Saturday, June 17, 2017

ECG Blog #140 – (PVC – Atrial Bigeminy – PAC – LAHB – RBBB – LPHB – Aberration).

The ECG in the Figure-1 was obtained from an otherwise healthy 20-year old man. The patient was asymptomatic. This ECG was obtained when an irregular heartbeat was noted on routine exam.
  • How would you interpret this­­ tracing?
  • Are these multifocal (multiform) PVCs?
  • How certain are you of your answer?
Figure-1: 12-lead ECG obtained from a previously healthy 20-year old man with an irregular heartbeat. Are these multiform PVCs? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
Interpretation: The underlying rhythm is sinus. Virtually every-other-beat occurs early and looks different, with at least some degree of QRS widening. That said, these are not PVCs (Premature Ventricular Contractions). Instead, the rhythm is atrial bigeminy, in that every-other-beat is a PAC (Premature Atrial Contraction).
     We know that the different-looking beats here are not PVCs — because: i) these early beats are preceded by premature P waves (RED arrows in lead II of Figure-2); and ii) QRS morphology of the early beats is highly characteristic for aberrant conduction (See below). Distinguishing between early-occurring wide beats that are ventricular in etiology (ie, PVCs) vs PACs that are wide because of aberrant conduction is at times a challenging task! We have previously reviewed this topic in detail in earlier ECG Blog posts (See ECG Blog #14 and Blog #15). This particular case applies principles brought forth from those previous ECG Blog posts that convincingly demonstrates the widened beats in Figure-1 are PACs with aberration.
Figure-2: The ECG from Figure-1 has been labeled (See text for full explanation).
Why We Know that Aberration is Present in Figure-2:
     The most convincing evidence for establishing that aberrant conduction is the etiology of early-occurring widened beats in this tracing lies with recognition of premature P waves. In contrast, PVCs are not preceded by premature P waves. RED arrows in lead II of Figure-2 highlight the presence of a premature P wave with constant PR interval before each early beat (ie, beats #1,3,5,7).
  • The fact that deflections highlighted by red arrows in lead II occur at this exact point in virtually all other simultaneously-recorded limb leads establishes that these deflections are real and not artifact.
  • Note: It is common to see PR interval prolongation for PACs (as is the case here) — since early-occurring atrial activity is clearly more likely to encounter some delay as it traverses an AV node that may not yet have recovered full conduction properties.
Aberrant Conduction is most likely to take the form of some type of bundle branch block and/or hemiblock pattern. As a result — attention to QRS morphology may sometimes help to distinguish between aberrancy vs ventricular beats.
  • By far — the most common form of aberrant conduction manifests a RBBB (Right Bundle Branch Block) pattern. This is because under normal circumstances, the right bundle branch tends to have the longest RP (Refractory Period) — which means, that an early-occurring impulse (ie, a PAC) has the greatest chance to arrive at the AV node at a time when the right bundle branch is still refractory. That said, any form of conduction defect may be seen with aberrant conduction — depending primarily on the relative length of the RP for the various conduction fascicles in a given patient. As a result — there may be LBBB (Left Bundle Branch Block) aberration; aberration of either hemifascicle ( = LAHB or LPHB = Left Anterior HemiBlock or Left Posterior HemiBlock aberration) — or, any combination thereof (ie, RBBB/LAHB or RBBB/LPHB aberration).
  • KEY POINT: If early beats manifest highly typical QRS morphology for any one or any combination of conduction defect — this is highly suggestive that the widened beat (or run of beats) is supraventricular with aberrant conduction. The converse, however — is not true! That is, aberrant conduction is still possible even if QRS morphology of early beats does not resemble any form of conduction defect(s). In such cases — other ECG criteria will have to be used for distinguishing between ventricular vs supraventricular etiology. 
Unfortunately, Figure-2 does not provide us with an uninterrupted long-lead rhythm strip. That said, it should be obvious that every-other-beat (ie, each odd-numbered beat) manifests a different and widened QRS morphology.
  • Attention to premature beats #9 and 11 in lead V1 reveals a highly characteristic RBBB morphology, especially for beat #9 — which shows initial small, narrow r wave; followed by S wave that descends below the baseline in V1; followed by a terminal tall R’ (ie, taller “right rabbit ear”).
  • Note the presence of a terminal wide S wave in simultaneously-occurring beats #9 and #11 in lead V6. In contrast, beat #13 in lead V1 is only minimally different in morphology from normally conducted beats #8,10 and 12. As might be expected, there is no terminal wide S wave for beat #13 in simultaneously-occurring lead V6. ECG recognition of this very highly characteristic RBBB morphology in leads V1 and V6 for early-occurring beats #9 and 11 is virtually diagnostic of RBBB aberration.
  • Turning our attention to the limb leads — we know (even without seeing a simultaneously-recorded lead V1) that beats #1, 3, 5 and 7 are also all conducted with a typical RBBB pattern, because each of these beats manifests a terminal wide S wave similar to that we have already intermittently seen in lead V6. What is especially fascinating about this tracing — is that while early beats #1 and 3 only manifest RBBB aberration — beat # 5 manifests RBBB/LPHB aberration — and, beat #7 manifests RBBB/LAHB aberration. We say this, because of the typical very deep straight S wave in lead I of beat #5 that occurs in association with a qR pattern in leads II,III (highly typical of LPHB!) — whereas we see an rS complex with predominant negativity in leads II and III for beat #7 (highly typical of LAHB!).
  • And then there is beat #13 — which despite being early, occurs without a RBBB pattern, and with no more than minimal aberration.
BOTTOM LINE: PVCs do not do what we see here. More than the already diagnostic presence of premature P waves preceding each early beat (best seen in the limb leads) — changing QRS morphology of every-other-beat manifesting multiple variations of highly typical conduction defect morphology establishes with 100% certainty that the rhythm in Figures-1,2 is Atrial Bigeminy with varying forms of Aberrant Conduction.
  • Otherwise, judging from QRST morphology in the normally conducted beats — there do not appear to be any acute changes on this tracing.

Additional Reading: 

Saturday, December 24, 2016

ECG Blog #139 (Atrial Flutter – AV Block – Artifact – Sinus Rhythm)

The rhythm in Figure-1 was diagnosed as AFlutter (Atrial Flutter) with 4:1 AV conduction. Do you agree?
  • What could be done to confirm your answer?
Figure-1: Lead II rhythm strip. Is this AFlutter? NOTE — Enlarge by clicking on the Figure.
Interpretation: As emphasized in ECG Blog #137 — the most common ventricular response to untreated atrial flutter is with 2:1 AV conduction. But the next most common ventricular response is with 4:1 AV conduction. At first glance, the rhythm in Figure-1 appears to be atrial flutter with this latter conduction ratio. However, close inspection reveals this is not the case!
  • Use of calipers demonstrates that the small upright deflections on the baseline between QRS complexes are definitely not regular. This makes it extremely unlikely that these deflections represent flutter activity, since flutter waves (by definition) should be extremely regular.
  • There is also a changing relationship between these small vertical deflections (that are seen throughout the baseline on this rhythm strip) — and neighboring QRS complexes. In contrast, with atrial flutter — there is usually a constant relationship between atrial deflections and neighboring QRS complexes. This is because with the exception of the variable conduction variant of flutter — there will usually be a readily identifiable repetitive pattern of atrial activity with respect to each QRS complex that results in a predictable conduction ratio.
  • Finally, if one steps back a bit from this tracing — underlying upright (sinus) P waves can be seen to precede each QRS complex with a fixed (and normal) PR interval (red arrows in Figure-2). The fact that these sinus P waves are unaffected by the smaller, irregularly occurring upright deflections proves that these smaller pointed deflections are the result of artifact.
Figure-2: We have labeled Figure-1 by adding red arrows to highlight underlying regularly-occurring sinus P waves (See text).
Comment: The best way to prove artifact — is to go to the bedside to observe the patient as the ECG is being recorded. Tapping, scratching, coughing, shaking, shivering, seizing and tremor are but a few of the common causes of artifactual arrhythmias. The patient in this case had Parkinson’s disease, which characteristically produces a tremor at a frequency that approximates the rate of atrial flutter. Bottom Line: It is easy to be fooled by artifact. It is well to develop a healthy respect for the gamut of “real appearing” arrhythmias that artifact distortion may produce.
For More on this Subject:

ECG Blog #138 (SVT – AV Block – Atrial Flutter – Atrial Tachycardia – Digoxin)

How would you interpret the rhythm in Figure-1? What is your differential diagnosis? Can you be sure of your answer from looking at this lead MCL-1 rhythm strip?
  • Why is it important to know if this patient is on Digoxin?
Figure-1: Lead MCL1 rhythm strip. Is this AFlutter or ATach? NOTE — Enlarge by clicking on the Figure.
Interpretation: The rhythm in Figure-1 is regular with a ventricular rate of ~115/minute. P waves outnumber QRS complexes by two to one (Figure-2) — making the atrial rate ~230/minute. The QRS complex is narrow, implying a supraventricular mechanism — and each QRS complex is preceded by a P wave with a constant PR interval. Thus P waves are related to the QRS complexes, albeit only one of every two P waves is conducted to the ventricles. Therefore, this is an SVT (SupraVentricular Tachycardia) rhythm with 2:1 AV conduction. The differential diagnosis is between AFlutter (Atrial Flutter) vs ATach (Atrial Tachycardia).
Figure-2: We have labeled Figure-1 by adding red arrows for the regular atrial activity. There are 2 P waves for each QRS complex (See text).
Diagnostic Considerations:
  • In favor of AFlutter — is regular and rapid atrial activity with a peaked upward deflection in this right-sided MCL-1 monitoring lead. That said, the atrial rate of 230/minute is a bit below the usual atrial rate range for untreated atrial flutter (of 250-350/minute) — and, the expected “sawtooth” pattern of atrial flutter is missing in this lead.
  • In favor of ATach — is the atrial rate (below 250/minute) and, the isoelectric baseline (rather than sawtooth) in this lead.
  • Note: We are not told if this patient is taking an antiarrhythmic agent (such as flecainide, amiodarone, sotalol, etc.) that might slow the atrial rate of flutter. We are also not told if this patient is taking Digoxin. This is important because SVT with 2:1 conduction in a patient taking Digoxin should strongly suggest the possibility of digitalis toxicity. Given greatly reduced use of this drug at the current time — atrial tachycardia with block due to digitalis toxicity is no longer commonly seen — but it remains important to inquire about this medication since you may occasionally encounter patients who are still taking Digoxin.
Bottom Line: It is impossible to be certain of the rhythm diagnosis in Figure-2 from this single rhythm strip without the benefit of additional information (ie, previous clinical history; knowing what medications the patient is taking, etc.). Seeing a full 12-lead ECG might help by revealing a typical sawtooth pattern in other leads. That said, the clinical reality is that neither rate nor baseline appearance (sawtooth vs isoelectric baseline) have been shown to reliably distinguish between ATach vs AFlutter. Fortunately, from a non-cardiologist’s perspective — both initial and long-term management of these two SVT rhythms is similar (once you have ruled out the possibility of digitalis toxicity).  Initial efforts entail slowing the ventricular response, with consideration of EP = electrophysiology referral if the arrhythmia is persistent or recurs.
Clinical Note: Assuming this patient is not on Digoxin — the terminology used to describe the arrhythmia seen in Figure-1 is far less important than the overall clinical concepts involved. This is because what used to be classified as “atrial tachycardia” in non-Digoxin toxic patients is now often referred to as an “atypical” form of AFlutter.
  • Included within the broad category of “atypical” AFlutter rhythms are various types of atrial tachycardias that may arise from anywhere within the atria or neighboring pulmonary veins.
  • Some atrial tachycardias may be “focal” or automatic (often recognizable by non-sinus P wave appearance — “warm up” phenomenon until the ectopic tachycardia is established — relatively slower rateand on occasion slightly variable P-P intervals).
  • Other atrial tachycardias may be much faster, perfectly regular, lack an isoelectric baseline — and be clinically indistinguishable from AFlutter based on ECG appearance. That said, since practically speaking both persistent ATach as well as persistent AFlutter are indications for EP referral — definitive diagnosis from the initial ECG is not essential.
For More on this Subject:
  • See also ECG Blog #40 — for review of a relevant SVT case.

ECG Blog #137 (SVT – AV Block – Atrial Flutter – Atrial Tachycardia – Atrial Fibrillation)

The rhythm in Figure-1 was diagnosed as AFlutter (Atrial Flutter). Do you agree? If so — Is there anything unusual about this rhythm strip?
Figure-1: Lead MCL1 rhythm strip. Is this typical atrial flutter? NOTE — Enlarge by clicking on the Figure.
Interpretation: Atrial flutter is characterized by a special pattern of regular atrial activity that in adults almost always occurs at a rate of 300/minute (250-to-350/minute range). The most common ventricular response to atrial flutter (by far! ) — is with 2:1 AV conduction. As a result, the ventricular rate with untreated atrial flutter will usually be close to 150/minute (ie, 300÷2) — although the ventricular rate may be slower if the patient is taking antiarrhythmic drugs.
  • Less commonly with atrial flutter — there is 4:1 AV conduction (ventricular rate ~75/minute) — or a variable ventricular response.
  • Odd conduction ratios (ie, 1:1: 3:1; 5:1) are possible, but extremely uncommon unless the patient is on antiarrhythmic medication or has WPW (Wolff-Parkinson-White) Syndrome.
  • Atrial flutter typically manifests a sawtooth appearance that is usually best seen in the inferior leads. That said, flutter waves may sometimes be subtle and only seen in a handful of leads (if at all).
  • Distinction between ATach (Atrial Tachycardia) and AFlutter may be difficult. This is especially true when the characteristic sawtooth appearance of flutter is missing, and the rate of atrial activity is at least slightly below the usual range for flutter.
The ventricular response in Figure-1 is regular at a rate of ~85/minute. Regular atrial activity is seen — but instead of 2 P waves for each QRS, there are 3 P waves for each QRS complex (Figure-2). Note that the PR interval preceding each QRS complex is the same! This tells us that there is conduction — in this case with a 3:1 ratio (ie, only one out of every 3 P waves seen within each R-R interval is being conducted to the ventricles).
  • Since we know that there are 3 times as many P waves as QRS complexes in this example — the easiest way to accurately calculate the atrial rate is to multiply the ventricular rate (85/minute) by 3. This yields an atrial rate of ~255/minute, which is above the usual range rate for atrial tachycardia (which generally doesn’t exceed 240/minute). As a result, the rhythm in Figure-2 most probably represents the unusual case of AFlutter with an odd conduction ratio (here with 3:1 AV conduction).
Figure-2: We have labeled Figure-1 by adding red arrows for the regular atrial activity. There are 3 P waves for each QRS complex (See text).
PEARL: There will usually be “something else” going on medically with the patient when you encounter AFlutter with an odd conduction ratio. Many such patients will be receiving one or more antiarrhythmic drugs (that may slow the flutter rate and affect the AV conduction ratio) — or perhaps the patient has already undergone ablation for one or more previous episodes of AFlutter.
  • The unusual situation of AFlutter with 1:1 AV conduction (ventricular rate close to 300/minute) — should lead one to inquire IF the tracing is from a child who may have congenital heart disease and/or a patient of any age with WPW. Bottom Line: Non-cardiologists will probably only rarely see AFlutter with an odd conduction ratio, if at all.
For More on this Subject:
  • See also Section 14.4 (from our ACLS-2013-ePub) — on Atrial Flutter.

Friday, December 23, 2016

ECG Blog #136 (AVNRT – Vagal Maneuver – PVC – Couplet – Salvo - SVT

The rhythm in Figure-1 was observed as a previously healthy young adult was being treated for his “palpitations”. He was hemodynamically stable at the time. Interpret the rhythm.
  • What happened? Should what we see be cause for alarm?
Figure-1: Lead II rhythm strip during treatment (obtained from a patient with palpitations). Should what you see be cause for alarm? NOTE — Enlarge by clicking on the Figure.
Note: Discussion of this tracing is far easier if beats are labeled (Figure-2).
Figure-2: We have labeled all beats in Figure-1.
Interpretation: The patient is hemodynamically stable. The first 9 beats show a regular SVT rhythm (SupraVentricular Tachycardia) at a rate between 185-190/minute. No atrial activity is seen during this run. The rhythm changes beginning with beat #10.
  • After the run of SVT — it is easiest to look next at beats #11,12. Both beats are clearly ventricular in etiology — since the QRS complex is wider and completely different in appearance from QRS complexes during the SVT run at the beginning of the tracing.
  • Beat #10 manifests an intermediate morphology between the narrow beats before it — and the ventricular couplet that follows. Beat #10 is a fusion beat — which means it is due to simultaneous occurrence of a supraventricular and ventricular beat. Therefore, beats #10-through-12 constitute a 3-beat salvo of ventricular tachycardia. PEARL: Recognition of fusion beats can be facilitated by looking not only to see if QRS appearance is intermediate between beats occurring before and beats that come after — but also by looking to see if ST-T wave appearance is intermediate! This clearly is the case here — as T wave shape and amplitude of beat #10 is indeed intermediate between T wave shape and amplitude of beats #9 and #11.
  • Note that there is conversion to sinus rhythm beginning with beat #13. Another ventricular couplet follows (beats #14,15) — with the tracing ending in a regular sinus rhythm at a normal rate.
IMPRESSION: The rhythm in Figure-2 begins with a 9-beat run of AVNRT (AV Nodal Reentry Tachycardia). The rate of this SVT rhythm is too fast for atrial flutter with 2:1 conduction. It is also must faster than the usual rate range of sinus tachycardia. Abrupt conversion to sinus rhythm (beat #13) supports the diagnosis of AVNRT, which is a common cause of “palpitations” in the young adult age group.
  • We do not know if conversion to sinus rhythm was achieved by a vagal maneuver, by medication — or by a combination of the two. Regardless — the point to emphasize is that it is a common and normal phenomenon to see PVCs (including ventricular couplets or salvos) at the time of conversion from a reentry tachycardia to sinus rhythm. Therefore, there is no cause for alarm from the rhythm in Figure-2, and assuming no other concerning features, additional workup would not be indicated at this time.
For More on this Subject: