Sunday, November 29, 2020

A woman in her 40s with acute chest pain

Case written by Neha Ray MD, Brandon Fetterolf MD, and Pendell Meyers MD


A woman in her 40s with a history of rheumatoid arthritis, anemia, and thrombocytopenia presented to the ED with acute onset chest pain starting around 5am on the morning of presentation.  It woke her from sleep. The chest pain was midsternal, severe, sharp, and constant. 

On the previous night she had had a mild version of the same pain that she thought was heartburn (esophageal reflux). She reported some radiation to the left arm. She also reports 3 episodes of non-bloody vomiting over the course of the morning. She had a recent admission for endoscopy and colonoscopy which failed to show any source of bleeding. She denied any fevers, chills, sick contacts, diarrhea, or abdominal pain.

Here is her triage ECG:

What do you think?








An old ECG from 4 years ago was available:




The current triage ECG shows normal sinus rhythm with:

 - New pathologic QS-waves ("QS-wave" means there is no R-wave at all; the entire QRS is negative) in the anterior, lateral, and inferior leads.  These QS-waves alone are all but diagnostic of infarction of indeterminate age.

 - In the anterolateral leads, the are QS-waves with obliteration of the previously normal R wave progression

 - Very slight STE in leads II, III, aVF, V3-V6 that does not meet STEMI criteria

 - T waves in V3 and V4 are not consistent with old MI, but rather are hyperacute.  (They are not consistent with chronic, old LV aneurysm morphology as the the T/QRS ratio is 4.5 mm/ 6mm = 0.75 in lead V3 and 3.0mm/4.5mm = 0.67, both greater than our studied cutoff of 0.36 (see discussion below regarding Dr. Smith's derived and validated rules for differentiating chronic LV aneurysm morphology from acute anterior OMI)


Although QS waves are a sign of decreased acuity, the persistent pain and hyperacute T waves definitively mean that there is ongoing ischemia and more viable myocardium that can be salvaged with reperfusion therapy and which will infarct if emergent reperfusion is not achieved quickly.


In these cases, it is important and sometimes difficult to decide between several possibilities:


1) Old anterior MI with no active ischemia (old LV aneurysm morphology)

2) Old anterior MI with superimposed acute occlusion

3) Subacute MI (no prior MI at that location, and now at least 6-12 hours into full thickness infarction)


T waves are tall and hyperacute (use the ratios below) in both #2 and for at least a few hours in #3, then fall with time, loss of tissue, and rising troponin.


Troponin will be positive already in #3, will quickly become positive in #2, and will be negative in #1.



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


We have derived and validated a rule to differentiate "LV aneurysm" ST elevation from STEMI.  The rule depends on the principle that acute STEMI has a tall T-wave and LV aneurysm does not.  There are two versions:

In the first rule, if there is any single T/QRS ratio in V1-V4 that is greater than 0.36, it is likely STEMI:  for the ECG from 3 years prior, that would be lead V2.  At 5mm/21mm, the ratio is less than 0.36 and would indicate LV aneurysm.  But for the first acute ECG above, lead V2 is 8.5/15 which is 0.56 and would NOT indicate LV aneurysm.

In the second rule, one takes the sum of T-wave amplitudes in V1-V4 and divides by the sum of the QRS amplitude in V1-V4.  A value less than 22 indicates LV aneurysm.  In the second ECG from 3 years ago, that comes to 10/47 = 0.215, consistent with LVA.


T/QRS ratio to differentiate anterior STEMI from anterior LV aneurysm:


These studies showed that acute anterior MI (symptoms less that 6 hours) almost always had a T/QRS ration greater than 0.36 in at least one of leads V1-V4.  A subacute MI (symptoms of at least 6 hours) and Old MI both had ratios less than 0.36.  This just demonstrates that in acute MI, the T-wave is large.


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


Case continued


The team called cardiology immediately via our "high risk ECG alert" pathway (this gets immediate consultation with the on-call interventionalist, to decide if immediate cath lab activation is appropriate). 


While waiting for the arrival of cardiology, we obtained a beside ultrasound looking for wall motion abnormalities.


ED bedside limited cardiac echo (performed by Drs. Dominic Nicacio and Gabriela Rivera-Camacho):




The parasternal long axis view above appears to show hypokinesis of the anterior septum. 





The parasternal short axis view above appears to show hypokinesis of anterior septum and anterior wall.


With the ECG as it is, there will always be a wall motion abnormality. The question is: is it new or old? It can be very difficult to tell on bedside echo. If it is old (i.e. aneurysm) a very high quality echo might see wall thinning and diastolic distortion. If it is new, there will be a thick wall and no distortion. But usually bedside echo would not be able to make this distinction.  


Repeat ECG about 1.5hrs later:



 


The repeat ECG shows worsening STE and persistent hyperacute T waves. The QRS complexes especially in the inferior leads are proportionally tiny compared to the ST segments and T waves.



The initial troponin (high sensitivity troponin I) returned highly elevated at 5,478 ng/L. This is consistent with the Q-waves on the ECG, and together they confirm some irreversible myocardial necrosis.  However, this in no way means that there is no remaining salvagable myocardium if the patient undergoes emergent reperfusion therapy.


The patient was taken for emergent cath which showed a fully occlusive spontaneous coronary artery dissection of the proximal LAD. There was also an acute spontaneous nonocclusive dissection of the distal RCA. There was no aortic dissection. The occlusive LAD dissection underwent PCI with 3 overlapping stents. The nonocclusive RCA dissection was treated conservatively without PCI.


The next four serial troponin measurements were all greater than 25,000 ng/L (the assay does not report higher concentrations). 


Her formal echocardiogram showed an EF of 25-30% with akinesis of the anteroseptal, apical, anterior, and lateral myocardium. 


Her medical regimen was complicated by platelets of 2,000/uL (history of chronic low platelets). Hematology was consulted and the patient was transfused platelets with a goal of greater than 5,000/uL, at the same time he was continued on ticagrelor (the reasoning being that ticagrelor may have favorable pharmacokinetics in the setting of platelet transfusion). Aspirin was considered contraindicated.


Repeat echocardiogram on day 3 showed improvement of the EF to 43%, but still with severe hypokinesis in the same location.


She remained on ticagrelor monotherapy and had no bleeding issues. She was discharged home but long term follow-up is unavailable.




See these related cases:


Subtle Anterior STEMI Superimposed on Anterior LV Aneurysm Morphology






 

 

 

Hyperacute T waves examples:


10 Cases of Inferior Hyperacute T-waves





http://www.emdocs.net/hyperacute-t-waves/

https://www.emra.org/emresident/article/stemi-equivalents/

 





Friday, November 27, 2020

Chest pain, ST Depression maximal in V2-V4, and a Blood Pressure of 238/118.

A Middle-aged male had sudden onset severe substernal chest pain that woke him from sleep.

His BP was 238/118 on arrival.

Here is his first ED ECG:

What do you think?











There is ST depression maximal in V2-V4, which normally would be all but diagnostic for posterior MI.  However, the extremely elevated BP makes it likely that this STD is really subendocardial ischemia from high oxygen demand.  (There are also incidentally large U-waves -- the K was 4.1).

It is best to first manage the BP and then repeat the ECG.

So the physician did just that.  He obtained a chest CT to rule out aortic dissection (which was negative).

He also gave nitroglycerine to bring the Systolic BP down to 180 mmHg, at which time the chest pain resolved.  Then he recorded another ECG:

The ST depression and pain is gone!  It must have been demand ischemia, right?



He gave aspirin, heparin and transferred to the nearest PCI center.

The initial troponin at that referral center was "negative", so they observed the patient.  A later troponin returned at 0.346 ng/mL (unfortunately, I don't have the assay -- don't even know if TnI or TnT.  In any case, that level is elevated and diagnostic of either type 1 or type 2 MI).

Shortly thereafter, the patient had sudden onset 10/10 pain again.  Another ECG was recorded:


The ST depression is back!

He went for emergent angiogram and was found to have a 100% proximal circumflex occlusion with TIMI-0 flow.


Comment:

The physician was worried that he had made a mistake here.

I disagreed.  

One must manage very abnormal vital signs first.  There is no way to know whether the initial chest pain + EKG findings were not subendocardial ischemia due to high oxygen demand due to the extremely elevated BP.

The correct management is to manage the BP, then assess symptoms and a repeat ECG.

As it turned out, the ischemia was indeed due to ACS.

It is an unfortunate coincidence that the artery spontaneously opened (reperfused) at the same time that the BP was managed.  The physician could not have known that.

It was only when the ischemia returned (both symptoms AND ECG findings, in this case) WITHOUT an elevated blood pressure that it could be ascertained that this was all due to coronary occlusion.

The ECG did indeed look more like posterior OMI than subendocardial ischemia

One certainly might strongly suspect that this is ischemia is due to posterior OMI rather than subendocardial ischemia, since posterior OMI usually has maximal STD in V2-V4, and subendocardial ischemia usually has STD in I, II, V4-V6, with reciprocal STE in aVR

See here for a case of LAD subendocardial ischemia that presented like a posterior OMI; it even had STE on posterior leads.  Guess the culprit with ST Elevation in posterior leads

Summary: The physician was thrown a curveball, but he managed it very well.  (That is a baseball metaphor, for those outside the U.S.!)

A particularly difficult issue, obstacle, or problem. Named after the equally tricky baseball pitch.
The professor really threw me a curve ball with that last exam test.









Wednesday, November 25, 2020

Barcelona Rule on Left Bundle Branch Block: Lots of Issues.

By the time we read the paper on the Barcelona rule, it was too late to write a letter to the editor or a commentary. So we are posting it here.


Here is the paper:

New Electrocardiographic Algorithm for the Diagnosis of Acute Myocardial Infarction in Patients With Left Bundle Branch Block

https://www.ahajournals.org/doi/10.1161/JAHA.119.015573




Diagnosis of Acute Occlusion Myocardial Infarction in the Setting of Left Bundle Branch Block: Thoughts on the Barcelona vs. the Modified Sgarbossa Rules


H. Pendell Meyers

Kenneth W. Dodd

Stephen W. Smith



Di Marco et al.1 performed a multicenter retrospective cohort study to derive and internally validate a new electrocardiographic algorithm known as the Barcelona algorithm for the ECG diagnosis of AMI in the setting of LBBB, and to compare the new algorithm against prior strategies including the original2 (OSC) and modified Sgarbossa criteria (MSC)3,4. For the diagnosis of any type 1 MI (equivalent in normal conduction to any NSTEMI or STEMI), they report the Barcelona algorithm to be superior to the MSC with higher sensitivity (93 vs. 68%, p<0.01) and equal specificity (94%). In this review we examine the compatibility of the results with prior data and discuss some major methodologic flaws of the study.


Results of Barcelona algorithm study compared to prior data


There are three differences between the Barcelona algorithm and the MSC:


1) While the MSC includes concordant ST depression (STD) in only leads V1-V3, the Barcelona algorithm considers concordant STD in any lead.


2) The MSC does not include excessively discordant STD, whereas the Barcelona criteria does.


3) For the definition of excessively discordant ST deviation (either ST elevation or STD), both strategies require at least 1.0 mm, but the MSC uses a quantified ratio of the discordant ST deviation to R or S wave amplitude of 20-25% in any lead, regardless of QRS voltage, whereas the Barcelona algorithm applies only to leads with maximum R/S voltage 6 mm and at least 1mm of ST deviation (meaning a minimum ratio of 1mm / 6mm = 17%).


If one of the two strategies is superior, then the improvement must originate from these three differences. Therefore it should be helpful to consider the prior data available for these differences. 


1) Concordant STD in all 12 leads vs. V1-V3 only:

Concordant STD was studied in all 12 leads previously by Dodd and Smith.5 When the MSC (using concordant STD in V1-V3 only) were compared with an alternate version including concordant STD in any lead, the sensitivity of the rule remained unchanged (91%) while the specificity decreased (from 90% to 76%). Thus, the best prior evidence does not support extending concordant STD to all leads.


2) Excessively discordant STD

Excessively discordant STD in LBBB was first studied in the derivation study3 of the MSC by Smith et al, in which the optimal cutpoint for discordant ST deviation was calculated to be 30% (STD of at least 30% of the preceding R wave), which produced sensitivity and specificity of 100% and 88% for acute coronary occlusion myocardial infarction (OMI, not for any AMI). Meyers and Smith replicated the study design in a validation study4 and found lower sensitivity of only 64%, but with 98% specificity. Thus, although the specificity was even higher in this separate validation sample by the same author group, the sensitivity of excessively discordant STD was not replicated, and it was therefore not incorporated into the MSC. The new data from Di Marco et al. offer renewed interest in the role of excessively discordant STD in future validation studies. 


3) MSC’s 20-25% ratio for excessive discordance vs. Barcelona algorithm’s 1 mm ST deviation in leads with R/S voltage 6 mm

The Barcelona algorithm uses a ratio of 1 mm / 6 mm = 17%, similar to the MSC’s lower studied ratio of 20%. However, the Barcelona algorithm’s ratio is not applied in leads with > 6mm maximum R/S component. Thus, we do not know what percent of patients in this algorithm require concordant STE to be positive. It is difficult to fathom how excluding all patients with excessive discordance who have an R- or S-wave greater than 6 mm could improve sensitivity.


For example Figure 1 below shows the ECG of a patient with 100% acute thrombotic LAD occlusion. The ECG has no concordant STD or STE, and is positive by the MSC due to excessively discordant STE (of > 25%) in V2, V3, and V4. However, the ECG contains no leads with maximum R or S wave 6 mm or less (other than aVR), and therefore is a false negative by the Barcelona algorithm (aVR has a 2mm R wave and a 2 mm S wave, with < 1 mm ST deviation).


Figure 2 shows the ECG of another patient with LBBB and an acute TIMI-0 LAD occlusion. There is no concordant STE or STD. There is discordant STE in V1-V5 which meets the MSC criterion in all 5 consecutive leads, but meets the Barcelona algorithm criterion only in lead V5, because V1-V4 have predominant S waves which are greater than 6 mm in amplitude, whereas the S wave in V5 is exactly 6 mm. Thus, a realistic and imperfect practitioner has five consecutive leads to identify using the MSC versus only one lead using the Barcelona criteria (assuming the practitioner measures the S wave perfectly and does not exclude the lead due to a perceived S wave of 7.0 mm). For these reasons, it is unclear how these new criteria could improve the ECG diagnosis of OMI in LBBB.


Figure 1


Figure 2



It is hard to imagine why limiting proportionally excessively discordant ST Elevation only to leads with an R- or S-wave of less than 6 mm could improve the rule. In both our derivation and validation studies of the MSC, many cases were only identified by a high ST/S ratio in leads with large S-waves. The answer lies most likely in the methodologic flaws outlined below.



Methodologic flaws of Di Marco et al.


Patient Population

Unlike the derivation and validation studies of the MSC which used a control group of ED patients with potential ischemic symptoms, Di Marco et al. used a control population of patients with no clinical concern for ACS, which likely overestimates the specificity of all strategies studied. Furthermore, all case patients (non-control patients) used in Di Marco were identified by referral for primary PCI, which does not appropriately represent the entire population of ED patients with LBBB and possible ACS. Thus, cases have an extremely high, and controls an extremely low,  pretest probability, which, contrary to conventional wisdom, does affect sensitivity and specificity.6


Outcome Definitions

In contrast to the MSC studies, which used angiographic occlusion (diagnosed by TIMI 0/1 or any culprit withy very high troponin) as the primary outcome, the primary outcome used in Di Marco et al., was “AMI” with any culprit lesion of any TIMI flow score and any rise and/or fall of troponin above the upper reference limit (essentially, any type 1 MI, equivalent in normal conduction to all type 1 STEMI and all type 1 NSTEMI).


Although the Barcelona algorithm appears to show very high sensitivity for any type 1 MI (both STEMI and NonSTEMI), all previous studies of ST Elevation in normal conduction (no LBBB) have shown much lower sensitivity for any type 1 MI. For example, among a prospective, real world population of 2486 patients in the ED with ACS symptoms, of whom 438 had type 1 MI, Hillinger et. al. reported sensitivity of only 17% for any Type 1 MI (STEMI or NonSTEMI) in normal conduction, with cardiologists using formal STEMI criteria7. This is not surprising because the ECG is known to be very insensitive for any MIs, no matter whether in LBBB or normal conduction. Since the ECG is so insensitive, and troponin can be used to diagnose MI that does not need the cath lab emergently, the current role of the ECG is to diagnose OMI, which needs emergent reperfusion. The fact that the Barcelona algorithm was found to have 93 and 94% sensitivity and specificity for any type 1 MI in LBBB is therefore impossible to reconcile with previous data on the ECG in the diagnosis of AMI. Thus, Di Marco’s primary outcome definition was not an appropriate or reasonable goal to ask of the ECG, and it is unclear how such a high degree of accuracy was possible for this outcome.


Even if the ECG could accurately predict any MI, the standard management of patients with NSTEMI who are pain free and without OMI is to wait up to 36 hours for angiography and PCI. Thus, Di Marco’s outcome definition including TIMI 3 flow and minimal troponin rise and fall is unlikely to represent patients who require emergent reperfusion. While many STEMIs do not have complete occlusion (TIMI 0) at the time of angiography, the majority have large troponin elevations.8 For this reason, the MSC studies used full occlusion (TIMI 0/1 flow) but also used a surrogate endpoint for an acute coronary occlusion that may have been present at the time of the ECG, but not at the time of angiography: any culprit, even with TIMI 2-3 flow if there was also a “highly elevated” troponin defined as troponin I >10.0 ng/mL or troponin T > 1.0 ng/mL. 


In their supplemental information, Di Marco et al. provide a secondary outcome definition which they state was modeled after the outcome definition used in the MSC studies, however the troponin cutoffs used are markedly different. Di Marco et al. used a troponin ratio (peak level divided by upper reference limit) of 10, referencing Gonzalez et al.9 Moreover, this is a mistaken representation of Gonzalez et al. who instead stated that 11.3% of STEMI patients had a peak troponin I of 7.1 ng/mL. Moreover, Gonzalez et al. erroneously state that their troponin assay has an 99% URL of >0.001 µg/L, a critical mistake: there is no assay on the market which has a URL of 0.001 µg/L. Using this URL, a peak troponin ratio of 10 gives a cutpoint of 0.010 ng/mL, which is not only a very low cutoff for occlusion, it is too low even to make the diagnosis of MI, as it lower than the URL for almost all assays.



In the MSC validation study, by comparison, the vast majority of troponin I measurements were done using an assay with URL of 0.032 to 0.050 ng/mL (µg/L). Thus, the troponin I ratio in our study was 10.0 / 0.05 ng/mL (µg/L) = 200, far greater than 10 as in Di Marco et al. Similarly, the most appropriate equivalent troponin T cutpoint is estimated at 1.0 ng/mL.10 The proven TIMI 0-1 Occlusion MI groups in our studies consistently show mean peak troponin T levels in the 2.0-6.0 ng/mL (µg/L) range, despite the fact that the two sites have assays with a 10-fold difference in the URL (0.01 vs. 0.10 ng/mL). This highlights the inappropriateness of fixed troponin ratios for comparing the peak troponin levels in STEMI and Occlusion MI among assays with vastly different URLs.


As expected with the inappropriately low troponin threshold in Di Marco et al, the online supplemental information reveals that 95% of all AMIs in the study were considered “STEMI equivalents.” Obviously not all AMIs should be considered “STEMI equivalents”, and this is not in keeping with the known prevalence of true STEMI among AMI in normal conduction. For example, Hillinger et al. found only 81 STEMIs (18%) and 135 Occlusion MI (31%) among 438 AMIs in their large, prospective, real world chest pain cohort.7



Conclusion

Despite the profound methodological flaws, there may be utility of some  components of the Barcelona algorithm vs. those of the MSC. If such individual components are confirmed by external validation studies, perhaps a rule with better overall performance could be formulated. Most importantly, we must understand that no ECG rule will likely ever identify all AMI in either LBBB or normal conduction, and so seek to maximize the potential of the ECG to identify Occlusion MI.  




References:

1.    Di Marco, A. et al. New Electrocardiographic Algorithm for the Diagnosis of Acute Myocardial Infarction in Patients With Left Bundle Branch Block. J. Am. Heart Assoc. e015573 (2020) doi:10.1161/JAHA.119.015573.

2.    Sgarbossa, E. B. et al. Electrocardiographic Diagnosis of Evolving Acute Myocardial Infarction in the Presence of Left Bundle-Branch Block. N. Engl. J. Med. 334, 481–487 (1996).

3.    Smith, S. W., Dodd, K. W., Henry, T. D., Dvorak, D. M. & Pearce, L. A. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann. Emerg. Med. 60, 766–776 (2012).

4.    Meyers, H. P. et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am. Heart J. 170, 1255–1264 (2015).

5.    Dodd, K. W., Elm, K. D. & Smith, S. W. Comparison of the QRS Complex, ST-Segment, and T-Wave Among Patients with Left Bundle Branch Block with and without Acute Myocardial Infarction. J. Emerg. Med. 51, 1–8 (2016).

6.    Leeflang, M. M. G., Rutjes, A. W. S., Reitsma, J. B., Hooft, L. & Bossuyt, P. M. M. Variation of a test’s sensitivity and specificity with disease prevalence. CMAJ 185, E537–44 (2013).

7.    Hillinger, P. et al. Prospective validation of current quantitative electrocardiographic criteria for ST-elevation myocardial infarction. Int. J. Cardiol. (2019) doi:10.1016/j.ijcard.2019.04.041.

8.    Karwowski, J. et al. Total coronary occlusion of infarct-related arteries in patients with non-ST-elevation myocardial infarction undergoing percutaneous coronary revascularisation. Kardiol. Pol. 75, 108–116 (2017).

9.    Gonzalez, M. A. et al. Quartiles of Peak Troponin Are Associated with Long-term Risk of Death in Type 1 and STEMI, but Not in Type 2 or NSTEMI Patients. Clinical Cardiology vol. 32 575–583 (2009).

10.    Baro, R., Haseeb, S., Ordoñez, S. & Costabel, J. P. High-sensitivity cardiac troponin T as a predictor of acute Total occlusion in patients with non-ST-segment elevation acute coronary syndrome. Clin. Cardiol. 42, 222–226 (2019).

Tuesday, November 24, 2020

A Fall and a Rhythm to Recognize

 

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

MY Comment by KEN GRAUER, MD (11/24/2020):

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

The 12-lead ECG and accompanying long-lead rhythm strip shown in Figure-1 — was obtained from an elderly man who experienced a minor fall without serious injury. The patient had no cardiac symptoms — and this ECG was recorded as part of a “thorough assessment”. The patient was on long-term Digoxin — but other than this, no additional information about this case was available.

  • NOTE: Although both the 12-lead and long-lead rhythm strip are angled (slightly distorted) — the quality of these tracings is adequate for interpretation — and — there are important lessons to be learned from this case!


QUESTIONS:

  • WHAT is the rhythm in Figure-1?
  • From a clinical perspective — WHAT does this rhythm tell you until you prove otherwise?


Figure-1: 12-lead ECG and accompanying long-lead rhythm strip from an elderly man who fell — but who had no symptoms at the time these tracings were recorded (See text).



MY Thoughts regarding Figure-1: The rhythm is complex — and I’ll discuss it step-by-step below. What can be said at a glance — is that the rhythm is supraventricular (ie, the QRS is narrow everywhere) — and — that the rhythm is not regular, and not overly fast.

  • Looking at the rest of the 12-lead ECG — the axis is horizontal (about 0 degrees) — there is probable LVH (deep S ~19-20 mm in V2 and cut off S wave after 15 mm in lead V3). The T waves in leads V2-thru-V4 are peaked — although my sense is that given deep anterior S waves and an asymptomatic elderly patient — that this may reflect LV “strain” (that sometimes appears as ST-T wave peaking in anterior leads with LVH). ST-T waves in other leads are not “normal” (ie, some ST-T “scooping” in leads I, V5,V6 — and some ST segment flattening in several limb leads) — but my sense is that there probably are no acute ST-T wave changes in this elderly patient without any chest pain.
  • The interesting component in Figure-1 is the rhythm, which we see best in the long-lead rhythm strip ...



QUESTION:

  • Did YOU see evidence of atrial activity in Figure-1?
  • HINT: WHY did I reach for my calipers to answer this question?




ANSWER: In general — the BEST lead to look for atrial activity in is lead II. We define sinus rhythm by the presence of an upright P wave in lead II that is conducting. That said — it’s important to remember that the 2nd-best lead to see atrial activity in is lead V1.

  • I do not see P waves in lead II of the 12-lead tracing in Figure-1. I also do not see P waves in 9 of the other leads. But we definitely do see evidence of regular atrial activity in lead V1 (RED arrows in Figure-2).
  • Calipers allow us to instantly prove that the multiple small-amplitude deflections in lead V1 are truly P waves— because: i) Calipers show these deflections are perfectly regular; andii) We see similarly-timed regular deflections in lead V2 in the 12-lead tracing.
  • Note that regular atrial deflections are seen throughout the long-lead V2 rhythm strip (RED arrows in Figure-2). Some of these deflections are more subtle than others (sometimes being partially hidden within various parts of the T wave) — but using calipers allows us to “walk out” regular P waves throughout the entire long-lead rhythm strip!
  • To further assess this rhythm — it’s important to determine the atrial rate. As I’ve illustrated in a number of prior posts in Dr. Smith’s ECG Blog — this is easy to do using the Every-other-Beat Method (See My Comment at the bottom of the page of the April 15, 2020 post). Vertical YELLOW lines in lead V1 of Figure-2 show the starting and stopping point in the interval measuring the amount of time needed to record 2 P waves. It takes just over 3 large boxes (YELLOW numbers) to record 2 P waves (RED numbers) in Figure-2. Therefore — HALF of the atrial rate is a little slower than 300/3 = about 95/minute. This means that the atrial rate is ~95 X 2 = about 190/minute.
  • PEARL #1: A regular atrial rate of ~190/minute is too fast to be sinus tachycardia. The differential diagnosis is between AFlutter vs ATach (Atrial Tachycardia). The isoelectric baseline between P waves (instead of a “sawtooth” patternand an atrial rate well below 300/minute combine to strongly favor ATach as the underlying atrial arrhythmia.


Figure-2: I’ve labeled the P waves in ECG #1 (RED arrows). I also illustrate the every-other-beat Method for determining the atrial rate (See text).



QUESTIONS:

  • WHY is the rhythm in the long-lead rhythm strip in Figure-2 irregular?
  • HINT: Is there a PATTERN to this rhythm? (ie, Are there any elements that repeat?).




ANSWER: As I said at the outset — this rhythm is complex. Nevertheless — certain points can be made about what we see in the long-lead V2 rhythm strip:

  • There is the suggestion of group beating. By this I mean that there are elements of this rhythm that repeat. For example — the 3 short “pauses” that we see (ie, between beats #1-2; between #6-7; and between #8-9) are all about the same duration — and the PR interval for the P wave that appears before the 1st QRS complex at the end of each pause is equal (ie, the PR intervals before beats #2, 7 and 9 is the same!).
  • Virtually all of the other R-R intervals on this long-lead rhythm strip are of very similar duration (if not, the same duration)!
  • The PR intervals preceding beats #3, 4, 5; 8; 10, 11, 12 all look to be the same.
  • The PR interval preceding beat #6 — is the same as the PR interval preceding beat #13 (albeit these 2 PR intervals are a little bit longer than the PR intervals preceding beats #3,4,5,8,10,11,12).
  • CONCLUSION: The above bullets point out too many findings to be by chance. Therefore, these consistent relationships that are highly unlikely to be by chance tell us — there must be some type of conduction going on in this irregular, long-lead rhythm strip.


PEARL #2: It is sometimes very helpful to “step back” a little bit from the tracing — to gain an overall perspective of the pattern of a complex rhythm. PROVE THIS to yourself. Go BACK to my unlabeled Figure-1— and take another look at the long-lead rhythm strip. Realizing that there is some distortion from the angling in this picture — Isn’t it now easier to appreciate the relationships I highlighted in the bullets of my previous section?

  • Becoming comfortable recognizing group beating and other patterns of beats that repeat — provides an invaluable initial clue that can tell you within seconds that there is some type of conduction.


PEARL #3: It is very common to see Wenckebach conduction in association with both AFlutter and ATach. In today’s case — it was the combination of group beating + multiple PR and R-R intervals that are the same that strongly suggested to me that there was Wenckebach conduction, in this case out of the AV node.

  • An important “Take-Home” point from today’s case — is that even without working out a specific mechanism for how such conduction is occurring — we should strongly suspect that the rhythm is ATach with AV Block (in this case with some type of Wenckebach conduction out of the AV node).


PEARL #4: We were told at the beginning of today’s case that this elderly man has been on long-term Digoxin.

  • The combination of Atrial Tachycardia with Wenckebach Block in a patient taking Digoxin has to strongly suggest Digoxin Toxicity until you prove otherwise!


A Few Words on Digoxin:

Digoxin is not used nearly as commonly as it had been in the past. During my training and early practice years — it seemed like a majority of patients with heart failure and/or atrial fibrillation were on this drug. No longer. That said — selected indications for Digoxin remain — and emergency providers will still encounter a certain number of patients taking the drug. This is important — because Digoxin Toxicity may predispose patients to any of a number of potentially life-threatening arrhythmias.

  • Always inquire what medications the patient in front of you is taking. This is especially important if Digoxin is among the medications your patient is taking — because there is a narrow “therapeutic window” between beneficial vs toxic effects of Digoxin. And, if your patient is on Digoxin — be sure to ask if they may have missed any doses — or if they instead might have taken some “extra doses” of their “heart medication" because they weren’t doing so well. You’ll sometimes be surprised by the answers you receive.
  • For those of us who trained in years past — Digoxin taught many of us more about cardiac arrhythmias than any other factor. This is because Dig excess may cause virtually any arrhythmia (except rapid AFib). Certain rhythms are especially suggestive of Dig toxicity = frequent and/or multiform PVCs; VT; ATach (atrial tachycardia) with block; accelerated junctional rhythm; rhythms with Wenckebach block; very slow AFib. Other rhythm disturbances that may be seen include marked bradycardia, PR interval prolongation, and sometimes complete AV block.
  • A wide range of trough serum Digoxin levels has been cited as “therapeutic”. In years past, this range had been ~0.8-to-2.0 ng/ml — but lower ranges (ie, keeping the trough level ≤1.2 ng/ml — if not below 0.8 ng/ml) are now more commonly recommended. KEY Point: There is a wide “overlap range” between serum Digoxin levels that fall within the “therapeutic range” — and serum Digoxin levels that may precipitate serious Dig toxicity arrhythmias. Acutely ill patients, especially those with renal impairment and/or serum electrolyte disorders (low serum K+ or Mg++) — are especially vulnerable to developing Dig toxic arrhythmias despite serum Digoxin levels that fall within the therapeutic range.


NOTE: All of the above is relevant to today’s case. Unfortunately, we don’t have follow-up for this patient — but given that today’s patient was on long-term Digoxin and presented with ATach + Wenckebach block — we need to strongly suspect Dig Toxicity until proven otherwise (even if the serum Digoxin level were to fall within the “therapeutic” range).

  • P.S.: Much has been made about looking for “Dig effect” on ECG. The literature describes ST segment “scooping” with a relatively short QT interval as the ST-T wave response to high serum levels of this drug. This picture is seen for the ST-T wave in leads V5 and V6 of ECG #1 — but it is not seen in other leads on this tracing.
  • Having worked as full-time faculty for 30 years in an ambulatory primary care center in which we worked closely with our pharmacology colleagues — I had extensive experience interpreting numerous ECGs on patients whose serum Digoxin levels were carefully monitored over time. Doing so taught me the following: iPatients on long-term Digoxin may manifest ST “scooping” in at least several leads (as is seen in leads V5 and V6 of ECG #1) — but not all patients taking Digoxin show such ST-T wave changes; andii) Despite what the literature says — there is no reliable correlation between how high the serum Digoxin level is and the presence or absence of “Dig effect” on ECG. Patients can be Dig toxic despite having normal ST-T waves.


MORE on the Rhythm:

As I noted from the outset — the mechanism of the rhythm in the long-lead rhythm strip is complex.

  • Recognition of Atrial Tachycardia with group beating and the similar R-R and PR interval relationships that I detailed earlier is sufficient to strongly suggest there is Wenckebach conduction (and Wenckebach block) out of one or more levels in the AV node.
  • I propose the Laddergram I show in Figure-3 as the mechanism operative in this case. The laddergram suggests there is dual-level Wenckebach conduction out of the AV node (2:1 and 3:2 conduction at the upper level — with longer Wenckebach cycles in the lower level).
  • Other proposed mechanisms from any of our readers are welcome!


Figure-3: My proposed laddergram for the rhythm in today’s case (See text).



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  • NOTE: My sincere THANKS to Edward Brunacci (Australia) for sharing the tracings and this case with us!

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ADDENDUM (11/25/2020):
As I've indicated in previous posts in which I have proposed laddergram solutions — there can often be more than a single possible explanation for a given complex arrhythmia. I therefore wanted to publish David Richley's proposed alternative laddergram to the one I show above in Figure-3:
  • Dave writes: I offer an alternative laddergram which proposes that there are long Wenckebach sequences in the upper AV node and 2:1 block at the lower AV node (See Figure-4).
  • Dave adds: I don't know if my proposed alternative laddergram is more or less likely to be true than your explanation, Ken — and I merely offer it as an alternative for consideration!
  • BOTTOM Line: I also don't know if Dave's proposed laddergram is more or less likely than mine — but regardless — the KEY points to this case are unchanged = this elderly patient who is on long-term Digoxin manifests with ATach + some form of multi-AV-nodal level Wenckebach block — and should therefore be considered to have Dig Toxicity until proven otherwise.


Figure-4: David Richley's proposed alternative laddergram (See text).







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