weaned from mech

Ventilation then underwent an EP study d a dual av nodal pathway was found with reproduction of avnrt 

Finally succeessful ablation of the pathway done. 

Case finally considered tyical AVNRT. 

With tachy induced cardiomyopathy. 

MOHAMMED (7/14/2026) 

Yes, dramatic improvement after maintenance of sinus rhythm — proves this was tachycardia-induced cardiomyopathy — because EF improved after the WCT was treated !!!!

Of course u can use this case as a blog — Thanks ken. 

MY REPLY:

GREAT case! I want to use this for an ECG Blog — it may be a while — but I'll let you know when I publish this. So LV function improved once AVNRT was ablated? If so — then YES, this was a tachycardia-induced cardiomyopathy!

 

Always good to consider the possibility of an underlying abnormal ECG with similar morphology as during the WCT — which sometimes you just don't know when you first see the patient!

 

GREAT WORK on your part! 

Tha

EXTRA COPY — ECG Blog #542 — Why is the Rhythm Irregular? — EXTRA COPY

The ECG in Figure-1 was obtained from a man in his 60s — who is aware of his "irregular heart beat".

Relevant history: 

• The patient is overall healthy — with the exception of some "kidney issues" for which he periodically has "low potassium" and sees a nephrologist.
• The patient notes that his "skipped beats" tend to increase when he is lying down — and generally go away when he stands up.

 

QUESTIONS:

• How to interpret the rhythm in Figure-1?
• What is your differential diagnosis for the irregularity?
• How does the 12-lead ECG help in diagnosing the rhythm?

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

ANSWER:

By the Ps, Qs, 3R Approach to systematic rhythm interpretation (See ECG Blog #185) — I note the following:

• The QRS is narrow everywhere. This tells us that the rhythm is supraventricular.
• The Rate is controlled, averaging ~60/minute — but the rhythm is not Regular. Instead, there is a bigeminal rhythm (ie, Every-other-beat occurs early — such that we see a repetitive pattern with groups of 2 beats followed by a short pause). See ECG Blog #232 for more on the types of bigeminal rhythms.
• P waves are present. These P waves precede each of the 9 beats in the long lead II (as per the RED arrows in the long lead II rhythm strip in Figure-2).
• These P waves are "Related" to neighboring QRS complexes — because the PR interval before each QRS complex is constant (as well as being normal = not more than 1 large box in duration).

Figure-2: I've added RED arrows to highlight regularly occurring P waves that precede each QRS with a constant (conducting) PR interval.

Our Differential Diagnosis:

We've arrived at a relatively common situation in that there is a bigeminal rhythm — in which all QRS complexes are preceded by P waves that appear to be conducting because they have a constant PR interval. At this point — my diagnostic considerations were the following:

• Atrial bigeminy (in which every other beat is a PAC). I thought this to be unlikely — because as I look at all 12 leads in the simultaneously-recorded ECG above the long lead rhythm strip — P wave morphology looks to be identical for the early beats ( = beats #1,3,5,7,9) — and for the normal sinus-conducted beats ( = beats #2,4,6,8). Because PACs arise from a different place in the atria — P wave morphology of PACs should differ from the P wave morphology of normal sinus-conducted P waves.
• Atrial trigeminy with blocked PACs (ie, in which every 3rd beat is a non-conducted PAC). This is also unlikely, because as I look at all 12 leads in the ECG above the long lead II — the T waves of beats #1,3,5,7,9 do not manifest any notching or extra peaking that would alert to hidden, non-conducted P waves.
• 2nd-degree AV block of the Mobitz I Type (which is the same thing as AV Wenckebach) is not present because: i) The  PR interval is not increasing within each of the 2-beat groups; — and, ii) The P-P interval is not regular (or at least almost regular) — as it should be if AV block was present.
• 2nd-degree AV block of the Mobitz II Type is not present. This is because the P-P interval is not regular (or at least almost regular) — as it should be if there was some form of AV block.
• Sinus arrhythmia is unlikely to be present here. This is because the rhythm in Figure-2 represents a fixed pattern of group beating, in which the duration of each of the longer, and each of the shorter R-R intervals is remarkably consistent. In contrast — the duration of R-R interval variation is generally longer with sinus arrhythmia, and manifests much more variability than what we see in Figure-2.
• 
  
• SA (SinoAtrial) block . . .

Conclusion: Having ruled out my top 5 diagnostic considerations that I list above — We are left with the last consideration on my list = SA Block!

• The reason I put SA block last on my list — is that true SA block is the least common of the above entities that I encounter. That said — it "fits best" for the characteristics of today's ECG.
• My proposed laddergram in Figure-3 illustrates what appears to be the mechanism of this patient's SA block. 

Figure-3: My proposed laddergram for today's rhythm.

Laddergram Illustration:

I review how to read laddergrams (as well as presenting a primer for how to draw them) — with numerous examples of laddergrams in ECG Blog #188.

• As I illustrate in Blog #188 — it's EASY to read laddergrams that have already been drawn for you. All the laddergram does — is follow the electrical impulse as it records the cardiac rhythm, showing the path of electrical activity as it makes its way through the Atria — then the A-V Node — and finally through the Ventricles.
• In today's case, since the mechanism of the rhythm is SA Block — the problem arises from within the SA Node.

We show this schematically in Figure-3:

• Beginning with beat #2 — We see that only 2 out of every 3 SA nodal impulses ( = the RED circles at the very top of the laddergram) — are able to make it through the SA Node to arrive in the Atria.
• Keeping in mind that time is recorded horizontally — We can see that once an impulse arrives in the atria, that conduction speeds up. We schematically depict this by drawing the lines that pass through the Atrial Tier vertically (representing fast conduction through specialized atrial fibers).
• Conduction of each impulse then slows down as the impulse passes through the AV Nodal Tier (which is why there is slight increase in angulation of the RED lines within the AV Nodal Tier).
• On arrival in the ventricles — conduction again speeds up due to fast conduction through specialized His-Purkinje fibers (less angulation of the RED lines within the Ventricular Tier).

Return for a moment to the SA Nodal Tier at the top of the laddergram: 

• Note the increase in angulation between the 1st and 2nd RED circles in each group — with the 3rd RED circle being blocked — after which the sequence begins again. This is Wenckebach conduction! (ie, There is 3:2 SA block of the Wenckebach Type).
• For more on SA Block — See the ADDENDUM below!

Clinical Correlation in Today's CASE:

Going back to the brief history presented at the beginning of this case — We were told that today's patient has a history of hypokalemia — and that he noticed a tendency for his "skipped beats" to increase when lying down, and to go away when standing up.

• In my experience of having looked for true examples of SA block over decades — this phenomenon is not common in the general population.
• At times I've observed incidental SA block, seemingly without clinical consequence (almost like a normal variant).
• At other times, this rhythm is clearly pathologic — accompanying inferior infarction with 2nd-degree AV block of the Wenckebach (Mobitz I) Type — or — as a component of the arrhythmias seen with SSS (Sick Sinus Syndrome).
• In today's case — I suspect that this patient's periodic hypokalemia was at least contributing to development of his SA block, if not frankly causative.
• Holter monitoring showed this patient's SA block to be without hemodynamic consequence, although persistent through much of the day that the Holter was done. I lack the follow-up to know if the rhythm resolved once serum K+ normalized.
• Otherwise — selected patients with cardiac arrhythmias have been known to observe a change in the frequency of certain rhythm disorders depending on body posture. This effect is highly individualized — with literature on the subject scarce, and the mechanism uncertain. Theories include variation in vagal tone, which tends to increase when resting supine. Other theories involve changes in intrathoracic pressure occurring with changes in body position — and/or increased "stretch" on cardiac tissue seemingly being more likely when supine.
• Bottom Line: It's hard to know what to do with a history that the patient notes of a change in arrhythmia frequency depending on body position — other than to accept that in some selected patients, there is evidence that arrhythmias may increase or decrease depending on body position.

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Acknowledgment: My appreciation to Stewart (from Los Angeles, USA) — for allowing me to use this case and this tracing.

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ADDENDUM:

Figure-4: Essentials of SA Block (Modified from Grauer: ACLS-2013-ePub).

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #312 and ECG Blog #488 — for additional examples of SA block. 
• ECG Blog #147 — Reviews a case showing blocked PACs. 
• ECG Blog #57 — Reviews a case showing atrial bigeminy with blocked PACs.