Chest pain and rapid pacing followed by an unexplained wide complex tachycardia. Time for cardioversion?

Written by Willy Frick with edits by Ken Grauer

An older man with a history of non-ischemic HFrEF s/p CRT and mild coronary artery disease presented with chest pain. He said he had had three episodes of chest pain that day while urinating. The following ECG was obtained in the emergency department during active chest pain.

ECG 1 

What do you think?

There is a lot going on in this ECG. No evidence for ischemia jumps out. The confusing part here is the rhythm. The ventricular pacing spikes are easy to notice. Standard ventricular pacing occurs in the right ventricle. The electrical wavefront then spreads in sequence from the tip of the lead in the RV over to the LV, so that the left lateral wall of the LV is the last part to depolarize. Consider that this is the same sequence that occurs in a patient with LBBB -- right bundle (and right ventricle) depolarize rapidly, and then the area subtended by the left bundle is the last to depolarize. This is why standard pacing produces a LBBB morphology.

In this ECG, we see more of a RBBB morphology. Even if we had not learned from chart review that the patient had a CRT ("cardiac resynchronization therapy") device, we could have discerned this from ECG due to RBBB morphology following the pacer spikes. How does a pacemaker accomplish RBBB morphology? The most common way is by delivering a lead into the coronary sinus ostium in the RA, which wraps around the posterolateral portion of the LV. This permits LV pacing from within the venous system.

Here is a representative CXR from a different patient showing a typical CRT-D

• The blue dotted line overlies the right atrial lead

• The red dotted line overlies the RV lead. Specifically, it overlies a thicker radiopaque segment. This is the shock coil and identifies this device as a defibrillator.

• The black arrow heads point to the electrodes on the coronary sinus ("CS") lead. It is very common for these leads to have four electrodes.

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Quick aside on device terminology (feel free to skip):

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• A "single chamber" pacemaker is a device with only one lead. The most common single chamber device would be a ventricular lead only, but occasionally patients have single chamber atrial pacemakers, e.g. sick sinus syndrome with intact AV node.

• A "dual chamber" pacemaker is a device with an atrial lead and a ventricular lead. This is not the same as a biventricular device as described below.

• A "biventricular pacemaker" is a pacemaker with an RV lead and an LV lead (usually via the coronary sinus) as in the above chest X-ray.

• "Conduction system pacing" is a newer technique that is being studied as a way of delivering more physiologic pacing, typically by inserting a lead into the area of the left bundle branch, or the bundle of His.

• A "cardiac resynchronization therapy" device is one capable of delivering left ventricular pacing, either with biventricular pacing or conduction system pacing as above.

• CRT-D is cardiac resynchronization therapy with defibrillation capability, like the CXR above.

• CRT-P is cardiac resynchronization therapy with pacing only, without the ability to defibrillate.

More on CRT later in the post

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Returning to our patient:

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When I was sent this ECG, I was asked whether the last part could be VT. The ECG can be divided into two parts morphologically as shown below

The first part of the ECG (contained within the blue arrows) is morphologically consistent, as is the second part of the ECG (within the red arrows). But something happens in the middle, producing the transition. Let's begin by focusing on the first section. Here is a representative beat from that section.

The black arrow points to a native (i.e. not paced) P wave. The dotted black arrow points to a pacing spike producing a QRS. If you had no ECGs to compare to, you might suspect the P wave to be sinus in origin, but comparison to a tracing from a week prior shows this is not the case.

ECG 2

ECG 2 is clearly sinus rhythm -- Upright P wave in leads I, II, aVF with pretty typical morphology, with the typical biphasic P-wave in V1. By contrast, ECG 1 has a different morphology. Additionally, the patient had no other apparent reason to have sinus tachycardia (such as volume depletion, bleeding, fever). So the most likely rhythm in ECG 1 is ectopic atrial tachycardia.

Therefore the first part of ECG 1 shows ectopic atrial tachycardia with biventricular pacing. So, what happens later in the tracing to change this? Here is a zoomed in view of the transitional period.

Can you figure out what changed here?

Hint: Focus on the T waves!

Observe that the R2 T wave is taller than the R1 T wave, likely due to a buried P wave. The most likely explanation is that the P wave following R2 had a shorter coupling interval (i.e. was earlier than expected) and fell within the PVARP (post ventricular atrial refractory period of the pacer), hence was not sensed. Since it was not sensed, no pacing followed. But it was able to conduct natively.

There are two important points to tease out here.

Point 1:

What is PVARP? Answer: PVARP is a programmable feature in pacemakers designed to prevent pacemaker mediated tachycardia. PMT AKA endless loop tachycardia is explained in this video:

Here is a still image taken from the video for ease of reference. Test yourself by seeing if you can recite the steps in your head without looking at it.

Summary of steps in PMT (Pacemaker Mediated Tachycardia) — from the above video.

During normal dual chamber pacemaker function, ventricular events rarely conduct retrograde into the atrium. In normal dual chamber pacemaker function, most ventricular events fall into one of the two following categories:

1. Natively conducted from the atrium, through the AV node, and down into the ventricle. In this case, since the AV node just permitted antegrade conduction, it is refractory and will not permit retrograde conduction.
2. Ventricular paced due to failure of antegrade conduction in the setting of heart block. In this case, heart block is almost always bidirectional. In particular, there is retrograde block.

PVCs disrupt this by possibly occurring at a time when the AV node is recovered and therefore able to permit retrograde conduction.

The PVARP is a period of time (often around 250 ms) after a ventricular event where the pacemaker ignores all atrial activity. The idea being that atrial activity occurring shortly after ventricular activity is likely to be a retrograde P wave. By ignoring this, the pacemaker reduces the likelihood of PMT. In particular, it disrupts step 3 (and 7) in the video.

Point 2:

Why was the atrial event able to conduct natively through the AV node in the first place? You might be thinking: "Shouldn't that P wave have been blocked in the AV node? Why else does the patient have a pacemaker?" But cardiac resynchronization therapy (CRT) devices are often implanted in patients with intact antegrade AV conduction. A typical CRT patient is someone with EF 35% or less and a wide LBBB (greater than 150 ms). The device helps the patient by restoring mechanical synchrony to a diseased conducting system. Consider the following analogy:

Imagine you are in a rowboat and want to get to shore as fast as possible. Would you:

1. Row on the right, wait 10 seconds, then row on the left
2. Row on the left, wait 10 seconds, then row on the right
3. Row on both sides at the same time

Of course, the most effective way to travel is by rowing on both sides synchronously. This is what Olympic rowers do. Just like a rowboat, the left ventricle is most effective as a pump when the whole ventricle contracts synchronously. In patients with very wide LBBB (particularly > 150 ms), a lot of mechanical effort is wasted because the septum contracts first and actually starts relaxing by the time the lateral wall contracts. Pacing both sides at the same time improves mechanical synchrony of the left ventricle.

Importantly, CRT only works when it is pacing. In contrast to conventional dual chamber pacemakers where we often try to limit the amount of pacing, the goal with CRT is 100% ventricular pacing. Otherwise you are not getting the benefit of the device!

This patient has intact AV conduction. If there is a P wave in the PVARP, the pacemaker will not detect it, and therefore will not pace. But there will be native conduction. The picture below depicts the PVARP as a gray box (which in this example = 300 ms). The red arrow points to the "on time" atrial tachycardia P wave which is outside of the PVARP (hence successfully detected, and followed by a pacing spike), and the black arrow points to a premature atrial tachycardia P wave which falls within the PVARP. Since it is within the PVARP, the pacemaker ignores it. The P wave is followed by native conduction, and hence a different morphology QRS without any pacing spikes.

The natively conducted P wave has a longer PR interval. (In fact, it is quite long -- about 310 ms. This is due to a property of the AV node called "decremental conduction," where a premature stimulus conducts more slowly.) And since the underlying atrial tachycardia has a relatively constant cycle length, this translates mathematically into a shorter RP interval. The cardiac cycle duration can be expressed in the following way.

Cardiac cycle duration = PR + RP

If the cycle duration is unchanged and PR is increased, then RP must decrease. As a result, every subsequent P wave falls within the PVARP and is therefore ignored by the pacemaker and allowed to conduct natively.

The effect of the PVARP is also represented diagrammatically with the following example of another sequence from the patient's device interrogation.

• AS = atrial sensed event (e.g. a P wave)
• AR = atrial refractory event (e.g. a P wave within the PVARP)
• VP = ventricular pacing (e.g. paced QRS)
• VS = ventricular sensed event (e.g. native QRS)

The blue arrows point to what are likely sinus P waves. The red arrows point to what are likely ectopic atrial tachycardia P waves (with associated abrupt increase in rate). Notice that the pacemaker stops pacing at the onset of tachycardia due to the P waves falling within the PVARP.

BACK TO THE CASE:

The patient had serial troponin testing that was within normal limits. Due to symptoms during wide complex tachycardia, there was a question about whether the patient should undergo cardioversion.

But ectopic atrial tachycardia is most commonly an automatic arrhythmia. The cycle length variability (called "wobble") in this case also supports an automatic mechanism. Cardioversion will momentarily reset the AT, but it will likely recur immediately.

Cardioversion is most beneficial for reentrant arrhythmias (e.g. VT, atrial flutter, AVNRT, atrial fibrillation) because it terminates the reentry circuit. Atrial tachycardia can occasionally be due to reentry, but reentrant circuits usually have a more stable cycle length without so much beat to beat variability.

The patient was treated with amiodarone which suppressed his atrial tachycardia, and his symptoms resolved. It should not be surprising that his symptoms were associated with micturition, as atrial tachyarrhythmias are known to produce polyuria (Kinney et al., Kaye et al., Canepa-Anson et al.) perhaps due in part to enhanced natriuretic peptide production.

Learning points:

• Serial ECG comparison to discern sinus activity vs ectopic atrial activity

• Understand pacemaker mediated tachycardia

• Understand the purpose of PVARP

• Differences between conventional dual chamber pacemaker and CRT

Another case of Pacemaker Mediated Tachycardia:

Ventricular Fibrillation, ICD, LBBB, QRS of 210 ms, Positive Smith Modified Sgarbossa Criteria, and Pacemaker-Mediated Tachycardia

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MY Comment, by KEN GRAUER, MD (12/20/2024):

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Troubleshooting pacemaker ECGs continues to be increasingly challenging for clinicians who do not regularly encounter such tracings in their practice. Gone are the days when it was easy at a glance to determine if the device was sensing and pacing appropriately.

• It is precisely because current pacemakers are such amazingly efficient devices — that recognizing problems with the pacemaker can be so difficult.

Confession: I found today's case fascinating and insightful. I was fooled by a number of aspects in the case and base my comments on my improved understanding. My appreciation to Dr. Frick for his superb insights and discussion.

As per Dr. Frick — there is a lot going on in today's initial ECG, that I've reproduced in Figure-1: 

• Given that today's patient presented with active CP (Chest Pain) — high priority must be given to assessing for ECG signs of ischemia. But to do this — we need to separate paced beats from conducted QRS complexes.

As per Dr. Frick — this initial ECG is morphologically divided into 2 parts:

• Part 1 of this rhythm strip consists of beats #1-thru-14. As per Dr. Frick — PINK arrows in Figure-1 highlight the ectopic P waves of this patient's ectopic ATach (Atrial Tachycardia) — which manifests a rapid atrial rate of ~135/minute.
• But as shown above by Dr. Frick — since these PINK arrow P waves occur beyond the limits of the PVARP — these ectopic atrial P waves are sensed by the pacemaker — which is why each of these ectopic atrial impulses results in a paced beat.

I thought the BLUE arrow that is seen to peak the T wave of beat #14, to be a premature atrial impulse from another atrial site (ie, a PAC). 

• Although ectopic ATach may manifest some degree of P-P interval variability — there is no more than minimal (if any) P-P interval variation in the rest of the tracing in Figure-1 — which is why I thought this much-earlier-than-expected P wave to be a PAC.
• The clinical significance of the BLUE arrow P wave being a PAC — is that this PAC now "lands" within the limits of the PVARP — which means that the pacemaker does not sense this PAC — which is WHY the next QRS complex ( = beat #15) is not paced, but instead is a conducted beat (albeit with a very long PR interval).
• KEY Point: Were it not for this PAC — pacing of each ectopic atrial impulse would continue.
• It is because the underlying rhythm in ECG #1 is ectopic ATach — that after the very brief pause brought about by the PAC (ie, the BLUE arrow P wave) — ectopic ATach resumes in Part 2 of this rhythm strip, as shown by the RED arrow P waves that are evidenced by extra "peaking" of the preceding T waves.
• Note that the P-P interval between these RED arrow ectopic P waves is virtually the same as the P-P interval we saw earlier between the PINK arrow P waves. However, the PR interval preceding beats #15-thru-22 is longer than the PR interval preceding beats #1-thru-14 because these initial beats were paced (the pacer being activated soon after it sensed the PINK arrow P waves) — whereas all beats after beat #15 are conducted by the ectopic atrial P waves.

What Confused Me ...

• When I first saw today's tracing — I thought the very linear notching seen in lead II beginning with beat #15 (within the dotted RED circles) represented a pacing spike, since it closely resembles the appearance of pacer spikes seen just before the QRS for beats #1-thru-14. That said — I could not figure out why a pacer spike should occur in the middle of the QRS of beats #15-thru-22.
• This was my error. Whereas pacing spikes are well seen in all leads that show paced complexes — the only lead with conducted beats that shows the notching (which I highlight within the dotted RED circles) is lead II. No such notching is seen within the QRS of conducted beats #15 and 16 in leads V1,V2,V3 — nor for conducted beats #17-thru-22 in leads V4,V5,V6. I therefore completely agree with Dr. Frick that this notching in lead II simply reflects fragmentation of the QRS from this patient's severe underlying heart disease.

Are there Acute ST-T Wave Changes?

Now that we know the rhythm — it's much easier to assess for QRST changes. Looking at QRS morphology of all conducted complexes (ie, beats #15,16 in leads V1,V2,V3 — beats #17-thru-22 in the long lead II rhythm strip and in leads V4,V5,V6) — We can say the following: 

• The QRS of conducted beats is wide. Whether this reflects an underlying conduction defect (probable) — vs reflecting rate-related aberrant conduction (the heart rate is ~135/minute with this ATach) — is uncertain.
• There is fragmentation in lead II — and no more than the tiniest of r waves in leads II,V5,V6 — with QS complexes in the remaining leads. 
• The above findings suggest previous extensive infarction. That said — ST-T wave appearance in all of these leads with conducted beats does not suggest an ongoing acute event.
• P.S.: Search through this patient's chart for a prior non-paced ECG might prove insightful as a source for comparison with QRST morphology of conducted beats in today's tracing.

"12 Leads are Better than One" ... 

As a final illustration of optimal use of simultaneously-recorded leads — Consider QRS morphology of all 22 beats in the long lead II and long lead V5 rhythm strips.

• Both paced and conducted beats in leads II and V5 look similar, in that all beats show a virtually all negative, widened QRS complex.
• That said — it's EASY to recognize how different the QRS looks in the long lead V1, beginning with beat #15 (as well as in simultaneously-recorded leads V1,V2,V3) ==> "12 Leads are Better than One".

Figure-1: I've labeled the initial ECG in today's case.

Proposed Laddergram:

I propose the laddergram I've drawn in Figure-2 — in the hope of clarifying my understanding of events in today's initial tracing. In order to make events in the key transitional period larger — I focused on beats #12-thru-18 from lead II.

• PINK arrow P waves indicate ectopic ATach P waves. Because these P waves occur beyond the limits of the PVARP — these ectopic P waves are sensed by the pacemaker (dotted PINK lines from atria-to-ventricles) — which thereby produces ventricular paced beats #12,13,14.
• The BLUE arrow P wave occurs much earlier than expected (therefore most probably a PAC arising from elsewhere in the atria). This PAC conducts to the ventricles (albeit with a very prolonged PR interval) to produce beat #15.
• After a brief pause — the ectopic ATach resumes. But due to the shorter coupling interval of these ectopic RED arrow P waves (which places these P waves now within the PVARP) — the pacemaker is no longer able to sense these P waves. As a result, the ectopic ATach resumes with beat #16, with all ectopic atrial P waves now being conducted.

Figure-2: Laddergram of the transitional period in the long lead II rhythm strip.

Which Chest Pain patient needs a CT scan?

Which patient needs a CT Scan?

Case 1: 20-something woman with chest pain

Case 2: 50-something man with chest pain

Case 1

A 20-something yo woman presented in the middle of the night with severe crushing chest pain.  It had begun 4 hours before arrival and was initially dull, but became severe and "unbearable" 2 hours prior to arrival.  She was a walk-in at triage. She has no SOB and no prior medical history.  Her initial BP was 203/124.

She had this ECG recorded:

Obvious massive anterior STEMI

She was quickly brought to the critical care area and the cath lab was activated.

The blood pressure was 170/100 in the critical care area.

Cardiology wanted a CT of the aorta to rule out dissection, presumably partly due to the very high blood pressure readings, but also because it is hard for people to believe that a 20-something woman could have acute thrombotic coronary artery.

They also recommended a NTG drip, after which she reported complete resolution of pain.  No ECG was recorded after pain resolution.  

Here is the ECG at 25 minutes:

Terrible LAD STEMI (+) OMI

So a CT scan was done which of course showed a normal aorta.  But it also shows a massive area of total ischemia in the LAD territory:

CT shows the infarct

The CT is with contrast, which increases density (which looks more white).  Myocardium that does not have blood flow does not get the contrast, and therefore looks more dark.  

See the dark area in the septum and apex, highlighted with the white circle:

First hs troponin I returned at 256 ng/L.

 Angiogram

Door to balloon time was 120 minutes (much too long) because of time taken for a CT.

Coronary angiogram showed 100% mid LAD occlusion for which she received a DES with excellent angiographic result.  This was ruptured plaque with thrombus.  It was not SCAD (coronary dissection)

Highest troponin I was 37,000 ng/L, but it was not measured to peak.

Echo:

--Normal left ventricular cavity size, mild to moderately increased wall thickness, and moderate LV systolic dysfunction.

--The estimated left ventricular ejection fraction is 37%.  (if she does not get a lot of recovery over the ensuing weeks, that is a lot of lost myocardium)

--Regional wall motion abnormality- mid and apical anterior, apical septum, apical anterolateral, apical inferior, and apex, hypokinetic to akinetic.

Important:

It is exceedingly rare for an anterior STEMI to be due to Aortic Dissection.  And almost all of them could be detected by bedside ultrasound.

Conclusion: you may take a few moments to look for dissection with your bedside ultrasound, but when it is a clear STEMI, do NOT waste time with a CT scan.

Case 2

A 50-something y.o. male who hasn't doctored in several years presented to the emergency department by ambulance for chief complaint of chest pain.  

Here is the prehospital ECG:

There is some minimal STE in inferior leads with reciprocal STD in aVL, and also minimal STE in lead V1.  

This is very suggestive of OMI, but not diagnostic. 

Queen of Hearts: "STEMI or STEMI Equivalent detected" (that is, "OMI detected")

The Queen is not wrong very often, so maybe it is an OMI?

History

Patient complains of a 24-hours of chest pain of sudden onset, sharp in nature.  Pain started day before and it started on the left side of his face, descended down his neck, and remained mainly in his chest before radiating down his back to his left lower extremity.   It persisted through the night (for at least 18 hours), and nothing made the pain better or worse. He had never experienced a similar pain at rest or upon exertion.  He reported chest pain 9/10 at the time of evaluation. Denies SOB. Vomited 3 times overnight, not currently feeling nauseous. He denies history of HTN, HLD, DM, smoking. He does not take any medications chronically. 

Vital signs were normal.

An ED ECG was recorded:

Very Similar

Mild ST elevations in leads II, III, aVF with reciprocal changes in the lateral leads, along with ST elevation in V1 raising concern for RVMI. 

This time the Queen of Hearts interpreted: No STEMI or Equivalent. (Interesting!)

Initial hs troponin I returned at > 60,000 ng/L

Cardiology was consulted and the cardiology fellow palpated both radial pulses and found that they were very assymetric.

They recommended a CT of the aorta.

Here it is:

Type A Aortic Dissection

Why was the troponin so elevated?  And why does the ECG show subtle signs of OMI?

See here that the dissection is very close to the ostium of the RCA.  Most dissections which cause coronary ischemia are into the RCA ostium 

("ostium" = locations of takeoff of the vessel).

Going from the upper left to farther upper left is the RCA, which is open.

   The CT showed extensive type A aortic dissection which starts at the ostium of the RCA and extends all the way to the left iliac artery.  

Trop > 60,000 ng/L

Thus, at the onset of the dissection, it almost certainly occluded the RCA and led to OMI that is now reperfused.  

Thus, it was a PROXIMAL RCA occlusion (at the ostium) which resulted in right ventricular OMI (RVMI, RVOMM) with ST Elevation in V1

A dissection can break through the flap and reperfuse the true lumen

Here you can see some ischemic myocardium:

The dark areas are not perfused with contrast.  Most of it is subendocardial in the septum, apex, and even lateral wall, but mostly posterior (bottom of image)

What if the patient had cath lab activation?

That could have been troublesome.  It would delay diagnosis and treatment and perhaps not resulted in the correct diagnosis at all.

There were many clinical clues to dissection.  

The assymetric pulses mandated a CT scan.

But what if pulses were symmetric?  The strange history also mandates CT scan.

But what if you did not have either of the above?

Ultrasound

Here is one easy way to look for it when you think there is OMI but want to be certain that it is not dissection.

Bedside Ultrasound by the emergency physician of the aortic arch through the sternal notch:

The bright line in the middle of the aorta is the dissection flap. This is easy to see.

This patient had symptoms all the way to his leg, so an abdominal view is likely to show something.  Here is the abdomincal aorta transverse view:

On the left is the IVC, on the right is the aorta with a dissection flap across the middle.

Learning Points:

1. When there is a slam dunk diagnosis of OMI on the ECG, it will almost always be a waste of valuable myocardium (time because time is myocardium) to get a CT scan.

2. It is not a waste of time to use bedside ultrasound to look for dissection

3. Dissection is rare.  OMI is common.  Pretest probability is important.

4. Most Dissection that causes OMI is in the RCA

5. Only ~1% of STEMI are due to dissection

6. Only about 5% of dissection result in OMI

7. Check pulses!

8. When there is an unusual history ("started in face, went down to leg"), pay attention.  Not all chest discomfort is the same.

9. Young women have large MI and the worst thing you can be if you have OMI is to be a young woman: no one will believe that you have OMI. 

Some Literature

1.3% of STEMI are due to Aortic Dissection.

Wang J-L, Chen C-C, Wang C-YW, Hsieh M-J, Chang S-H, Lee C-H, Chen D-Y, Hsieh I-C. Acute type A aortic dissection presenting as ST-segment elevation myocardial infarction referred for primary percutaneous coronary intervention. Acta Cardiol. Sin. [Internet]. 2016;32:265–272. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4884753/   

The incidence of STEMI in the US is 100 per 100,000 per year (300,000 STEMI per year in the U.S.)

The incidence of Aortic Dissection in the US is 3 per 100,000  (maybe up to 6 per 100,000)

Yin J, Liu F, Wang J, Yuan P, Wang S, Guo W. Aortic dissection: global epidemiology. Cardiol. Plus [Internet]. 2022;7:151–161. Available from: https://journals.lww.com/cardioplus/fulltext/2022/12000/aortic_dissection__global_epidemiology.1.aspx   

5% of Aortic Dissection result in STEMI, and the majority are RCA occlusions.  When they are due to left coronary artery, the are left main, and rarely present as Anterior STEMI

Kawahito K, Adachi H, Murata S-I, Yamaguchi A, Ino T. Coronary malperfusion due to type A aortic dissection: mechanism and surgical management. Ann. Thorac. Surg. [Internet]. 2003;76:1471–6; discussion 1476. Available from: https://www.sciencedirect.com/science/article/pii/S0003497503008993   

Wang: Transthoracic echo is 85% sensitive for type A dissection.

Wang Y, Yu H, Cao Y, Wan Z. Early screening for aortic dissection with point-of-care ultrasound by emergency physicians: A prospective pilot study: A prospective pilot study. J. Ultrasound Med. [Internet]. 2020;39:1309–1315. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1002/jum.15223   

Good Review:

Loftus A, Abou-Arbid S, Marshall D, Suszanski J, Clark C. Resuscitative transesophageal echocardiography identifies aortic dissection intussusception as the cause of aVR STEMI. JEM Reports [Internet]. 2023;2:100029. Available from: https://www.sciencedirect.com/science/article/pii/S2773232023000251   

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MY Comment, by KEN GRAUER, MD (12/16/2024):

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Today's post features 2 highly insightful cases. I focus My Comment on Case #1. Dr. Smith’s discussion covers all aspects of Case #2 in fascinating fashion.

Regarding Case #1:

• It is insightful seeing how Aortic CTA (Computed Tomography Angiography) so clearly showed this patient's infarction — thereby confirming the diagnosis of acute MI prior to cardiac catheterization (even though the primary reason for aortic CTA was to rule out aortic dissection).
• It is humbling to realize that bedside Echo revealed normal LV function — whereas formal Echo showed significantly reduced ejection fraction with multiple regional wall motion abnormalities. The accuracy of bedside Echo is clearly a function of operator skill and experience — and at times it may be difficult to exclude the possibility of WMA (Wall Motion Abnormality) from bedside Echo alone.
• The clinical presentation of the patient in Case #1 qualifies as a hypertensive emergency (with the difference between HT "urgency" vs "emergency" being whether or not there is acute end-organ damage — which clearly was present given the large acute infarction).
• Sublingual NTG (nitroglycerin) X3 was no more than minimally effective in relieving this patient's CP (Chest Pain). As a result — IV NTG was started, with complete resolution of the patient's CP (and presumably significant improvement in her marked hypertension)! This raises the question as to how much this patient's hypertensive emergency contributed to her ongoing severe CP prior to initiation of IV NTG — vs — how much her acute MI contributed to her ongoing severe hypertension? (See below).
• And — this patient's initial ECG (that I've reproduced and labeled in Figure-1) shows some interesting findings (See below).

Hypertensive Urgency/Emergency and CP in the ED:

Although accurate data is hard to come by — true hypertensive emergency is rare (most probably well under 1% of ED visits).  

• As noted above — the presence of acute target organ damage in today's case (ie, acute MI) in association with marked sustained hypertension (this patient's BP at times exceeding 200 mm Hg systolic and >110 mm Hg diastolic) — qualifies her as a true hypertensive emergency (Janke et al — JAHA 5(12); 2016 — and — Cardiology Advisor — Feb. 29, 2024). Fortunately — today's patient rapidly responded to initiation of IV NTG.
• It is not always appreciated that chest pain is one of the most common associated symptoms of hypertensive crisis presenting to the ED (occurring in more than half of the patients with HT urgency — and in an even greater percentage of those with HT emergency in the study by Salkic et al — Mater Sociomed 26(1):12-16, 2014).
• PEARL: Case #1 in today’s post provides superb illustration of the synergistic effect that IV NTG may have in the patient who presents with severe CP in association with the combination of hypertensive emergency and acute MI.

Figure-1: I've labeled the initial ECG in Case #1.

The Initial ECG in Case #1:

The ECG in Figure-1 — shows sinus tachycardia at ~110/minute with markedly increased QRS amplitude and marked chest lead ST elevation.

• We have often made the point in Dr. Smith's ECG Blog that in general — it is not common to see tachycardia with an uncomplicated MI. As a result — the finding of sinus tachycardia in today's case should immediately suggest that something else might also be going on (which in today's case was this patient's severe CP and her hypertensive emergency).

QRS voltage is markedly increased in ECG #1 (with an S wave in lead V3 of 36 mm — as shown by the QRST complex outlined in RED in Figure-1). This extremely deep S wave is consistent with this patient's severe hypertension and increasd LV wall thickness on formal Echo.

• This degree of increased S wave amplitude made me initially stop to consider proportionality of the amount of chest lead ST elevation relative to the increase in chest lead voltage.
• Double RED arrows in leads V3,V4,V5 highlight what I considered the point of inflection defining the J-point for determining the amount of ST elevation. Even in lead V3 (in which the S wave attains a depth of 36 mm) — the 8 mm of J-point ST elevation is inappropriately increased, and indicative of acute MI in this patient with severe new CP.
• S wave depth is much less in neighboring leads V4 and V5 — which clearly show disproportionate J-point ST elevation (of 12 mm and 9 mm in lead V4 and lead V5, respectively) — compared to more modest S wave depth in these leads (ie, of 20 mm and 11 mm). As per Dr. Smith — the overall ECG picture in Figure-1 indicates an anterior STEMI in progress in this patient with acute hypertensive emergency.
• While difficult to know what to make of inferior lead ST-T wave appearance — the inappropriate T wave inversion in lead aVL adds further support to the diagnosis of an ongoing STEMI.