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 — so 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 occurrence — which 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 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 simultaneously-recorded 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.
• Finally — Sinus arrhythmia is not present here. I say this 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 (whereas some variability would seem almost certain to creep in when there is simple sinus arrhythmia).

Conclusion: Having ruled out the above the above 5 entities — We are left with the least common remaining explanation = SA Block!

• My proposed laddergram in Figure-3 illustrates the mechanism of this patient's SA block. 

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

Laddergram Illustration:

I review interpretation (as well as a primer with more than 140 examples of how to draw laddergrams) in ECG Blog #188.

• As I demonstrate in Blog #188 — it is EASY and takes minimal time to learn how to read laddergrams.
• It takes practice and more time to become comfortable drawing laddergrams — but drawing laddergrams is not needed to become a skilled interpreter.
• Laddergrams usually only contain 3 Tiers. These are the Atrial Tier — the AV Nodal Tier — and the Ventricular Tier.
• When the mechanism of the arrhythmia is SA Block — we add a 4th ( = SA Nodal) Tier, as I have done in Figure-3.

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I should add links to cases of SA block, as well as bigeminal group beating !!!!

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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:

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

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StonePillar stonepillar2006@yahoo.com — E-mail on 6/7/2024 — 

Stewart Kayle (from Los Angeles, USA)

—    Why is the Rhythm Irregular? —

Hi Dr. Grauer,  I have a brand-new ECG for you that was just done today, June 7, and is similar to the ECG in "ECG Blog #339."

 

MY REPLY:

Hi. Great tracing — This looks like SA Block (Type 1 — with 3:2 conduction out of the SA node! = 3 SA nodal impulses, but only 2 of them get out of the SA node)

• There is perfect "Wenckebach periodicity” ( = Group beating — Pause is less than twice the shortest R-R interval
• Unlike Blog #339 — P wave morphology STAYS THE SAME throughout. Note virtually identical P wave morphology in all 12-leads — a pattern that seemed to hold through for the numerous periods of bigeminy on 24 our Holter moniorin
• Although SA block can be a normal variant — I suspect the hypokalemia is the cause!

Hi Stewart. Thanks for the Holter. Looks like this patient is in this bigeminal rhythm a LOT! Also, P wave morphology here looks IDENTICAL — so I think this has to be 3:2 SA Block, Type I (which is the Wenckebach type of SA block) — : ) Ken

• YES — It is possible for there to be atrial bigeminy so very close to the SA node that we do not recognize a difference in P wave morphology — but I think that even less common than SA block (and SA block is rare in my experience). So I do think this is a true example of SA block.
• K+ disorders are known to potentiate AV conduction defects — so while I of course can not prove anything — I suspect the hypokalemia in your patient IS a potential cause. One way to find out is to see what happens after correcting serum K+ levels.
• Way back when I wrote up a piece for FPR (Family Practice Recertification) based on the experience of an ICU nurse educator who polled numerous nurses nationwide. I “informally” confirmed her conclusions by asking a number of ICU nurses that I worked with. Many of them had patients in whom certain body positions (most commonly lying on their left side — probably because of the effect this has on the apex of the heart ) can result in certain arrhythmias. I’ve seen periodic reference to this in the literature, though to my recollection, not all that well documented … But I do think change in body position can influence certain arrhythmias in certain patients.

You said that if you can clearly see that the P wave morphology is the exact same in all the recorded leads, then you can determine that the P waves are coming from the SA node and therefore rule out PACs in a pattern of bigeminy and consider SA block of the Wenckebach type.

Also, while low intracellular potassium is likely contributing to the arrhythmias, it's also interesting that the arrhythmias are triggered by lying down when the heart rate slows down and stop when the patient stands up. Vagally mediated? Increased vagal tone during relaxed state? Changes in intrathoracic pressure while lying down? Change in body position affecting fluid and electrolyte distribution?

= = = =

Yes, atrial bigeminy can be positional. Many people notice extra heartbeats or skipped-beat sensations when lying down, particularly on their left side. [1, 2, 3, 4]

Why Position Matters

Increased Pressure: Lying on your side or back can increase physical strain and stretch on the heart's upper chambers (the atria).
Vagal Tone: Lying down changes your nervous system tone (vagal tone), which can make premature atrial contractions (PACs) more likely to fire in a bigeminal pattern.
Sleep Position Effects: Positions that trigger mild breathing strain or positional sleep apnea can also spark extra atrial beats

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ECG Blog #321

https://ecg-interpretation.blogspot.com/2022/06/ecg-blog-312-bigeminy-but-not-mobitz-i.html

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How would YOU interpret the lead II rhythm strip shown in Figure-1?

Figure-1: How would you interpret this rhythm strip?

MY Approach to the Rhythm in Figure-1:

As always — I favor a systematic approach to every arrhythmia that I encounter, encompassed by the memory aid, "Watch Your Ps, Qs and the 3Rs" (See ECG Blog #185). That said, looking at this rhythm — I could not fail to notice that there is "group beating" in a supraventricular (ie, narrow QRS) bigeminal pattern.

PEARL #1: As discussed in ECG Blog #232 — recognition of a bigeminal supraventricular pattern when the 1st beat in each pair is conducted, should suggest the following differential diagnosis:

• Sinus rhythm with atrial or junctional bigeminy (ie, every-other-beat is a PAC or a PJC).
• Sinus rhythm with atrial trigeminy — in which every-third P wave is a PAC that is "blocked" (non-conducted).
• Some form of SA ( = Sino-Atrial) Block.
• Mobitz I, 2nd-Degree AV Block ( = AV Wenckebach) with 3:2 AV conduction.
• Mobitz II, 2nd-Degree AV Block (with non-conduction of every 3rd P wave).

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Beyond-the-Core: Technically, there are a few additional causes of a bigeminal rhythm that need not be considered in today's case, because the rhythm is either not strictly supraventricular — or — because the 1st beat in each group is not sinus-conducted. These additional causes include:

• Ventricular bigeminy (ie, every-other-beat is a PVC).
• Atrial fibrillation, atrial tachycardia or atrial flutter with Wenckebach conduction.
• "Escape-Capture" (the 1st beat in each group is a junctional or ventricular escape beat — followed by a conducted beat).

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PEARL #2: Another way to look at the bigeminal pattern of group beating that we see in Figure-1 — is that each group of 2 beats is separated by a short pause.

• The commonest cause of a pause is a blocked PAC. In clinical practice — the finding of blocked PACs is far more common than any form of AV block.
• As a result, within seconds of seeing today's tracing — my thoughts were that statistically, the most likely cause of the bigeminal rhythm with short pauses that is seen in Figure-1 — would be atrial trigeminy, in which every-third P wave is a blocked PAC. I'd therefore want to address this possibility early in my assessment. 

 

At this point — I applied the Ps, Qs, 3R Approach:

• P waves — are present (RED arrows in Figure-2 highlight upright sinus P waves in lead II).
• The QRS is narrow — which confirms that the rhythm is supraventricular.
• The rhythm in Figure-2 is not "Regular" — so the Rate varies. That said — there is group beating, with a repetitive pattern of alternating short-long intervals. P waves are Related to neighboring QRS complexes — in that each QRS complex in this tracing is preceded by a sinus P wave with a fixed and normal PR interval. However, the P-P interval is not regular.

Figure-2: I've added RED arrows to Figure-1 to highlight sinus P waves.

Continuing with My Systematic Approach to the Rhythm:

Now that we have systematically assessed the 5 parameters in the Ps, Qs, 3R Approach — it's time to consider the entities included in the differential diagnosis for a bigeminal rhythm that was presented above in PEARL #1:

• Despite the clinical reality expressed in PEARL #2 above — there is no evidence that the rhythm in Figure-2 represents atrial trigeminy, with every third beat being a PAC that is non-conducted. That is — there is no deflection suggestive of a non-conducted PAC in the T wave of beats #1, 3, 5, 7 and 9.
• The rhythm in Figure-2 is neither Mobitz I nor Mobitz II 2nd-degree AV block. The reason we can easily exclude 2nd-degree AV block — is that the atrial rhythm is not regular! (RED arrows in Figure-2). With rare exceptions, for there to be AV block — the P-P interval should at least be fairly regular, and this is definitely not the case in this tracing That is — no P wave is seen near the mid-point of each pause, as would be expected if some form of 2nd-degree AV block was present.
• Additional reasons why the rhythm in Figure-2 is not a form of AV block are: i) The PR interval is not increasing (as it should be if this was Mobitz I); and, ii) The QRS is not wide (as it should be if this was Mobitz II).
• 
  
• The rhythm in Figure-2 is not junctional bigeminy — because the P wave in lead II is positive everywhere (The P wave in lead II would be negative if there were junctional beats). This also rules out "escape-capture" — because there are no junctional escape beats.
• The rhythm is not atrial bigeminy — because P wave morphology of every P wave is the same (ie, with a distinct notch at its midpoint). In addition — the PR interval in front of every beat remains the same.
• 
  
• By the process of elimination — this leaves us to consider some form of SA block as a likely etiology for the rhythm in Figure-2.

CAVEATS (Beyond-the-Core): 

Unfortunately — We only have access to the 7 second rhythm strip that is shown in Figure-2. We do not have access to a simultaneously-recorded 12 lead ECG.

• It is true that PACs which originate near the SA node may closely resemble sinus P waves in one or more leads. Technically speaking, without the benefit of a 12-lead ECG — I can not completely rule out the possibility of atrial bigeminy, in which the reason the P waves before beats #1,3,5,7 and 9 so closely resemble the P wave of sinus beats — is that the PACs originate so near to the SA node.
• For the same reason — I can not completely exclude the possibility that the reason for the short pauses in Figure-2 might be blocked PACs that are not evident in the single lead being monitored. And although no notched deflection suggestive of a blocked PAC is seen in Figure-2 — it is true that the ST-T wave of beats #1,3,5,7 and 9 appears to be flatter than the ST-T wave of beats #2,4,6,8.
• 
  
• That said — I think the rhythm in Figure-2 is most consistent with SA Block.

The Concept of SA Block:

Wenckebach phenomena, in which there is progressive delay in conduction until conduction fails — is not limited to the Mobitz I type of 2nd-degree AV block that occurs out of the AV node.

• Among the other types of Wenckebach conduction — is SA Block of the Wenckebach type. Instead of progressive delay in the PR interval until eventually a P wave fails to conduct to the ventricles (as occurs with the Mobitz I form of 2nd-degree AV block) — with SA Wenckebach, there is progressive delay in the time it takes sinus node impulses to get out of the SA node — until eventually, exit of an impulse out of the SA Node is completely blocked.
• Because this progressive delay in sinus node impulses is completely contained within the SA node — SA block is not seen on the surface ECG. This makes it much more challenging to diagnose SA block.

The mechanism of SA Wenckebach is best explained by use of a Laddergram. I illustrate this concept in Figure-3 — in which I propose a laddergram to explain the ECG findings for today's rhythm:

• Note the addition in Figure-3 of an "extra" Tier to the laddergram — to illustrate progressive delay of sinus node impulses trying to get out of the SA Nodal Tier. Note that every-third SA nodal impulse is blocked.
• Of the 2 sinus node impulses in each group that are able to make it out of the SA Node — conduction of these impulses on their way to the ventricles now proceeds normally, as these impulses pass through the Atria — the AV Node — and the Ventricles. Thus, my proposed laddergram suggests that the rhythm in today's case represents SA Wenckebach with 3:2 SA conduction (ie, 2 out of every 3 SA nodal impulses is able to make it out of the SA Node).

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

NOTE: It may be easiest to think of SA block as an "exit" block that occurs at the level of the SA Node. In the same way that 2nd-degree AV block may be of the Mobitz I and Mobitz II types — so it is with SA block:

• With the Mobitz II form of AV block — instead of progressive increase in the PR interval until a beat is dropped, the PR interval remains constant until one or more on-time P waves is non-conducted.
• 
  
• With SA block of the Mobitz II type — sinus node impulses are conducted out of the SA Node without progressive delay — until suddenly, one or more on-time sinus node impulses is not able to make it out of the SA Node. As a result, with SA block of the Mobitz II type — the pause due to non-conduction of one or more P waves out of the SA Node will be some "fixed ratio" of the shortest P-P interval (ie, the result of 2:1, 3:1 or other ratio "exit" block). This is in contrast to SA Wenckebach — in which the pause is less than twice the shortest P-P interval

The "essentials" of SA Block are summarized in Figure-4. I emphasize the following:

• SA block is not common! I count on my fingers and toes the number of times I've seen true SA block over my decades of looking for this rhythm disorder. But as per my proposed laddergram in Figure-3 — I believe this is the most logical explanation for the mechanism of today's rhythm.
• The significance of SA block depends on the clinical setting in which it occurs. This may be a benign conduction disturbance when the pause containing non-conducted sinus impulses is short and occurs in an otherwise healthy and asymptomatic individual. In contrast — when associated with other conduction system disorders in a symptomatic patient with underlying heart disease — clinical outcome may be significantly influenced by the presence of SA block. In older individuals with syncope — SA block may be a component of Sick Sinus Syndrome. That said, given the absence of information in today's case — clinical significance (if any) of the rhythm in Figure-3 is unknown.

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 #185 — Reviews the Ps, Qs and 3R Approach to Systematic Rhythm Interpretation.
• ECG Blog #188 — for Review on how to Read (and/or Draw) Laddergrams (with links to more than 50 examples of explained laddergrams).
• 
  
• ECG Blog #232 — Reviews the concept of a Bigeminal Rhythm (which may be due to Atrial or Ventricular Bigeminy, Wenckebach conduction — or other causes — Listen to Audio Pearl #47).
• 
  
• ECG Blog #163 — Reviews a case of "escape-capture" bigeminy, in which SA block might be operative.
• ECG Blog #256 — Reviews another case of "escape-capture" bigeminy (in which retrograde conduction from junctional escape results in "capture").
• 
  
• ECG Blog #164 — Reviews a case Mobitz I 2nd-Degree AV Block, with detailed discussion of the "Footprints" of Wenckebach.
•  
• ECG Blog #33 — Reviews a case showing blocked and aberrantly-conducted PACs. 
• ECG Blog #66 — Reviews a case showing blocked and aberrantly-conducted PACs. 
• ECG Blog #147 — Reviews a case showing blocked PACs. 
• ECG Blog #57 — Reviews a case showing atrial bigeminy with blocked PACs.

EXTRA COPY — ECG Blog #543: A 24-Hour Holter was Done- EXTRA COPY

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

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Figure-2: XXX

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Figure-3: XXX

Figure-4: XXX

Figure-5: XXX

Figure-6: XXX

Figure-7: XXX

Figure-8: XXX

Figure-9: XXX

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

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Passang Jinpa — Guayaquil, Ecuador (Cardiologist at a free clinic! ) – 7/31/2026

THE CASE — Passang Jinpa

An 80-year-old woman presented with mild dizziness and fatigue, denying chest pain or dyspnea. Resting12-lead ECG showed marked sinus bradycardia with biphasic T-wave changes in anterior precordial leads, suggestive of a Wellens pattern. Ambulatory heart rate response was preserved. Echocardiography revealed regional wall motion abnormalities in the basal and mid-anteroseptal segments with sinus bradycardia throughout. A 24-hour Holter monitor was ordered.

 

Clinical Timeline: Day 1: Resting 12-lead ECG. Day 2: 24-hour Holter monitoring initiated. Day 3: Patient found deceased while wearing the Holter monitor. Retrospective review of the Holter recording captured the entire electrocardiographic evolution of the acute myocardial infarction, from initial ischemic changes through ST-segment elevation to the terminal arrhythmia.

 

What should I've done at first? Cath lab activation?

On Day-2 when she came to clinic no chest pain, absolutely fine.

 

MY REPLY:

Be sure to carefully review my ECG Blog #350 (https://ecg-interpretation.blogspot.com/2022/12/ecg-blog-350-severe-cp-not-much-on-ecg.html ) that reviews what Wellens' Syndrome truly is. Be sure to also review material in the Addendum (including the 8 minute Audio Pearl). So your patient did not have a true "Wellens' Syndrome" — because there was no history of chest pain that then went away. But it's important to remember the pathophysiology of Wellens' Syndrome (which I review in Blog #350) — as well as the fact that an IDENTICAL ECG may be seen AFTER an infarction. And in older patients — a "silent" MI (ie, an MI but without any chest pain) is the probable explanation for the T wave inversions that we see in your patient's ECG. So my main questions would relate as to WHEN the patient had those symptoms of mild dizziness and fatigue. It is a very fine line as to which older patient who you strongly suspect has had a "silent MI" needs to be hospitalized until you can be comfortable that their condition has stabilized. So — IF this patient's symptoms were in the last day or two — and especially since the heart rate on this ECG is SLOW (about 50/minute) — a period of monitoring in the hospital would seem warranted. Were Troponins done? If so — and if still elevated, that's another clue that this patient's MI was recent — and if this is a fully functioning 80-year old — cardiac cath should probably have been done before sending the patient home. P.S. Again, the history here is very subtle — but serial Troponins and serial ECGs may have provided insight as to WHEN the MI occurred (and the need for cath). Finally — Before I'd want to send this patient home — I would want to see if she is able to walk at a level comparable to doing her everyday activities. Ideally she is monitored when you do that. The point is that many patients don't want to stay in the hospital — but if this 80 yo woman normally is able to walk everywhere — and now she gets fatigued on much less activity — that's one more sign that she has had a recent MI that may not yet have "completed" (such that cath may be indicated before she goes home). TOUGH case. I hope the above is 

helpful ...

 

 

PASSANG Reply:

Dear Guru KEN, Thank you very much for your thoughtful comments and for taking the time to review my case. I really appreciate your insights. This was actually the patient's first medical evaluation. She had never previously seen a physician. I work in a charitable foundation that provides free outpatient cardiology consultations. Although it functions as a private clinic, patients are responsible for any additional investigations or hospital care, and many have significant financial limitations. Clinically, she looked remarkably well. She was an active 80-year-old woman who came with a friend in her 90s. They were both independent, regularly went shopping together, and she denied chest pain or dyspnea. She only mentioned mild fatigue. Because she appeared so functional and stable, I did not initially suspect an acute coronary syndrome. On the first day, I obtained a 12-lead ECG and observed an abnormal T-wave pattern. I ordered routine laboratory tests, but unfortunately I did not obtain troponin levels. Immediate coronary angiography was also not a realistic option because of the patient's financial situation. What makes this case particularly fascinating is what happened afterward. A 24-hour Holter monitor had been placed, and sadly, the patient was found deceased the following day before returning to have it removed. During my retrospective analysis of the Holter recording, I was able to observe the complete electrical evolution—from the initial ischemic T-wave abnormalities, through progressive ST-segment elevation, and ultimately to the terminal rhythm. The transition began at approximately 11:00 PM. To my knowledge, it is uncommon to have continuous Holter documentation of the entire evolution of an untreated myocardial infarction ending in sudden death. I believe this provides a unique opportunity to correlate the initial 12-lead ECG with the continuous ischemic progression. Do you think this case would be suitable for publication as a case report? If so, I would greatly appreciate any suggestions regarding the best way to present it or which aspects should be emphasized.

 

MY REPLY:

Hi. I can totally relate to ALL that you describe. Knowing more of the details — I may have done what you did.

My training is in family medicine. I was faculty in a Family Medicine Residency for 30 years — so we would see ambulatory patients and on occasion we'd get a history similar to what you describe, in which you suspect that an MI occurred days earlier. So the question then arises as to HOW MUCH to do for a "completed MI?" in an older patient who doesn't want to come into the hospital.

I am also familiar with free clinics as you describe (but for which funding is lacking if additional investigations are needed. You deserve CREDIT for providing care to people who otherwise have NO care .... but situations like this one are clearly frustrating!

In retrospect — the only thing I could say is that subtle change in symptoms (ie, development of some new "fatigue" in recent days in an older person with the initial ECG that you show is suggestive that a recent MI may have occurred, and that we are now seeing reperfusion T waves. What to do with this IF the patient otherwise "seems well" is a difficult question and "Ya gotta be there!" because there is NO certain answer.

In my capacity as hospital Attending for 3-4 months each year — I would read all of our service ECGs and I'd see the Holter Monitors. I will NEVER forget reading ECGs one day — and seeing a Holter monitor of a hospitalized patient, when I suddenly saw on the Holter that the rhythm was getting slower and slower — and then stopped. So I ran up to the floor where this patient was — only to find everyone at the bedside treating her cardiac arrest. It was an EERIE feeling seeing that Holter, and then seeing the patient (just like the eerie feeling that I'm sure you have when you saw these tracings!).

The above said — YES, this is rare to catch this — but I'm not sure you have best exposure by writing an article. Instead — I propose that you let me write an ECG Blog Case that I will publish within a couple weeks. I will show the 12 lead ECG that you sent me and ask the reader how they will interpret this?

I will write up the case giving enough basic info to "set the scene" — but I will not give specific details that may identify the patient. And then I will show the sequential tracings you sent me (that I put into a PDF here).

When I was on faculty — I would "collect" code tracings and later went thru them for insight while I was writing my books on ACLS. So these sequential tracings that you sent me show a similar sequence of events as this unfortunate woman evolved her huge extensive LAD occlusion.

These are TOUGH cases. Given age, vague symptoms (!!!) and lack of resources — there is no right or wrong answer — but the fact that you are soul searching events is sign that YOU are truly a good, caring physician doing the best you can given limited resources for the best you can do for your patients. Many clinicians would not give this case a second thought ....

Is it OK with you that I write this case up as an ECG Blog? I would be happy to acknowledge you if you like? — or the case can be anonymous — JUST LET ME KNOW. It will be published as a Blog post on-line, so it can be referenced by a link to my Blog.

Let me know what you prefer. THANK YOU for sharing this very difficult case with me. I believe it IS worthwhile to soul search events and think IF there is anything for you to learn from this OR if in fact you considered everything and from the information you had simply thought this was a completed MI with not much to gain by hospital admission in an older, minimally symptomatic patient. Putting older patients in a hospital is NOT benign, as "things happen" in the hospital ...

Should I acknowledge you as Passang Jinpa from Guayaquil, Ecuador — Dejame saber lo que quieres que hago por este caso — Ken