The
ECG in Figure-1 was obtained from a middle-aged woman who
presented with a syncopal attack and hypotension. No
chest pain.
- How would you interpret this ECG?
- What is the “culprit” artery?
- What is the rhythm?
Confession: I am still not
completely certain about all that is going on with the cardiac rhythm in this
tracing. That said — several statements about the rhythm can be
made with certainty. And, I have a theory …
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Figure-1: 12-Lead ECG and
simultaneously-recorded long lead II rhythm strip, obtained from a
middle-aged woman with syncope and hypotension. (See text). |
COMMENT: This is a complex
tracing! As I fully acknowledge above — I am still not certain of
all aspects of the arrhythmia, details of which I’ll address a little bit
later. For the moment — suffice it to say that: i) All beats on this tracing are
supraventricular; ii) There are lots
of P waves; iii) Some of these P
waves look like they may be conducting; and, iv) There appears to be some form
of AV block.
- PEARL #1: Although the
arrhythmia in Figure-1 is fascinating (!) — Recognizing that more
detailed analysis beyond what I state above in i), ii), iii) and iv) is not needed
at this point in order to initiate the most important priorities
in management!
- Therefore
— it is BEST not to spend any more time trying to decipher
this rhythm until you have completed your Systematic Approach
for assessment of QRS and ST-T wave morphology!
Descriptive Analysis of the ECG
in Figure-1: Focusing attention on QRS morphology in the 12-lead tracing —
there is GOOD reason for this woman to have presented with syncope and
hypotension!
- Rate
& Rhythm — Sinus tachycardia with what appears to be some complex form
of AV block (Details in a moment! ).
- Intervals — The PR
interval varies (See below). The QRS complex for all beats on
this tracing is narrow. The QTc interval appears to be normal.
- Axis — The mean QRS
axis is normal (about +70 degrees).
- Chamber
Enlargement — None.
Looking
next at Q-R-S-T Changes:
- Q Waves — There is a small, but fairly wide Q
wave in lead III.
One of the 2 complexes in lead aVF appears to have a small Q wave.
- R Wave Progression — Transition occurs normally (here, between leads V3-to-V4).
Regarding ST-T Wave Changes:
- There
is hyperacute ST
elevation in each of the inferior leads!
ST elevation is clearly more marked in lead III compared to lead II. There may
be beginning T wave inversion in lead III, but not yet in other inferior leads.
- There
is mirror-image
(reciprocal) ST depression in lead aVL
when one compares this to the shape
of the ST elevation in lead III. To a
lesser degree — there is also reciprocal ST-T wave depression in lead I.
PEARL #2:
As we have discussed in previous ECG Blogs (most recently in ECG Blog#167) — there is an almost “magic” mirror-image
relationship between leads III and aVL
in many (most) cases of acute inferior MI.
- Otherwise
— there is marked ST depression, that rises to hyperacute T
waves in leads V2, V3 and V4.
- Surprisingly
— there is slight-but-real ST elevation in lead V1 (usually there is no ST elevation in lead V1).
Putting It All
Together: QRS morphology
for the ECG shown Figure-1 is diagnostic of acute
infero-postero
STEMI. Note the following:
- Acute
posterior involvement is diagnosed
by the presence of unexpected ST depression in anterior leads. Anterior leads
show the “mirror-image” of what one expects to see in posterior leads (such
as leads V7, V8, V9). Isn’t the “shelf-like” ST depression rising to
prominent T wave in lead V2 virtually the mirror-image of the
ST elevation + T wave inversion expected with acute MI? (See ECG Blog #80 for application of the “mirror test” for diagnosing posterior
MI).
- The “culprit” artery
(See ECG Blog #80) — is almost certain to be acute RCA (Right Coronary Artery)
occlusion because: i) Statistics (~85%
of patients have a dominant right system — so that acute RCA occlusion is much
more likely than LCx [Left Circumflex]
occlusion to be the cause of inferior MI); ii) ST elevation in
lead III > lead II; iii) there is
marked reciprocal ST depression in lead aVL; and, iv) there is no sign of associated lateral
infarction (ie, no ST elevation in any of the lateral leads).
- NOTE: In addition to
being an anterior lead — lead V1
is also a right-sided
lead. The unexpected finding of ST
elevation in lead V1 tells us that in addition to acute infero-postero
STEMI — there is also acute RV (Right Ventricular) involvement.
- PEARL #3: Most of the time, right-sided leads
will be needed to diagnose acute RV MI. However, when there is definite
ST elevation in lead V1 in a patient with acute inferior MI — this almost
certainly indicates that ST elevation from acute RV MI has cancelled out
the ST depression that you would otherwise have seen in lead V1 from ongoing
posterior MI.
- Recognition
of acute RV MI in association with acute infero-postero MI localizes the
“culprit” artery to the RCA — because the LCx does not
vascularize the right ventricle. This further establishes the proximal RCA
as the “culprit” artery in Figure-1.
- FOLLOW-UP: Cardiac cath confirmed
acute occlusion of the proximal RCA — and, reperfusion was
achieved by stenting this vessel. Presumably, the degree of AV block improved
as the patient recovered (although I’m not privileged to those details).
My Purpose — in presenting this case was 3-fold:
i) This case provides an excellent
example of how to recognize acute OMI (Occlusion-related Myocardial
Infarction) in a patient without chest pain — despite
distraction from the presence of a complex form of AV block; ii) How to assess a complex form of AV block,
such as is evident in Figure-1; — and, iii) How use of a Laddergram
can assist in this assessment.
- As I
have already emphasized — detailed assessment of this rhythm is not
essential for initiating the key priorities of management. I would be
HAPPY — if you simply recognize the presence of a complex form
of AV block — and, that the cause of this arrhythmia and the patient’s
syncope/hypotension is acute OMI in need of immediate cath + reperfusion.
- PEARL #4: Don’t even bother
trying to assess this rhythm unless you are using a pair of calipers. In my opinion — it is virtually impossible
to assess a complex rhythm such as this one without calipers. The
cardiologist who tries to assess complex arrhythmias without using calipers — is
a cardiologist who will miss the diagnosis of many complex
rhythms.
Looking Closer at the Rhythm: While
admittedly not certain about all aspects of the rhythm in Figure-1
— there are a number of Observations
that we can make:
- The rhythm is supraventricular
— since all QRS complexes on this tracing are narrow.
- Using calipers — We can say that Sinus P waves
are present (RED arrows in the long lead II rhythm
strip in Figure-2). This sinus rhythm is fast (ie, sinus
tachycardia) — and fairly (but not completely)
regular. Since it would be unlikely to “miss” occasional P waves — I’ve added
WHITE arrows in Figure-2 where I suspect additional sinus P waves are
located (partially or totally hidden by simultaneously-occurring QRS
complexes).
- In addition to
sinus arrhythmia — there is a phenomenon known as ventriculophasic sinus arrhythmia
— in which severe bradycardia from AV block may cause variation in
the P-P interval. When this happens — the P-P interval that “sandwiches” a
QRS complex tends to be shorter than P-P intervals without enclosed QRS
complexes (thought to be due to better perfusion following cardiac
contraction that occurs just after a QRS). Using calipers verifies the presence of ventriculophasic
sinus arrhythmia in Figure-2.
- There are a
number of consecutively-occurring P waves in Figure-2 that are not
followed by QRS complexes. This suggests that at the least
— there is high-grade
AV block
in this tracing (which I define as AV block in which more than one
sinus P wave in a row fails to conduct despite having adequate
opportunity to conduct).
- The ventricular
rhythm is not regular! This suggests that complete
(3rd-degree) AV block is not likely — since the ventricular
escape rhythm is usually at least fairly regular when AV block is
complete. This defines the rhythm in Figure-2 as high-grade 2nd-Degree
AV block.
PEARL — Common things
are common! In the presence of acute inferior MI (as this patient
has) — AV Wenckebach
is by far (!!!) the most common type of 2nd-Degree AV Block.
- Therefore — whenever
I see acute inferior STEMI with a fast-but-irregular sinus rhythm in
which there are intermittent pauses — I specifically look for Wenckebach conduction.
In my experience — this almost always turns out to be the cause of the
irregularity! (For an example of this — See ECG Blog #55).
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Figure-2: I’ve added ARROWS to indicate definite (and probable)
atrial activity. WHITE arrows indicate where I suspect there are P waves,
albeit hidden by the QRS complex (See text). |
Is there Any Conduction in Figure-2?
As I stated at
the outset — this is a complex rhythm! We’ve already established that
there is high-grade 2nd-degree AV block with numerous non-conducted
P waves. The next step in determining specifics of this rhythm to establish IF
there is any conduction? This is best accomplished by use of a Laddergram (Figure-3):
- NOTE: Although learning to draw laddergrams is challenging (it
literally took me many years to become comfortable doing so! )
— learning to read laddergrams is easy and intuitive! (IF
you would like Review on using Laddergrams — See ECG Blog #69 and
Blog #164).
- The 1st Step in
drawing a laddergram is filling in the Atrial Tier where
you see P waves (Figure-3). Since conduction of the
electrical impulse through the atria is fast (passing over
specialized atrial conduction tracts) — we represent atrial conduction
on a laddergram by a vertical line through the Atrial Tier.
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Figure-3: Step #1 in drawing a laddergram = Filling in the Atrial
Tier where you see P waves. Since conduction of impulse through the
atria is fast — we represent atrial conduction by a vertical line
through the Atrial Tier (See text). |
PEARL #5: You’ll be amazed at how much EASIER it becomes to see
relationships (or lack thereof) between P waves and neighboring QRS
complexes the moment you highlight P waves (RED arrows in Figure-4).
- The EASIEST way
to determine IF there is any conduction in the rhythm you are assessing
— is to see IF there are any identical
PR intervals?
- NOTE — The PR intervals preceding beats #1, 4, 6 and 9 are all
identical. This tells us that these 4 beats must be
conducting. Figure-4 shows how we represent conduction through the AV
node and through the ventricles for these 4 beats. The reason there is a greater
slant (ie, greater angulation) for conduction through the AV Nodal Tier
compared to conduction through the Atria and through the Ventricles — is that
conduction of the electrical impulse is slowest going through the AV
node.
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Figure-4: The PR intervals preceding beats #1, 4, 6 and 9 are identical.
Therefore — these 4 beats must be conducting (See
text). |
Are Any Other Beats Conducted in
Figure-4?
Following
through with the KEY principle that identical PR intervals are unlikely
to be due to chance — We look next at Figure-4 to see IF any other
PR interval duration repeats.
- Caliper
measurement of the PR interval preceding beats #5 and #7 is identical. This
strongly suggests that these 2 beats are also conducted, albeit
with a longer PR interval than for beats #1,4, 6 and 9. We illustrate
this in Figure-5.
- This leaves us
with uncertainty about beats #2, 3 and 8 (QUESTION MARKS in
Figure-5).
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Figure-5: Beats #5 and 7 also appear to be conducting, albeit with a longer
PR interval than for beats #1, 4, 6 and 9 (See text). |
PEARL #6: The longest R-R interval in this rhythm strip is between beats
#2-3. When working with a complex conduction disturbance — unexpected
shortening of the R-R interval often tells you that earlier-than-expected
beats are being conducted!
- I do not know
if beat #3 that terminates the longest R-R interval — is a junctional escape
beat or a sinus-conducted beat. We cannot know this for certain without
additional monitoring …
- However — Since
beats #2 and #8 in Figure-5 are both preceded by an R-R interval that is
shorter than the R-R interval between beats #2-3 — I suspect beats #2 and #8 are
probably conducting!
What then is the
Mechanism of the Rhythm?
At this point
— I admittedly was not sure how to draw in lines
representing conduction of beats #2 and 8 (and possibly also beat #3).
- After pondering
this arrhythmia for longer than I care to admit … — I decided that I
needed to think “out of the box”. (I said this rhythm was complex
… ).
- NOTE — Some forms of AV Wenckebach may exhibit Wenckebach conduction at multiple
levels within the AV Node.
What IF there were 2 Levels of Block within the
AV Node?
The BEST way to
illustrate the concept of a dual-level block within
the AV Node — is by clicking successively on the magnified view of the next 5
Figures. The legends of these Figures describe my ladder problem-solving
approach.
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Figure-6: The horizontal black DOTTED line pictorially represents the initial
(upper) level of block within the AV node. Imagine each
of the sinus impulses reaches this level within the AV node. Our task in
completing this laddergram — will be to connect impulses
at this upper level within the AV node — with the 9 QRS complexes below
that are conducted through the ventricles (which I’ve drawn in the
Ventricular Tier). SUGGESTION: Click on THIS Figure-6 to enlarge this
tracing. Then ADVANCE on your device through the next 4 Figures (ie, Figures
7-thru-10) to BEST appreciate my approach for laddergram problem-solving. |
|
Figure-7: As we have previously deduced — since the PR intervals preceding
beats #1, 4, 6 and 9 are all identical — these beats must
be conducting. I’ve illustrated this by connecting these P waves
preceding beats #1, 4, 6 and 9 — with their respective QRS complexes in the
Ventricular Tier of Figure-7. |
|
Figure-8: I’ve made an assumption that all 9 beats in Figure-8
are conducting. As stated earlier — I can’t rule out the possibility that beat
#3, which is preceded by the longest R-R interval, might represent a junctional
escape beat. But as we’ll see in a minute — a more logical rhythm mechanism can
be postulated by assuming that beat #3 is also being conducted (albeit with
a greatly prolonged PR interval). PEARL #7: Although admittedly not perfectly
symmetric — Isn’t there a pattern of grouped
beats with PR interval lengthening within the 2nd level of block
within the AV Nodal Tier? |
|
Figure-9: Let’s now make the assumption that there is also some form of
Wenckebach conduction at the initial level of block within the AV node.
IF this is so — then there will need to be non-conduction of 1
atrial impulse at the end of each group. I pictorially represent this by
the BUTT ENDs that I have drawn in within the initial level of block in the AV
Nodal Tier. |
|
Figure-10: To complete the laddergram — Let’s make a final assumption
that for those impulses that successfully get through the upper (initial)
level of block in the AV node — that 4 of these impulses fail to make it
through the 2nd (lower) level of block in the AV node (pictorially
represented by the BUTT ENDs drawn within the lower level of block in the AV
Nodal tier of Figure-10). |
BOTTOM LINE: My favorite
quote about complex arrhythmias is by Rosenbaum, who said: “Every
self-respecting arrhythmia has at least 3 possible interpretations”. While
I cannot prove that my interpretation of this complex arrhythmia is the
only correct one — IF you are able to construct a laddergram that makes
sense (as I have done in Figure-10) — then my theory qualifies as
at least one possible mechanism for this complex rhythm. Other
theories from anyone reading this blog are welcome!
- To Emphasize — Deriving a
precise mechanism for this complex arrhythmia (as I propose in Figure-10)
— is not nearly as important as the other TAKE-HOME Points
from this case!
- TAKE-HOME Points from
this Case: What is most
important to appreciate from this case is the following: i) Although this patient did not have chest pain
— she did have other symptoms (ie, syncope; hypotension)
that could be consistent with acute MI; ii) The rhythm is supraventricular — with
lots of sinus P waves, some of which are conducting — and others, which
are not conducting. Therefore, the rhythm represents some form
of 2nd-Degree AV Block; iii) QRS
morphology is diagnostic for an acute STEMI. Management
priorities include prompt activation of the cath lab with the goal of achieving
timely coronary reperfusion; iv) Since
this patient has an acute inferior MI — and, there is
2nd-Degree AV Block with group beating and a narrow QRS
complex — the mechanism of this AV block statistically (ie, over 90%
likelihood) is almost certain to represent some form of AV
Wenckebach (Mobitz I); and, v) Chances are, that IF you are
able to promptly achieve coronary reperfusion (which should be your
highest priority) — that this very complex form of AV Wenckebach will improve,
if not completely resolve.
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Acknowledgment: My appreciation to Wai Shein (from Myanmar) for the case
and this tracing.
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