ECG Blog #384 — Why So Fast?

The ECG in Figure-1 was obtained from a young man with a history of rheumatic heart disease — who presented with “palpitations”. He was hemodynamically stable at the time this tracing was recorded.

• How would YOU interpret the ECG in Figure-1?
• How would you treat the patient?

Figure-1: The initial ECG in today’s case. What is the rhythm? How would you treat the patient? (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The “good news” about today’s case — is that the patient was hemodynamically stable at the time the initial ECG in Figure-1 was recorded. By definition, this means that despite the fast heart rate — providers had at least “a moment in time” to contemplate the etiology of the rhythm before initiating treatment. By the Ps, Qs, 3R Approach (See ECG Blog #185):

• The rhythm in Figure-1 is fast and Regular.
• By the Every-Other-Beat (or in this case Every-3rd-Beat) Method (See ECG Blog #210) — the Rate of the rhythm is ~250-260/minute (ie, As shown in Figure-2 —  the R-R interval of every 3rd beat is 3.6 large boxes — which means 1/3 the rate = ~85/minute X 3 ~250-260/minute).
• The QRS complex is wide (ie, ~0.13-0.14 second).
• There is no clear sign of P waves (and therefore no indication of any Relation between atrial activity and neighboring QRS complexes).

Putting It All Together: The rhythm in Figure-1 is an extremely fast (ie, ~250-260/minute) — and regular WCT (Wide-Complex Tachycardia) rhythm, without clear sign of atrial activity.

• The KEY determination to make for ECG #1 — is between VT (Ventricular Tachycardia) — vs some form of SVT (SupraVentricular Tachycardia).
• Statistically, in an unselected adult population — VT is much more common than an SVT rhythm, especially in a patient such as the one in today’s case who has underlying heart disease. That said — since today’s patient is a “young man” — and the rate of today’s rhythm is extremely fast (ie, 250-260/minute — which is faster than is usually seen in a VT rhythm that maintains a well-defined QRS morphology) — we clearly can not discount the possibility of an SVT rhythm.
• IF today’s rhythm was an SVT — a rate of 250-260/minute is clearly too fast to be sinus tachycardia. While AFlutter (with 1:1 AV conduction) and ATach are possibilities — a reentry SVT rhythm (either AVNRT or AVRT) would seem far more likely. The extremely rapid rate increases the chance of an AP (Accessory Pathway)-dependent reentry circuit (ie, of AVRT).
• 
  
• BOTTOM Line: To Emphasize — The above “thought process” should take no more than seconds to complete! That said — I could not be sure of the etiology of today’s rhythm on the basis of my analysis thus far. KEY Point: It is common for even the most experienced clinician not to be 100% certain of the etiology of a regular WCT rhythm at the time that they need to begin treatment.

Figure-2: I've labeled the ECG in Figure-1 — to illustrate use of the Every-Other-Beat Method for accurate estimation of the heart rate.

Does QRS Morphology Help?

Take another look at the regular WCT rhythm in Figure-2:

• Does QRS morphology in ECG #1 favor VT? — or — an SVT with either preexisting BBB (Bundle Branch Block) or aberrant conduction?

ANSWER: Does QRS Morphology Help?

QRS morphology in Figure-2 could be consistent with supraventricular conduction (ie, from either preexisting BBB — and/or — from aberrant conduction):

• The RsR’ triphasic QRS complex seen in lead V1 of ECG #1 (with S wave that descends below the baseline — and taller right “rabbit ear”, together with wide, terminal S waves in lateral leads I, V6) — is consistent with rbbb conduction.
• The predominant S wave in lead I, with steep downslope — in association with predominant positivity of the QRS in lead iII — is consistent with lphb conduction.
• 
  
• BOTTOM Line: Use of QRS morphology is not perfect for distinguishing VT from an SVT rhythm. Sometimes it helps. At other times — it does not help. Most of the time — QRS morphology provides clues that “move the likelihood” of VT vs an SVT rhythm in one direction or the other, albeit without 100% certainty. QRS morphology is most helpful when either: i) A completely typical RBBB morphology is seen (ie, an rsR’ in lead V1, with S wave that descends below the baseline and taller, slender R’ = “right rabbit ear” in this lead V1 — with wide terminal S waves in lateral leads I and V6); or, ii) An ill-defined QRS morphology is seen that is not consistent with any known form of conduction defect.
• The “Long” ANSWER: In today's case — QRS morphology in ECG #1 clearly could be consistent with supraventricular conduction showing RBBB/LPHB. That said — I thought there were a few slightly atypical features for expected QRS morphology with LPHB — including: i) Absence of a typical qR pattern in both leads II and III (ie, the QRS complex is nearly equiphasic in lead II — and there is no clear initial q wave preceding the upright R wave in lead III); and, ii) The QRS is all negative in lead aVL (whereas typically lead aVL would show a similar rS complex, as we see here in lead I). Given statistical prevalence of VT in patients with a regular WCT rhythm — I suspected fascicular VT for the rhythm in today's case. That said — I was not at all certain about the diagnosis (See ECG Blog #197 — as well as other references listed below for more on this topic).
• 
  
• The “Short” ANSWER: The patient in today’s case presents in a regular WCT rhythm, without clear sign of atrial activity. Although I initially suspected fascicular VT — there is no way to be certain that the rhythm is not a reentry SVT from the single tracing shown in Figure-2. Since the patient was initially stable hemodynamically — a trial of IV Verapamil could be the initial treatment of choice, given that IV Verapamil is often effective for both fascicular VT and reentry SVT rhythms (AVNRT, AVRT). Alternatively (and equally appropriate given the extremely rapid ventricular rate) — one might opt for sedation and immediate synchronized cardioversion.

CASE Follow-Up:

An initial trial of low-dose IV Verapamil was given — but was not successful. At this point, the decision was made for synchronized cardioversion — which converted to the rhythm shown in ECG #2. 

QUESTIONS:

• How would you interpret the repeat ECG shown in Figure-3?
• Does ECG #2 help to tell us what the rhythm in ECG #1 was?

Figure-3: Comparison between the initial ECG — and the repeat tracing obtained following synchronized cardioversion. (To improve visualization — I've digitized the original ECG using PMcardio).

Case CONCLUSION:

The repeat ECG in Figure-3 shows conversion of the rhythm in ECG #1 to sinus tachycardia (restoration of upright sinus P waves in lead II — at a rate of ~110/minute).

• Comparison of QRS morphology between the 2 tracings shown in Figure-3 (ie, during and after the WCT rhythm) — reveals remarkable similarity in virtually all 12 leads! Especially remarkable — is the virtually identical initial deflection in all leads (ie, small, thin initial r wave in lead I — similar shape and slope of the biphasic R wave in lead II; identical-looking initial r waves in leads V1,V2 — and more of the same in the other 8 leads).
• 
  
• BOTTOM Line: The finding of near-identical QRS morphology during and after the WCT rhythm — confirms that the etiology of the WCT rhythm in ECG #1 was supraventricular, here with preexisting RBBB/LPHB. The very rapid ventricular rate attained (ie, ~250-260/minute) — with need for synchronized cardioversion suggests: i) That the rhythm in ECG #1 was probably orthodromic AVRT; and, ii) That this young man with established rheumatic heart disease and underlying bifascicular block (RBBB/LPHB) will probably best be served by referral to EP Cardiology for ablation. 

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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Qatar) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.
• ECG Blog #210 — reviews the Every-Other-Beat Method for rapid estimation of heart rate.
• 
  
• ECG Blog #220 — reviews the approach to a Regular WCT (Wide-Complex Tachycardia).
• 
  
• ECG Blog #323 — WCT with RBBB Morphology = Fascicular VT.
• ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm.
• 
  
• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 

• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
• 
  
• ECG Blog #197 — Review of Fascicular VT.
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• 
  
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT.
• ECG Blog #42 — Comprehensive review of criteria for distinguishing VT vs Aberration.
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• See ECG Blog #240 — for Review on the ECG assessment of the patient with a regular SVT rhythm (including distinction between the various types of SVT reentry). 

• See ECG Blog #250 — for Review of another case of regular SVT with ST depression.
• 
  
• ECG Blog #220 — reviews my LIST #1: Causes of a Regular WCT and — HOW to assess Hemodynamic Stability.
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• González-Torrecilla et al: Ann Noninvasive Electrocardiol 16(1):85-95, 2011 — Reviews distinction between AVNRT vs AVRT and other regular SVT rhythms in patients without WPW.
• Please check out the November 12, 2019 post in Dr. Smith's ECG Blog — in which I reviewed the case of a different kind of regular SVT Rhythm (AFlutter).

ECG Blog #383 — Is this Coronary Disease?

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Please NOTE: 

• After today — No new ECG Blog posts for 2-to-3 weeks ...
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— I'll be back! —

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ECG Blog #383 — Is this Coronary Disease?

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The ECG in Figure-1 — was obtained from a previously healthy 70-year old man who presented to the ED (Emergency Department) with new CP (Chest Pain).

• How would YOU interpret this tracing?
• 
  
• Should you activate the cath lab? (ie, Is the ST elevation in lead V1 — in association with the ST-T wave changes in lateral chest leads suggestive of Precordial "Swirl" from proximal LAD occlusion, as discussed in ECG Blog #380)?

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

MY Thoughts on the Initial ECG:

I thought ECG #1 was both fascinating and a bit bizarre ...

• The rhythm overall looks to be a fairly regular sinus rhythm with a PAC — although P waves in lead II are extremely small. P waves are probably best seen in lead V2, which is unusual for sinus rhythm — so possibly this is an ectopic atrial rhythm.
• Intervals overall (PR, QRS, QTc) appear to be normal. That said — lack of a well defined P wave in lead II makes assessment of the PR interval difficult — and — the QRS looks a little wide in lead V3, albeit QRS duration does not appear to exceed 0.10 second in any particular lead.
• The frontal plane axis is slightly leftward (ie, the QRS being more negative than positive in lead aVF) — but not leftward enough to qualify for LAHB (ie, the QRS in lead II is not predominantly negative).

Regarding Chamber Enlargement:

• There is marked LVH! As shown in Figure-2 by coloring of the QRS complexes in leads V4,V5,V6 — there is abundant overlap, with marked increase in QRS amplitude in these leads (ie, the RED-colored R wave in lead V5 = 27 mm — and the GREEN-colored R wave in lead V6 = 25 mm).

Regarding Q-R-S-T Changes:

• There is a small Q wave in lead aVL — and a very large Q wave in lead V1.
• Regarding R Wave Progression — Transition is early! That is, a predominant R wave is already seen by lead V2.
• There is marked J-point ST depression (of ≥3 mm in leads V5,V6 — with lesser degrees of ST depression in 4 limb leads and leads V3,V4). ST segments are downsloping — terminating in symmetric T wave inversion that is deep in the inferior and lateral chest leads.
• There are 2 mm of ST elevation in lead V1 — with ST segment coving and a hint of elevation in neighboring lead V2.

Putting It All Together:

As noted — I found today's tracing fascinating, but a bit bizarre!

• What we know — is that the rhythm in ECG #1 is fairly regular and supraventricular (probably sinus with a PAC — albeit upright P waves are not clearly seen in lead II). 
• There is marked LVH — with dominant R waves in each of the lateral chest leads. ST-T waves.
• There are profound ST-T wave changes. Part of the ST depression with deep T wave inversion in the lateral chest leads clearly reflects LV "strain" from the marked LVH — but despite the very large QRS amplitudes, this ST-T wave appearance looks disproportionate, suggesting at least a component of ischemia.
• The above said — LVH and ischemic coronary disease does not explain the ST-T wave depression in the inferior leads (BLUE arrows in leads II,III,aVF) — that is much more commonly seen as a sign of acute RV "strain".
• However — ECG #1 is not especially suggestive of RVH. Tall, peaked and pointed inferior P waves of RAA (Right Atrial Abnormality) are not seen — although this might be the result of a non-sinus rhythm (ie, As noted earlier — a clearly defined upright sinus P wave is not seen in lead II). There is no rightward axis — and no predominant R wave in lead V1. The persistent S wave in lead V6 that attains 13 mm is deeper than is normally seen — but by itself, this does not satisfy criteria for RVH.

And then — there is the Qr' pattern in lead V1 with ST elevation:

• The Qr' pattern in lead V1 with ST elevation was the most challenging part of today's tracing for me to explain.

PEARL #1: I like my ECGs to "tell a story". By this I mean that all ECG findings over serial tracings and the course of the patient's evaluation make sense when correlated clinically to the history and physical exam.

• The Qr' in lead V1 does not look like simple RBBB conduction. The QRS is not wide enough for a complete RBBB — and, lateral limb leads I and aVL both lack terminal S waves.
• I've previously discussed the interesting correlation of a qR pattern in lead V1 in patients with RVH — as strongly suggesting associated pulmonary hypertension (See ECG Blog #234 and Blog #248). However, today's case lacks a dominant R wave in lead V1 — and lacks other ECG evidence of clear RVH.
• Then there is the significant ST elevation we see in lead V1 ... But limitation of this ST elevation to a single lead is not consistent with any distribution of a STEMI.
• And then — IF we "forget" about the initial Q wave in lead V1, and instead just focus on the r' with upward sloping ST elevation — Doesn't the shape of this r' followed by upward sloping ST elevation with an upright T wave resemble the saddleback of a Brugada-2 ECG pattern (See ECG Blog #238 — for review of Brugada patterns and Phenocopy).
• Finally — there is the bizarre-looking initial positive "hump" just before the Q wave in lead V1. I had no idea what this represents, given that this small positive "hump" occurs before the QRS (The vertical dotted BLUE line in Figure-2 marks the beginning of the QRS) — yet after the onset of the clearly seen P wave in lead V2.
• 
  
• BOTTOM Line: I could not come up with any logical "story" that would correlate all ECG findings of today's tracing with the limited history I was given of "new CP". I would not be at all surprised if prompt cardiac cath was performed — since the patient did present with new CP — and there is marked ST-T depression on this ECG — but I felt sure that "something else" must be going on.

Figure-2: I've labeled key findings from Figure-1 (See text).

The CASE Continues:

The bizarre appearance of the QRST complex in lead V1 was not the result of any lead misplacement (Repeat ECGs verifying placement were similar).

• I never got to see a prior tracing — which could have been extremely insightful explaining how this current tracing compared to this patient's baseline ECG.
• 
  
• Cardiac Cath showed patent coronary arteries!
• An Echo on this patient was revealing! It showed reduced LV function — significant concentric LVH — a dilated left atrium — severe aortic stenosis (seemingly in need of prompt valve replacement) — and at least moderate pulmonary hypertension, with resultant moderate pulmonary regurgitation.
• 
  
• The plan was to proceed as soon as possible with aortic valve replacement. Unfortunately — the patient abruptly developed hypoxemia, followed by cardiac arrest with PEA. He could not be resuscitated.

PEARL #2: Although always difficult to retrospectively "look back" after a patient dies, trying to better understand events that happened — doing so is immensely helpful in learning from the experience in the hope of optimizing future care.

• Apparently while waiting on the hospital floor for the decision regarding optimal aortic replacement — the patient took one of his sublingual NTG (nitroglycerin) tablets. As may happen with critical AS (Aortic Stenosis) — the vasodilating effect of NTG may further reduce systolic pressure. It was thought that this action precipitated the patient's desaturation, and led to his cardiac arrest.
• In patients with severe valvular disease (such as this patient's critical AS) — the finding of significant pulmonary hypertension (as was found on this patient's Echo) — often indicates a decompensated state, in which left ventricular and left atrial compensation is no longer able to prevent backward transmission (to the pulmonary circuit) of elevated left atrial pressure. A point may be reached in which even with valve replacement — pulmonary hypertension persists, which serves as a marker for a poor longterm prognosis (Maeder et al — Frontiers in Cardiovasc Med 5(40):1-15, 2018). 

ECG Findings in Today's Tracing Now Make Sense!

In view of the knowledge that cardiac cath revealed no significant coronary disease — and Echo indicated critical aortic stenosis with reduced LV function and significant pulmonary hypertension — the ECG findings in today's tracing now make sense!

• Severe AS is a common cause of marked LVH with LV "strain" on ECG. This explains the marked increased in QRS amplitude in the lateral chest leads — as well as some of the ST-T wave depression in these leads.
• Whereas excessive ST-T wave depression in the lateral chest leads probably reflects a superimposed ischemic component to this patient's marked LVH — the inferior lead T wave inversion (BLUE arrows in leads II,III,aVF of Figure-2) is consistent with RV "strain".
• In the context of RV "strain" — the Qr' pattern in lead V1 most probably reflects this patient's significant pulmonary hypertension (See ECG Blog #248).
• 
  
• I suspect that the saddleback ST elevation that we see isolated to lead V1 may reflect a Brugada-2 Phenocopy pattern (See ECG Blog #238) in this hemodynamically decompensated patient.
• Perhaps the small positive "hump" that appears just before the QRS complex in lead V1 reflects a similar phenomenon as can be seen with the Spiked Helmet Sign — in which with conditions of excessive endogenous catecholamines (as may occur with hemodynamically compromised patients) — there may be some elevation of the isoelectric line that begins before the QRS complex (See ECG Blog #310).

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"Take Home" Lessons from Today's Case:

This is not a simple case! As I emphasized — This complex ECG did not initially make sense to me until I learned more about the clinical history. 

• The most important "Take-Home" Points about today's case — are not about these complex ECG findings — but rather to highlight the need to clinically correlate ECG findings. Many ECGs "tell a story" — and recognizing: i) That despite this patient's presentation of new chest pain (and despite the deep ST-T wave depression in lateral chest leads) — this was not ACS (it was not an Acute Coronary Syndrome); ii) There is marked LVH; and, iii) That the inferior lead T wave inversion and Qr' with ST elevation in lead V1 point to RV "strain" with pulmonary hypertension — which in association with this patient's critical aortic stenosis explain the principal pathology. This patient needed prompt aortic valve replacement. Although this was recognized by the treating health care team — the patient unfortunately expired before this could be accomplished. 

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for making me aware of this case and allowing me to use this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
• 
  
• ECG Blog #380 — Reviews what is "Precordial Swirl" (LOTS of links to blog posts on various aspects of acute OMI/ischemia).
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• ECG Blog #234 — and ECG Blog #248 — Review of ECG diagnosis of RVH and the qR Pattern for recognition of Pulmonary Hypertension.
• ECG Blog #77 — Reviews ECG criteria for the diagnosis of RVH and RV “Strain”.
• ECG Blog #75 — Reviews the ECG criteria for the diagnosis of RAA & LAA.
• ECG Blog #233 — Reviews the ECG diagnosis for acute PE (Pulmonary Embolism).
• ECG Blog #156 — Reviews a case of Tetralogy of Fallot in an adult (with marked RAA, RVH, pulmonary hypertension).
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• ECG Blog #310 — Reviews the Spiked Helmet Sign! (Catecholamine excess).
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• ECG Blog #238 — Reviews Brugada Patterns and Phenocopy.

 

An Example of RVH in a 21yo Woman:

• See My Comment at the BOTTOM of the page in the September 1, 2020 post on Dr. Smith’s ECG Blog (as I comment in detail on the 1st of the 6 cases that Dr. Smith presents).

• ECG Blog #245 — Reviews assessment of LVH on ECG.
• ECG Blog #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
• ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
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• ECG Blog #75 — Reviews "My Take" on the ECG Diagnosis of LAA & RAA. 
• ECG Blog #234 — Reviews "My Take" on the ECG Diagnosis of RVH.
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• The November 4, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews 3 ECG Clues for rapid recognition of erroneous lead V1,V2 placement. 
• The March 31, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates the potentially misleading effect the pre-hospital ECG may have in patients with LVH (ie, by cutting off S wave voltage in the anterior leads).
• The March 29, 2019 post in Dr. Smith's ECG Blog — My Comment regarding Tracing A (at the bottom of the page) illustrates how LVH is a common mimic of acute ischemia. 
• The December 27, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates a case with anterior ST elevation from LVH that may falsely suggest acute anterior infarction.

 

ECG Blog #382 — What Does the Holter Show?

I was sent the Holter monitor tracing in Figure-1 — but without the benefit of any clinical information.

QUESTIONS:

A total of 9 QRS complexes are seen in the 2 simultaneously-recorded monitoring leads.

• How would YOU interpret the rhythm in Figure-1?
• How many P waves do you see?
• Why do the QRS complexes of beats #4 and 5 in the bottom lead look different than the other 7 beats?
• 
  
• What do you suspect as the clinical diagnosis?

Figure-1: The initial 15-second rhythm strip in today’s case.

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NOTE: The recording system used in rhythm strips from today’s post may be different from what you are accustomed to. In Figure-2 — I've labeled some of these differences — and I highlight atrial activity.

• Note in Figure-2 — in the upper right corner of this rhythm strip (within the RED rectangle) — that the recording speed is 12.5 mm/second (instead of the 25 mm/sec. speed that many of us are used to) — BUT — that the width of each large box on the ECG grid paper has been reduced by 50% (so that each small rectangular box on this ECG grid paper still represents 200 msec. = 1/5 second — as shown by the RED arrow).
• As a result — the time to record 5 of these small rectangular boxes on each rhythm strip in today’s post is still 1.0 second (with each increment of 1.0 second separated by vertical dotted GRAY lines).
• The advantage of this system of recording is that QRS amplitude of each complex is maintained — while an easier-to-read longer rhythm strip can be displayed (ie, ECG Rhythm #1 displays a full 15 seconds of today’s rhythm! — instead of the usual 6-10 second rhythm strips many of us are used to).
• 
  
• Finally — Note that each R-R interval in Figure-2 has been precisely calculated for you. For example — the R-R interval between beats #1-2 = 1820 msec. ( = 1.82 second = 9.1 little boxes, as per the GREEN arrows ==> which corresponds to a heart rate of 300 ÷ 9.1 = 33 beats/minute). 
• 
  
• PEARL #1: This computer-determined calculation allows us to instantly appreciate small changes in heart rate (ie, The R-R interval before beat #4 = 1679 msec. — which is significantly shorter than the 1820 msec. R-R interval for the first few beats in this tracing). 

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How Many P-Waves are there in ECG Rhythm #1?

The benefit of having 2 simultaneously-recorded leads in a given rhythm strip — is that this allows us to see ECG findings that may only be visibile in one of the 2 leads being monitored.

• Sinus P waves with a constant PR interval are clearly seen to precede beats #4-thru-9 (RED arrows in the upper monitoring lead in Figure-2).
• P waves in the upper lead of Figure-2 are upright, albeit small in amplitude. These P waves that precede beats #4-thru-9 — are larger and biphasic in the lower monitoring lead.
• 
  
• The QRS complexes of beats #1,2,3 are wider — and look very different in both monitoring leads in Figure-2, than the QRS morphology of sinus beats #4-thru-9. These wider beats are not preceded by sinus P waves — which suggests they are ventricular escape beats! The R-R interval that separates these ventricular beats = 1820 msec. — which corresponds to a ventricular rate of ~33/minute (which fits perfectly within the usual range of an idioventricular escape rhythm).
• 
  
• PEARL #2: The fact that the R-R interval preceding return of the 1st sinus-conducted beat ( = beat #4) is shorter ( = 1679 msec.) than the 1820 msec. R-R interval of the 3 ventricular escape beats — suggests that the reason sinus rhythm resumes beginning with beat #4, is that the rate of sinus discharge sped up sufficiently to surpass the rate of idioventricular escape!
• 
  
• PEARL #3: Note that the R-R interval varies significantly between sinus-conducted beats #4-thru-9 (ie, from 1679 msec. to 1828 msec.) — which corresponds to a variation in the rate of sinus bradycardia from 36-to-33/minute. This suggested to me from this initial rhythm strip — that additional rhythm strips from this patient's 24-hour Holter recording will probably show episodes of varying duration of ventricular escape when the rate of sinus bradycardia slows below the ventricular escape rate!
• 
  
• PEARL #4: In view of the etiology I suspected for the mechanism of explaining the rhythm change in Figure-2 — I looked closer at the lower monitoring lead for partially hidden atrial activity. Note tiny-but-real differences in QRS morphology for the first 3 beats in the lower lead (ie, a pseudo r' notch at the end of the QRS for beats #1 and 2 that is not seen at the end of beat #3 — and an extra initial positive deflection at the beginning of beat #3 that is not seen at the beginning of beats #1 and 2). This strongly suggests that sinus P waves are occurring throughout this rhythm strip — and are partially hidden under the PINK arrows!

Figure-2: I've labeled the initial rhythm strip in today’s case (See text).

Why Do Beats #4 and 5 Look Different?

Although QRS morphology for each of the sinus-conducted beats in the upper monitoring lead in Figure-2 look similar — beats #4 and 5 clearly look different than the other 7 beats in the lower monitoring lead!

• Beats #4 and 5 manifest a narrow biphasic (almost equal R wave and S wave) morphology in the lower lead. This is an intermediate morphology between the predominantly upright QRS of sinus-conducted beats #6-thru-9 — and the wider predominantly negative QRS of beats #1-thru-3, which are the ventricular escape beats.
• 
  
• PEARL #5: The most logical explanation for why the QRS complex of beats #4 and 5 in the lower monitoring lead look different and intermediate in morphology between QRS morphology of the initial 3 ventricular escape beats and the pure sinus-conducted beats that follow ( = beats #6-thru-9) — is that beats #4 and 5 must be Fusion beats! Identification of beats #4 and 5 as "fusion" beats (F) confirms a ventricular etiology for beats #1,2,3. This makes sense given that the underlying rhythm in today's case appears to be marked sinus bradycardia and arrhythmia, with a ventricular escape rhythm appearing when the SA node rate drops below 33/minute.
• 
  
• NOTE: The rhythm strip in Figure-2 is a Holter tracing — so baseline artifact undulations that we see, in addition to some variation in QRS amplitude for sinus beats #6-thru-9 is not unexpected. That said — the difference in QRS morphology between beats #4,5 vs beats #6-thru-9 in the lower lead is clearly real, and most logically explained by interpreting beats #4 and 5 as fusion beats.

What Do YOU Suspect as the Clinical Diagnosis?

As mentioned above — I had no clinical information (not even the age of this patient) at the time I was sent this initial tracing. That said — Common things are Common.

• Although there are a number of ECG findings that characterize SSS (Sick Sinus Syndrome) — by far, the most common initial rhythm of this syndrome will be sinus bradycardia and arrhythmia. There is often a long subclinical period (of up to a decade or more!) — during which sinus bradycardia and arrhythmia may be seen as the only indication of SSS, albeit not yet to a degree that produces symptoms.

PEARL #6: As I discuss in my review of SSS (See ECG Blog #342 for details) — establishing a diagnosis that sinus bradycardia indicates SSS — will depend on the following:

• Finding out the age of the patient (ie, SSS is most common in older individuals) — and learning whether the patient has been symptomatic? (ie, with syncope-presyncope, fatigue, dyspnea, chest pain?).
• Checking the rest of the Holter to see if episodes of bradycardia primarily occur at night? (since sleep apnea is a readily treatable cause of nighttime bradycardia, as well as of other arrhythmias).
• Checking all medications that the patient is taking (including herbal products). You are looking for potential rate-slowing medication — that may be the cause of bradycardia (Not to forget inquiry about beta-blocker eye drops — which are partially absorbed, and which can be an easily overlooked as an iatrogenic cause of bradycardia). 
• Ruling out other potential causes of bradycardia (ie, recent ischemia-infarction; hypothyroidism).
• 
  
• BOTTOM Line: Although many questions remain to be answered regarding clinical correlation of today's case — I immediately considered SSS as being statistically the most common cause of a rhythm like the one we see in Figure-2.

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What Else did the 24-Hour Holter Show?

I was sent a number of additional 15-second rhythm strips from this patient's 24-hour Holter Monitor. In addition — I was provided with the Holter Summary Report. Pertinent ECG findings from this summary included the following:

• An overall average heart rate for the day of monitoring of between 45-50/minute. The rate did not drop below 30/minute — and it did not exceed 100/minute. Bradycardia was not limited to nighttime hours.
• No pause beyond 2.0 second.
• 
  
• Occasional PVCs throughout the day without sustained repetitive forms.
• 2 short runs of SVT (presumably atrial tachycardia).
• Periodic transition from wide-to-narrow QRS complexes (similar to that seen in Figure-2).

Below in ECG Rhythms #2-thru-6 — are selected additional rhythm strips I received. Do these tracings support my initial impression?

ECG Rhythm #2:

ECG Rhythm #3:

ECG Rhythm 4:

ECG Rhythm #5:

 ECG Rhythm #6:

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MY Thoughts on ECG Rhythms #2-thru-6:

Overall — these additional rhythm strips support my initial impression.

ECG Rhythm #2:

Amazingly — We see no less than 7 variations in QRS morphology for the 9 beats shown in ECG Rhythm #2. For clarity in Figure-3 — I've labeled P waves in this tracing (RED arrows in Figure-3).

• I find it difficult to determine which (if any) of the 9 beats in Rhythm #2 are purely sinus-conducted.
• Although the QRS complex of beat #8 occurs earlier-than-expected and looks similar to the QRS of sinus-conducted beats in Figure-2 — this beat is biphasic in the lower monitoring lead, and we previously determined that biphasic beats #4 and 5 in the lower lead of Figure-2 were fusion beats (F).
• For this reason — I suspect beat #2 in Figure-3 is also a fusion beat (because beat #2 is also biphasic in the lower lead).
• Beats #3-thru-7 in Figure-3 represent various degrees of ventricular etiology, with-or-without some component of fusion. Note that the PR interval for beats like #3,4,5 is clearly too short for normal conduction (therefore predisposing to a certain amount of fusion). 
• Beat #9 is different — and shows us a different shape (V) for this wide beat in both the upper and lower monitoring lead (compared to the shape of previous ventricular escape beats in these 2 leads). Therefore — There appear to be at least 2 different ventricular sites for the ventricular escape rhythm!
• Finally — I put a question mark (?) above beat #1 — because I can't figure out what this beat represents (ie, Ventricular escape, possibly with fusion from perhaps yet another ventricular site?).

PEARL #7: The specific etiology of each beat in these selected tracings is not important. Instead — What counts is the "theme" of the overall rhythm disturbance in today's Holter report.

• The overall "theme" of these rhythm strips — is that there is an underlying marked sinus arrhythmia and bradycardia, with frequent escape rhythms arising from one or more ventricular sites. This results in a variety of fusion beats between sinus-conducted beats and ventricular escape rhythms.

Figure-3: I've labeled P waves (RED arrows) and selected beats in ECG Rhythm #2. Note that the PR interval is clearly too short to conduct normally for a number of beats (that therefore must represent fusion between sinus and ventricular beats).

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ECG Rhythm #3:

The overall "theme" of today's Holter monitor recording continues. For clarity in Figure-4 — I've labeled P waves in this tracing (RED arrows in Figure-4).

• None of the P waves in Figure-4 come before the QRS. Therefore — there are no sinus-conducted beats in ECG Rhythm #3. Instead — all beats in Figure-4 must be of a ventricular etiology!
• Beat #3 clearly manifests an intermediate QRS morphology (Best appreciated in the lower monitoring lead — where beat #3 is intermediate in shape to the wide positive QRS of beats #1,2,4 — and the wide negative QRS of beats #7 and 8). Therefore — Beat 4 represents a fusion beat between 2 different ventricular escape foci!
•  
• Negative but narrow beats #5 and 6 are also clearly intermediate in QRS morphology between the wide upright QRS of beats #1,2,4 — and the wide negative QRS of beats #7 and 8. Therefore — beats #5 and 6 also represent fusion between 2 different ventricular escape foci!

Figure-4: I've labeled ECG Rhythm #3.

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ECG Rhythms #4, 5 and 6:

The "theme" of today's Holter monitor continues with these last 3 rhythm strips.

• There is marked bradycardia throughout — with frequent ventricular escape from different ventricular foci — often for extended periods without return of sinus rhythm.

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Putting It All Together:

I have subsequently found out that the patient in today's case is a woman in her 80s — so the likelihood of Sick Sinus Syndrome increases! I previously mentioned that the Holter Summary showed the following:

• An overall average heart rate for the day of monitoring of between 45-50/minute. The rate did not drop below 30/minute — and it did not exceed 100/minute. Bradycardia was not limited to nighttime hours.
• No pause beyond 2.0 second.
• 
  
• Occasional PVCs throughout the day without sustained repetitive forms.
• 2 short runs of SVT (presumably atrial tachycardia).

Clinically — the degree of persistent marked bradycardia is worrisome, even if prolonged pauses (of >2.5-to-3.0 second) are not yet seen — and even if this patient is not yet reporting "symptomatic bradycardia".

• Failure of the heart rate to go over 100/minute during the course of a day suggests there may be chronotropic incompetence — another concerning sign of SSS.
• The short runs of SVT are consistent with possible "Tachy-Brady" Syndrome — in which many patients with SSS alternate between marked bradycardia and various tachyarrhythmias.
• 
  
• Follow-Up: Our interpretation of this Holter was passed on to the patient's primary physician. I would bet that this patient will soon receive a permanent pacemaker.

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Acknowledgment: My appreciation to Andreas Röschl (from Neumarkt, Germany) for the case and this tracing.

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ADDENDUM (June 3, 2023): 

• The Audio PEARL (2:45 minutes) below reviews the ECG findings of SSS.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs and 3R Approach to Systematic Rhythm Interpretation.
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• ECG Blog #342 — reviews the ECG diagnosis of SSS (Sick Sinus Syndrome)
• ECG Blog #256 — Reviews another case of SSS.
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• ECG Blog #128 — ECG Blog #129 — and ECG Blog #133 — for review on Fusion Beats (that also show AV dissociation).
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• ECG Blog #295 — Reviews the concept of bradycardic-induced BBB ( = Phase 4 block). This is discussed near the bottom of the page (ie, in Pearl #5 — that appears just under Figure-6).
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• The July 5, 2018 post in Dr. Smith's ECG Blog — (Please see My Comment at the bottom of the page for Review on the ECG diagnosis of Sick Sinus Syndrome).