Thursday, May 17, 2012

ECG Interpretation Review #43 (AFib - PACs - Acute MI - STEMI - "smiley" - reciprocal changes)

The 12-lead ECG shown in the Figure was obtained from an older woman who was extremely anxious about her home situation. She felt some “heart sensations”. 
  • Is she in atrial fibrillation? 
  • Is anything else going on? 

Figure 1 – 12-lead ECG from an older woman with anxiety and “heart sensations”. Is she in atrial fibrillation? NOTE Enlarge by clicking on FiguresRight-Click to open in a separate window.
INTERPRETATION: At first glance – the patient appears to be in atrial fibrillation. The rhythm in Figure 1 is irregular, and normal upright P waves are not seen preceding each QRS complex in lead II. That said – artifact is present, and there is some baseline wander in lead II.
  • Ideally there would be a simultaneously-recorded lead II rhythm strip available for rhythm determination …
  • Even without a lead II rhythm strip – We feel this is not AFib (Atrial Fibrillation). Figure 2 explains why.  
Figure 2 – Despite irregularity of the rhythm and lack of a consistently upright P wave in lead II – this is not AFib. We have added red arrows to the ECG from Figure 1 showing clear evidence of atrial activity in other leads (See text).
DISCUSSION OF FIGURE 2: Addition of red arrows to the ECG shown in Figure 1 strongly suggests that despite the irregular appearance in lead II – the underlying rhythm is sinus:
  • Note that the overall rhythm becomes fairly regular after the first few beats (the main irregularity being beats #2,3,4 in lead II …). 
  • Careful inspection before the QRS complex in lead aVF and in lead V4 does suggest the presence of an upright P wave with fixed PR interval (red arrows in these leads). 
Thus, although impossible to know for sure without a longer lead II rhythm strip – We strongly suspect an underlying sinus mechanism with frequent PACs (Premature Atrial Contractions) as the rhythm. 
  • The occurrence of frequent PACs is clearly one cause of “heart sensations”. 
  • Up to half of all patients with AFib have the intermittent form (= PAF = Paroxysmal Atrial Fibrillation). Patients with PAF often manifest a series of PACs prior to precipitation of sustained AFib (presumably when one of the PACs falls within the atrial vulnerable period and “sets off” the episode of AFib) – so it is of course possible that the older woman in this case was having intermittent episodes of AFib … 
Is Anything Else Going On?
Much more than the rhythm – there are other concerns about the ECG in Figure 1, obtained from this older woman with anxiety and “heart sensations”. Continuing on with our systematic interpretation we note: 
  • The PR, QRS and QT intervals are normal. 
  • The mean QRS axis is normal (at about +60 degrees). 
  • There is no chamber enlargement. 
  • Assessment of Q-R-S-T Changes reveals definite abnormalities (Figure 3)
Figure 3 – We have labeled Figure 1 to illustrate ST-T wave abnormalities in this older woman with “chest sensations” (See text).
Assessment of Q-R-S-T Changes
Especially when assessing complex tracings such as this one – it is best to systematically complete Descriptive Analysis (making note of all findings seen) – before attempting to render a Clinical Impression. Only in this way will you avoid overlooking potentially important findings. We note the following: 
  • Q Waves: – Q waves are present in the inferior (II,III,aVF) and lateral precordial (V5,V6) leads. The Q waves in leads III and aVF are relatively deep and wide. The Q wave in lead V6 is wider than anticipated for a normal septal q wave. 
  • R Wave Progression: Transition occurs at a normal point (between leads V2-to-V3) – however, there is a fairly abrupt increase in R wave amplitude in lead V3
  • ST and T Wave Changes: The most concerning finding on this tracing is ST segment elevation in each of the inferior leads. Although the amount of ST elevation varies from beat-to-beat in simultaneously recorded leads II and III (due to baseline wander) – the finding of coved ST elevation above the PR segment baseline is unmistakable (horizontal red lines in in the inferior leads of Figure 3). 
  • There is also a hint of ST elevation in lead V6. This is subtle (red line in V6) – and suggested more by shape of the ST segment in lead V6 (which looks to be elevated) – rather than by amount of ST elevation (which at most is minimal). Baseline wander in lead V6 makes ST-T wave assessment especially challenging in this lead. 
  • Support that the above findings are truly acute is forthcoming from the presence of reciprocal ST segment depression in multiple leads (I,aVL; V2,V3,V4)
  • An additional subtle reciprocal change is disproportionate peaking of the T wave in leads V3 and V4
Each of the findings we note above in our Descriptive Analysis of Q-R-S-T Changes contributes in this case to our Clinical Impression
  • We are strongly suspicious of acute evolving infero-postero-lateral MI. Although impossible to “date” the infarction in this case (lack of a history of new-onset chest pain) – there clearly is ST elevation suggesting possible benefit from acute reperfusion. This should be considered as a possible intervention within the context of this case (perhaps assisted by serial tracings, troponins, comparison with prior tracings, and this patient’s clinical course). 
  • ST elevation in all 3 inferior leads (II,III,aVF) suggests acute inferior MI
  • The fact that inferior Q waves are deep and wide – and – the lack of a definite history of new-onset chest pain makes us question “how acute” these changes are … 
  • That said – the presence of definite reciprocal ST depression in several lead areas (blue circles in leads I,aVL,V2,V4 of Figure 3) supports the possibility that STEMI (ST-Elevation Myocardial Infarction) may be acutely evolving. 
  • ST depression in leads V2,V3 suggests acute posterior involvement. Supporting this finding is the abrupt increase in R wave amplitude between V2-to-V3 and the disproportionately tall T waves in V3,V4. Because none of the standard 12 leads directly view the posterior wall – we generally infer posterior involvement when the clinical setting is “right” (ie, associated inferior MI – since both inferior and posterior walls of the left ventricle are usually supplied by the right coronary artery) – and – when the Mirror Test” is positive (See Figure 4 below). 
  • Awareness that a “left dominant” circulation may be present in the minority of patients whose right coronary artery is relatively smaller – increases our index of suspicion for associated lateral precordial involvement in Figure 3. That is, in approximately 10% of patients – it is the left circumflex artery that is dominant – wrapping around the lateral wall to continue on while supplying blood flow to the posterior and inferior walls of the left ventricle. Thus, in the context of a deeper-and-wider-than-expected Q wave in lead V6 in association with a hint of ST elevation in this lead – we suspect acute infero-postero-lateral MI in Figure1
Figure 4 – We illustrate the concept of “mirror-image” reciprocal deflections by means of the colored inserts in leads I,aVL,V2,V3,V4 (See text).
Figure 4: The “MIRROR Test”for Posterior MI/Reciprocal Changes: 
The concept of reciprocal changes is based on the simplified assumption that the left ventricle acts as a cylindrical structure. With acute injury (from acute coronary occlusion) – ST segments elevate in leads directly over the area that is infarcting. In opposite areas of the heart – instead of ST elevation, there is “reciprocal” ST depression. Given the basic cylindrical structure of the left ventricle – reciprocal changes may be seen in any non-infarcting lead area, since all walls are in a sense “opposite” to one another. Thus, ST depression in lateral limb (I,aVL) and anterior (V2,V3,V4) leads in Figure 4 may reflect “reciprocal changes”
  • The posterior wall of the left ventricle sees “mirror-image” opposite electrical activity compared to the anterior wall. As shown by the colored inserts in leads V2,V3 of Figure 4 – instead of an RS complex with ST depression – the mirror-image in V2,V3 shows a Q wave, ST elevation and deep symmetric T wave inversion. The “mirror image” of the abrupt increase in R wave amplitude by V3 is a deepening Q wave – and the “mirror-image” of disproportionately tall T waves in V3,V4 is deep symmetric T wave inversion. In the setting of associated acute inferior MI – these changes are virtually diagnostic of accompanying acute posterior MI
  • Realizing that “reciprocal” ST segment depression is merely the mirror-image of ST elevation in another area of the heart helps with recognition. Note the mirror-image appearance of the QRST complex for the colored inserts in leads I and aVL of Figure 4. There can be little doubt that the ST depression in these high lateral leads represents reciprocal changes occurring in association with this patient’s acute inferior MI. 
BOTTOM LINE: Many of the changes in this case are subtle and represent advanced concepts. At the least – the “take home” messages from this interesting case study are the following: 
  • The cause of “heart sensations” in this older woman with anxiety but no chest pain is not AFib. Instead – her underlying rhythm is sinus with PACs. 
  • Some of this patient’s “heart sensations” probably relate to her acute inferior MI. Although lack of clear history (no definite onset of chest pain) precludes determination of the age of her MI – the presence of inferior ST elevation with reciprocal changes in several other lead areas strongly suggests at least relatively recent onset (that may therefore potentially benefit from acute reperfusion). This needs further evaluation. 
  • Whether the deep and wide Q waves that are already present in leads III and aVF represent prior inferior MI in this older patient (with superimposed new inferior injury) – orongoing damage from her acute event that continues to evolve – or – some combination of these possibilities – is impossible to know for sure from the “snapshot” we are given in Figure 1. Time, serial tracings and troponins, exam findings and clinical course will be needed to sort this out. 
  • In addition to the inferior wall – other areas of the heart may be involved (posterior and possible lateral precordial area). Regardless of whether ST depression in V2,V3,V4 respresents reciprocal changes – associated posterior infarction – or some combination of these two possibilities is much less important than awareness that the findings of significant ST elevation with associated ST depression in multiple leads signals involvement of a relatively larger area of myocardium (with more urgent need for immediate attention). 

NOTE: - Relevant PDF on ECG diagnosis of acute MI:


  1. Could also be possible that this is WAP? Since this is only a 10 sec strip, P wave morphology can be changing. I have seen patients before they convert to AF had P waves of different morphology. When a 12L is done or just a 6 sec strip it looks like a PAC but when P wave morphology is analyzed they in fact vary.

  2. Hi Nel. Your question is a good one - which is why I state above under Discussion of Figure 2 that it is impossible to know for sure what the rhythm is without a longer lead II rhythm strip.

    That said - the reason that I strongly suspect this is sinus rhythm (and not WAP = wandering atrial pacemaker) - is that in Figure 2 - IF you look at simultaneously recorded leads aVR-aVL-aVF - the shape and PR interval for each of the 3 beats in these leads is identical. Similarly - in simultaneously recorded leads V4-V5-V6 - the shape and PR interval for the 4 beats in these leads is the same. With wandering pacemaker - there is generally variation (gradually) in rate and in P wave morphology as the site of the pacemaker shifts. Granted - because I do not show a longer lead II rhythm strip - it is impossible to be certain that the P wave site of origin in different lead sets is the same ... but the PR interval for the one definite sinus beat in lead II (red arrow) is the same as the PR in aVR-L-F and the same as the PR in V4-5-6, which I wouldn't expect with WAP.

    Finally - WAP would not be expected to produce those 2 quick beats following the sinus beat in lead II (with the P wave in front of this 3rd and 4th beat in lead II being different - which shouldn't manifest this quick a change in P wave morphology with WAP).

    So - the above all based on hunches (lacking a longer lead II rhythm strip) - but I think the best bet is sinus rhythm with PACs ... THANKS for your excellent question!

  3. Hello
    Doing a 2D echo will be of help to determine the need for acute reperfusion in this case????

    1. This ECG strongly suggests acute evolving STEMI. I don’t know that 2D Echo is necessarily needed for clinical decision-making ..