Welcome to the second session in the ECG review.

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The topics covered in todays session are included on this slide.

We will cover three topic areas, including

1. Axis deviation/bundle branch block

2. Chamber enlargement and hypertrophy
3. Myocardial infarction

For each topic, we will review a small series of ECGs as unknowns with a primary
focus on the pathophysiologic concept relevant to that topic area.

The last section of todays session will be a series of unknown tracings selected
from all topic areas covered in both sessions.

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We will start with bundle branch block and axis deviation.

The learning objectives for this first block are the following:

1. Identify the characteristic patterns associated with bundle branch block

2. Distinguish between the different types of bundle branch block (RBBB, LBBB,
IVCD)
3. Identify the key features of axis deviation and be able to determine if the axis in
any given tracing is normal or abnormal.

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For your reference, we have included a brief summary of some commonly described
features of bundle branch block.

For all types of bundle branch block, a widened QRS complex of 120 msec or longer is
expected.

Location of the block (right bundle, left bundle, or both) will lead to characteristic
patterns that are listed here.

Please note that if you observe a characteristic RBBB or LBBB pattern, but with QRS
duration between 110 and 120 msec, an incomplete bundle branch block is
present.

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Before going into the reasons why certain bundle branch blocks produce
characteristic patterns on the ECG, I would like to start by providing you with a basic
description of the sequence of ventricular depolarization under normal
circumstances. This description is based on a series of slides provided by Dr. P.
Yurchak.

The first part of the ventricles to depolarize is the proximal septum (Phase I).

This is followed by depolarization of the distal septum and the antero-apical

segments of both ventricies (Phase II).

Next, septal depolarization is completed as well as the remaining lateral segments of

both ventricles (Phase III).

Last, the basal segments of both ventricles depolarize (Phase IV).

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This depolarization leads to a series of individual depolarization vectors, here viewed
with respect to the placement of the precordial leads. The QRS complex viewed on
the typical 12-lead ECG is therefore the sum of all of these indivicual vectors.
Because of the time sequence, we observed characteristic notching in certain leads.

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This is a detailed view of the typical QRS complexes viewed in leads V1-V6, on which
the specific phase of ventricular depolarization has been superimposed.

Direction of the depolarization vector with respect to individual leads makes sense
anatomically (septal depolarization toward the anterior precordial leads, away from
the lateral precordial leads, and so forth).

Before we discuss the pattern changes associated with bundle branch block, I would
like to offer a brief description of the normal axis as viewed in the limb leads.

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In the limb leads, these summed vectors lead to an axis between -30 and 90 degrees,
as shown on this diagram.

It is possible to calculate the numerical value of the sum vector from the data
provided on a 12-lead ECG, but we will focus on a much more simple method of
determining whether or not the axis is normal.

This simplified system utilizes the QRS complex in leads I and II.

If the QRS complex is positive in both, the axis is normal.

If the QRS complex is negative in I, right axis deviation is present.

If the QRS complex is negative in II, left axis deviation is present.

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In order to discuss the alterations in ventricular depolarization associated with RBBB,
we will return to our vector-based description of ventricular depolarization.

In RBBB, the initial depolarization still involves the proximal interventricular septum
(Phase I).

Because of block in the RBB, Phase II involves depolarization of mostly the left side of
the interventricular septum and the apico-anterior segment of the left ventricle.

Phase III involves completion of LV depolarization, including the base.

Phase IV then involves depolarization of the right section of the interventricular

septum and the remainder of the right ventricle.

Below this phase diagram is a diagram of the vectors produced in the context of
RBBB, with respect to the precordial leads.

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On this slide, I have included both the vector diagram and a diagram of the QRS
complexes viewed in the anterior precordial leads in which the vector contributions
are labelled.

The largest difference observed here is depolarization of the right ventricle at the end
of the QRS complex, leading to a large R wave in V1 and an S wave in lead V6.

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Difference in the conduction patterns during normal conduction and RBBB are
displayed side-by-side in this diagram.

The first half of the QRS complex is very similar in both the normal and RBBB
circumstances.

In RBBB, the terminal vectors point toward the right ventricle and not the base. This
leads to the characteristic rightward vector viewed in V1 as well as the
complimentary S wave in V6.

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Now that we have covered the physiologic basis for the difference in the
depolarization pattern, we can summarize the changes in the precordial leads that
are characteristic of RBBB.

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We will now move on to LBBB.

Because of a block in the left bundle, the left ventricle is last to depolarize. This leads
to the following sequence of events.

The first tissue to depolarize is in the right side of the interventricular septum and the
antero-apical segment of the RV. This reflects the anatomical insertion site of the
RBB (Phase I).

This is followed by depolarization of the remainder of the RV and interventricular

septum (Phase II).

Then the posterolateral and anterolateral segments of the LV (Phase III and Phave IV).

The altered vector sequence is illustrated at the bottom of the slide.

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The altered vector sequence is displayed here in conjunction with labelled QRS
complexes viewed in the precordial leads.

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The changes from the normal sequence of events are illustrated by this side-to-side
comparison.

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Now that we have an understanding of the alteration of the activation sequence, the
characteristic ECG changes associated with LBBB in the precordial leads make more
sense.

You see here a deep S wave in V1 as well as a broad R wave in V6 (with no Q wave)
that reflect conduction from the RBB first, with depolarization of the lateral aspect of
the LV last.

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This is a comparison of RBBB and LBBB that includes not only the characteristic
features in the precordial leads, but the characteristic features in the limb leads as
well (note lead I in particular).

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As we mentioned, incomplete bundle branch block is defined to be present when the
ECG pattern is typical of RBBB or LBBB but the QRS width is between 110 and 120
msec.

Hemi-block is a different situation, involving block of only one of the two segments of
the left bundle, as shown in this anatomic diagram.

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Hemi-block results in axis deviation.

I have included this slide as a reminder of the cues in the limb leads that will help you
determine axis (as well as right and left axis deviation).

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LAFB results in terminal depolarization of the antero-lateral aspect of the LV, resulting
in left axis deviation.

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LPFB results in terminal depolarization of the distal interventricular septum and
posterior LV, leading to right axis deviation.

Note that this is less frequently encountered due to the dual blood supply received by
the posterior fascicle.

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This slide summarizes the anatomic basis for the changed depolarization sequence
for LAFB and LPFB and the associated changes in the limb leads.

Note that the LAFB and LPFB sequences will not lead to the ECG changes
characteristic for LBBB in the precordial leads.

RBBB may be present simultaneously, so care should be taken when viewing ECGs
with RBBB to determine if there is evidence of simultaneous block of the LAFB or
LPFB.

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Normal axis as the QRS complexes in I and II are upright.

Other noteworthy features include sinus bradycardia (rate 50 bpm) with 1st degree AV
block.

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LBBB is present qS in V1, broad/notched R in V6, no Q wave in lead I.

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There is evidence of left axis deviation in this ECG (QRS positive in I, negative in II).

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The learning objectives for this first block are the following.

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This four-chamber view of the heart displays key segments of the cardiac conduction
system, including the SA and AV nodes.

Atrial depolarization originates in the RA. Although the depolarization front moves
rapidly to the LA, note that the RA still depolarizes slightly before the LA.

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Consequently, the first segment of the P wave is the result of RA depolarization and
the second segment is the result of LA depolarization.

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This table highlights the contributions of the RA and LA depolarization to the
observed P wave in the context of normal atria, right atrial enlargement, and left
atrial enlargement.

Some relevant definitions are included: right atrial enlargement for P wave >2.5mm in
lead II (P pulmonale), left atrial enlargement for a greater than 40 msec spread
between peaks in the P wave (P mitrale).

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ECG criteria for LA enlargement also include size of the terminal segment of the P
wave in leads V1 (> 40 msec in duration, greater than 1mm in depth).

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Evidence of LA enlargement in both lead II and V1

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Evidence of RA enlargement in lead II.

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In order to describe the ECG changes that accompany LVH, it is helpful to revisit the
normal propagation of the wavefront in the ventricles.

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With an increased mass of the ventricle (either RV or LV), the amplitude of the QRS
complex will increase.

Depolarization is not the only phenomenon affected: changes in the repolarization of

the hypertrophied ventricle are often reflected in ST and T wave changes also.

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Presence of ventricular hypertrophy is not typically determined by a single, standard
set of criteria. There are a number of analysis tools present, each with their own
sensitivities and specificities.

This slide contains a recommended set of tools that you can use as a reference.

Note that determining the presence or absence of ventricular hypertrophy will often
be an integrative assessment.

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Left ventricle:

Cornell voltage criteria satisfied and there is evidence of a strain pattern in the
precordial leads.

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Right ventricle:

Tall R wave in lead V1

Right axis deviation

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The third section involves the characteristic ECG patterns associated with myocardial
infarction.

The learning objectives of this session are listed.

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Depolarization changes associated with MI include formation of Q waves acutely.

If a baseline ECG is available, presence/evolution of these Q waves can be tracked.

In those patients in whom dynamic changes are not observed (or when you are
observing the consequences of an MI after the event has passed), Q waves are
deemed to be pathological if the following criteria are satisfies:
-Greater than 40 msec wide, greater than 1mm deep
-Or, Q wave whose depth is at least 25% of the amplitude of the associated QRS
complex

Q waves will be observed in the leads that are closest to the affected territory.

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Repolarization changes are also affected by acute MI, and include either depression
or elevation of the ST segment. Elevation of the ST segment is typically associated
with a larger territory of injury (previously termed as transmural).

Significant ST elevations are by definition greater than 1mm in elevation and are
present in at least two adjoining leads

As with Q waves, the leads in which ST elevations are observed are typically the leads
closest to the affected territory. In fact, ST elevations are typically used as a reliable
guide to determine the affected wall/coronary vessel.

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T wave changes are also observed in the context of acute injury. T waves are typically
concordant with the QRS complex, but may become discordant or inverted in the
context of an acute infarction. Location of T wave inversions is a good indicator for
the location of the infarct, but is not considered as good as ST elevation.

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Infarct localization can be determined using Q waves, ST elevations, and T wave
inversions.

This diagram shows the surfaces of the heart in a right sagittal view, along with some
of the leads that can be used as references. Note that the posterior wall does not
have overlying leads in the standard configuration and may require application of
additional leads in appropriate clinical situations.

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This slide illustrates the concept of reciprocal ST segment changes in an acute MI.

In the upper part of this slide, an anterior MI with evidence Q wave and ST elevation
in an overlying precordial lead are shown.

In the lower part of this slide, a posterior MI is shown. This is manifest as ST

depressions in the precordial leads, but a lead applied to the posterior wall of the
chest will reveal ST elevations.

Note that if an ST elevation marks the location of an infarct, ST depressions may be

visible in the leads overlying the opposite wall.

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Location of ST elevations can assist in determining which wall of the heart is affected.
This, in turn, can provide a pointer toward the coronary vessel most likely to be
implicated.

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This slide of the ECG changes associated with anterior and inferior infarcts
summarizes two concepts: reciprocal changes observed with infarction and the
evolution of the ECG changes with time after the acute event.

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ST elevations and Q waves in the inferior limb leads with reciprocal ST depressions in
the precordial leads.

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ST elevations and Q waves in the precordial leads with reciprocal ST depressions in
the inferior limb leads.

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Look at Q wave in inferior leads, tall R wave in V2 could be IPMI but more
information is required. Posterior leads may help, as may historical data and
laboratory data.

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ST elevations of comparable height across multiple leads in a non-coronary
distribution are highly suggestive of pericarditis.

Also note the upward sloping (concave) ST segments, which are reassuring (as distinct
from the convex/tombstone ST segments suggestive of MI)

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This is a general review, and is also a good opportunity for the students to ask any
topic-specific questions that remain.

End by referring the students to the available resources for ongoing study.

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These sessions build upon material that you have already seen as part of the
Homeostasis I course. You will therefore see some familiar material, especially during
todays session.

These sessions are but an introduction to ECG analysis. We know that your study of
the topic will continue throughout your training.

In order to facilitate future study, these sessions reference other resources available
at HMS.

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rate: 17*6
rhythm:
intervals: OK
axis: OK

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 Q in II, II, aVF, 4,5,6
Atrial fibrillation irreg irreg QRS
Moderate ventricular response
Evidence of CAD: Q waves in inferior limb leads and lateral precordial leads

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 subtle RsR'
interventric
conduction
delay...
looks like RBBB
but not quite wide
enough @ QRS

less happy STs

right axis dev---I is neg "scoopy happy"

ST area...might
make you think
it's not concering,
but still w/ST
elev, send to cath
lab

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Sinus rhythm
Lateral myocardial infarction with ST elevations, no Q waves
Right axis deviation

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 is this LBBB?
right dev so
posterior LPFB

is there a P buried
here?

Rate: brady--54 another

immediate drop
Clustered beats? and then resets

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Sinus rhythm
Second degree AV block (Wenckeback/Mobitz I)
RBBB

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2:1 block...atria @ 300
ventricle @ 150

this is NOT irreg irreg

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 Atrial flutter with rate of 300 bpm
Variable AV conduction

side note: 3 or more dif p-wave morphologies=

multifocal a-tach "wandering atrial pacemaker"
WAP

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Sinus rhythm
Left atrial enlargement (suggestive of underlying LVH)
LBBB

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Normal sinus rhythm
LVH by voltage criteria, strain pattern is also present

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Normal sinus rhythm
Complete heart block with junctional escape rhythm (calculate the rate)
Ventriculophasic variation in P-P intervals

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AF with moderate ventricular response
RBBB
Left axis deviation suggesting LAFB
Second-to-last beat on the tracing is a PVC

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Normal sinus rhythm
Long QT interval

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Right ventricular hypertrophy: tall R wave in V1, right axis deviation, NS ST TWA in
anterior precordial leads
Peaked P waves in lead II consistent with RA enlargement
Also with evidence of LA enlargement in lead V1

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