A woman in her 60s with syncope and vomiting. Does she need a pacemaker?

 Written by Pendell Meyers with some edits by Steve Smith

A woman in her 60s on chemotherapy presented to the Emergency Department for a syncopal episode just prior to arrival. She was walking to the bathroom when she suddenly felt nauseous and passed out. EMS was called by the patient's daughter, and en route to the ED she vomited twice. On arrival to the ED, she adamantly denies chest pain but says she's "just still not feeling well." She had no prior known cardiac disease.

Triage at 0755:

The rhythm is most either atrial fibrillation with complete heart block and resulting junctional escape, or atrial flutter with very high degree (but constant) block. Remember, atrial fibrillation cannot result in regular ventricular rhythm if it is conducted through the AV node.

The QRS has narrow normal morphology. There is almost 1 mm STE in III, but no STE at all in II or aVF. The T wave in III is hyperacute, and is biphasic up-down. Leads aVL and I show reciprocal findings (STD and TWI biphasic down-up). Through the baseline wander, you can see the impression of downsloping STD in V2 indicating posterior extension. Interestingly, V3 then appears to have a hyperacute biphasic down-up T wave, with hyperacute Ts in V3 and V4, but then V5 and V6 do not.  All the biphasic T-waves suggest that there is some early spontaneous reperfusion happening.

Overall, it is diagnostic of inferoposterior OMI, likely RCA occlusion, likely also explaining the acute bradydysrhythmia.

The rhythm was noticed as pathologic, but none of the ischemic findings discussed above were initially noticed. It seems as though the providers felt that the problem was a primary bradydysrhythmia.

Initial troponin returned at 520 ng/L, and another ECG is recorded at that time (0900):

Findings are very similar to the first ECG. There is ongoing active transmural (full thickness) infarction. Still no STEMI criteria.

Anther ECG was done at 1000 (reason unknown):

This ECG shows some interval reperfusion compared to the prior ones, including slight deflation of the hyperacute T waves and terminal T wave inversion in III, and the opposite in V2.

At this point the patient was persistently hypotensive and bradycardic requiring epinephrine drip to maintain heart rate above 50 bpm. She was described as uncomfortable and short of breath. She continued to deny chest pain. 

The ED team consulted cardiology for symptomatic bradycardia, asking whether the patient should go for an emergent pacemaker. The cardiology team evaluated the patient, reviewed all the ECGs above, and apparently found no concern for ischemia and agreed that the primary problem was just the bradydysrhythmia.

They were in the process of consenting the patient for a pacemaker when I contacted the ED provider in real time (I happened to be actively reading ECGs for the department from home at that time). I explained my concern for RCA occlusion as the cause of her OMI findings on ECG, and as the cause for her bradydysrhythmia (because the RCA almost always supplies the AV node).

The ED team performed a bedside echo which showed an inferior wall motion abnormality.

The repeat troponin I was 595 ng/L.

Another ECG was performed at 1055:

The end of the T wave in III is difficult to see through the atrial waves. There are some features of reperfusion, but also some leads that seem to show ongoing ischemia.

I was told the patient was still persistently symptomatic despite some features of reperfusion on ECG. She still required epinephrine and norepinephrine drip and was short of breath.

The ED provider was  able to convince the skeptical cardiologist to perform an angiogram before placing a pacemaker. 

The angiogram showed an acute thrombotic proximal RCA occlusion (TIMI 0 flow). After PCI, there was 0% residual stenosis with TIMI 3 flow.  

Comment: TIMI-0 flow does not rule out some degree of microvascular reperfusion; collateral flow may account for the minimal ECG features of reperfusion.  In fact, in Wellens' studies which established Wellens' syndrome, in all cases there was perfusion, but 20% of these cases were in spite of an occluded artery, but through collateral circulation.) This is precisely the reason why we conceptually define OMI as: "Acute coronary occlusion or near-occlusion with insufficient collateral circulation, resulting in imminent full-thickness myocardial infarction."

The first ECG after cath was performed hours later, in the cardiac ICU:

Sinus rhythm with PACs. There is resolution of the STE and hyperacute T waves, as well as terminal T wave inversion in III. This confirms reperfusion. Not to mention the dramatic improvement in AV node function.

The ICU staff noted that, after PCI, her heart rate rapidly improved and she never required even a temporary pacemaker. Her epinephrine and norepinephrine requirement resolved within hours of PCI. 

In fact, within 24 hours the patient required metoprolol and amiodarone for rate control of intermittent atrial fibrillation with rapid ventricular response:

Later she was back in sinus rhythm:

She had several minor complications unrelated to ACS during her stay, but was ultimately discharged on day 5.

Learning Points:

The most important, deadly, reversible causes of bradycardia include acute RCA occlusion (OMI), hyperkalemia, and toxicity from beta blockers, calcium channel blockers, or digoxin. We in the ED must be the experts at recognizing these conditions on the ECG. 

If this patient had instead received a pacemaker rather than RCA reperfusion, her ECG would have shown a ventricular paced rhythm. Providers who cannot recognize OMI in normal QRS conduction may be even less likely to recognize it in ventricular paced rhythm, although we have shown that it can be reliably done with proper training: 

New Review: Diagnosis of Occlusion Myocardial Infarction in Patients with Left Bundle Branch Block and Paced Rhythms

Until we get AI that can learn ECG patterns, we might need human ECG experts to act like radiologists, so that EM physicians and cardiologists can have access to expert interpretation.

You must learn to recognize hyperacute T waves. 

This patient is STEMI(-) OMI that clearly benefits from emergent reperfusion.

A 50s year old man with lightheadedness and bradycardia

 Written by Pendell Meyers with edits by Smith and Grauer

A man in his 50s with history of end stage renal disease on dialysis, prior bradycardia episode requiring transvenous pacemaker, diabetes, and hypertension, presented to the ED for evaluation of acute onset dizziness and lightheadedness starting several hours prior to arrival. These symptoms prevented him from going to dialysis, and his last session was three days ago. EMS found him with a heart rate of 30 bpm but normal blood pressure. He received 0.5 mg atropine with increased in heart rate to the 60s with improvement in symptoms. He denied chest pain or shortness of breath. 

Here is his triage ECG at 1533:

There is a regularly irregular rhythm with RBBB and possibly also LAFB morphology. The T waves are definitively peaked in many leads. The rhythm is possibly junctional with pauses or block, I'm not exactly sure. I asked Ken Grauer for help with this rhythm and he agrees it cannot be atrial fibrillation due to the irregular regularity, but with the artifact present also cannot definitively find atrial activity. His bottom line: "This rhythm is not 'following the rules' - so either hyperkalemia - or some other toxicity - or very severe and diffuse conduction system disease producing junctional escape with bifascicular block with some complex form of exit block." See his full comments reproduced at the end of the post. 

This ECG is diagnostic of significant hyperkalemia.

He was immediately given 2gm calcium gluconate, insulin and dextrose. Shortly after those therapies his heart rate is documented as improved to the 70s.

Initial labs showed a potassium level of 7.7 mEq/L.

Repeat ECG at 1801:

Improved heart rate and narrower QRS.

He later received a second dose of 2 gm calcium gluconate for down-trending heart rate.

He was emergently dialyzed and did well.

No more ECGs were recorded from this visit, unfortunately.

Approximately 1 year prior to this event, he had a similar event and presented with this ECG:

Junctional escape with similar RBBB and LAFB morphology, and peaked T waves. Notice the flat ST segments and narrow base of the T waves. This ECG was apparently not recognized as hyperkalemia (!). In my experience, these are some of the most commonly missed and dangerous hyperkalemia ECGs because many practitioners rely heavily on strikingly peaked T waves to start considering hyperkalemia on ECG. These T waves are in fact peaked, but they are more subtle than the textbook hyperkalemia ECG.

During this visit, the patient received transcutaneous pacing and an emergent transvenous pacemaker before the labs showed a potassium level of 7.3 mEq/L!

After treating his hyperkalemia, the pacemaker was successfully discontinued. He never received a permanent pacemaker.

After dialysis during that visit, a repeat ECG was recorded showing resolution of the RBBB/LAFB:

Notice the marked difference in the T-waves

Learning Points:

In medical school, I worry that the only consistent teaching you get about hyperkalemic ECG findings is peaked T waves and QRS widening. What should be taught includes the "Killer B's of Hyperkalemia": Broad (QRS widening), Brady (bradycardias), Blocks (AV blocks, bundle branch blocks), and Bizarre (bizarre morphology, OMI mimics, etc.). Some of the most important hyperkalemia ECGs are like the above: QRS widening that can be subtle or falsely blamed on RBBB alone, and T waves that are not perceived as classically peaked. Yet this ECG above is far more dangerous and far more hyperkalemic than the classic hyperkalemia ECG with only peaked T waves in the textbook.

Before you consider pacing a patient, consider hyperkalemia. I would go so far as to say that every patient about to be paced should receive calcium, unless there is certainty of a non-hyperkalemia diagnosis as the cause.

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Ken Grauer's comments on the rhythm in the first ECG of this case (he was completely blinded to all case details, just the ECG):

This is tough — and I do NOT have a definite answer. I labeled the tracing (Figure-1):

Figure-1: The 1st tracing in today's case.

Artifact makes it difficult to assess for the presence of atrial activity. I thought BLUE arrows might represent retrograde P waves (as their placement seems pretty consistent) — but there is a lot of “noise” in the baseline — so I’m not sure if this really represents retrograde atrial activity or not …

What we DO know — is that the QRS is wide, and NO P wave precedes any QRS. We also know (as per Pendell) — that this isn’t AFib, because there is a definite pattern ( = a “regular regularity” to the rhythm) — with both the short intervals (between #1-2; 4-5; 6-7) all equal — and the long intervals (between #2-3; 5-6; 7-8) also all equal.

My #1,2,3 questions are what is the serum K+ level? We have a wide QRS and T waves really are peaked in multiple leads (even though the base of these T waves isn’t as narrow as is usually seen with hyper-K+) — but Hyperkalemia is notorious for QRS widening, brady rhythms and ALL SORTS of conduction disorders that do not “obey the rules” …

So if K+ is normal — then we really have an RBBB/LAHB configuration without sinus P waves — so suggesting perhaps origin of a ventricular rhythm near the left anterior hemifascicle — vs junctional escape with bifascicular block … (the surprisingly narrow initial part of the QRS suggests origin not directly from ventricular myocardium).

What is unusual for a simple block (or “exit block”) — is that the duration of the pauses. You can have an ectopic ventricular focus (even VTach) with various degrees of “exit block” out of the ventricular focus — but against the usual form of exit block is the fact that the long intervals (between #2-3; 5-6; 7-8) is clearly MORE than twice the shortest interval …

Of note — the R-R interval between beats #3-4 is LONGER than that between #4-5. I do not think this is for chance — and this is what you tend to see with Wenckebach phenomenon — but unlike typical Wenckebach phenomena is the overly long pauses (more than twice the shortest R-R interval). NOTE — You CAN have a ventricular rhythm (including VTach) with a Wenckebach-type of exit block … 

BOTTOM LINE: This rhythm is not “following the rules” — so either hyperkalemia — or some other toxicity — or very severe and diffuse conduction system disease producing junctional escape with bifascicular block (vs ventricular escape near the anterior hemifascicle) with some complex form of exit block …

Hope the above is helpful. Let me know if you find out more clinically about the patient — :) Ken

==============================

Here are a couple other cases of hyperkalemia with small, but peaked, T-waves:

Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer. (Physician also reads it as normal)

This is on a previous visit with K = 6.6:

After treatment: 

ST Elevation in I and aVL, with reciprocal ST depression in lead III

"It isn't a STEMI," so cath lab refusal (again). Were they right?

Sent by Anonymous, written by Pendell Meyers

An elderly female called EMS for acute epigastric pain. EMS arrived and recorded this ECG on the way to the hospital:

This case was sent to me with only the details above, and my response was: 

"It's posterolateral (and probably also inferior) OMI until proven otherwise. I'd also give a little calcium because it's slow, wide, and a couple leads have almost pointy Ts. But I don't really think it's hyperK. This one is OMI. Either LCX or RCA, or perhaps an Obtuse Marginal that supplies those regions."

Interpretation: There is an absence of sinus activity, including an absence of retrograde P waves. The rhythm is probably a junctional escape at a rate of approximately 45, with RBBB and likely also LAFB (given the leftward axis despite RBBB). Alternatively, it could be a posterior fascicular escape. There is STD in V2-V5 that is maximal in V2 and V3. This STD is excessively discordant in V2, and concordant in V3. The inferior leads show Q waves with STE in lead III, and there is some slight reciprocal STD in I and aVL. Interestingly, many of the T waves have a slightly peaked appearance. Along with bradycardia and conduction block, this would be alarming for potential hyperkalemia, which of course can also cause OMI mimics. We have shown several cases on this blog that appear to have both OMI and severe hyperkalemia.

Additionally, both 1) no spontaneous sinus activity (sinus arrest or extreme sinus brady) and 2) no retrograde activity, which implies AV block as well

Cardiology was summoned immediately to bedside but they thought that this ECG "isn't a STEMI" and refused to take the patient to the lab. 

The initial troponin T returned highly elevated at 4.04 ng/mL. The potassium was 4.1 mEq/L. Cardiology was recalled to bedside to reevaluate.

Smith comment: When Pendell texted this to me, I thought it was both hyperkalemia and inferior posterior OMI.  V4 and V5 especially have the appearance of hyperK.  This just goes to show that there are always false positives and false negatives.

Another ECG was recorded:

These are almost certainly posterior leads, though they were not labelled as such (V4-V6 are really V7-V9 on the posterior thorax). 
How do we know? We can tell this because of the very low QRS amplitude and the Q-waves.  The slight ST elevation is diagnostic of posterior STEMI, which in posterior leads only requires 0.5 mm in just one lead to meet "criteria."

There are possible atrial waves but it is not definitive with this low quality ECG. If the possible atrial waves are real, it could be sinus bradycardia with 2:1 AV block. Otherwise, this would be complete heart block with junctional escape. The rate is approximately 30 bpm. Apparently the patient was mentating and had a normal blood pressure with this, and did not require pacing at that moment.

We do not recommend posterior leads in this situation because they are unnecessary (the initial ECG is diagnostic of posterior MI) but they might be falsely negative and dissuade you from your diagnosis. 

Why are posterior leads falsely negative?  2 reasons: 

1) they are often recorded at a later time, after the artery has reperfused.  It is easy to recognize this if you are aware: V1-V3 will still be recorded and visible, and the STD in these leads will be gone.

2) the voltage of posterior leads may be very small because the signal needs to traverse the lungs.

Outcome

The patient was taken to cath where a 100% (TIMI 0) LCX occlusion was found and stented. No further troponins were ordered.

The patient survived so far.

Learning Points:

RBBB should have a small, proportional amount of appropriately discordant STD and T wave inversion in leads with large R' wave (usually just V1 and V2). At some point, STD in these leads becomes out of proportion. This case is an excellent example of excessively discordant STD in RBBB, maximal in V2-V4, which signifies posterior OMI in RBBB.

Make sure to keep hyperkalemia on the differential for any sick patient with bradycardia, wide QRS, AV blocks, and bizarre morphology. It would have been an excellent choice to give this patient IV calcium on arrival to see if the ECG responded, while also treating for OMI simultaneously.

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MY Comment by KEN GRAUER, MD (9/28/2020):

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Superb interpretation of the presenting ECG in this case by Dr. Meyers!

• As per Dr. Meyers — the combination of QRS widening + bradycardia + lack of sinus P waves should immediately suggest the possibility of Hyperkalemia — especially since T waves in no less than 8/12 leads (ie, in leads I,II,aVL,aVF; and in V3-thru-V6) in the initial ECG look more-peaked-than-they-normally-should-be. For this reason — Dr. Meyers appropriately suggests that empiric Calcium would be a reasonable option in this circumstance, even before knowing the serum K+ level.
• NOTE — I would bet that No One who regularly follows Dr. Smith’s ECG Blog has trouble recognizing hyperkalemia when all of the typical findings are present. That said, many of our patients simply “don’t read the textbook” — and recognition of hyperkalemia becomes much more challenging when T wave peaking isn’t obvious (ie, when T waves aren’t so pointed with such a narrow base — or, when other abnormalities such as RBBB are present). For this reason — I thought it worthwhile to review some less appreciated ways in which hyperkalemia may present.

Regarding HyperKalemia & Brady Rhythms: We have previously discussed on numerous occasions in Dr. Smith’s ECG Blog, the multiple ECG manifestations of various degrees of HyperKalemia. Among these:

• Review of sequential ECG changes of Hyperkalemia — in My Comment at the bottom of the January 26, 2020 post.
• And, relevant to the bradycardia and lack of P waves in today’s tracing — My review of the mechanism for the various ECG changes (My Comment in the July 3, 2020 post) — which I restate here: The characteristic T wave peaking of hyperkalemia is seen early in the process — due to an acceleration by elevated K+ levels of terminal repolarization. With more severe K+ elevation — there is depression of conduction between adjacent cardiac cells, eventually with depression of SA and AV nodal conduction. This may result in a series of conduction defects, including PR and QRS interval prolongation — frontal plane axis shift — fascicular and/or bundle branch block (including interventricular conduction defects) — and/or AV block with escape beats and rhythms. Ultimately, QRS widening may lead to a sine-wave appearance (fusion of the widened QRS with the ST-T wave — such that distinction between the two is no longer possible). If this severe hyperkalemia remains untreated — VT, VFib or asystole are likely to result as the terminal event.
• As serum K+ increases — P wave amplitude decreases. Ultimately, P waves may disappear. This is because atrial myocytes are exquisitely sensitive to the extracellular effects of hyperkalemia (much more so than the SA node, AV node, the His, and ventricles). As a result — despite lack of atrial contraction (ie, loss of P waves on ECG) — there may still be transmission of the electrical signal from the SA node over the conduction system and to the ventricles. Thus, rather than a junctional rhythm or fascicular escape rhythm — a bradycardic rhythm without visible P waves in severe hyperkalemia may be a Sino-Ventricular Rhythm (in which despite lack of P waves on ECG — the rhythm IS still initiated in the SA node, with electrical transmission through to the ventricles). But because P waves disappear and the QRS is often wide with a hyperkalemic sino-ventricular rhythm — it is EASY to mistake this rhythm as either AIVR (Accelerated IdioVentricular Rhythm) or VT.
• BOTTOM Line: The bradycardia, altered P wave activity and the different forms of widened QRS morphologies may make for multiple potential ECG manifestations when there is severe hyperkalemia. The only way to prevent overlooking the diagnosis in some of these patients — is to always consider the possibility of HyperKalemia whenever presented with a tracing such as the one that was seen in today’s case.

— BUT — Serum K+ in this case turned out to be normal! Therefore — the ST-T wave appearance in today’s case is not the result of hyperkalemia.

QUESTION: If I were to show you the ECG that appears in Figure-1 — Would you have any doubt that this is an acute STEMI?

• HINT: The answer is “No”.

Figure-1: How would YOU interpret this tracing?

MY Thoughts on ECG #1: In the context of the obvious acute STEMI-like ST elevation in leads V1, V2 and V3 of Figure-1 — supportive ECG findings that we see in other leads should become unmistakably obvious:

• There is definite ST elevation in lead III — with reciprocal ST depression in high lateral leads I and aVL. These high lateral leads also manifest suspicious-looking terminal T wave positivity of surprisingly high amplitude.
• The T wave in lead II is obviously hyperacute (much more “voluminous” than-it-should-be, given modest depth of the S wave in this lead).
• In this context — the T wave in lead aVF is probably also hyperacute (given small depth of the S in this lead).
• All 3 of the lateral chest leads (leads V4,5,6) manifest clearly hyperacute T waves given modest QRS amplitude of the complexes in each of these leads. In addition, ST segments leading up to these hyperacute T waves are abnormal (depressed in V4; straightened in V5; and straightened with a rising takeoff in V6).

COMMENT: Despite the above described obvious abnormalities in 11/12 leads (actually in all 12 leads if you count the ST elevation in aVR) — in this elderly patient with new-onset potential chest pain “equivalent”symptoms — this case presents yet one more instance of the cardiology team stating, “Not a STEMI — therefore NO indication for acute cath.” I have to admit that I just do not understand this refusal ... (We’ve published many similar examples of this type of oversight — the most recent of which in our September 21, 2020 post).

CONFESSION: The 12-lead tracing I show above in Figure-1 was altered by me. I simply inverted the 3 leads within the RED rectangle (to project the mirror-image of leads V1, V2 and V3).

• I show the actual initial ECG in today's case in Figure-2 — to which I’ve added the inverted (mirror-image) view of leads V1, V2 and V3 to the right of ECG #1.
• As I’ve described in many prior posts on Dr. Smith's ECG Blog (See especially My Comment from Sept. 21, 2020) — the Mirror Test is no more than a simple visual aid that inverts anterior leads, thereby facilitating recognition of the shape of an acute posterior MI. It is based on the principle that the mirror-image of anterior leads provides insight into the appearance of ongoing electrical activity in the posterior wall. With a little practice — you’ll find posterior leads are rarely (if ever) needed — because use of the Mirror-Test allows instant recognition of virtually all cases when there is acute posterior MI.
• NOTE: Regardless of whether you call the ST-T wave appearance in the anterior leads of ECG #1 (in Figure-2) a “STEMI-equivalent” (since technically there isn’t ST “elevation” ) or simply an OMI — this pattern in a patient with new symptoms reliably identifies acute Occlusion-based MI.
• Final POINTS: The shape of the ST-T waves in leads V2 and V3 of ECG #1 in Figure-2 is clearly abnormal! Note how much J-point ST depression there is for the ST segment in lead V2. This is not seen with simple RBBB. The 2 mm of J-point ST depression with shelf-like straightening of the ST segment in lead V3 is also not a “normal accompaniment” of simple RBBB. Some ST-T wave depression is expected with uncomplicated RBBB — but generally this should be maximal in lead V1 (and not increasing as we move laterally toward leads V2, V3, as we see in Figure-2).

Figure-2: The initial ECG in this case, with the mirror-image of leads V1, V2 and V3 placed to right of ECG #1 (See text).

What do you think of this elderly man with "possible seizure"?

Written by Pendell Meyers

(with really great and thorough explanation of this finding by Ken Grauer).

At my hospital, patients with any symptoms which could be vaguely interpreted as a possible stroke during the triage process are brought to the high acuity area and a provider is asked to do a "neuro check", which involves a quick H and P and exam to determine if we should activate our stroke protocol.

A man in his 70s was brought to me for a neuro check, and the triage providers commented that they were worried about a possible seizure as well. The patient was alert and oriented with normal vitals at triage. He stated that the last thing he remembers was sitting at his desk working on some paperwork, then he remembers being on the ground looking up at paramedics. His wife heard a noise and found him on the floor next to his desk. He could not recall feeling anything unusual prior to the event, was in good health earlier that day, and felt completely normal at the time of my evaluation with no complaints. Of note, he had an identical episode last week for which he did not seek medical attention.

So I asked for an ECG as syncope was high in the differential.

Here is his initial ECG:

What do you think?

Interpretation: Sinus rhythm with extreme 1st degree AV block (PR interval roughly 500 msec!)

There is a narrow, regular QRS which could arguably meet morphology criteria for LAFB. The ST segments and T-waves are normal, but they are followed immediately by another wave that at first may be confused in some leads (especially in lead II rhythm strip) for a U-wave. However, looking in all 12 leads reveals that this wave has textbook P-wave morphology (biphasic up-down in V1, upright in II). In addition, there is no other wave which could be a P-wave, therefore if it were a U-wave then the rhythm would have to be junctional (the computer mistakenly thought this was junctional rhythm by the way). The width of the P-wave and the "second bump" of the P-wave in lead II may suggest atrial enlargement, but this is not particularly relevant clinically in this case.


Assuming there are no extra P-waves hidden inside the QRS complexes (I don't see any), then there is a 1:1 relationship of P-waves to QRS complexes. There are no dropped beats, and the PR interval is not prolonging. This pattern has two possible etiologies:

1) Sinus rhythm with 1st degree AV block
2) Sinus rhythm with complete 3rd degree AV block, with a junctional rhythm that exactly matches the rate of the SA node (the two rhythms are dissociated due to the complete AV block, and the result is called "isorhythmic dissociation")

It is extremely unlikely that two separate, dissociated rhythms are at EXACTLY the same rate, and thus #1 is far more likely than #2. As this pattern persists for more and more time, the chances of isorhythmic dissociation (#2) approach zero.

So to be sure, I stood by the bedside and watched the cardiac monitor carefully for a few minutes. There was never a single dropped beat, and the PR interval never changed.

The diagnosis is sinus rhythm with 1st degree AV block, with extremely long PR interval.

All ECGs with bradycardia and/or heart block should be considered for hyperkalemia and inferior OMI (because the RCA supplies the SA and AV nodes) as a cause, but this ECG shows no evidence of these etiologies.





So what is the cause of the patient's event?


The most likely explanation is that he had transient 2nd or 3rd degree heart block resulting in bradycardia and decreased cardiac output leading to syncope. Between these episodes his ECG shows only first degree heart block as a clue of what happened.

We carefully reviewed his medications and found no beta blockers, calcium channel blockers, digoxin, or any other medications which could cause or contribute to bradycardia. We kept him on the cardiac monitor with pacer pads just in case, but never had to use them. His potassium returned normal, and his troponin negative. He had no further syncopal events. He was admitted to cardiology.

He received a pacemaker and is doing well so far.


Learning Points:

Any time seizure or syncope is on the differential, the other one is also on the differential.

1st degree AV block is defined as PR interval greater than 200 msec. Most cases are between 200-300 msec, with 500 msec (as in this case) being extraordinarily long.

Although 1st degree AV block is often inconsequential in the ED, it should be taken seriously when the patient has symptoms compatible with intermittent higher grade AV blockade. I am not aware of specific PR cutoffs that indicate especially high risk in asymptomatic patients.

Use all 12 leads to see more examples and morphologies of a wave to distinguish whether it is a P-wave with 1st degree AVB versus a U-wave.

Make sure to look for an extra set of P-waves hidden within the QRS complex.

When the P to QRS ratio is 1:1, isorhythmic dissociation is an unlikely possibility which becomes less and less likely as time goes on.

1st degree AV block is usually thought to be inconsequential, however in some cases it is an indicator of serious AV node disease and an indicator of intermittent higher-grade AV block.

In the emergency department, the most important etiologies of bradycardia and AV block are remembered by the mnemonic "DIE": Drugs (CCBs, BBs, digoxin, etc), Ischemia (usually of the RCA which supplies the SA and AV nodes), and Electrolytes (hyperkalemia).

Detailed ECG interpretation is vital in syncope. I personally use and teach the WOBBLER mnemonic.

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MY Comment by KEN GRAUER, MD (5/24/2020):

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Interesting case presented by Dr. Meyers! The patient was a man in his 70s, who presented to the ED with possible syncope and an abnormal ECG. The following QUESTIONS were raised during Dr. Meyers’ discussion:

• HOW CAN WE TELL if the small upright deflection that we see after the T wave, and near the middle of each R-R interval is a P wave or a U wave?
• In ECG #1 — HOW can we rule out the possibility of complete (ie, 3rd-degree) AV block?
• Could there be “isorhythmic AV dissociation?” — in which atrial and AV nodal pacemakers manifest a nearly identical heart rate?
• Is the rhythm regular?
• HOW can calipers help you to rapidly answer the questions in the 4 bullets above this?

Exploration of this case also poses the following Clinical QUESTIONS:

• What is the clinical significance of 1st-degree AV block?
• How long can the PR interval be, and still conduct?
• Does 1st-degree AV block become more “dangerous” once the PR interval becomes “very” long? IF so — WHY?

My Comment below is aimed at providing another perspective at answering the above questions.

• For clarity — I’ve reproduced the initial ECG in this case in Figure-1:

Figure-1: The initial ECG in this case (See text).

MY THOUGHTS: Did YOU think that the rhythm in ECG #1 was regular? Although easy to assume from rapid inspection that the rhythm in ECG #1 is regular — it is not regular!

• Using calipers will tell you within seconds that the rhythm in ECG #1 is not regular (Figure-2).

Figure-2: I’ve numbered the beats in ECG #1 — and, have added RED arrows to highlight each of the P waves. I fully acknowledge that there is some variability in P wave morphology in the long lead II (especially those P waves highlighted by PURPLE arrows) — but judging from P wave appearance in the simultaneously-recorded long lead V1, and in the 12-lead tracing above the 2 rhythm strips (PINK arrows in Figure-2) — I believe each of the RED and PURPLE arrows in the long lead II truly indicates a sinus P wave (Sometimes, for whatever reason — you just see some variation in sinus P wave morphology). Finally — I’ve added the duration of each of the R-R interval in milliseconds. From these numbers — it is obvious that the R-R interval in ECG #1 is not regular (See text).

HOW to Distinguish P waves from U waves?

On occasion — it can be difficult to distinguish P waves from U waves. The KEY for making this distinction — is to determine IF the deflection in question is related to what comes before it (ie, to the QRS complex and T wave to the left of the deflection in question) — or, to what comes after it (ie, to the next QRS complex, that lies to the right of the deflection in question)?

• Using calipers — I carefully measured the PR interval before each beat in Figure-3.
• NOTE that the PR interval before each beat in Figure-3 remains constant ( = 460 msec). The fact that despite a changing R-R interval — the PR interval in Figure-3 remains constant, means that each of these P waves is conducting (albeit with marked 1st-degree AV block).

Figure-3: Note that the PR interval remains constant at 460 msec throughout the long lead rhythm strips — despite the change in R-R intervals. This tells us that each of the P waves in Figure-3 are conducting, albeit with a markedly prolonged PR interval (See text).

In contrast — the RP interval does not remain constant — as shown by the different RP interval durations that appear in PURPLE numbers in Figure-4.

• This means that each of the deflections under the RED arrows in Figure-4 must be related to the QRS complex ahead of it — and not to the QRS complex and T wave that came before ...
• This confirms that the deflections under the RED arrows in Figure-4 are P waves. IF they were U waves — then the R-"U" interval would be constant.

Figure-4: I’ve added in PURPLE numbers the RP interval in milliseconds. The fact that the RP interval continually varies (ie, from 340 msec — up to 470 msec) proves that the deflections under the RED arrows can not be U waves! (See text).

Why We Know the Rhythm in ECG #1 is Not 2nd- or 3rd-Degree AV Block?

We have established that each of the P waves in ECG #1 are conducting with an extremely prolonged PR interval (of 460 msec). But HOW can we rule out the possibility of some higher degree of AV block?

• PEARL #1 — Dr. Meyers showed us this “Pearl” — which is simply to observe the monitor for a period of time — until it becomes clear IF the rhythm is changing (ie, in this case — whether the relationship between each P wave and the next QRS complex to follow it, maintains the same PR interval of 460 msec).
• As per Dr. Meyers — it would be exceedingly unlikely for there to be isorhythmic AV dissociation without apparent change in the PR interval, for so many beats from simultaneously firing AV nodal and SA nodal pacemakers.

WHAT IS “Isorhythmic” AV Dissociation?

The general term of AV dissociation simply means, that for a certain period of time sinus P waves are not related to neighboring QRS complexes. That is, P waves preceding one or more QRS complexes are not being conducted to the ventricles.

• AV Dissociation may be intermittent, recurrent and/or short-lived — or — it may be complete and persistent/permanent, as occurs with 3rd-degree AV block.
• AV Dissociation is said to be “isorhythmic” — when there are 2 independent pacemakers (usually sinus P waves from the SA node and an accelerated junctional focus) — with these 2 pacemaker sites having identical (or nearly identical) rates. In Figure-5 — a “picture” tells 1,000 words.

Figure-5: To quote Dr. Marriott’s description of what is happening here in this rhythm strip = “After 1 conducted sinus beat ( = beat #1) — an accelerated junctional rhythm usurps control from the sinus and holds dissociated sway at a rate of 74/minute to the end of the strip.” So, although it looks like the first 3 beats are conducting — if you look closely, you’ll see the PR interval is getting shorter (which means that beats #2 and #3 are not conducting). After this, you progressively lose the P wave (ie, the P wave is barely seen by the onset of beat #7) — before regaining the P wave toward the end of the rhythm strip. The reason for this continual subtle change in the PR interval — is that there is “isorhythmic AV dissociation”, in which atrial and accelerated junctional escape rates are very close to one another (Figure adapted from Marriott HJL: Pearls & Pitfalls in Electrocardiography — Lea & Febiger, PA; Page 91, 1990).

NOTE: True “isorhythmic” AV dissociation is like a horse race — in that rather than persistent near-equal rates for SA nodal and AV nodal pacemakers — there is a given-and-take — with first one horse (ie, one pacemaker) taking the lead by a tiny amount — then the other horse (ie, the other pacemaker) taking back that ever-so-slim margin of lead — and back-and-forth.

• This back-and-forth can be seen in Figure-5 — in which there is an ever-so-slight-but-real change in both the sinus and accelerated AV nodal escape rate. As a result — the PR interval in Figure-5 continually changes from beat-to-beat.
• In contrast — the relationship in Figure-4 between P waves and the next QRS complex remains the SAME (ie, the PR interval remains constant = 460 msec) in ECG #1.
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• PEARL #2 — AV dissociation is never a “diagnosis”. Instead — it is a condition caused by “something else”. There are 3 Causes of AV Dissociation: i) AV Block itself (of 2nd- or 3rd-degree); ii) Usurpation — in which P waves transiently do not conduct because an accelerated junctional rhythm takes over (ie, “usurps” control of the rhythm); and, iii) Default — in which a junctional escape rhythm takes over by “default” (ie, because of SA node slowing) — as may occur if a medication such as a ß-blocker is being used.
• The task for the clinician is to figure out what the cause of AV dissociation is for any given rhythm. This task is far more than academic — since appropriate management depends on figuring out the cause of AV dissociation. Active treatment may or may not be indicated. For example — optimal treatment of complete AV dissociation by “usurpation”, say with an accelerated junctional rhythm due to digitalis toxicity is simple: Stop digoxin!
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• PEARL #3 — Complete AV Dissociation is not the same as 3rd-degree AV block! This is one of the most commonly misunderstood concepts in all of arrhythmia interpretation! Complete AV block is just one of 3 possible causes of AV dissociation. Patients with “complete AV dissociation” may actually have no degree of AV block at all. This is the case in Figure-5 — in which after beat #1, none of the other 8 P waves in this tracing are conducted. But since none of these 8 P waves ever has a chance to conduct (ie, because the PR interval preceding beats #2-thru-9 is too short to conduct) — we have NO WAY of knowing whether P waves could conduct IF given the chance! Thus, the correct diagnosis for the rhythm in Figure-5 is not “AV dissociation” — but rather, “Sinus rhythm with AV dissociation as a result of “usurpation”, produced by a slightly accelerated junctional pacemaker at 74/minute”.
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• PEARL #4 — Complete (or 3rd-degree) AV Block is said to be present when none of the impulses from above (P waves) are able to conduct to the ventricles. KEY to this definition is the need to demonstrate that P waves fail to conduct despite being given adequate opportunity to do so — which requires that we must see P waves occurring in all phases of the R-R cycle (ie, having opportunity to conduct — but failing to do so). Note that none of the 8 P waves that fail to conduct in Figure-5 have any “chance” to conduct — which is why we are unable diagnose any degree of AV block from this particular tracing.
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• PEARL #5 — Most of the time, IF the degree of AV block is complete (3rd-degree) — then the ventricular rhythm should be at least fairly regular. This is because escape rhythms arising from the AV node, the His or ventricles are usually fairly regular rhythms. Exceptions may occur (ie, during cardiopulmonary resuscitation) — but even then, there will usually be a recognizable pattern of ventricular regularity. Going BACK to Figure-2 — the obvious irregularity of the ventricular rhythm (R-R interval varying from 800-to-930 msec) is yet another clue telling us that complete AV block is highly unlikely for ECG #1!
• IF interested in more on “My Take” of the Basics of AV Block — CLICK HERE. To go directly to the section that distinguishes AV Dissociation from Complete AV Block — CLICK at 49:25 in the video.

PEARLS about 1st-Degree AV Block:

Today’s case brings up a series of concepts regarding 1st-Degree AV Block:

• Traditionally — the diagnosis of 1st-degree AV block is defined as a PR interval of more than 0.20 second (ie, clearly more than 1 LARGE box in duration on ECG grid paper). That said — some individuals normally have PR intervals slightly above this upper range. This is especially true for athletic young adults, who often manifest increased vagal tone. As a result — I prefer the PR interval to be at least 0.22 second before saying 1st-degree AV block is present.
• Norms for the PR interval are different in children. Pediatric hearts are smaller. It therefore takes less time for the electrical impulse to travel through the conduction system of a child. For example — a PR interval of 0.18 second would be long for an infant.
• In younger adults — the cause of 1st-degree AV block is often the result of increased vagal tone. This can be a “training effect” — that goes way on deconditioning. In contrast — the causes of 1st-degree AV block in an older adult include fibrosis (aging) of the conduction system; coronary disease; myocarditis; rheumatic fever; infiltrative disease, Lyme disease; and neuromuscular disorders.
• The PR interval is defined as “short” — if it measures less than 0.12 second in lead II (as may occur with WPW when the AV node is bypassed). That said — some patients may normally have a PR interval slightly less than 0.12 second without necessarily having an accessory pathway (they may have an anatomically small AV node — or more-rapid-than-usual conduction through the AV node).
• HOW LONG can the PR interval be and still conduct to the ventricles? The answer is very long! I have seen PR intervals of greater than 1.0 second that still conduct to the ventricles in association with Mobitz I AV block.
• Clinically — Most patients with 1st-degree AV block remain asymptomatic and without need for intervention. This is especially true when the severity of 1st-degree AV block is not great (ie, a PR interval less than 0.30 second). Once the PR interval extends beyond 0.30 second — the delay in ventricular contraction that occurs may result in the atria contracting against closed AV valves, with reduction in cardiac output. This may lead to a series of symptoms similar to “pacemaker syndrome” (ie, dizziness, fatigue, light-headedness, presyncope/syncope, dyspnea and/or chest pain).
• On occasion — implantation of a permanent pacemaker may be needed in patients with marked 1st-degree AV block (ie, PR interval significantly greater than 0.30 second) who are symptomatic as a direct result of PR interval prolongation. This apparently is what happened in today's case — in which this man in his 70s presented with suspected syncope + a markedly prolonged PR interval of ~460 msec.
• Bottom Line: While the vast majority of patients with 1st-degree AV block are asymptomatic and do well without need for treatment — it is important to be aware of cardiac and other underlying disorders that the patient may have, as these may influence prognosis. As patients become older — 1st-degree AV block may progress to more prolonged PR interval prolongation, more advanced degrees of AV block and/or development of atrial arrhythmias including AFib. An occasional patient who presents with marked 1st-degree AV block + symptoms directly due to this, may need pacemaker placement.
• For a concise Review of 1st-Degree AV Block that appeared in NCBI StatPearls, 2019 — CLICK HERE.

Finally — Consider the rhythm shown in Figure-6. WHAT is going on?

• Can YOU guess WHY I am showing the rhythm in Figure 6 in this post that deals with 1st-degree AV block?

Figure-6: WHAT is going on in this rhythm? (See text).

INTERPRETATION of Figure-6: The rhythm is fairly regular — except for a brief pause after beat #7. The QRS complex is narrow — and P waves appear to be present. Can YOU identify all of the P waves?

• HINT: Using calipers should make it much easier to spot all of the P waves!

Identifying P Waves in Figure-6: I’ve added RED arrows in Figure-7 to highlight the location of all of the P waves:

• The atrial rhythm is actually quite regular at a rate of ~60-65/minute (RED arrows).
• Note that a P wave is hidden within the T wave of beat #6. The P wave that follows is more obvious — because it produces a spike in the T of beat #7.
• Final PEARL: This is a long Wenckebach cycle! On occasion with 2nd-degree AV block, Mobitz Type I ( = AV Wenckebach) — there will be a long series of beats before one is dropped. For example, in Figure-7 — it is difficult to appreciate that the PR interval is increasing as one moves from beat #2 — to beats #3, 4, 5, and 6. This is because the cycle of beats until one is dropped is long — and, the PR interval “increment” between one beat and the next is small. In such cases — the KEY that allows rapid identification of Mobitz I is to measure the PR interval at the beginning of the run (ie, the PR interval of beat #1) — and compare it to the PR interval at the end of the run just before the dropped beat. It should now be obvious that the PR interval of beat #7 is clearly much longer than the PR interval of beat #1. And then with the next cycle — the PR interval of beat #8 again shortens.
• P.S.: IF you'd like another Case Study on this phenomenon — CHECK OUT my ~11-minute ECG Video on this subject.

Figure-7: I’ve added RED arrows to highlight the regular atrial rhythm in this tracing. At first glance, it may appear that the rhythm is simply 1st-degree AV block with a markedly prolonged PR interval — because it is difficult to appreciate progressive lengthening of the PR interval if one just looks from one beat-to-the-next. However, closer inspection makes it clear that the PR interval at the beginning of the run (ie, the PR interval of beat #1) — is shorter than the PR interval at the end of the run (ie, the PR interval of beat #7) — and then, the spiked P wave that occurs in the T wave of beat #7 is not conducted. Following the brief pause between beats #7 and 8 — the next PR interval (before beat #8) shortens again as the next cycle begins (See text).

Our THANKS to Dr. Meyers for presenting this interesting case!