Ecg Utah Edu
Ecg Utah Edu
Ecg Utah Edu
INTERPRETATION
V9.0 (2016)
Frank G. Yanowitz, MD
Professor of Medicine
University of Utah School of Medicine
Director, IHC ECG Services
LDS Hospital & Intermountain Medical Center
Salt Lake City, Utah
[email protected]
Dedicated To:
INTRODUCTION
This booklet is dedicated to the memory of Alan E. Lindsay, MD (1923-1987) master
teacher of electrocardiography, friend, mentor, and colleague. Many of the excellent
ECG tracings illustrated in this learning program are from Dr. Lindsay's personal
collection of ECG treasures. For many years these ECG's have been used in the training of
medical students, nurses, housestaff physicians, cardiology fellows, and practicing
physicians in Salt Lake City, Utah as well as at many regional and national medical
meetings.
2012 Intermountain Healthcare. All rights reserved.
The materials presented in the Introduction to ECG Interpretation Booklet are for your information only. All of the
materials are provided "AS IS" and without any warranty, express, implied or otherwise, regarding the materials'
accuracy or performance. You accept all risk of use of, and reliance on, the materials contained in the Booklet.
TABLE OF CONTENTS
1. The Standard 12 Lead ECG (p. 4)
In 2001 a joint committee of the American College of Cardiology and the American Heart
Association published a list of ECG diagnoses considered to be important for developing
basic competency in ECG interpretation. This list is illustrated on the following page and
is also illustrated on the website with links to examples or illustrations of the specific
ECG diagnosis. Students of electrocardiography are encouraged to study this list and
become familiar with the ECG recognition of these diagnoses. Most of the diagnoses are
illustrated in this document.
Normal ECG
TECHNICAL PROBLEM
Lead misplaced
Artifact
SINUS RHYTHMS/ARRHYTHMIAS
Sinus rhythm
Sinus tachycardia
Sinus bradycardia
Sinus arrhythmia
Sinus arrest or pause
Sinoatrial block, type I
Sinoatrial block, type II
OTHER SV ARRHYTHMIAS
PAC's (nonconducted)
PAC's (conducted normally)
PAC's (conducted with aberration)
Ectopic atrial rhythm or tachycardia (unifocal)
Multifocal atrial rhythm or tachycardia
Atrial fibrillation
Atrial flutter
Junctional prematures
Junctional escapes or rhythms
Accelerated Junctional rhythms
Junctional tachycardia
Paroxysmal supraventricular tachycardia
VENTRICULAR ARRHYTHMIAS
PVC's
Ventricular escapes or rhythm
Accelerated ventricular rhythm
Ventricular tachycardia (uniform)
Ventricular tachycardia (polymorphic or torsade)
Ventricular fibrillation
AV CONDUCTION
INTRAVENTRICULAR CONDUCTION
HYPERTROPHY/ENLARGEMENTS
Interior MI
Inferoposterior MI
Inferoposterolateral MI
Posterior MI
Anteroseptal MI
Anterior MI
Anterolateral MI
Extensive anterior MI
High lateral MI
Non Q-wave MI
Right ventricular MI
CLINICAL DISORDERS
PACEMAKER ECG
Atrial-paced rhythm
Ventricular paced rhythm
AV sequential paced rhythm
Failure to capture (atrial or ventricular)
Failure to inhibit (atrial or ventricular)
Failure to pace (atrial or ventricular)
Behold: Einthoven's Triangle! Each of the 6 frontal plane or "limb" leads has a negative
and positive pole (as indicated by the '+' and '-' signs). It is important to recognize that
lead I (and to a lesser extent aVL) are right -to- left in direction. Also, lead aVF (and to a
lesser extent leads II and III) are superior -to- inferior in direction. The diagrams on page 6
further illustrate the frontal plane and chest lead hookup.
Note: the actual ECG waveform in each of the 6 limb leads varies from person to person
depending on age, body size, gender, frontal plane QRS axis, presence or absence of
heart disease, and many other variables. The precordial lead sites are illustrated below.
2. RHYTHM ANALYSIS:
State the basic rhythm (e.g., "normal sinus rhythm", "atrial fibrillation", etc.)
Identify additional rhythm events if present (e.g., "PVC's", "PAC's", etc)
Remember that arrhythmias may originate in the atria, AV junction, and ventricles
3. CONDUCTION ANALYSIS:
4. WAVEFORM DESCRIPTION:
Carefully analyze each of the12-leads for abnormalities of the waveforms in the order
in which they appear: P-waves, QRS complexes, ST segments, T waves, and. Don't
forget the U waves.
P waves: are they too wide, too tall, look funny (i.e., are they ectopic), etc.?
QRS complexes: look for pathologic Q waves, abnormal voltage, etc.
ST segments: look for abnormal ST elevation and/or depression.
T waves: look for abnormally inverted T waves or unusually tall T waves.
U waves: look for prominent or inverted U waves.
5. ECG INTERPRETATION:
This is the conclusion of the above analyses. Interpret the ECG as "Normal", or
"Abnormal". Occasionally the term "borderline" is used if unsure about the
significance of certain findings or for minor changes. List all abnormalities.
Examples of "abnormal" statements are:
HR=67 bpm; PR=0.18 s; QRS=0.09 s; QT=0.40 s; QRS axis = -50 (left axis
deviation)
Normal sinus rhythm; normal SA, AV, and IV conduction; rS waves in leads II,
III, aVF (this means small r waves and large S waves); SIII > SII
Interpretation: Abnormal ECG: 1) Left anterior fascicular block (see p.16)
If there is a previous ECG in the patient's file, the current ECG should be compared
with it to see if any significant changes have occurred. These changes may have
important implications for clinical management decisions.
First find an isoelectric lead if there is one; its the lead with equal QRS forces in
both positive and negative direction (i.e., above and below the baseline). Often this
is also the lead with the smallest QRS complex.
The correct QRS axis is perpendicular (i.e., right angle or 90 degrees) to that lead's
orientation (see above diagram).
Since there are two possible perpendiculars for each isoelectric lead, one must chose
the one that best fits the direction of the QRS forces in other ECG leads.
Isoelectric
Lead
I
II
III
aVR
aVL
aVF
+90
-30
+30
-60
+60
0
-90
+150
-150
+120
-120
+/-180
If there is no isoelectric lead, there are usually two leads that are nearly isoelectric,
and these are always 30 apart on the diagram. Find the perpendiculars for each
lead and chose an approximate QRS axis within the 30 range.
Occasionally each of the 6 frontal plane leads is small and/or isoelectric. An axis
cannot be determined and is called indeterminate. This is a normal variant.
Lead aVF is the isoelectric lead (note: equal forces positive and negative).
The two perpendiculars to aVF are 0 and 180.
Note that Lead I is all positive (i.e., moving to the left).
Therefore, of the two choices, the axis has to be 0.
10
Analysis
1.
2.
3.
4.
5.
Analysis
1.
2.
3.
4.
Lead aVR is closest to being isoelectric (but slightly more positive than negative)
The two perpendiculars to aVR are -60 and +120.
Note that Lead I is mostly negative; lead III is mostly positive.
Therefore the axis is close to +120. Because aVR is slightly more positive, the axis is
slightly beyond +120 (i.e., closer to the positive right arm for aVR, ~ +125)
5. The differential diagnosis of RAD is listed on p16.
11
12
The ST segment is often elevated above baseline in leads with large S waves
(e.g., V2-3), and the normal configuration is concave upward. ST segment
elevation with concave upward appearance may also be seen in other leads;
this is called the early repolarization pattern, and is often seen in young,
male athletes (see an example of "early repolarization" in leads V4-6 in the
ECG below). J-point elevation is often accompanied by a small J-wave in the
lateral precordial leads. The physiologic basis for the J-wave is related to
transient outward K+ current during phase I of the epicardial and midmyocardial cells, but not present in the subendocardial cells. Prominent J
waves can also be seen in hypothermia (aka: Osborn waves)
13
14
Normal QT is heart rate dependent (upper limit for QTc = 0.46 sec)
Long QT Syndrome: LQTS (based on corrected QTc: QTc 0.45 sec for
males and 0.46 sec in females is diagnostic for hereditary LQTS in the
absence of other causes of long QT):
This abnormality may have important clinical implications since it usually
indicates a state of increased vulnerability to malignant ventricular
arrhythmias, syncope, and sudden death. The prototype arrhythmia of the
Long QT Interval Syndromes (LQTS) is Torsade-de-pointes, a polymorphic
ventricular tachycardia characterized by varying QRS morphology and
amplitude around the isoelectric baseline. Causes of LQTS include the
following:
Drugs (Class I and III antiarrhythmics, tricyclics, phenothiazines,
and many others)
Electrolyte abnormalities ( K+, Ca++, Mg++)
CNS insults (especially subarachnoid hemorrhage, stroke, head
trauma)
Hereditary LQTS (at least 7 genotypes are now known)
Coronary Heart Disease (some post-MI patients)
Cardiomyopathy
15
Right Axis Deviation (RAD): > +90 (i.e., lead I is mostly 'negative')
causes of right heart overload; these will also give same ECG picture
of LPFB)
Many causes of right heart overload and pulmonary hypertension
High lateral wall MI with Qr or QS complex in leads I and aVL
Some cases of RBBB
Some cases of WPW syndrome
Children, teenagers, and some young adults
Bizarre QRS axis: +150 to -90 (i.e., lead I and lead II are both
negative)
First, consider a limb lead error (usually right and left arm reversal)
Dextrocardia
Some cases of complex congenital heart disease (e.g., transposition)
Some cases of ventricular tachycardia
16
17
Single
Events
Sinus
Atria
Slow Rates
(<50 bpm)
Intermediate
Rates
(50-99 bpm)
Sinus
bradycardia
Sinus tachycardia
Paroxysmal SVT,
Atrial fibrillation,
Atrial flutter (2:1 block),
Ectopic atrial
tachycardia,
Multifocal atrial
tachycardia
PACs
AV Junction
(AVN, His)
PJCs
J- escape
beats
J- escape
rhythm
(~40-50 bpm)
Accelerated
J- rhythm
(~55-100 bpm)
Junctional tachycardia,
Paroxysmal SVT:
AVNRT,
AVRT (WPW)
Ventricles
(Wide QRS)
PVCs
V-escape
beats
V- escape
rhythm
(~35-45 bpm)
aka:
Idioventricular
Rhythm
Accelerated
V- rhythm
(~50-100 bpm)
Ventricular tachycardia,
Torsade de points,
Ventricular fibrillation
19
In the ladder diagram (p19), labeled 2, the cycle length has increased (i.e.,
heart rate is slower). This results in increased refractoriness in all the ventricular
conducting pathways. PAC 'b' now can't get through the AV node and is
nonconducted; PAC 'c' is now blocked in the right bundle branch and results in
a RBBB QRS complex (aberrant conduction); PAC 'd' occurs later and conducts
normally. RBBB aberration is generally more common because the right bundle
normally has a slightly longer refractory period (RP) than the left bundle. In
diseased hearts, however, either bundle branch or a left bundle fascicle may
have the longest RP and account for the particular aberration in QRS waveform.
The pause after a PAC is usually incomplete; i.e., the PAC can enter the sinus
node and reset its timing, causing the next sinus P to appear earlier than
expected. (PVCs, on the other hand, are usually followed by a complete pause
because the PVC usually does not disrupt the sinus node timing; see the next
ECG rhythm strip (p21) and the diagram on p29.)
20
Incomplete pause: The sinus PP interval surrounding the above PAC is less than
2 preceding normal PP intervals (because the PAC reset the sinus timing)
Complete pause: The PP interval surrounding the above PVC is equal to 2
normal PP intervals because the sinus continued to fire at its regular rate even
though it didnt conduct to the ventricle (see the sinus P hidden in the T wave of the
PVC).
21
Atrial activity is poorly defined; may see course or fine baseline undulations (wiggles)
or no atrial activity at all. If atrial activity is seen, it resembles the teeth on an old
saw (when compared to atrial flutter that often resembles a new saw or a clean
saw-tooth pattern especially in leads II, III, and aVF).
Ventricular response (RR intervals) is irregularly irregular and may be fast (HR
>100 bpm, indicates inadequate rate control), moderate (HR = 60-100 bpm), or
slow (HR <60 bpm, indicates excessive rate control medication, AV node disease, or
AV nodal blocking drugs including beta blockers and digoxin). Recent studies indicate
that resting HRs <110 bpm may be tolerated in atrial fibrillation, although not
optimal.
A regular ventricular response with A-fib usually indicates high grade or complete AV
block with an escape or accelerated ectopic pacemaker originating in the AV junction
or ventricles (i.e., consider digoxin toxicity or AV node disease). In the ECG shown
below the last 2 QRS complexes are junctional escapes indicating high-grade AV block
due (note: the last two RR intervals are the same indicating the escape rate).
22
Atrial flutter with variable HR response (note also LVH and left anterior fascicular block, LAFB)
Untreated A-flutter often presents with a 2:1 A-V conduction ratio. This a commonly
missed arrhythmia diagnosis because the all the flutter waves are often difficult to find.
Therefore, always think "atrial flutter with 2:1 block" whenever there is a
regular SVT @ approximately 150 bpm! (You arent likely to miss it if you look for it.)
In the 12-lead ECG shown above varying ratios are seen.
The ventricular response may be 2:1, 3:1 (rare), 4:1, or variable depending upon AV
conduction properties. A-flutter with 2:1 block is illustrated in the rhythm strip below;
one of the flutter waves occurs at the end of the QRS (pseudo RBBB pattern). Atrial
rate =280 bpm, ventricular rate =140 bpm.
Ectopic, discrete looking, unifocal P' waves with atrial rates <250/min (not to be
confused with slow atrial flutter).
Ectopic P' waves usually precede QRS complexes with P'R interval < RP' interval (i.e.,
not to be confused with paroxysmal supraventricular tachycardia with retrograde P
waves shortly after the QRS complexes).
23
The above ECG begins with a sequence of 3 sinus beats followed a PVC and
one more sinus beat; after this last sinus beat note the onset of an ectopic
atrial tachycardia (HR >100 bpm) and different P wave morphology).
Ventricular response may be 1:1 (as above ECG) or with varying degrees of
AV block (especially in the setting of digoxin toxicity).
Ectopic atrial rhythms are similar to ectopic atrial tachycardia, but with HR <
100 bpm. The ectopic P wave morphology is clearly different from the sinus
P wave.
Discrete, multifocal P waves occurring at rates of 100-250/min and with varying P'R
intervals (one usually sees at least 3 different P wave morphologies in a given lead).
Ventricular response is irregularly irregular (i.e., often confused with A-fib).
May be intermittent, alternating with periods of normal sinus rhythm.
MAT is seen most often in elderly patients with chronic or acute medical problems such
as exacerbation of chronic obstructive pulmonary disease.
If the atrial rate is <100 bpm, call it multifocal atrial rhythm.
MAT: Look at lead V1 for discrete multifocal conducted and nonconducted P waves, and how
other leads resemble atrial fibrillation (e.g., leads aVL and V4)
24
sudden, usually initiated by a premature beat, and the arrhythmia also stops abruptly - which
is why they are called paroxysmal tachycardias. They are usually narrow-QRS tachycardias
unless there is preexisting bundle branch block (BBB) or aberrant ventricular conduction (i.e.,
rate related BBB). There are several types of PSVT depending on the location of the reentry
circuit. The diagram below illustrates the mechanism for AV nodal reentrant tachycardia
(AVNRT), the most common form of PSVT.
25
The above ECG begins with 2 sinus beats followed by PAC (black arrow) that initiates the
onset of PSVT. Retrograde P waves (red arrow) immediately follow each QRS (seen as a
little dip at onset of ST segment resembling a pseudo r )
If an early PAC is properly timed, AVNRT results as seen in the diagram on p25. Rarely,
an atypical form of AVNRT occurs with the retrograde P wave appearing in front of the
next QRS (i.e., RP' interval > 1/2 the RR interval), implying antegrade conduction down
the faster alpha, and retrograde conduction up the slower beta pathway.
This type of PSVT can also occur in the absence of the typical WPW pattern if the
accessory pathway only allows conduction in the retrograde direction (i.e.,
concealed WPW). Like AVNRT, the onset of PSVT is usually initiated by a PAC that
finds the bypass track temporarily refractory, conducts down the slower AV junction
into the ventricles, and reenters the atria through the bypass track. In this type of
PSVT retrograde P waves usually appear shortly after the QRS in the ST segment
(i.e., RP' < 1/2 RR interval). Rarely the antegrade limb for this PSVT uses the bypass
track, and the retrograde limb uses the AV junction; the PSVT then resembles a wide
QRS tachycardia and must always be differentiated from ventricular tachycardia.
Sino-Atrial Reentrant Tachycardia: This is a rare form of PSVT where the reentrant
circuit is between the sinus node and the right atria. The ECG looks just like sinus
tachycardia, but the tachycardia is paroxysmal; i.e., it starts and ends abruptly.
Junctional Escape Beats: These are passive, protective beats originating from
subsidiary pacemaker cells in the AV junction. The pacemaker's basic firing rate is 40-60
bpm; junctional escapes are programmed to occur whenever the primary pacemaker
(i.e., sinus node) defaults or the AV node blocks the atrial impulse from reaching the
ventricles. The ECG below shows marked sinus arrhythmia with two junctional escapes
(arrows). Incomplete AV dissociation is also seen during the junctional escapes.
26
27
In the above diagram A illustrates single PVCs and PVC couplets; B illustrates interpolated
PVCs (sandwiched between 2 regular sinus beats without a pause; the PR interval after the PVC
is prolonged because the PVC retrogradely enters the AV junction slowing the subsequent
antegrade sinus conduction); C illustrates late or end-diastolic PVCs with and without fusion.
PVCs may occur early in the cycle (R-on-T phenomenon), after the T wave, or late in the cycle often fusing with the next QRS (called a fusion beat; see 2nd PVC in C above). R-on-T PVCs may
be especially dangerous in acute ischemic settings, because the ventricles are more vulnerable to
ventricular tachycardia or fibrillation. In the ECG strip below, late (end-diastolic) PVCs are
illustrated with varying degrees of fusion. For fusion to occur the sinus P wave must have
entered the ventricles to begin the ventricular activation sequence. Before ventricular activation is
completed, however, the "late" PVC occurs, and the resultant QRS looks a bit like the normal
QRS, and a bit like the PVC; i.e., a fusion QRS (see arrows). Also, see the second PVC with
fusion in strip C above.
28
The events following a PVC are also of interest. Usually a PVC is followed by a complete
compensatory pause, because the sinus node timing is usually not interrupted by the PVC; one
sinus P wave occurs in the ST-T of the PVC and cant get to the ventricles because the ventricles
are refractory after the PVC; the next sinus P wave occurs on time based on the basic sinus
frequency. In contrast, PACs are usually followed by an incomplete pause because most PACs
can reset the sinus node timing; this enables the next sinus P wave to appear earlier than
expected. These concepts are illustrated in the diagram below as well as in the example on p21.
Not all PVCs are followed by a pause. If a PVC occurs early enough (especially when the sinus
rate is slow), it may appear sandwiched between two normal sinus beats. These PVCs are
called interpolated PVCs as discussed on p28. The sinus P wave following the PVC usually has
a longer PR interval because of retrograde concealed conduction by the PVC into the AV junction
slowing subsequent conduction of the sinus impulse (see B on p28).
Rarely a PVC may retrogradely conduct all the way back to the atria and reset the sinus node
timing resulting in an incomplete pause. Often the retrograde P wave can be seen hiding in the
ST-T wave of the PVC.
A most unusual post-PVC event occurs when retrograde activation of the AV junction (or atria)
re-enters (or comes back to) the ventricles as a ventricular echo. This is illustrated below. The
"ladder" diagram under the short ECG strip helps us understand the mechanism. The P wave
following the PVC is the next sinus P wave, but the PR interval is too short for it to have caused
the next QRS. (Remember, the PR interval following an interpolated PVC is usually longer than
normal, not shorter!). The PVC must have conducted retrogradely into the AV junction (but not
the atria) and then reentered the ventricles resulting in a normal QRS complex (e for ventricular
echo). Note the timing of the sinus P waves is not interrupted. Amazing, isnt it?
29
PVCs usually stick out like "sore thumbs" or funny-looking-beats (FLBs), because they are wide
and bizarre in appearance compared to the normal QRS complexes. However, not all premature
sore thumbs are PVCs. In the example below 2 PACs are seen: #1 has a normal QRS, and #2
has RBBB aberrancy - which looks like an FLB. The challenge, therefore, is to differentiate
sore thumbs for what they are or are not; that's the next topic for discussion!
30
Before we can understand aberrant ventricular conduction we must first review how normal
conduction of the electrical impulse occurs in the heart (Figure 1). What a magnificent
design! Impulses from the fastest center of automaticity (SA node) are transmitted through the
atria and over specialized fibers (Bachmanns bundle to the left atrium and three inter-nodal
tracts) to the AV node. The AV node provides sufficient conduction delay to allow atrial
contraction to contribute to ventricular filling. Following slow AV node conduction high velocity
conduction tracts deliver the electrical impulse to the right and left ventricles (through the His
bundle, bundle branches and fascicles, and into the Purkinje network). Simultaneous activation
of the two ventricles results in a NARROW, NORMAL QRS COMPEX (0.06-0.1 sec QRS
duration). Should conduction delay or block occur in one of the two bundle branches an
ABNORMAL WIDE QRS COMPLEX will be the result of sequential activation of the ventricles.
(A delay or block in a fascicle of the left bundle branch will also result in an abnormal QRS that is
not necessarily a wide QRS but of a QRS of different shape (e.g., a change in frontal plane QRS
axis) from the persons normal QRS morphology).
Figure 1 (note the left bundle branch also has a middle, or septal fascicle not shown
in the figure)
Figure 2 below illustrates a basic principle of AVC. AVC is a temporary alteration of QRS
morphology when you would have expected a normal QRS complex. Permanent bundle branch
block (BBB) is NOT AVC.
In this discussion we will concentrate on AVC through normal bundle branch and fascicular
pathways and not consider conduction through accessory pathways (e.g., as in WPW syndrome).
The ECG illustrated in Figure 2 from lead V1 shows two normal sinus beats followed by a
premature atrial complex (PAC, first arrow). The QRS complex of the PAC is narrow resembling
the normal QRS morphology of the sinus beats. After an incomplete pause, another sinus beat is
followed by a slightly earlier PAC. Now, because of this slightly increased prematurity (and the
longer preceding RR cycle), the QRS morphology is wide and different (rsR morphology of
RBBB). One who is not careful might mistake this wide funny looking beat (FLB) as a PVC and
attach a different clinical significance (and therapy). The diagram and examples on p19-20 also
illustrate the different fates of PACs. The key clues to recognizing AVC in Figure 2 are:
1. Finding the premature P-wave (P) or Cherchez le P (in French)
2. Recognizing the typical RBBB QRS morphology (rsR in lead V1)
31
Lead V1
Figure 2
ABERRANT VENTRICULAR CONDUCTION
A term that describes a temporary alteration of QRS morphology under conditions
where a normal QRS might be expected. The common types are:
1. Through normal conduction pathways:
Cycle-length dependent (Ashman phenomenon)
Rate-dependent tachycardia or bradycardia
2. Through accessory pathways (e.g., Kent bundle)
Five features or clues help identify AVC of the right bundle branch block variety, the most
common form. It should be emphasized that although RBBB morphology is the commonest form
of AVC, LBBB or block of one of its three fascicles may also occur, particularly in persons with
more advanced left heart disease or those taking cardiovascular drugs. In healthy people the
right bundle branch has a slightly longer refractory period than the left bundle at normal heart
rates and, therefore, is more likely to be unavailable when an early PAC enters the ventricles.
The second-in-a row phenomenon will be illustrated later in this section.
FEATURES FAVORING RBBB ABERRANT CONDUCTION
1. Preceding atrial activity (premature P wave)
2. rSR or rsR morphology in lead V1
3. qRs morphology in lead V6
4. Same initial r wave as normal QRS complex (in lead V1)
5. Second-in-a-row phenomenon
The Ashman Phenomenon is named after the late Dr. Richard Ashman who first described, in
1947, AVC of the RBBB variety in patients with atrial fibrillation. Ashman reasoned, from
observing ECG rhythms in patients with a-fib, that the refractory period (during which conducting
tissue is recovering and cannot be activated) was directly proportional to the cycle length or
heart rate. The longer the cycle length (or slower the heart rate) the longer the refractory period
is. In Figure 3 below a premature stimulus (PS) can be normally conducted if the preceding cycle
length is of short or medium duration but will be blocked if the preceding cycle length is long.
Ashman observed this in atrial fibrillation when long RR cycles were followed by short RR cycles
and the QRS terminating the short RR cycle was wide in duration (looking like RBBB).
Look at the ECG rhythm strips in Figure 3. Simultaneous Lead II and Lead V1 are recorded. The
first PAC (first arrow in V1) conducts to the ventricles with a normal QRS because the preceding
cycle was of normal or medium length. The second PAC (next arrow) conducts with RBBB (rsR
in V1) because the preceding cycle was LONGER. Both PACs have identical coupling intervals
from the preceding sinus P wave. Thus, a long cycle-short cycle sequence often leads to AVC.
Unfortunately this sequence helps us UNDERSTAND AVC but is not DIAGNOSTIC OF AVC.
32
PVCs may also occur in a long cycle-short cycle sequence. It is important, therefore, to have
other clues to the differential diagnosis of funny looking QRS beats (FLBs).
Figure 3
Years ago Dr. Henry Marriott, a master teacher of electrocardiography and author of many
outstanding ECG textbooks offered valuable guidelines regarding aberrant QRS morphologies
(especially in lead V1). These morphologies contrasted with the QRS complexes often seen with
PVCs and enhanced our ability to diagnose AVC. For example, if the QRS in lead V1 is
predominately up-going or positive (Figure 4) the differential diagnosis is between RBBB
aberrancy and ventricular ectopy usually originating in the left ventricle. A careful look at each of
the 5 QRS morphologies in Figure 4 will identify the Las Vegas betting odds of making the
correct diagnosis.
Figure 4
QRS #1 and #2 are classic RBBB morphologies with rsR or rSR triphasic QRS shapes. When
either of these is seen in a V1 premature beat we can be at least 90% certain that they are
33
aberrant RBBB conduction and not ventricular ectopy. Examples #3 and #4 are notched or
slurred monophasic R wave QRS complexes. Wheres the notch or slur? Think of rabbit ears. If
the notch or slur is on the downstroke of the QRS (smaller right rabbit ear in Example #4),
then the odds are almost 100-to-1 that the beat is a left ventricular ectopic beat (or PVC). If, on
the other hand, the notch or slur is on the upstroke of the QRS (smaller rabbit ear on the left in
Example #3), than the odds are 50:50 and not helpful in the differential Dx. Finally if the QRS
complex has just a qR configuration (Example #5) than the odds are reasonably high that the
beat in question is a left ventricular ectopic beat and not AVC. Two exceptions to this last rule
(#5) need to be remembered. Some normal ECGs do not have an initial little r-wave in the QRS
of lead V1 (i.e., just a QS morphology). If RBBB occurs in such a person the QRS morphology in
V1 will be a qR instead of an rsR. Secondly, in a person with a previous anterior or anteroseptal
infarction the V1 QRS often has a QS morphology, and RBBB in such a person will also have a qR
pattern.
Now consider mostly down-going or negative wide QRS morphologies in lead V1 (Figure 5). Here
the differential diagnosis is between LBBB aberration (Example #1) and right ventricular ectopy
(Example #2). Typical LBBB in lead V1 may or may not have a thin initial r-wave, but will
always have a rapid descending S-wave as seen in #1. On the other hand any one of three
features illustrated in #2 is great betting odds that the beat in question is of ventricular origin
and not AVC. These three features are: 1) fat initial r-wave, 2) notch or slur in the descending
limb of the S wave, and 3) a 0.06 sec or more delay from the beginning of the QRS to the nadir
of the S wave.
Figure 5
Figure 6
34
Now, lets look at some real ECG examples of the preceding QRS morphology rules. We will
focus on the V1 lead for now since it is the best lead for differentiating RBBB from LBBB, and
right ventricular ectopy from left ventricular ectopy.
Figure 6 (above) illustrates two premature funny-looking beats (FLBs) for your consideration.
FLB A has a small notch on the upstroke of the QRS complex resembling #3 in Figure 4.
Remember, thats only a 50:50 odds for AVC and therefore not helpful in the differentiating it
from a PVC. However, if you look carefully at the preceding T wave, you will see that it is more
pointed than the other T waves in this V1 rhythm strip. There is very likely a hidden premature
P-wave in the T before A, making the FLB a PAC with RBBB aberrancy. Dr. Marriott likes to say:
Cherchez le P which is a sexy way to say in French Search for the P before the FLB to
determine if the FLB is a PAC with AVC. FLB B, on the other hand, has a small notch or slur on
the downstroke of the QRS resembling #4 in Figure 4. Thats almost certainly a PVC (and
originating in the left ventricle (because its moving in an anterior direction).
Alas, into each life some rain must fall! Remember life is not always 100% predictable. In
Figure 7, after 2 sinus beats with incomplete RBBB, a bigeminal rhythm develops. The 3
premature FLBs have TYPICAL TRIPHASIC RBBB MORPHOLOGY (rSR) and yet they are
PVCs! How can we tell? They are not preceded by premature P-waves, but are actually followed
(look in the ST segment) by the next normal sinus P-wave which cannot conduct because the
ventricles are refractory at that time. The next sinus P wave comes on time (i.e., a complete
pause). Well, you cant win them all!
Figure 7
The rhythm illustrated in the six leads of Figure 8 was actually interpreted as Ventricular
bigeminy in our ECG lab by a tired physician reading late at night. Try to see if you can do
better. The first thing to notice is that the two premature beats in lead V1 have RBBB (rsR)
morphologyalready a 10:1 odds favoring AVC. Note also that some the T waves of the sinus
beats look a little funny particularly in Leads 1, 2, and V2. They are small, short, and peak
too early, a very suspicious signal that they are, indeed, hidden premature P-waves in the T
waves (Cherchez-le-P).
The clincher, however, is that the premature beats are followed by INCOMPLETE
COMPENSATORY PAUSES. How can you tell in a bigeminal rhythm? One lead (aVF) has no
premature beats, so you can measure the exact sinus rate (P-P interval). Taking 2 sinus cycles
from this lead (with your calipers), you can now tell in the other leads that the P wave following
the FLBs comes earlier than expected suggesting that the sinus cycle was reset by the
premature P waves (a common feature of PACs, but not PVCs). The correct diagnosis, therefore,
is atrial bigeminy with RBBB aberration of the PACs.
35
Figure 8
As discussed on p29, the diagram now reproduced in Figure 9 helps us understand the difference
between a complete compensatory pause (characteristic of most PVCs) and an incomplete
pause (typical of most PACs). The top half of Figure 9 shows (in ladder diagram form) three
sinus beats and a PAC. The sinus P wave after the PAC comes earlier than expected because the
PAC entered the sinus node and reset its timing. In the bottom half of Figure 9 three sinus beats
are followed by a PVC. As you can see the sinus cycle is not interrupted, but one sinus beat
cannot conduct to the ventricles because the ventricles are refractory due to the PVC. The next
P wave comes on time making the pause a complete compensatory pause.
Figure 9
36
The top ECG strip in Figure 10 illustrates 2 PACs conducted with AVC. Note how the premature
ectopic P-wave peaks and distorts the preceding T-wave (Cherchez-le-P). The first PAC conducts
with LBBB aberrancy and the second with RBBB. In the second strip atrial fibrillation is initiated by
a PAC with RBBB aberration (note the long preceding RR interval followed by a short coupling
interval to the PAC). The aberrantly conducted beat that initiates atrial fibrillation is an example of
the second-in-a-row phenomenon which is frequently seen in atrial tachyarrhythmias with AVC.
Its the second beat in a sequence of fast beats that is most often conducted with AVC because of
the long-short rule (Ashman phenomenon).
Figure 10
In Figure 11 you can see Ashman beats at their finest. RBBB beats in lead V1 follow the long
cycle-short cycle sequence. Since the atria are fibrillating, you cant identify a PAC or preceding
atrial activity so you have to presume that all QRSs are conducted from the atria. Note that the
2nd Ashman beat in the top strip is followed by a quicker but narrow QRS beat the right bundle is
now responding to a short cycle-short cycle sequence and conducts normally. Dr. Ashman first
published this observation in 1947! His name has become a permanent icon in the ECG world.
Figure 11
If youre ready for some fun, consider the next ECG rhythm illustrated in Figure 12. This
unfortunate man suffered from palpitations and dizziness when he swallowed. What you see is the
onset of an ectopic atrial tachycardia (after the first 2 sinus beats) with intermittent RBBB aberrant
37
conduction. The arrows point to ectopic P-waves firing at nearly 200 bpm. Note how the PR
intervals gradually get longer until the 4th ectopic P-wave in the tachycardia fails to conduct
(Wenckebach phenomenon). This initiates a pause (longer cycle), and when 1:1 conduction
resumes the second and subsequent QRS complexes exhibit upright QRS complexes of atypical
RBBB. This is truly a cool ECG rhythm strip! The man was told to stop swallowing so much!
Figure 13
Figure 14 shows another example of acceleration-dependent RBBB, this time in the setting of atrial
fibrillation. Even the normal beats have a minor degree of incomplete RBBB (rsr). At critically
short cycles, however, complete RBBB ensues and remains until the rate slows again. You can tell
that these are not PVCs and runs of ventricular tachycardia because of the typical RBBB
morphology (rsR in lead V1) and the irregular RR cycles of atrial fib.
Figure 14
38
Things can really get scary in the coronary care unit in the setting of acute myocardial infarction.
Consider the case illustrated in Figure 15 (lead V1) with intermittent runs of what looks like
ventricular tachycardia. Note that the basic rhythm is irregularly irregular indicating atrial
fibrillation. The wide QRS complexes are examples of tachycardia-dependent LBBB aberration, not
runs of ventricular tachycardia. Note the morphology of the wide beats. Although there is no
initial thin r-wave, the downstroke of the S wave is very rapid (see #1 in Figure 5, p34).
Figure 15
Finally we have an example in Figure 16 of a very unusual and perplexing form of AVC --deceleration or bradycardia-dependent aberration. Note that the QRS duration is normal at
rates above 65 bpm, but all longer RR cycles are terminated by beats with LBBB. What a paradox!
You have to be careful not to classify the late beats ventricular escapes, but in this case the QRS
morphology of the late beats is classic for LBBB (see #1 in Figure 5, p33) as evidenced by the
thin r-wave and rapid downstroke of the S-wave. This type of AVC is sometimes called Phase 4
AVC because its during Phase 4 of the action potential that latent pacemakers (in this case located
in the left bundle) begin to depolarize. Sinus beats entering the partially depolarized left bundle
conduct more slowly and sometimes are nonconducted (resulting in LBBB).
Figure 16
The actual rhythm in Figure 16 is difficult to recognize because sinus P-waves are not easily seen in
this V1 lead. P-waves were better seen in other leads from this patient. The rhythm was sinus
arrhythmia with intermittent 2nd degree AV block.
The ECG strips in Figure 17 summarize important points made in this section. In strip 1
intermittent RBBB is seen with atrial fibrillation. The first two RBBB beats result from an
accelerating rate (tachycardia-dependent RBBB) while the later triplet of RBBB beats are a
consequence of the Ashman phenomenon (long cycle-short cycle sequence). Strip 2 from the
same patient (in sinus rhythm) shows two premature FLBs. The first FLB has a QR configuration
similar to #5 in Figure 4 (p33) and is most certainly a PVC as the pause following it is a complete
compensatory one. The 2nd FLB has the classic triphasic rsR morphology of RBBB AVC (#1 in
Figure 4). The pause following this beat is incomplete which is expected for PACs.
39
40
Figure 18
Unfortunately the ECGs that you end up interpreting will not have arrows pointing at the interesting
findings. You just have to imagine where they should be!
AVC SUMMARY
The differential diagnosis of FLBs is intellectually challenging and has important clinical implications.
This section has provided clues that help distinguish wide QRS complexes that are supraventricular
in origin with AVC from ectopic beats of ventricular origin (PVCs and ventricular rhythms). When
looking at single premature FLBs always search for hidden premature P-waves in the ST-T wave of
the preceding beat (Cherchez-le-P). Measure with calipers the pause after the FLB to determine if
its compensatory or not. Remember the lead V1 morphology clues offered in Figures 4 and 5
(pp33, 34) that provide reliable (although not perfect) betting odds that a particular beat in
question is supraventricular or ventricular in origin. These morphology clues may be the only way
to correctly diagnose wide QRS-complex tachycardias.
Dont be fooled by first impressions.
The next section focuses on ECG aspects of ventricular tachycardia and the differential
diagnosis of wide QRS tachycardias. Other ventricular rhythms are also briefly
discussed.
41
Ventricular Tachycardia
Differential Diagnosis: just as for single premature funny-looking beats, not all wide
QRS tachycardias are ventricular in origin (they may be supraventricular
tachycardias with bundle branch block or WPW preexcitation)!
Although this is an ECG tutorial, let's not forget some simple bedside and
clinical clues to ventricular tachycardia:
Presence of advanced heart disease (e.g., coronary heart
disease and heart failure) favors ventricular tachycardia
Cannon 'a' waves in the jugular venous pulse suggests
ventricular tachycardia with AV dissociation. Under these
circumstances atrial contraction from on-going sinus rhythm may
sometimes occur when the tricuspid valve is closed causing
retrograde blood flow into the jugular veins (giant a wave).
Variable intensity of the S1 heart sound at the apex (mitral
closure); again this is seen when there is AV dissociation
resulting in varying position of the mitral valve leaflets
depending on the timing of atrial and ventricular systole.
If the patient is hemodynamically unstable, its probably
ventricular tachycardia and act accordingly!
ECG Clues:
Regularity of the rhythm: Sustained monomorphic (i.e., all QRSs look the same)
ventricular tachycardias are usually regular (i.e., equal RR intervals); an
irregularly-irregular wide-QRS rhythm suggests atrial fibrillation with aberration
or with WPW preexcitation.
A-V Dissociation strongly suggests ventricular tachycardia! Unfortunately AV
dissociation only occurs in approximately 50% of ventricular tachycardias (the
other 50% have retrograde atrial capture or "V-A association"). Of the V-tachs
with AV dissociation, it can only be easily recognized when the tachycardia rate is
<150 bpm. Faster heart rates make it difficult to detect the dissociated P waves.
Fusion beats or captures often occur when there is AV dissociation and this also
strongly suggests a ventricular origin for the wide QRS tachycardia.
QRS morphology in lead V1, illustrated in Figures 4 and 5 (pp33, 34), is often the
best clue to the origin, so go back and check out these clues! Also consider a
few additional morphology clues:
Bizarre frontal-plane QRS axis (i.e. from +150 degrees to -90 degrees or NW
quadrant) suggests ventricular tachycardia
42
Nonsustained VT (note the first beat in the run is a fusion beat, and the LV origin of the VT)
The ECG shown below illustrates several features of typical VT: 1) QRS morphology in lead
V1 looks like #4 in Figure 4, p33; the notch is on the downstroke of the R wave; 2) the QRS
is mostly negative in lead V6; 3) bizarre northwest quadrant frontal plane QRS axis of -180
degrees (both leads I and II are predominately negative. This VT is most likely from the left
ventricle (note the direction of QRS forces is rightward and anterior; i.e., the QRS originates
in the leftward, posterior LV).
43
The ECG illustrated on the below shows another typical sustained monomorphic VT, but this
time originating in the right ventricle. Note the V1 QRS morphology has all the features of a
left ventricular VT origin (see Figure 5, p34) including 1) fat, little R wave; 2) notch on the
downstroke or the S-wave; and 3) >0.06 s delay from QRS onset to the nadir (bottom) of the
S-wave. The direction of QRS forces is leftward and posterior (i.e., coming from a rightward
and anterior RV)
44
A "passive" wide QRS rhythm that occurs by default whenever higher-lever pacemakers
in AV junction or sinus node fail to control ventricular activation.
Escape rates are usually in the range of 30-50 bpm.
Seen most often in complete AV block with AV dissociation or in other bradycardia
conditions.
The QRS morphology is clearly of ventricular origin (see Figures 4 and 5, p34).
Ventricular Parasystole
Parasystolic PVCs come from protected ectopic pacemaker cells in the ventricles that fire
at a fixed rate unrelated to the underlying basic rhythm (usually sinus). As a result they
appear as PVCs with varying coupling intervals, and, if late enough in the cardiac cycle
they may fuse with the next sinus beat).
These non-fixed coupled PVCs have inter-ectopic intervals (i.e., timing between PVCs)
that are some multiple (i.e., 1x, 2x, 3x, etc.) of the basic rate of the parasystolic focus
The PVCs have uniform morphology unless fusion beats occur
There is usually an entrance block around the ectopic focus, which means that the
primary rhythm (e.g., sinus rhythm) cannot enter the ectopic site and reset its timing
(unlike a PAC that can reset the sinus pacemaker).
May also see an intermittent exit block just distal to the parasystolic site; i.e., the output
from the ectopic site may occasionally be blocked or non-conducted (i.e., no PVC occurs
when one is expected).
Fusion beats (F) are common when the ectopic site in the ventricle fires while ventricles
are already beginning activation from sinus beats. In the rhythm below non-fixed
coupled PVCs are seen with fusion beats (F). When the PVC occurs late enough in the
sinus cycle they can partially fuse with the sinus beats.
Parasystolic rhythms may also originate in the atria (i.e., with non-fixed coupled PAC's)
and within the AV junction.
Pacemaker Rhythms
Atrial pacing: note small pacemaker spikes before every P wave followed by normal
QRS complexes (used mostly for sinus node disease and related bradycardias)
45
A-V sequential pacing with ventricular pacing (note tiny spike before each QRS) and
atrial sensing of normal sinus rhythm (note: pacemaker spikes are sometimes difficult to
see):
A-V sequential pacing with both atrial and ventricular pacing (note pacing spikes before
each P wave and each QRS
Normal functioning ventricular demand pacemaker. Small pacing spikes (arrows) are
seen before QRS #1, #3, #4, and #6 representing the paced beats. There is marked
sinus bradycardia (thats the reason for the pacemaker), but when P waves are able to
conduct they do (see QRS #2 and #5). This is a nice example of incomplete AV
dissociation due to sinus slowing where the artificial pacemaker takes over by default.
Note also, in this V1 rhythm strip the morphology of the paced beats resemble QRS #2 in
Figure 5 (p32) indicative of a RV ectopic pacemaker focus (notched downstroke).
within the cardiac conduction system (see diagram on page 29). Heart block can be
conceptualized in terms of three cardiac regions where heart block occurs and three degrees of
conduction failure in each region. The three regions of heart block include the sino-atrial
connections (SA), the AV junction (AV Node and His Bundle), and the bundle branches including
their fascicles. The three degrees include slowed conduction (1st degree), intermittent
conduction failure (2nd degree), or complete conduction failure (3rd degree). In addition, there
are two varieties of 2nd degree heart block: Type I (or Wenckebach) occurring mostly in the
Ca++ channel cells of the AV node and Type II (or Mobitz) usually found in the Na+ channel
cells of the bundle branches and fascicles. In Type I (2nd degree) block decremental
conduction is seen where the conduction velocity progressively slows beat-by-beat until failure
of conduction occurs. This is the form of conduction block in the AV node. Type II block is all or
none and is more likely found in the His bundle or in the bundle branches and fascicles. The
term exit block is used to identify a conduction delay or failure immediately distal to a
46
pacemaker site. Sino-atrial (SA) block, for example, is an exit block. The table below summarizes
the three degrees and three general locations of heart block.
2nd Degree SA Block: Although three degrees of SA block can occur only 2nd degree SA
block can be recognized on the surface ECG because the sinus discharge doesnt appear
on the surface ECG. (i.e., one can only see an intermittent conduction failure between
the sinus node and the right atrium). Two types of 2nd degree SA block have been
described but, unlike 2nd degree AV block, differentiating type I from type II is
unimportant. Also sinus arrhythmia makes the differential diagnosis a wasted time.
Type I SA block (SA Wenckebach): the following 3 rules represent the classic rules of
Wenckebach which were originally described for Type I 2nd degree AV block. The
rules are the result of decremental conduction where the increment in conduction
delay for each subsequent impulse gets smaller and smaller until conduction failure
occurs. For Type I SA block (in the absence of sinus arrhythmia) the three rules are:
1. PP intervals gradually shorten until a pause occurs (i.e., when the blocked
sinus impulse fails to reach the atria and a sinus P-wave isnt seen on the ECG)
2. The PP interval of the pause is less than the two preceding PP intervals
before the pause
3. The PP interval just following the pause is greater than the PP interval just
before the pause (not seen on the ECG example below). The dotted red
arrows point to an educated guess as to when the sinus fired before each P
wave. Note how it takes longer and longer to the P wave, and then a P wave
doesnt appear.
47
Both Type I and Type II SA block indicate sinus node disease (intrinsic or drug induced).
48
2nd Degree AV Block: The ladder diagrams below illustrate the differences
between Type I (Wenckebach) and Type II 2nd degree AV block.
In "classic" Type I (Wenckebach) AV block the PR interval gets longer and longer (by
smaller and smaller increments) until a nonconducted P wave occurs. The RR
interval of the pause is less than the two preceding RR intervals, and the RR interval
after the pause is greater than the RR interval just before the pause. These are the 3
classic rules or footprints of Wenckebach (described on p48 for the PP intervals in SA
Wenckebach). In Type II (Mobitz) AV block the PR intervals are constant (for at least 2
consecutive PR intervals) until a nonconducted P wave occurs. The RR interval of the
pause is equal to the two preceding RR intervals (assuming a regular sinus rate). In 2:1
AV block one cannot distinguish type I from type II block (because PR is fixed in both
cases). There are often other ECG clues to the correct diagnosis in 2:1 AV block:
Wide QRS complexes (BBBs) suggest type II; narrow QRS complexes suggest type I.
Prolonged PR intervals (conducted beats) suggest type I (Wenckebach).
NOTE: Type I AV block is almost always located in the AV node itself, which
means that the QRS duration is usually narrow unless there is also a preexisting
bundle branch block. Note also the 4:3 and 3:2 groupings of Ps and QRSs.
Group beating is common in type I 2nd degree AV block.
49
Type II (Mobitz) 2nd degree AV block: (note: the constant PR for two
consecutive PR's before the blocked P wave, and the wide QRS of LBBB)
Type II AV block there is almost always a preexisting bundle branch block (LBBB in
the ECG strips above and below), which means that the QRS duration is wide
indicating complete block of one bundle The nonconducted P waves are blocked in
the other bundle (i.e., a 2nd degree block in the right bundle branch). Also, in Type
II block several consecutive P waves may be blocked as illustrated below:
50
The location of the block may be in the AV junction or bilaterally in the bundle
branches. Look carefully in B for dissociated P waves that are independent of the
pacemaker rhythm.
51
3. 2nd or 3rd degree AV block with an escape rhythm from a junctional or ventricular
site:
In the example (below) of complete AV dissociation (3rd degree AV bock with a
junctional escape pacemaker) the PP intervals are alternating because of
ventriculophasic sinus arrhythmia (phasic variations in vagal tone depending on
the timing of ventricular contractions effect the sinus rate or PP intervals).
52
First, consider left bundle branch block (LBBB) in the above figure. The vertical dotted lines
divide the QRS into two parts with the 2nd half representing the activation of the ventricle with
the blocked bundle branch. Since the left ventricle is to the left and posterior to the right
ventricle the 2nd half of the QRS is downgoing in lead V1 (posterior) and upgoing in leads I, aVL,
and V6 (leftward). Similarly in right bundle branch block (RBBB) the 2nd half of the QRS is
upgoing in lead V1 (anterior), and downgoing in leads I, aVL, and V6 (rightward). Note also the
first part of each QRS in BBB moves more quickly than the 2nd part because activation of the
ventricle with the intact bundle branch proceeds normally through the bundle branch and
subsequent Purkinje network. Activation of the ventricle with the blocked bundle is slower
because of the aberrant nature of the activation sequence.
Now lets consider the 12-lead ECGs of complete BBB.
The frontal plane QRS axis in RBBB is usually in the normal range (i.e., -30 to +90
degrees). If left axis deviation is present, one must also consider left anterior
fascicular block, and if right axis deviation is present, one must consider left
posterior fascicular block in addition to the RBBB (i.e., bifascicular block). ECG
criteria for the fascicular blocks are discussed later in this outline (pp55-57)
"Incomplete" RBBB has a QRS duration of 0.10 - 0.12s with the same 2nd half QRS
features. This is often a normal variant, but could be seen in people with RVH.
The "normal" ST-T wave morphology in RBBB is oriented opposite to the direction of
the late QRS forces or last half of the QRS; i.e., in leads with terminal R or R' forces
(e.g., V1) the ST-T should be downwards (negative); in leads with late S forces (e.g.,
I, V6) the ST-T should be positive. If the ST-T waves are in the same direction as
the terminal QRS forces, they should be labeled primary ST-T wave
abnormalities because they may be related to other conditions affecting ST-T
wave morphology (e.g., ischemia, drug effects, electrolyte abnormalities)
53
The "normal" ST-T waves in LBBB should be oriented opposite to the direction of the
terminal QRS forces; i.e., in leads with terminal R or R' forces the ST-T should be
downwards (negative) (see I, aVL); in leads with terminal S forces the ST-T should
be upwards (positive) (see III, V1-3). If the ST-T waves are in the same direction
as the terminal QRS forces, they should be labeled primary ST-T wave
abnormalities. In the above ECG the ST-T waves are "normal" for LBBB; i.e., they
are secondary to the change in the ventricular depolarization sequence.
"Incomplete" LBBB looks like LBBB but QRS duration is 0.10 - 0.12s, with less ST-T
change. This is often the result of long standing LVH.
54
Usually see poor R progression in leads V1-V3 and deeper S waves in leads V5 and
V6
May mimic LVH voltage in lead aVL, and mask LVH voltage in leads V5, V6
In the above ECG, note -45 QRS axis, rS complexes in II, III, aVF, tiny q-wave in I,
aVL, S in III > S in II, R in aVL > R in aVR, and late S waves in leads V5-6. QRS
duration is normal, and there is a slight slur to the R wave downstroke in lead aVL.
This is classic LAFB!
Left Septal Fascicular Block (LSFB): This new and somewhat controversial ECG
diagnosis has recently become a credible entity as there is increasing anatomical evidence
that the left bundle has three divisions that simultaneously initiate left ventricular activation
in three distinct areas. The following ECG criteria have been proposed (Perez Riera et al
Ann of Noninvasive Electrocardiol 2011; 16:196).
o QRS duration up to 0.11s
o Normal frontal plane QRS axis (unless additional LAFB or LPFB)
o Prominent anterior forces (PAF)
R wave voltage in V1 >5 mm)
RS ratio V1-2 >2
R wave voltage V2 >15 mm
o Intermittent PAF in setting of ischemia (acute MI or positive stress test)
o Transient PAF in an aberrantly conducted PAC
o Small q-waves V1-2, or V2-3
o Absence of q-waves in left precordial leads
55
New onset LSFB immediately following CABG (severe L-main and LAD disease). Note that PAF
was not seen in prior ECGs from this patient.
Bifascicular Blocks
RBBB plus either LAFB (common) or LPFB (uncommon) or LSFB (very uncommon)
Features of RBBB plus frontal plane features of the fascicular block (frontal plane axis
deviation, prominent anterior forces, etc.)
The ECG below shows classic RBBB (note rsR' in V1) plus LAFB (QRS axis = - 60, rS
in II, aVF; and small q in I and aVL).
Bifascicular blocks are clinically important precursors of complete (3rd degree) AV
block. Before 3rd degree block occurs there may be episodes of 2nd degree AV block
(Mobitz) indicating intermittent block in the remaining fascicle. These episodes
often cause symptoms of syncope or presyncope.
56
The ECG shown below is classic RBBB and LPFB (bifascicular block) in a patient with
chronic heart failure. Note the unusual frontal plane QRS axis of +150 (isoelectric lead
II), the rS complex in lead I, and the small q-waves in II, III, aVF. There is rsR in V1
indicative of RBBB.
57
WPW Preexcitation (note short PR and delta waves best seen in I, V5-6)
7. ATRIAL ENLARGEMENT
P wave amplitude >2.5 mm in II and/or >1.5 mm in V1 (these criteria are not very
specific or sensitive)
Frontal plane P-wave axis 90 (isoelectric in lead I)
Better criteria can be derived from the QRS complex; these QRS changes are due to
both the high incidence of RVH when RAE is present, and the RV displacement by an
enlarged right atrium.
58
QR, Qr, qR, or qRs morphology in lead V1 (in absence of coronary heart disease)
QRS voltage in V1 is <5 mm and V2/V1 voltage ratio is >6 (Sensitivity = 50%;
Specificity = 90%)
Why are these P waves (see lead II below) sometimes called Viagra P-waves?
59
8. VENTRICULAR HYPERTROPHY
Introductory Information:
The ECG criteria for diagnosing right or left ventricular hypertrophy are very insensitive
(i.e., sensitivity ~50%, which means that ~50% of patients who have ventricular
hypertrophy cannot be diagnosed by ECG criteria). When in doubt.Get an ECHO!
However, the criteria are very specific (i.e., specificity >90%, which means if the ECG
criteria are met, it is very likely that ventricular hypertrophy is present).
+ECG Criteria
Voltage Criteria (any of):
a. R or S in limb leads 20 mm
b. S in V1 or V2 30 mm
c. R in V5 or V6 30 mm
Points
3 points
60
ST-T Abnormalities:
On digitalis Rx
Not on digitalis Rx
Left Atrial Enlargement in V1
Left axis deviation -30
QRS duration 0.09 sec
Delayed intrinsicoid deflection in V5 or V6 (0.05 sec)
1 point
3 points
3 points
2 points
1 point
1 point
CORNELL Voltage Criteria for LVH, assuming correct precordial lead placement
(sensitivity = 42%, specificity = 95%)
S in V3 + R in aVL > 28 mm (men)
S in V3 + R in aVL > 20 mm (women)
Other Voltage Criteria for LVH (note that voltage criteria alone cant make a definite
ECG diagnosis of LVH)
Limb-lead voltage criteria:
R in aVL 11 mm or, if left axis deviation, R in aVL 18 mm
R in I + S in III >25 mm
R in aVF >20 mm
S in aVR > 14 mm
Chest-lead voltage criteria:
S in V1 + R in V5 or V6 35 mm
R + S in any leads > 45 mm
Example 1: (Limb-lead Voltage Criteria; e.g., R in aVL >11 mm, or R in I + S in III > 25 mm;
note downsloping ST segment depression in leads I and aVL).
61
Example 2: (ROMHILT-ESTES Criteria: 3 points for precordial lead voltage, 3 points for ST-T
changes; also LAE (possibly bi-atrial enlargement). This pattern is classic for LVH due to severe
LV pressure overload as seen in aortic stenosis.
62
Example #1: RVH in patient with mitral stenosis. Note qR pattern in V1, marked RAD (+140),
large P-terminal force in V1 (LAE), slight increased QRS duration (incomplete RBBB), deep S
wave in V5-6.
Example #2: 18 yr. old patient with primary pulmonary hypertension. Note: marked RAD
(+140), R in V1 >7mm, prominent anterior forces in V1-3, increased P amplitude of RAE, and
the typical RV strain pattern in precordial leads (ST depression, T wave inversion)
63
Example #3: RVH in patient with an atrial septal defect. Note the incomplete RBBB pattern in V1
(rsR), and the slight RAD (+105).
9. MYOCARDIAL INFARCTION
Introduction to ECG Recognition of Acute Coronary Syndrome (ACS)
The ECG changes of ACS are the result of a sudden reduction of coronary blood flow to a
region of ventricular myocardium supplied by a coronary artery with a ruptured
atherosclerotic plaque and intracoronary thrombus formation. Depending on how quickly
the patient gets to the hospital for definitive treatment (usually percutaneous
revascularization or thrombolytic Rx) myocardial necrosis (infarction) may or may not
occur. The diagram below shows four possible ECG outcomes of myocardial ischemia in
the setting of an acute coronary syndrome. On the left side no myocardial necrosis (or
infarction) occurs (negative troponins) but there is either subendocardial ischemia
manifested by reversible ST segment depression or transmural ischemia manifested
by reversible ST segment elevation. On the right are two types of myocardial infarction
(with elevated troponins indicative of cellular damage), one manifested by ST segment
elevation (STEMI) and one without ST segment elevation (NonSTEMI). Either of these
can evolve into Q-wave or non-Q-wave MIs. Because Q waves may not appear initially,
early treatment decisions are based on the presence or absence of ST segment elevation,
and if revascularization is accomplished quickly Q-waves may never appear as the
residual damage or scar is small (time is muscle says the interventional cardiologist).
64
No-MI
Non-Q MI
Non-ST elevation MI
ST depression or
T-wave changes or
Normal ECG
Subendocardial Ischemia
Transient ST ,
New onset angina
Myocardial
Ischemia
No-MI
Transmural Ischemia
Transient ST ,
Variant Angina
Q-wave MI
ST elevation MI (STEMI)
Typical evolution of
ST-T changes
The following discussion will focus on ECG changes during the evolution of a STEMI
All MIs involve the left ventricular myocardium. In the setting of a proximal right
coronary artery occlusion, however, there may also be a component of right
ventricular infarction as well. Right sided chest leads are usually needed to recognize
RV MI.
In general, the more leads of the 12-lead ECG with MI changes (Q waves and/or ST
elevation), the larger the infarct size and the worse the prognosis (i.e., more damage).
The left anterior descending coronary artery (LAD) and it's branches supply the anterior
and anterolateral walls of the left ventricle and the anterior two-thirds of the septum.
The left circumflex coronary artery (LCx) and its branches supply the posterolateral wall
of the left ventricle. The right coronary artery (RCA) supplies the right ventricle, as well
as the inferior (diaphragmatic) and posterior-lateral walls of the left ventricle, and the
posterior third of the septum. The RCA also gives off the AV nodal coronary artery in 8590% of individuals; in the remaining 10-15%, this artery is a branch of the LCX.
The usual ECG evolution of a STEMI with Q-waves is illustrated in the diagram below.
Not all of the 6 patterns may be seen; the time from onset of MI to the final pattern is
quite variable and is related to the size of MI, the rapidity of reperfusion (if any), and the
location of the MI. (This example might be seen in lead II during an acute inferior MI)
A. Normal ECG prior to the onset of plaque rupture
B. Hyperacute T wave changes - increased T wave amplitude and width; QT
prolongs; may also see some ST segment elevation
C. Marked ST elevation with hyperacute T wave changes (tombstone pattern)
D. Pathologic Q waves appear (cell necrosis), ST elevation decreases, T waves begin
to invert (this is also called the "fully evolved" phase)
E. Pathologic Q waves, T wave inversion (necrosis and fibrosis)
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I. Inferior MI Family of STEMIs (Q-wave MI's); includes inferior, true posterior, and
right ventricular MI's
Inferior MI
Pathologic Q waves and evolving ST-T changes in leads II, III, aVF
Q waves (if they appear) are usually largest in lead III, next largest in lead aVF, and
smallest in lead II. Q wave 30ms in aVF is diagnostic.
Example #1: Acute inferior MI injury pattern. Note hyperacute T waves with ST elevation in II,
III, aVF (ST in III > ST in II suggests RCA occlusion); reciprocal ST depression is seen in I,
and aVL. ST depression in V1-3 represents posterior or lateral injury pattern and not a reciprocal
change (see posterior MI patterns below). The V4 and V5 electrode sites in this ECG are
interchanged (this is an ECG technician error; it doesnt alter the diagnosis however).
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Example #2: Old inferior MI (note largest Q in lead III, next largest in aVF, and smallest in lead
II). Axis = -50 (LAD); T wave inversion is also present in leads II, III, and aVF
True posterior MI: (note, recent terminology renames this location as lateral)
ECG changes are seen in precordial leads V1-3, but are the mirror image of an anteroseptal
MI (because the posterior or lateral LV wall is behind the anterior wall)
Increased R wave amplitude and/or duration 40 ms in V1-2 (i.e., a "pathologic R wave"
is the mirror image of a pathologic Q on the posterior wall seen in V8 and V9)
PAF: R/S ratio in V1 or V2 >1 (i.e., prominent anterior forces; need to R/O RVH, LSFB,
etc.)
Hyperacute ST-T wave changes: i.e., ST depression and large, inverted T waves in V1-3
Late normalization of ST-T with symmetrical upright T waves in V1 to V3
Often seen with an inferior wall MI (i.e., "infero-posterior MI")
Example #3: Acute infero-posterior MI (note tall R waves V1-3, marked ST depression V1-inferior
ST elevation in II, III, aVF)
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Example #4: Old infero-posterior (infero-lateral) MI: Note tall, wide pathologic R in V1-3 (this
is a Q wave equivalent), upright T waves, and inferior Q waves with residual ST segment
elevation)
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Right Ventricular MI (only seen with proximal right coronary occlusion; i.e., with inferior
family of left ventricular MI's)
ECG findings usually require additional leads on right chest; Criteria: ST elevation,
1mm, in right chest leads, especially V4r (see below).
Example #6: Acute inferior MI also involving the right ventricle; 15-lead ECG (adding V4r, V8,
V9). Note ST segment elevation in V4r indicative of proximal RCA occlusion causing right
ventricular infarction in addition to the acute inferior left ventriclar MI.
Anteroseptal MI
Q, QS, or qrS complexes in leads V1-V3
Evolving ST-T changes
Example #7: Hyperacute anteroseptal MI; marked ST elevation in V1-3 before Q waves
developed (note convex-up ST elevation in V1-3)
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Example #8: Fully evolved anteroseptal MI (note QS waves in V1-2, qrS complex in V3, resolving
ST elevation with deep inverted T waves)
Example 9: Acute extensive anterior injury; note tombstone ST elevation V2-6, I, aVL;
note reciprocal ST depression in II, III, aVF. This is a really big infarct!
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Note: new Q waves V2-4 and resolving ST changes indicative of successful reperfusion.
Comment: The precise identification (and terminology) of MI locations on the ECG is evolving
as new heart imaging (e.g., MRI) better defines the ventricular anatomy. New terminology has
been suggested (see Circulation 2006;114:1755). While not universally accepted, the following
new Q-wave MI patterns have been defined for left ventricular segments seen on MRI imaging:
Septal MI: Q (or QS) waves in V1-2
Mid-Anterior MI: Q waves in aVL, sometimes in lead I, V2, V3, but not in V5-6.
Apical-Anterior MI: Q waves in V3, V4, and sometimes in V5-6. No Q waves in I, aVL
Extensive Anterior MI: Combination of above 3 locations.
Lateral MI: Prominent R waves (PAF) in V1-2 (this replaces the true posterior MI
terminology; MRI imaging of the left ventricle shows no posterior wall). Q waves may
also be present in I, aVL, V5-6.
Inferor MI: Q waves in II, III, aVF, but without prominent R waves in V1-2
(It remains to be seen whether or not this new terminology of infarct location will become
accepted in the ECG literature of the future)
The ECG (Example #11) illustrated below is a tragic case of missed acute left main subtotal coronary occlusion. It was inappropriately diagnosed as a non-STEMI because of
the absence of typical ST segment elevation in 2 or more contiguous ECG leads.
Instead of proceeding to emergent coronary intervention, the patient was treated with
the non-STEMI protocol in the CCU for 12 hrs. until a disastrous cardiac arrest occurred.
The ECG findings of left main sub-total coronary occlusion seen in the following ECG
include:
ST segment elevation in aVR > any ST elevation in V1
ST segment depression in 7 or more leads of the 12-lead ECG
This ECG represents circumferential subendocardial ischemia due to left main
coronary artery occlusion. Although technically a non-STEMI, the extent of
ischemia is sufficient to consider this a STEMI equivalent and Rxed emergently.
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Note: ST depression in at least 7 leads; ST elevation aVR > any ST elevation in V1.
Example #12: Inferior MI + RBBB (note Q's in II, III, aVF and typical rSR' in lead V1)
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Example #13: Extensive anterior MI with RBBB + LAFB; note pathologic Q's in leads V1-V5,
terminal fat R wave in V1-4, fat S wave in V6 of RBBB). Axis = -80 (rS in II, III, and aVF:
indicative of left anterior fascicular block; RBBB+LAFB indicates bifascicular block!
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Example #14: Acute anterior MI with LBBB. Note exaggerated convex-upwards ST elevation in
V1-3 with reciprocal increased ST depression in V-6.
Example #15: Old MI (probable septal location) with LBBB. Remember LBBB without MI should
have monophasic R waves in I, aVL, V6). This ECG has abnormal q waves in I, aVL, V5-6
suggesting a septal MI location. Note also the notching on the upslope of S wave (arrow) in V4
(sign of Cabrera) and the PVC couplet.
ECG changes may be minimal, or may show only T wave inversion, or may show ST
segment depression with or without T wave inversion.
Although it is tempting to localize the non-Q MI by the particular leads showing ST-T
changes, this is probably only valid for the ST segment elevation MIs (STEMI)
Evolving ST-T changes may include any of the following patterns:
ST segment depression in 2 or more leads (this carries the worse prognosis)
Symmetrical T wave inversion only (this carries a better prognosis)
Combinations of above changes
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OR the ECG may remain normal or only show minimal change (this has the best
prognosis)
V. The Pseudoinfarcts
These are ECG conditions that mimic myocardial infarction either by simulating
pathologic Q or QS waves or mimicking the typical ST-T changes of acute MI.
WPW preexcitation (negative delta wave may mimic pathologic Q waves; see the
ECG below. This is an interesting ECG with intermittent WPW preexcitation. The
WPW pattern is seen only on the first half of the ECG, but disappeared when the
precordial leads V1-6 were recorded. Note the deep Q and QS waves in leads II, III,
and aVF. These are not really Q waves but negative (down-going) delta waves.
Note also the slurred upstroke of the QRS complex in leads I, and the first half of the
V5 rhythm strip (bottom channel). In the 2nd half of the ECG tracing the pseudo Q
waves in the lead II rhythm strip disappear and a qR wave QRS complex appears
indicating the return of normal conduction through the ventricles. Also the delta
wave in lead V5 goes away on the bottom channel during the 2 nd half of the ECG.
Finally, the PR interval is shorter during the 1st half of the ECG when preexcitation is
occurring.
Intermittent WPW Preexcitation (1st half of ECG) with pseudo Q-waves II, III, aVF
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Central nervous system disease (may mimic non-Q wave MI by causing diffuse ST-T
wave changes)
Poor R Wave Progression arbitrarily defined as small, or absent r-waves in leads V13 (R <2mm, plus R/S ratio V4 <1). Differential diagnosis includes:
Normal variant (if the rest of the ECG is normal; frequently seen in women due to
inaccurate precordial lead placement (under the breast interspace lower)
LVH (look for voltage criteria and ST-T changes of LV "strain")
Complete or incomplete LBBB (also see increased QRS duration)
Left anterior fascicular block (should see LAD -45 in frontal plane)
Anterior or anteroseptal MI (look for evolving ST-T changes)
Emphysema and COPD (look for R/S ratio in V5-6 <1)
Diffuse infiltrative or myopathic processes
WPW preexcitation (look for delta waves and short PR)
Prominent Anterior Forces (PAF) - defined as R/S ratio >1 in V1 or V2. Differential
diagnosis includes:
Normal variant (if the ECG is otherwise normal)
True posterior MI (look for additional evidence of inferior MI; see Example 4, p64)
RVH (should see RAD in frontal plane and/or P-pulmonale; see Example 2, p60)
Complete or incomplete RBBB (look for rSR' in V1)
WPW preexcitation (look for delta waves, short PR)
Left septal fascicular block
the clinical circumstances in which the ECG changes are found than by the particular
changes themselves. Thus the term, nonspecific ST-T wave abnormalities, is
frequently used for ST segment depression and T wave abnormalities when clinical data
are not available to correlate with the ECG findings. This does not mean that the ECG
changes are unimportant! It is the responsibility of the clinician providing care
for the patient to ascertain the importance of the ECG findings.
Secondary ST-T wave changes are the result of alterations in the sequence of
ventricular depolarization (e.g., bundle branch blocks, WPW preexcitation and ventricular
ectopic beats or paced beats). These changes are not abnormalities; they are
appropriate in the setting of altered ventricular activation sequence. ST-T wave changes
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are called primary if they are independent of the sequence of ventricular depolarization
(e.g., ischemic ST changes, electrolyte abnormalities, drug effects, etc.). These changes
are repolarization abnormalities.
I.
Acute Pericarditis
Concave upwards ST elevation in most leads except aVR
No reciprocal ST segment depression (except in lead aVR)
Unlike "early repolarization", T waves in leads with ST elevation are usually lower in
amplitude, and heart rate is usually increased.
May see PR segment depression which is a manifestation of atrial injury.
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Acute Pericarditis
The ECG changes of acute pericarditis evolve over time through the following stages (not
all stages are seen in every patient):
Stage I: concave upwards ST segment elevation in most leads with reciprocal ST
segment depression in aVR. During this stage there is also atrial injury represented
by PR segment depression in many leads and PR segment elevation in aVR (see
above example, p74).
Stage II: resolution of ST segment and PR segment changes
Stage III: diffuse T wave inversion in many leads
Stage IV: resolution of the T wave changes or persistent T wave inversion (chronic
pericarditis)
Hypothermia: In this interesting condition the onset of the ST segment (called the Jpoint) turns into a wider J-wave as a result of increased transmural dispersion of
ventricular repolarization. The ECG below illustrates prominent J-Waves following most
of the QRS complexes (also called Osborn waves). This homeless person was found
comatose outdoors in a park in December. Note also atrial fibrillation.
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The above diagram illustrates possible ischemic ECG changes during treadmill
exercise testing as seen in lead V5; this is the best lead for identifying
subendocardial ischemia as demonstrated by the sequence C-D-E.
A. Normal V5 ECG at rest before exercise (note normal ST-T and U waves)
B. J-junctional ST depression due to increased HR (this is not an ischemic change, but
represents atrial repolarization extending through the QRS into the ST segment)
C. Early subendocardial ischemia (increased J-junctional depression, slowly upsloping ST)
D. Horizontal ST segment depression (1mm, horizontal, lasting 80 ms)
E. Downsloping ST depression (usually seen during recovery from exercise as HR slows)
F. ST segment elevation (this is a manifestation of transmural ischemia)
G. U-wave inversion (a very unusual manifestation of ischemia suggesting LAD or L-main
disease). When seen, it occurs during recovery when HR slows down.
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Normal ECG
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II. QT Interval Prolongation (increased probability of sudden cardiac death; see p15
for causes):
Example 1: Hereditary long QT syndrome (note the unusual bifid, humped T waves in V2-3)
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ARVC is a rare cause of sudden cardiac death in athletes. The disease usually involves the right
ventricular outflow tract; normal myocardium is replaced by fatty infiltration and fibrosis. ECG
manifestations include the very difficult to recognize epsilon wave as well as right precordial T
wave inversions as seen above.
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Congenital coronary artery anomalies (e.g., anomalous origin of the left coronary artery
from the right coronary cusp). Sudden death is due to acute ischemic events.
Coronary artery disease
Myocarditis
Hereditary channelopathies (long QT, short QT, Brugada syndrome, et al)
Electrolyte abnormalities
Hypercalcemia (abbreviated ST segment with short QT intervals
Hypocalcemia and hypomagnesaemia (long ST segment with prolonged QT intervals)
Hyperkalemia (peaked T waves, prolonged QRS duration; see ECG below)
Hypokalemia (usual triad of: ST depression, low T waves, and large U waves)
Digoxin effect: scooped ST depression, low amplitude T waves, short QT intervals.
Brugada type ECG is seen in the hereditary Brugada syndrome and the acquired
Brugada sign due to Na+ channel blockers such as flecainide and tricyclic
antidepressants. This unusual pattern consists of right precordial ST segment elevation
with or without T wave inversion. An example is seen in the ECG below. Note that leads
V1 and V2 might be misinterpreted as RBBB, but the QRS duration is not prolonged in
other leads. Like the long QT syndromes, there is an increased incidence of malignant
ventricular arrhythmias and sudden cardiac death in this condition.
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The ECG below illustrates resolution of the acquired Brugada sign due to an overdose of a
tricyclic antidepressant, a Na+ channel blocker (by Day 4 the ECG has returned to normal).
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Normal U waves are illustrated in the precordial leads below. Look closely after the T
waves in V2 and V3 and note the small upward deflections. Thats looking at U !!
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Nonischemic causes: some cases of LVH or RVH (usually in leads with prominent
R waves)
Some patients with LQTS (see below: Lead V6 shows giant negative TU
fusion wave in patient with LQTS; a prominent upright U wave is seen in
Lead V1)
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