ECG Blog #16 — 23 yo Woman; Atypical Chest Pain

QUESTION: The ECG in Figure-1 was ordered on a 23 year old woman who was seen in the office a day earlier. No history was given.  No prior tracing was available for comparison.

• How would you interpret this ECG?
• Clinically — What would you do if you were reading this ECG the day after without the benefit of any history to go on?

Figure-1: ECG from a 23 yo woman with atypical chest pain.

INTERPRETATION: The rhythm is sinus at a rate just under 100/minute. All intervals (PR, QRS, QT) are normal. The mean QRS axis is normal (at +75 degrees). There is no chamber enlargement.

• Q-R-S-T Changes:  — There is definite baseline wander in several leads on this tracing (most notably in leads III, aVL, aVF, and lead V2). There appears to be a tiny q wave in lead III. Transition is normal (occurs between leads V2-to-V3).  There is subtle but real ST segment elevation in a number of leads.

CLINICAL IMPRESSION: Although one might want to be "lulled" into a sense of security by the young age of this patient — this is not a normal tracing in a 23 year old woman. The ST segment elevation is real (Figure-2).  Clearly — the baseline wander (especially in lead V2) makes assessment of ST segment position difficult.  That said — one is struck by the straight takeoff with almost hyperacute T waves and suggestion of subtle ST segment elevation in many of the leads on this tracing.

Figure-2 — Blow-up of the precordial leads from Figure 1. Despite baseline wander (blue double arrow in V2) — the J-point is elevated above the PR segment baseline in leads V2-thru-V5 (short red lines).

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COMMENT: Given the age of this patient, the diffuse nature of the ST-T wave change, and the lack of any reciprocal ST depression — myocardial infarction is unlikely. However, young adults do get acute pericarditis — and the constellation of a relatively rapid heart rate with subtle but diffuse ST elevation and morphology seen here is certainly consistent with a diagnosis of acute pericarditis. We felt a need to review the chart and contact the treating physician. Turns out the history was of atypical chest pain of relatively recent onset that was initially attributed to a musculoskeletal cause (with the patient being sent home on a short course of NSAID therapy). In view of this history — a more likely diagnosis was acute pericarditis, with our revised plan for more careful follow-up, repeat ECG in 1-2 weeks, and to continue the course of NSAIDS (appropriate for both musculoskeletal pain and pericarditis).

• There are many causes of acute pericarditis. These include cancer (metastasis); viral and bacterial causes; autoimmune disorders; associated myocarditis; drugs; radiation pericarditis; trauma; post-MI; tuberculosis; uremia; and “idiopathic” when no cause can be found. 
• By far — the most likely etiology in a previously healthy young adult is a viral disorder. Most of the time — history, physical exam and the clinical setting will suggest the probable etiology.

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ECG Recognition:  Pericarditis is often a difficult clinical entity to detect — especially when there is no preceding viral illness, no rub is heard, and the entity is not actively considered. The ECG can be helpful in diagnosis. Typically — there are 4 Stages to Acute Pericarditis, which we simplify as follows (Figure-3):

• Stage I -— everything is "up" (ST elevation is seen in almost all leads).
• Stage II — transition ( = "pseudonormalization" ).
• Stage III — everything is "down" (inverted T waves).
• Stage IV — normalization.

Figure-3 — The 4 Stages of Acute Pericarditis.

ST Segment Elevation: Figure-4 shows a schematic example of Stage I Acute Pericarditis. Note how diffuse the ST segment elevation is in Stage I ("everything up" stage) - being seen in virtually all leads (except the "far away" leads = blue shaded leads III, aVR, and V1).

• ST-T wave morphology with acute pericarditis may resemble that seen with early repolarization — in that the ST segment tends to manifest an upward concavity (“smiley” configuration) rather than the coved (downward convexity) more commonly seen with acute MI. 
• ST elevation with acute pericarditis is more generalized than that usually seen with early repolarization (that tends to be localized to one or two lead areas). 
• J-point notching is characteristically seen in one or more leads with early repolarization — though overlap in the ECG picture between acute pericarditis and early repolarization may certainly be seen (since after all — acute viral pericarditis is commonly seen in a previously healthy young adult population who may develop this disorder superimposed on a baseline ECG showing early repolarization changes …). Look for tachycardia — a history of pleuritic-type chest pain worse on recumbency — listen carefully for pericardial friction rub — and inquire about recent viral illness. 
• The ST elevation seen with acute MI differs from the picture of acute pericarditis in several ways: i) it is more localized — with reciprocal ST depression in other areas of the heart; ii) Q waves may be seen (absent from pericarditis, with possible exception of baseline small septal q waves); iii) leads II and III tend to look similar with acute MI (inferior changes) — vs — with acute pericarditis, leads I and II tend to look more similar (See Figure 4); and iv) the associated history will be very different for the two entities. 
• NOTE: ST elevation (and PR segment depression) is typically absent with acute pericarditis from uremia (since the diffuse ECG changes of pericarditis are attributable to acute epicardial inflammation which is not a feature of pericarditis from uremia).

Figure-4 — Schematic example of Stage I Acute Pericarditis.

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PR Segment Depression: In addition to the diffuse ST segment elevation seen in Figure-4 — PR segment depression is also seen.

• PR segment depression — may be a subtle sign that supports the diagnosis of acute pericarditis. It is not always seen. It may be seen in some leads, but not in others. Close inspection of Figure 4 shows PR segment depression present in leads I, II, V2, and V3 — but not in aVL,aVF; V4,V5,V6 (You may want to click on Figure-4 to enlarge the tracing).
• We emphasize that PR depression may be subtle — although it will be seen in at least some leads in many (not all) cases of acute pericarditis IF it is looked for. PR depression is helpful when seen — though its absence does not rule out the diagnosis ...
• We do not seen PR depression in Figure-1 for the 23-year-old woman in this case ...
• Acute pericarditis is one of those conditions in which we pay special attention to lead aVR. This most distant recording electrode often manifests the opposite ST/PR segment picture of most other leads (Note PR segment elevation and ST depression in lead aVR for Figure-4).
• A final caveat regarding PR segment depression is that it may occasionally be seen in normal subjects ... Thus, both sensitivity and specificity of PR depression are imperfect indicators of acute pericarditis. That said — this sign may be very helpful IF found in selected cases when symptomatic patients present with subtle ECG findings.

To clarify how to recognize PR depression — we add a blow-up of 4 leads taken from another patient with acute pericarditis (Figure-5). Note subtle but real PR segment depression in leads II, III, and aVF (as judged with respect to the R-P baseline).

Figure 5 — 4-lead blow-up taken from a patient with acute pericarditis. There is PR segment depression in leads II,III,aVF — as judged with respect to the R-P baseline (arrow in lead II shows the PR is below this baseline — while the ST segment is above it).

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CONCLUSION (Bottom Line):  A history is needed for accurate ECG interpretation. If the 23-year-old woman presented in this case in question asymptomatic — then the tracing seen in Figure-1 could conceivably represent a normal repolarization variant. Knowing that this young woman instead had atypical chest pain of recent onset makes it much more likely that the constellation of ECG findings seen represents acute pericarditis. Given transition between the "everything up" ST elevation stage (Stage I in Figure-3) — and the "everything down" T wave inversion stage (Stage III) — it may be that another reason for the subtle findings in Figure-1 is that this tracing caught the patient in transition (Stage II) between diffuse ST elevation returning to the baseline on its way to evolving toward diffuse T wave inversion. The findings of acute pericarditis may indeed be subtle.

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Final CAVEAT (Clinical Pearl ):  A common differential diagnosis is between acute pericarditis vs ACS (Acute Coronary Syndrome). Keep in mind that in practice — ACS is far more common than acute pericarditis. Despite this clinical reality — acute pericarditis tends to be greatly overdiagnosed ... The onus of proof is on US to rule out ACS as the cause of ST elevation, rather than the other way around. BOTTOM LINE: It's best not to diagnose acute pericarditis until you have ruled out ACS!

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  — See also ECG Blog Review #12 — and — this pdf from Section 12.0 of ECG-2014-ePub—
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ECG Interpretation Review #15 (Run of WCT - VT vs Aberrant Conduction)

QUESTION: Interpret the Lead MCL-1 rhythm strip in the tracing shown in Figure-1.

• Is this a run of VT?
• How certain are you of your diagnosis?

Figure 1 - What is the cause of the run of beats #6-thru-#14?

INTERPRETATION: The underlying rhythm (as suggested by the first 5 beats) — is sinus tachycardia at ~105/minute (regular, narrow QRS with R-R interval of just under 3 large boxes; P waves with fixed PR interval precede each QRS for beats #1-5 in this right sided MCL-1 lead). Sinus rhythm is then interrupted by a run of a WCT (Wide-Complex Tachycardia). Despite QRS widening — the run of beats #6-thru-#14 in Figure 1 is not ventricular tachycardia.

ABERRANT CONDUCTION: 

The 3 possibilities for conduction of PACs (Premature Atrial Contractions) are shown in Figure-2:

• Premature Impulse A — occurs so early as to fall within the ARP (Absolute Refractory Period). Because the entire conduction system is still in an abolute refractory state — premature impulse A is "blocked" (ie, non-conducted to the ventricles).
• Premature Impulse C — occurs after the refractory period is over.  As a result — a PAC occurring at Point C will conduct normally (with a narrow QRS that looks identical to other sinus beats on the tracing).
• However — Premature Impulse B occurs at an intermediate point during the RRP (Relative Refractory Period).  A PAC occurring at Point B will therefore conduct aberrantly (ie, with QRS widening) — because only part (but not all) of the ventricular conduction system has recovered. Most often PACs that occur during the RRP will conduct with some form of bundle branch block and/or hemiblock (reflecting that part of the conduction system which has not yet recovered).

Figure-2: Absolute and Relative Refractory Periods (ARP & RRP) — explaining why beat A is blocked — and beat B is conducted with aberration.

Returning to the Questions in this Case:  

It is important to emphasize that by far, the most common cause of a WCT is ventricular tachycardia. That said — there are times when one can definitively exclude VT from consideration.  This is one of those times. The best way to diagnose aberrant conduction is by identifying a premature P wave at the onset of the tachycardia. The RED arrow in Figure-3 does just this. Note notching in the T wave of beat #5 just before the run begins. None of the sinus-conducted beats at the beginning of the tracing show such notching, confirming that this finding is real and indicative of a PAC.

Figure-3: Answer to Figure 1.

Two additional findings consistent with a supraventricular etiology for beats #6-thru-#14 are: 1) that QRS widening though present is not marked; and, 2) that the initial deflection (both the small, slender r wave and the downslope of the S wave) is very similar in morphology to the initial part of the QRS of sinus beats.

• Final POINT: Note that there is atrial activity during the run in the form of a small point at the peak of the T wave (Note thin RED circles in the T wave of beats #6,7). Because VT may sometimes manifest 1:1 retrograde conduction back to the atria — the atrial activity that we see in Figure 3 is not helpful diagnostically in distinguishing between VT and SVT with aberration.

IMPRESSION:  

Sinus tachycardia for the first 5 beats. This is interrupted by a PAC (in the T wave of beat #5) — and followed by a wide tachycardia that is supraventricular with aberrant conduction. This is not VT.

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NOTE: See also ECG Blog Review #14 -
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ECG Blog #14 — The Cause of the Pause?

QUESTION: Interpret the Lead MCL-1 rhythm strip that is shown below in Figure-1.

• What is the cause of the pauses in this tracing?  Is there AV block?
• Why is the PR interval preceding beat #7 shorter than the PR for other sinus beats?

Figure-1: What is the cause of the pauses? (between beats #2-3 and between #6-7).

INTERPRETATION: The rhythm in Figure-1 is irregular in a pattern of group beating (with short pauses between beats #2-3 and #6-7). The QRS complex is narrow (ie, not more than half a large box in duration). The underlying rhythm appears to be sinus, with similar-looking P waves showing a fixed PR interval preceding beats #1, 2, 3, 4, 5, 6, 8, and 9 in this right-sided Lead MCL-1 rhythm strip.

• Despite the presence of group beating — there is no evidence of Wenckebach or other form of AV block on this tracing.  Instead, the "cause" of the pause lies within the T waves of beats #2 and 6.

The Most Common Cause of a Pause: 

Although most premature supraventricular beats (PACs or PJCs) are conducted normally to the ventricles (ie, with a narrow QRS complex) — this is not always the case.  Instead, PACs (or PJCs) may sometimes occur so early in the cycle as to be "blocked" (non-conducted) — because the conduction system is still in an absolute refractory state.

• This is the situation for premature impulse A in schematic Figure-2 (which shows A occurring during the ARP = Absolute Refractory Period).

Figure-2: Absolute and Relative Refractory Periods (ARP & RRP) — explaining why beat A is blocked — and beat B conducts with aberration.

• At other times — premature (early) beats may occur during the RRP (Relative Refractory Period) — in which case aberrant conduction (with a wide and different-looking QRS) occurs.  This is the situation for premature impulse B in Figure 2.  Because impulse B occurs during the RRP — part (but not all) of the ventricular conduction system has recovered. Most often PACs occurring at Point B will conduct with some form of bundle branch block and/or hemiblock (reflecting that part of the conduction system which has not yet recovered).
• Premature impulse C in Figure 2 occurs after the refractory period is over.  As a result — a PAC occurring at Point C will conduct normally (with a narrow QRS that looks identical to other sinus beats on the tracing).

KEY Clinical Point: 

The most common cause of a pause is a blocked PAC (corresponding to a PAC occurring at Point A in Figure 2). Blocked PACs occur much more often than any form of AV block.

• Blocked PACs are often subtle and difficult to detect. That said — they will be found IF looked for (they'll often be hiding/notching a part of the preceding T wave).

Returning to the Questions in this Case: 

We illustrate our Answers in Figure 3:

• The cause of the pause in this case is a blocked PAC (arrow in the T wave of beat #6 highlights the "telltale notching" of a PAC buried in this T wave).  A similar very early-occurring PAC (corresponding to a PAC at point A in Figure 2 can be seen notching the T wave of beat #2).
• The occurrence of a PAC resets the sinus cycle, usually with a brief pause after the early beat. The reason the PR interval preceding beat #7 is shorter - is that beat #7 is a junctional escape beat that occurs just before before the P wave that precedes it is able to conduct to the ventricles. Normal sinus rhythm then resumes with beat #8.
• Finally — is the subtle finding that the escape interval preceding beat #3 (ie, the distance between beats #2-3) is slight longer than the distance between beats #6-7. This accounts for why beat #3 is sinus-conducted (with a normal PR interval) — whereas slightly earlier occurring beat #7 is a junctional escape beat (that occurs just before the P wave preceding it is able to conduct to the ventricles).

Fgure 3: Answer to Figure 1 (See text).

BOTTOM Line: 

The commonest cause of a pause is a blocked PAC. Remembering this truism will hopefully remind you to always look carefully in the T wave at the onset of all pauses to see if the "telltale" notching of a blocked PAC is in hiding. 

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NOTE: See also ECG Blog Review #15 - and - Section 20.0 from ACLS-2013-ePub on AV Block - 

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ECG Interpretation Review #13 (BBB, Wide QRS, Is this LBBB vs RBBB vs IVCD)

 

QUESTION: Interpret the 12-lead ECG below.

• What type of conduction defect is present?  - Is this LBBB?
• Clinically - Is anything else going on?  (Has there been anterior infarction?)

Figure 1: What type of conduction defect is present?

INTERPRETATION:  The rhythm is regular with the exception of the 4th beat which is early (See Lead II Rhythm Strip at bottom of tracing).  Upright P waves are present in lead II with a fixed PR interval. Thus, the rhythm is sinus at a rate of 75/minute with a PAC (Premature Atrial Contraction). The PR interval is approximately one large box (or at most a tad more) in duration. The QRS is obviously long.  Recognition of QRS widening at this point is indication to STOP (and figure out WHY the QRS is wide) - before going any further:

• Assessment of QRS Widening: The 3 KEY leads to assess in order to determine the reason for QRS widening are leads I, V1, and V6.  Practically speaking - IF the QRS complex is wide and the rhythm is supraventricular (ie, not wide due to ventricular tachycardia or WPW) - then there are 3 possibilities: 1) Typical RBBB; 2) Typical LBBB; or 3) IVCD (Figure 2).

Figure 2: Assessment of QRS Widening — for which there are 3 possibilities.

• Figure 2 in ECG Review #3 showed the expected morphology for typical RBBB = Right Bundle Branch Block (an rSR' complex in right-sided lead V1 - and wide terminal S waves in left-sided leads I and V6). Clearly, Figure 1 above does not manifest the morphology of RBBB.
• Figure 2 in ECG Review #11 showed expected morphology for typical LBBB = Left Bundle Branch Block (upright, monophasic QRS in left-sided leads I and V6 - and a predominantly negative QRS in right-sided lead V1). Although QRS morphology in Figure 1 above is consistent with LBBB in lead V1 - it is clearly not consistent with it in either I or V6. 
• By the process of elimination - the conduction defect in Figure 1 above is IVCD (IntraVentricular Conduction Delay).

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About IVCD: The ECG appearance of IVCD is difficult to characterize.  This is because IVCD is often the end result of a number of different pathophysiologic processes - rather than reflecting a discrete defect in the conduction system (as usually occurs with RBBB or LBBB).  Examples of conditions that may lead to IVCD include myocardial infarction; cardiomyopathy with ventricular fibrosis; chamber enlargement; and/or any combination of these (with or without a component of bundle branch block).  Thus, many patients with IVCD have at least some type of underlying heart disease. The "beauty" of the above algorithm (Figure 2) - is that it greatly simplifies the diagnosis of conduction defects.  IVCD is present IF:

• The QRS complex is wide (ie, at least 0.11 second).
• Neither typical RBBB nor typical LBBB is present.

Figure 3 - Schematic example of IVCD. QRS morphology is not typical for  either RBBB or LBBB.

Thus, in Figure 3 - the rsR' pattern in V1 and the wide terminal S wave in lead I are both consistent with RBBB.  However, the notched, upright complex in lead V6 is clearly not consistent with RBBB (but rather with LBBB).  Since typical morphology for either RBBB or LBBB is not present in all 3 of the KEY leads (leads I,V1,V6) in Figure 3 - the reason for QRS widening must be IVCD . . .

Returning to Our Systematic Approach: The QT interval is difficult to interpret and less relevant in the setting of conduction defects such as IVCD. The axis in Figure 1 is indeterminate (negative QRS in leads I and aVF). That said - the concept of axis is elusive with IVCD, and there is really no need to comment on it in this setting. 

• Chamber Enlargement - None that we can call (given the presence of IVCD).
• Q-R-S-T Changes - Nonspecific changes (Nothing more can be said given IVCD).

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Note - In Figure 3 of ECG Review #11 - we illustrated a KEY rule for assessment of ST-T wave changes with typical RBBB or LBBB (that the ST segment and T wave should be oppositely directed to the last QRS deflection in the 3 key leads).  This rule does not work for IVCD. With rare exceptions - it is extremely difficult to assess ST-T wave changes for ischemia or infarction in the setting of IVCD.
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CLINICAL IMPRESSION:  Our final interpretation of the ECG in this case (Figure 1) is as follows: "NSR. Occasional PAC. IVCD. Non-specific ST-T wave changes. Suggest clinical correlation."

•  Despite the deep QS complexes in leads V1,V2,V3 of this tracing - one cannot call prior anterior infarction because there is IVCD

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   - See also ECG Blog Review #3 - and Review #11 - 
   - Please also check out our ECG Video on the Basics of Bundle Branch Block (www.bbbecg.com).

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ECG Interpretation Review #12 (Computerized ECG Interpretation, Normal Variant vs ST Elevation)

QUESTION: The ECG below was one of many in "the pile to be read".  It was from a middle-aged adult.  No history was given. No prior tracing was available for comparison. The computerized interpretation of this tracing was the following: "Sinus rhythm. Normal ECG."

• How would you interpret his ECG?  — Do you agree with the computer?
• Clinically — How would you proceed?

Figure 1 - This ECG was read by the computer as "within normal limits". Do you agree?

INTERPRETATION:  The rhythm is sinus at a regular rate of 80/minute. All intervals (PR, QRS, QT) are normal.  The mean QRS axis is normal (at +70 degrees). There is no chamber enlargement.

•  Q-R-S-T Changes:  — There are small and narrow q waves in infero-lateral leads (II,III,aVF; and V5,V6). Transition occurs early (between leads V1-to-V2). Subtle but real ST segment elevation is seen in multiple leads (II,III,aVF,V1-thru-V6). There is symmetric T wave inversion in lead aVL and to a lesser extent in lead V1.

CLINICAL IMPRESSION:  Despite the computerized interpretation — this is not a "normal tracing". The findings of small, inferolateral q waves, early transition, and fairly shallow T wave inversion in leads aVL and V1 by themselves all could be normal variants. However — one cannot discount the small amplitude but real ST elevation seen in multiple leads. The differential diagnosis includes:

1. Acute MI (less likely given the diffuse nature of the changes; acute MI is most often localized to a given lead area).
2. Acute Pericarditis (a definite possibility given diffuse ST segment elevation).
3. Early Repolarization as a Normal Variant (a diagnosis of exclusion to be made only after #1 and #2 considerations above are ruled out).

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COMMENT:  — It is sometimes difficult to recognize subtle ST segment elevation (as seen in leads V4,V5,V6 in Figure 1). To assist in this task — it is well to remember that it is the PR segment baseline (Figure 2) that serves as the landmark for judging ST segment deviations (elevation or depression). With this in mind — we can clearly identify the takeoff of the ST segment as being elevated with respect to the preceding PR segment for each of the leads mentioned above.

Figure 2 - Use of the preceding PR Segment as a baseline to judge ST elevation or depression.

We make several additional points:

1. Computerized ECG Interpretations are not always correct (and this case is a glaring example of how they can go wrong). That said - computerized ECG interpretations can have utility IF used correctly (Click HERE for a link to download our pdf Review on "Optimal Use of Computerized ECG Interpretations").
2. This case also illustrates the tremendous importance of knowing the history. We are literally lost without it — as we have no idea if the patient in question was having new-onset crushing chest pain, having pleuritic-type chest pain with pericardial friction rub on exam — or was entirely asymptomatic. Our clinical interpretation would vary dramatically based on answers to these questions. Having a prior ECG for comparison would also be invaluable for determining if the ST elevation seen here is new or old.
3. As we note above, without a history of new-onset cardiac-sounding chest pain — the diffuse nature of the ST changes makes us less suspicious of acute infarction. That said — each of the inferior leads show q waves with ST elevation, and the symmetric T wave inversion in lead aVL could be a reciprocal change. The onus remains on us to rule out acute MI as a possibility.
4. We would be very suspicious of acute pericarditis - IF the history was fitting (especially if a pericardial friction rub was heard). In addition to diffuse ST elevation — PR segment depression can be a helpful clue suggestive of acute pericarditis — and this appears to be present (albeit subtly) in the inferior leads.
5. Finally - the findings in Figure 1 could reflect a normal repolarization variant. In favor of this is the upward concavity (ie, "smiley") shape to the elevated ST segments (See ECG Blog Review #2 for review of Early Repolarization). In addition — J-point notching is seen in leads V2, V6, and intermittently in other leads.

BOTTOM Line:  We ignore the computerized ECG interpretation in this case. Small q waves and diffuse ST elevation is noted. History (and ideally a prior ECG for comparison) is needed to know how to interpret this tracing in context.

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• NOTE — For a Review on Use of Computerized ECG Interpretations — GO TO our ECG Blog #126 — Click HERE for a pdf copy of this material.

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