Monday, September 10, 2012

ECG Interpretation Review #51 (Chamber Enlargement - LVH - Cardiomyopathy)


The ECG shown in Figure 1 was obtained from a 50-year-old man who presented to the office with dyspnea on exertion. No chest discomfort. He is a chronic smoker with a longterm history of alcohol consumption. The patient says he, “doesn’t see doctors”. He takes no medications. There is no obvious heart failure or wheezing on exam.
  • Should the patient be admitted to the hospital because of his ECG?
  • What clinical diagnosis do you strongly suspect?
Figure 1: ECG obtained from a 50yo smoker/drinker with dyspnea on exertion. What diagnosis is suggested by this ECG? NOTE - Enlarge by clicking on Figures - Right-Click to open in a separate window.
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INTERPRETATION:  The ECG shows sinus rhythm at a rate of about 85/minute. The PR and QRS intervals are normal; the QT is no more than borderline prolonged. The axis is normal (approximately +50 degrees). Beyond this point – a variety of interpretations are possible. We make the following points:

Point #1: There appears to be evidence of at least 3 chamber enlargement:
  • RAA (Right Atrial Abnormality) – is diagnosed by the tall, peaked and pointed P wave in the inferior leads (that is >2.5 mm tall in lead II).
  • LAA (Left Atrial Abnormality) – is suggested by the deep, negative component to the P wave in lead V1.
  • Voltage for LVH (Left Ventricular Hypertrophy) – is diagnosed by the finding of deepest S wave in V1 or V2 + tallest R wave in V5 or V6 ≥35mm.
  • True LV (left ventricular) chamber enlargement is strongly suggested (with ≥90% specificity) by the finding of voltage for LVH in an adult over 35 years of age when underlying heart disease is likely – IF there are ST-T wave changes consistent with “strain” (Figure 2). The difficult-to-describe ST-T wave abnormalities seen in leads V5,V6 of Figure 1 are clearly not normal findings in these lateral precordial leads. While they do not quite manifest a typical “Strain” pattern – they do qualify as a “strain equivalent” pattern that overwhelmingly favors a diagnosis of LVH in this patient.
Figure 2: Schematic depiction of LV "strain" and "strain equivalent" patterns. When either is present in addition to voltage for LVH - the specificity of the diagnosis is greatly increased.
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Point #2: The QRS complex and ST segments in Figure 1 are not normal:
  • There is ST segment coving ("frowny" configuration) with some amount of ST elevation in leads V1,V2 (difficult to be sure where the J point begins in these 2 leads).
  • The ST-T waves in leads V4,V5 are clearly abnormal (with appearance of at least some T wave inversion). There is abnormal ST-T flattening in other leads.
  • In addition – the QRS complex looks abnormal in Figure 1 (with notching and slurring in several leads). That said – the QRS is really not widened, so no definite conduction defect is present.
  • In the absence of a prior ECG – We can not rule out something acute going on (given the ST coving and elevation in leads V1,V2,V3). That said – Our "sense" is that the changes seen in Figure 1 are more likely to be longstanding and not acute.  Supporting this supposition is the lack of reciprocal changes.
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Point 3: The clinical diagnosis that we strongly suspect when we encounter an ECG such as seen in Figure 1 is of a cardiomyopathy (based on the history and ECG findings of abnormal though not necessarily prolonged QRS complex; multi-chamber enlargement; and clearly abnormal ST-T wave morphology).
  • We would not necessarily admit this patient to the hospital on the sole basis of this ECG.  We would obviously feel better IF we could find an old ECG showing similar changes.  We'd use clinical judgement in the context of the clinical setting to guide our decision. 
  • This patient would most likely be admitted to the hospital IF he presented in the middle of the night to an ED (Emergency Department).  IF he however presented to the office without any objective evidence of heart failure and without any chest discomfort – and his dyspnea was not new, not severe, and associated with a good office oxygen saturation – we would probably feel comfortable managing his presumed cardiomyopathy on an ambulatory basis.  One just has to be there to decide . . .
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  • See ECG Blog #73  – for more on ECG diagnosis of LVH -
  • See ECG Blog #75  – for more on Atrial Enlargement - 
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Wednesday, August 8, 2012

ECG Interpretation Review #50 (Syncope - STEMI - MI - Brugada - RBBB - Early Repolarization)

The ECG shown was obtained from a 62-year-old man who presented to the ED (Emergency Department) with a history of several presyncopal episodes in recent months. His ECG was diagnosed as showing acute anterior STEMI (ST Elevation Myocardial Infarction). 
  • Do you agree? 
  • What treatment is indicated?

Figure: ECG obtained from a 62 year-old man with a history of presyncopal episodes. 



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INTERPRETATION: The ECG shows sinus bradycardia at a rate just under 60/minute. All intervals and the axis are normal. There is no chamber enlargement. There may be slight J-point ST elevation in lead I, and some nonspecific ST depression in inferior and lateral precordial leads. That said – the area of most concern clearly relates to findings in leads V1 and V2.
  • There appears to be an rSr’ complex in V1,V2.
  • There is an elevated J-point in each of these leads – with an unusual type of downsloping ST segment that is especially marked in lead V2. The ST segment terminates in shallow T wave inversion.
  • The ECG findings in the Figure are highly suggestive of Brugada Syndrome. First described in 1992 — the Brugada syndrome is important to recognize because of an associated very high risk of sudden death. The prevalence of this disorder is approximately 1/2000 in the general population. Brugada syndrome is a leading cause of sudden death in adults under 40.
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BOTTOM LINE: Although serial tracings and troponins are advised — the ECG in the Figure is not suggestive of acute STEMI. It is also not representative of RBBB (Right Bundle Branch Block). Instead, especially in view of the history of several recent presyncopal episodes (!) — the tracing suggests Brugada Syndrome. 
  • Cardiology consult should be obtained.
  • ICD (Implantable Cardioverter-Defibrillator) placement should be considered, pending results of careful evaluation.

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ACKNOWLEDGMENT: My appreciation goes to Dr. Harsha Nagarajarao (of Cardiology Boards) for allowing me to use this tracing.
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For more on Brugada Syndrome – See ECG Blog #238 —

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Wednesday, August 1, 2012

ECG Interpretation Review #49 (Chest Pain - STEMI - Culprit Artery - LAD - RBBB - LAHB - AFib - Nodal)

The 12-lead ECG and lead II rhythm strip shown in Figure 1 were obtained from 55-year-old man with “chest pressure”. He is hemodynamically stable.
  • What is the rhythm?
  • Can you identify the “culprit artery” ?
Figure 1 – 12-lead ECG from a 55-year-old man with chest pressure. 

INTERPRETATION: The first problematic aspect of the tracing in Figure 1 is to determine the rhythm. Given that the patient is hemodynamically stable – there is at least a moment to contemplate what is seen.
  • The QRS complex looks slightly widened. Assessing QRS duration in leads where the complex appears to be widest (ie, leads V4,V5,V6) – we estimate QRS duration at 0.11 second (just over half a large box). That said – QRS morphology looks to be supraventricular (as we’ll discuss momentarily).
  • The rhythm is not sinus. There is no upright P wave in lead II. In fact – there are no P waves anywhere … There are fine undulations of the baseline – although we can’t be sure if this represents baseline artifact, fine “fib waves”, or both.
  • The rate is ~100/minute.
  • The rhythm is not completely regular. This tracing provides an excellent example of how easy it is to be fooled into thinking a rhythm is regular when one does not measure (with calipers) consecutive complexes. Admittedly – variation in R-R interval from beat-to-beat is minimal – and there are a number of consecutive beats with the same R-R interval. But there is some variation.
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BOTTOM LINE: What is the Rhythm?
We are not certain what the rhythm in Figure 1 is based on this single tracing. Additional rhythm strips would be needed to know for sure. The differential diagnosis includes:
  • Fascicular Tachycardia or VT (Ventricular Tachycardia).
  • Accelerated AV Nodal (Junctional) Rhythm.
  • AFib (Atrial Fibrillation).
We favor AFib with a controlled but regularized ventricular response as the most likely etiology of this rhythm – given supraventricular appearance, irregularity, and absence of P waves.
  • We doubt the rhythm is VT or fascicular tachycardia – given its supraventricular appearance (See below).
  • We can’t rule out the possibility of an accelerated junctional rhythm – given the “almost regularity” of the rhythm.
  • We fully acknowledge that we are not certain of the rhythm.
  • Given that this patient is at the moment hemodynamically stable – there are much more pressing problems than determination of the rhythm!
  • Additional rhythm strips will almost certainly clarify rhythm diagnosis.

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What is Going On with the Rest of the Tracing? 
QRS morphology in Figure 1 suggests RBBB (Right Bundle Branch Block).
  • The QRS complex is widened. Although a typical rSR’ pattern is not seen in lead V1 - the QR pattern that is seen serves as a “right bundle equivalent” in a patient who has lost the small initial positive r wave deflection due to septal infarction.
  • S waves are seen in left-sided leads I and V6 (although admittedly the S in lead I is not nearly as wide as is usually the case with RBBB).

In addition – there is LAHB (Left Anterior HemiBlock), as determined by the rS complexes in the inferior leads producing a markedly leftward axis. The presence of RBBB/LAHB qualifies as “bifascicular block”.
     Of most concern – the ECG in Figure 1 suggests ongoing evolution of a large acute STEMI (ST Elevation Myocardial Infarction):
  • Q waves are seen in septal leads V1 and V2.
  • There is significant ST segment elevation in leads V1-thru-V4. There is also ST segment coving and elevation in lead aVL. ST elevation in lead V3 shows straightening of the ST upstroke and elevation of the J point by at least 4mm.
  • There is also ST segment elevation in lead aVR.
  • Reciprocal ST segment depression is clearly seen in each of the inferior leads (II,III,aVF).
  • There appear to be hyperacute T waves in the inferior and lateral precordial leads.

IMPRESSION: The ECG shown in Figure 1 suggests acute proximal occlusion of the LAD (Left Anterior Descending) coronary artery causing an extensive anterior STEMI. Acute reperfusion is urgently needed for this patient.
  • ST elevation in leads V1-thru-V4 suggests antero-septal involvement.
  • ST elevation also in lead aVL suggests involvement of the 1st Diagonal Branch of the LAD.
  • Septal necrosis with extensive damage is suggested by: i) RBBB (especially in view of the loss of the initial positive r wave deflection in lead V1 with this RBBB); ii) Q waves in leads V1,V2; iii) ST elevation in lead aVR; iv) presumably new bifascicular block (RBBB/LAHB); v) AFib. 
  • This patient is at high risk of developing complete heart block and/or cardiogenic shock.
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ACKNOWLEDGMENT: My appreciation goes to Dr. Harsha Nagarajarao (of Cardiology Boards) for allowing me to use this tracing.
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NOTE: - Relevant PDF on ECG diagnosis of acute MI:
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Monday, July 9, 2012

ECG Interpretation Review #48 (Chest Pain - STEMI - 1st Degree - 2nd Degree AV Block - Infero-lateral - 2-to-1 - Wraparound)

The 12-lead ECG shown in Figure 1 was obtained from 50-year-old woman with “chest tightness”.
  • What two major conclusions should be reached regarding ECG interpretation of this tracing? 
Figure 1 – 12-lead ECG from a 50-year-old woman with chest tightness. (Reproduced from ECG-2014-ePub). – NOTE – Enlarge by clicking on Figures – Right-Click to open in a separate window.
INTERPRETATION: The two conclusions to be reached are: i) that there is a large acute evolving STEMI (ST-Elevation-Myocardial Infarction) in progress; and ii) there is 2nd degree AV block. It may be easiest to first interpret the changes of acute MI:
  • The QRS complex is narrow.
  • The axis is normal.
  • There is no chamber enlargement.
  • Q Waves/R Wave Progression: Q waves are present in each of the inferior leads (II,III,aVF). After a small (but definitely present) initial r wave in lead V1 – there is loss-of-R-wave – with a probable QS in V2 and a definite QS (with notch in downslope of S wave) by lead V3. Abnormal Q waves persist in leads V4-thru-V6.
  • ST-T Wave Changes: There is marked ST elevation in each of the inferior leads. In addition – there is ST segment coving and elevation that appears to begin in lead V2, and persist through to lead V6. T wave inversion (sometimes marked) is seen in each of the leads with ST elevation.
  • Reciprocal Changes – are seen in leads I and aVL. These reciprocal changes entail not only ST depression in lead aVL – but also T wave peaking (which is the “mirror-image” of the deep inferior symmetric T wave inversion).
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WHAT IS THE RHYTHM in FIGURE 1?
An extra P wave appears to be hiding in the tail portion of each QRS complex on this tracing (Figure 2). This extra P wave is most evident in lead II (RED arrows in Figure 2) – but it is also seen in other leads (BLUE arrows).
  • The underlying atrial rhythm is rapid (~140/minute) and regular.
  • The PR interval preceding each QRS complex is fixed (albeit prolonged to 0.26 second). Thus, every-other-P-wave is conducting – and the rhythm is 2nd degree AV block with 2:1 AV conduction.
Figure 2 – Addition of red and blue arrows to Figure 1 – revealing 2:1 AV conduction in the underlying rhythm (See text).
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IMPRESSION:  The ECG in Figure 1 suggests a large acutely evolving STEMI involving inferior, anterior and lateral precordial lead areas. Large Q waves have already developed in anterior leads (loss or r between V1-to-V2 – and QS in V2,V3). ST segment coving and elevation persists in these anterior lead areas – though ST elevation is not as marked as it is in inferior leads.
  • Whether the extensive pattern of injury seen indicates acute occlusion of a large dominant circumflex artery vs an LAD (Left Anterior Descending) artery with “wraparound” (an LAD that also supplies the inferior wall) vs some combination of lesions (perhaps with collateralization affecting distribution) – is uncertain. What is certain – is that an extremely large infarction with AV block is acutely evolving.
We define the type of AV conduction disturbance seen in Figures 1,2 as 2nd degree AV block with 2:1 AV conduction:
  • In theory – the conduction disturbance could be either Mobitz I (AV Wenckebach) or Mobitz II AV block. The reason we cannot absolutely distinguish between these two possibilities is that one never sees two beats conducted in a row (so that we can’t tell IF the PR interval would lengthen if it did have an opportunity to do so).
  • That said – we strongly suspect the conduction disturbance represents 2nd degree AV block, Mobitz Type I (Wenckebach) – because: i) Mobitz I is far more common than Mobitz II – especially in the setting of acute inferior MI when there is also 1st degree AV block for conducting beats; and  ii) the QRS complex is narrow (as it almost always is with Mobitz I – vs QRS widening that is usually seen with Mobitz II).
  • PEARL: It would be easy to overlook 2:1 AV block in this tracing. Awareness that various forms of AV Wenckebach commonly occur with acute inferior MI should increase your index of suspicion that this conduction disturbance may be “in hiding” whenever ST segment elevation is marked – and you either see: i) a pattern of grouped beating; or ii) a longer-than-expected PR interval preceding those beats that are conducting (as seen here). Use of calipers may prove invaluable for confirming your suspicion.
BOTTOM LINE: Acute reperfusion is urgently needed for this patient.
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NOTE: - Relevant PDFs on ECG features in this case
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Thursday, July 5, 2012

ECG Interpretation Review #47 (Normal Variants - Early Repolarization - Benign - ST Elevation - Pericarditis - ERP - STEMI)

The 12-lead ECG shown in Figure 1 was obtained from 50-year-old man with chest discomfort.
  • Is this ECG likely to reflect acute anterior STEMI? – acute pericarditis? – or ERP (Early Repolarization Pattern) without acute process?

Figure 1 – 12-lead ECG from a 50-year-old man with chest discomfort.



INTERPRETATION: Using our systematic sequential approach (rate-rhythm-intervals-axis-hypertrophy-QRST changes) – We interpret the 12-lead ECG in Figure 1 as follows:
  • The QRS complex is narrow.
  • There is slight but definite variability in the R-R interval throughout the tracing. The rhythm is sinus arrhythmia.
  • All intervals (PR,QRS,QT) are normal; the axis is normal (approximately +70 degrees).
  • There is voltage for LVH (deepest S in V1,2 + tallest R in V5,6 ≥35). No other sign of chamber enlargement.
  • Q-R-S-T Changes: There are small q waves in the inferior and lateral precordial leads.  R wave progression is normal (ie, transition occurs between leads V3-to-V4 ).  T waves are peaked.  There is some J-point ST segment elevation (with upward concavity = "smiley" configuration) in multiple leads - and there is shallow symmetric T wave inversion in lead aVL.
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IMPRESSION: There is some baseline artifact (seen most in leads I, II, III, aVL . . . - albeit not enough to impede our interpretation). Sinus arrhythmia. Voltage for LVH. Shallow T wave inversion in lead aVL – plus – 1-2mm of J-point ST segment elevation with upward concavity in a number of leads … STOP! ...
  • Interpretation of the ECG in Figure 1 beyond the “STOP” depends greatly on the clinical setting.
  • IF this ECG was obtained from an otherwise healthy young adult without cardiac symptoms – we would interpret the isolated shallow T inversion in lead aVL as normal given the relatively vertical QRS axis and predominantly negative QRS complex in this lead (See Figure 2 below).
  • Similarly – We would interpret the slight (but real) upward concavity (“smiley”) precordial ST elevation as consistent with ERP (See Figure 3 below).

HOWEVER – The situation in this case is different – because the patient whose ECG is shown in Figure 1 is 50 years old and IS having chest discomfort ...
  • Consideration therefore HAS to be given to the possibility that the precordial lead ST elevation seen could represent an early stage of acute anterior STEMI (ST Elevation Myocardial Infarction) – especially given the T wave inversion in lead aVL.
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NOTE: We complete our interpretation of this case (and the ECG in Figure 1) at the bottom of this Blog post. Before doing so – we address a number of key concepts relating to clinical assessment of anterior lead ST elevation.
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Normal T Wave Inversion:
Five leads (III,aVF,aVL,aVR,V1) – may normally display moderate-to-large Q waves and/or T wave inversion in otherwise healthy adults. Thinking of a “reverse Z” (à la Zorro) may help recall which leads these are (Figure 2):
  • While we cannot rule out the possibility that the shallow T wave inversion in lead aVL of Figure 1 reflects ischemia – this T inversion is much more likely to be normal in this patient because: i) T wave inversion is isolated (it is only seen in lead aVL); ii) T inversion is shallow; iii) the QRS complex in aVL is predominantly negative in this patient with a relatively vertical QRS axis (conditions that predispose to the normal finding of some T inversion in aVL); and iv) no acute change is seen in other limb leads.

Figure 2 – Schematic tracing showing those leads that may normally manifest even large Q waves or deep T wave inversion (leads III,aVF,aVL,aVR,V1). Thinking of a “reverse Z” may facilitate recall.


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ST Segment SHAPE:
The shape of ST elevation is more important than the amount of elevation (Figure 3). Acute MI may occur with only minimal ST elevation:
  • ST elevation with an upward concavity (ie, “smiley” configuration) is usually benign – especially when seen in an otherwise healthy, asymptomatic individual (especially when seen with notching or slurring of the J point in one or more leads). This ST segment variant is known as ERP (Early Repolarization Pattern).
  • In contrast – ST elevation with coving or a downward convexity (“frowny” ) – is much more likely to be due to acute injury (from ischemia/MI).
  • KEY POINT: History is ever important. Although ST elevation with a “smiley” configuration and J-point notching often reflects a normal variant – this is only true IF the patient is asymptomatic. An identical ST-T wave pattern from a patient with chest pain must be assumed acute until proven otherwise.
  • IF in doubt – Admit the patient! Look at old tracings to compare. Repeat the ECG.

Figure 3 – Schematic showing upward concavity (“smiley” ) ST elevation that is usually benign – especially when J-point notching is seen in one or more leads. In contrast – ST segment coving (“frowny” ) – is much more likely to be due to acute injury/infarction.


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Are ST Segments Truly Elevated in Figure 1? 
ST segment elevation in Figure 1 is subtle but real (Figure 4):
  • We judge ST segment deviations with respect to the PR segment baseline. In Figure 4 – the blowup of leads V1,V2 shows the J-point to be clearly elevated above the PR segment baseline. We estimate 1-2mm of upward concavity ST elevation in lead V2 (although we admit that subtle rounding of the J-point area in this lead makes precise determination of the amount of ST elevation difficult).

Figure 4 – Second look at the ECG shown in Figure 1 from this 50 year-old man with chest discomfort. Blowup of leads V1,V2 illustrates subtle but real upward concavity ST elevation above the PR segment baseline (See text).


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Putting It All Together:
As stated earlier – the ECG in Figure 1 shows sinus arrhythmia; voltage for LVH; shallow T wave inversion in lead aVL – plus – 1-2mm of J-point ST segment elevation with upward concavity in a number of leads … Our impression is probable ERP (and not anterior STEMI or pericarditis) because:
  • ST elevation manifests and upward concavity (“smiley” ) configuration (albeit no J-point notching is seen).
  • ST elevation is seen (at least in small amount) in all precordial leads. IF acute anterior STEMI was evolving – one would expect additional ST-T wave abnormality elsewhere on this tracing given the extent of ST elevation.
  • The shallow T wave inversion in lead aVL is isolated and probably normal given the patient’s relatively vertical QRS axis and predominantly negative QRS in lead aVL.
  • The q waves seen on this tracing are small and narrow. They most probably are normal septal q waves (which are typically seen in lateral leads and sometimes also in inferior leads in patients with a vertical axis).
  • The ECG picture in Figure 1 is not suggestive of acute pericarditis (it lacks sinus tachycardia; ST elevation is absent in the limb leads; there is no PR depression).

We conclude our interpretation of the ECG in Figure 1 with the statement: “Urge clinical correlation”. The point to emphasize is that although we would be relatively comfortable that the ECG shown in Figure 1 is unlikely to represent early acute anterior STEMI – We can not rule out this possibility on the basis of this single tracing! How to proceed with only a ~90% comfort level that the ECG in Figure 1 is benign would depend:
  • IF this patient presented to the office with a history of chest discomfort that was relatively unconvincing for ischemic pain – we would probably manage the case on an ambulatory basis. We would be that much more inclined to do so IF history and physical exam suggested a non-cardiac cause (peptic ulcer disease; musculoskeletal chest pain, etc.).
  • Access to a prior ECG on this patient might prove invaluable (especially if it confirmed baseline anterior ST elevation and T wave inversion in aVL of similar nature to that seen in Figure 1).
  • On the other hand – IF this 50-year-old man presented to the ED (Emergency Department) with new-onset chest discomfort (and no prior tracing available) – he would almost certainly be admitted to the hospital. One simply can’t rule out the possibility of early anterior STEMI on the basis of this single tracing… (In our experience – such patients with new-onset chest discomfort are not sent home from the ED).


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Should the Cath Lab Be Activated?
Taking the 2nd scenario presented above (ie, that this 50-year-old man presented to the ED with the ECG in Figure 1 and a history of new-onset chest discomfort) – the question arises as to whether the cath lab should be activated for possible acute reperfusion on the basis of this tracing? IF Figure 1 in fact represents an early stage of anterior STEMI – then prompt reperfusion becomes a critical determinant of optimal prognosis.
  • At what point to activate the cath lab is difficult to say from the comfort of our home computer as we view this tracing …. Sometimes – “Ya just gotta be there …”. That said – We most probably would not activate the cath lab on the basis of what we see in Figure 1.
  • Access to a prior ECG on this patient might be revealing (if a prior tracing can be found…).
  • Repeating the ECG in short order may establish the diagnosis. With acute evolving infarction – significant change may be evident on ECG in as little as 20-to-30 minutes.
  • Obtaining an Echo at the bedside in the ED while the patient is having chest discomfort may provide invaluable assistance in determining the likelihood of an acute event. If an anterior wall motion abnormality is seen during symptoms — this becomes highly suggestive of an acute event. On the other hand, if during chest discomfort the Echo is entirely normal — this makes an acute event much less likely. (NOTE: We emphasize 2 points regarding ED use of Echo for this purpose: i) these Echos may be challenging to read, so expertise is needed to KNOW whether wall motion abnormality is or is not present; and ii) an Echo is only helpful IF obtained during chest discomfort. If chest discomfort has resolved and the Echo is normal — unfortunately nothing can be ruled out!)
  • STAT troponin values may confirm acute infarction (though even high-sensitivity troponins would not rule this possibility out if they were normal).
  • IF still in doubt after reexamining the patient and the above series of steps – Consider consulting the Cardiologist-On-Call to assist in the decision-making process. There are times when acute cath may be performed even without definitive diagnosis – although in this case, careful observation with close serial follow-up will almost certainly tell the tale over the next few hours. But at least the cardiologist is aware in the event a surprise occurs and the ECG evolves ...

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FINAL Thoughts: Is there Help in the Literature?
Smith et al have developed a multivariate equation to assist in acute evaluation of the patient with anterior ST elevation (Ann Emerg Med 60:45, 2012). Findings from their retrospective analysis of a large data set are insightful in this case – and further support our suspicion that the ECG in Figure 1 is most probably benign. These include relatively taller R wave amplitude and a QT interval that is not prolonged in Figure 1. That said – overlap exists in the parameters used in the calculated Smith equation, such that we are still left with being unable to exclude an acute process on the basis of the number score reported.  – END OF CASE –
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Please click on the icon below for a pdf Link to Section 09.0 (from our ECG-2014-ePub) on assessment of ST-T waves. The part on Early Repolarization begins in Section 09.14 in this pdf:


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