Sunday, July 1, 2018

ECG Blog #153 (LVH – RVH – WPW – RBBB)

The ECG in Figure-1 was obtained from an otherwise healthy and completely asymptomatic 39-year old man as part of his pre-employment physical exam.
  • How would you interpret this ECG?
  • Is there RVH? Is there LVH?
  • How would you advise this patient?
Figure-1: ECG obtained from a healthy and completely asymptomatic 39-year old man. NOTE — Enlarge by clicking on the Figure.
Interpretation: Our systematic approach to this ECG is as follows:
  • Rate & Rhythm — Normal sinus rhythm at a rate of ~60-65/minute. Unfortunately, there is no long-lead rhythm strip at the bottom of this tracing. However, the P wave is upright in lead II with a constant PR interval — and, this defines the rhythm as sinus.
  • Intervals The PR interval appears to be short (ie, less than 0.12 second in duration). Inspection of the QRS complex in all 12 leads suggests that there may be slight QRS widening (especially in leads V2 and V3). There appears to be slurring of the initial part of the QRS complex in several precordial leads.
  • Axis — N/A (Not Applicable) — given what we have just described ...
  • Chamber Enlargement — N/A (See below).
  • Q-R-S-T Changes — N/A (See below).
  • Clinical IMPRESSION — NSR ( = Normal Sinus Rhythm) with WPW. We emphasize that recognition of WPW in this case is subtle — and would be easy to overlook!
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COMMENT: This patient manifests the syndrome of WPW (Wolff-Parkinson-White— in which one or more accessory pathways exist that allow an alternate route for transmission of the electrical impulse from atria to ventricles. Thus, with WPW — sinus impulses bypass the AV node via an AP (Accessory Pathway) — and, therefore arrive early in the ventricles (Panel A in Figure-2).
Figure-2: With WPW — impulses bypass the AV node via AP conduction. Although the AP shown in Panel A is right-sided — it could be left-sided, anterior or posterior (and, at times there may be more than a single AP). The 3 ECG signs of WPW are seen in Panel B  ia delta wave (which may be positive or negative); iiQRS widening; and iiia short PR interval (See text).
ECG Recognition of WPW: It is usually easy to recognize WPW on a baseline ECG when conduction completely utilizes the AP (Accessory Pathway). There are 3 ECG features to look for (Panel B in Figure-2):
  • Delta waves.
  • A short PR interval.
  • QRS widening.
Delta Wave: The delta wave is recognized as a distortion of the initial portion of the QRS complex. It is due to the fact that the electrical impulse bypasses the AV node — and arrives at the ventricles directly via conduction over the accessory pathway.
  • Delta waves may be upright (positive) or downward (negative) — depending on where in the heart the AP is located. When delta waves are negative — they may simulate the Q wave of myocardial infarction (Panel B in Figure-2):
  • KEY Points: Even when conduction is entirely over the AP — delta waves will not always be seen in every lead. Moreover, delta waves may come and go — since conduction over the AP may be intermittent. At times — conduction may simultaneously occur over both the normal and accessory pathway. When this happens — the ECG characteristics of WPW may be subtle, because the contribution from conduction over the normal AV nodal pathway may predominate (and thereby mask) ECG features of preexcitation.
Short PInterval: The reason the PR interval is short with WPW — is that the AV node is bypassed. With normal conduction in sinus rhythm — the electrical impulse slows down as it passes through the AV node on its way to the ventricles. As a result — most of the PR interval normally consists of the time it takes for the impulse to traverse the AV node. The electrical impulse arrives at the ventricles sooner with WPW — because the usual relative delay that occurs when passing through the AV node is avoided by conduction over the AP.
QRS Widening: The QRS widens with WPW — because after the impulse arrives at the ventricles (via conduction over the AP) — it must travel over nonspecialized myocardial tissue until such time that it attains whatever distal portion of the conduction system that has not yet depolarized. Thus the delta wave may extend for 0.04 second or more (reflecting slow conduction over nonspecialized myocardial tissue). When the delta wave deflection is added to the rest of the QRS complex — the result is a widened complex.
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Bottom Line Regarding ECG Recognition: Many variations exist on the above theme. Remember the following:
  • WPW is not common in the general population. Its estimated incidence is ~2 per 1,000 subjects. This is just often enough that virtually every health care provider who deals with ECGs will at least occasionally encounter this syndrome.
  • When a patient with WPW is conducting over their accessory pathway — you can diagnose WPW by recognition of the following 3 ECG features in at least several of the leads in a 12-lead ECG: i) QRS widening; ii) a delta wave; and iii) a short PR interval. A problem with diagnosis is that preexcitation (ie, WPW conduction over an AP) can be intermittent. Thus, there may be no indication on a given ECG that a patient has WPW if conduction is entirely (or almost entirely) over the normal AV nodal pathway at the time the tracing is recorded.
  • NOTE about This Case: It is because of less-than-complete preexcitation that diagnosis of WPW is so challenging in Figure-1. Other than a slightly shortened PR interval — not much looks abnormal in the limb leads. Definite delta waves are only seen in leads V1, V2, V3 and V4.
Clinical Importance of WPW: There are 2 principal reasons why recognizing WPW is important:
  • Reason #1: WPW is often associated with cardiac arrhythmias — due in large part to availability of an accessory pathway (AP) that facilitates reentry tachycardias and exceedingly rapid conduction with atrial fibrillation or atrial flutter. Fortunately, the vast majority of patients with WPW have an excellent long-term prognosis — and, the overall incidence of sudden death with this syndrome is extremely low. That said, WPW-related arrhythmias can be potentially life-threatening — because extremely rapid rates (over 250/minute) may be attained if a patient with WPW develops AFib or AFlutter. These excessively rapid rates can precipitate deterioration of the rhythm to VFib.
  • Reason #2: WPW is often thought of as the “Great Mimic” of other conditions. The presence of QRS widening with resultant secondary repolarization changes in the ST-T wave may produce an ECG picture that simulates RBBB, LBBB, IVCD, LVH, RVH, and/or myocardial infarction or ischemia.
  • NOTE about This Case: The upright and slightly widened QRS complex in lead V1 of Figure-1 simulates RBBB and RVH. The markedly increased QRS amplitude present in lead V5 simulates LVH. That said, none of these conditions can be diagnosed on ECG — because this patient has WPW! Thus, we have no idea from this ECG if ventricular enlargement or bundle branch block is also present in this case.
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How Not to Overlook the Diagnosis of WPW? As emphasized, recognition of WPW in this case could be easy to overlook — because there is less-than-complete preexcitation. That said — strict adherence to a Systematic Approach to ECG interpretation should have allowed you to pick up the diagnosis of WPW in this case by at least one of 3 ways (Figure-3):
  • The PR interval in lead II is short (less than 0.12 second). While normal subjects sometimes manifest slight PR interval shortening — recognition that the PR interval is short should alert you to initiate a diligent search for subtle delta waves (RED arrows in Figure-3).
  • Several of the chest leads in Figure-3 suggest that the QRS complex is at least slightly widened. Remember: Determination of interval duration is assessed from whichever of the 12 leads show the longest interval — and, the QRS complex in lead V3 looks to be more than half a large box in duration.
  • Assessment of Q-R-S-T Changes: Note that transition in the chest leads occurs early — because the QRS complex is already all positivein lead V1 (within the RED rectangle)! Recognition of a Tall R Wave in Lead V1 should prompt immediate consideration of the Common Causes of this ECG Finding. WPW is one of these causes! (Please see ECG Blog #81).
Figure-3: ECG features suggesting WPW in this case (See text).
How Would You Advise this Patient? It is important to remember that the 39-year old man in this case has been healthy — and that he is completely asymptomatic. IF this patient had a prior history of symptoms suggestive of cardiac arrhythmia episodes — referral to an EP cardiologist would clearly be indicated. But he is asymptomatic!
  • Clinically — It is worthwhile to go back and question this patient again as to whether he has ever experienced symptoms possibly related to a cardiac arrhythmia. If done in an open-ended manner — a significant number of patients will then remember symptomatic episodes. Questioning might go like this: “Have you had episodes lasting 15 or more minutes, in which you felt dizzy, or felt strong a pounding in your chest?” Be sure to specifically inquire about syncopal (or presyncopal) episodes during exercise. A positive response to any of these questions merits further evaluation.
  • In 2018 — elective referral for RFCA (RadioFrequency Catheter Ablationhas become a standard procedure with a high success rate for potential “cure” of WPW-related arrhythmias. At established centers with experienced EP cardiologists — effective catheter ablation of the AP is generally achieved in >95-98% of cases, with complication rates of under 5%. Most complications are temporary, but complete AV block may occasionally occur. Thus, although EP testing and ablative procedures have become increasingly safe — they are not completely benign. Balanced by the overall favorable prognosis of most patients with WPW — risk stratification and patient preference enter prominently into the decision-making process.
  • Risk of developing symptomatic arrhythmias in patients with WPW varies with age. In many patients, the capacity for ventricular preexcitation is lost over time. Thus, the risk of developing malignant arrhythmias is significantly less for asymptomatic patients with WPW who are over 35-40 years of age, compared to the risk in younger adults and children.
  • In 2018 — detection of WPW on the ECG of an asymptomatic infant or child merits referral to a pediatric cardiologist. Another group that merits referral includes teenage and young adult competitive athletes. Risk stratification of these individuals can then assist in determining who among them will best be served by more invasive EP testing. In contrast, older adults who have remained asymptomatic from their WPW over the balance of their lives are at significantly lower risk — and do not necessarily need referral. Once again, patient preference and non-invasive risk stratification can facilitate decision-making.
  • The simplest form of risk stratification in patients with WPW is to determine IF preexcitation is lost on Holter monitoring or stress testing when there is physiologic increase in heart rate. Formal stress testing may be especially helpful. Because subtle preexcitation may be masked during exercise — only abrupt and complete loss of preexcitation during exercise reliably corresponds to a long APERP (accessory pathway effective refractory period), with resultant reduced risk of sudden death from deterioration of very rapid AFib.
  • For those WPW patients who have already developed one or more episodes of rapid AFib — the SPERRI (Shortest Pre-Excited R-RIntervalis a non-invasive indicator that provides excellent insight into anterograde conduction properties of the AP. Risk of developing VFib during AFib with WPW is greatly increased when a SPERRI of ≤220-250 msec is seen.
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Returning to This Case: The patient in this case is a healthy 39-year old man who as far as we know — has been entirely asymptomatic!
  • Assuming further questioning of this patient does not suggest a history of episodes potentially consistent with a cardiac arrhythmia — and, assuming the job this patient is about to be starting does not entrust him with the care of others (ie, flying a plane; driving a school bus) — the incidental finding of WPW on ECG should not disqualify him from work. We need to remember that the only reason an ECG was done — is that it was requested as part of this asymptomatic patient’s pre-employment physical exam.
  • The patient should be told that he has WPW. It may be helpful to give him a reduced-size copy of his ECG, so that he can carry this in his wallet should questions ever arise in the future from a visit to a medical facility.
  • One might consider non-invasive risk assessment with exercise testing — to see if there is abrupt and complete disappearance of preexcitation with physiologic increase in heart rate. If so, this would portend a favorable prognosis — and add further support to a decision not to pursue additional evaluation unless symptoms develop in the future.
  • Finally — the patient should be cautioned that if ever he does develop symptoms potentially related to a cardiac arrhythmia — that he should promptly seek medical assistance. In this case — further evaluation with EP testing would clearly be indicated.
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NOTE: The following blogs and reference materials provide more information on topics mentioned in this case:
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Some LITERATURE: How to proceed in an asymptomatic patient with WPW is the subject of much controversy. Here are a few relevant references:

ADDENDUM: 
This ECG Blog has generated numerous excellent comments on the EKG Club (by Alexander Nossikoff, Mario Parrinello, Paul Matera and others) — regarding distinction between “WPW” vs WPW "Syndrome”.
  • Technically — saying that a patient has WPW” implies the presence of an ECG pattern indicative of preexcitation (ie, presence of delta waves, short PR interval, wide QRS). For this “WPW pattern” to then qualify as WPW “Syndrome” — there must also be the presence of cardiac arrhythmias due to preexcitation.
  • Personally ( = MOpinion) — I think this is a semantic distinction of little (or no) clinical relevance. This is because the name (ie, use of WPW or WPW Syndrome) of whatever you say your patient has, does not in the least alter my clinical approach. That’s because each case must be individualized — and such individualization entails much more than designation of the word “Syndrome” after WPW … 
  • The field of EP cardiology has dramatically advanced in recent years. EP testing followed by ablation of one or more accessory pathways offers potential for “cure” from WPW-related arrhythmias. But determining which patients are to be referred to EP Cardiology does not (and should not) uniquely depend on whether the “Syndrome” of WPW has yet declared itself.
  • My impressions of the literature are that in 2018 — asymptomatic children with WPW (even when they have not yet demonstrated WPW-related cardiac arrhythmias) should still be referred to a pediatric cardiologist. At the least, there should be noninvasive evaluation by an expert in this area in an attempt to gage probable degree of risk for developing serious (potentially life-threatening) arrhythmias. 
  • I believe the same recommendation should apply for teenagers and young adults participating in competitive sports — at least in the United States in those areas of the country where a screening ECG is part of a pre-participation sports evaluation. And, once you detect a WPW pattern on the ECG on an asymptomatic young athlete — it becomes hard not to refer that individual to a cardiologist. 
  • NOTE #1: Is there any “defense” if you as a noncardiolgist find WPW in a young asymptomatic athlete but do nothing — and this athlete then develops a lethal episode of very rapid atrial fibrillation that leads to cardiac arrest? 
  • NOTE #2: If this young adult athlete is felt by an arrhythmia specialist to be of “lower risk”, with non-invasive stress testing demonstrating complete and abrupt resolution of preexcitation with physiologic increase in heart rate — nothing more might need be done other than long-term follow-up. But the point is, that despite not having WPW “Syndrome” — this is clearly a person who should be evaluated by a provider with expertise in cardiac arrhythmias.
  • In contrast — Consider the case of a 60-year old man or woman with WPW on ECG, and a history of rare episodes of reentry SVT that are easily controlled with intermittent use of AV blocking agents. By definition — this patient has WPW “Syndrome” — yet given the patient’s age, the nature of their arrhythmia and the ease of control with no more than intermittent medication — referral to EP Cardiology for an ablative procedure is clearly not mandatory. In fact, patient preference in this case is probably the most important factor in long-term decision-making. Clearly, management decisions in such a theoretical patient might quickly change (ie, if this patient developed atrial fibrillation with a very rapid response) — but the point is, that is that despite having WPW “Syndrome” — optimal management decision-making will depend more on other factors.
BOTTOM LINE: In my opinion — whether I describe the patient in front of me with WPW on his/her ECG as having (or not having) WPW “Syndrome” is not the determining factor in how I manage this patient. As for the asymptomatic 39-year old man in this case — individualization of each patient is essential. Depending on factors I outine above (under How Would You Advise this Patient?) — referral to an arrhythmia specialist may or may not be needed in this case (and may or may not be desired).
  • P.S.— I fully realize and acknowledge that others may disagree with my opinions. That’s fine. We ALL learn from healthy academic discussion! Your comments are welcome!

Monday, June 4, 2018

ECG Blog #152 (QTc – ECG Lists – Sinus Rhythm)

A 59-year old woman presented in an unresponsive state with presumed sepsis. A previous ECG was read as “normal”. How would you interpret this patient’s initial ECG? (Figure-1).
  • What is the rhythm?
  • What clinical entities should be considered as potentially contributing to the abnormal findings?
Figure-1: Initial 12-lead ECG obtained from a 53-year old woman who presented in an unresponsive state with presumed sepsis. What clinical entities are likely to be contributing to the ECG abnormalities seen? NOTE— Enlarge by clicking on the Figure.
Interpretation: We begin our systematic interpretation with assessment of the rhythm. This is somewhat challenging — since it is not immediately apparent whether an upright P wave is (or is not) present in lead II.
  • Lead II is typically the most helpful lead for rhythm assessment. In fact, we define a rhythm as of sinus origin, if P waves are similar in morphology are upright in lead II.
  • The ECG in Figure-1 provides one of the occasional instances in which the mechanism of the rhythm is not apparent from assessment of lead II alone — because the P wave in this lead is not clearly distinguishable from the end of the T wave. As a result, we need to look at other leads to determine the rhythm (Figure-2).
Figure-2: Determination of the rhythm by using other leads … (See text).
Confirming the Rhythm:
The lead that best displays P waves in Figure-2 is lead V1 (Blue arrow pointing to within the RED circle). There should be no doubt that P waves are regularly present in lead V1, and consistently conducting to the ventricles with a constant PR interval in this lead.
  • The other lead in this tracing, in which we clearly see conducting P waves with a constant PR interval is lead I. Using the concept of simultaneous leads — we can drop a time line (the vertical RED line in Figure-2) from P waves that we definitely see in lead I. Doing so confirms that the slight notching seen in the terminal portion of the T wave in lead II is in fact an upright P wave, that has fused with the end of this T wave. So the rhythm is sinus tachycardia, at a rate of ~100/minute.
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PEARL: Next to lead II — the 2nd-best lead to look for P waves in, is lead V1 (which anatomically, lies in close proximity to the right atrium). Other leads that are generally very helpful for visualizing atrial activity include leads III and aVR. If the nature of atrial activity is not apparent from these 4 leads — we then turn our attention to each of the remaining 8 leads. This case provides a nice example of how leads I and V1 were needed to confirm sinus origin of the rhythm.
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Intervals: Returning to our Systematic Approach, we next look at Intervals:
  • The PR interval is normal (ie, not more than 1 large box in duration = not more than 0.20 second in duration).
  • The QRS complex is narrow (ie, not more than 1/2 large box in duration = not more than 0.10 second in duration).
  • BUT — the QT interval is clearly long! (Figure-3).
Figure-3: The QTc is obviously prolonged (See text).
Assessing the QInterval: We review basic concepts for assessing the QT interval in our ECG Blog 89 (Turn to Figure-9 in this Blog post). We address more advanced concepts about the QTc in Section 6.0 from our ECG-2014-ePub.
  • For practical purposes, the QT= the QT interval, corrected for heart rateis prolonged  IF it clearly measures more than half the R-R interval.
  • That there is marked QTc prolongation in this case, should be obvious from Figure-3. We select lead V2 for our measurement. Another lead could have been chosen. Although admittedly difficult to be certain of where the T wave ends — we suggest the vertical PURPLE line as this landmark. The double RED arrow clearly reveals the QT in lead V2 to comprise much more than half the R-R interval in this lead.
Several caveats are in order:
  • Estimation of whether or not the QTc is prolonged is less accurate by the above “eyeball” method when the heart rate is faster (ie, over 90-100/minute). That said, despite a rate of ~100/minute in this case — the QT that we measure in lead V2 of Figure-3 is so much more than half the R-R interval, that despite the relatively fast rate, we still know that the QTc is very long.
  • There really is no lead on this 12-lead ECG that allows us to clearly define the end of the QT interval (ie, where the T wave ends). That said, there still should be no doubt in this tracing that the QTc is very long.
The Rest of our Systematic Interpretation: Having completed assessment of Rate, Rhythm and Intervals — we return to our Systematic Approach:
  • Axis — The mean QRS axis is about +40 degrees (a positive QRS complex, that is almost equally upright in leads I and aVF).
  • Chamber Enlargement — None.
  • QRST Changes — A small q wave is seen in lead III; transition is normal (occurs between lead V2-to-V4); and there are nonspecific ST-T wave abnormalities in multiple leads.
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Clinical IMPRESSION: Sinus tachycardia. Marked prolongation of the QT interval — seen here with nonspecific ST-T wave abnormalities that appear to be new (since we are told that a prior ECG on this patient was reportedly normal).
  • The principal abnormal finding on this ECG is the Long QT. The common Causes of QProlongation make up one of our KEY Lists. They are: iDrugs; ii“Lytes” (ie, electrolyte disorders — principally low serum K+ and/or Mg++ or Ca++); and iiiCNS catastrophes (including stroke, seizure, bleed, tumor, trauma, coma, etc.). We are told that the patient in this case has presumed sepsis — and, that she is unresponsive. Therefore, her altered mental status might account for the prolonged QT that we see on her ECG (Could there also be an as yet undiagnosed ongoing CNS catastrophe such as stroke or bleed?). Additional clinical information is needed on this patient, to determine IF drug effect and/or electrolyte disturbance might also be contributing to the ECG abnormalities we see in Figure-1.
  • ST segments and T waves are definitely not normal in this tracing. We’ve interpreted the diffuse abnormality seen here as a “nonspecific” ST-T wave change — because the ST segment is not elevated (with respect to the J point), and at most, is only minimally depressed. ST segment shape in this tracing is not diagnostic of any “specific” entity (ergo, the term “nonspecific” ST-T wave abnormality). We suspect that much of the ST-T wave abnormality that is seen may resolve if/as the QT interval normalizes. That said, Clinical Correlation over time will be needed to know if anything else is going on …
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  • Final NOTE: In addition to “Drugs-Lytes-CNS”  ischemia-infarction and/or conduction defects (ie, LBBB, RBBB, IVCDmay also produce QTc lengthening. That said, these findings will usually be obvious. But when the only (or the primary) ECG abnormality is a long QT interval — Think “Drugs-Lytes-CNS” as the likely cause(s).
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NOTE: The following blogs and reference materials provide more information on topics mentioned in this case.
  • Our suggested Systematic Approach to 12-Lead ECG Interpretation — See ECG Blog #93.
  • Basic Concepts for Assessment of the 3 Intervals (PR/QRS/QT) — See ECG Blog #89.
  • More on the QT Interval/Torsades de Pointes — Section 6.0 from our ECG-2014-ePub.

David Richley raised the following question in 12-Lead ECG: I’ve Got the Rhythm on Facebook:
  • “I’m not sure that the QT is prolonged, as stated in the blog. I think that a tall U wave is partially fused with the T wave, giving the impression that there is a very wide T wave (Figure-4). The main reason I suspect this is that there appears to be a ‘double- bump’ after the QRS in the chest leads. Based on the ECG alone, I would be suspicious of hypokalaemia."
Figure-4: Dave’s Figure that was included with his Comment.
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MReply to Dave’s Comment: Of course there may be a U wave within the deflection — even a very large one! The main point of this blog post is to highlight the importance of recognizing that there is a prolonged QT interval — and that awareness of this should “trigger” recall of my Key List = Think Drugs-Lytes-CNS !
  • Even if the deflection Dave labels is a huge U wave — the QT interval is still significantly prolonged (Figure-5).
Figure-5: What might represent T wave and U wave from Figure-4 (See text).
Assuming that the suggestion of an “extra hump” is in fact a large U wave, and being conservative — I have drawn a RED curve to postulate the likely path (and end point) of the T wave in lead V2 (Figure-5).
  • Using parameters of this RED T wave — the QT interval is still significantly prolonged. I measure a QT of 0.44 second, which corrected for the heart rate of ~100/minute — suggests a QTc ~0.56, which is still markedly prolonged.
  • If electrolyte disturbance is the cause of very large U waves in this case — then with correction of low K+/Mg++ — one would expect to see progressive decrease in U wave size, with reduction of the QT (QU) interval. Along the way, much clearer distinction between what is the end of the T wave and the beginning of the U wave will probably be seen.
  • Unfortunately, I do not have additional details from this case. Thus I do not know: i) What medications this patient was taking; ii) What serum K+, Mg++, and Ca++ were at the time this tracing was done; or iii) Whether this patient had additional CNS insult accounting for some of the QT lengthening we see on this tracing …
I suspect that in this 59-year old woman with sepsis and unresponsiveness — a combination of “Drug-Lytes-CNS” Factors accounted for the long QT (QU) interval. My THANKS to David Richley for his excellent comment!