ECG Blog #450 — A "Healthy" 30yo with Dizziness

The ECG shown in Figure-1 was obtained from a previously healthy 30-year old man — who had this ECG as part of a "routine" pre-employment physical exam. He has had a few episodes of "dizziness", but no syncope. He is otherwise well without medical problems.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• How to evaluate this patient?

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

MY Thoughts on the ECG in Figure-1:

This is a challenging tracing to interpret — because there is marked bradycardia with an irregular rhythm and a change in QRS morphology.

• There are only 8 beats recorded on this ~10 second rhythm strip — for an average rate of ~50/minute.
• The QRS complex is wide (ie, >0.10 second in duration).
• A number of sinus P waves are present — as well as what appears to be some P waves arising from a different atrial site.

At this point — I thought it would be most helpful to identify atrial activity — which I have done with colored arrows in Figure-2.

• Upright sinus P waves are seen before beats #1,2,3,4; and #7,8 in the long lead II rhythm strip (RED arrows) — with this rhythm strip having been simultaneously recorded with the 12-lead tracing above it. The PR interval in front of each of these 6 beats is constant at ~0.12 second — such that these are sinus-conducted beats (0.12 second being the lower limit of normal for conduction through the atria).
• The widened qRS complex that follows each of these sinus-conducted beats in left-sided leads I and V5,V6 — suggests that these beats are conducted with RBBB (Right Bundle Branch Block).
• Small amplitude negative deflections are seen to occur after the T waves of beats #4 and 5. These appear to be non-conducted P waves — since they are not followed by any QRS complex (PINK arrows in Figure-2). Since the shape of these negative deflections differs from the shape of the RED arrow sinus P waves — I though these PINK arrow P waves were arising from a different site in the atria.
• There is no P wave in front of beat #5. Since the QRS morphology of this beat #5 in the long lead II, looks to be the same as the QRS morphology of sinus beats #1,2,3,4; and 7,8 — beat #5 must be a junctional escape beat.
• Note that the rSr’ morphology of beat #5 in simultaneously-recorded lead V1 — supports my suspicion that sinus beats #1,2,3,4; 7,8 are conducted with RBBB.
• This leaves us with beat #6 — that is also wide, not preceded by any P wave in the long lead II rhythm strip — and different in QRS morphology than the other 7 beats in the long lead II rhythm strip that manifest RBBB conduction. This suggests that beat #6 is a ventricular escape beat.

IMPRESSION: Today’s initial ECG is a complex tracing that manifests marked sinus bradycardia and arrhythmia — underlying RBBB — and both junctional and ventricular escape beats when the heart rate drops below 50/minute.

• There also appears to be some non-conducted P waves arising from another atrial site (the PINK arrows in Figure-2).
• As to ST-T wave changes in the 12-lead ECG — although some leads show T wave inversion (ie, in leads III, V3 and V4) — I did not think this looked acute in this 30-year old man without chest pain.

Figure-2: I’ve labeled atrial activity from Figure-1 with colored arrows.

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What about the Repeat ECG?

A little later — this patient's ECG was repeated (Figure-3).

• How would YOU interpret ECG #2 (that is shown in Figure-3)?

Figure-3: The 2nd ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio)

MY Thoughts on the ECG in Figure-3:

The repeat ECG is as challenging to interpret, as was the initial tracing. Fortunately, the simultaneously-recorded long-lead rhythm strip at the bottom of ECG #2 — once again allows us to determine the etiology of the beats with a different QRS morphology.

• It also helps to know that in ECG #1 that was recorded a little earlier from the same patient (shown above in Figure-1) — the underlying rhythm was sinus bradycardia and arrhyhmia, with QRS widening due to RBBB — in which both junctional and ventricular escape beats were seen when the heart rate dropped below 50/minute. 

Putting both ECGs in Today's Case together:

To facilitate comparison — I've put both ECGs in today's case together in Figure-4. Once again, for ECG #2 — labeling P waves greatly facilitates identifying ECG features:

• Sinus P waves in the repeat ECG are slow and irregular (RED arrows in the long lead II rhythm strip shown in the lower tracing in Figure-4).
• Beats #3 and #4 in ECG #2 — are sinus-conducted beats with RBBB (with the same shape upright P waves, the same consistent PR interval, and the same QRS morphology as was seen for beats #1,2,3,4; 7,8 in the long lead II rhythm strip of ECG #1).
• 
  
• Beat #6 in ECG #2 is also sinus-conducted — but the PR interval before beat #7 is too short to conduct. This tells us that beat #7 in ECG #2 must be a junctional escape beat.
• Similarly — beat #5 in ECG #2 is wide, manifests RBBB morphology, and is not preceded by any P wave — which defines beat #5 as another junctional escape beat.
• 
  
• Note that a small amplitude negative deflection is seen after the T wave of beat #7 (PINK arrows in simultaneously-recorded leads V5,V6 and the long lead II from ECG #2). As was the case in ECG #1 — since this PINK arrow negative deflection is not followed by a QRS complex, it represents a non-conducted, non-sinus P wave.
• 
  
• This leaves us with beats #1, 2 and 8. Note in the long lead II rhythm strip in ECG #2 — that none of these beats is preceded by a sinus P wave with a normal PR interval (a sinus P wave occurs just after the QRS of beat #1 — just before the QRS of beat #2, with a PR interval too short to conduct — and no sinus P wave at all is seen in the vicinity of beat #8).
• A look at simultaneously-recorded leads I and III for beats #1 and 2 (and simultaneously-recorded leads V4,5,6 for beat #8) — confirms that these non-conducting QRS complexes are wide and very different in morphology from the other beats in this tracing that show RBBB conduction. This tells us that beats #1,2 and 8 must be ventricular escape beats.

IMPRESSION: Both ECGs in today's case manifest similar features of marked sinus bradycardia and arrhythmia — underlying RBBB — junctional and ventricular escape beats when the heart rate slows — and some non-sinus, non-conducted P waves (the PINK arrow P waves seen in both ECGs).

Figure-4: Comparison between the 2 ECGs in today's case.

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Laddergram Illustration:

To better illustrate the mechanism of the 2 ECGs in today's case — I've drawn laddergrams in Figure-5 for each of the long lead II rhythm strips.

Figure-5: Laddergram illustration for the rhythm in today's case.

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How do these ECGs "Fit" with the Clinical Scenario?

Before going further — I will offer the following quote from Dr. Harry Mond: "Today's ECGs would be impossible to understand unless we understand the eccentricities of vagal hypertonia".

• In my ECG Blog #61 — I addressed the issue of vagotonic block.
• For the interested reader wanting to know more — I highly recommend review of the October 1, 2021 post in Dr. Mond's CardioScan — in which Dr. Mond covers "the ECG Spectrum of Vagal Hypertonia", with a fascinating series of vagotonia examples in otherwise healthy individuals.
• CAVEAT: Although many of these rhythms are seen in seemingly healthy individuals — these are not always benign arrhythmias. 

Regarding Today's CASE:

The patient in today's case was a previously healthy 30-year old man — in whom the above 2 ECGs were recorded as part of a "routine" pre-employment physical.

• When questioned — this patient acknowledged a few episodes of "dizziness", but no syncope. As a result, both the patient and medical provider were surprised by what these ECGs revealed.

My Thoughts on Seeing this Case:

• Is the patient an endurance athlete? (who might therefore be predisposed to bradycardia and the training effect of increased vagal tone).
• Did the patient have some form of underlying heart disease?
• Was there a family history of sudden death or significant arrhythmia?

Suggested Evaluation:

• Echo and Cardiac MRI (Looking for underlying heart disease and assessing for LV function).
• ETT (Exercise Treadmill Test) — to see what happens to this patient's heart rate and how he handles progressively increasing levels of exercise.
• Cardiac Monitoring over ~48 Hours — to quantify and qualify the severity and duration of bradycardia and its correlation with symptoms (as well as to see if there were any prolonged pauses).
• LAB — including electrolytes, renal function, thyroid studies, etc.

CASE Follow-Up:

• Additional History: The patient used to play soccer — but has not engaged in endurance activities with any regularity for the past 8 years.
• Negative family history for sudden death or arrhythmia.
• No suggestion of sleep apnea.
• Echo — completely normal.
• ETT — excellent level of activity and heart rate response to exercise. No evidence of ischemia.

CASE Disposition:

Opinions of consulting cardiologists on this case were divided. Many favored pacemaker implantation at this time. But the question remained — Could this all simply be a result of "Vagal Hypertonia?"

• Ultimately (with completely informed patient consent) — the decision was made to implant a pacemaker. Pacing parameters were selected to encourage the patient's own rhythm. 

My Review of the Literature:

There is no perfect answer to the above questions. 

• Although the patient had not engaged in regular endurance training for a period of years — his arrhythmias could simply be the result of "Vagal Hypertonia".
• The diagnosis of enhanced vagal tone has to be a "diagnosis of exclusion" (ie, after ruling out underlying heart disease and/or a potentially "fixable" cause).
• What concerned me most about the patient's ECGs was the presence of non-conducted P waves (that should have been conducted). That said — vagotonic block can do this! (as per ECG Blog #61 and Dr. Mond's Vagotonia Review). 
• That said — enhanced vagotonia is not necessarily benign, as it can be one of the mechanisms for PAVB (Paroxysmal AtrioVentricular Block) — that can be potentially lethal (See the ADDENDUM in my ECG Blog #419 for detailed discussion of PAVB).
• The mechanisms associated with vagotonia and vasovagal-induced syncope are complex — involving a complex interplay between parasympathetic and compensatory sympathetic nervous system responses. These responses become even more complex in younger adults, especially when associated with endurance activity (Gopinathannair et al — Arrhythm & Electrophys Rev 7(2):95-102, 2018).
• 
  
• BOTTOM Line: Some patients with worrisome bradyarrhythmias due to intermittent or persistent enhanced vagal tone at some point do need permanent pacing. Unfortunately, there is no good medication for treatment of vagal hypertonia. There is research on attempting cardio-vagal nerve denervation — but this remains controversial, and not a perfect solution (Cai et al — Front Physiol 14:1088881, 2023). And — this patient is symptomatic (ie, with "dizziness" on a number of occasions).

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Acknowledgment: My appreciation to ضياء كمال (from Zagazig, Egypt) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — My Ps, Qs, 3R System for Rhythm Interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

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

• ECG Blog #192 — The 3 Causes of AV Dissociation. 
• ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.
• 
  
• ECG Blog #389 — ECG Blog #373 — for review of some cases that illustrate "AV block problem-solving".
• 
  
• ECG Blog #61 — on Vagotonic Block.
• ECG Blog #419 — on PAVB (Paroxysmal AV Block). 

 

ECG Blog #449 — Isorhythmic AV Dissociation?

The ECG in Figure-1 — was obtained from a 45-year old man with diabetes, who was being treated for septic shock.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• What is the rhythm?
• Why does QRS morphology in the long lead II rhythm strip change every-other-beat?

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

MY Thoughts on the ECG in Figure-1:

This is a challenging ECG to interpret because of: i) the changing QRS morphology; and, ii) the difficulty in seeing all of the P waves. That said — I was able to determine the rhythm within seconds because of the following observations:

• All beats on this ECG are supraventricular! The "beauty" of having a 12-lead tracing with a simultaneously-recorded long lead II rhythm strip — is that this allows us to view each of the 12 beats on this tracing in 3 other simultaneously-recorded leads. Doing so confirms that even though there are 2 distinct QRS morphologies in the long lead II rhythm strip (especially obvious in lead III) — the QRS is narrow in all 12 leads. Therefore — the rhythm is supraventricular!
• There is group beating! (seen in Figure-1 in the form of a bigeminal rhythm, in which the same shorter — then the same longer R-R interval alternates throughout the tracing).
• Regular P waves are present throughout the entire tracing. This KEY observation can be verified within seconds — simply by using calipers (See Figure-2).

Figure-2: I've added RED arrows to the initial ECG — showing that regular P waves are present throughout the entire tracing.

PEARL #1: The clinician who does not use calipers to interpret complex arrhythmias like today's tracing — will invariably take more time for their interpretation, only to discover that they will never be certain about the regularity of atrial activity.

• To optimally assess atrial activity — I simply set my calipers to the P-P interval between any 2 consecutive P waves that I can clearly identify. For example, in Figure-2 — 2 consecutive P wave deflections are clearly seen to occur at the same place within each of the longer R-R intervals (so that I chose to set my calipers to the P-P interval between the 3rd and 4th RED arrows in Figure-2).
• Once I set my calipers to this P-P interval — I was able to easily "walk out" regular P waves throughout the entire long lead II rhythm strip.
• PEARL #2: The reason today's tracing is so challenging — is that every 3rd P wave is so well hidden within the T waves of every odd-numbered beat. This is where awareness of simultaneously-recorded leads may prove invaluable! Although we do not see every 3rd P wave in the long lead II rhythm strip (because these P waves are hidden within the T waves of beats #1,3,5,7,9 and 11) — we do see an "on-time" tiny negative deflection right after the 1st T wave in lead V1 (2nd RED arrow in lead V1). This confirms that P waves are hidden at a similar point in the T wave of all odd-numbered beats. Therefore — there is an underlying regular atrial rhythm, with sinus P waves at ~110/minute.

PEARL #3: Today's rhythm does not represent complete AV block (and it does not represent isorhythmic AV dissociation). We can quickly determine this by focusing our attention on the PR interval just before the QRS complex of each beat that ends each of the longer R-R intervals (ie, the PR interval before beats #3,5,7,9 and 11).

• Labeling P waves (as we have done with RED arrows in Figure-2) — greatly facilitates this process — and expedites us being able to tell that although the PR interval before beats #1,3,5,7,9 and 11 is slightly prolonged (ie, ~0.22 second) — this PR interval in front of all odd-numbered beats remains constant! Therefore — there clearly is at least some conduction.
• PEARL #4: Despite the finding of a regular atrial rhythm — there are more P waves than QRS complexes (ie, there are 18 RED arrow P waves in Figure-2 — but only 12 QRS complexes). This means that some form of 2nd-degree AV block must be present — since not all P waves are being conducted to the ventricles.

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PEARL #5: At this point in my interpretation — I was virtually certain that today's rhythm represented some form of AV Wenckebach (ie, 2nd-degree AV block of the Mobitz I Type) — because of the information the above-described 5 Observations told me:

• Observation-1: The QRS complex for all beats in all 12 leads of Figure-2 is narrow. Therefore — today's rhythm is supraventricular.
• Observation-2: There is group beating (in the form of alternating longer-then-shorter R-R intervals). The presence of "group beating" should always raise the possibility of Wenckebach conduction — IF certain other features are also present.
• Observation-3: The underlying atrial rhythm is regular (RED arrows in Figure-2). Knowing there is a regular sinus rhythm rules out the non-Wenckebach causes of group beating, such as atrial bigeminy.
• Observation-4: At least some beats are being conducted to the ventricles (because the PR interval is constant before all of the beats that end longer R-R intervals). As per PEARL #3 — since at least some P waves are being conducted to the ventricles — this rules out 3rd-degree (complete) AV block!
• Observation-5: There are more P waves than QRS complexes. This means that some of the regularly-occurring sinus P waves are not being conducted (which means some form of 2nd-degree AV block must be present).

MY Impression of ECG #1: The above 5 Observations confer ECG features that characterize "the Footprints of Wenckebach!" — which is why within seconds of seeing today's ECG, I was virtually certain there was some form of 2nd-degree AV Wenckebach (See ECG Blog #164 — ECG Blog #55 — ECG Blog #347 — and ECG Blog #154).

• That said — I had not yet demonstrated cycles with progressive increase in the PR interval until an on-time sinus P wave is dropped (as should be seen with typical AV Wenckebach).

For Practical Purposes: I would be happy IF you stopped at this point, knowing that the above 5 observations make it virtually certain that today's rhythm represents 2nd-degree AV block of the Mobitz I Type ( = AV Wenckebach).

• Beyond-the-Core: Take a LOOK at Figure-3 — in which I have used 3 colors to label a certain P wave pattern in this tracing that repeats itself over the 12 beats in the long lead II rhythm strip. What does each color signify?

Figure-3: I've used 3 colors to label all P waves in today's rhythm. What does each color signify?

The Colors in Figure-3:

It's easiest to break down what is happening in Figure-3 — by starting with the RED arrow P waves.

• As noted above in Observation-4 — the RED arrow P waves in Figure-3 all manifest the same 0.22 second PR interval. Therefore — beats #1,3,5,7,9 and 11 are all conducted with 1st-degree AV block.
• IF the rhythm in Figure-3 is AV Wenckebach — then either the PINK or the YELLOW arrow P waves must not be conducted. Doesn't it seem more logical for the YELLOW arrow P waves to be non-conducted? (which would mean that the PINK arrow P waves would be conducting beats #2,4,6,8,10 and 12 with a very long PR interval of ~0.38 second).

PEARL #6: The last 2 features to explain regarding today's ECG are: i) Why QRS morphology changes slightly with every-other-beat; and, ii) What the rest of today's 12-lead ECG shows.

• Since we know that all beats in today's tracing are supraventricular (Observation-1 in PEARL #5) — and since all QRS complexes are conducted — the reason for slight change in QRS morphology every-other-beat must be the result of some aberrant conduction. As explained in ECG Blog #211 — whether a beat does or does not conduct with some aberration depends on the interplay between coupling intervals and the preceding R-R interval. Although I do not see a specific form of conduction delay in the slightly wider QRS complexes (which are the odd-numbered beats) — the differing R-R intervals most probably accounts for the aberrant conduction.
• Mobitz I 2nd-degree AV block is commonly seen in association with acute or recent inferior and/or posterior infarction. That said — I thought ST-T wave appearance in the rest of the 12-lead ECG showed nonspecific (nondiagnostic) abnormalities. I did not see evidence on this tracing for recent or acute MI (but it is always important to look for ECG signs of recent inferior and/or posterior MI whenever you encounter Mobitz I 2nd-degree AV block).

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Laddergram Illustration:

The BEST way to prove that today's rhythm is 2nd-degree AV block of the Mobitz I (AV Wenckebach) Type — is to construct a laddergram, which I illustrate step-by-step in Figures-4 thru -10.

Figure-4: I find the easiest 1st step in drawing a laddergram is to complete the Atrial Tier, that shows atrial activity.

Figure-5: I next fill in the Ventricular Tier — which corresponds to the timing of those ventricular beats I am sure about. Since we know in today's tracing that all 12 beats are supraventricular — I drew the arrow for each of these QRS complexes in the Ventricular Tier facing downward (representing normal conduction of supraventricular impulses through the ventricles).

Figure-6: We are now ready to begin solving the laddergram. I do this by connecting those P waves from the Atrial Tier — to those QRS complexes that I am certain each of these P waves is conducting to (BLUE lines that I've drawn within the AV Nodal Tier).

Figure-7: It seems logical that the next P waves to conduct to the ventricles are those that are highlighted by BLUE arrows in this Figure-7. It should now be easy to see that conduction of this 2nd P wave in each group takes a bit longer to be conducted, which is the principal characteristic of Wenckebach conduction (BLUE lines that I've drawn within the AV Nodal Tier).

Figure-8: By the process of elimination — this means that the remaining BLUE arrow P wave is not conducted (ie, there are no unconnected QRS complexes left). This therefore "completes" the laddergram — by the "butt end" that I've added to the remaining BLUE arrow P waves.

Figure-9: For clarity — I now labeled each of the P waves in the long lead II rhythm strip with the same colors that I used above in Figure-3.

Figure-10: Most of the time when I draw a laddergram — I use the same color for all lines in the illustration, as shown here.

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Acknowledgment: My appreciation to Vansh Verma (from New Delhi, India) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — My Ps, Qs, 3R System for Rhythm.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

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

• ECG Blog #192 — The 3 Causes of AV Dissociation. 
• ECG Blog #191 — AV Dissociation vs Complete AV Block.
• 
  
• ECG Blog #389 — ECG Blog #373 — for review of some cases that illustrate "AV block problem-solving".
• ECG Blog #236 — for an ECG Video Pearl on the 3 Types of 2nd-degree AV block.
• ECG Blog #344 — thoroughly reviews the Types of 2nd-degree AV block (Mobitz I vs Mobitz II vs 2:1 AV Block).
• 
  
• ECG Blog #267 — Reviews with step-by-step laddergrams, the derivation of a case of Mobitz I with more than a single possible explanation.
• ECG Blog #164 — Step-by-Step laddergram of Mobitz I.
• 
  
• ECG Blog #195 — reviews Isorhythmic AV Dissociation.

 

 

ADDENDUM (10/2/2024) — Based on Question by Akash

For those readers who enjoy the challenge of drawing laddergrams — I've decided to publish the Question sent to me from Akash (in the Comments below).

• As I've often emphasized — there may on occasion be more than a single possible explanation for the mechanism of a given complex arrhythmia!
• IF you are able to "draw" your theory for a potentially plausible mechanism — then consider yourself correct in proposing an alternative mechanism (in which case — the only way to verify which proposed mechanism is correct for the case at hand would be by EP study).
• The reason I thought it worthwhile to publish the excellent question that Akash asks — is that it illustrates the problem-solving process for complex rhythms, in which I have to "play" with a few potentially plausible laddergram solutions until I am able to come up with one that works.

This is the question by Akash (that I copied from the Comments below):

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Hello Dr. Grauer!
Long time lurker (and learner) here, posting for the first time.

• Could this be a 2:1 AV block?
• The first P wave (labelled with a RED arrow in Figure 3) is conducted (albeit with a slightly prolonged PR interval).
• The next P wave (the one hidden within the T wave = PINK arrow) is not conducted.
• The QRS complex labelled beat #2 is a junctional escape beat.
• The third P wave (YELLOW arrow) fails to conduct — because it finds the distal conduction system refractory (because of the junctional escape beat).

Is this a reasonable explanation of this rhythm? I’m sure I’m missing something, but am unsure what that is. Please throw light, Dr. Grauer!
Warm regards — Akash

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MY Reply to Akash:

Your question Akash is an excellent one — and I actually thought of the solution you propose when first working through this case.

• The problem however — is that if the 2nd P wave (first YELLOW arrow in Figure-11) was non-conducted because of 2:1 AV block and if beat #2 was a junctional escape beat — this would mean that you are proposing an accelerated junctional escape rate (because the R-R interval before beat #2 that you are proposing is junctional = 3.7 large boxes — which corresponds to an accelerated junctional escape rate of ~81/minute).
• And — this would mean that unless inhibited by a sinus-conducted beat — the next junctional escape beat would occur 3.7 large boxes later = where I placed the BLUE circle. But since the next sinus P wave is set to occur where the 3rd RED arrow occurs — we can see that this next junctional beat would prevent the 3rd sinus P wave from conducting .... (You'd have to propose "takeover" of the rhythm by an accelerated junctional rhythm — which I would not expect given the constant and reasonable PR interval before beats #1,3,5,7,9,11).
• 
  
• P.S.: Accelerated junctional rhythms and junctional tachycardia can occur — but they are relatively uncommon in adults unless there is some underlying cause (ie, ischemia, shock, electrolyte disorders, post-cardiac surgery, etc.).

BOTTOM Line: I thought it unlikely that there was 2:1 block with a "usurping" accelerated junctional rhythm. I also thought the laddergram that I derived in Figure-10 looked perfectly plausible for 2nd-degree AV Block, Mobitz Type I ( = AV Wenckebach).

Figure-11: Unsuccessful proposed laddergram (See above).

 

ECG Blog #448 — A Young Man with Chest Pain ...

The ECG in Figure-1 was obtained from a previously healthy man in his early 20s — who initially presented with GI symptoms, that then evolved into CP (Chest Pain).

• The patient was thought to have anxiety.

QUESTIONS:

• Given the above history — How would YOU interpret the initial ECG that is shown in Figure-1?
• Does the patient's age infuence your interpretation?

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

ANSWERS:

As emphasized in ECG Blog #205 — I favor a 2-Step Process for the interpretation of any ECG:

• STEP #1 = Descriptive Analysis — in which we simply assess the 6 KEY Parameters of Rate — Rhythm — Intervals (PR-QRS-QTc) — Axis — Chamber Enlargement — and Q-R-S-T Changes — but without yet commenting on what this assessment might mean clinically.
• STEP #2 = Clinical Impression — in which we correlate our assessment that we made in Step #1 to the clinical situation at hand. For example, considering whatever symptoms that the patient may have had (ie, chest pain, palpitations, shortness of breath, etc.) — what this might mean in view of the ECG we are looking at.

KEY Points:

• Use of this systematic 2-Step approach does not slow you down. On the contrary — it speeds you up, because once you routinely incorporate a sequential, systematic approach — you'll find you no longer go back-and-forth looking at the ECG to see if you missed anything.
• 
  
• PEARL #1: My assessment of the 6 KEY Parameters is the same — regardless of the age of the patient. That said — What (if anything) these ECG findings that you identify might mean — will depend on your clinical correlation in Step #2.
• 
  
• PEARL #2: The reason it helps to know the age of the patient and the reason the ECG was done as soon as possible — is that it greatly facilitates Clinical Correlation. For example, in today's case — Knowing the patient is a younger adult who developed chest pain immediately increases our need to consider acute myocarditis in the differential diagnosis.

Figure-2: I've labeled the initial ECG. 

MY Interpretation of Today's Initial ECG:

I've labeled key findings in Figure-2 for today's initial ECG:

• The rhythm is sinus tachycardia at ~105/minute. 
• All intervals (PR, QRS, QTc) are normal. 
• The frontal plane axis is normal at about +70 degrees. 
• Given the patient's young adult age — QRS amplitude does not satisfy criteria for chamber enlargement.

Regarding Q-R-S-T Changes:

• Small and narrow Q waves are seen in the inferior leads, and in lead V6. These are likely to be normal septal q waves. (The initial deflection in lead aVL is positive — so there is an rSr' complex, but no Q wave in this lead).
• R wave progression — is normal, with progressive increase in R wave amplitude (albeit transition is slightly delayed until lead V5, when the R wave finally becomes taller than the S wave is deep).

There are subtle-but-important ST-T wave findings:

• My "eye" was drawn first to the 2 leads within the RED rectangle (ie, leads V5 and V6 each show 2 millimeters of J-point ST elevation — which is more than is usually seen with a normal repolarization pattern).
• There is a lesser amount of ST elevation in lead V4 — but given my concern about leads V5,V6 — I thought the ST-T wave in lead V4 showed some ST segment straightening, and was disproportionately larger-than-it-should-be with respect to the modest-sized R wave in this lead (within the BLUE rectangle).
• Normally, there is slight, gently upsloping ST elevation in leads V2 and V3. While I thought the ST-T wave in lead V3 was non-diagnostic — lead V2 lacks the slight amount of gently upsloping ST elevation that is usually seen in this lead.
• In the limb leads — there is slight-but-real J-point ST elevation in the inferior leads and in lead I (BLUE arrows) — with ST segment straightening in these same leads (as shown by the light BLUE lines).

STEP #2 = My Clinical Impression of ECG #1:

I had been sent this ECG with only the information that I noted in the above history (ie, that the patient was a previously healthy man in his early 20s — who presented with GI symptoms — that evolved into chest pain thought to be the result of anxiety).

• I wrote back, "This is not a normal ECG". I then specified the findings I cite above in my Descriptive Analysis.
• The sinus tachycardia is a definite concern that something acute may be ongoing. Almost all leads show some ST elevation — with more ST elevation in leads V5,V6 than is usually seen with early repolarization and, with abnormal straightening of the ST segment takeoff in multiple leads.
• 
  
• To Emphasize: I was not at all certain about what might be going on here. But what I wrote back was the following: "This could be acute LAD occlusion (ie, acute LAD OMI). Given that this patient is having CP — more evaluation is clearly needed. Alternatively — this could represent acute infero-postero-lateral OMI. In any event — I'd repeat the ECG within 10-20 minutes (and serially thereafter) — check Troponin — and would definitely follow-up until a definite answer is forthcoming! 
• Pericarditis is rare — but myocarditis is not, so especially in this age group — more information is needed to quickly determine if this could be an acute MI, myocarditis, or none of the above. Let me know what happened".

CASE Follow-Up:

The emergency physician recognized the abnormal ECG findings that I highlight above — and sent the patient to a PCI-capable center.

• Unfortunately — the cardiologist at that center did not recognize the abnormal ECG findings. The patient was discharged without repeating the ECG.
• The patient arrested outside the hospital. He could not be resuscitated.

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There are Lessons-to-be-Learned from today's case:

• Treat the patient — Not the age of the patient!
• Acute MI can occur in a younger patient.
• There are other potentially serious causes of CP in a younger adult. Some of these other causes may also be potentially life-threatening.
• IF at all concerned by the history and/or appearance of the patient — Do not allow your decision-making to be determined by a single ECG. I fully acknowledge that I was not certain from today's initial ECG that this patient had a life-threatening problem. That said — a series of subtle but potentially concerning findings are present in today's initial tracing — and, this should signal the need for additional evaluation until a clear diagnosis is forthcominng.
• Be systematic in your ECG interpretation. If the interventionist would have been systematic — the abnormal ECG findings highlighted in Figure-2 would have been identified.
• Sometimes cardiac cath is needed to distinguish between an MI vs myocarditis.

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PEARL #3:  Acute MI Can Occur in a Younger Patient!

To quote Dr. Stephen Smith: "The worst risk factor for a bad outcome in acute MI is young age." This is because clinicians (including too many cardiologists) have trouble accepting the fact that a young patient can have an acute MI (See case discussion in the January 9, 2023 post in Dr. Smith's ECG Blog — with links at the bottom of this post to a series of more cases illustrating this phenomenon).

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I have excerpted a portion of My Comment from this same January 9, 2023 post — regarding acute MI in a younger patient:

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“Treat the patient — Not the age of the patient”

The tendency to discount new chest pain in a young adult as the 1st symptom of acute MI is understandable. Acute coronary occlusion almost always occurs in patients who are beyond their 20s. That said — acute MI does occur in younger patients.

• There is a literature on this subject (Sood et al — Cureus 15(4):e37102, 2023 — Gulati et al — Mayo Clin Proceed 95(1):136-156, 2020 — GGF van der Schoot et al: Neth Heart J 28(6):301-308, 2020 — and — Egred at al — Postgrad Med 81(962): 741-745, 2005 — to name just a few reports). 
• Acute MI in younger patients may result from acute coronary occlusion — which can be precipitated by conventional risk factors (such as smoking begun at an early age) — in individuals with special predisposition (ie, a factor V Leiden mutation — or nephrotic syndrome — both being correlated with a hypercoagulable state) — and/or in familial entities such as genetic hypercholesterolemia.
• In addition — there is a series of nonatherosclerotic potential causes of acute infarction in younger patients. These include coronary artery spasm (as may be precipitated by cocaine use or binge alcohol drinking) — myocardial bridging (that may be the cause of intermittent acute ischemia) — aberrant anatomy of a coronary artery (which may present with sudden rupture causing acute infarction or sudden death at any age!).
• Other types of nonatherosclerotic potential causes of acute infarction in younger patients include systematic inflammatory disease (ie, lupus, rheumatoid arthritis, Wegener granulomatosis) — thrombosis not due to coronary disease (ie, endocarditis, coagulation disorders) — pregnancy (with its hypercoagulable state).
• Causation of Endothelial damage is another potential mechanism of acute MI in a younger patient. This may occur as a result of blunt chest trauma or other acute stress that produces a sudden extreme shear force on a coronary artery (that can result in an intimal tear that leads to intraluminal thrombosis). Endothelial damage may also be seen with spontaneous dissection of a coronary artery — or result from “deceleration trauma (ie, from an auto or other vehicular accident).
• 
  
• BOTTOM LINE: While the above etiologies are not common causes of acute infarction in an adolescent or young adult — they do occur! And, like most diagnostic considerations in medicine — if the differential diagnosis excludes such "other potential etiologies" simply because they are not common, or because the patient is "too young to have a heart attack" — then these other potential etiologies will be missed!
• 
  
• RELEVANCE to this Case: Although the young adult in today’s case presented with GI symptoms (that were thought to be exacerbated by anxiety) — this did evolve into frank CP. So, while today's history by itself is not particularly suggestive of an acute coronary event — in association with the abnormal ECG findings and persistent CP — additional evaluation was clearly indicated.
• 
  
• P.S.: Given the history in today's case, and the abnormal ECG findings — acute myocarditis needs to be included in diagnostic considerations. There are times when distinction between acute myocarditis vs acute OMI in a younger patient with acute-looking ECG changes and troponin elevation can only be made by cardiac catheterization. At other times, when strongly suspecting acute myocarditis and not acute MI — cardiac MRI may yield a definitive enough picture to confirm acute myocarditis as the diagnosis.

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Acknowledgment: My appreciation to Kashif Aleem (from Sargodha, Punjab, Pakistan) for the case and these tracings.

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