Friday, October 4, 2024

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.
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