EXTRA COPY - ECG Blog #518 — WCT with Low Urine Output — EXTRA COPY

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The ECG in Figure-1 was obtained from a previously healthy middle-aged man — who presented to the ED (Emergency Department) with acute shortness of breath. The patient complained of malaise — but no chest pain or other bodily pain. He has had difficulty urinating.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• How would you treat this rhythm?

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

MY Thoughts on the Rhythm in Figure-1:

By the P's, Q's, 3R Approach (See ECG Blog #185) — the rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia):

• The rhythm is Regular.
• The QRS is obviously wide (at least 4 large boxes in duration ==> 0.16 second).
• The Rate of the rhythm is ~130/minute.
• P waves are absent.

As often emphasized in this ECG Blog — We need to assume VT until proven otherwise whenever we see a regular WCT rhythm without clear sign of P waves.

• BUT — Take another LOOK at QRST morphology in Figure-1.
• Consider that this patient has recently been ill — and has had trouble urinating ...

Figure-1: Take another LOOK at the ECG in Figure-1 ...

Taking Another LOOK: 

As noted above — the rhythm in Figure-1 is a regular WCT at ~130/minute, without clear sign of P waves.

• QRS morphology  in Figure-1 is consistent with LBBB conduction (Monophasic R wave in leads I and V6 — and predominantly negative QRS in the anterior leads).
• BUT — Aren't T waves in many of the leads tall and peaked (if not pointed)?
• Not only are positive T waves peaked (and quite pointed in leads II,III,aVF; and V3,V4,V5) — but the negative T waves in leads I and aVL are also pointed at their deepest part! (See this Eiffel Tower effect below in Figure-2).

Figure-2: Note the Eiffel Tower effect of both positive and negative T waves in many of the leads in today's ECG.

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I'll refer the reader to my recent ECG Blog #516 — in which I highlighted XXX — as well as indications for empiric treatment of suspected hyperkalemia with IV Calcium even before the serum K+ level returns from the laboratory.

https://ecg-interpretation.blogspot.com/2026/01/ecg-blog-516-patient-is-post-op.html

Hyperkalemia

ECG Blog #275

https://ecg-interpretation.blogspot.com/2022/01/ecg-blog-275-58-what-chart-audit.html

Review when to give empiric IV Calcium !!!! — and the sequence of ECG changes with hyperK

Also — Audio Pearl on HyperK

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ECG Blog #244

https://ecg-interpretation.blogspot.com/2021/07/ecg-blog-244-58-cath-lab-was-activated.html

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—  — 

ECG Media PEARL #58 (8:30 minutes Audio) — Reviews some lesser-known Pearls for ECG recognition of Hyperkalemia.

 

 

 

 

 

The 2nd ECG Diagnosis = Severe HyperKalemia:

For clarity — I've added Figure-2, which presents the "textbook" sequence of ECG findings seen with progressive degrees of hyperkalemia. While fully acknowledging that "not all patients read the textbook" — and that there will be variations in the various ECG findings from one patient-to-the-next — I have found awareness of the generalizations for these ECG signs in Figure-2 to be extremely helpful.

• The usual earliest sign of hyperkalemia ( = T wave peaking) may begin with no more than minimal K+ elevation (ie, K+ between 5.5-6.0 mEq/L) — although in some patients, T wave peaking won't be seen until much later.
• I love the image of the Eiffel Tower. With progressive degrees of hyperkalemia — the T wave becomes tall, peaked (pointed) with a narrow base. While patients with repolarization variants or acute ischemia (including the deWinter T wave pattern) often manifest peaked T waves — the T waves with ischemia or repolarization variants tend not to be as pointed as is seen with hyperkalemia — and, the base of those T waves tends not to be as narrow as occurs with hyperkalemia.
• P.S. — As helpful as I find Figure-2 is for providing insight to the ECG changes we look for when suspecting clinically significant hyperkalemia — progression from sinus rhythm to VFib as the 1st ECG sign of hyperkalemia has been documented. Not all patients read the textbook. (emDocs, 2017 — Management of Hyperkalemia).

 

 

Figure-2: The "textbook" sequence of ECG findings with hyperkalemia.

 

 

ECG Changes of Hyperkalemia in Today's Case:

The reasons I instantly suspected severe hyperkalemia in today's case were:

• Significant QRS widening (to at least 0.11 second in leads I, II, aVL and others).
• T wave morphology that is typical for hyperkalemia. As shown in Figure-3 — the T waves in multiple leads resemble the Eiffel Tower (ie, not only are the T waves in leads I, II, aVL; V4, V5 and V6 tall, peaked and pointed — but these T waves are symmetric with an equally steep angle of rise and fall — with a narrow T wave base).
• There is a Brugada-1 ECG pattern in leads V1, V2 and V3. As emphasized above — it is common to see Brugada Phenocopy in association with severe hyperkalemia.

 

 

 

PEARL #3: Assessment of the rhythm with severe hyperkalemia is often extremely difficult because: i) As serum K+ goes up — P wave amplitude decreases, and eventually P waves disappear (See Panels D and E in Figure-2); ii) As serum K+ goes up — the QRS widens; and, iii) In addition to bradycardia — any form of AV block may develop, and AV conduction disturbances with severe hyperkalemia often do not "obey the rules" (See Figure-4).

• THINK for a MOMENT what the ECG will look like IF you can't clearly see P waves (or can't see P waves at all) — and the QRS is wide? ANSWER: The ECG will look like there is a ventricular escape rhythm, or like the rhythm is VT if the heart rate is faster.
• NOTE: We do not see P waves in most of the leads in Figure-3 — and it's difficult to be certain if the deflection in lead II is a sinus P wave (RED arrow). Fortunately — a definite P wave is seen in lead aVF, which confirms that the rhythm is still sinus (ie, sinus tachycardia at ~135/minute). But without lead aVF — I would not have been at all certain what the rhythm was.

 

Figure-4: Why assessing the rhythm with hyperkalemia is difficult (See text).

 

 

Follow-Up to the Case:

The cardiac cath was negative (Clean coronary arteries! ). That said — the patient's condition precipitously declined after catheterization — and he was emergently intubated. Pertinent lab findings on admission included a pH = 6.94 — glucose over 1,100 mg/dL — serum K+ = 7.5 mEq/L.

• Fortunately — the patient's DKA (Diabetic KetoAcidosis) responded to treatment, with normalization of lab values.
• I was unable to obtain follow-up ECGs that could have confirmed my suspicion of Brugada Phenocopy.

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Hello Dr. Grauer I am Hamid. Working as Emergency Medicine Doc in Slovakia. I would love to get your insight on an ECG. The patient 42 years old, past history only hyperlipidemia (No hypertension!), presenting to ER with difficulty breathing for the past two days. Malaise. No chest pain. No complaint of pain. Stool normal. Urine he says for the past few days he has increased urgency with low urine output. Obj: GCS 15, diaphoretic, pale, breathing: crackles bilaterally. Blue protocol: Sliding present, B-Lines diffusely bilat.

MY REPLY:

This is an interesting tracing. I see a regular WCT ( = Wide-Complex Tachycardia at ~135/minute. There are NO sinus P waves ( = NO upright P wave in lead II. I really do not see sign of 2:1 atrial activity. T waves are PEAKED in many leads — so I'd be concerned about HyperK+ (ie, the patient may need IV Calcium ... — which depending on the clinical situation, I might even give empirically here ...) If serum K+ is normal — then QRS morphology could potentially be consistent with LBBB conduction (finding a prior tracing would help) — so I could not rule out a supraventricular etiology based on this single tracing — but HyperK is my suspicion. What happened?

HAMID HIMAT REPLY:

Thank you. I will keep that in mind for the future. You are absolutely spot on. I administered calcium before the lab values were available, based on the fact that the patient urinated approximately 1.5 liters within minutes after the Foley catheter was inserted. The assumption was hyperkalemia due to post-ren AKI with pulmonary edema. Following repetitive doses of calcium IV, the QRS complexes started to shorten, and the patient was taken for urgent dialysis. The potassium level was 8.71 mmol/L. Unfortunately, I do not have access to the ICU ECGs, but the system indicates the patient is stable. My specific question is, how do you differentiate between a wide QRS tachycardia that is V-tach versus one that is metabolic or supraventricular tachycardia with aberrancy in such patients?

MY REPLY:

Great question you ask! And often it is VERY difficult !!!

#1) Does the clinical setting predispose? Your patient's history is subtle — but inability to urinate — a history of HTN (What MEDS was he taking ???) — and now pulmonary edema DO potentially predispose him to HyperK.

#2) The ECG shows a wide QRS — without really showing indication of what it is! Always USE calipers when you have a moment to reflect (obviously you can't use calipers if your patient is crashing in front of you) — and doing so, I do NOT see any indication of 2:1 atrial activity (so NOT AFlutter). 

QRS morphology does resemble LBBB conduction (all upright in leads I, V6 — and predominantly negative in V1-thru-V4 — so I can't rule out a supraventricular etiology (finding a prior ECG would be VERY helpful in assessing this!) — but looking carefully, I see peaked T waves in 7 leads! (RED rectangles).

I also see a "point" to the negative T waves in 2 leads (BLUE rectangles).

When suspicious and in doubt — there is minimal morbidity from prudent Ca++ administration — and you can cure the patient — so you diid the RIGHT THING by giving IV Ca++ BEFORE the serum K+ value came back.

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Acknowledgment: My appreciation to Hamid Himat (from Bratislava, Slovakia) — for allowing me to use this case and these tracings.

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EXTRA COPY — ECG Blog #517: Recurrent Syncope — EXTRA COPY

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The ECG in Figure-1 was obtained from an older woman who presented to the ED (Emergency Department) after suddenly waking up from sleep dyspneic, dizzy, and convinced she was "about to die".

QUESTIONS:

• How would YOU interpret her initial ECG shown in Figure-1?
• What do you think is the cause of her symptoms?

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

CASE Follow-Up:

Over the next few weeks — this patient was again seen in the ED on 2 occasions.

• On her 2nd-ED-Visit — She presented after syncope and a fall. She reported several episodes of "dizziness" in the days prior to this 2nd ED visit.
• Her exam in the ED was "normal".
• Her repeat 12-lead ECG was virtually identical to that seen in Figure-1.
• Basic lab was unremarkable.
• The patient was discharged home.

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• On her 3rd-ED-Visit — She presented to the ED with a presyncopal episode and ongoing dizziness.
• Her initial exam was unremarkable.
• Her repeat 12-lead ECG was once again unchanged from that seen in Figure-1.
• Basic lab was again unremarkable.
• The patient was placed on a monitor for a period of observation in the ED. Suddenly — the patient became unresponsive! The rhythm strip shown in Figure-2 was recorded.

QUESTIONS:

Realizing that Figure-2 is limited to a brief, single lead rhythm strip ...

• How would you interpret the rhythm in Figure 2?
• What diagnosis is suggested by the history in today's case — given the 2 tracings shown in Figures-1 and -2?

Figure-2: Brief telemetry recording on the patient's 3rd ED visit (normal 25 mm/sec calibration).

ANSWER:

The rhythm in Figure-2 shows marked bradycardia (21 large boxes = 4.2 seconds separate the 2 beats in the middle of the rhythm strip). The tracing ends with nearly 4 seconds of asystole (We don't know if another QRS complex ever occurred).

• It looks like very low amplitude but almost regular P waves are seen throughout the tracing

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COMMENT:

This sequence of events should not have happened. In Figure-3 — I've labeled the initial tracing to illustrate the ECG diagnosis that could have been made at the time of this patient's 1st ED visit.

• The rhythm is sinus at ~80-85/minute.
• The PR interval is at the upper limit of normal ( = 0.21 second).
• The QRS is wide (3 little boxes in duration = 0.12 second).
• QRS morphology in the chest leads is consistent with RBBB conduction (ie, predominant R wave in right-sided lead V1 — with a wide terminal S wave in lead V6).
• QRS morphology in the limb leads is consistent with LBBB conduction (ie, all upright QRS in left-sided leads I and aVL). In addition — there is marked LAD (Left Axis Deviation).

BOTTOM Line: The ECG in Figure-3 is consistent with MBBB (Masquerading Bundle Branch Block).

Figure-3: I've labeled today's initial ECG.

PEARL #1: ECG criteria for the diagnosis of MBBB are described by Dhanse et al (J Clin Diag Research: 10(9), 2016) — and Buttner and Cadogan (LITFL, 2021) — and include the following: 

• An ECG pattern consistent with RBBB in the chest leads (ie, with a widened, predominantly positive QRS in lead V1).
• An ECG pattern consistent with LBBB in the limb leads (ie, with a widened, monophasic QRS in leads I and aVL).
• 
  
• NOTE: Variations on this above "theme" of MBBB are common. Thus, the S wave that is typically associated with RBBB patterns in lateral chest leads V5,V6 may or may not be present. In the limb leads, rather than a strict LBBB pattern — more of an extreme LAHB (Left Anterior HemiBlock) pattern will often be seen (ie, with wide and predominantly [if not totally] negative QRS complexes in the inferior leads — and with a smaller [blunted] terminal s wave in leads I and aVL).
• 
  
• BOTTOM Line: Knowing the clinical history may aid in recognition of IVCD patterns that are consistent with MBBB (ie, if the patient has a known history of severe, underlying heart disease). Distinction from simple bifascicular block (ie, with RBBB/LAHB) — may be facilitated by seeing one or more of the following: i) More of a monomorphic upright QRS in lead V1 (which lacks the neatly defined, triphasic rsR' with taller right "rabbit ear" seen with typical RBBB); ii) Lack of a wide terminal S wave in lateral chest lead V6; iii) Seeing an all-positive (or at least predominantly positive) widened QRS in leads I and/or aVL, with no more than a tiny, narrow s wave in these leads; and/or, iv) Seeing widened, all-negative (or almost all-negative) QRS complexes in the inferior leads.

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Retrospective Reflection on Today's CASE:

Hindsight is 100% in the "retrospectoscope". That said — I think it instructive to reflect back on events in today's case.

• Given the history — one might not have chosen to insert a permanent pacemaker after this patient's 1st ED visit. However, the diagnosis of MBBB should be recognized from this initial ECG shown above in Figure-1 because the rhythm is sinus — the QRS is wide — and as shown in Figure-2, QRS morphology "looks" like RBBB conduction in the chest leads, but LBBB conduction with left axis in the limb leads.
• IF one recognizes MBBB on this 1st ED visit — and then given the feeling this patient had on awakening "that she was going to die" — the astute clinician should have suspected that the patient may have had a bradyarrhythmic form of AV block and monitored the patient in the ED (and depending on the history — potentially admitting the patient for 24 hours to monitor her rhythm).
• And even if nothing showed on those 24 hours of telemetry — given the diagnosis of MBBB — the patient should have been warned to promptly report any "dizzy episodes". Especially given subsequent "several dizziness episodes" over the next few weeks — the patient would have been diagnosed and paced long before her 3rd ED visit. 
• PEARL #2: As per the famous aphorism by Sir William Osler, "Listen to your patient; He/she is telling you the diagnosis". All too often the diagnosis is there being told to us by our patient, if we only listen (ie, Today's patient waking up, feeling she was "about to die" — and then having episodes of "dizziness" in the days prior to her 2nd ED visit).
• PEARL #3: The entity of MBBB is often cited in the literature as being "rare". But since I've become aware of this entity — in my experience, it is not rare. Instead, I find this similar to the frequency of Brugada ECG patterns — Takotsubo Cardiomyopathy — and blocked PACs — in that each of those entities seemed "rare" to me until I became aware of them. And now that I've become experienced recognizing these entities — they are no longer "rare" (See ECG Blog #394 and Blog #419 for 2 more examples of MBBB).

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Is the QRS in today's ECG truly wide?

It's worth spending a moment reviewing the question as to whether the QRS complex in today's initial ECG is truly wide? After all, the QRS doesn't look that wide — Does it?

• Many textbooks describe QRS widening as being defined by a QRS ≥0.12 second in duration. But is this truly the best defining limit for QRS widening when there are cases of fascicular VT in which QRS duration is less than 0.12 second? (Kapa et al — Circ: Arrhythm and Electrophys 10(1), 2017).
• The definition of QRS widening is different in children. It takes less time to depolarize a smaller heart. Therefore, QRS duration will normally be ≤0.10 second up to ~12 years of age (Rijnbeek et al — Eur Heart J 22:702-711, 2001— See Table-2).
• 
  
• PEARL #4: For practical purposes — I find the easiest way to define the QRS as being "wide" in an adult — is if the QRS complex in any lead is clearly more than half a large box in duration. Since each large box on ECG grid paper = 0.20 second — more than half a large box is ≥0.11 second.
• 
  
• Returning to today's initial ECG — although the QRS does not "look" to be overly wide — it actually measures 3 little boxes in duration in a number of leads ==> the QRS is wide in today's initial ECG (See Figure-3).

Figure-3: I've added enlarged inserts of leads V2 and V6 from today's initial ECG that was shown in Figure-1. The vertical RED lines in leads V2 and V6 mark the onset and offset of the QRS in these leads — which = 3 little boxes in duration = 0.12 second, therefore confirming a wide QRS.

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CASE Follow-Up:

• Today's patient has MBBB. This woman was extremely symptomatic with recurrent syncopal episodes, and an extended episode of profound bradycardia consistent with PAVB (Paroxysmal Atrio-Ventricular Block). 
• She was referred for permanent pacing.
• 
  
• See the ADDENDUM below for more on PAVB.

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Acknowledgment: My appreciation to Ahmed Marai (from Irak) and Amr Elhelaly (from the UK) — for allowing me to use this case and these tracings.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
• 
  
• ECG Blog #282 — reviews a user-friendly approach to the ECG diagnosis of the Bundle Branch Blocks (RBBB, LBBB and IVCD).
• 
  
• ECG Blog #203 — reviews ECG diagnosis of Axis, Hemiblocks and Bifascicular Blocks.
• 
  
• ECG Blog #394 and ECG Blog #419 — for 2 more examples of MBBB.

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ADDENDUM (The Addendum below reproduced from ECG Blog #419): 

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In follow-up to the Comment I have just received from H.S.Cho — I would expand on my description of the cardiac rhythm in ECG #1 from today's case.

• Given the history in today's case (ie, Sudden onset of the rhythm seen in ECG #1 — that within a minute spontaneously resolved) — Rather than "near ventricular standstill" — this rhythm is best described as PD-PAVB (Pause-Dependent Paroxysmal AtrioVentricular Block).
• 
  
• For clarity — I have reproduced Figure-1 from today's case.

Figure-1: The 2 ECGs in today's case. 

Paroxysmal AtrioVentricular Block (PAVB):

As described by Bansal et al (J Arrhythmia 35:870-872, 2019) — Bosah et al (Cureus 14[7]: e27092, 2022) — and Uhm et al (Heart Rhythm Case Rep 4(5):197-199, 2018) — the entity known as PAVB is a potential cause of syncope that is easily overlooked and which is potentially lethal (probably more often than is commonly realized).

• PAVB is characterized by the sudden, unexpected onset of complete AV block with delayed ventricular escape — therefore resulting in a prolonged period without any QRS on ECG. Prior to the prolonged pause — the patient manifests 1:1 AV conduction without other evidence of AV block (which is why onset of PAVB is typically so unsuspected!).
• Because of its totally unexpected onset and propensity to result in sudden death — PAVB is difficult to document and significantly underdiagnosed.
• Three mechanisms for producing PAVB have been described: i) Vagally mediated (ie, Vagotonic Block — as described in ECG Blog #61, with the references listed at the end this Blog post citing instances of transient asystole from excessive vagal tone!); ii) Intrinsic (Phase 4 = pause- or bradycardic-dependent) PAVB; — and, iii) Idiopathic.

i) Vagotonic AV Block:

This form of PAVB is potentially benign when it results from a transient profound surge of parasympathetic tone in an otherwise healthy individual (as might occur with an episode of severe vomiting; a fit of severe coughing; vasovagal reaction from a blood draw).

• The problem with vagotonic PAVB is localized to within the AV Node.
• There will often be a "prodome" of diaphoresis, nausea, dizziness — with the patient aware of imminent fainting.
• 
  
• Characteristic ECG findings of vagotonic PAVB include progressive sinus rate slowing — often associated with an increasing PR interval and a narrow-QRS escape focus — followed by recovery with progressive return to a normal sinus rate and normal PR interval.

ii) Intrinsic PAVB:

Several names have been attached to this mechanism of PAVB — including most commonly "Phase 4 AV block" and/or PD-PAVB (Pause-Dependent Paroxysmal AtrioVentricular Block).

• PD-PAVB is the most likely mechanism for the cardiac rhythm in ECG #1 from today's case. The underlying pathology is severe His-Purkinje System disease (strongly suggested by the presence of MBBB in ECG #2 of today's case). This form of PD-PAVB is likely to be fatal unless the patient receives a permanent pacemaker.
• The interesting pathophysiology of PD-PAVB results from chance occurrence of an "appropriately-timed" PAC or PVC that partially depolarizes the diseased HPS (His-Purkinje System) at a specific point in the cycle that renders the poorly-functioning HPS unable to complete depolarization. The resultant prolonged pause in ventricular depolarization may only resolve if another "appropriately-timed" PAC or PVC occurs at the precise point needed to "reset" the HPS depolarization cycle (which presumably explains why the patient in today's case spontaneously recovered).
• Of note — although severe underlying HPS disease is evident from the MBBB seen in ECG #1 of today's case — up to 1/3 of patients with PD-PAVB do not show evidence of conduction defects on ECG, thereby complicating documentation of this diagnosis.
• 
  
• PEARL #4: In addition to seeing MBBB in ECG #2 — the fact that the atrial rate remains the same in both ECG #1 and ECG #2 is yet one more reason why the rhythm in ECG #1 does not represent simple vagotonic PAVB.

iii) Idiopathic PAVB:  

This is the most recently described form of PAVB — in which findings are not consistent with either of the other 2 forms.

• The baseline ECG before idiopathic PAVB tends to be normal.
• No "trigger" for PAVB is evident (ie, no source of excessive vagal tone — and no precipitating PACs/PVCs are seen).

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NOTE: The conduction disturbance shown in ECG #1 from today's case differs from that shown in ECG Blog #342 — in which the initial rhythm was AFib (ie, no P waves present for the first 6 beats in this tracing) — followed by a prolonged flat line pause (nearly 5 seconds in duration) — until finally a QRS complex preceded by a P wave (that may or may not have been conducting) was seen.

• Whether the prolonged flat line pause in this Blog #342 example represents another variation of PD-PAVB due to severe underlying disease of the His-Purkinje System — or reflects severe SA Node disease (ie, Sick Sinus Syndrome) — or most likely represents some combination of the two, is uncertain from the single ECG I was provided with.
• That said — the BOTTOM Line remains the same, namely that assuming nothing "fixable" is found — permanent pacing will be needed.

EXTRA-MAGNUS- Why the Sudden Shock after a Few Days of Malaise? -SSmith (9-5-2024)

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Written by Magnus Nossen - Edits by Grauer and Smith

The patient in today’s case is a woman in her 70s with a previous medical history of HTN and hyperlipidemia. She presented to an outside hospital after several days of malaise and feeling unwell. At the time of admission, her vital signs were normal. Heart rate was in the 80s. She had a very elevated troponin T at 12,335 ng/L at the time of presentation. (This is a value typical for a large subacute MI, normal value < 0-14ng/L.)  

Below is the presentation ECG.

The patient initially denied chest pain, but when questioned directly — did admit to vague "chest discomfort" in previous days. She was transferred to our facility for angiography. On arrival she was without distress. Due to acute renal failure and the duration of her symptoms over a number of days — it was decided to perform angiography the following day. Serial Troponin T values were decreasing, consistent with subacute completed MI. The ECG on admission showed sinus rhythm with a heart rate in the 80s — and was consistent with a subacute completed inferior, lateral and posterior transmural infarction, with Q waves and ST elevation in the inferiolateral leads — and ST depression in lead V2. The patient was put on telemetry while waiting for angiography the following day.

The patient awoke suddenly during the night — stating that she felt "strange". The ECG below was recorded at this time. What do you think?

This ECG is consistent with infero-postero-lateral infarction — with persistent inferior lead ST elevation and reciprocal high-lateral ST depression — ST depression in lead V2 — and some terminal T wave inversion in inferior and lateral chest leads. It is not significantly different from the admission ECG. Perhaps the most remarkable change — is the increase in heart rate, with this ECG now showing sinus tachycardia at 118/minute! Also of note is the still upright (not inverted) T waves. Persistent ST elevation with upright T waves >48 hours after myocardial infarction is associated with Post-Infarction Regional Pericarditis (PIRP).

Sinus tachycardia has many potential causes. In my experience, for the patient at rest and not anxious — it often signifies severe illness. This is especially true for the elderly patient with sinus tachycardia. The patient in today’s case suddenly became tachycardic while sleeping. The heart rate almost doubled within a minute. What might account for the sudden rate change in this patient? See if you can identify the problem in the below parasternal view of the heart.

The above video file was recorded from a subcostal «window» and it shows the heart with all four chambers. Right atrium, right ventricle, left atrium and left ventricle viewed through the liver. What is the cause of the sudden tachycardia? 

Below is a still image from the above video. The heart chambers are annotated. From the subcostal "window" the heart is viewed through the liver and thus the liver parenchyma is closest to the transducer (top of the image). Below the liver is the heart with the right atrium (RA), right ventricle (RV), left atrium (LA) and left ventricle (LV) The red arrow points to a large opening in the basal region of the interventricular septum. This is a ventricular septal rupture (VSR). As already mentioned, this patient could have post-infarction regional pericarditis from a large completed MI. PIRP is strongly associated with myocardial rupture. This patient developed a rupture of the basal portion of the interventricular septum (VSR). The VSR is what is causing the cardiogenic shock!

A Short Comment on PIRP and T Waves: 

Oliva et al found a strong association of myocardial rupture with postinfarction regional pericarditis. PIRP was associated with persistent upright T waves. He found two types of atypical T wave development in PRIP

1) Persistently positive (upright) T waves beyond 48 hours in a patient with acute MI

2) Premature change from inverted T waves to pseudonormal T waves (within 48-72 hours) 

In our case, PIRP is a likely explanation for the continued positive T waves. Since serial ECGs are not available so either of the two patterns described above could be present (only serial ECG could differentiate). 

Another possible cause of pseudonormalization of T waves mentioned many times on this blog is the pseudonormalization caused by re-occlusion of an infarct related reperfused coronary artery. This does not fit with the clinical scenario in today's case. 

Below are two more video files. These images were obtained  from the parasternal short axis which transects the left and right ventricles. The VSR is located in inferior and basal portion of the ventricular septum and is readily visible. The second video file below shows the shunt by color doppler. 

Discussion: The patient in today’s case experienced a mechanical complication secondary to completed OMI. Troponin at presentation was very significantly elevated and T waves were still upright. She had atypical symptoms which made her postpone seeking medical attention. Mechanical complications secondary to myocardial infarction are infrequent due to most patients receiving revascularization quite rapidly. The patient in today’s case developed a large basal septal ventricular septal rupture (VSR) as a complication of an untreated OMI. Auscultation of a NEW harsh holosystolic murmur lead to rapid evaluation with echocardiography that confirmed the clinical suspicion. 

A VSR will lead to sudden left to right shunt and if large enough can lead to low output left sided failure. The RV acts as a conduit and does not necessarily become acutely dilated. Left ventricular afterload reduction is essential to decrease the trans-septal pressure gradient and thus decrease shunt volume, making a larger proportion of the blood flow from the left ventricle through the aortic valve.

For the patient in today's case nitroprusside (vasodilator) infusion was started to lower systemic vascular resistance (SVR), and an intra aortic balloon pump (IABP) was placed to further decrease afterload and better the hemodynamics. Surgical repair of the VSR was eventually done. The patient needed short term dialysis post surgery, but she eventually made a full recovery.

Mechanical complications are dreaded sequela of myocardia infarctions and can  come in the form of free wall rupture, ventricular septal rupture or papillary muscle rupture. The true incidence of the three mechanical complications may differ from reported incidence due to underreporting, miscoding, or variation in the populations studied. It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. Among patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common. 

Mechanical complications occur acutely and significantly alter hemodynamics leading to compensatory mechanism which usually involve vasoconstriction and tachycardia, both hallmarks of cardiogenic shock. 

A VSR is more likely to occur in patients who are older, female, hypertensive, have chronic kidney disease, and have no prior history of smoking. It commonly occurs in the setting of a first myocardial infarction (MI) in the background of delayed or absent reperfusion therapy. Angiography usually reveals an absence of collateral circulation to the infarct zone. 

Because previous ischemia induces myocardial preconditioning, decreasing the likelihood of transmural myocardial necrosis and myocardial rupture, patients with evidence of diabetes mellitus, chronic angina or previous MI are less likely to experience a rupture. VSR may develop within 1-14 days post MI, however it’s incidence usually shows a bimodal peak which is within 24 hours and after 3-5  days post MI.

Survival after ventricular septal rupture may occur only after surgical repair. Thus, the diagnosis of ventricular septal rupture should prompt a heart team discussion of options. This discussion should take into account that, for some patients, surgery is futile as mortality approaches 100 percent. Older patients and those with poor right ventricular function often fall into this group. The timing of ventricular septal rupture repair is controversial.

Subacute AnteroSeptal STEMI, With Persistent ST elevation and Upright T-waves

Learning Points:

1. Sinus tachycardia (especially in the elderly) often signifies serious illness as it did in today’s case.
2. Mechanical complications of transmural infarction are rare and dreaded sequela and have high morbidity and mortality. 
3. Post infarction regional pericarditis (PIRP) can be suspected from the ECG and is associated with an increased risk of myocardial rupture.

Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis

Oliva PB.  Hammill SC.  Edwards WD.  Cardiac rupture: a clinically predictable complication of acute myocardial infarction

Ventricular septal rupture

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MY Comment, by KEN GRAUER, MD (9/5/2024):

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As I emphasized in My Comment in the December 6, 2022 post and the August 19, 2023 post of Dr. Smith's ECG Blog — Not all patients with acute MI report chest pain. I thought the presentation of today's case makes it worthwhile to review the data regarding this issue.

• As per Dr. Nossen — today's patient concerns an older woman with a several day history of malaise and "not feeling well". Mention of vague "chest discomfort" over a period of recent days was only elicited when specifically requestioned. By history — providers were not expecting her initial ECG to show recent completed infarction with marked Troponin elevation.

The Framingham studies from many years ago taught us that the incidence of “Silent MI” is as high as ~30% of all MIs (Kannel & Abbott: N Engl J Med 311(18):1144-1147, 1984 — Kannel: Cardiol Clin 4(4):583-591, 1986).

• The interesting part of this data is that in about half of this 30% (ie, ~15% of all patients with MI) — patients found on yearly follow-up ECGs to manifest clear evidence of infarction had NO symptoms at all — therefore truly “silent” MIs.
• But in the other half of this 30% (ie, in ~15% of all patients with MI) — although these patients found on follow-up ECG to have had infarction did not have chest pain — they did have "something else" thought to be associated with their MI.
• The most common “something else” symptom was shortness of breath. Other non-chest-pain equivalent symptoms included — abdominal pain — “flu-like” symptoms (ie, myalgias; not “feeling” good) — excessive fatigue — syncope — mental status changes (ie, as might be found in an elderly patient wandering from home).
• 
  
• BOTTOM Line: It's especially important for emergency providers to be aware of the entity of “Silent MI” — which can either be completely “silent” — or, associated with a non-chest-pain equivalent symptom. The incidence of both types of silent MI is more common than is often appreciated. Not all patients with acute (or recent) MI have chest pain with their event.

Application to Today's Case: Today's patient developed ventricular septal rupture the evening after she was admitted to the hospital. Her nonspecific symptoms that brought her to the hospital began a number of days before she finally sought medical assistance. 

• Awareness that this patient's malaise and her "not feeling well", as well as her vague chest discomfort might represent a cardiac problem — could have resulted in more timely initiation of treatment, that potentially might have averted the severe mechanical complication of her initially unrecognized extensive infarction.