SSmith-DRAFT (KG- not done) - Solana Case with CT Scan (11-20.21-2024)-DRAFT- AWAIT SSmith-to-Finish

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MY Comment, by KEN GRAUER, MD (11/20/2024):

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Figure-1: The initial ECG in today's case. I've labeled KEY findings that give us the "Quick" Answer. (To improve visualization — I've digitized the original ECG using PMcardio).

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

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 SSmith DRAFT (11/19/2024):

The worst thing you can be is a young woman.

You will not be treated as rapidly as possible.

arrived 0130

5947582

30 y.o. female presents to the stabilization room for crushing chest pain. Patient reported she had chest pain at 9pm which woke her up, it was initially dull, however 2 hours prior to arrival, it became unbearable prompting her to present to the ED. Denies any SOB, or prior pmh

25 minutes

CT shows the infarct

 Patient's EKG was done in triage where she was quickly stabbed from

 This patient presented with concern for OMI. EKG with marked ST elevation in anterolateral leads. 

 Bedside cardiac ultrasound demonstrated normal function. Cath lab activated. 

 Aspirin, nitro, ticagrelor 180 given, and heparin load given.

 Patient vitals remarkable for hypertension to systolic's 180s> denies any history of this and no prior diagnosis

○ Given sublingual nitroglycerin x3 with minimal chest pain improvement

○ Nitro drip was started and patient had resolution of her pain

 Dr. Driver talked to cardiology staff who recommended CTA aorta> which had no dissection, however, obvious hypodensity of the anterior and septal wall of the myocardium. 

 Notable labs and events highlighted below in ED course 

 

In the ED she was fth anterolateral STE and hyperacute T waves, she was hypertensive in the 170s/100s for which she was started on NTG gtt with complete resolution of her chest pain. She was loaded with ASA 324, Ticagrelor 180mg and given 5k U of heparin at the time of cath lab activation. Initial hsTn 262.

Coronary angiogram showed 100% mid LAD occlusion for which she received a DES with excellent angiographic result. 

Angiogram:

Start time 0315

Acute anterior STEMI

Culprit is 100% occlusion in the mid LAD, No angiographic features of

SCAD.

Echo:

Normal left ventricular cavity size, mild to moderately increased wall

thickness, and moderate LV systolic dysfunction.

3. The estimated left ventricular ejection fraction is 37 %.

4. Regional wall motion abnormality- mid and apical anterior, apical

septum, apical anterolateral, apical inferior, and apex, hypokinetic to

akinetic.

SSmith-DRAFT- (KG- not done) - XXXX (11-14.1-2023)-DRAFT- ME_to_DO

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My Comment, by KEN GRAUER, MD (11/11/2024):

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

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SSmith Pearls on RV MI — May 30, 2023

Chest pain and shock: Is there a right ventricular OMI on this ECG?

https://hqmeded-ecg.blogspot.com/2023/05/chest-pain-and-shock-is-there-right.html

 

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

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SSmith DRAFT as of 11-10.1-2024:

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SSmith- DRAFT (KG-done -AWAIT SSmith)- 10 Serial ECGs (10-20.1-2024)- DRAFT- I_am_DONE

 

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NOTE — Steve waiting for final version of QOH before publishing this!

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MY Comment, by KEN GRAUER, MD (11/7/2024):

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Today’s case is a study in important subtlety — from which much can be learned in retrospect.

• The 1st question that arises — Is whether or not either of the first 2 ECGs might be diagnostic of an acute inferior OMI?
• Perhaps the more clinically important question is — How can we learn retrospectively what might have been done better. While fully acknowledging that, "Hindsight is 100% in the retrospectoscope" (ie, from the comfort of my computer desk chair)  — I think it insightful to relook at the 4 serial tracings shown in this case.
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• NOTE: Mention is made that a total of 10 serial ECGs were recorded in today's case over an 11-hour span. I only have access to the 4 ECGs that I show in Figure-1 — plus the final ECG done at T = 11 hours, at which time dramatic and diffuse hyperacute ST elevation is seen. I limit my comments to the history provided and the 4 ECGs shown in Figure-1.

Figure-1: I've labeled the first 4 ECGs shown in today’s case.

My Initial Thoughts on Today's CASE:

The history in today's case is of a mid-50s man with CP (Chest Pain) that apparently had been going on intermittently for some period of time (weeks?) — with a more severe episode the night before presentation. The patient noted a "brief syncopal period". His CP returned that morning — but CP was not present at T = 0 when ECG #1 was recorded.

• Given this history (with the intermittent nature of this patient's symptoms) — anything might be seen on the initial ECG. It is therefore important to realize that even IF this patient was having an ongoing cardiac event — We might not necessarily see obviously acute changes. 
• Instead, what might be seen — is a certain amount of "pseudo-normalization" (ie, if some degree of spontaneous reperfusion had at some point occurred). We should therefore be prepared to look for subtle ECG findings that may be important — with need to correlate the presence and severity of symptoms with each of these serial ECGs in order to optimally understand what happened.

The Initial ECG in Figure-1 (done at T = 0):
The rhythm in ECG #1 is sinus at ~65/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal. There is no chamber enlargement.

• As will become important momentarily — the PR interval = 0.20 second in ECG #1 — the frontal plane axis = +50 degrees — and the patient had no CP at the time this tracing was recorded.
• In ECG #1 — 3 leads show findings of potential concern: i) The most concerning finding is seen in lead III (within the RED rectangle) — in which there is slight-but-real ST elevation (RED arrow), with a biphasic T wave ending in terminal negativity.
• ii) That this ST-T wave abnormality is "real" — is supported by reciprocal changes in high-lateral leads aVL and I (BLUE arrows highlighting ST segment straightening, with a hint of ST depression in these leads).
• In the chest leads — there is T wave "imbalance", in that the upright T wave in lead V1 is taller than the upright T wave in lead V6. As I emphasize in My Comment in the June 1, 2022 post in Dr. Smith's ECG Blog — such "T wave imbalance" is a nonspecific finding that I have on occasion found useful as a "tip-off" to an acute coronary syndrome that I might not otherwise have recognized.
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• BOTTOM Line: While I found interpretation of ECG #1 to be non-diagnostic for OMI as a single tracing — given the history, I thought the subtle abnormal findings in leads I,III,aVL and the precordial T wave "imbalance" — could reflect a certain amount of "pseudo-normalization" (from spontaneous reperfusion) in a patient with a recent event, especially since the patient had no CP at the time ECG #1 was recorded!
• Suggestion: Given how quickly ECG findings may change in an acute coronary syndrome of uncertain duration — I favor not waiting more than ~20 minutes for the initial repeat ECG (with additional repeat tracings in short succession until there is clear indication of no progression).

The 2nd ECG in Today's Case (ECG #2 was done at T = 82 minutes):

While unknown if the patient was (or was not) having CP at the time ECG #2 was recorded — the initial Troponin came back significantly elevated at 1300 ng/L.

• My reason for noting the slight shift in frontal plane axis in ECG #2 (ie, from +50 to +70 degrees) — is because there is subtle-but-real change in ECG appearance for the leads mentioned above in ECG #1 — and we want to ensure that a change in frontal plane axis is not responsible for this (I did not think this slight change in axis was the cause for the change in limb lead ST-T wave appearance).
• Specifically: i) Despite no significant difference in QRS morphology — there is no longer any ST elevation in lead III; — and, ii) There is no longer any hint of ST depression in leads I and aVL — and T wave amplitude has increased slightly in both of these leads.
• While fully acknowledging the subtlety in these limb lead ST-T wave changes — the fact that 3 leads show similar evolution to me suggests that these changes are "real" — and may reflect "dynamic" ST-T wave change. Given the elevated Troponin (= 1300 ng/L) — Hasn't the diagnosis of acute OMI (and the need for prompt cath) been made?

The 3rd and 4th ECGs (done at T = 8.3 hours — and T = 9 hours):

The patient apparently continued to have ongoing stuttering symptoms (recurrence of a "heartburn" sensation) during the night. At some point — the patient became bradycardic and developed a "Mobitz II pattern" — but he remained asymptomatic and hemodynamically stable.

In the interest of pointing out subtle but relevant issues in today's case — I'll note the following:

• Despite no more than slight axis adjustments — the limb leads in ECG #3 and ECG #4 continue to show ongoing changes of coronary reperfusion. These include: i) Progressive increase in T wave amplitude in leads III and aVF (compared to ECG #2); — and, ii) Progressive decrease in T wave amplitude in lead aVL (compared to ECG #2).
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• Note the serial change in the ST-T wave appearance in lead V1 over the course of the 4 ECGs in Figure-1. Although we usually associate development of a Wellens'-like sharp T wave descent into terminal T wave negativity in leads V2,V3,V4 with Wellens' Syndrome — here we see this evolution only in lead V1. In retrospect — I interpreted these serial lead V1 ST-T wave changes as support of the early precordial T wave "imbalance" as a "tip-off" finding that I noted when interpreting ECG #1.
• Note also development of distinct J-point notching in leads V3,V4 that was not seen earlier. As per My Comment in the February 2, 2024 post — knowing the results of today's cardiac catheterization, I retrospectively interpreted this finding as representing ischemic Osborn waves.

The Patient developed AV Block, "Mobitz Type II" during the Night ...

Realizing that no definitive diagnosis of the nature of the conduction block referred to in description of today's case can be made without seeing the actual ECG rhythm strips — I'll suggest that statistical odds that the type of AV block seen was Mobitz I (and not Mobitz II) are well over 90-95%.

• Today's patient was found on cath to have RCA OMI. Mobitz I is common in this clinical setting. Mobitz II is not. This is especially true because: i) The QRS complex is narrow in all 4 ECGs seen in Figure-1 (whereas the QRS is usually wide with Mobitz II); — and, ii) The first 2 ECGs in today's case show a normal PR interval ( = 0.20 second) — whereas ECG #3 and ECG #4 now show 1st-degree AV block (PR interval = 0.24 second). It is common for Mobitz I in the setting of inferior OMI to evolve from a normal PR interval — to 1st-degree AV block — to 2nd-degree, Mobitz I. This sequence of evolution is not seen with Mobitz II — that typically presents with abrupt failed conduction despite a constant (and usually normal) PR interval.
• What most likely was seen during the night — was 2nd-degree AV block with 2:1 AV conduction, which is often mistakenly interpreted as Mobitz II (because the PR interval remains constant as every-other-beat is non-conducted). Technically — one can not distinguish between Mobitz I vs Mobitz II when there is 2:1 AV conduction — because you never see 2 consecutively conducted beats (so you never know whether the PR interval would progressively increase before dropping a beat IF given a chance to do so). That said — in the setting of acute inferior OMI with a narrow QRS and evolution from a normal to a prolonged PR interval — the odds that 2:1 AV block represent Mobitz I are overwhelming. (For more on ECG recognition and clinical significance of 2nd-degree AV blocks — Please check out My Comment at the bottom of the page in the November 12, 2024 post in Dr. Smith's ECG Blog).
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• Clinical Relevance: On seeing PR interval lengthening during the night — that evolved into 2:1 AV block — We had at that time, yet one more piece of evidence diagnostic of acute inferior OMI in progress.

 

 

Statistical odds that the type of AV Block developed was Mobitz I instead of Mobitz II are probably at least 95%.

— can't tell without the rhythm

— probably 2:1 block - which usually is Mobitz I (esp. with acute inf MI — narrow QRS — and new 1st degree av block!)

MAKE FIGURE of 4 ECGs 

— add axis in degrees 

— add PR interval

— RED and BLUE rectangles in limb leads!

• I don’t know what to make of the chest leads — I don’t see clear evidence of post MI ….
• Focus on limb leads
• Me to figure out frontal plane axis in all 4 tracings (I can WRITE this ON the actual ECGs) – slight changes but not enough to produce the ST-T wave changes we see.
• True that none of the 4 ECGs is “diagnostic” of OMI.
• But — given the history and given the changes — these are “dynamic” ST-T wave changes that are diagnostic of OMI (or at the very least — clearly indicative of the need for prompt cath.
• Excellent move by the providers to keep ECG leads attached! Catching the ST elevation tracing is a superb illustration of how quickly things can change once the “threshold” for “adequate” coronary perfusion is superceded. It also is a powerful lesson that the 1st ECG alone could have been enough to justify prompt cath — but clearly once the 2nd ECG was done — this already DOES show enough ST-T wave dynamic change to justify prompt cath.
• That 2nd ECG could have been ordered sooner.
• Was first Troponin value increased ??? (What are limits of normal?)

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— Me to see if Steve ever finds the Mobitz II tracings.

— I doubt Mobitz II — RCA OMI with inf. MI — narrow QRS — Mobitz II usually wide QRS, ant. MI — and given that it is a much more severe conduction defect — less likely to be subject to the intermittent AV nodal ischemia that clearly was occurring in this case.

— Statistically before you look at the rhythm strip — given acute inf. MI with narrow QRS — about 95% (at least) of 2nd degree will be Mobitz I — Add in the 1st degree and even more than that

— Also — normal PR for ECG-1,2 — but 1st degree for ECG #3 — and Mobitz II does not do that (but Mobitz I does!)

 

Magnus-DRAFT-BLANK- XXX (4-28.1-2023)-BLANK DRAFT

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

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SSmith Draft (11-6.1-2024) 

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5965104

This patient had 10 ECGs recorded over 11 hours, and then had to have continuous 12-lead monitoring, in order to prove a STEMI. We only show 5 of the ECGs.

A mid-50s male came to the ED with a burning sensation that was acutely worse while at home. He had recently returned from overseas travel where these symptoms had been intermittently bothersome over the preceding weeks and had been attributed to heartburn.

The previous evening, he was at rest and developed severe pain with associated shortness of breath, diaphoresis and a brief syncopal episode. He had ongoing pain following the syncopal event but went to bed and awoke in the morning with ongoing pain.

He came to the ED at the urging of his wife. At ED presentation, he was asymptomatic but developed extremely brief periods of recurrent burning discomfort that were centered about the sternal notch.

Given his history, an EKG, labs including high sensitivity troponin, and chest radiograph were ordered. 

Here is the first ECG at Time zero:

Here is his initial EKG: What do you think?

A bedside cardiac ultrasound revealed grossly preserved left ventricular function, no appreciable wall motion abnormality, pericardial effusion, or obvious valvular abnormality. His initial high sensitivity troponin returned at 1300 ng/L and given that his cardiac workup was otherwise unremarkable, a CT was obtained to evaluate for pulmonary embolism and aortic aneurysm or dissection but this too was unrevealing. Another EKG was also obtained.

ECG at time 82 minutes:

What do you think? 

Cardiology was consulted and agreed that his history was high risk for ACS and a next-day angiogram was merited. He was started on intravenous heparin and given aspirin. His care was signed out to the overnight team with a plan to continue to obtain serial troponin measurements and admit the patient to the hospital for an angiogram. 

Overnight, his troponin continued to rise, but he remained asymptomatic and was resting between cares. When pressed, he endorsed mild, very brief periods of a retrosternal burning sensation and serial ECGs were obtained. 

ECG at 8.3 hours

What is noticeable now? 

These EKGs were concerning for a Wellen’s-like pattern of subtle reperfusion changes in the setting of stuttering anginal-equivalent symptoms, but none were diagnostic of STEMI or OMI. Later in the night, the patient became bradycardic and developed a Mobitz II pattern, but he remained asymptomatic and hemodynamically stable. Very early in the morning, he reported recurrence of a heartburn sensation, so another EKG was obtained. 

ECG at 9 hours:

This was also non-diagnostic for OMI. However, with the development of Mobitz II and ongoing stuttering symptoms, the 12-lead EKG was left attached to the patient and was observed. After about 10-15 minutes, there was a significant change and very large inferior ST elevation with reciprocal ST depression in the lateral leads was observed and the patient was moved to the stabilization room. 

ECG at 11 hours:

Given this EKG with diagnostic findings, his heparin infusion was stopped, and he was given a 5000 unit heparin bolus and 180 mg of ticagrelor while the cardiac catheterization laboratory was activated and interventional cardiology was emergently consulted. 

Angiography was performed and found a normal LAD, a large co-dominant LCX, and 95% disease at the mid-RCA. A large RPDA and a small RPAV giving rise to RPL1 was seen. The RCA was stented successfully with TIMI III flow noted post-procedure and the patient has done well with a post-PCI TTE demonstrating good LVEF and no wall motion abnormality. Given the right coronary anatomy seen during angiography, it is particularly interesting that subtle T wave changes were seen on the previous EKGs in the high lateral leads that would otherwise only be expected with a more proximal RCA lesion. 

This case highlights the importance of maintaining a high degree of suspicion for clinically important disease even in the absence of classic symptoms or an EKG without STEMI despite an initially high troponin. Uptrending troponin should prompt immediate reassessment and serial EKGs are an essential tool for the patient with stuttering symptoms and concerning biomarker findings. Changes in the cardiac rhythm, as was seen in this case with the development of bradycardia and intermittent heart block should prompt extremely careful monitoring and serial EKGs. This case also highlights the value of continuous 12-lead EKG monitoring, which is not routinely available in many institutions but proved invaluable in making a timely diagnosis at the time that the EKG became diagnostic. 

ECG Rhythms- MIS-C Case Report (9-15.21-2024) - DRAFT

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Review of ECG Rhythms — MIS-C Case Report (9/5/2024):

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What follows below are my first impressions of the ECG rhythms sent to me from the Case Report by Dimah Jarmakani et al — of a 12-year old boy with MIS-C (Multisystem Inflammatory Syndrome in Children).

• For full discussion of the case — CLICK HERE —

ECG Rhythm Overview:

A 12-year-old boy was admitted to our hospital with severe myocardial dysfunction and chaotic rhythm with tachy- and bradycardic arrhythmias. What follows are the ECG tracings of our patient:

• ECGs #1 and #2 were performed on the 2nd and 4th hospital days, respectively — at which time the patient had severe myocardial dysfunction. 
• ECGs #3,4,5,6 were done one week later — at which time the patient began to respond to the medical treatment, with recovery of myocardial function. 

We requested assistance from Dr. Grauer for interpretation of the ECG tracings, This is his response to us:  

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My impressions of representative tracings from this case follow below:

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ECG #1:

Figure-1: ECG #1 is from the 2nd hospital day.

MY Thoughts on ECG #1:

This clearly is a challenging series of arrhythmias — obtained from this acutely ill 12-year old boy with MIS-C:

• I put limb leads and chest leads from this first tracing togeter (these tracings were sequentially recorded). Note that this tracing was recorded at half standardization. 
• The rhythm is highly variable. The RED arrow looks like a sinus P wave in front of beat #2. We really do not see more sinus P waves in this ECG #1 — but having glanced ahead at ECG #2, there clearly are sinus-appearing P waves in this next tracing (below) — so I’ll suppose that the RED arrow in front of beat #2 in ECG #1 is a sinus P wave (or possibly a P wave from another atrial focus).
• Given that this RED arrow P wave is pointed — I think we are seeing the opposite picture under each of the YELLOW arrows! I therefore suspect these YELLOW arrows highlight the location of retrograde conduction from ventricular beats.
• QRS morphology of beats #3,4; 6,7; 9,10; 12,13 and 15 shows marked right axis with an rS in lead I — and qR pattern in leads III,aVF.
• Unfortunately — we do not know for certain which beats in the limb leads correspond to which beats in the chest leads — but my guess is that beats #3,4; 6,7; 9,10; 12,13 and 15 with LPHB-like conduction — correspond to the RBBB-like beats in lead V1 of the chest leads. These beats are very wide and not preceded by P waves — so I think these are all PVCs (with a bunch of ventricular couplets) and with the YELLOW-arrow retrograde conduction. RBBB-LPHB-like conduction suggest they may be fascicular beats from the left anterior hemifascicle (although the QRS is wider than fascicular beats usually are).
• In the chest leads of ECG #1 — we also see a LBBB-like etiology for beats #6 and 13 in the chest leads (and perhaps for beats #16,17 in the limb leads). It is hard to say if these are PVCs from another ventricular focus (though their close resemblance to LBBB conduction to me suggests they are supraventricular with aberration.
• I think the BLUE arrows in ECG #1 represent conducted beats from a different atrial focus (ie, negative or not well seen in lead II — but better seen in other leads).
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• BOTTOM LINE — I do not think any of the above details really matter clinically … As you say — the rhythm is chaotic — but not necessarily unexpected given the history of a sick, symptomatic 10-year with severe dilated cardiomyopathy … I’d guess this is sinus rhythm, perhaps with a wandering atrial pacemaker and very frequent ventricular ectopy with multiple couplets. It is not quite MAT — because pure MAT should show a different-shape P wave with every beat, and we don’t quite have that. That said — in my experience, there is a spectrum of disorders with sinus rhythm and PACs at one end — and true MAT at the other end. This rhythm is somewhere in between.

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ECG #2:

Figure-2: ECG #2 is from the 4th hospital day.

Figure-1: I've - ECG-1

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ECG #2 — I again put both pieces together. I’m not quite sure when ECG #2 was done with respect to ECG #1 — nor whether clinical circumstances were different — but this ECG looks VERY different than ECG #1.

RED arrows show what looks to be sinus P waves that are HUGE !!!! = consistent with RAA (which is consistent with this patient’s underlying heart disease. Perhaps the patient has pulmonary hypertension and/or tricuspid regurgitation?

After 2 sinus beats — we see junctional escape at a SLOW escape rate — followed by 2 more sinus beats, and then 2 slow junctional escape beats.

As you suspect — this could reflect SSS ( = Sick Sinus Syndrome) — with need to rule out effect from rate-slowing medication and/or something potentially “fixable” (ie, hypoxemia).

I suspect BEST treatment for these rhythm disturbances is correction of this patient’s underlying heart disease — but that of course is easier said than done …. In the meantime, a pacemaker may be needed.

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ECG #3:

Figure-3: ECG #3 — obtained 1 week later during recovery.

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ECG 3: (HAS 4 tracings):

I am glad your patient is getting a little better. It became difficult to know which tracing was which — so I am placing below what I think are the 4 new tracings. Some of the leads are not labeled — and I don’t know if any 2 make up a complete ECG — but clinically, that really isn’t important since your patient has heart failure from cardiomyopathy and NOT and acute infarction. Whether there is a component of myocarditis is another question …

So I’ll put the 4 tracings I see below with my thoughts. Overall — it DOES look like the patient may be a little better — though still with a chaotic rhythm. There definitel are periods of bradycardia (so pacing may be needed for that). There is an underlying sinus rhythm — with the “theme” being LOTS of ectopics including many different PAC shapes (therefore multiple PAC sites) and some PVCs.

Overall — I think this rhythm “acts” like MAT. By strict definition — each P wave should change in shape with “true MAT” — and that does not quite happen, since there are periods of sinus rhythm. But as I think I mentioned earlier — there is a “spectrum” of supraventricular arrhythmias — and sinus rhythm with lots of different looking PACs as we see here “acts” clinically like MAT. Typically — this may be cause by a very “sick” patient (as is the case for your patient) and/or hypoxemia, electrolyte disorders, heart failure, etc.

BOTTOM LINE — It’s hard to be sure of every single beat — but this is not important. It is the “theme” that counts — which as I describe above, seems to be “acting clinically” like MAT + PVCs — for which best treatment is support and to do the best you can with the patient’s heart failure. Hope this helps — :)

ECG-3 — I see sinus bradycardia and arrhythmia. Beat #4 is a PAC (Note that the P looks different in lead aVL) — and then beat #5 is junctional escape (the sinus P in front of beat 5 has a PR too short to conduct!)

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ECG #4:

Figure-4: ECG-4 — obtained 1 week later during recovery. 

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ECG-4 — I see sinus rhythm for beats #1,2. Beats #3 and 6 look like PVCs. Since the QRS is different and we see retrograde P waves — I think beats #4,5,9,11,13,15,17 are PVCs. The other beats are PACs with different-looking P waves. The fixed coupling for beats #4,5,9,11,13,15,17 supports these being PVCs.

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ECG #5:

Figure-5: ECG-5 — obtained 1 week later during recovery.

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ECG-5 — Now that we know that the tall, pointed P-Pulmonale P waves in lead II are the sinus beats — we can identify the P waves in front of beats #2,6-thru-9 as being sinus P waves. Once again — the P in front of #6 is too short to conduct, so this is junctional escape. After beat #9 — we see the same thing that we saw in ECG #1 ...

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ECG #6:

Figure-6: ECG-6 — obtained 1 week later during recovery.

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ECG-6 — I see sinus brady until the ?. I cannot tell for certain if the “dip” under the BLUE line is a PAC.

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Figure-1: I've