Thursday, September 29, 2022

ECG Blog #335 — Is there Proof?

You are given the ECG shown in Figure-1 — and told only that the patient is a 40-year old man, who was hemodynamically stable.

  • How would YOU interpret this tracing?

NOTE: Unfortunately — no long lead rhythm strip was recorded. That said — it turns out that a long lead rhythm strip was not needed for definitive diagnosis.

Figure-1: 12-lead ECG obtained from a 40-year old man. He was hemodynamically stable at the time this ECG was recorded.

MY Approach to the ECG in Figure-1:
As always – I favor beginning interpretation with assessment of the long lead rhythm strip — using the Ps, Qs & 3R Approach to recall the KEY Parameters (See ECG Blog 185). I find it easiest (and most productive) to delay assessing the 12-lead ECG until after I’ve had a chance to look at the rhythm.
  • The rhythm is fast and regular (although not quite as fast as one might think from initial inspection = about 115/minute). The QRS is wide. Regular sinus P waves that conduct are not seen (ie, there is no upright P wave with constant and normal PR interval before each QRS complex in lead II).

What Have We Described for the Rhythm in Figure-1?
We have described a regular WCT ( = Wide-Complex Tachycardia) rhythm at ~115/minute — but without clear sign of normally conducting sinus P waves.
  • PEARL #1: As emphasized often on these ECG Bogs — the most common cause (by far!) of a regular WCT rhythm without sinus-conducting P waves is VT (Ventricular Tachycardia). Depending on clinical circumstances of the case at hand — between 80-to-90+% of such rhythms will turn out to be VT. For that reason — ALWAYS assume VT until proven otherwise!

  • PEARL #2: Prominent among ECG features that may assist in the diagnosis of a regular WCT — is QRS morphology. VT is favored IF — QRS morphology does not resemble any known form of conduction defect (ie, LBBB or RBBB, with or without a hemiblock). This is the case with the ECG in Figure-1. Although the predominantly upright qR pattern in lead V1, with wide terminal S wave in lead V6 resembles RBBB (Right Bundle Branch Block) conduction in the chest leads — the indeterminate frontal plane axis (ie, leads I,II,III all predominantly negative) is not typical for RBBB conduction in the limb leads. That said — I thought QRS morphology in ECG #1 was clearly not definitive for a ventricular etiology.

  • NOTE: For review of "My Take" on the ECG approach for assessing the regular WCT rhythm — Check out ECG Blog #196Blog #220Blog #263 — and Blog #283

Returning to today's case — there is 1 ECG feature that is all but definitive for VT in Figure-1. What might this be?
  • HINT: Take Another LOOK at the ECG in Figure-1WHY might QRS morphology in lead II be changing?

  • See Figure-2 ...

Figure-2: RED arrows highlight why QRS morphology in lead II is subtly changing (See text).

Why QRS Morphology in Lead II is Changing:
There are 5 RED arrows in Figure-2. These arrows represent atrial activity — that is best seen under the 1st RED arrow — partially seen under the next 3 RED arrows (as these P waves distort the initial part of the QRS complex) — and almost completely hidden within the QRS under the last RED arrow.
  • PEARL #3: The fact that the position of the 5 P waves highlighted by these RED arrows is constantly moving with respect to its neighboring QRS complex — tells us that these P waves are unrelated to QRS complexes (ie, there is complete AV dissociation for these 5 beats). This finding of complete AV dissociation of a regular atrial rhythm from the wide tachycardia (at least for a significant portion of the WCT rhythm)is virtually diagnostic of VT (See ECG Blog #133Blog #134and Blog #151 for additional examples illustrating how AV dissociation allows you to confirm the diagnosis of VT!).

  • PEARL #4: Although the ECG finding of AV dissociation provides invaluable assistance for confirming the diagnosis of VT — it will usually not be seen with the most problematic forms of VT (which are those VTs that occur at faster heart rates). This is because the faster the ventricular rate of VT — the more likely it is that underlying sinus P waves will be hidden (ie, within QRS complexes or within ST-T waves). It is because the ventricular rate of the WCT rhythm in today's case was relatively slow (ie, only ~115/minute) — that we are able to identify AV dissociation for the 5 P waves highlighted by RED arrows in Figure-2 (Note that we do not see evidence of AV dissociation in the rest of today's tracing).

  • PEARL #5: In my experience — AV dissociation is greatly overdiagnosed! There is a tendency to label as "AV dissociation" any (and sometimes all) unexpected deflections seen in a WCT tracing. Most of the time (in my experience) — these "extra" deflections are not underlying P waves — but rather reflect artifact that is so common in symptomatic patients with marked tachycardia. Because of the clinical implications of identifying true AV dissociation in a regular WCT rhythm (ie, it virtually proves the rhythm is VT!) — I favor only diagnosing AV dissociation when you can be certain it is present (ie, when you can reliably identify at least a series of regular underlying P waves at a constant rate — as is possible for the 5 consecutive RED arrows seen in Figure-2).

  • PEARL #6: As I've emphasized — the rate of the regular WCT rhythm in today's tracing is not fast. It is ~115/minute — which lies at the limit between a "slower" form of VT = AIVR (Accelerated IdioVentricular Rhythm  which is often benign and associated with reperfusion) — and a "faster" VT rhythm (with much higher risk of deterioration to VFib and cardiac arrest). As a result — the clinical significance of today's rhythm will depend on the patient's hemodynamic stability — and — on clinical factors such as whether this rhythm represents a positive (and transient) sign that reperfusion of the "culprit" artery has just occurred. KEY POINT: Depending on these factors — the risk of today's rhythm deteriorating to VFib and cardiac arrest might be limited — and cardioversion or antiarrhythmic treatment might not necessarily be needed (See ECG Blog #108 and Blog #125 for more on AIVR).

CASE Follow-Up:
My follow-up to today's case is limited. I know that this patient had a recent MI — which suggests that the rhythm in Figure-2 may represent AIVR that developed in response to coronary reperfusion. Unfortunately — I lack confirmation of this.
  • In the absence of more clinical information — I'd consider optimal interpretation of today's rhythm = "Ventricular Tachycardia at a rate of 115/minute"
  • I'd emphasize the need for clinical correlation to determine IF antiarrhythmic treatment, cardioversion — or — a "tincture of time" (ie, with no active treatment) is likely to represent the BEST approach to initial management.


Acknowledgment: My appreciation to Ahmed Shaaban (from Cairo, Egypt) for the case and this tracing.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation
  • ECG Blog #185 — Reviews my Systematic Approach to Rhythm Interpretation.

Saturday, September 24, 2022

ECG Blog #334 — What do the 12 Leads Show?

The ECG in Figure-1 — was obtained from an older woman. Unfortunately — No other clinical information was available.
  • How would YOU interpret this ECG?

Figure-1: 12-lead ECG obtained from an older woman. No clinical history was available.

MY Thoughts on the ECG in Figure-1:
Many readers of this blog encounter the same situation that I often find myself in — namely, having to interpret tracings without the benefit of any clinical history. That was the case for me with today's tracing. (I initially did not even have the benefit of a long lead rhythm strip).
  • The rhythm in Figure-1 (for the 11 beats that we see on this tracing) — appears to be fairly regular at a rate just under 70/minute.
  • The QRS complex is narrow everywhere.

  • P waves are absent in lead II!

  • What is the rhythm in ECG #1?

  • See Figure-2 ... 

Figure-2: I've labeled atrial activity from Figure-1 (which is confirmed by provision of a long lead rhythm strip).

Continuing My Interpretation of Today's Tracing:
The fact that there is no upright P wave in lead II in Figure-1 — tells us that the rhythm is not sinus!
  • PEARL #1: Although lead II is clearly the most helpful of the 12 leads on a standard ECG for determining the cardiac rhythm — this lead will not always show atrial activity. When no clearly upright P wave is seen in lead II — then: i) The rhythm is not sinus (assuming there is neither dextrocardia nor lead reversal); and, ii) We need to focus on the remaining 11 leads in our search for atrial activity. Of these remaining 11 leads — I have found lead V1 to be 2nd-best for detecting atrial activity — followed by leads III, aVR, aVF, and/or lead V2 — followed by taking a close look at the 6 leads that remain.

The Rhythm is Revealed in Figure-2:
The 12-lead ECG in today's case provides an excellent example of how lead V1 may sometimes reveal atrial activity not evident in any of the other 11 leads. RED arrows in Figure-2 suggest there is 2:1 AV conduction for the 3 beats that occur in lead V1!
  • The long lead rhythm strip at the bottom of Figure-2 (with simultaneously-recorded leads V1 and II) — confirms 2:1 atrial activity throughout!
  • Note that the PR interval before each of the 11 beats on the long lead rhythm strip is constant — which confirms that 1 out of every 2 P waves are conducted to the ventricles.
  • The RHYTHM: Since the ventricular rate is just under 70/minute — this means that the atrial rate = 2X this, or ~135-140/minute. Since this atrial rate is well below the atrial rate usually seen with AFlutter — and since the baseline between P waves is flat (ie, there is no "sawtooth" pattern) — the rhythm in ECG #1 = ATach (Atrial Tachycardia) with 2:1 Block.

Continuing Interpretation of the Rest of the 12-Lead:
Now that we've interpreted the rhythm in Figure-2 — we can complete interpretation of the rest of this tracing:
  • Intervals (PR - QRS - QTc): We've already established that the QRS complex is narrow in all 12 leads. The PR interval looks to be a little long (ie, >0.20 second) — although the non-sinus origin of atrial activity may account for this. The QTc does not appear prolonged (ie, clearly less than half the R-R interval).

  • Axis: The frontal plane axis is normal (ie, about +40 degrees).

  • Chamber Enlargement — There is probable LVH (ie, the deepest S wave is in lead V2 [ =19 mm] + the tallest R wave, which is in lead V5 [ =18 mm] is ≥35 mm).

Regarding Q-R-S-T Changes:
  • Q waves: There is a QS complex in lead V1 (though by itself — this is not abnormal — and a small-but-definitely-present initial r wave is present in lead V2).
  • R Wave Progression — is normal (with Transition occurring between lead V3-to-V4).

  • ST-T Wave Changes: There is slight J-point ST depression in a number of leads (most marked in leads V4,V5,V6) — with T wave inversion in at least 9/12 leads (most marked in leads V3,V4,V5).
  • There is slight ST elevation in lead aVR.
  • The most "eye-catching" lead — is lead V3, which shows a straightened (almost coved) ST segment takeoff that terminates in a deep and symmetrically inverted T wave.
  • The T wave in lead V2 appears to be biphasic (ie, positive-negative) — with rapid descent from the initially positive portion of the T wave.

Putting It All Together:
Fully aware that we lack clinical information — My Thoughts on today's tracing were as follows:
  • There is an abnormal rhythm = ATach with 2:1 AV Block (with an atrial rate of ~135-140/minute).
  • Voltage criteria for LVH are satisfied.
  • J-point ST depression is seen in multiple leads — with symmetric T wave inversion (that is quite deep in leads V3,V4,V5) — with an ST-T wave shape that resembles a Wellens'-type morphology.

  • PEARL #2: Although the shape of the ST-T wave depression that we see in lateral leads I, aVL and V5,V6 is consistent with LV "strain" (in association with LVH voltage criteria) — ST-T wave changes of "strain" do not normally extend as far over as lead V3 (and should certainly not be maximal in mid-precordial leads V3,V4 when this is solely the result of LVH). So, while a component of the ST-T wave changes we see in today's tracing may reflect LVH — the Overall Picture (ie, with ST depression and T wave inversion in at least 9/12 leads) clearly suggests ischemia (which depending on the history, could be recent or acute).

  • PEARL #3: While the shape of the ST-T wave in leads V2 and V3 is consistent with what may be seen with Wellens' Syndrome — this diagnosis can not be made without a history of previous chest pain that has now resolved at the time the ECG being looked at is recorded (See ECG Blog 254).

  • PEARL #4: A number of conditions may result in similar ST-T wave changes as are seen in Figure-2. These include: i) Diffuse cardiac ischemia (given ST-T wave changes in 10/12 leads!); ii) Wellens' Syndrome (IF the history is consistent) from a tight, proximal LAD (Left Anterior Descending) stenosis; iii) Recent infarction — in which there are now ST-T wave changes from reperfusion of the "culprit" artery (See ECG Blog #294); iv) Hypertrophic cardiomyopathy (See ECG Blog 309); v) Myocarditis — or other underlying cardiac problem; vi) A "memory" effect from sustained arrhythmia (if the ATach has been present for an extended period of time); and/or, vii) Some combination of the above factors!

  • BOTTOM Line: There are multiple possible reasons that may account for the ECG findings described above. The task falls on us to correlate this tracing with the clinical situation to determine IF an acute cardiac process is ongoing.


ADDENDUM (9/24/2022): In the following 2 Figures — I post written summary from my ECG-2014-ePub regarding Wellens’ Syndrome

  • CLICK HERE — for a PDF of this 3-page file on Wellens’ Syndrome that appears in Figure-3 and Figure-4.



Figure-3: Regarding Wellens’ Syndrome (from my ECG-2014-ePub).

Figure-4: Wellens’ Syndrome (Continued). 

ECG Media PEARL #26a (7:40 minutes Audio) — Reviews what Wellens' Syndrome is — and what it is not (from ECG Blog #254).




Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).  

  • ECG Blog #209 — Reviews a case of marked LVH that results in similar ST-T wave changes as may be seen with Wellens' Syndrome.
  • ECG Blog #254 — Reviews what Wellens' Syndrome is and is not.
  • ECG Blog #309 — Reviews distinction between LVH, Wellens' Syndromevs — HCM (Hypertrophic CardioMyopathy).

  • See My Comment at the bottom of the page in the August 12, 2022 post in Dr. Smith's ECG Blog — for review on the History of Wellens' Syndrome (with reference to the original 1982 article by Zwaan, Bär & Wellens).

  • ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subect of Audio Pearl MP-59 in Blog #245).

  • ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused (with Audio Pearl MP-11 in Blog #294).

Monday, September 19, 2022

ECG Blog #333 — An Elderly Man with a Stroke

The ECG in Figure-1 — was recorded pre-hospital by the EMS (Emergency Medical Services) team, obtained from an elderly man with an acute stroke. There was no chest pain. The patient was hemodynamically stable.
  • How would YOU interpret this ECG?
  • Clinically — What do you suspect as the cause of these ECG findings? Does this explain the cardiac rhythm?

Figure-1: The 12-lead ECG recorded by the EMS team in today's case.

NOTE: Interpretation of today's tracing is especially challenging because (as is common with pre-hospital ECG machines): i) There is no simultaneously-recorded long lead rhythm strip; and, ii) QRS amplitude is often "cut off" — such that in Figure-1, full amplitude of some QRS complexes in leads II, III, aVL, aVF and V3 is simply not seen.
  • Also complicating interpretation of the ECG in Figure-1 — is the constantly changing QRS morphology.

MY Thoughts on the Rhythm in Figure-1:
As noted — constantly changing QRS morphology and lack of a long lead rhythm strip complicate interpretation. For clarity in Figure-2 — I've numbered the 15 beats in today's tracing.
  • Beats #1, and 8 (which is partially hidden by the vertical black lead change marker) — and beats #12-thru-15 all manifest a narrow QRS. Although this makes for a total of only 7 narrow-complex beats — this appears to be the underlying rhythm. This underlying rhythm looks to be irregular (ie, with variable R-R intervals— and, I do not see any P wave in lead II (and IF there were sinus P waves — I would expect to see one in lead II between beats #1-2). Therefore — the underlying rhythm in Figure-2 appears to AFib (Atrial Fibrillation), here with a controlled ventricular response.
  • In support that the underlying rhythm in Figure-2 is AFib — are the irregularly irregular undulations between QRS complexes that appear in the baseline, and which are best seen in lead V1. These are "fib waves".

  • This leaves us with beats #2-thru-6 and beats #9,10,11 — which all manifest a wide QRS complex. These wide beats are surprisingly regular (with no more than minimal variation in the R-R interval) — with a ventricular rate of ~85/minute

  • PEARL #1: The fact that in the setting of underlying AFib — these 8 wide beats manifest an almost regular rhythm strongly suggests that these beats represent a ventricular rhythm (which at a rate of ~85/minutequalifies this rhythm as AIVR = an Accelerated IdioVentricular Rhythm — See ECG Blog #108).

  • PEARL #2: The wide beats in Figure-2 are not the result of aberrant conduction. There simply is no reason for beats #2-thru-6 and #9,10,11 to conduct with a wide QRS complex — because these beats occur late in the cycle (whereas aberrant conduction almost always occurs with a much shorter coupling interval that falls within the relative refractory period). Instead — the R-R interval preceding the 1st ventricular beat in each run (ie, the R-R interval before beat #2 and before beat #9) — is virtually the same as the R-R interval between consecutive ventricular beats (which is exactly what we'd expect for an escape rhythm!).
  • PEARL #3: QRS morphology of the wide beats in Figure-2 is not consistent in all leads with LBBB (Left Bundle Branch Block) conduction. Although the monophasic R wave in high-lateral leads I and aVL does resemble LBBB conduction — the equiphasic (R=S) complex in lead V2 for beats #9,10,11 is not consistent with this, or any other form of conduction defect.
  • PEARL #4: In final support that the wide beats in Figure-2 represent an accelerated ventricular rhythm — is the finding that beat #2 is a fusion beat! (See ECG Blog #128). This is best seen by comparing the shape and width of the QRS complex and T wave of beat #2 in leads I and II — with the shape and width of the supraventricular beat before it ( = beat #1) — and the ventricular beat after it ( = beat #3). The only way to produce the intermediate appearance of beat #2 — is if beat #2 represents near-simultaneous occurrence of both a supraventricular and ventricular beat!

Figure-2: I've numbered the beats in Figure-1.

Interpreting the Rest of the 12-Lead ECG:
Now that we've established that the underlying rhythm in Figure-2 is AFib (that is twice interrupted by runs of AIVR) — we can focus attention on interpreting the remainder of today's tracing.
  • PEARL #5: The KEY to assessing acute ST-T wave changes in association with an intermittent ventricular rhythm — is to focus attention in each of the 12 leads on all supraventricular beats (which in Figure-2 entails assessing ST-T wave morphology for each of the narrow beats).
  • In leads I,II,III — beat #1 is supraventricular. In leads aVR,aVL,aVF — beat #7 and beat #8 are supraventricular (but we unfortunately do not see the ST-T wave for beat #8). Both beats #1 and 7 reveal T wave inversion in the inferior leads for these 2 supraventricular beats.
  • There are no supraventricular beats in leads V1,V2,V3 (so we can not reliably assess for ST-T wave changes in these leads).
  • There are 4 supraventricular beats in leads V4,V5,V6 — all of which show modest T wave inversion, with what appears to be modest J-point ST depression.

  • BOTTOM LINE: There is a small-to-modest amount of symmetric T wave inversion in 6/9 leads that we were able to assess for this in. A number of these leads also show slight J-point ST depression. These ST-T wave changes may represent: i) Ischemia (which could be recent or acute); — and/orii) These ST-T wave changes may represent reperfusion T waves following recent infarction.

Putting It All Together:
Although today's patient did not complain of chest pain — this elderly man was having an acute cardiovascular event in the form of an acute stroke. Clearly age and the underlying AFib rhythm predisposed this patient to developing stroke.
  • In a small-but-significant percentage of patients with acute thromboembolic stroke — an acute MI is the precipitating cause. Perhaps the most common clinical setting for seeing AIVR — is as a reperfusion arrhythmia following acute OMI ( = Occlusion-based Myocardial Infarction).

  • PEARL #6: On occasion (ie, when the clinical setting is "right") — the 1st ECG clue that a patient is having an acute MI may be the unexpected development of AIVR. Given the age of today's patient — his ongoing acute stroke — diffuse T wave inversion (with some ST depression) — and runs of AIVR — spontaneous reperfusion from acute MI should be suspected!

  • PEARL #7: As emphasized in ECG Blog #228Not all patients with acute MI have chest pain. Instead, the estimated incidence of "Silent" MI may be as high as between 20-40% of all MIs (depending on the definition used). As a result — lack of chest pain in today's case does not rule out the possibility of acute MI given predisposing factors of advanced age and acute stroke, in association with diffuse T wave inversion and runs of AIVR. 

CASE Conclusion:
Unfortunately — I do not have follow-up on this case. That said — the "Lesson-to-be-Learned" — is that despite the absence of chest pain in today's case — serial troponins and repeat ECGs were indicated as soon as the patient arrived at the hospital.  



Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).  

  • ECG Blog #108 — Reviews the concept of AIVR.
  • ECG Blog #321 — Reviews another case of an AIVR rhythm.

  • ECG Blog #128 — Reviews the concept of how Fusion Beats can help to prove a wide-complex rhythm is ventricular (and not the result of aberrant conduction).

  • ECG Blog #228 — Reviews the concept of "Silent" MI (How common this is — and How these patients present).

  • ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused (with Audio Pearl MP-11 in Blog #294).

Wednesday, September 14, 2022

ECG Blog #332 — 3rd-Degree with Double BBB?

The ECG in Figure-1 — is from a woman in her 60s, who presented with “chest tightness” over several days. This tracing was diagnosed as showing complete AV block.

  • Do YOU agree with the interpretation? OR — Is this “trifascicular" block?
  • Is there evidence of infarction on this tracing?

Figure-1: 12-lead ECG and long lead II rhythm strip — obtained from a woman with "chest tightness" over several days. Is this complete AV block? — Is it "trifascicular" block? (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:
As always – I favor beginning interpretation with assessment of the long lead rhythm strip — using the Ps, Qs & 3R Approach to recall the KEY Parameters (See ECG Blog 185). I find it easiest (and most productive) to delay assessing the 12-lead ECG until after I’ve had a chance to look at the rhythm.

PEARL #1: As I have often emphasized — It does not matter in what sequence you choose to assess the KEY Parameters — and I often START with whichever of these parameters is easiest to assess.
  • Today's tracing is extremely complicated. On initial inspection of this rhythm — it simply is not immediately evident: i) Why QRS morphology is changing? (ie, Bundle branch block or ventricular escape beats?); ii) Why the ventricular rate is changing? — and, iii) What kind of AV block is present?

  • As a result of the above complexities — My "eye" focused on beat #4 in Figure-1 because: i) This beat occurs earlier-than-expected; ii) The QRS complex of beat #4 is not as wide as the QRS in the first 3 beats; and, iii) The PR interval preceding beat #4 = 0.18 second, which makes it the only one of the 6 beats on this tracing that is preceded by a PR interval with a reasonable chance of conducting. 
PEARL #2: When a complex form of AV block is present — my favorite CLUE that a beat is likely to be conducted — is IF you see a beat that occurs earlier-than-expected.
  • In addition to its earlier-than-expected occurrence — further support that beat #4 in Figure-1 is probably conducted is forthcoming from: i) The fact that QRS morphology changes from that of the 3 preceding beats; ii) A look at simultaneously-recorded lead V1 for beat #4 suggests a very typical RBBB (Right Bundle Branch Block) morphology — in the form of an rSR' (with S wave descending below the baseline in lead V1 — and a terminal "taller right rabbit ear" R' deflection); and, iii) Beat #4 is the only beat preceded by a normal PR interval — whereas the none of the other PR intervals preceding the remaining 5 beats on this tracing seem likely to conduct.

  • NOTE: For more on HOW to tell if a P wave is (or is not) likely to conduct — Check Out the Audio Pearl in the ADDENDUM below.

PEARL #3: As I often emphasize — the simple step of labeling P waves is amazingly helpful for: i) Determining IF there is an underlying regular (or almost regular) atrial rhythm; andii) Facilitating assessment as to whether some (or all) of the P waves you identify are (or are notRelated to neighboring QRS complexes.
  • In Figure-1 — I began my “Search for P Waves” — by labeling those P waves that I was certain are present. I have done this with RED arrows in Figure-2.
  • Accounting for slight variation in the P-P interval that is so often seen — it seems logical to anticipate that 2 additional sinus P waves are likely to be hiding within the QRS of beats #1 and 2 (PINK arrows in Figure-2).

PEARL #4: It is common to see slight variation in the atrial rate when there is 2nd- or 3rd-degree AV block. This phenomenon is known as ventriculophasic sinus arrhythmia — and is thought to be due to better perfusion for those P waves that "sandwich" a QRS complex (with resultant slight shortening of the P-P interval). There may then be slight lengthening for P-P intervals that do not contain a QRS between them.
  • To Emphasize: The above relationship showing slight shortening of the P-P interval for those P waves that "sandwich" a QRS complex between them — does not always hold. That said — we do for the most part see this relationship hold true for most P-P intervals shown in Figure-2.

  • Doesn't the labeling of P waves with ARROWS in Figure-2 — facilitate determining which of the P waves in today's tracing are likely to have a chance to conduct?

Figure-2: I have added RED arrows over those P waves that I am certain are present in the long lead II rhythm strip.

Is There Complete AV Block in Figure-2?
Ideally — we would have a much longer period of monitoring for determining the rhythm in Figure-2. That said — I find it helpful to break down our assessment of the rhythm into several Parts:
  • Part-1: Look at the first 3 beats in Figure-2. The QRS complex for these first 3 beats is wide — with a morphology potentially consistent with LBBB (Left Bundle Branch Block).
  • The 6 P waves associated with these first 3 beats appear completely unrelated to the QRS (ie, with a constantly changing PR interval). The 1st, 3rd and 5th P waves in the long lead II rhythm strip ( = the first 3 RED arrows) have clearly had more than adequate opportunity to conduct — yet failed to do so. This suggests that at the least — there is high-grade 2nd-degree AV Block.

  • Part-2: As we have already deduced (ie, in Pearls #1 and #2 above) — the degree of AV block for the rhythm in Figure-2 can not be "complete" — because beat #4 is conducted! We know this — because beat #4 occurs earlier-than-expected — beat #4 is preceded by a normal PR interval and QRS morphology of this beat #4 changes from the LBBB-like appearance of the first 3 beats in Figure-2 — to a QRS morphology consistent with RBBB conduction.

  • Part-3: The remaining 2 beats in Figure-2 ( = beats #5 and 6) are not conducted. We know this because: i) None of the P waves associated with these last 2 QRS complexes occur at a point in the cardiac cycle when they would be expected to conduct; and, ii) The R-R intervals between beats #4-5 and beats #5-6 are equal to each other — and — these R-R intervals are significantly longer than the R-R interval preceding beat #4 that we know is conducting. This suggests that beats #5 and 6 must be "escape" beats that manifest (at least in lead II) a similar QRS morphology as conducted beat #4.

Figure-2: Putting It All Together
  • High-grade 2nd-degree AV Block is present in the long lead II rhythm strip in Figure-2 — because there are many P waves that clearly have more than adequate opportunity to conduct, yet fail to do so. But because at least 1 QRS complex is conducted (ie, beat #4) — the degree of AV block can not be complete!

  • The 1 beat in Figure-2 that is conducted ( = beat #4) — is conducted with an underlying RBBB (based on the typical rSR' morphology of this beat in lead V1 — as was highlighted in Pearl #2 above).
  • Because QRS morphology of "escape" beats #5 and 6 in the long lead II rhythm strip is similar to QRS morphology of conducted beat #4 — this suggests that the site of these escape beats is from the AV Node. The wide terminal S wave in simultaneously-recorded lateral leads V5 and V6 for beat #6is consistent with RBBB conduction.
  • Presumably — the first 3 beats in this tracing, that manifest AV dissociation with more pronounced QRS widening (ie, beats #1,2,3) — are arising from an "escape" site below the AV Node (ie, either from the right bundle branch or from ventricular myocardium).

  • What do the measurements that I've added in Figure-3 show?

Figure-3: I've measured the R-R intervals between each of the beats in today's rhythm. I've also dropped 3 vertical BLUE lines to show where the QRS complex begins for beats #1, 4 and 6 in simultaneously-recorded leads.

Figure-3: What Do My Measurements Show?
When I first saw today's tracing — I wondered if beats #1,2,3 might be supraventricular, given the close resemblance of QRS morphology for these beats to LBBB conduction. As a result — I initially wondered if alternating BBB (Bundle Branch Block) might be present — with change from LBBB to RBBB conduction beginning with beat #4?
  • I found it interesting that caliper measurement reveals an equal R-R interval between beats #1-2 and beats #2-3 ( = 1480 msec.) — and — that this R-R interval is different than the R-R interval between beats #4-5 and beats #5-6 ( = 1530 msec.). The fact that these 2 R-R intervals are different — suggests there are 2 different "escape" rhythm sites.
  • The finding of similar (if not identical) QRS morphology for conducted beat #4 — and non-conducted "escape" beats #5,6 — essentially localizes the site of this "escape" focus to the AV Node.
  • I thought this finding made it much more likely that beats #1,2,3 represent a ventricular escape focus (possibly arising from the right bundle branch).

  • Finally — I dropped verticle BLUE lines passing through simultaneously-recorded leads for beats #1, 4 and 6. These lines begin just before the onset of the QRS complex. They explain why despite RBBB conduction — the QRS complex does not look overly wide for beats #4,5,6 in the long lead II rhythm strip (ie, the initial part of the QRS in lead II lies isoelectric with the baseline).

Is There Evidence of Infarction in Figure-3?
Common things are common. Given the presence of bradycardia + high-grade 2nd-degree AV block + underlying RBBB — recent infarction has to be strongly considered as the potential precipitating factor for these multiple conduction defects.
  • Assessment of ST-T wave changes during a ventricular rhythm is usually difficult (and often not possible). As a result — I did not think much could be said about the possibility of recent infarction from assessment of ST-T wave appearance of beats #1,2,3 in Figure-3 — because these first 3 beats in the rhythm presumably arise from a ventricular escape focus.
  • Beats #4,5,6 manifest RBBB conduction. While not definitive — I thought the appearance of ST-T waves in several of the chest leads leads in which this supraventricular RBBB conduction morphology appears was potentially suspicious for a recent (or acute) cardiac event. That is: i) Usually the ST segment in lead V1 with RBBB is depressed — and not at the baseline, as it is in Figure-3. There is also usually no terminal T wave positivity with RBBB in lead V1; ii) ST depression with RBBB is usually also seen in lead V2 — so the distinctly flat ST segment that we see in lead V2 of Figure-3 is not typical; and, iii) The T waves in leads V5,V6 appear larger-than-expected given R wave amplitude in these leads (ie, These T waves may be hyperacute).

  • To Emphasize: The above described ST-T wave changes are not definitive. Instead — they are subtle! But in the setting of the advanced conduction defects that we see in today’s tracing — these subtle ST-T wave changes are suspicious for a possible recent event — and — this suspicion justifies obtaining serial tracings and troponins, and possibly performing cardiac catheterization (depending on specifics of the clinical situation).

Is There Tri-Fascicular Block?

The term, “trifascicular” block — implies impaired conduction in all 3 of the major conduction fascicles: i) the right bundle branch; ii) the left anterior hemifascicle; andiii) the left posterior hemifascicle.

  • The term, “trifascicular block” is no longer recommended (Surawicz et al — JACC: Vol. 53, No. 11, pp 976-981, 2009). This is because of “the great variation in anatomy and pathology producing this pattern” — as well as the fact that one will usually not be able to make a definitive diagnosis of trifascicular block from the surface ECG. We simply can not tell IF PR interval prolongation in a patient with bifascicular block is due to AV Nodal disease or disease in the remaining conducting fascicle.
  • The Exception: Rarely, one may be able to diagnose involvement in all 3 conduction fascicles — if for example, there is RBBB and LAHB that alternates with RBBB/LPHB. But even in this circumstance — current recommendations favor clarity in description by avoiding the term “trifascicular block” — and instead noting each of the conduction defects that are present.
  • Regarding Today’s Tracing: As stated above — the conduction defects in today’s tracing include: i) High-grade 2nd-degree AV block (but not complete AV block!); and, ii) Underlying RBBB for the 1 conducted beat, and for the 2 AV Nodal escape beats. Since there is no indication of either left anterior or posterior hemiblock — there is no evidence in today's tracing for “trifascicular” block.

Final Confirmation of the Rhythm in Today's Case:
The BEST way to demonstrate the etiology of a complex cardiac rhythm — is by construction of a Laddergram — which I illustrate in Figure-4.

  • NOTE: For more on how to read (and/or draw) Laddergrams — Please check out our ECG Blog #188 (which includes teaching aids + LINKS to more than 50 illustrated laddergrams I have published).   

Figure-4: My proposed laddergram for explaining the mechanism of today’s rhythm (See below).

Explanation of the Laddergram in Figure-4:
  • The first 3 beats in the long lead II rhythm strip most likely represent a ventricular escape rhythm (which is why these beats originate from the bottom of the Ventricular Tier). None of the first 6 P waves (labeled "a"-thru-"f") are able to conduct to the ventricles — so there is AV dissociation during the first half of this tracing.
  • The KEY to interpreting today’s rhythm lies with recognition that beat #4 is conducted, albeit with RBBB. The fact that at least 1 on-time P wave (this being the P wave labeled “gis able to conduct — tells us that the degree of AV block is not complete.

  • Following beat #4 — there is again AV dissociation, as none of the next 5 on-time P waves (labeled "h"-thru-"l") are conducted to the ventricles.
  • While true that the on-time P waves labeled “i” and “k” do not have a reasonable “chance” to conduct (because they either occur with a PR interval that is too short to conduct — or they occur right after the QRS during the absolute refractory period) — the P waves labeled “h”, and especially “jshould be able to conduct, but fail to do so. This supports our conclusion that there is high-grade 2nd-degree AV block.
  • Since the R-R intervals between beats #4-5 and beats #5-6 are equal to each other, and clearly longer than the R-R interval preceding conducted beat #4 — and — since QRS morphology of beats #5 and 6 is similar (if not identical) to QRS morphology of conducted beat #4 — beats #5 and 6 presumably represent a junctional escape focus that also manifests RBBB conduction.

CASE Follow-Up:
Unfortunately, my follow-up to today’s case is limited. I know that troponin was normal — and that the patient did not have hyperkalemia. A permanent pacemaker was placed — and the patient was discharged from the hospital after several days without further complication.


Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.


Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. (This block post also reviews the concept of "Trifascicular Block").
  • ECG Blog #185 — Use of a Systematic Approach to Rhythm Interpretation

  • ECG Blog #188 — Reviews how to read (and/or drawLaddergrams (plus LINKS to more than 50 clinical examples of laddergrams I have drawn).

  • ECG Blog #203 — Reviews the ECG diagnosis of Axis and Hemiblocks.
  • ECG Blog #204 — Reviews a user-friendly approach for diagnosis of the Bundle Branch Blocks.

  • ECG Blog #186 — and ECG Blog #236 — for review on the basics of 2nd-degree AV Block.
  • ECG Blog #192 — Reviews the 3 Causes of AV Dissociation — and emphasizes why AV Dissociation is not the same thing as Complete AV Block. 
  • ECG Blog #191 — Emphasizes the difference between AV Dissociation vs Complete AV Block.
  • ECG Blog #202 — and ECG Blog #257 — Review cases regarding HOW to tell if there is (or is not) Complete AV Block.

  • ECG Blog #247 — Reviews a complex case with AV Dissociation.

ADDENDUM (9/14/2022): I've reviewed some KEY material related to today's case:
  • Audio Pearl on HOW to tell if a given P wave in an AV block tracing is likely to be conducting.
  • 3 figures below (from my ECG-2014-PB) — that review "My Take" on the ECG diagnosis of Bifascicular Block.

ECG Media PEARL #61 (5:45 minutes Audio) — Reviews HOW to Tell IF a P Wave is Conducting? Being able to answer this question is KEY for determining the etiology of complicated AV Block/AV Dissociation tracings.



Figure-6: RBBB/LPHB (cont.) — ECG examples of bifascicular block.


Figure-7: Trifascicular Block? — Isolated LPHB vs marked RAD.