Thursday, June 30, 2016

ECG Blog #128 (VT – Fusion – WCT – Sinus Tachycardia)

How would you interpret the lead II rhythm strip shown in Figure-1?
  • How certain are you of your diagnosis?
  • Are the P waves preceding beats #6 and #7 conducting?
  • Challenge Question: How many different-shaped beats are there on this tracing?
Figure-1: Long lead II rhythm strip showing a changing rhythm. Can you explain what is happening? NOTE — Enlarge by clicking on the Figure.
Interpretation: This is a challenging case. The easiest way to approach the interpretation of more difficult arrhythmias such as this one, is to begin with that part of the tracing that is easiest to interpret. 
  • To do this — Mentally block out the first 7 beats on this tracing. If ALL you had to worry about was the last 6 beats in Figure-1 (ie, beats #8-thru-13) — How would you interpret the rhythm in Figure-2?
Figure-2: The first 7 beats from Figure-1 have been blocked out. How would you interpret the arrhythmia represented by beats #8-thru-13?
Answer to Figure-2:
Beats #8-thru-13 are regular at a rate of 110 beats/minute. The QRS complex is narrow, and each QRS is preceded by normal appearing (upright) P waves with a normal PR interval. Beats #8-thru-13 represent Sinus Tachycardia.
  • Now mentally block out the last 8 beats on this tracing. If all you had to worry about were the initial 5 beats — How would you interpret the arrhythmia in Figure-3?
Figure-3: The last 8 beats (#6-thru-13) from Figure-1 have been blocked out. How would you interpret the arrhythmia represented by beats #1-thru-5?
Answer to Figure-3:
Beats #1-thru-5 are regular at a rate of just over 100 beats/minute (the R-R interval is just under 3 large boxes in duration). The QRS complex of these beats is wide, bizarre, and not preceded by atrial activity. This suggests a ventricular etiology. Since the usual rate of an idioventricular escape rhythm is much slower (in the range of 30-40 beats/minute) — We describe the arrhythmia represented by beats #1-thru-5 in Figure-3 as an Accelerated IdioVentricular Rhythm ( = AIVR).
  • Return to Figure-1. Now focus on the more difficult part of the tracing = beats #5-thru-8. Can you figure out what is going on in Figure-4?
Figure-4: Beats #1-thru-4 and #9-thru-13 from Figure-1 have been blocked out. Can you figure out what is happening with the remaining beats #5-to-8?
HINT to Figure-4: Sequential consideration of the following 4 questions may lead you to the diagnosis:
  • What kind of beat is beat #8? (See Answer to Figure-2).
  • What kind of beat is beat #5? (See Answer to Figure-3).
  • Would you expect the P wave preceding beat #6 to be able to conduct normally? If not — Why not?
  • Think of beats #5 and #8 as “parent beats”. If these parent beats (#5 and #8) were to mate (ie, combine) and “have children” — What would you expect the children to look like?
Answer to Figure-4:
Since the rhythm in Figure-2 is sinus tachycardia, beat #8 must be a sinus-conducted beat. Similarly, since the rhythm represented by Figure-3 is AIVR — beat #5 must be a ventricular beat.
  • Note that the PR interval preceding beat #6 is shorter than the PR interval preceding other sinus-conducted beats (beats #8-thru-13 in Figure-1). It is too short to conduct normally.
  • Note also that although the QRS complex of beat #6 is entirely upright — it is not nearly as wide as the other upright (ventricular) beats (beats #1-thru-5 in Figure-1). Beat #6 is a Fusion Beat.
Fusion beats occur as a result of simultaneous occurrence of supraventricular and ventricular impulses. This concept is illustrated in Figure-5.
  • Panel A in Figure-5schematically shows the pathway of normal conduction (SA Node–to–AV Node – to bundle branches). This results in a sinus-conducted beat (S) with a normal PR interval and a narrow QRS complex.
  • In contrast, Panel B — begins in the ventricles (V). This results in a wide QRS complex without preceding atrial activity.
  • The phenomenon of Fusion is represented in Panel C — in which there is simultaneous (or near simultaneous) occurrence of a supraventricular and ventricular complex. Depolarization wavefronts meet before they are able to complete their path, and the ECG appearance of the resultant fusion beat takes on characteristics of both the supraventricular and ventricular complex (F).
Figure-5: Illustration of the concept of fusion beats. Panel A — Sinus-conducted beat (S). Panel B — Ventricular beat (V). Panel C — Fusion beats (F1 and F2).
NOTE: Depending on whether the wavefronts in Panel C of Figure-5 meet high or low in the ventricles — the fusion beat will take on more characteristics of either the supraventricular complex (F2 in Panel C) — or, of the ventricular complex (F1 in Panel C).
  • Clinically — the reason recognition of fusion beats is important, is that it proves anomalous complexes in a tracing must be of ventricular etiology!
SUMMARY: Now look at Figure-6 — in which we have labeled Figure-1 with RED arrows to indicate the series of regularly-occurring sinus P waves which are clearly seen to begin just before beat #6.
  • Close inspection just before widened beat #5 reveals a subtle-but-definite small hump at the onset of the R wave of this beat. This small hump is almost certainly one more P wave (BLUE arrow) — that occurs right on time (ie, at the appropriate P-P interval distance just before the last RED arrow). No sinus P waves are seen before this blue arrow ...
Figure-6: Long lead II rhythm strip taken from Figure-1. We have labeled the regularly-occurring sinus P waves that are clearly seen with RED arrows. The BLUE arrow indicates yet one more on-time P wave that deforms the initial part of beat #5.
From Figure-6 — It should now be apparent that the arrhythmia begins with a 5-beat run of AIVR (at ~100-105/minute). Sinus tachycardia at a slightly faster rate (~110/minute) then takes over (beats #8-thru-13). Beats #6 and #7 manifest a QRS morphology intermediate between that of the ventricular and supraventricular beats, with the former beat (#6) more closely resembling the morphology of ventricular beats (as was the case for F1 in Panel C of Figure-5) — and the latter ( = beat #7) most closely resembling the morphology of the QRS complex during sinus tachycardia (as was the case for F2 in Figure-5).
  • The appearance of beats #6 and #7 in Figure-6 is as might be anticipated considering the PR interval that precedes each of these fusion beats. That is, the very short PR interval preceding beat #6 would not be expected to allow sufficient time for deep penetration of the supraventricular impulse (P wave) into the ventricles. Thus, beat #6 much more closely resembles the beats of ventricular etiology.
  • In contrast — the PR interval preceding beat #7 is almost normal. As a result, this supraventricular impulse (P wave) should have had time to travel relatively far down the conduction system before fusion occurred (explaining why the beat more closely resembles the morphology of supraventricular beats).
  • KEY POINT — Clinically, recognition that beats #6 and #7 in this tracing are fusion beats confirms the ventricular etiology of beats #1-thru-5.
CHALLENGE Question — Return a final time to Figure-6. In addition to beats #6 and #7 — there are 3 more fusion beats in this tracing. Can you spot them?
  • PEARL — One looks for fusion beats not only by examining the QRS complex — but also by close inspection of each T wave!
ANSWER to Challenge Question:  Beats #5, #8 and #9 are all fusion beats! The KEY to recognizing fusion beats is to look for the ever-so-slight subtle differences that may be present in either the QRS complex and/or the T wave between the beat(s) in the question and the complexes of known etiology.
  • Careful inspection of beat #5 reveals that its R wave is not quite as tall and its T wave not quite as deep as the other ventricular beats. Note also that the very initial portion of the upstroke of this R wave is deformed. A P wave is hiding here — and accounts for the slight degree of fusion that this beat manifests (BLUE arrow in Figure-6).
  • Beats #8 and #9 are also fusion beats. Careful comparison of these beats with beats #10-thru-13 reveals that they have a slightly narrower QRS complex and, a T wave that is smaller and less peaked.

Monday, June 27, 2016

ECG Blog #127 (Acute STEMI – Lead Malposition – LVH – Reciprocal Changes)

This 12-lead ECG was obtained from a 61-year old man who was seen by EMS for new-onset chest discomfort. How would you interpret this ECG? Should you call to activate the cath lab en route to the hospital?
Figure-1: 12-lead ECG obtained from a 61-year old man with new-onset chest discomfort. Would you activate the cath lab for suspected acute anterior STEMI? NOTEEnlarge by clicking on the Figure.
Interpretation: There are a number of findings on this ECG that make it difficult not to immediately activate the cath lab. We note the following:
The rhythm is sinus. Intervals are normal. The axis is slightly leftward (at about -15 degrees). Voltage for LVH is satisfied by an R wave in lead aVL that clearly exceeds 12mm in amplitude.
  • There is a Q wave in lead V1, a QS in V2 — and no more than the tiniest of r waves in lead V3. Thus, R wave amplitude is clearly reduced in the anterior leads — and Q waves in V1,V2 could be consistent with septal infarction.
  • The T wave in leads V2-thru-V5 looks like it may be hyperacute. T wave amplitude in lead V2 seems disproportionately tall compared to the QRS complex in this lead. In addition, the amount of J-point elevation in leads V4 and V5 seems more-than-is-normally-expected in these leads, especially given relatively small R waves in V4,V5.
  • There is ST elevation in lead aVL that looks to be the mirror-image of lead III.
  • There appears to be reciprocal change in the inferior leads (more subtle in lead II, since there is only some ST-T flattening in this lead …).
Considering the above findings together — one needs to be concerned about the possibility of acute LAD occlusion in this 61-year old man with new-onset symptoms. That said, there are a number of features against this being an acute anterior STEMI. These include:
  • Probable Lead Malposition — It is surprising how frequently leads V1 and V2 are placed too high on the chest. Doing so may give false impression of anterior infarction. Clues that precordial leads have probably been placed one (or even two) interspaces too high include: i) a significant negative component to the P wave in lead V1 and/or V2; and ii) the finding of an r’ deflection in either V1 and/or V2. Both of these findings are present in Figure-1. Perhaps lead V3 is then also malpositioned? So maybe there is not loss of r wave (and development of Q waves) after all in the anterior leads?
  • The mean QRS Axis is Leftward. This might account for normal T wave inversion in predominantly negative limb leads III and aVF.
  • Early Repolarization in Leads I, aVL? — Shape of the J-point ST elevation in these lateral leads is concave-up (ie, “smiley”-configuration) with small, narrow septal q waves and J-point notching. This has the appearance of early repolarization.
  • There is LVH. As mentioned, voltage criteria for LVH are clearly met in lead aVL (that easily surpasses an R wave amplitude of ≥12mm). What about R wave amplitude in lead V6? Close vertical placement of lateral chest leads with resultant overlap makes it very difficult to discern just how tall the R wave in lead V6 is, but I suspect it surpasses 18mm once one mentally “subtracts” the overlap. LVH is notorious for producing a reciprocal “strain” pattern in anterior leads — and this could account for at least some of the suspicious T wave appearance in leads V2,V3.
BOTTOM LINE — If the history in this case was worrisome, then this patient most likely needs timely cardiac catheterization. One has to be able to rule out acute stemi with more certainty than I have from looking at this single tracing. But my thought on seeing this ECG was that I would not be surprised if cath turned out to be unremarkable.
  • That said, there DOES seem to be more ST elevation-than-I-would-expect given QRS appearance in leads V4,V5 — so I would also not be surprised if cath showed acute LAD occlusion.
  • It is FINE not to be certain from review of a single tracing as to whether or not acute infarction is occurring. Depending on clinical circumstances — one might either decide to repeat the ECG and obtain stat Echo (looking for wall motion abnormality) in the Emergency Department — or, simply proceed to cath for definitive diagnosis.
  • Follow-Up — This patient did not have acute infarction ...
Acknowledgment: — My thanks to Dustin Carter and James Criscitiello (from New York, New York) for their permission to use this case and ECG.

Tuesday, May 24, 2016

ECG Blog #126 (Computerized ECG Interpretations - DeWinter - HyperK)

NOTE: This Blog post is a reproduction of Section 13.0 from my ECG-2014-ePub (
13.0 – Computerized ECG Interpretations:
A frequent question that arises is, “How best to use (or not use) the computerized ECG interpretation?” Opinions vary. We feel the answer depends on the goals and experience level of the interpreter.
  • Computerized ECG analysis systems are not infallible. Although they clearly have merit in certain regards — they are far from perfect at ECG interpretation. Our task is to appreciate the positives of computer systems while being aware of their drawbacks.
13.1 – Computerized Systems: Pros & Cons
At the current time — virtually all modern ECG machines automatically provide a computerized interpretation. This has benefits and drawbacks. Consider the following:
  • Computerized systems excel at computing values. This is because that’s what computers do. As a result — computerized systems are extremely accurate in calculating: i) Rate; ii) Intervals (PR/QRS/QT intervals); and iii) Axis.
  • Computerized systems are usually reliable in recognizing sinus rhythm mechanisms and normal tracings.
  • For the Expert Interpreter — the best feature of computerized systems is that they save time! There is no longer need to calculate rate, intervals or axis — since the computer instantly provides legible and accurate print-out of these values. IF the computer says, “Normal ECG” — it may literally take no more than 2-3 seconds for an experienced interpreter to peruse the tracing and sign the report (provided there is agreement with the computer interpretation).
  • For the Non-Expert Interpreter — the major benefit of computerized systems is the backup opinion the system provides. The computer may suggest findings not initially thought of by a less experienced interpreter. This encourages more careful, targeted review of the tracing. It may also be educational by the suggestions it makes. Finally — confidence is boosted when computer analysis agrees with the clinician’s interpretation.
NOTE: The computer backup opinion may also help the expert-in-a-hurry by reducing the chance that any ECG findings will be overlooked.
  • Interpretation of any one ECG by an expert provided with: i) a moment of time to sit down and give full attention to interpretation; and ii) the clinical history — will always be superior to interpretation by a machine. That said — this is not reality.
  • Reality in the “real world” — is that the clinician assigned to interpret all tracings on a given hospital or ambulatory service usually has limited time to interpret a large number of ECGs and is often asked to do so without the benefit of clinical history. As a result — it becomes easy for even an expert interpreter to overlook certain findings on occasional tracings. Knowing how to use the computerized interpretation as a “backup opinion” can be invaluable even for the most experienced of interpreters! (Grauer, Nelson, Marriott et al: J Am Bd Fam Prac 1:17-24, 1989).
CAVEATS (What the Computer May Miss): Computerized systems do not do nearly as well in evaluation of abnormal tracings as they do in assessing ECGs with minimal abnormalities. The more complex the abnormal ECG is — the more difficult it becomes for a computerized system to render an entirely accurate interpretation.
  • Computerized systems are far less accurate interpreting rhythms that do not have a sinus mechanism.
  • They may miss subtle infarctions.
  • They tend to overinterpret the J-point ST elevation that is commonly seen with early repolarization patterns. As a result — computerized systems may be prone to mislabel these normal variants as “acute MI”.
  • Computerized systems may miss pacemaker spikes/WPW/tall R in V1. They are unlikely to appreciate certain clinical entities such as Wellens’ syndrome or DeWinter T waves.
  • Many hospitals do not utilize special computer programs for interpretation of ECGs obtained on pediatric patients. Obvious problems with interpretation will arise IF a pediatric ECG is interpreted by a computer program using adult criteria.
  • Finally computerized systems by definition lack the “human Gestalt” by an expert of the overall tracing.
13.2 – Suggested Approach: How to Use the Computer
The most important point to emphasize in this Section — is that clinical use of the computerized report by non-expert interpreters should be very different than use of this same report by the expert who regularly interprets a large volume of tracings. Expertise of the interpreter therefore dictates the approach we recommend (Grauer: Practical Guide to ECG Interpretation; Mosby, St. Louis; pp 375-379, 1998).
  • For the Non-Expert Interpreter — Do not initially read the computer report. Instead — WRITE OUT (or at least think out) your interpretation first. Check findings you note with each computer statement. Then delete, modify and/or add to the computer interpretation as needed.
  • For the Expert Interpreter — Review the computer report either before or after evaluation of the ECG itself. Minimize time devoted to determination of heart rate, intervals and axis (since the computer is very accurate for these parameters). Consider more careful evaluation IF the rhythm is not sinus — or IF the ECG is interpreted by the computer as abnormal. Overread each computer statement. Place a check mark next to those that are accurate. Delete, modify or add to incorrect statements.
KEY Point: The expert interpreter is not using the computerized report to “learn”. This is because by definition — the interpretation of an expert electrocardiographer is the “gold standard”. Since computerized systems are programmed by experts — the best they can realistically hope for is to put out interpretations that equal the level of accuracy of the expert that programmed them.
  • The Expert uses the computer: i) to save time; and ii) to prevent overlooking findings when forced to read many ECGs in a limited period of time.
  • Less Experienced Interpreters do look to the computer to assist in accuracy. They are usually called on to read no more than one ECG at any one time. Therefore — the most important step for the non-expert is to first COVER UP the computerized report. It is otherwise all too easy to be biased by what the computer says. Used in this way — comparing one’s own interpretation with what the computer says optimally incorporates potential benefit from any discrepancy in interpretation that may exist.
13.3 – FIGURE 13.3-1: Do You Agree with the Computer?
Perhaps the best way to illustrate potential pros and cons of computerized interpretations — is by clinical example. Consider the ECG shown in Figure 13.3‑1 — obtained from a 78 year old woman with atypical chest pain.
  • The computerized interpretation was: Sinus rhythm; left axis (-10 degrees) — but otherwise “normal” ECG.
  • Do you agree with the computerized interpretation?
  • HINT: Be sure to interpret this ECG in its entirety by the systematic approach first — before you compare what the computer said with your interpretation.
Figure 13.3-1: ECG obtained from a 78 year old woman with atypical chest pain. The computerized report interpreted this tracing as, “left axis but otherwise normal”. Do you agree with the computerized report? NOTE — Enlarge by clicking on the Figure.
Answer to Figure 13.3-1: The rhythm is sinus. All intervals are normal. The axis is leftward (predominantly negative QRS in lead aVF) but not negative enough to qualify as LAHB (since the QRS in lead II is still upright). No chamber enlargement.
  • Regarding Q-R-S-T Changes — There are QS complexes in leads V1,V2. An r wave develops by lead V3 — and transition occurs normally between lead V3-to-V4. Although there is no more than minimal (at most) ST elevation — T waves are dramatically peaked in anterior precordial leads (especially in lead V2). There is shallow T inversion in lead III, and perhaps some nonspecific ST‑T wave flattening in lead aVF.
IMPRESSION: This example highlights the importance of overreading the computerized interpretation after you have independently arrived at your own conclusion. This is not a “normal” ECG. That statement should be crossed out on the computerized report. This is because the computerized interpretation is a medical record — and statements you disagree with should therefore be crossed out.
  • Clinical correlation is needed to determine the meaning of the abnormal findings you identified. Of Concern — is the fact that i) this woman is of a “certain age” (78 years old — so clearly old enough to have coronary disease); — and ii) she is having “chest pain” (even though it is described as “atypical” in nature).
  • While not definitive — the QS complexes in leads V1,V2 could reflect septal infarction of uncertain age. This should at least be noted in your interpretation (it was ignored by the computerized report).
  • There is marked T wave peaking — especially in leads V2,V3. This is not normal (despite also being ignored by the computerized report). Possible explanations for this abnormal T wave peaking include: i) Hyperkalemia (less likely because T wave peaking is not generalized and the base of these T waves is not narrow — but a serum K+ level should nevertheless be checked to rule this out); ii) Ischemia (which when posterior in location sometimes manifests as anterior T wave peaking); and iii) DeWinter T waves. Given the history of chest discomfort — we are most concerned with this 3rd possibility. While the J‑point ST depression that is usually seen with DeWinter T waves is missing in Figure 13.3‑1 — the ECG picture in this tracing is otherwise perfectly compatible with this harbinger sign of possible impending proximal LAD occlusion.
BOTTOM Line: It might be easy to overlook the QS complexes in leads V1,V2 of this tracing IF you allowed the computerized report to bias you prior to rendering your own independent interpretation. Hopefully — you did not overlook the obviously abnormal T wave peaking in anterior leads that somehow escaped detection by the computer. Recognition of DeWinter T waves is indication for immediate cath/acute reperfusion — so this possibility mandates immediate attention. This would have been missed had the computer report been accepted without overread. Computerized interpretations can be extremely helpful to both expert and non-expert interpreters — but knowing HOW to use the computer report always assumes first priority.
  • NOTE: For more on DeWinter T waves — Please see our ECG Blog #53
  • We refer to Computerized ECG Interpretations in our ECG Blog #12 — 
EDITORIAL COMMENT by the AUTHOR:  Prior to researching this topic (references of my work below) — I thought computerized interpretations were a waste of time. However, once I learned to appreciate their benefits and drawbacks — I learned to love computerized interpretations. They literally tripled my speed of interpretation — especially when sinus rhythm and minimal abnormalities are present. On the other hand — I ignore what the computer says when the rhythm is anything other than sinus. I’m fully aware of the need to carefully overread early repolarization patterns and tracings on patients with chest pain. Finally — I’ve observed that when less experienced interpreters truly make an honest attempt to interpret the ECG first before they look at what the computer says — that accuracy is increased.
—  —
Our Publications on Computerized ECG Interpretation include the following:
  • Grauer K: Chapter 21  Does the Computer Know Better? – from Grauer K: Practical Guide to ECG Interpretation (2nd Edition) – Mosby, St. Louis, 1998, pp 374-379.
  • Grauer K, Kravitz L, Ariet M, Curry RW, Nelson WP, Marriott HJL: Potential Benefits of a Computer ECG Interpretation System for Primary Care Physicians in a Community Hospital. J Am Bd Fam Prac 1:17-24, 1989.
  • Grauer K, Kravitz L, Curry RW, Ariet M: Computerized Electrocardiogram Interpretations: Are They Useful for the Family Physician? J Fam Prac 24:39-43, 1987.
  • Grauer K, Curry RW: Chapter 11: Use of Computerized ECG Interpretation Programs. — from Clinical Electrocardiography (Grauer & Curry Blackwell Scientific Publications, Boston, 1992, pp 418-425.