Saturday, September 9, 2017

ECG Interpretation Review #142 (Ischemia - MI - Posterior - Dating Infarction - Chest Pain).

The ECG in Figure-1 was obtained from a 48-year old man who presented to the ED (Emergency Department) with a 3-day history of chest discomfort. It shows evidence of a MI (Myocardial Infarction).
  • How would you “date” this MI?
  • Which areas of the heart are involved?
Figure-1: 12-lead ECG obtained from a 48-year old man with 3 days of chest discomfort. NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
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Interpretation: The rhythm is fairly regular at 85-90/minute. Upright sinus P waves are seen in lead II. The PR, QRS, and QT intervals are normal. The axis is leftward, but not by enough to qualify as LAHB (ie, the net QRS deflection in lead II is not predominantly negative). There is no chamber enlargement.
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  • Terminology Definitions: Before assessing for Q-R-S-T Changes in Figure-1 — it may be helpful to review terminology (See ECG Blog #94). We favor use of the lower case designation “q” wave when the initial negative deflection of a QRS complex is relatively smaller (ie, <3mm in depth). If the initial negative deflection of the QRS complex is larger (ie, ≥3mm in depth) — we favor the upper case designation “Q” wave. When the QRS deflection is entirely negative — the designation “QS” complex is used, since without any upright deflection in the QRS, one can’t tell if the all-negative deflection occurs “before” or “after” the R wave.
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Returning to Figure-1: Regarding Q-R-S-T Changes ...
  • Q waves are present in multiple leads. Small, narrow (probably septal) q waves are seen in leads I and aVL. The Q wave in lead II is narrow but deep (ie, it is virtually as deep as the height of the R wave in this lead). Of note, there may be a tiny initial positive deflection (r wave) in at least some of the beats in lead III. However, in lead aVF — the QRS complex is clearly all negative, which defines this as a QS complex. There is also a distinct notching (called fragmentation) on the upslope of this QS complex in lead aVF. Finally, there are Q waves in leads V4, V5, and V6. Although narrow, the Q waves in leads V5, V6 are somewhat deeper-than-expected to be simple “septal” q waves.
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  • Clinical Note on Q Wave Significance: In general, the larger and wider a Q wave is — the more likely this Q wave is to be “significant” (ie, indicative of infarction at some point in the patient’s history). That said, numerous exceptions exist — such that reliable generalizations about the clinical significance of Q wave appearance are difficult to make. It is common to see small narrow q waves in one or more of the lateral leads. These “normal septal q waves” reflect the normal direction of septal activation, which moves from left-to-right. That said, distinction between normal septal q waves and Q waves indicative of previous lateral infarction may be challenging when q wave width and/or depth appears to be more-than-expected, as is seen here for the 3mm deep Q waves in leads V5 and V6. On the other hand, we can definitely say that QRS appearance in the 3 inferior leads (leads II, III, aVF) in Figure-1 IS strongly suggestive of prior infarction. In the context of a surprisingly deep Q wave in lead II and, an all-negative QS complex with notching (fragmentation) in lead aVF — even if a tiny initial positive deflection is present in some of the beats in lead III, the most likely explanation for this combination of findings has to be prior inferior infarction.
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Returning to Figure-1:
  • R Wave Progression — is not normal in the chest leads. Normally, there should be a predominant negative deflection (S wave) in lead V1 — with the area of “transition” (where R wave amplitude supersedes S wave depth) not occurring until after V2,V3. Instead, R wave amplitude in lead V1 = S wave depth in this lead, and relatively prominent R waves are already seen by lead V2. Although there are a number of entities that may produce a Tall R Wave in Lead V1 (See ECG Blog #81) — recent posterior infarction should be at the top of this list, considering the ECG evidence of previous inferior infarction we have just discussed, and the ST-T wave changes we are about to assess.
  • ST-T Waves — There is ST segment coving, with fairly deep T wave inversion in each of the inferior leads. In addition, there is 1-2mm of ST depression in leads V3-thru-V6, with a definite ST segment “shelf” in these leads. This strongly suggests ischemia. A final, admittedly subtle finding — is ST segment straightening with angulation of the junction between the straight ST segment and the beginning of the T waves in leads I and aVL. This makes these T waves (especially in lead aVL) appear more prominent than one might normally expect, given R wave amplitude in this lead.
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  • Dating an Infarct: A picture “tells 1,000 words”. Rather than QRST appearance in one or two leads — it is the composite picture of the entire 12-lead tracing, in context with the clinical history that “tells a story”. That said, it is good to appreciate that our ability to “date” an infarct from assessment of a single 12-lead ECG is far from perfect. Practically speaking, we are limited to classifying ECG signs of MI as being: i) Acute ( = onset within the past few hours); ii) Old (occurrence more than several days ago); or iii) of Uncertain Age (ie, likely onset being intermediate between “acute” and “old” ) — which includes MIs that may be fairly recent, or of completely uncertain duration.
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Impression: The overall ECG picture that we see in Figure-1 is strongly suggestive of infero-postero (and possible lateral) infarction of uncertain age. In view of the history (ie, that chest pain began 3 days earlier) — there is an excellent chance that onset of the event corresponds to the onset of symptoms that began several days earlier.
  • Against calling this infarction “acute” (ie, onset within the past few hours) — is the lack of ST elevation in Figure-1, and the presence already of large inferior Q waves. Yet persistence of ST coving with deep T wave inversion in these inferior leads — in conjunction with ST segment flattening and depression in many of the remaining leads strongly suggests that the event may indeed be recent. Careful questioning of this patient regarding the precise onset and nature of his symptoms over the past week is likely to be revealing.
  • PEARL: With acute and/or relatively recent inferior infarction — there is almost always a reciprocal relationship in ST-T wave appearance between leads III and aVL. This is because electrical activity assessed by these 2 leads is almost completely opposite (lead aVL at -30 degrees; lead III lying 150 degrees away at +120 degrees in the frontal plane). Awareness of this relationship often provides an invaluable clue as to whether subtle ST elevation in inferior leads is likely to indicate an acute or recent event. Early repolarization should not produce reciprocal ST depression in lead aVL. Although subtle — there is a reciprocal ( = “mirror” image) relationship in this tracing between the ST coving with deep T wave inversion that is seen in lead III — and the subtle ST segment straightening with somewhat prominent T wave appearance in lead aVL.
  • ST-T wave changes of “reperfusion” typically manifest the appearance seen here — that is, with no more than minimal residual ST segment elevation, and with deep T wave inversion in lead groups that overlie the area of infarction. Since anterior leads (ie, leads V1, V2, V3) provide a mirror-image perspective of posterior events — the prominent T waves we see in leads V2, V3 are most likely to represent recent posterior reperfusion. This is consistent with the presence of a disproportionately tall R wave in lead V1, with prominent R wave forces already evident by V2, V3. These findings all support the presence of recent posterior as well as inferior infarction.
  • As suggested earlier, deeper-than-expected Q waves in leads V5, V6 may indicate lateral infarction of uncertain age. It is difficult to know if the lateral chest lead ST depression reflects reciprocal change or ongoing ischemia.
  • The “Culprit” Artery: Statistically, we would suspect the RCA (Right Coronary Artery) to be the “culprit” artery of infarction in this case — since the large majority of patients have a right dominant circulation (See ECG Blog #141). That said, given the lack of ST segment elevation at this time, the criterion that compares the relative amount of ST elevation in lead III vs lead II cannot be used. Given the possibility of lateral infarction, and absence of ECG evidence suggesting right ventricular infarction — one cannot rule out the possibility of recent LCx (Left Circumflex) occlusion without cardiac catheterization.
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Case Follow-Up: Cardiac catheterization revealed severe multi-vessel disease, including diffuse involvement of the LAD (Left Anterior Descending) artery, diffuse LCx disease with prior occlusion of obtuse marginal branches that now show collateral filling — and, 100% occlusion with fresh thrombus in the RCA. Thus, the RCA was the “culprit” artery in this patient with preexisting extensive and severe coronary disease.
  • BOTTOM LINE: The process of determining the onset of acute infarction is not always straightforward. The answer may not be forthcoming from assessment of a single ECG. Instead, careful integration of the clinical history, interpreted in light of the timing of troponin rise and ECG evolution on serial tracings is often needed. The process may be further complicated when a new event is superimposed on severe preexisting coronary disease. This case illustrates how helpful the history can be — even in a patient with preexisting disease, for deducing the likely onset of the most recent event.
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Acknowledgment: My thanks to MG for allowing me to use this tracing and clinical case.
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NOTE: The following ECG Blogs review material relevant to this case:
  • ECG Blog #94 (regarding Q wave terminology; assessment of QRST Changes).
  • ECG Blog #81 (regarding differential diagnosis of a Tall R in Lead V1).
  • ECG Blog #80 (regarding distinction between LCx vs RCA culprit; Coronary Circulation; the "Mirror Test" ).
  • ECG Blog #141 (regarding assessment of the "culprit" artery).


Saturday, September 2, 2017

ECG Interpretation Review #141 (Ischemia - STEMI - Coronary Anatomy - Lat - Post - Inf - MI)

The ECG in Figure-1 was obtained from a man in his 50s, who presented with new severe chest pain.
  • How would you interpret this­­ tracing?
  • What area(s) of the heart are involved?
  • What is the likely “culprit” artery?

Figure-1: 12-lead ECG obtained from a man in his 50s with chest pain. What is the likely “culprit” artery? NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
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Interpretation: The underlying rhythm is sinus at a rate of 75-80/minute. Intervals and axis are normal. There is no chamber enlargement. Regarding Q-R-S-T Changes:
  • Narrow but fairly deep Q waves are seen in leads III and aVF. There is also a small and narrow q wave in lead II, and a tiny q wave in lead V6.
  • Overall R wave progression across the chest leads is appropriate — although R wave amplitude in lead V2 is a bit taller-than-expected. Small s waves persist through to leads V5, V6.
  • There is dramatic ST elevation in each of the inferior leads (leads II,III,aVF) with a “check-mark” appearance that strongly suggests acute injury. As a subtle finding, there appears to be slight ST segment elevation in lead V1. The ST segment in this lead is coved and clearly more prominent than is usually the case.
  • There is marked reciprocal ST depression in leads I and aVL. Note how the shape of this ST depression in lead aVL is a precise “mirror-image” picture of the ST elevation in lead III.
  • There is at least 4mm of “shelf-like” ST depression in lead V2 — which surprisingly largely resolves by lead V3. There is a hint of J-point depression in leads V3-thru-V6.
Impression: In a patient with new-onset chest pain — the ECG appearance in Figure-1 is virtually diagnostic of a large acute infero-postero STEMI (ST Elevation Myocardial Infarction). In addition, there is almost certainly acute RV (Right Ventricular) involvement. This strongly suggests acute RCA (Right Coronary Artery) occlusion. In support of this conclusion — we make the following points:
  • Statistically, approximately 80-90% of patients have a “right-dominant” circulation (Figure-2). This means that after supplying the RV (right ventricle) — the RCA continues as the PDA (Posterior Descending Artery) along the undersurface of the heart to supply the posterior and inferior walls of the LV (left ventricle). In contrast, about 15% of patients have a left-dominant circulation, in which the RCA is less prominent. To compensate, the LCx (Left Circumflex) artery is a relatively larger vessel, and it (rather than the RCA) provides most (or all) of the blood supply to the PDA. As a result not only the lateral, but also the inferior and posterior walls of the LV are predominantly supplied by LCx artery in patients with a left-dominant circulation. Bottom Line — Statistically then, even before looking at the ECG, we can predict that the “culprit artery” for the vast majority of patients with acute inferior STEMI is likely to be the RCA (See also ECG Blog #80).
Figure-2: Overview of normal coronary anatomy. Panel A — the most common situation (80-90%), in which the RCA is a dominant vessel that supplies the RV as well as the posterior and inferior walls of the LV. The RCA also provides blood supply to the RV. The LAD (Left Anterior Descending) artery normally supplies the anterior wall of the heart (via diagonal branches); part of the cardiac apex; and a major portion of the conduction system (via septal perforators that run vertically down through the septum). The LCx (Left Circumflex) artery supplies the lateral wall of the LV. Panel B — represents a left-dominant circulation, in which the LCx (rather than the RCA) supplies the posterior and inferior walls of the left ventricle.
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ECG features in Figure-1 that further support the likelihood of the RCA as the “culprit artery” are: i) ST elevation in lead III > II; ii) Marked reciprocal ST depression in lead aVL; iii) Relatively less (or no) lateral ST elevation, with the amount of ST elevation in lead III > V6; and iv) Evidence of acute RV involvement.
  • PEARL: The LCx does not supply the right ventricle. Therefore, if there is ECG evidence suggesting acute RV involvement in association with inferior STEMI — this is virtually diagnostic of the RCA being the culprit artery. While ST elevation in right-sided leads (especially in lead V4R) is clearly the best indicator of acute RV MI — lead V1 is a right-sided lead, and on occasion it may provide insight as to whether or not there is likely to be significant associated RV infarction. Normally the ST segment in lead V1 is flat or slightly depressed. With acute inferior STEMI — ST segments in leads V1, V2 and V3 often show ST depression due to accompanying posterior infarction and/or reciprocal changes due to the inferior STEMI. Typically, such ST depression is maximal in lead V2 — but it should also be present in V1. If ever there is ST segment coving (especially if accompanied by some ST elevation) in lead V1 — there is almost certainly acute RV involvement.
  • In this case, the marked ST depression in lead V2 (Figure-1) indicates acute posterior involvement. This is supported by the taller-than-expected R wave in lead V2 (positive “mirror test”See Figure 2 in ECG Blog #80). However, rather than ST depression in lead V1 — there is prominent ST segment coving with suggestion of slight elevation. In the setting of acute inferior STEMI — this is almost certainly the net result of right-sided ST elevation from acute RV infarction attenuating (opposing) the ST depression that should also be seen in lead V1 from acute posterior infarction. And, since the LCx does not provide blood supply to the RV — this finding of ST coving with slight elevation in lead V1, but with marked ST depression by V2 incriminates the RCA as the culprit vessel. It most often indicates proximal RCA occlusion.
  • Note that the extent of acute infarction is obviously large in this case — since the amount of ST elevation is profound; ST elevation is accompanied by marked reciprocal ST depression; inferior Q waves have already formed; and inferior, posterior and right ventricular walls are involved.
BOTTOM LINE: Due to the possibility of anatomic variants and/or collateral circulation — definitive identification of the “culprit” artery is only possible with cardiac catheterization. That said, recognition of probable proximal RCA occlusion in this case with associated acute RV involvement is clinically important — because hemodynamics may differ compared to predominant LV infarction (ie, nitroglycerin is not advised because it may excessively lower BP; hypotension in the setting of acute RV involvement responds well to volume infusion).
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Acknowledgment: My thanks to MG for allowing me to use this tracing and clinical case.
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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.
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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).
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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.

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Additional Reading: 
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