Thursday, January 31, 2019

What is the Rhythm?

Presentation by KEN GRAUER, MD:
The Case: A previously healthy young man presented to the ED for shortness of breath and chest pressure that occurred ~3 hours earlier, when he suddenly felt his heart “skip a beat”, and then begin “racing”. He felt “lightheaded” (presyncopal) during the episode — with the “strong sensation of his heart beating”. He did not feel better until ~45 minutes later. Similar episodes had occurred over the past month — but none lasted as long.  Of note, the patient is an active athlete. There is a family history of a “junctional or other abnormal rhythm”.

Figure-1 shows his initial ECG that was obtained in the ED.

  • Use of calipers is strongly advised for interpreting the rhythm!
Figure-1: The initial ECG in this case (See text). 

  • What is the rhythm in Figure-1?
  • Why is this not, strictly speaking, “isorhythmic” AV dissociation?
  • Might the family history of an abnormal rhythm have anything to do with this case?
  • Clinically — What would you do for this patient?
PEARL #1: The easiest way to instantly enhance your arrhythmia interpretation skills is by using CALIPERS. The cardiologist who does not regularly use calipers for interpretation of complex arrhythmias — is a cardiologist who will miss the diagnosis on more than a few occasions.
  • Obviously, not all arrhythmias are amenable to use of calipers. You’ll often know the etiology of a particular rhythm without the need for calipers. And, in an acute emergency situation — there is often no time to stop and pull out calipers until you’ve taken care of the patient. That said, calipers instantly make you smarter. They excel for assessment of AV blocks and AV dissociation — they allow instant determination if a rhythm is or is not regular — and, calipers are invaluable for deducing whether or not various beats are being conducted.
  • Using calipers will NOT slow you down. On the contrary — with a little bit of practice, you’ll find they dramatically speed up the interpretation of many complex arrhythmias — because you can instantly measure and compare intervals.
PEARL #2: When discussing a complex rhythm — Numbering the beats is of invaluable assistance for clarifying which beat is being referred to (Figure-2).
Figure-2: We have numbered the beats in the long lead II rhythm strip at the bottom of the tracing (See text).
Initial Assessment of the Rhythm: When confronted with a complex arrhythmia — I always like to begin with WHAT I KNOW to be true.
  • I know that the PR interval in front of beat #6 is too short to conduct. The PR interval in front of beat #2 is also too short to conduct. This suggests that there is at least transient AV dissociation — which simply means that there are sinus P waves present that are not related to neighboring QRS complexes.
  • The longest PR interval in Figure-2 appears before beats #8 and 9. The PR interval preceding these 2 beats is equal and normal — and the P wave in this lead II is upright. This suggests that beats #8 and 9 are most probably sinus-conducted.
  • There seems to be indication of LOTS of P waves on this long lead II rhythm strip. PEARL #3: Clarification of a complex rhythm is often much EASIER to attain IF you are able to label underlying atrial activity. We do so in Figure-3.
Figure-3: RED arrows indicate what we believe is the underlying atrial rhythm (See text). 
Assessment of Figure-3: Although some of the P waves highlighted by RED arrows in Figure-3 are partially hidden by neighboring QRS complexes — overall P wave morphology appears to be the same throughout this tracing. Therefore, there is an underlying sinus mechanism.
  • BUT — the P-P interval of these RED arrows varies throughout the tracing! This tells us that the underlying rhythm is a fairly marked sinus arrhythmia. It should be emphasized that of itself — sinus arrhythmia is not an abnormal rhythm in an otherwise healthy young adult.
  • All 10 QRS complexes in this tracing are narrow. These QRS complexes all look similar — although there are slight differences in QRS morphology for some of the beats. But the fact that there are some sinus-conducted beats — as well as many other beats with PR intervals that are definitely too short to conduct — tells us that there are junctional escape beats (ie, beats #3, 4, 5 and 6 at least — are all junctional beats).
Putting Together What WKnow Thus Far: The underlying rhythm is sinus bradycardia with marked sinus arrhythmia. As a result of slowing of the sinus pacemaker — the sinus rate occasionally drops below the intrinsic rate of the AV nodal escape pacemaker. This results in transient AV dissociation — until the sinus node speeds up enough to exceed the intrinsic AV nodal escape rate. This phenomenon is best known as, ADissociation by “Default” — ie, “default” of the sinus pacemaker due to marked sinus bradycardia, which transiently allows the AV nodal escape pacemaker to take over. We emphasize the following KEY points:
  • The rhythm in Figure-3 is not “AV dissociation”. AV dissociation is never the etiology of a rhythm. Instead, as we state above — the rhythm is sinus bradycardia with marked sinus arrhythmia. It is because of marked slowing in the rate that AV dissociation arises.
  • There is absolutely no evidence of any form of AV block. This is because we never see any P waves that fail to conduct despite adequate opportunity to conduct! Instead, the reason why certain P waves do not conduct — is simply that the PR interval is too short.
  • This is not “isorhythmic” AV dissociation. The word “iso” — is from the Greek word “isos” — which means “equal”. True isorhythmic” AV dissociation is an uncommon phenomenon, in which there are independent atrial and ventricular pacemakers that are beating at nearly identical (ie, “equal” ) rates. Most often, there is an underlying sinus (atrial ) rhythm competing with an AV nodal rhythm beating at an almost identical rate. The effect is like a horse race — in which one rhythm temporarily “takes the lead” (ie, takes over the rhythm) — until it either slows slightly, or until the other rhythm accelerates just enough to take over the rhythm — and then this back-and-forth process begins anew. This is not what we see in Figure-3 — as there is an obvious marked difference in P-P and R-R intervals for much of the long lead II rhythm strip.
NOTE — It is important to appreciate that there are 3 potential Causes of ADissociation:
  • AV dissociation due to some form of 2nd or 3rd degree AV Block;
  • AV dissociation by “Usurpation” — in which P waves transiently do not conduct because an accelerated junctional rhythm takes over the pacemaking function (because it is faster than the underlying sinus rhythm); and/or,
  • AV dissociation by Default” — in which a junctional escape rhythm takes over by “default” (ie, because of SA node slowing — as occurs in this case).
But there is MORE to this case … (WARNING: What follows involves advanced arrhythmia concepts! ).

  • What is atypical about the rhythm in the long lead II of Figure-3, compared to what we most often see when there are junctional escape beats?
  • The answer is revealed in Figure-4, in which careful caliper measurement provides the duration of all P-P intervals (in PURPLE lettering) — and the duration of the R-R interval preceding each of the first 6 beats (in BLUE lettering). What do you see?
Figure-4: We have carefully measured the number of large boxes for the critical intervals illustrated above (See text). 
Assessment of Figure-4: Most of the time, the intrinsic rate of the escape junctional pacemaker is constant. We are generally able to use this finding to help determine which beats are junctional vs conducted — because the R-R interval preceding most beats in a junctional escape rhythm is the same. But this is not the case in Figure-4 — because despite our thought that beats #2-thru-6 are all junctional escape beats (since they are all preceded by a PR interval too short to conduct) — the preceding R-R interval varies from 4.8-to-5.1 large boxes.
  • PEARL #4: The QRS complex of junctional escape beats sometimes looks a little bit different than the QRS of sinus-conducted beats. The reason is that the path of the electrical impulse for a sinus beat — may differ slightly from the path of a junctional beat that begins lower down or more to one side or the other of the AV node. We see this in Figure-4. We know beats #8 and 9 are sinus-conducted. We see a small-but-definitely-present initial q wave in these beats that is not seen in junctional beats #3, 4, 5 and 6. In addition, R wave amplitude of junctional beats #4 and 5 is clearly taller than the R wave of sinus-conducted beats #8 and 9! This PEARL is sometimes invaluable for telling us which beats in a tracing with AV dissociation are sinus-conducted vs of junctional origin vs fusion beats.
  • Then WHY does the QRS complex of beat #10 look exactly like the QRS of sinus-conducted beats #8 and 9, despite being preceded by a shorter PR interval? I believe the answer is that this patient manifests a component of Vagotonic AV Block (albeit not yet with clear demonstration of AV block ... ).
I discuss in detail the phenomenon of Vagotonic ABlock in THIS CASE. In the interest of brevity here — Suffice it to say that some otherwise completely healthy individuals manifest a marked increase in vagal tone, to the point that significant bradycardia with various forms of AV block may sometimes be seen despite complete absence of underlying structural heart disease. Among the characteristics of this syndrome are marked sinus arrhythmia, variation in the rate of escape pacemakers, variable PR intervals for sinus-conducted beats (that is otherwise hard to explain) — and at times, various forms of transient AV block.
  • Returning to Figure-4 — I believe the fact that the QRS complex of beat #10 is identical to the QRS of known sinus-conducted beats #8 and 9 — tells us that beat #10 is most probably sinus-conducted with a slightly shorter PR interval. The same is likely to be true for beats #1 and 7 — each of which is preceded by a PR interval slightly shorter than the PR interval of known sinus-conducted beats #8 and 9. It’s hard to know about beat #2 (the QRS looks like a sinus-conducted beat — but the PR interval is exceedingly short ... ). But overall, considering variation in the R-R intervals preceding known junctional escape beats #3, 4, 5 and 6 — the composite of findings suggest profound vagal influence affecting this patient!
  • The fact that there is a family history of some "abnormal" rhythm — suggests there may be a familial component to this patient’s inherently increased vagal tone.
  • Finally — this patient’s symptoms almost seem out of proportion to the rhythm we see in Figure-4. After all, there are no runs of tachycardia, no profound bradycardia, and as yet no sign of AV block. Close follow-up is essential. Holter monitoring may well reveal other more worrisome arrhythmias over the course of a day. That said, even though vagotonic AV block most often has a benign prognosis — the fact that this patient is so symptomatic (with what sounds like presyncope) merits referral to an EP cardiologist for more thorough evaluation and risk assessment.
BOTTOM LINE — Complete explanation of all findings present in the ECG shown in this case is indeed complex! I would be ecstatic for anyone assessing the rhythm in Figure-1 as showing marked sinus bradycardia and arrhythmia, that sometimes results in sufficient sinus slowing to produce AV dissociation with junctional escape beats. I think it important to appreciate that there is no evidence of AV block in Figure-1. That said — I think it helpful to be aware of the phenomenon of vagotonic AV block, that although uncommon — will be seen from time-to-time by emergency providers (Review of THIS CASE may prove insightful). In this particular case, even though AV block is not seen in Figure-1 — there are a number of ECG findings that in the context of the significant symptoms experienced by this patient, point to an inherent increase in vagal tone that merits referral for more complete assessment.

For More Info:
  • For another example of my step-by-step approach to assessing a case of AV dissociation — CLICK HERE
  • For those wanting a VIDEO Review (58 minutes) of the ECG Diagnosis of AV Blocks & AV Dissociation CLICK HERE. If you click on SHOW MORE (under the video on the YouTube page) — you’ll see a linked Contents of all that is covered in the video. The part regarding AV Dissociation BEGINS HERE.

Wednesday, January 30, 2019

Hyperthermia and ST Elevation

This was submitted by Alexandra Schick.  Dr. Schick is a PGY3 at the Brown Emergency Medicine Residency in Rhode Island.  I remember Allie well from her days in the Research volunteer program at Hennepin.

The article is edited by Smith.

Title: Is it just hot in here or is it a OMI? 

An elderly woman presents with altered mental status; she was found by her family lying on her bed in her apartment on a hot (103 F) summer day and was last seen three hours before.  She was obtunded, not following commands, hypoxic, and in respiratory distress. She was ventilated by bag-valve-mask by EMS on arrival and was quickly intubated with etomidate and succinylcholine. A rectal temperature was obtained which read 107.9 F. Otherwise vitals after intubation were only notable for tachycardia. 

An initial EKG was obtained: 
Computer read: sinus tachycardia, early acute anterior infarct.

There is sinus tach with rate of 124, normal axis, QRS 92, QTc 460, upsloping STD in I, aVL, V4 – V6 with concave STE in V1 (3mm) and V2 (5mm), and III (1mm) with Q wave in V1, V2, III. T wave inversion III, aVR, TWF in aVF.

Here is her prior EKG:
When compared to the old EKG – Q waves present before, TWI in aVR present before, but all other changes are new. 

What is the differential for this EKG? Is this an OMI? 

We considered OMI, as there are elevations with reciprocal changes (III and aVL), but the STE in III does not fit with this pattern.

The pattern of STE and STD reminded us of Brugada Type 1 morphology.

Smith comment:
1) Brugada ECG may have ST shifts in limb leads as well as precordial leads.  See additional image at the bottom of this post.
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI.
3)  Similar downsloping ST elevation in V1 and V2 with an rsr' is also found in hyperkalemia (See several cases at this post):

This ECG is NOT Pathognomonic of Brugada Syndrome

Case continued:
A bedside cardiac POCUS did not reveal and regional wall motion abnormalities, LV function was hyperdynamic.

Could this be induced by elevated core temperature? Or possibly a medication or metabolic effect?

We started active cooling of the patient and within one hour her temperature had come down to 101.1 F (rectal).

A repeat EKG was performed at that time and showed this:
The STE had almost completed resolved and the STE depression is improved as well.  All that remains is an incomplete RBBB.

By this time, some labs had returned, which showed a troponin I of 0.348 ng/mL (normal in our lab is less than 0.060)
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The only other abnormal labs were: 
pH 7.18, pCO2 61, K 5.1, Bicarb 20, Lactate 4.2, Ammonia 100.

Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab.

The Troponin I was cycled over time and was 0.353 followed by 0.296.

A formal echocardiogram was completed the next day and again showed a normal ejection fraction without any focal wall motion abnormalities to suggest CAD.  The elevated troponin was attributed to either type 2 MI or to non-MI acute myocardial injury.

There is no further workup at this time.

Smith: Here is a case that was just texted to me today from a former resident.  It was from a patient with chest pain:
Note the obvious Brugada pattern.
Also note that there is also: STE in aVL and inferior reciprocal ST depression.
This patient ruled out for MI. 
The limb lead abnormalities appear to be part of the Brugada pattern, as described in this article:
Inferior and Lateral Electrocardiographic RepolarizationAbnormalities in Brugada Syndrome


Brugada Type 1 ECG changes are associated with sudden cardiac death (SCD) and the occurrence of ventricular dysrhythmias. Patients that develop a Type 1 pattern without any precipitating or provoking factors have a risk of SCD of 0.5-0.8% per year. In patients that only have this pattern induced by a sodium channel blocking agent have a lower rate of SCD (0 - 0.35% per year)[1]. Drugs that have been associated with Brugada ECG patterns include tricyclic antidepressants, anesthetics, cocaine, methadone, antihistamines, electrolyte derangements, and even tramadol. [2]. 

Our patient had a Brugada Type 1 pattern elicited by an elevated core temperature, which is also a documented phenomenon. She was on amitriptyline 50 mg/day but no other medications that would affect the sodium channel. There are many case reports of ST elevation with Brugada pattern related to fevers related to infections [3, 4]. It is hypothesized that the rate of sodium channel inactivation can be temperature sensitive and that fever can impair the conductance through the sodium channels [5, 6]. In the largest study looking at this topic by Mizusawa et al., 88 patients with fever induced Brugada Type 1 ECG changes without history of syncope or VF/VT were analyzed. There was a 0.9% per year incidence of SCD in this cohort [1]. 

Prior to Mizusawa's study, it was thought that the incidence of syncope, arrhythmia, or SCD in this cohort was low [7]. Of those that had fever induced Type 1 pattern, approximately 80% also had drug induced Type 1 changes with provocative testing. Only 26% of the group carried the SCN5A mutation and 20% had family history of SCD [1]. It appears as though having Brugada Type 1 ECG patterns unmasked only by fever portends a similar risk of SCD to spontaneous Brugada syndrome, but the studies on this rare clinical entity are still quite small. For now, the 2017 AHA/ACC/HRS guidelines for asymptomatic patients that have inducible types of Brugada syndrome recommend observation without any specific therapies or interventions [8]. In light of the risk of arrhythmia events observed in the Mizusawa trial, a formal EP study might be reasonable to obtain in those with fever induced asymptomatic Brugada ECG changes to help risk stratify these patients. 

Fever in those with spontaneous Brugada Type 1 syndrome has been known to induce Type 1 EKG changes; it is recommended to aggressively treat any fever in this patients when identified. Recently the rate of true arrhythmic events related to fevers in the classic Brugada Type 1 syndrome was explored by Michowitz et al. In a cohort of 588 patients with diagnosed Brugada syndrome who had an arrhythmic event, 6% were associated with a febrile illness. Pediatric and elderly patients were more predisposed to developing an arrhythmic event in the setting of fever [7]. 

As for our patient, on discharge, her EKG had completed returned to her baseline morphology and she has been doing well in follow-up. She has not had a heart catheterization or after this event so the presence or absence of CAD is still unknown. She has not yet been seen by electrophysiology or had further genetic testing for Brugada syndrome. 

[1]: Mizusawa Y, Morita H, Adler A, Havakuk O, Thollet A, Maury P, Wang DW, Hong K, Gandjbakhch E, Sacher F, Hu D, Amin AS, Lahrouchi N, Tan HL, Antzelevitch C, Probst V, Viskin S, Wilde AA. (2016). Prognostic significance of fever-induced Brugada syndrome. Heart Rhythm, 13(7): 1515-1520.

[2]: Junttila MJ, Gonzalez M, Lizotte E, Benito B, Vernooy K, Sarkozy A, Huikuri HV, Brugada P, Brugada J, Brugada R. (2008). Induced Brugada-type electrocardiogram, a sign for imminent malignant arrhythmias. Circulation, 117, 1890–1893.

[3]: Lamelas P, Labadet C, Spernanzoni F, Lopez Saubidet C, and Alvarez PA. (2012). Brugada electrocardiographic pattern induced by fever. World Journal of Cardiology, 4(3): 84-86.

[4]: Antzelevitch C and Brugada R. (2002). Fever and Brugada syndrome. Pacing Clin Electrophysiol, 25(11), 1537-1539.

[5]: Dumaine R, Towbin JA, Brugada P, Vatta M, Nesterenko DV, Nesterenko VV, Brugada J, Brugada R, Antzelevitch C. (1999). Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ Res, 85(9), 803-809.

[6]: Deschênes I and Laurita KR. (2007). How can a single mutation cause such arrhythmic havoc? Heart Rhythm, 4(2), 198-199.

[6] Michowitz Y, Milman A, Sarquella-Brugada G, Andorin A, Champagne J, Postema PG, Casado-Arroyo R, Leshem E, Juang JJM, Giustetto C, Tfelt-Hansen J, Wijeyeratne YD, Veltmann C, Corrado D, Kim SH, Delise P, Maeda S, Gourraud JB, Sacher F, Mabo P, Takahashi Y, Kamakura T, Aiba T, Conte G, Hochstadt A, Mizusawa Y, Rahkovich M, Arbelo E, Huang Z, Denjoy I, Napolitano C, Brugada R, Calo L, Priori SG, Takagi M, Behr ER, Gaita F, Yan GX, Brugada J, Leenhardt A, Wilde AAM, Brugada P, Kusano KF, Hirao K, Nam GB, Probst V, Belhassen B. (2018). Fever-related arrhythmic events in the multicenter survey on arrhythmic events in Brugada syndrome. Heart Rhythm, 15(9): 1394-1401.

[7] American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. (2017). 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Heart Rhythm, 15(10), e73-e189.

Comment by KEN GRAUER, MD (1/30/2019):
Superb presentation and discussion by Dr. Alexandra Schick (with edits by Dr. Smith) of an elderly woman who was seen in the ED for altered mental status, hyperthermia, and the initial ECG shown above. This case provides an excellent example of a “pseudo-infarction” ECG produced by a hyperthermia-induced Brugada-1 ECG pattern. My comments are limited to a few additional clinical points:
  • It is important to distinguish between a Brugada-ECG pattern (as manifest in leads V1, V2 of the initial ECG in this case— vs the “Brugada Syndrome”. In addition to a spontaneous or induced Brugada-1 ECG pattern, criteria for Brugada Syndrome require one or more of the following: History of cardiac arrest, of polymorphoic VT, or of non-vagal syncope — positive family history of sudden death at an early age — a similar ECG in close relatives.
  • ECG criteria for diagnosis of either a Brugada-1 or Brugada-2 pattern are summarized in Figure-1, which I have excerpted from the Bayés de Luna reference shown at the top of the Figure. Note how leads V1 and V2 in the initial ECG (above) clearly satisfy criteria for a Brugada-1 ECG pattern.
  • It is important to clarify distinction between Brugada Syndrome” vs Brugada Phenocopy”. Many factors may induce a Brugada-1 or Brugada-2 ECG pattern. These include certain drugs (ie, calcium channel blockers; ß-blockers; antianginals; psychotropics; ETOH; cocaine; others …); — acute febrile illness (especially with markedly elevated body temperature); — variations in autonomic tone — hypothermia — electrolyte imbalance (ie, common in hyperkalemia); — ischemia/infarction — bradycardia — after cardioversion or defibrillation. The designation Brugada Phenocopy” is given when an otherwise healthy patient has none of the factors associated with Brugada Syndrome — but only develops a Brugada-1 ECG pattern as a result of one of the above conditions — and, resolves this Brugada-1 pattern once the precipitating condition has been corrected. This appears to be what happened in this case — as Brugada-1 ECG changes resolved once this elderly woman’s core temperature was lowered.
  • The clinical significance of distinguishing between Brugada Phenocopy vs a patient with a Brugada-1 ECG that may be due to a true Brugada Syndrome — is that prognosis appears to be significantly better with the former. That said — risk is still present for any patient with a Brugada-1 ECG pattern, which is why referral is merited for more formal risk assessment by an EP cardiologist.
Our THANKS again to Dr. Schick for sharing this case with us!
Figure-1: ECG criteria for diagnosis of a Brugada-1 or Brugada-2 pattern (See text).
NOTE: There are numerous additional cases regarding Brugada pattern ECGs by Dr. Smith on this blog (Simply search for Brugada Syndrome!).
  • For those wanting more — I’ve summarized “My Take” on the Basics of Brugada Pattern ECGs in an ECG VIDEO on this subject.

ADDENDUM (10/24/2020): In the past, the diagnosis of Brugada Syndrome required not only the presence of a Brugada-1 ECG pattern — but also a history of sudden death, sustained VT, non-vasovagal syncope or a positive family history of sudden death at an early age. This definition was changed following an expert consensus panel in 2013 — so that at the present time, all that is needed to diagnose Brugada Syndrome is a spontaneous or induced Brugada-1 ECG pattern, without need for additional criteria.

Monday, January 28, 2019

What is going on here?? (The computer called it "STEMI" and "Intraventricular Conduction Delay"!!)

I was asked by my partner to interpret this ECG because the Veritas algorithm had called it "STEMI" and Intraventricular Conduction Delay (IVCD), and he could not see why.
He also was confused by what looked like possible delta waves with short PR interval.
What do you think?

This is simply an accelerated junctional rhythm at a rate of approximately 100.  It is high enough in the junction that it initiates an atrial beat before it initiates a ventricular beat, and of course it does so in a retrograde fashion.  So the P-wave is before the QRS, is inverted, and there is a very short PR interval.  The junction is going faster than the sinus node.

Alternatively, it could be a low atrial rhythm.

Usually an accelerated junctional rhythm is seen with Digoxin toxicity, but that is primarily when there is underlying atrial fibrillation: the AV node is blocked from conducting the AF impulse, and the junction is accelerated. 

See this case for AF, Dig toxicity, and accelerated junctional rhythm:

Looks like a Posterior STEMI. Is it?

If the sinus node were firing faster than 100, then it would take over, there would be an upright P-wave and a normal PR interval.

Low atrial rhythm can also have short PR interval.

Our electrophysiologist, Rehan Karim, explains this simply: 

Essentially PR interval would have 3 components:
1.       Time from impulse origin to the area of input into AV node.
2.       Time within AV node

3.       His-Purkinje system

He did not say how much is attributable to each segment, although there is no doubt that the most time is spent traversing the AV node.

There is of course no STEMI and there is no Intraventricular conduction delay (and no delta wave/no WPW!)

I found this very nice laddergram on Arnel Carmona's site (high Arnel! We have not been in touch for a long time!).

It is:
Our case here is analogous to (a) above.

Comment by KEN GRAUER, MD (1/28/2019):
Interesting case presented by Dr. Smith about the misinterpretation of a less common rhythm as being due to a “STEMI” with “IVCD”. I’ll add the following thoughts to those presented by Dr. Smith.
  • For clarity, I’ve reproduced and labeled the initial ECG in Figure-1.

Figure-1: The initial ECG in this case (See text).

THOUGHT #1 — What is the rhythm in Figure-1?
  • The rhythm in Figure-1 is not sinus — because there is no upright P wave in lead II. Instead, the P wave in lead II (as well as in the other 2 inferior leads) is negative (RED arrows). The only exceptions to the rule that “if the P wave is not upright in lead II, then you don’t have sinus rhythm” — are dextrocardia and lead misplacement. But the upright QRS in lead I and the large initial Q in lead aVR tell us the limb leads are correctly placed — and, the normal R wave progression in the chest leads tells us this is not dextrocardia.
  • The QRS complex is narrow.
  • The long lead II rhythm strip at the bottom of the tracing tells us that each QRS complex is preceded by a negative P wave in lead II with a fixed and shortened PR interval. Since this supraventricular rhythm is not sinus — there are 2 other possibilities: ian AV Nodal (or Junctional) Rhythm; or, iia Low Atrial Rhythm (often also referred to as a Coronary Sinus Rhythm).

The negative P waves in lead II of Figure-1 are the result of retrograde conduction. As schematically shown by the light RED arrows in Panels A and B of Figure-2 — atrial depolarization will be directed opposite from the +60 degree vantage point of standard lead II when impulse origin is either from the AV Node (“X” in Panel A of Figure-2) — or from a site low in the atria, such as the ostium of the coronary sinus (“Y” in Panel B).
  • Precise localization of the site of an ectopic atrial impulse is beyond the scope of this ECG Blog, and rests in the domain of the cardiology electrophysiologist. Suffice it to say that assessment of P wave morphology (positive, negative, biphasic, or null deflection) in multiple leads of the 12-lead tracing assists in location prediction. The ECG picture in Figure-1, in which inferior lead P waves are negative and P waves are positive in leads aVR and aVL (BLUE arrows) is consistent with either a Junctional or Low Atrial Rhythm.
  • What can be said — is the large size of the negative P waves in the inferior leads suggests the impulse is arising from a considerable distance away (ie, from either low in the atria or from the AV node).
  • P wave morphology in lead V1 is often helpful in further clarification of impulse origin. That said, I fully acknowledge my confusion about how to interpret P wave morphology in leads V1 and V2, as highlighted by the thin, vertical blue line in Figure-1 (which I drew corresponding to what I perceived as the end of the P wave in simultaneously-obtained lead II). BOTTOM LINE: The rhythm in Figure-1 is either Low Atrial or Junctional at a rate of ~100/minute.

Figure-2: Illustration how either a low atrial or junctional rhythm might produce the P wave morphology seen in Figure-1 (See text). Figure reproduced from Grauer K: ECG-2014-ePub (KG/EKG Press).

THOUGHT #2 — What accounts for a negative P wave in front of the QRS with AV nodal beats or rhythm?
  • I expand on the laddergram above in Figure-3. The legend explains all.

Figure-3: Laddergram of the 3 possibilities for P wave appearance in lead II with junctional beats or junctional rhythm. Panel A illustrates the normal forward conduction of sinus rhythm. The impulse originates in the SA Node — travels through the atria — slows down a bit as it passes through the AV Node — and is then transmitted down through the conduction system to the ventricles. NOTE: With junctional beats (or junctional rhythm) — the impulse originates from the AV Node. It then travels back (retrograde) to the atria, and down to the ventricles. As a result — the P wave in lead II may be negative appearing either before (Panel B) or after (Panel D) the QRS — or — no P wave at all may be seen (Panel C). Clinically — Situation C is most common, whereas it is rare to see a P wave after the QRS (situation D). NOTE: Whether a negative P wave is seen before, after, or is hidden within the QRS is determined not only by location of origin of the AV nodal impulse, but by the relative speed of conduction back to the atria compared to down the ventricles. (Figure reproduced from Grauer K: ECG-2014-ePub [KG/EKG Press]).

THOUGHT #3 — Why did the computer interpretation call a “STEMI” with “IVCD”?
  • Computerized ECG interpretations have pros and cons. They are only as good as what they have been programmed for. The better we understand what the computerized system in our facility is capable of — the more effective we can be in using the computer. As a result — I always try to understand what the computer missed. In Figure-1 — my hunch is that the computer interpreted the negative inferior P waves as Q waves, and as a part of the QRS complex — in which case it might call an MI with IVCD. I see nothing that could be misconstrued as acute ST-T wave changes. That said — I’m not quite sure why the computer said what it did ...
  • For “My Take” on the Pros & Cons of Computerized Interpretations — and how I suggest they might best be used — CLICK HERE.

THOUGHT #4 — Clinically, regardless of whether the rhythm is junctional or low atrial — WHY is there a rate of ~100/minute?
  • Practically speaking, distinction between a junctional vs low atrial rhythm is largely academic, since clinical significance of these 2 entities is similar. In either case — the rate here is faster than anticipated ( = “accelerated” ). The point to emphasize is that there are NOT that many reasons for an accelerated junctional rhythm. As a result — recognition of this rhythm should immediately prompt consideration of the following: iDig toxicity (if a patient is on Digoxin and manifests an accelerated junctional rhythm — then almost regardless of the Dig level, they are Dig toxic!); iiIschemia/infarction; iiiPost-operative state; ivCongenital heart disease (if the patient is a child); and, v“Sick” patient.
  • Unfortunately, we are not given any History in this case. Clearly, this would be important to know before proceeding further with clinical management! All we can say is that there is an accelerated junctional (or low atrial) rhythm with LVH (R in lead V6 ≥18 mm) — but no acute ST-T wave changes.The QTc interval looks like it may be prolonged — though this is harder to interpret in view of the rapid rate and generalized ST-T wave flattening.

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